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"explanation": "This is incorrect because fluoxetine should be tapered down slowly on discontinuation. This avoids unwanted side effects caused by withdrawal of SSRIs, including restlessness, sweating, anxiety, insomnia, and unsteadiness.",
"id": "53281",
"label": "e",
"name": "Fluoxetine should be discontinued immediately once the treatment course is completed",
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"explanation": "Symptoms may start improving after 2-4 weeks (SSRIs do not work instantly), but the medication must not be stopped once the symptoms improve due to risk of relapse. They must be continued for 6 months, and then reviewed at this stage.",
"id": "53279",
"label": "c",
"name": "Take fluoxetine for 6 weeks",
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"answer": true,
"explanation": "Patients may see an improvement in their mood earlier than 6 months from remission, but it is important they are advised they do not discontinue their SSRI medication before the 6 month period is over, due to risk of relapse. Guidelines therefore state they must be taken for a minimum of 6 months. SSRIs should never be stopped suddenly, but gradually tapered, to reduce the risk of withdrawal.",
"id": "53277",
"label": "a",
"name": "Fluoxetine may be weaned 6 months after remission if he has improved clinically",
"picture": null,
"votes": 4018
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"__typename": "QuestionChoice",
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"explanation": "Symptoms may start improving after 2-4 weeks (SSRIs do not work instantly), but the medication must not be stopped once the symptoms improve due to risk of relapse. They must be continued for at least 6 months, and then reviewed at this stage. Furthermore, SSRI medication must never be stopped suddenly due to risk of withdrawal symptoms, such as restlessness, sweating, anxiety, insomnia, and unsteadiness.",
"id": "53278",
"label": "b",
"name": "Take fluoxetine once daily until his depressive symptoms improve",
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"explanation": "If a dose of fluoxetine is missed at the usual time, it should be taken as soon as the patient remembers. It is important to advise patients that they should not be taking 2 doses together unless the dose has been increased by their GP. If it is nearly time to take the next dose, he should leave out the dose he has forgotten and take the next scheduled dose as normal. This option says he must always respond by taking the next dose as scheduled and skip the missed dose; this is not true, since this only needs to be done if the next dose is due soon. Otherwise, the missed dose should be taken.",
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"name": "If he misses a dose of fluoxetine, take the missing dose with the dose due ",
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"comment": "doesnt fluoxtine not need to be tapered due to its long half life??",
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"comment": "It says you can start weaning at 6 months post-remission but yes the tapering is a longer process with fluoxetine.",
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"explanation": "# Summary\n\nDepression is a common mental health disorder typified by low mood, anhedonia, significant weight change, sleep and activity changes, fatigue, feelings of guilt or worthlessness, or poor concentration. It is defined by the DSM as the presence of 5 out of 8 symptoms for at least 2 weeks. It is more prevalent in females. Key investigations include FBC, TFT, U+E, LFT, Glucose, B12/folate, cortisol, toxicology screen, and CNS imaging to rule out organic causes. Management strategies encompass low to high intensity psychological interventions, pharmacotherapy including anti-depressants, and in severe cases, lithium or ECT.\n\n# Definition\n\nDepression is a mental health disorder characterised by:\n\n- **ICD-11 Criteria:**\n - Depressive Episode: Depressed mood, loss of interest (anhedonia), and reduced energy (fatigue) persisting for at least two weeks.\n\n- **DSM-V Criteria:**\n - Major Depressive Disorder (MDD): Presence of a major depressive episode lasting at least two weeks, with specific criteria regarding mood, cognitive, and physical symptoms.\n - Persistent Depressive Disorder (Dysthymia): A chronic form of depression lasting for at least two years. \n\nThis consists of the presence of at least five out of a possible eight defining symptoms, during the same two-week period, where at least one of the symptoms is depressed mood or loss of interest or pleasure\n\n**Severity:**\n\n- Mild: Few, if any, symptoms in excess of those required to make the diagnosis (associated symptoms, see below), and the symptoms result in minor functional impairment.\n- Moderate: Symptoms or functional impairment between \"mild\" and \"severe.\"\n- Severe: The number of symptoms, intensity, and impairment are all greatly increased.\n\n\n# Epidemiology\n\nDepression is a highly prevalent mental health disorder. It represents the third most common reason for consulting a general practitioner in the UK. Depression demonstrates a higher prevalence in females.\n\n# Aetiology\n\nThe aetiology of depression involves a complex interplay of genetic and environmental factors. History of previous mental health issues, physical illnesses, and social challenges like divorce, poverty, and unemployment can all contribute to its development.\n\n# Clinical Features\n\nDepression is defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM) as the presence of 5 out of the following 9 symptoms, occurring nearly every day for at least 2 weeks:\n\n1. **Depressed mood or irritability** for most of the day, indicated by either subjective report (feels sad or empty) or observation by others (appears tearful).\n2. **Anhedonia:** Decreased interest or pleasure in most activities, most of the day.\n3. Significant **weight change** (5%) or change in appetite.\n4. **Sleep alterations:** Insomnia or hypersomnia.\n5. **Activity changes:** Psychomotor agitation or retardation.\n6. **Fatigue** or loss of energy.\n7. **Guilt or feelings of worthlessness:** Excessive or inappropriate guilt or feelings of worthlessness.\n8. **Cognitive issues:** Diminished ability to think or concentrate, or increased indecisiveness.\n9. **Suicidality:** Thoughts of death or suicide, or formulation of a suicide plan.\n\n### Additional Features (Severe Depression)\n- **Psychotic Features:** Delusions (e.g. nihilistic delusions, Cotard's syndrome) and hallucinations.\n- **Depressive Stupor:** Profound immobility, mutism, and refusal to eat or drink, sometimes necessitating electroconvulsive therapy (ECT).\n\n# Differential Diagnosis\n\nThe main differentials and their key signs and symptoms include:\n\n- **Bipolar Disorder:** Characterised by periods of mania/hypomania (elevated mood, inflated self-esteem, decreased need for sleep, increased talkativeness, distractibility, increased goal-directed activity) alternating with depressive episodes.\n- **Anxiety Disorders:** Persistent and excessive worry, restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and sleep disturbance.\n- **Psychotic Disorders:** Hallucinations, delusions, disorganised speech, grossly disorganised or catatonic behaviour.\n- **Substance/Medication-Induced Mood Disorder:** Mood disturbance associated with intoxication or withdrawal from substances or side effects of medications.\n- **Adjustment Disorders:** Development of emotional or behavioural symptoms in response to identifiable stressors.\n\n\nVarious organic causes should be considered and ruled out through careful history-taking, physical examination, and relevant investigations. These include:\n\n- Neurological disorders such as Parkinson's disease, dementia, and multiple sclerosis.\n- Endocrine disorders, especially thyroid dysfunction and hypo/hyperadrenalism (e.g., Cushing's and Addison's disease).\n- Substance use or medication side effects (e.g., steroids, isotretinoin, alcohol, beta-blockers, benzodiazepines, and methyldopa).\n- Chronic conditions such as diabetes and obstructive sleep apnea.\n- Long-standing infections, such as mononucleosis.\n- Neoplasms and cancers - low mood can theoretically be a presenting complaint in any cancer, with pancreatic cancer being a notable example.\n\n\n# Investigations\n\n- Standard investigations for depression may include Full Blood Count (FBC), Thyroid Function Test (TFT), Urea and Electrolytes (U&E), Liver Function Test (LFT), Glucose, B12/folate levels, cortisol levels, toxicology screen, and imaging of the Central Nervous System (CNS).\n- These help rule out organic causes (listed above) such as endocrine disorders (e.g. thyroid disorders).\n- There are several questionnaires that can also be used to help assess depressive symptoms, such as the Hospital Anxiety and Depression (HAD) Scale and Patient Health Questionnaire (PHQ-9).\n\n# Management\n\nDepression is usually managed in primary care. GPs can refer to secondary care (Psychiatry) if there is a high-suicide risk, symptoms of bipolar disorder, symptoms of psychosis, or if there is evidence of severe depression unresponsive to initial treatment.\n\r\n**Persistent subthreshold depressive symptoms or mild-to-moderate depression:**\n\n- 1st line = Low-intensity psychological interventions (individual self-help, computerised CBT). \r\n- 2nd line = High-intensity psychological interventions (individual CBT, interpersonal therapy) \r\n- 3rd line = Consider antidepressants \r\n\r\n**Mild depression unresponsive to treatment and moderate-to-severe depression:**\n\n- 1st line = High-intensity psychological interventions + antidepressants (1st line = SSRI)\r\n- 2nd line (Treatment-resistant depression) – switch antidepressants and then use adjuncts \r\n\r\n**Severe depression and poor oral intake/psychosis/stupor:**\n\n- 1st line = ECT \n- Although the exact mechanism remains elusive, it is thought that the induced seizure, rather than the ECT procedure itself, has therapeutic benefits. Short-term side effects of ECT include headache, muscle aches, nausea, temporary memory loss, and confusion, while long-term side effects can include persistent memory loss. Due to the induced seizure, there is a risk of oral damage, and due to the general anaesthetic, a small risk of death.\r\n\n**Recurrent depression:** \n\n- Treated with antidepressant + lithium \r\n\n\nMedical management of depression - additional notes:\n\n- First-line pharmacological treatment typically involves a Selective Serotonin Reuptake Inhibitor (SSRI) such as sertraline. SNRIs such as venlafaxine can also be used first-line, but are less preferable due to the risk of damage from overdose, which is less likely with SSRIs.\n- In people aged 18-25 there is an increased risk of impulsivity and suicidal risk upon commencing antidepressant medication and so they should have a follow-up appointment arranged after one week to monitor progress. Initial reviews can otherwise be arranged 2-4 weeks after starting medication in patients >25.\n- Continuation of antidepressants for at least six months post-remission is recommended to mitigate relapse risk. Tapering should be done gradually over a four-week period when discontinuing antidepressants.\n\n\n\n# NICE Guidelines\n\n[NICE Guidance on the Management of Depression](https://www.nice.org.uk/guidance/cg90)",
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"question": "A 33-year-old male presents to the GP with low mood and low energy for the past 4 weeks. He has been trying to follow psychological self-help at home, but this has not improved his symptoms. His appetite is now increasingly poor and he is struggling with his sleep. This is affecting his performance at work. The GP commences him on fluoxetine.\n\nWhich of the following is the most appropriate to advise this patient regarding his anti-depressant medication?",
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"explanation": "This is incorrect because ITU admission is considered for patients with a CURB-65 score of 3 and above. This is because they are likely to require close monitoring, inotropic, or vasopressor support. The outreach team in the hospital are useful points of contact for patients who are critically unwell. This patient doesn't currently display any need for ITU support; she is slightly hypotensive but a trial of intravenous fluids will be needed in the first instance, and her hypoxia is likely correctible with a small amount of oxygen therapy.",
"id": "53284",
"label": "c",
"name": "Contact the outreach team and consider ITU admission",
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"explanation": "This is incorrect because DOACs are not the correct treatment for community-acquired pneumonia. DOACs are the correct treatment for a pulmonary embolism, which could present in a similar manner. However, given the chest X-ray findings, the clinical presentation is better explained by a pneumonia at this moment.",
"id": "53286",
"label": "e",
"name": "Admit patient to the medical ward and start a direct oral anti-coagulant (DOAC)",
"picture": null,
"votes": 30
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"explanation": "This is incorrect because she has a CURB-65 score of 2. Patients with a score of 0 or 1 can be discharged for management within the community with oral antibiotics, such as amoxicillin (or doxycycline/clarithromycin if there is a penicillin allergy.) This patient also requires intravenous fluids due to the hypotension.",
"id": "53283",
"label": "b",
"name": "Discharge with a 5 day course of oral antibiotics",
"picture": null,
"votes": 204
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"__typename": "QuestionChoice",
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"explanation": "This is incorrect because this patient should not be discharged home unless they are clinically well and have a CURB-65 score of 0 or 1. It is important to give all patients correct safety netting if they go home, however this patient needs IV antibiotics and fluids and has a confirmed source of infection, which needs treatment.",
"id": "53285",
"label": "d",
"name": "Discharge patient with safety netting advice",
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"votes": 7
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is the correct answer because this patient has community-acquired pneumonia and a CURB-65 score of 2 for confusion and systolic blood pressure <90mmHg. The CURB-65 score is used to guide management and prognosticate in community acquired pneumonia. Pneumonia typically presents as shortness of breath, productive cough, pleuritic chest pain, and fever. On examination, you can hear focal coarse inspiratory crepitations. This patient should be admitted as she will need IV antibiotics and fluids, which she cannot have within the community.",
"id": "53282",
"label": "a",
"name": "Admit patient to the medical ward and start intravenous antibiotics",
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"comment": "Am I being thick why is here creatinine on the floor?",
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"comment": "Shush AD",
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"comment": "idk bro she seems septic to me..id still be checking in with ITU just in case",
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"explanation": "# Summary\n\n\nPneumocystis Pneumonia (PCP) is a fungal infection caused by _Pneumocystis Jirovecii_ that affects immunocompromised patients. Key symptoms include fever, a dry cough, and exertional breathlessness. Desaturation on exertion is characteristic of PCP pneumonia. Chest X-ray may be normal or show bilateral infiltrates, and a definitive diagnosis is reached with either sputum samples or bronchoscopy with bronchoalveolar lavage. Management involves antibiotics, usually co-trimoxazole as the first line treatment, with steroids added for more severe cases.\n\n\n# Definition\n\n\nPneumocystis Pneumonia (PCP) is an infection caused by the fungus _Pneumocystis Jirovecii_. It usually affects patients who are immunocompromised, for example patients with late-stage HIV or those on immunosuppressant medications after an organ transplant.\n\n\n# Epidemiology\n\n\nIn the UK, rates of PCP are falling in patients with HIV due to improvements in antiretroviral therapies. However, there has been an increase in PCP in patients immunosuppressed for other reasons (such as transplant or haematological malignancies). Currently around half of patients with PCP have HIV and half do not.\n\n\nPatients at risk of PCP should be treated with prophylaxis (usually oral co-trimoxazole) - this includes all patients with HIV with a CD4 count of below 200. \n\n\n# Aetiology\n\n\nPCP is caused by _Pneumocystis Jirovecii_, a fungus that causes pulmonary infections. Patients at risk of PCP are those who are immunocompromised (it is classed as an opportunistic infection, and an AIDS-defining illness in those with HIV). \n\n\nRisk factors include:\n\n\n- HIV with a CD4 count below 200\n- Steroids or other immunosuppressive medications\n- Previous organ transplant\n- Congenital immunodeficiencies (e.g. hypogammaglobulinaemia)\n- Severe malnutrition\n- Comorbid lung disease\n- Haematological malignancies\n\n\n# Signs and Symptoms\n\n\n- Fever\n- Dry cough\n- Exertional breathlessness\n- Chest pain\n\n\nOn examination, the chest may be clear, or end-inspiratory crackles and wheeze may be present.\n\n\n# Differential Diagnosis\n\n\n- Bacterial or viral pneumonia: similar symptoms, more likely to have a productive cough.\n- Tuberculosis: chronic cough, haemoptysis, weight loss, night sweats and fever. \n- Pulmonary embolism: less likely to have fevers, dry cough and shortness of breath on exertion typical, may have haemoptysis.\n\n\n# Investigations\n\n\n**Bedside tests include:**\n\n\n- Oxygen saturations on exertion \n- Arterial blood gas for hypoxia, important to grade severity and determine if steroids are indicated\n- Sputum samples (may need to be induced e.g with saline nebulisers): **silver staining** is used to confirm the diagnosis of PCP (shows a characteristic Mexican hat appearance), also send sputum for routine and mycobacterial culture (to rule out TB or other infections)\n\n\n**Blood tests include:**\n\n\n- Routine bloods for FBC and CRP (looking for infection markers) and baseline liver and renal function prior to starting antibiotics\n- HIV testing\n- CD4 count if HIV positive\n\n\n**Imaging includes:**\n\n\n- Chest X-ray: often shows bilateral hilar interstitial infiltrates, however 10% have a normal chest X-ray.\n- High-resolution CT scan: if chest X-ray is normal and PCP is suspected, a high-resolution CT is more sensitive.\n\n\n**Other investigations:**\n\n\n- Bronchoscopy with bronchoalveolar lavage: if sputum samples are negative, this is the definitive investigation to gain a respiratory sample for staining. \n\n\n[lightgallery]\n\n\n# Management\n\n\n- Supportive treatment with analgesia, oxygen if hypoxic, consider holding immunosuppressant treatment (with liaison with specialist teams as needed)\n- Patients with mild disease (only mild changes on CXR, normal oxygen saturations) can be treated as outpatients; moderate and severe cases should be admitted\n- High dose co-trimoxazole is the primary treatment\n- Alternative therapies if co-trimoxazole is contraindicated or not tolerate include: atovaquone, dapsone with trimethoprim or pentamidine. \n- Steroids should be given in all patients with moderate or severe PCP (i.e.PaO2<11kPa) - either oral prednisolone or IV hydrocortisone. \n\n\n# NICE Guidelines\n\n\n[NICE CKS - HIV infection and AIDS](https://cks.nice.org.uk/topics/hiv-infection-aids/)\n\n\n# References\n\n\n[Patient UK - Pneumocystis Jirovecii Pneumonia](https://patient.info/doctor/pneumocystis-jirovecii-pneumonia)\n\n\n[BNF treatment summary - Pneumocystis Pneumonia](https://bnf.nice.org.uk/treatment-summary/pneumocystis-pneumonia.html)",
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"question": "A 52-year-old female presents to A&E with her partner as he has concerns regarding a recent change in behaviour. He reports she has been confused at home for the past 2 days. She is unable to give a history. Observations: HR 95bpm, RR 21, O2 saturation 93% on room air, BP 89/65mmHg, temperature 38.1. On examination, she has coarse inspiratory crackles at the right base. Her blood test results show the following:\n\n||||\n|-------|:-------:|-------|\n|Sodium|145 mmol/L|135 - 145|\n|Potassium|3.6 mmol/L|3.5 - 5.3|\n|Urea|6.5mmol/L|2.5 - 7.8|\n|Creatinine|21 µmol/L|60 - 120|\n\n\nA chest radiograph demonstrates right lower zone airspace opacification with air bronchograms.\n\n\nWhich of the following is the next best step in management?",
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"explanation": "Myelofibrosis presents with constitutional symptoms such as fatigue, weight loss, fever, and night sweats, alongside splenomegaly. Blood tests show potential pancytopenia due to bone marrow failure secondary to fibrosis, which usually results in dry taps during bone marrow aspiration. Blood film findings are tear-drop poikilocytes.",
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"label": "c",
"name": "Myelofibrosis",
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"explanation": "This is incorrect because primary polycythaemia is due to the spontaneous proliferation of red blood cells in the bone marrow. This is less likely, though is an important differential, given the normal platelet and white cell count, which are also usually deranged in polycythaemia rubra vera, and an otherwise clear and logical explanation ie. chronic hypoxia in COPD. There is also no history of itching on hot baths, which is more likely in polycythaemia rubra vera.",
"id": "53288",
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"explanation": "Blood tests show a raised haemoglobin, which is suggestive of polycythaemia. This patient has got a disorder (COPD) leading to chronic hypoxia, and as a result has developed secondary polycythaemia. Primary polycythaemia, such as polycythaemia rubra vera, indicates a primary bone marrow disorder, and given the normal platelet and white cell count values, this is less likely, though an important differential. There is also no history of itching on hot baths, which is more likely in polycythaemia rubra vera. It is important to note that a pO2 of <7.3 is the usual criteria for LTOT, but between 7.3-8 he would qualify if he had complications related to chronic hypoxia, such as polycythaemia. He would now most likely fuflfil LTOT criteria, and referral back to the LTOT service will be indicated. Symptoms of polycythaemia include dizziness and fatigue.",
"id": "53287",
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"name": "Secondary polycythaemia",
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"explanation": "# Summary\n\nChronic obstructive pulmonary disease (COPD) is a chronic obstructive disease of the airways with the two main components being chronic bronchitis and emphysema. It usually develops due to smoking, with other risk factors including occupation exposures and air pollution. Patients present with breathlessness, a chronic productive cough and wheeze. Key investigations are spirometry (to confirm obstruction), full blood count (to identify anaemia or polycythaemia) and a chest X-ray to exclude lung cancer or other causes of symptoms. Management includes smoking cessation, pulmonary rehabilitation, consideration of long term oxygen therapy, inhaled or nebulised medical treatment and consideration of other medications e.g. mucolytics. Acute exacerbations of COPD may be infective or non-infective, and can be treated by increasing bronchodilator therapy, oral prednisolone and antibiotics (if an infective cause is suspected).\n\n# Definition\n\nChronic obstructive pulmonary disease (COPD) involves airway obstruction that is usually progressive. It encompasses both emphysema (where alveolar wall destruction leads to enlargement of the distal airspaces) and chronic bronchitis (persistent or recurrent productive cough usually due to mucus hypersecretion). \n\n# Epidemiology\n\nIn the UK 1.2 million people have a diagnosis of COPD, with an estimated 2 million people living with it undiagnosed. It is the 5th commonest cause of death in the UK, causing almost 30,000 deaths per year. \n\nAround 90% of COPD cases in the UK are caused by smoking, with household pollution being a bigger contributing factor in low and middle income countries.\n\n# Risk Factors\n\n- Tobacco smoking and passive smoke exposure\n- Marijuana smoking \n- Occupational exposure to dusts and fumes\n- Household air pollution from wood or coal burning\n- Alpha-1 antitrypsin deficiency\n\nPrognosis is variable, with the following factors associated with higher morbidity and mortality:\n\n- Poor exercise tolerance\n- Smoking\n- Low body mass index\n- Multi-morbidity and frailty\n- Exacerbations requiring admission to hospital or frequent exacerbations\n- Severe obstruction on spirometry (as measured by a lower FEV1)\n- Chronic hypoxia\n- Cor pulmonale\n\n# Pathophysiology\n\nChronic Bronchitis:\n\n- As a protective reaction to smoke or other pollutants, goblet cells hypersecrete mucus in the bronchi and bronchioles of the lungs.\nCilia are not able to remove the excess mucus and so it obstructs the small airways.\nOngoing inflammation causes remodelling and thickening of the airway walls that also contributes to obstruction.\n\nEmphysema:\n\n- Inflammation in the lungs is usually countered by antiproteases such as alpha-1 antitrypsin, however the activity of these is reduced by smoke and other pollutants. \n- Without sufficient antiprotease activity, proteolytic enzymes produced by inflammatory cells break down the walls of the alveoli.\n- This causes enlargement of the terminal airspaces and reduces the surface area available for gas exchange.\n\n# Classification\n\nThe Global Initiative for Chronic Obstructive Lung Disease (GOLD) classifies COPD severity using airflow limitation (as measured by FEV1), severity of symptoms and frequency of exacerbations. \n\n| GOLD Grade | Severity | Post-Bronchodilator FEV₁ (% Predicted) |\n|------------|--------------------------|----------------------------------------|\n| 1 | Mild | ≥ 80% |\n| 2 | Moderate | 50-79% |\n| 3 | Severe | 30-49% |\n| 4 | Very Severe | < 30% |\n\n\nThe two measures used to quantify symptom severity are the CAT (COPD Assessment Test) and the mMRC (modified Medical Research Council) dyspnoea scale which is given below:\n\n| Grade | Description |\n|-------|----------------------------------------------------------------------------------------------------|\n| 0 | I only get breathless with strenuous exercise. |\n| 1 | I get short of breath when hurrying on level ground or walking up a slight hill. |\n| 2 | On level ground, I walk slower than people of the same age because of breathlessness, or I have to stop for breath when walking at my own pace. |\n| 3 | I stop for breath after walking about 100 yards or after a few minutes on level ground. |\n| 4 | I am too breathless to leave the house, or I am breathless when dressing or undressing. |\n\n# Signs and symptoms\n\n- Shortness of breath that worsens with exertion\n- Reduced exercise tolerance\n- Chronic productive cough\n- Recurrent lower respiratory tract infections\n- Wheeze\n- In more advanced cases, systemic symptoms such as weight loss and fatigue may be present\n\nExamination may be normal, though signs may include:\n\n- Wheeze or crackles on auscultation\n- Accessory muscle usage\n- Pursed lip breathing (this creates a small amount of positive end expiratory pressure to prevent the alveoli from collapsing)\n- Cyanosis \n- Hyperinflation of the chest\n- Cachexia\n- Raised JVP and peripheral oedema (indicating cor pulmonale has developed)\n\n# Investigations\n\n- **Spirometry** - the diagnostic investigation for COPD and key to classification of severity, may be used to monitor progression of the disease. A FEV1/FVC ratio <0.7 confirms obstruction.\n\n- **Bloods** - Full blood count looking for polycythaemia (resulting from chronic hypoxaemia) or anaemia (usually anaemia of chronic disease), consider BNP to assess for heart failure (with an **echocardiogram** if suspected, alpha-1 antitrypsin in young patients/minimal smoking history/strong family history\n- **ECG** - the following ECG changes are often seen in advanced COPD with features of e.g. cor pulmonale, and include:\n\t- Right axis deviation\n\t- Prominent P waves in inferior leads\n\t- Inverted P waves in high lateral leads (I, aVL)\n\t- Low voltage QRS\n\t- Delayed R/S transition in leads V1-V6\n\t- P pulmonale\n\t- Right ventricular strain pattern\n\t- RBBB\n\t- Multifocal atrial tachycardia\n\n- **Chest X-ray** - used to rule out other causes of symptoms (e.g. lung cancer, bronchiectasis), may show features of COPD including hyperinflation of the chest with flattening of the hemidiaphragms and bullae.\n\n[lightgallery1]\n\n- **Sputum culture** - during exacerbations to target antibiotic therapy\n\n# Differential diagnosis\n\n- **Asthma:** may coexist with COPD, suspect if onset of symptoms <35, history of atopy, non-smoker, variable or nocturnal symptoms.\n- **Bronchiectasis:** copious secretions and coarse crepitations on examination, triggering factors include severe childhood respiratory tract infections.\n- **Heart Failure:** suspect in patients with ischaemic heart disease, may have orthopnoea and paroxysmal nocturnal dyspnoea.\n- **Interstitial Lung Disease:** dry rather than a productive cough, fine crackles on examination.\n- **Lung cancer:** patients with COPD are usually at higher risk due to smoking history, need to investigate for malignancy in cases with a persistent cough/haemoptysis/weight loss.\n- **Tuberculosis:** similar symptoms, systemic manifestations include fevers and weight loss, consider in at-risk groups.\n\n# Management of Chronic COPD\n\n**Conservative:**\n\n- Patient education, ensure all patients have a personalised self-management plan\n- Smoking cessation support\n- Nutritional support and dietician referral if malnourished\n- Annual influenza and one-off pneumococcal vaccination\n- Pulmonary rehabilitation (refer if grade 3 and above on mMRC dyspnoea scale or a recent admission for an acute exacerbation)\n- Consider referral for respiratory physiotherapy to help with sputum clearance and breathing techniques\n\n**Medical:**\n\n\n- For patients whose activities are limited by breathlessness, start a short-acting beta-2 agonist (SABA, e.g. salbutamol) or short-acting muscarinic antagonist (SAMA, e.g. ipratropium) inhaler\n- The next step depends on if they have features of asthma or steroid responsiveness: if these are present then add a long-acting beta-2 agonist (LABA, e.g. formoterol) and an inhaled corticosteroid (ICS, e.g. beclomethasone). If these are not present then add a LABA and a long-acting muscarinic antagonist (LAMA, e.g. tiotropium). \n- If patients do not respond adequately to this, the third inhaler can then be trialled (i.e. all patients would be on a SABA/SAMA + LABA + LAMA + ICS).\n\nPatients who require further therapy should be referred to a specialist for ongoing management which may include oral steroids, oral theophylline or oral phosphodiesterase-4 inhibitors (e.g. roflumilast).\n\nManagement of stable COPD is can be tailored according to the patient’s clinical phenotype. The following groups are defined according to 2024 NICE guidance:\n\n**Group A**\n \n- **Definition**: Patients with minimal symptoms (mMRC grade 0–1 or CAT score <10) and no history of exacerbations requiring hospitalisation or oral corticosteroids in the last year. \n- **Management**:\n - Start with a **short-acting bronchodilator (SABA or SAMA)** as needed for symptom relief.\n - If symptoms are not controlled, consider switching to a long-acting bronchodilator: \n - **LAMA** or **LABA**, depending on individual tolerance and symptom profile. \n\n**Group B**\n \n- **Definition**: Patients with significant symptoms (mMRC grade ≥2 or CAT score ≥10) but no exacerbations requiring hospitalisation or oral corticosteroids in the last year. \n- **Management**: \n - Initiate treatment with a **LAMA** or **LABA** as maintenance therapy. \n - If symptoms persist despite monotherapy, escalate to **dual therapy (LABA + LAMA)**. \n\n**Group E**\n \n- **Definition**: Patients with frequent exacerbations (≥2 per year or ≥1 requiring hospitalisation) regardless of symptom burden. \n- **Management**: \n - First-line therapy is **LAMA** for exacerbation prevention. \n - If exacerbations persist, escalate to: \n\t - **Dual therapy (LABA + LAMA)**. \n\t - If asthmatic features or steroid responsiveness are present (e.g., eosinophilia or a history of asthma), consider **LABA + ICS**. \n - For patients who continue to experience exacerbations despite dual therapy, switch to **triple therapy (LABA + LAMA + ICS)**. \n\n\n\n| **Group** | **Phenotype** | **Initial Therapy** | **Escalation Therapy** | \n|-------------|--------------------------------|------------------------------|------------------------------------| \n| **Group A** | 0 or 1 moderate exacerbation not leading to hospitalisation | SABA or SAMA as needed | LAMA or LABA | \n| **Group B** | 0 or 1 moderate exacerbation not leading to hospitalisation| LAMA or LABA | LABA + LAMA | \n| **Group E** | 2 or more moderate exacerbations or 1 or more exacerbations leading to hospitalisation\t | LAMA | LABA + LAMA or LABA + LAMA + ICS | \n\n\nOther medical treatments that may be considered include:\n\n- Oral mucolytic therapy - for patients with a chronic cough productive of sputum.\n- Prophylactic antibiotics - in cases of frequent infective exacerbations, should be discussed with a specialist, a common choice would be azithromycin 3x per week.\n- Nebuliser therapy - for patients with disabling breathlessness despite optimised use of inhalers.\n- Long-term oxygen therapy (LTOT) - see below for more details\n\n\n**Surgical:**\n\n- In certain cases of severe COPD when patients have not responded to maximal medical therapies, surgical intervention may be considered. \n- Both the NICE recommended options involve lung volume reduction (which involves removing emphysematous areas of the lung so that the healthy lung can expand) - this can be done either by surgical resection or using bronchoscopy to site a one-way valve in one of the larger airways to collapse the diseased lung. \n\n### Long term oxygen therapy (LTOT)\n\n**The following patients should be referred for assessment for LTOT:**\n\n- Oxygen saturations <92% in air or cyanosis\n- FEV1 <30% predicted (consider referring if <49%)\n- Polycythaemia\n- Peripheral oedema or raised jugular venous pressure (suggesting cor pulmonale)\n\nThis assessment involves ensuring that patients are medically optimised and their COPD is stable (i.e. they’re not recovering from a recent exacerbation). Patients who are current smokers cannot be offered LTOT because of the risk of burns and fires. \n\nPatients then have two ABGs in air at least 3 weeks apart and the following patients should be offered LTOT (with the advice to use the oxygen for at least 15 hours per day):\n\n- PaO2 below 7.3kPa\n- PaO2 7.3-8kPa with any of secondary polycythaemia, peripheral oedema or pulmonary hypertension\n\n# Complications\n\n## Acute exacerbations\n\n- These present with worsening breathlessness, productive cough and wheeze, and patients may be febrile, tachycardic and tachypnoeic. \n- Patients who are clinically well may be treated at home with an increase in their usual inhalers, a short course of oral steroids (usually 30mg prednisolone for 5 days) and oral antibiotics if bacterial infection is suspected. \n- Those who have frequent exacerbations may be given a “rescue pack” of steroids and antibiotics to keep at home and start using in case of an exacerbation (alongside seeking medical help).\n\n- Patients requiring hospital admission should also receive steroids and antibiotics if indicated. \n- They may require nebulised bronchodilators, supplementary oxygen and in case of deterioration respiratory support with non-invasive ventilation may be required. \n- Advanced care planning and ensuring that escalation status is discussed with patients is therefore key, so that if they deteriorate to the point of needing intensive care support it is established whether or not this is appropriate and in line with their wishes.\n\n## Polycythaemia\n\n- Chronic tissue hypoxia as seen in COPD leads to a compensatory overproduction of erythropoietin, which leads to increased red blood cell production (i.e. secondary polycythaemia). \n- This causes an increase in blood viscosity that in turns increases risk of both arterial and venous thrombosis. \n\n\n## Cor Pulmonale\n\nCor pulmonale refers to right ventricular dilation or hypertrophy in response to pulmonary hypertension caused by chronic lung disease - COPD is not the only cause of this but it is the most common.\n\nThe pathophysiology is as follows:\n\n- Changes in the lungs and chronic hypoxaemia cause the walls of the pulmonary arteries to thicken.\n- This increases vascular resistance in the lungs.\n- The right ventricle then has to pump against greater resistance, which causes it to either dilate or hypertrophy.\n- Ultimately this leads to right heart failure, with resulting peripheral oedema, hepatomegaly and elevated jugular venous pressure (JVP).\n\nPeripheral oedema may be treated symptomatically with diuretics and long-term oxygen therapy has been shown to reduce morbidity and mortality. All patients with suspected cor pulmonale should be referred to secondary care.\n\n## Pneumothorax\n\n- COPD is a common cause of secondary pneumothoraces (i.e. a pneumothorax secondary to underlying lung disease). These occur when a bulla ruptures, releasing air into the pleural cavity. \n- Investigations and treatment are as per the BTS guidelines (see Pneumothorax chapter for more details).\n\n## Depression and anxiety\n- Over 1 in 3 people with COPD report symptoms of depression and anxiety so screening for this is important during patient reviews. \n- The COPD Assessment Test (CAT) can be used to assess the impact of COPD on everyday life. \n- Referral to psychological services for support may be appropriate, as well as holistic assessment and management.\n\n# NICE Guidelines\n\n[Click here for the NICE Guidelines](https://www.nice.org.uk/guidance/ng115)\n\n[NICE CKS - COPD](https://cks.nice.org.uk/topics/chronic-obstructive-pulmonary-disease/)\n\n# References\n\n[Patient UK - COPD](https://patient.info/doctor/chronic-obstructive-pulmonary-disease-pro)\n\n[GOLD report 2023](https://goldcopd.org/2023-gold-report-2/)\n\n[Radiopaedia - COPD](https://radiopaedia.org/articles/chronic-obstructive-pulmonary-disease-1?lang=gb)\n\n[Patient UK - Cor Pulmonale](https://patient.info/doctor/cor-pulmonale)",
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"explanation": "This is incorrect because p-ANCA (antibody against myeloperoxide (MPO)) is positive in microscopic polyangiitis and Churg-Strauss. p-ANCA stands for perinuclear anti-neutrophil cytoplasmic antibodies, whereas c-ANCA refers to cytoplasmic anti-neutrophil cytoplasmic antibodies. The terminology originates from the pattern of staining seen during immunoflouresence. Churg-Strauss is also known as eosinophilic granulomatosis with polyangiitis, and can present with a nephritic/rapidly progressive glomerulonephritis picture, as well as other clinical features such as eosinophilia and poorly controlled asthma. Microscopic polyangiitis has a less well defined constellation of clinical features, and may present non-specifically with virtually any organ system involved, as one would expect of a vasculitis disorder.",
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"comment": "lets be honest it was a 50/50 between PANCA and CANCA like always",
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"comment": "W - Wegener's granulomatosis (now GPA)\n\nE - Early respiratory symptoms (sinusitis, nasal ulcers, ear infections)\n\nG - Glomerulonephritis (kidney involvement)\n\nE - Elevated ANCA (anti-neutrophil cytoplasmic antibodies)\n\nN - Nodules and granulomas (formation of small inflamed nodules)\n\nE - Early diagnosis and treatment are essential\n\nR - Respiratory and renal manifestations are common",
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"explanation": "# Summary\n\nGranulomatosis with polyangiitis (GPA), previously known as Wegener's granulomatosis, is an ANCA associated vasculitis affecting small and medium sized vessels. The classic triad of manifestations is of upper respiratory tract involvement, lower respiratory tract involvement, and pauci-immune glomerulonephritis. Additional organs may be involved, including the skin, the eyes and the peripheral nerves. Key investigations are blood tests including ANCA (c-ANCA is usually positive), chest X-ray or CT showing nodules +/- cavitation and biopsy (showing necrotising granulomas with associated vasculitis). Acute management is usually with steroids with another immunosuppressive agent, the choice of which is dependent on the severity of disease. Steroids should be tapered once remission is achieved whilst another immunosuppressant is continued.\n\n# Definition\n\nGranulomatosis with polyangiitis (GPA), formerly known as Wegener's granulomatosis, is a chronic granulomatous ANCA-associated vasculitis that primarily involves the upper and lower respiratory tracts and the kidneys. \n\n# Epidemiology\n\n- GPA is a rare disease with an annual incidence of 8.4 per million\n- Men are slightly more likely to be affected\n- Onset peaks between the ages of 35 to 55\n- There is a higher incidence of cases seen in the winter, suggesting that environmental exposures such as infections may trigger GPA\n- There is also a slightly increased risk in first degree relatives of people with GPA, indicating a genetic predisposition\n\n# Signs and Symptoms\n\nThe classic triad involved in GPA is as follows:\n\n- **Upper respiratory tract** \n- Chronic sinusitis with nasal obstruction and facial pain\n- Rhinorrhoea which is often bloody\n- Epistaxis\n- Ulceration and crusting in and around the nose\n- Destruction of nasal cartilage leading to a saddle-nose deformity \n- Subglottis stenosis may present with hoarseness, stridor or airway obstruction\n- Otitis media causing ear pain and fullness\n- Hearing loss\n- **Lower respiratory tract**\n- Cough\n- Haemoptysis due to pulmonary haemorrhage\n- Dyspnoea\n- Pleuritic chest pain\n- Wheeze\n- **Necrotising glomerulonephritis**\n- Haematuria\n- Frothy urine due to proteinuria\n- Oliguria\n\n**Systemic signs and symptoms** are common:\n\n- Fatigue\n- Malaise\n- Fevers\n- Night sweats\n- Anorexia\n- Weight loss\n- Arthralgia or arthritis\n\nOther organs may also be affected, for example:\n\n- **Skin**\n- Palpable purpura\n- Nodular, papular or vesicular rashes\n- Ulcers\n- **Eyes**\n- Granulomatous disease may cause an inflammatory mass in the orbit leading to proptosis \n- The optic nerve may also be compressed\n- Vasculitis may cause conjunctivitis, episcleritis, scleritis, uveitis, retinitis or optic neuritis\n- Eye pain, redness and visual loss may occur\n- **Peripheral nerves**\n- Mononeuritis multiple is the usual pattern seen\n- Sensory and motor deficits are seen in the distribution of particular peripheral nerves\n- Pain and paraesthesias of affected areas are common\n- **Central nervous system**\n- Granulomatous lesions\n- Vasculitis causing infarction\n- Intracranial haemorrhage\n- Symptoms include headaches, cranial nerve lesions, seizures, focal neurological deficits and altered consciousness\n- **Gastrointestinal (GI) tract**\n- Mouth ulcers\n- Strawberry gums (hyperplastic gingival lesions)\n- Ulceration elsewhere in the GI tract leading to bleeding or perforation\n- Ischaemic bowel disease\n- Symptoms include abdominal pain, vomiting and diarrhoea\n- **Heart**\n- Pericarditis or myocarditis\n- Coronary arteritis\n- Valvular disease\n- Conduction deficits\n- Symptoms include chest pain, dyspnoea, palpitations and dizziness\n\n# Differential Diagnosis\n\n- **Eosinophilic granulomatosis with polyangiitis** is another ANCA-associated systemic vasculitis which may share features of sinusitis, lung and renal involvement however almost all patients have asthma and eosinophilia\n- **Microscopic polyangiitis** is also an ANCA-associated systemic vasculitis which classically involves the lungs and kidneys, as well as the eyes, peripheral nerves, GI tract and skin, however features of sinusitis are not present\n- **Anti-GBM disease** (also known as Goodpasture's syndrome) causes diffuse pulmonary alveolar haemorrhage and rapidly progressive glomerulonephritis; antibodies against the glomerular basement membrane (GBM) are the key differentiating investigation; ANCA may also be positive\n- **Polyarteritis nodosa** also causes systemic symptoms and commonly involves the kidneys, however pulmonary involvement is very rare unlike in GPA\n- **IgA vasculitis** is an immune complex-mediated small vessel vasculitis that typically affects children; palpable purpura on the legs, abdominal pain and renal involvement are all shared features\n- **Infective endocarditis** causes similar systemic symptoms (e.g. fevers, malaise, weight loss) and septic emboli can affect the lungs and kidneys as well as the central nervous system\n- **Malignancy** may cause similar systemic symptoms of weight loss, fatigue, malaise and low-grade fevers, and specific malignancies may cause symptoms that mimic GPA (e.g. haemoptysis due to lung cancer, haematuria due to urological malignancies)\n\n# Investigations\n\n**Bedside tests:**\n\n- **Urine dip** for blood and protein\n- **Urinary protein:creatine ratio** if proteinuria present on urinalysis\n- **Urine microscopy** may show red blood cell casts\n\n**Blood tests:**\n\n- **Full blood count** which may show a normocytic anaemia and thrombocytosis due to chronic inflammation, or a microcytic anaemia due to alveolar haemorrhage or GI bleeding\n- **U&Es** looking for renal impairment due to glomerulonephritis\n- **LFTs** may show hypoalbuminemia due to inflammation or proteinuria\n- **CRP** and **ESR** are raised due to systemic inflammation\n- **Bone profile** is typically normal, hypercalcaemia should raise suspicion of malignancy as an important differential\n- **ANCA** is usually positive - anti-PR3 or c-ANCA is most commonly seen but a small proportion of people are anti-MPO or p-ANCA positive\n\n**Imaging tests:**\n\n- **Chest X-ray**\n- The most common finding is multiple nodules of various sizes throughout both lung fields\n- These may cavitate\n- Pulmonary haemorrhage may also be seen with patchy or diffuse opacification\n- Focal areas of alveolar consolidation may occur and can also cavitate\n- Pleural effusions may be seen secondary to cardiac or renal GPA\n- **CT chest** is more sensitive for the above findings and may also show:\n- Micronodules due to bronchial wall involvement or retained blood in the distal airways\n- Mild bronchiectasis\n- Ground glass changes secondary to haemorrhage\n- Tracheobronchial wall thickening\n- **CT of the sinuses** may show:\n- Mucosal thickening\n- Soft tissues nodules\n- Erosions +/- perforation of the cartilage and bones\n- Sclerosis and calcification may also be present\n- **CT** or **MRI** of the head and orbits may show central nervous system involvement or granulomatous disease of the orbits\n- **CT** of the kidneys typically shows a hypovascular mass\n- **FDG-PET CT** can be used to identify occult sites of disease and investigate for differentials such as chronic infection or malignancy\n\n**Special tests include:**\n\n- **Renal biopsy** shows crescentic and necrotising glomerular lesions with no or few immune deposits (pauci-immune)\n- Other affected sites may also be amenable to biopsy, including skin, nasal mucosa and lung tissues \n- **Flexible nasendoscopy** may be done to look for features such as ulceration, septal perforation, crusting and subglottic stenosis\n- **Lung function testing** with **flow-volume loops** may show evidence of fixed upper airway obstruction in subglottic stenosis\n- **Nerve conduction studies** and **electromyography** may be useful in the investigation of mononeuritis multiplex\n- **Endoscopy** may be required in GPA associated with gastrointestinal bleeding\n- **Bronchoalveolar lavage** may be indicated in evaluating pulmonary infiltrates e.g. alveolar haemorrhage\n\n# Management\n\n- Organ or life-threatening GPA should be treated with high dose steroids (usually 1mg/kg prednisolone or equivalent) with either rituximab or cyclophosphamide\n- Avacopan (an oral C5a-receptor antagonist) may be substituted for steroids in severe GPA\n- Plasma exchange is another option that may be used for salvage therapy, especially in severe renal impairment due to rapidly progressive glomerulonephritis\n- Patients may require supportive treatment e.g. intensive care admission with intubation and ventilation and/or renal replacement therapy\n- If GPA is not organ or life-threatening, steroids and rituximab (in some cases methotrexate or mycophenolate mofetil may be used instead of rituximab) are recommended\n- Prednisolone should be tapered over several months\n- Options for maintenance treatment once remission is achieved include rituximab, azathioprine or methotrexate \n- Maintenance immunosuppressive treatment is usually continued for 2 to 4 years (longer in relapsing disease)\n- Patients should be counselled on the risks of immunosuppressive treatments, and prophylactic co-trimoxazole given to patients on rituximab, cyclophosphamide or high-dose steroids\n- In some cases, surgical treatment is required e.g. reconstructive surgery for nasal deformities or for subglottic stenosis\n- Long-term renal replacement therapy (haemodialysis or transplant) may be required for patients who develop end-stage renal disease\n\n# Complications\n\n- Renal failure due to rapidly progressive glomerulonephritis \n- Respiratory failure due to diffuse pulmonary haemorrhage\n- Hearing loss\n- Vision loss\n- Septal perforation or saddle nose deformity\n- Increased cardiovascular risk due to chronic inflammation\n- Increased risk of bladder cancer in patients treatment with cyclophosphamide - patients should have regular urinalysis as part of follow up\n- Side effects of immunosuppression e.g. osteoporosis, diabetes, peptic ulceration with prolonged steroid courses\n- Psychological distress and negative impacts on quality of life due to the burden of disease and its treatments\n\n# Prognosis\n\n- Without treatment, GPA is usually fatal\n- Patients with both renal and respiratory tract involvement have an increased risk of early death\n- Mortality with effective treatment is 14% at 1 year\n- The majority of patients respond to treatment although relapses are frequent (50% at 8 years)\n\n# References\n\n[EULAR recommendations for the management of ANCA-associated vasculitis](https://ard.bmj.com/content/83/1/30)\n\n[Radiopaedia - Granulomatosis with polyangiitis](https://radiopaedia.org/articles/granulomatosis-with-polyangiitis?lang=gb)\n\n[Patient UK - Granulomatosis with polyangiitis](https://patient.info/doctor/granulomatosis-with-polyangiitis-wegeners-granulomatosis-pro)\n\n[DermNet - Granulomatosis with polyangiitis](https://dermnetnz.org/topics/granulomatosis-with-polyangiitis)\n\n[StatPearls - Granulomatosis with polyangiitis](https://www.ncbi.nlm.nih.gov/books/NBK557827/)",
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"question": "A 43-year-old male presents to the GP with a 5-day history of cough on a background of lethargy and weight loss. He denies any recent unwell contacts. He is concerned as he saw blood in his urine for the first time this morning. He denies any regular medication but he says he has recently started to depend on nasal decongestants over-the-counter, due to chronic nasal congestion.\n\nGiven the most likely diagnosis, which of the following tests are most specific in this condition?",
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"explanation": "This is incorrect because this patient's breast cancer is 1.5cm which is small. This means that she can have a wide local excision without the need for a mastectomy. However, patients can have a mastectomy depending on their preference as breast-conserving surgery such as a wide local excision can give an unacceptable cosmetic result to some females, for example if the breast is small and a wide local excision would actually represent a significant proportion of the breast tissue being removed. Another indication for mastectomy is if the patient is unsuitable for radiotherapy, since radiotherapy is usually required to the whole breast after having breast conserving surgery (i.e. a wide local excision.)",
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"explanation": "This patient has a malignant breast mass isolated to the breast with no distant spread, and as such has a potentially curable cancer. These patients undergo wide local excision with sentinel lymph node biopsy. A sentinel lymph node biopsy is carried out when there are no palpable lymph nodes on examination or on ultrasound imaging. This helps to identify whether any cancer cells are present within these lymph nodes, which are not yet detectable using imaging/examination; if positive, the patient will subsequently have axillary lymph node clearance. If there were palpable lymph nodes/ultrasound identified any lymphadenopathy, these would be biopsied directly. If the biopsy subsequently confirms the cancer has spread to involve the lymph nodes, then an axillary clearance will be performed without need for a sentinel lymph node biopsy.",
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"explanation": "Letrozole is an aromatise inhibitor used for post-menopausal women in the management of oestrogen receptor breast cancer, either neo-adjuvantly or adjuvantly. It works by reducing peripheral aromatisation of androgens to estrogens in fat, and so is only effective in post menopausal women, since in pre-menopausal women the ovaries (rather than fat) produce the bulk of the oestrogen. This patient is oestrogen receptor negative, and as such would not benefit from tamoxifen. Furthermore, due to the reasonably small size of the lump, she likely does not require neo-adjuvant treatment prior to surgery. Aromatase inhibitors may cause osteoporosis, so careful monitoring of the bone mineral density is required.",
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"explanation": "Trastuzumab, also known as Herceptin, is used in HER2+ (human epidermal growth factor receptor) breast cancer, either as neo-adjuvant or adjuvant therapy. This patient has triple-negative breast cancer so it is not indicated in this case. Furthermore, due to the reasonably small size of the lump, she likely does not require neo-adjuvant treatment prior to surgery. Serious side effects of trastuzumab involve cardiac dysfunction and teratogenicity.",
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"explanation": "# Summary\n\n\nBreast carcinoma is the most prevalent form of cancer among women and the second leading cause of cancer death in the UK. It manifests in various histological subtypes including ductal, lobular, medullary, and phyllodes tumours, each displaying distinct characteristics. Certain genetic mutations, especially BRCA1 and BRCA2, can increase the risk for breast carcinoma. Notable signs and symptoms include unexplained breast mass, nipple discharge, retraction, or skin changes suggestive of breast cancer. Key investigations comprise a triple assessment—clinical examination, radiological examination, and biopsy. Treatment strategies encompass surgical management (wide local excision or mastectomy), radiotherapy, chemotherapy, biological therapy, and hormonal therapy. Risk factors for breast cancer include increased hormone exposure, susceptibility gene mutations, advancing age, and lifestyle factors like obesity, physical inactivity, and alcohol and tobacco use.\n\n\n# Definition\n\n\nBreast carcinoma refers to a malignant tumour originating from the cells of the breast tissue. It exhibits different subtypes each with unique cellular properties and clinical implications. The carcinomas can be invasive, indicating they have broken through the basement membrane of the tissue of origin and have the potential to metastasize, or non-invasive (in situ), suggesting they are confined to the initial location.\n\n\n# Epidemiology\n\n\nBreast carcinoma is the most common type of cancer in women and accounts for approximately 15% of new cancer cases, representing 50,000 new cases annually. It is the second most common cause of cancer death in the UK.\n\n\n# Aetiology\n\nMost breast cancers are either ductal (arising from the epithelial lining of the ducts) or lobular (originating from epithelial cells in the terminal ducts of the lobules).\n\n\nRisk factors for breast carcinoma include:\n\n\n- Being female\n- 99% of breast cancer cases occur in women\n- Increased hormone exposure\n- Early menarche or late menopause\n- Nulliparity or late first pregnancy\n- Oral contraceptives or Hormonal Replacement Therapy\n- Susceptibility gene mutations\n- Most commonly BRCA mutations (BRCA1/BRCA2)\n- Advancing age\n- Caucasian ethnicity\n- Obesity and lack of physical activity\n- Alcohol and tobacco use\n- History of breast cancer\n- Previous radiotherapy treatment\n\n\n# Classification\n\n\nBreast cancer is not a single disease, but a collection of several subtypes, each with its unique characteristics, prognosis, and treatment options.It can be classified based on its origin cell type such as:\n\n\n- **Invasive ductal carcinoma (IDC)**: This is the most common type, accounting for about 80% of all breast cancers. It starts in a milk duct, breaks through the wall of the duct, and invades the fatty tissue of the breast.\n- **Invasive lobular carcinoma (ILC)**: This type begins in the milk-producing glands (lobules) and can spread to other parts of the body.\n- **Ductal carcinoma in situ (DCIS)**: This is a non-invasive or pre-invasive cancer where the cells are confined to the ducts in the breast and have not spread into the surrounding breast tissue.\n- **Lobular carcinoma in situ (LCIS)**: This is not a cancer but an area of abnormal cell growth that increases a person's risk of developing invasive breast cancer later.\n- **Paget's disease of breast**: Infiltrating carcinoma of nipple epithelium.\n\n\nIt can also be classified based on the hormone receptors present on the surface of the breast cancer:\n\n- **Inflammatory breast cancer (IBC)**: This is a rare but aggressive type of breast cancer that causes the lymph vessels in the skin of the breast to become blocked.\n\n- **Triple-negative breast cancer (TNBC)**: This type lacks estrogen receptors, progesterone receptors, and does not have an excess of the HER2 protein on the cancer cell surfaces. It tends to be more aggressive and has fewer targeted treatments available.\n\n- **HER2-positive breast cancer**: This is a cancer that tests positive for a protein called human epidermal growth factor receptor 2 (HER2), which promotes the growth of cancer cells. It tends to be more aggressive than other types of breast cancer, but it may respond well to targeted therapies that can block HER2.\n\n\n# Signs and Symptoms\n\n\nCommon clinical manifestations of breast carcinoma include:\n\n\n- Unexplained breast mass in patients aged 30 and above, with or without pain\n- In those aged 50 and older, nipple discharge, retraction/inversion, or other concerning symptoms\n- This can also include eczema-type changes surrounding the nipple as seen in Paget's disease of the breast\n- Skin changes suggestive of breast cancer\n- This includes skin retraction, peau d'orange appearance or ulceration of the skin above an underlying mass.\n- Unexplained axillary mass in those aged 30 and above\n\n\nApproximately 25% of cases are found in routine breast cancer screening (mammography).\n\n\n# Differential Diagnosis\n\n\nWhile an unexplained breast mass is a key indicator of breast carcinoma, it can also represent various other conditions, each characterized by distinct signs and symptoms:\n\n\n- **Fibroadenoma**: Typically presents as a solitary, painless, and well-circumscribed breast lump in young women\n- **Breast Cyst**: Characterized by a round or oval, well-defined, and movable mass. It may be painful and size may vary with the menstrual cycle.\n- **Mastitis**: Typically presents in breastfeeding women, characterized by a painful, warm, red breast often accompanied by systemic symptoms like fever.\n- **Lipoma**: Presents as a soft, mobile, and painless lump.\n\n\n# Breast Cancer Screening in the UK\n\n\nIn the United Kingdom, the NHS Breast Screening Programme provides free breast screening services for all women registered with a GP. The programme invites women between the ages of 50 and 70 for breast screening every three years, with the first invitation to screening usually sent to women before they turn 53.\n\n\nThis screening process involves a mammogram, which is an X-ray of the breasts that can help detect breast cancers early, often before they can be felt. The aim of breast cancer screening is to find cancer at an early stage when treatment is most effective.\n\n\nIn 2018, the age range for screening was extended as part of a trial, and some women were invited for screening from the age of 47 up to the age of 73. Women over 70 can still self-refer for screening every three years.\n\n\n# Investigations\n\nCriteria for 2-week wait:\n\n- Age 30 or more with unexplained breast lump (with or without pain)\n- Age 50 or more with nipple discharge, retraction or other changes\n- Consider a 2-week wait if a patient is 30 or over with skin changes suggestive of breast cancer or an unexplained lump in the axilla\n\nNB: a non-urgent referral should be considered for patients under the age of 30 with an unexplained breast lump.\n\n### Triple Assessment\n\nTriple assessment is used to investigate suspected breast carcinoma:\n\n\n1. Clinical examination: of the breast and surrounding lymph nodes\n2. Radiological examination:\n\t- Ultrasound is used for women under the age of 40 or those with higher breast density.\n\t- A mammogram is commonly used for women over 40 years.\n\t- If there are concerns of metastatic disease, a CT or PET scan may be done.\n3. Biopsy: often a core needle biopsy or fine needle aspirate (FNA)\n\t- Fine needle aspiration (FNA): Often combined with mammography, however, has a high rate of false negatives.\n\t- Core needle biopsy: method of choice, can be combined with imaging to aid accuracy.\n\t- DCIS biopsy will show cellular atypia and hyperchromatic nuclei involving the ducts, but not passing the basement membrane\n\t- In invasive breast cancer, these abnormal cells will pass the basement membrane\n\t- In lobular carcinoma, the abnormal cells will be found within the lobular acini\n\n### Further Investigations\n\nFollowing the triple assessment, further investigations will include:\n\n- Biopsies to determine\n- Oestrogen and progesterone receptor status\n- Epidermal growth factor receptor status\n- Routine blood tests (i.e. LFTs)\n- CXR\n- MRI is not routinely used. It is used for women with:\n- Discrepancy between the extent of disease between clinical examination and imaging\n- Dense breast tissue limiting mammography\n- Invasive lobular carcinoma to evaluate tumour size when planning breast-conserving surgery\n- BRCA1/2 testing is done for women < 50 years with triple-negative breast cancer regardless of family history\n\n\n### Staging\n\nStaging involves the TNM system considering the size of the tumour (T), the spread to the lymph nodes (N), and the presence of metastases (M). For locally invasive breast cancer, this can include:\n\n- Axilla ultrasound with needle sampling if abnormal lymph nodes are identified\n\nIf the cancer is deemed to be advanced, staging investigations should include:\n\n- CT, MRI or bone scintigraphy to determine the presence and extent of visceral and bony metastasis\n- PET CT is only used to diagnose metastasis\n\n\n# Management\n\n\nThe management strategy for breast carcinoma can vary based on several factors including the subtype of carcinoma, stage, hormonal receptor status, and the patient's overall health and preferences.\n\n\n- Surgical management: Wide local excision (WLE) or mastectomy, with sentinel node biopsies for invasive cancers and possible axillary node clearance for positive nodes. Breast reconstruction can be done concurrently or later.\n- Radiotherapy: Adjuvant radiotherapy is commonly offered following WLE to reduce recurrence. It may also be given to patients with higher-stage cancers post-mastectomy.\n\n**Chemotherapy:**\n\n- Suggested for hormone receptor-negative and HER2 over-expressing patients. Neoadjuvant chemotherapy may be given to downstage tumours before surgery. This commonly includes an anthracycline (i.e. doxorubicin) and a taxane (i.e. paclitaxel)\n- Biological Therapy:\n\t- Trastuzumab (Herceptin) should be given to HER2-positive patients with tumour size T1c and above in combination with surgery, chemotherapy and radiotherapy. Patients should have regular cardiac function assessments.\n\t- Abermaciclib (selective inhibitor of cyclin-dependent kinases 4 and 6) for HER2-negative, hormone receptor-positive breast cancer\n\t- Pembrolizumab for triple-negative breast cancer\n\t- Olaparib (PSTP inhibitor) for BRCA positive, HER2 negative high-risk early breast cancer\n- **Hormonal Therapy** for oestrogen-positive breast cancer:\n\t- Anastrozole (aromatase inhibitor) for postmenopausal women\n\t- Tamoxifen (oestrogen receptor antagonist) for premenopausal patients\n\t- Bisphosphonates: May be used for reducing occurrence in node-positive cancers.\n\t- Zoledronic acid has been shown to improve disease-free survival in postmenopausal women with node-positive invasive breast cancer.\n\t- Bisphosphonates are also advised for treatment-induced menopause in women treated with aromatase inhibitors\n\n\n# Complications\n\n### Complications of Breast Carcinoma\n\n- Fatigue\n- Bone metastases\n- Brain metastases\n- Psychological difficulties: Anxiety, depression and damage to the individual's self-esteem.\n- Recurrence:\n\t- Local: recurrence in the same breast as the original tumour\n\t- Regional: recurrence in the axillary or sub-clavicular lymph nodes draining the breast cancer\n\t- Distant: recurrence once already metastasized to other parts of the body (i.e. liver, lungs, brain, bone)\n\n\n### Side Effects of Medication Used to Treat Breast Cancer\n\n\nTreatment for breast cancer often involves medication, including chemotherapy, hormone therapy, and targeted drug therapy. Each of these can have different side effects.\n\n\n**Chemotherapy** drugs are powerful medications that aim to destroy rapidly dividing cells, such as cancer cells. However, they can also affect healthy cells, leading to a range of side effects, including fatigue, hair loss, easy bruising and bleeding, infection, anaemia, nausea and vomiting, appetite changes, peripheral neuropathy, and problems with concentration or memory.\n\nChemotherapy agents can have specific side effects such as:\n\n- Doxorubicin is associated with cardiac toxicity (e.g. cardiac arrhythmias, myopericarditis)\n- Paclitaxel is associated with lung fibrosis.\n\n\n**Hormone therapy** drugs, such as tamoxifen and aromatase inhibitors, are used to treat hormone receptor-positive breast cancers. Common side effects include hot flushes, vaginal dryness or discharge, menstrual changes, fatigue, mood changes, and osteoporosis. In rare cases, tamoxifen can increase the risk of serious conditions like endometrial cancer and blood clots.\n\n\n**Targeted drug therapies** such as trastuzumab (Herceptin), pertuzumab (Perjeta), and ado-trastuzumab emtansine (Kadcyla), are designed to interfere with specific proteins or processes that contribute to cancer growth.\n\nSide effects include:\n\n- Infections\n- Bruising and easy bleeding\n- Anaemia\n- Cardiac (i.e. arrhythmias)\n- Insomnia\n- GI side effects (i.e. diarrhoea, vomiting, constipation, appetite loss, weight loss)\n- Runny nose\n- Conjunctivitis\n- Hair loss\n- Nail changes\n- Hand foot syndrome: the palms and plantar surfaces become sore, peel, crack and blister.\n- Hepatotoxicity\n\n\n\n### Surgical Complications\n\nKey surgical complications include:\n\n- Venous thromboembolism\n- Lymphoedema\n- Pain\n\n\n### Breast Cancer in Pregnancy\n\nBreast cancer is the most common malignancy to occur during pregnancy. Radiotherapy and chemotherapy are most commonly delayed until completion of pregnancy, but surgical intervention can be considered.\n\n# Prognosis\n\nThe prognosis for individuals with breast cancer has vastly improved, almost doubling over the past 50 years. The ten-year survival for breast cancer in England is 75.9%\n\nA poorer prognosis is associated with:\n\n- Advancing age\n- Being male\n- Stage III or IV\n- Tumour size\n- Tumour grade\n- Hormone receptor-negative tumours (oestrogen or progesterone receptor-negative)\n- HER 2 positive tumours\n\n\n# NICE Guidelines\n\n[NICE Guidelines on Early and Locally Advanced Breast Cancer](https://www.nice.org.uk/guidance/ng101)\n\n[NICE Guidelines on Advanced Breast Cancer](https://www.nice.org.uk/guidance/cg81)\n\n# References\n\n[Patient Info Breast Cancer](https://www.nice.org.uk/guidance/cg81)\n\n[BMJ Best Practice Breast Cancer](https://bestpractice.bmj.com/topics/en-gb/718?q=Metastatic%20breast%20cancer&c=suggested)\n\n[NHS Breast Cancer in Women](https://www.nhs.uk/conditions/breast-cancer-in-women/)\n\n[Cancer Research UK Breast Cancer](https://www.cancerresearchuk.org/about-cancer/breast-cancer/survival)",
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"question": "A 37-year-old woman presents to the triple assessment breast clinic following a GP referral regarding a new breast lump. She denies itching, bleeding, or abnormal nipple discharge. On examination, she has a 1.5cm breast lump in the 7 o'clock position in the left breast. There are no palpable axillary lymph nodes. An axillary ultrasound scan shows no evidence of axillary lymphadenopathy. Tissue biopsy shows evidence of an invasive ductal carcinoma and the breast cancer is triple-negative for oestrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2. A subsequent staging CT scan of the chest, abdomen, and pelvis confirms no distant metastases.\n\nWhich of the following is the next best step in the management of this patient?",
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"explanation": "A displaced apex beat can occur in a variety of conditions that result in left ventricular dilation, including a volume overloaded left ventricle as in mitral or aortic regurgitation, chronic right-left shunt, eventual decompensation in concentric hypertrophy secondary to pressure overload, or dilated cardiomyopathy. This patient may develop a displaced apex beat, but it is not specific.",
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"explanation": "This patient has aortic regurgitation caused by infective endocarditis, as indicated by the presence of fever and a new murmur. Her risk factors include current intravenous drug use. De Musset's sign is a rhythmic head nodding or bobbing in-sync with each heart beat, which is associated with aortic regurgitation. She also has a wide pulse pressure, which is also associated with aortic regurgitation. This patient should have an urgent echocardiogram.",
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"comment": "Could the subcutaneous painless nodules not be Janeway lesions (i.e. supportive of endocarditis)?",
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"comment": "May be being pedantic but think the question may benefit from some rephrasing: \"Which clinical sign is most likely to be seen in this patient?\". \n\nThe question asks for the a specific sign for the diagnosis. The diagnosis is infective endocarditis, not aortic regurgitation (which has other causes).",
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"explanation": "# Summary\r\n\r\nInfective endocarditis (IE) is a rare infection of the inner surface of the heart (endocardium), usually the valves. Various risk factors contribute to its development, including age, sex, intravenous drug use, poor dentition, valvular disease, congenital heart disease, prosthetic valves, and certain medical conditions like HIV. Symptoms can be diverse and non-specific including fevers, night sweats, weight loss, and myalgia. Diagnosis is based on the modified Duke Criteria, which include major and minor criteria. Treatment involves prolonged courses of intravenous antibiotics, and surgical intervention may be necessary in certain cases. Complications can be severe, and without appropriate treatment, IE can lead to heart failure and death. Prevention through antibiotic prophylaxis is no longer recommended.\r\n\r\n# Definition \r\n\r\nInfective endocarditis (IE) is the infection of the inner surface of the heart (endocardium), usually the valves. \r\n\r\n# Epidemiology \r\n\r\nInfective endocarditis is a rare disease, impacting approximately 2-6 per 100,000 people every year. There are many risk factors implicated in the development of IE. \r\n\r\nRisk factors for IE: \r\n\r\n* Age >60 years\r\n* Male sex\r\n* IVDU: predisposition to _Staph. aureus_ infection and right-sided valve disease e.g. tricuspid endocarditis.\r\n* Poor dentition and dental infections\r\n* Valvular disease: rheumatic heart disease, mitral valve prolapse, aortic valve disease and any other valvular pathology. \r\n* Congenital heart disease: bicuspid aortic valve, pulmonary stenosis, and ventricular septal defects.\r\n* Prosthetic valves\r\n* Previous history of infective endocarditis\r\n* Intravascular devices: central catheters and shunts.\r\n* Haemodialysis\r\n* HIV infection\r\n\nAntibiotics have previously been prescribed to at-risk patients undergoing interventional procedures, frequently in dentistry, with the rationale that resultant bacteraemia could threaten to cause infective endocarditis. However, the evidence for this is inconclusive, and **NICE therefore do not advise antibiotic prophylaxis for IE.**\r\n\r\n# Pathophysiology\r\n\r\nA damaged endocardium can contribute to the development of IE. When part of the endocardium is damaged, the heart valve forms a local blood clot known as non-bacterial thrombotic endocarditis (NBTE). The platelets and fibrin deposits that form as part of the clotting process allows bacteria to stick to the endocardium leading to the formation of vegetations. The valves do not have a dedicated blood supply and so the body is unable to launch an appropriate immune response to the vegetations. The combination of damaged endocardium, vegetation development, and lack of an appropriate immune response results in infective endocarditis. \r\n\r\n# Classification \r\n\r\nIE can be considered according to different classification systems. \r\n\r\n## Acute vs. Subacute vs. Chronic IE \r\n\r\nIE can be considered according to duration of symptoms. \r\n\r\n* *Acute IE*: patient has signs or symptoms for days up to 6 weeks. Theoretically, a fulminant illness with rapid progression and so is most likely due to *S.aureus* infection. \r\n* *Subacute IE*: patients has signs or symptoms for 6 weeks up to 3 months. \r\n* *Chronic IE*: patients has signs or symptoms that persist for longer than 3 months. \r\n\r\n## Valve Type \r\n\r\nIE can be considered according to the type of valve involved. \r\n\r\n- *Native-valve endocarditis*: patient without prosthetic valve implant. \r\n- *Prosthetic-valve endocarditis*: \r\n\t- Early prosthetic valve endocarditis occurs within 1 year of surgery. This is usually due to intra-operative contamination or post-operative nosocomial contamination. \r\n\t- Late prosthetic valve endocarditis occurs beyond 1 year of surgery. This is usually due to community-acquired infections. \r\n\r\n# Common organisms \r\n\r\nThe most common organisms involved in infective endocarditis (in order of incidence) are:\r\n\r\n* _Staph. aureus_: now the most common cause of IE. Coagulase positive.\r\n* _Strep. viridans_: used to be the most common cause of IE. Implicated in patients with poor dental hygiene. \r\n* Enterococci\r\n* Coagulase negative _staphylococci_ e.g. _staph. epidermidis_: common culprit of prosthetic valve endocarditis. \r\n* _Strep. bovis_: important link with colorectal cancer. Need to consider colonoscopy and biopsy in these patients.\r\n* Fungal \r\n* HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella): culture negative causes of IE. \r\n* Non-infective: marantic endocarditis (malignancy - pancreatic cancer), Libman-Sacks endocarditis (SLE). \r\n\r\n# Symptoms\r\n\r\nClinical features of IE are diverse and variable. It may present acutely with a rapid deterioration or it can present subacutely/chronically with non-specific symptoms. \r\n\r\n* Common presenting symptoms: \r\n\t* Fever: most common symptom. \r\n\t* Night sweats \r\n\t* Anorexia \r\n\t* Weight loss \r\n\t* Myalgia\r\n\r\n* Others: \r\n\t* Headache \r\n\t* Arthalgia\r\n\t* Abdominal Pain \r\n\t* Cough \r\n\t* Pleuritic pain \r\n\r\n# Signs\r\n\r\n**Systemic signs**: \r\n\r\n* Febrile \r\n* Cachectic \r\n* Clubbing\r\n* Splenomegaly \r\n\r\n**Cardiac**: \r\n\r\n* Murmur: fever + new murmur is infective endocarditis until proven otherwise. \r\n* Bradycardia: aortic root abscess tracks down to the AVN causing heart block. \r\n\r\n**Vascular phenomena**: \r\n\r\n* Septic emboli: abdominal pain due to splenic infarct/abscess, focal neurology due to stroke, gangrenous fingers. \r\n* Janeway lesions: painless haemorrhagic cutaneous lesions in the palms and soles. \n* Splinter haemorrhages\r\n\r\n**Immunological phenomena**: due to immune-complex deposition. \r\n\r\n* Osler's nodes: painful pulp infarcts on end of fingers. \r\n* Roth spots: boat-shaped retinal haemorrhages with pale centres seen on fundoscopy. \r\n* Glomerulonephritis: identified on urine dip. \r\n\r\n# Differential Diagnoses\r\n\r\n* Non-infectious endocarditis/Nonbacterial thrombotic endocarditis (NBTE)\r\n\t* Similarities: both present with new murmurs and both may have constitutional symptoms including fevers and weight loss. \r\n\t* Differences: blood cultures will likely be positive in infective endocarditis and may identify microorganisms that are commonly associated with IE. NBTE is often associated with advanced malignancy (pancreatic cancer and marantic endocarditis), SLE (Libman Sacks endocarditis) or hypercoagulable states and will not have positive blood cultures. \r\n\r\n* Rheumatic Fever\r\n\t* Similarities: may both present with similar symptoms including fever, heart murmur and joint pain. \r\n\t* Differences: rheumatic fever is an autoimmune response triggered by a Group A strep infection and ASOT titres may be high. In comparison, infective endocarditis will likely have positive blood cultures that identify a particular micro-organism. \r\n\r\n\r\n# Modified Duke Criteria \r\n\r\nFor the diagnosis of IE, the modified Duke Criteria needs to be followed. \r\n\r\nA useful mnemonic to remember the criteria is **'BE FIVE PM'**:\r\n\r\n* Major Criteria: \r\n\t* **B**lood Cultures\r\n\t* **E**vidence of Endocardial Involvement: **E**cho\r\n\r\n* Minor Criteria: \r\n\t* **F**ever\r\n\t* **I**mmunological phenomena\r\n\t* **V**ascular phenomena\r\n\t* **E**chocardiogram minor criteria\r\n\t* **P**redisposing features\r\n\t* **M**icrobiological evidence that does not meet major criteria. \r\n\r\nFor a definitive diagnosis of IE two major criteria, or one major and three minor criteria, or all five minor criteria must be present. \r\n\r\n## Major Criteria \r\n\r\n**Blood culture positive for IE**\r\n\r\n* 2x separate positive blood cultures showing typical microorganisms consistent with IE (S viridans, S bovis, HACEK organisms, enterococcus). \r\n* Persistent bacteraemia with 2x blood cultures >12 hours apart or =>3 positive blood cultures with less specific microorganisms (S.aureus or S. epidermidis). \r\n* Single positive blood culture for Coxiella burnetti or positive antibody titre\r\n\r\n**Evidence of endocardial involvement with imaging positive for IE**\r\n\r\n* Echocardiogram (1st line TTE, then TOE) demonstrating vegetation, abscess, partial dehiscence of prosthetic valve or new valvular regurgitation. \r\n* Abnormal activity around site of prosthetic valve implantation on PET-CT\r\n* Paravalvular lesions on cardiac CT\r\n\r\n## Minor Criteria \r\n\r\n* **Fever**: >38.0 degrees celsius. \r\n* **Immunological phenomena**: Roth spots, Olser's nodes, immune complex-mediated glomerulonephritis, positive rheumatoid factor.\r\n* **Vascular phenomena**: Evidence of septic embolis (splenic infarct/abscess), Janeway lesions, conjunctival haemorrhages, mycotic aneurysm, intracranial haemorrhage. \r\n* **Echocardiogram minor criteria**: not meeting above criteria. \r\n* **Predisposing features**: known valvular disease, IVDU, prosthetic valves etc. \r\n* **Microbiological evidence that does not meet major criteria**: blood culture not meeting major criteria, or serological evidence of active infection with organism consistent with IE\r\n\r\n# Investigations\r\n\r\nBedside:\r\n\r\n- **ECG**: increasing prolongation of PR interval suggests development and worsening of aortic root abscess. \n- **Urine dip**: look for haematuria which may suggest development of glomerulonephritis. \r\n\r\nBlood tests:\r\n\r\n- **Routine bloods**: significant elevation of inflammatory markers and acute phase response is in line with infective endocarditis. If subacute/chronic process there may be a normocytic anaemia. \r\n- **Blood cultures**: required as per the modified Duke criteria. At least 3 sets of blood cultures taken at different times and sites. \r\n\r\nImaging:\r\n\r\n- **Echocardiogram**: \r\n\t* **1st line**: transthoracic echocardiogram \r\n\t* **2nd line**: transoesophageal echocardiogram; more invasive, but better view of mitral valve lesions and aortic root abscesses. It is the most sensitive diagnostic test. \r\n- **PET CT**: used to look for evidence of septic emboli. \r\n\r\n# Management\r\n\r\n## Medical \r\n\r\nMainstay of treatment for infective endocarditis is a prolonged course of IV antibiotics (approximately 6/52). Patients commonly require midline insertion to enable administration of IV antibiotics long-term. \r\n\r\nExamples of antibiotic choice demonstrated below: \r\n\r\n**Blind Therapy** when the organism and sensitivities are not yet known: \r\n\r\n* Native valve: amoxicillin (+/- gentamicin) \r\n* Pen-allergy/MRSA: vancomycin (+/- gentamicin) \r\n* Prosthetic valve: vancomycin + rifampicin + gentamicin \r\n\r\n**Native Valve S. aureus IE**\r\n\r\n* 1st line: flucloxacillin \r\n* 2nd line: vancomycin + rifampicin \r\n\r\n**Prosthetic Valve S. aureus IE**\r\n\r\n* 1st line: flucloxacillin + rifampicin + gentamicin \r\n\r\n\r\n**Strep viridans IE**\r\n\r\n* 1st line: benzylpenicillin \r\n* 2nd line: vancomycin + gentamicin \r\n\r\n**HACEK IE**: 1st line: ceftriaxone \r\n\r\n## Surgical \r\n\r\nDespite the main-stay of treatment for IE being medical management. The following scenarios are indications for surgical intervention: \r\n\r\n* Haemodynamic instability\r\n* Severe heart failure\r\n* Severe sepsis despite antibiotics/failed medical therapy\r\n* Valvular obstruction\r\n* Infected prosthetic valve\r\n* Persistent bacteraemia\r\n* Repeated emboli\r\n* Aortic root abscess\r\n\r\n**Common exam question**: PR interval prolongation in a patient with Infective Endocarditis is an indication for surgery as it can be secondary to aortic root abscess\r\n\r\n# Complications\r\n\r\nComplications of infective endocarditis can also be the initial presenting complaint\r\n\r\n* Acute valvular insufficiency causing heart failure\r\n* Neurologic complications e.g. stroke, abscess, haemorrhage (mycotic aneurysm)\r\n* Embolic complications causing infarction of kidneys, spleen or lung\r\n* Infection e.g. osteomyelitis, septic arthritis\r\n\r\n\r\nWithout timely and appropriate treatment, IE can rapidly lead to heart failure and death. The mortality rate within the first 30 days has been estimated at approximately 20%. Long-term survival for IE has been estimated at 50% at 10 years. The mortality in IE remains high. \r\n\r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines on Prophylactic Antibiotics in IE](https://www.nice.org.uk/guidance/cg64/ifp/chapter/infective-endocarditis)\r\n\r\n# References \r\n\n[American Heart Association Summary on Heart Valves and Endocarditis](<https://www.heart.org/en/health-topics/heart-valve-problems-and-disease/heart-valve-problems-and-causes/heart-valves-and-infective-endocarditis#:~:text=What%20is%20infective%20endocarditis%3F,greater%20risk%20of%20developing%20it.>)",
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"question": "A 34-year-old woman presents to A&E with a three day history of fevers and joint pains. She denies any unwell contacts. She has a history of intravenous drug use but no other past medical history. Her vital signs are: HR 101bpm, RR 17 breaths per minute, O2 saturations of 98% on air, BP 157/61mmHg, and temperature 39.5. On examination, there is an early diastolic murmur on auscultation of the aortic area.\n\nWhich of the following clinical signs is specific to his diagnosis?",
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173,459,030 | false | 88 | null | 6,494,981 | null | false | [] | null | 10,723 | {
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"explanation": "This is a sensible and potentially useful option, but it is not the best next step in management, since the oral glucose tolerance test at 24-28 weeks will detect cases of gestational diabetes more sensitively than routine glucose monitoring at home.",
"id": "53314",
"label": "c",
"name": "Advise patient to self-monitor their own blood glucose levels at home",
"picture": null,
"votes": 336
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "An immediate oral glucose tolerance test at booking is offered in patients with previous gestational diabetes. If this is normal, then it is repeated at 24-28 weeks. This is the patient's first pregnancy and so she has never been diagnosed with gestational diabetes in the past.",
"id": "53313",
"label": "b",
"name": "Offer an oral glucose tolerance test immediately",
"picture": null,
"votes": 624
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"answer": true,
"explanation": "This patient is at risk for developing gestational diabetes as she has a BMI greater than 30kg/m². All patients with a risk factor should be offered an 2 hour 75g OGTT at 24-28 weeks. As per NICE guidelines, other risk factors include a previous macrosomic baby weighing 4.5kg or above, previous gestational diabetes, a first-degree relative with diabetes, or minority ethnic family origin with a high prevalence of diabetes. It is important to diagnose gestational diabetes early in order to get good control, to reduce risk of foetal macrosomia, neonatal hypoglycaemia, and shoulder dystocia. NICE suggests a diagnosis of gestational diabetes can be made if: a fasting blood sugar is 5.6 mmol/litre or above, or a 2-hour plasma glucose level is 7.8 mmol/litre or above",
"id": "53312",
"label": "a",
"name": "Offer an oral glucose tolerance test at 24 weeks",
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"votes": 3360
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Metformin may be used used if gestational diabetes is confirmed, which is not the case at present in this patient. Lifestyle advice is offered first in patients with gestational diabetes, and if adequate glucose targets are not met within 1-2 weeks, metformin is started. Insulin is the next step or alternative if metformin cannot be used.",
"id": "53315",
"label": "d",
"name": "Start metformin",
"picture": null,
"votes": 52
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This may be a suitable plan if the patient had confirmed gestational diabetes. However, in this case, the diagnosis has yet to be confirmed.",
"id": "53316",
"label": "e",
"name": "Advise patient regarding diet and exercise, and prescribe insulin",
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"comment": "Worth noting that those with previous gestational diabetes also have an OGTT at booking, since neither the explanation or notes clarify this...",
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"comment": "Can you diagnose T2D in pregnant patients? ",
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"comment": "pretty sure its just gestational diabetes at that point ",
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"explanation": "# Summary\n\nGestational Diabetes Mellitus (GDM) is a condition of glucose intolerance that begins or is first detected during pregnancy, leading to insulin resistance. It affects approximately 5% of pregnancies and poses an increased risk of type 2 diabetes development. The condition is more prevalent among women from ethnic backgrounds with a high prevalence of type 2 diabetes, those with a previous history of GDM, and obese women. GDM may lead to complications such as macrosomia, shoulder dystocia, pre-term delivery, neonatal respiratory distress syndrome, and maternal hypertension, including perinatal complications. Management strategies typically involve a low glycemic index diet, regular physical activity, medication (metformin or insulin) based on specific glucose levels, and postpartum glucose testing to ensure resolution.\n\n\n# Definition \n\nGestational Diabetes Mellitus (GDM) is defined as glucose intolerance with fasting blood glucose levels equal to or above 5.6 mmol/L or 2-hour plasma glucose levels equal to or above 7.8 mmol/L on a 75g Oral Glucose Tolerance Test (OGTT).\n\n\n# Epidemiology\n\nApproximately 5% of pregnancies are affected by GDM. Women diagnosed with GDM have an increased risk of developing type 2 diabetes, with up to a 50% chance within 5-10 years postpartum.\n\n\n# Risk Factors\n\n\n\n- Ethnic backgrounds with a high prevalence of type 2 diabetes (e.g., Middle Eastern, South Asian, and Afro-Caribbean)\n- Prior history of GDM\n- Prior delivery of macrosomic babies (>4.5kg)\n- History of stillbirth or perinatal death\n- Maternal obesity (BMI>30)\n- Diabetes in first-degree relatives\n\n\n# Signs and Symptoms\n\n\n\nGDM often presents with no noticeable symptoms. However, some women may experience:\n\n- Polyuria\n- Thirst\n- Fatigue\n\n\n# Differential Diagnosis\n\n\n- Type 1 or Type 2 Diabetes Mellitus: Generally presents with symptoms outside of pregnancy, including potential weight loss\n- Other forms of gestational hyperglycaemia: These can be identified through early pregnancy HbA1c testing\n\n# Investigations\n\n\nDiagnosis of GDM is based on a 75g OGTT:\n\n- Fasting blood glucose level (fasting glucose ≥5.6 mmol/L)\n- 2-hour plasma glucose level (2-hour glucose ≥7.8 mmol/L)\n\nThis can be remembered as 'diagnosis of GDM is as easy as 5678'\n\nAdditional tests may include:\n\n- HbA1c: Helpful in distinguishing between gestational and pre-existing diabetes early in pregnancy\n- Urinalysis: To check for glycosuria\n\n# Foetal Complications\n\n- Macrosomia (birthweight >4kg): Excess maternal glucose crossing the placenta and inducing increased fetal insulin production can lead to macrosomia, increasing the risk of shoulder dystocia, birth injuries, and emergency caesarean section\n- Increased risk of sacral agenesis in the developing foetus\n- Pre-term delivery: May cause neonatal respiratory distress syndrome\n- Neonatal hypoglycaemia: High fetal insulin levels after delivery may lead to hypoglycaemia, which if severe, may result in seizures in the baby\n- Long-term risk: Increased risk of the baby developing type 2 diabetes later in life\n\n# Maternal Complications\n\n- Increased risk of hypertension and pre-eclampsia\n- Future risk: Increased risk of developing type 2 diabetes and GDM in subsequent pregnancies\n\n# Management\n\nManagement of GDM depends on specific glucose levels:\n\n- Lifestyle modifications, such as adopting a low glycemic index diet and regular physical activity, are the initial approach when fasting glucose levels are <7 mmol/L.\n\t- If blood glucose targets are not met with diet and exercise changes within 1 to 2 weeks, offer metformin.\n- If fasting glucose levels are ≥7 mmol/L, insulin therapy with or without metformin is often the first-line treatment.\n- Advise pregnant women with any form of diabetes to maintain their capillary plasma glucose below the following targets, if these are achievable without causing problematic hypoglycaemia:\n\t- Fasting: 5.3 mmol/litre\n\t- 1 hour after meals: 7.8 mmol/litre\n\t- 2 hours after meals: 6.4 mmol/litre\n- Postpartum management includes glucose testing to ensure resolution of GDM and long-term follow-up due to the increased risk of future type 2 diabetes.\n\n\n# NICE Guidelines\n\n[NICE CKS on Gestational Diabetes](https://www.nice.org.uk/guidance/ng3)\n\n",
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"question": "A 27-year-old pregnant female presents to the maternity unit for her booking appointment. This is her first pregnancy and she is currently fit and well. She has no significant past medical history and is currently taking folic acid tablets daily. Her height and weight is recorded by the nurse and her body mass index (BMI) is calculated as 32kg/m². Her fasting blood sugar is 5.2 mmol/litre (3.5-5.5 mmol/L).\n\n\nWhich of the following is the next best step in the management of this patient?",
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"explanation": "A pulmonary embolism is an important differential for post operative hypoxia, especially in the context of orthopaedic patients where mobility may be dramatically reduced. However, pulmonary emboli usually present later in the post-operative period, with the highest risk being 1-5 weeks after an operation. This is since it takes time for the deep vein thrombus to form. Furthermore, pulmonary emboli are not associated with petechial rashes.",
"id": "53318",
"label": "b",
"name": "Pulmonary embolism",
"picture": null,
"votes": 236
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Atelectasis post operatively may result in lung collapse and respiratory distress. It is a good differential diagnosis, but the presence of equal breath sounds, a central trachea (which may be deviated in a collapse), and a petechial rash, make this less likely.",
"id": "53321",
"label": "e",
"name": "Atelectasis",
"picture": null,
"votes": 76
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"explanation": "Compartment syndrome presents with pain out of proportion to any clinical signs and passive stretch in the early stages. Progression leads to pallor, pulselessness, and paraesthaesia as the bloody supply to the limb is compromised. The pain typically does not responding to any analgesia. This can occur after limb trauma because muscle swelling and inflammation increases the pressure in the muscle compartment. This is an orthopaedic emergency which must be diagnosed and treated immediately as it can potentially result in loss of blood supply to the limbs if untreated. Patients with compartment syndrome would not present primarily with respiratory distress as in this case.",
"id": "53319",
"label": "c",
"name": "Compartment syndrome",
"picture": null,
"votes": 79
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"__typename": "QuestionChoice",
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"explanation": "A pneumothorax is an important differential to exclude in this context, especially after trauma. It is likely this patient would have had a trauma series CT scan performed on presentation, which would image the thorax, and he would also likely get repeat chest imaging after being observed to be more short of breath during the ward round to rule this out. However, given the equal breath sounds on clinical examination and the presence of a petechial rash, this is unlikely. A tension pneumothorax may present with haemodynamic instability and shock, and warrants immediate needle decompression without delay. This patient has a central trachea, making this unlikely.",
"id": "53320",
"label": "d",
"name": "Pneumothorax",
"picture": null,
"votes": 31
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"explanation": "A fat embolism is a potential complication of long bone fractures. Patients present with respiratory distress, a petechial rash, and haemodynamic instability. It may occur 24-72 hours after the initial injury. Management is supportive.",
"id": "53317",
"label": "a",
"name": "Fat embolism",
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"explanation": "# Summary\n\nFat embolism refers to a medical condition characterized by the entry of fat fragments into the systemic circulation, subsequently lodging in the small vessels of the lungs or other tissues. This typically occurs due to fractures, especially long bone fractures. Clinical manifestations vary depending on the site of embolism, with breathlessness being a common symptom in pulmonary fat embolism. Investigations may include radiographic imaging and serum markers. The mainstay of management is supportive care, focused on oxygenation and symptomatic relief.\n\n# Definition\n\nFat embolism is a clinical syndrome resulting from the dissemination and subsequent lodgment of fat droplets or fat globules in the small vessels of the systemic and/or pulmonary circulation. This event typically follows trauma, particularly fractures of long bones or pelvic bones, but it can also occur after non-traumatic events such as orthopedic surgery or severe burns.\n\n# Epidemiology\n\nThe incidence of fat embolism varies and is largely dependent on the context. It is estimated to occur in 1-3% of all long bone fractures, but the incidence can be as high as 10-30% in patients with polytrauma or after major orthopedic surgeries. Fat embolism syndrome, a severe manifestation of fat embolism characterized by multisystem involvement, is estimated to occur in approximately 10% of all cases of fat embolism.\n\n# Aetiology\n\nThe aetiology of fat embolism generally involves:\n\n- Trauma, particularly long bone and pelvic fractures\n- Non-traumatic events such as orthopedic surgeries (hip or knee arthroplasty)\n- Severe burns\n- Liposuction\n- Prolonged corticosteroid therapy\n\n# Signs and Symptoms\n\nThe signs and symptoms of fat embolism are largely determined by the site of embolization:\n\n- Pulmonary: Breathlessness, hypoxia, tachycardia, tachypnea, and fever\n- Neurologic: Altered mental status, seizures, focal deficits, or coma\n- Dermatologic: Petechial rash predominantly on the upper body\n\n# Differential Diagnosis\n\nDifferential diagnosis for fat embolism includes conditions that present similarly such as:\n\n- Pulmonary embolism: Presents with sudden onset shortness of breath, chest pain, and hemoptysis.\n- Acute respiratory distress syndrome (ARDS): Presents with severe shortness of breath, rapid breathing, and bluish skin coloration (cyanosis).\n- Pneumonia: Presents with cough (often productive), fever, shortness of breath, and chest discomfort.\n- Sepsis: Presents with fever, increased heart rate, increased respiratory rate, and confusion.\n\n# Investigations\n\nThe diagnosis of fat embolism is typically clinical, supported by relevant investigations:\n\n- Imaging studies: Chest X-ray may reveal diffuse bilateral infiltrates; CT of the chest may show fat within the vessels.\n- Laboratory tests: Serum markers such as fat macroglobulinemia, increased serum lipase, and increased serum LDH.\n- Bronchoalveolar lavage: To identify fat droplets in macrophages.\n\n# Management\n\nManagement of fat embolism is primarily supportive and includes:\n\n- Oxygen therapy: To relieve hypoxia and dyspnea.\n- Fluid resuscitation: To maintain hydration and support circulatory function.\n- Pharmacological therapy: Prophylactic low-molecular-weight heparin may be considered to prevent thromboembolic events.\n- Fracture stabilization: Early immobilization of fractures can reduce the incidence of fat embolism.\n\n# References\n\n- [Ortho Bullets: Fat Embolism Syndrome](https://www.orthobullets.com/basic-science/9055/fat-embolism-syndrome)",
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"question": "A 32-year-old male presents with bilateral fractures of the tibia following a road traffic accident. He undergoes operative management and is reviewed the following day on the ward round. On examination, he is unable to speak in full sentences and is visibly short of breath. There are equal breath sounds bilaterally on chest auscultation and his trachea is central. He has a petechial rash across his body. His vital signs are: HR 120bpm, oxygen saturations 90% on room air, RR of 33, BP 95/43, and temperature 36.5.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "Normal pressure hydrocephalus is a cause of secondary dementia and presents with a triad of urinary incontinence, dementia, and falls. It is treatable by shunting away the excess CSF from the ventricles. This patient does not have these clinical features, but is instead presenting with the characteristic features as associated with Dementia with Lewy Bodies.",
"id": "53325",
"label": "d",
"name": "Normal pressure hydrocephalus",
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"explanation": "Vascular dementia is the second commonest cause cause of dementia after Alzheimer's and presents with a step-wise decline in cognitive function due to accumulation of ischaemic infarcts over time (or small vessel disease.) Risk factors such as hypertension, hypercholesterolaemia, and diabetes should be managed. This patient has none of these risk factors, and the characteristic features are that of Lewy Body Dementia and not vascular dementia.",
"id": "53323",
"label": "b",
"name": "Vascular dementia",
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"explanation": "Parkinson's Disease Dementia and Dementia with Lewy Bodies are on a spectrum with one another, presenting with similar clinical features due to a common pathophysiological basis (alpha synucleinopathy.) If the dementia precedes or begins at the same time as the movement disorder (Parkinsonism), then the diagnosis is Dementia with Lewy Bodies (also known as Lewy Body Dementia), but if the dementia occurs a year or more after the movement disorder/diagnosis of Parkinson's Disease, then the diagnosis is referred to as Parkinson's Disease Dementia.",
"id": "53326",
"label": "e",
"name": "Parkinson's Disease Dementia",
"picture": null,
"votes": 344
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"__typename": "QuestionChoice",
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"explanation": "Alzheimer's disease is the commonest cause of dementia but does not present with movement issues or hallucinations.\nPatients present with gradual loss of memory, difficulty with word-finding, poor recognition of objects and people, and an inability to carry out tasks which require fine motor function.",
"id": "53324",
"label": "c",
"name": "Alzheimer's disease",
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"explanation": "Dementia with Lewy Bodies is a progressive neurodegenerative disorder caused by deposits of alpha-synuclein within the brain. Patients develop cognitive decline, hallucinations (typically of little people or animals, 'Lilliputian bodies'), and Parkinsonism. If the dementia precedes or begins at the same time as the movement disorder (Parkinsonism), then the diagnosis is Dementia with Lewy Bodies (also known as Lewy Body Dementia), but if the dementia occurs a year or more after the movement disorder/diagnosis of Parkinson's Disease, then the diagnosis is referred to as Parkinson's Disease Dementia.",
"id": "53322",
"label": "a",
"name": "Dementia with Lewy bodies",
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"comment": "De mention started 2 years ago and Parkinson’s movements last month. Isn’t this F least a year apart?",
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"explanation": "# Summary\n\nDementia with Lewy bodies (DLB) is a progressive, complex condition, accounting for approximately 10-15% of dementia cases. DLB is characterised by the presence of Lewy bodies, abnormal protein deposits, within brain cells, particularly in the substantia nigra, paralimbic, and neocortical areas. The clinical picture is often characterised by fluctuating cognition, Parkinsonism, and visual hallucinations. A diagnosis is primarily clinical, although dopamine uptake scanning can provide supplementary data. Patients with DLB are highly sensitive to neuroleptics, potentially exacerbating Parkinsonism. \n\n# Definition\n\nDementia with Lewy bodies (DLB) is a type of progressive dementia caused by deposits of an abnormal protein, alpha-synuclein, forming cytoplasmic inclusions known as Lewy bodies within brain cells. These aggregates disrupt normal cell functioning and eventually lead to neuronal death.\n\n# Epidemiology\n\nDLB is the third most common type of dementia, following Alzheimer's disease and vascular dementia. It represents around 10-15% of all dementia cases.\n\n# Aetiology\n\nThe primary pathological feature of DLB is the presence of Lewy bodies in the brain's substantia nigra, paralimbic, and neocortical areas. However, the exact cause of this accumulation remains unknown. An association with Parkinson's disease has been noted, with many patients exhibiting overlapping symptoms. \n\nNew research suggests that LBD and Parkinson’s disease have much more overlap than originally thought. Parkinson’s disease starts in the basal ganglia/brainstem and then progresses upwards towards cerebral cortex (hence dementia is late), whereas in LBD the process progresses downwards from the cerebral cortex.\n\n# Clinical Features\n\nThe clinical features of DLB include:\n\n- Fluctuating cognition: Changes in attention and alertness may occur\n- Parkinsonism: Rigidity, bradykinesia, and postural instability are common\n- Visual hallucinations: Patients often experience complex and recurrent visual hallucinations\n\t- Classically, patients complain of seeing small mammals around them \n- High sensitivity to neuroleptics: These drugs can induce or worsen parkinsonism\n\nA general rule of thumb that can help with distinguishing LBD form Parkinson's disease (PD) is if cognitive impairment and parkinsonism develop <1 year of each other, it is likely LBD. If diagnosed with PD and dementia develops >1 year later this is Parkinson’s disease.\n\n# Differential Diagnosis\n\nDifferential diagnoses for DLB include:\n\n- Alzheimer's disease: Characterised by gradual memory loss, difficulties with problem-solving, and changes in mood or behaviour. However, Alzheimer's patients do not typically exhibit the severe sensitivity to neuroleptics seen in DLB.\n- Parkinson's disease dementia: While it shares many symptoms with DLB, Parkinson's disease dementia typically starts with motor symptoms before cognitive decline. \n- Vascular dementia: This condition features stepwise cognitive decline and evidence of cerebrovascular disease. Parkinsonism and hallucinations are less common.\n\n# Investigations\n\nDiagnosis is primarily clinical, involving a careful medical history and physical examination. However, some additional investigations may be useful, such as:\n\n- Dopamine transporter (DaT) scan: This can help distinguish DLB from other types of dementia.\n- Neuropsychological testing: To assess cognitive functioning and fluctuations.\n- Electroencephalography (EEG): Although not diagnostic, a slowing background rhythm may be seen in DLB.\n\n\n# Management\n\nManagement of DLB includes should follow the biopsychosocial model - please see our Dementia section for holistic management principles.\n\n- Non-pharmacological interventions: These include cognitive stimulation, physical therapy, and occupational therapy.\n- Supportive care: As DLB is a progressive disorder, palliative and end-of-life care considerations are essential.\n- Medications: Cholinesterase inhibitors can help manage cognitive symptoms. However, caution is required with antipsychotic medications due to neuroleptic sensitivity.\n\n\n# NICE Guidelines\n\n[Click here to see information on NICE CKS on dementia](https://cks.nice.org.uk/topics/dementia/)",
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"question": "A 63-year-old woman presents to the GP with her daughter. Her daughter reports a gradual deterioration of her mother's memory over the last two years, which is concerning her. During this time period, her mother has frequently been found to be talking to small children sitting by the foot of the bed, who her daughter cannot see. Over the last month, she has also noticed that her mother's movement has slowed down significantly, which is limiting her mobility, as well as a new resting tremor in her mother's hands. She has no past medical history.\n\nWhich of the following is the most likely diagnosis?",
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173,459,033 | false | 91 | null | 6,494,981 | null | false | [] | null | 10,726 | {
"__typename": "QuestionSBA",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Frontotemporal dementia typically affects patients who are younger than 65 years and causes changes in their behaviour and personality. Memory and visuospatial skills are relatively preserved. This patient has personality change and is young, but frontotemporal dementia is not a feature of Down's syndrome, and Alzheimer's dementia is therefore more likely.",
"id": "53330",
"label": "d",
"name": "Frontotemporal lobe dementia",
"picture": null,
"votes": 1595
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Dementia pugilistica is a type of dementia caused by repetitive head injuries. It is also known as chronic traumatic encephalopathy. It is associated with professions where repeated head injury occurs, such as boxing or playing football. This patient has no history of repeat head injury and this therefore does not represent a likely differential.",
"id": "53331",
"label": "e",
"name": "Dementia Pugilistica",
"picture": null,
"votes": 75
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Depression is an important differential since the loss of sociability may represent anhedonia. However, the verbal aggression and low MMSE are not clinical features of depression and as such, Alzheimer's disease should be considered. In severe depression, a pseudo-dementia type picture may occur, but there are no clinical features here to suggest this patient has a severe depressive illness.",
"id": "53328",
"label": "b",
"name": "Depression",
"picture": null,
"votes": 134
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Delirium is an acute confusional state characterised by fluctuating consciousness. Delirium has several causes which can be remembered with the mnemonic PINCHME: pain, infection, nutrition, constipation, hydration, medications and the environment. It is important to exclude causes of delirium in patients with acute onset confusion. However, in this patient, the decline has been gradual, over months, as opposed to acute.",
"id": "53329",
"label": "c",
"name": "Delirium",
"picture": null,
"votes": 10
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "Patients with Down's syndrome are at a high risk of developing early-onset Alzheimer's disease. This is because they have a greater quantity of amyloid plaques and tau protein within their brain cells at a younger age. Changes in personality and behaviour are especially associated with Alzheimer's disease in the context of Down's syndrome. Note that his MMSE score is less than 27 which indicates there is cognitive decline.",
"id": "53327",
"label": "a",
"name": "Alzheimer's disease",
"picture": null,
"votes": 3111
}
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"__typename": "QuestionComment",
"comment": "Amyloid precursor protein (APP) is found on chromosome 21 (which people with downs have 3 copies of). Hence more amyloid will be made increasing their risk of Alzheimer's",
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"explanation": "# Summary\n\nFrontotemporal dementia (FTD) is a neurodegenerative disorder primarily affecting the frontal and temporal lobes of the brain. It characteristically presents at a younger age compared to other forms of dementia, with early personality changes and language impairments being key signs and symptoms. Investigations often involve neuroimaging and genetic testing, particularly in cases of suspected hereditary conditions. The management of FTD includes symptom-targeted strategies, with behavioural and psychological interventions playing a crucial role. One specific cause of FTD is Pick's disease, characterised by the accumulation of TAU proteins in neurons, identified post-mortem.\n\n# Definition\n\nFrontotemporal dementia (FTD) is a heterogeneous group of neurodegenerative disorders characterised by progressive atrophy of the frontal and/or temporal lobes of the brain, leading to impairments in behaviour, personality, language, and motor functions.\n\n# Epidemiology\n\nFTD is one of the most common forms of early-onset dementia, with the age of onset typically occurring during the sixth or seventh decade of life. The prevalence and incidence rates of FTD vary globally due to genetic and environmental factors.\n\n# Aetiology\n\nThe precise aetiology of FTD is unknown; however, the condition is thought to result from the atrophy of the frontal and temporal lobes of the brain. Genetic mutations can play a role, particularly in familial cases. One specific cause is Pick's disease, characterised by the presence of \"Pick's bodies\" - accumulations of TAU protein within neurons. FTD is associated with ALS - 40% of people with FTD carry same genetic mutation which is commonest cause of ALS.\n\n# Signs and Symptoms\n\nFTD typically presents with:\n\n- Personality changes: Patients often exhibit disinhibited behaviour and apathy early on.\n- Language impairments: Early language difficulties can be present, varying from mild problems with word finding to severe aphasia.\n- Cognitive decline: Although memory may be relatively preserved in the early stages, executive function is frequently impaired.\n- Motor abnormalities: Some patients may develop features of motor neuron disease, including muscle weakness and dysarthria.\n\n# Differential Diagnosis\n\nThe differential diagnosis for FTD includes other forms of dementia and neurological disorders, such as:\n\n- Alzheimer's disease: Characterised by memory loss, confusion, trouble handling money and paying bills, and mood changes. Pathology is defined by the presence of beta-amyloid plaques and neurofibrillary tangles.\n- Vascular dementia: Presents with step-wise cognitive decline, focal neurological signs, and evidence of cerebrovascular disease on neuroimaging.\n- Creutzfeldt-Jakob disease: Rapidly progressive dementia with neurological signs such as myoclonus, ataxia, and visual disturbances. Periodic sharp wave complexes on EEG are suggestive.\n- Primary progressive aphasia: Characterised by gradual, insidious decline in language abilities with relative preservation of other cognitive functions, at least in the early stages.\n\n# Investigations\n\nDiagnosis of FTD often involves:\n\n- Neuroimaging: Structural imaging (MRI or CT) can show atrophy of the frontal and/or temporal lobes. Specifically, MRI can show focal gyral atrophy and knife-blade appearance.\n- Genetic testing: This may be used in cases where an inherited form of FTD is suspected, especially if there is a strong family history.\n\n# Management\n\nThere is currently no cure for FTD; management focuses on alleviating symptoms and providing support. Strategies include:\n\n- Behavioural interventions: Counselling, behaviour modification strategies, and caregiver support can help manage behavioural symptoms.\n- Pharmacotherapy: Selective serotonin reuptake inhibitors (SSRIs) and antipsychotics can help control behavioural symptoms, though their use must be carefully balanced against side effects.\n- There is no good evidence that the cholinesterase inhibitors or memantine help people with FTD, including Pick's disease. In some people they may make symptoms worse.\n- Supportive care: Speech and language therapy, physiotherapy, and occupational therapy can help manage the impacts of the disease on daily functioning.\n \n# NICE Guidelines\n\n[Click here to see information on NICE\nCKS on dementia](https://cks.nice.org.uk/topics/dementia/)",
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"learningPoint": "Individuals with Down's syndrome have an increased risk of early-onset Alzheimer's disease, often presenting with cognitive decline and behavioural changes.",
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"question": "A 51-year-old male presents to the GP with his sister as she has concerns regarding his memory. She says he is getting increasingly forgetful over the past 6 months, with periods of verbal aggression towards her. He is also less interested in socialising. He has a past medical history of Down's syndrome which was diagnose during childhood. On examination, his Mini-mental state examination is 21/30.\n\nWhich of the following is the most likely diagnosis?",
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"a"
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173,459,034 | false | 92 | null | 6,494,981 | null | false | [] | null | 10,727 | {
"__typename": "QuestionSBA",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "ITP is a disorder resulting in an isolated low platelet count and a tendency to bruise/bleed. A purpuric rash may be present but it is not typically palpable. Children may develop ITP post virally and recovery often occurs spontaneously. The additional clinical features here of joint pain and dipstick positive urine suggest an alternative diagnosis.",
"id": "53333",
"label": "b",
"name": "Immune thrombocytopenic purpura (ITP)",
"picture": null,
"votes": 314
},
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "Henoch-Schonlein Purpura is a small vessel vasculitis characterised by IgA deposition. It is associated with nephrotic and nephritic syndromes, as well as a rapidly progressive glomerulonephritis, due to glomerular IgA deposition. It presents with a triad of joint pain, abdominal pain, and palpable purpura.\n\nA typical history involves a recent viral upper respiratory tract infection in a child, followed by the development of the characteristic clinical features. HSP is usually managed supportively as it often resolves spontaneously. Severe renal involvement (for example rapidly progressive, crescentic glomerulonephritis, or persistent nephrotic syndrome), or intractable symptoms not responding to analgesia may necessitate management with steroids.",
"id": "53332",
"label": "a",
"name": "Henoch-Schonlein Purpura",
"picture": null,
"votes": 2906
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Microscopic polyangiitis is a small vessel vasculitis associated with p-ANCA. It is a systemic condition that can affect any organ including the lungs, kidney, skin and nervous system, and may present with a palpable purpuric rash. However, the clinical features here are that of HSP, with a classical triad of abdominal pain, joint pain, and purpura, in a child who has recently recovered from a viral infection.",
"id": "53336",
"label": "e",
"name": "Microscopic polyangiitis",
"picture": null,
"votes": 66
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect because meningitis classically presents with a fever, headache, photophobia and neck stiffness. It can be difficult to elucidate these symptoms in children so it is important to distinguish between a vasculitic rash compared to a non-blanching purpuric rash in meningitis. There is increased awareness and education amongst parents about how to use the glass test to determine if their child's rash is non-blanching.",
"id": "53335",
"label": "d",
"name": "Meningitis",
"picture": null,
"votes": 6
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect because ALL presents with symptoms of anaemia, infection and bleeding. This is secondary to bone marrow failure. It can also present with infiltrative symptoms such as bony pain. It is very important to elucidate any red flag symptoms which point towards cancer such as weight loss or night sweats. The question stem points towards HSP due to the triad of proteinuria, joint pain and a palpable, purpuric rash.",
"id": "53334",
"label": "c",
"name": "Acute lymphoblastic leukaemia (ALL)",
"picture": null,
"votes": 53
}
],
"comments": [
{
"__typename": "QuestionComment",
"comment": "Triad: HSP\n\nHinge pain (arthralgias)\nStomach pain (abdo pain associated w/ intussusception)\nPalpable purpura on buttocks / legs",
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"explanation": "# Summary\n \n\nHenoch-Schonlein Purpura (HSP) is the most common type of small vessel vasculitis in children, particularly in those aged 3-5 years. It is often preceded by a viral upper respiratory tract infection and presents with purpura or petechiae, abdominal pain, arthralgia, and nephritis. Investigations primarily involve physical examination and urine tests. Management strategies involve NSAIDs for analgesia and inflammation control, potential use of antihypertensives for blood pressure management, and long-term renal function monitoring post-episode.\n \n\n# Definition\n \n\nHenoch-Schonlein Purpura (HSP), also known as IgA vasculitis, is an immune-mediated small vessel vasculitis. It predominantly affects children, especially those aged 3-5 years, and is characterised by palpable purpura, arthritis or arthralgia, abdominal pain, and renal disease.\n \n\n# Epidemiology\n \n\nHSP is the most common vasculitis in children. Its peak incidence occurs in the age group of 3-5 years, affecting 10-20 per 100,000 children annually in the UK. The disease is slightly more common in males than females. Many cases occur in the fall and winter months, often following an upper respiratory tract infection.\n \n\n# Aetiology\n\nHSP is the result of IgA immune complex deposition in small blood vessels of the skin, kidneys, joints and gastrointestinal tract.\n \nWhile the exact aetiology of HSP is unknown, it is thought to be immune-mediated. Often, the onset of HSP is preceded by an upper respiratory tract infection, suggesting a potential infectious trigger. Other proposed triggers include medications, vaccinations, and insect bites.\n \n\n# Signs and Symptoms\n \n\nThe primary presentation of HSP includes:\n \n\n - Purpura or petechiae, primarily located on the buttocks and lower limbs\n - Diffuse abdominal pain\n - Arthralgia or arthritis, predominantly in the knees and ankles\n - Renal involvement: Nephritis (haematuria and/or proteinuria)\n - Patients may present with a fever\n - Scrotal pain\n - Often, a history of a recent upper respiratory tract infection\n \n\n# Differential Diagnosis\n \n\nDifferential diagnoses for HSP based on its signs and symptoms include:\n \n\n - **Leukocytoclastic vasculitis**: Presents with palpable purpura, but typically lacks the systemic features of HSP\n - **Idiopathic thrombocytopenic purpura (ITP)**: Presents with petechiae and purpura, but lacks abdominal pain, arthralgia, and renal involvement\n - **Meningococcaemia**: Presents with purpuric rash and fever but also includes symptoms like rapid disease progression, severe illness, and potential neurological symptoms.\n \n\n# Investigations\n \n\nThe diagnosis of HSP is primarily clinical, based on the characteristic presentation and the EULAR criteria:\n\n- Palpable purpura **AND** at least one of the following:\n\n - Diffuse abdominal pain\n - Arthritis or arthralgia \n - Renal involvement\n - Haematuria +/- proteinuria \n - Biopsy showing IgA deposition \n\nHowever, investigations can be used to monitor disease progression and complications:\n \n\n - Urinalysis: To monitor for nephritis (haematuria and proteinuria)\n - Blood pressure: To assess for hypertension secondary to renal involvement\n - Bloods may include U&Es, ESR and creatinine\n - In severe cases, a kidney biopsy may be necessary\n \n\n# Management\n \n\nThe management of HSP involves symptom control and monitoring for complications:\n \n\n - Analgesia and anti-inflammatory effects are typically achieved with paracetamol \n - Avoid Ibuprofen if significant proteinuria or hypertension\n - Prednisolone is not routinely used. It may be used in cases of severe or persistent abdominal or joint pain. \n - Antihypertensives may be needed to control blood pressure in cases of significant renal involvement\n - Following an episode of HSP, regular urine tests and blood pressure monitoring should be conducted for 12 months to monitor for potential renal impairment.\n\nHSP is not communicable, so children can return to school when they feel well enough.\n \n# Complications\n \n - Oliguria \n - Hypertension \n - End-stage renal disease may occur in a small number of patients \n - Myocardial infarction\n - Intussusception \n - Seizures \n \n\n# Prognosis\n \n\n - The majority of HSP cases recover completely within 4 weeks.\n - A recurrence of HSP is seen in about 50% of patients. \n - Long-term renal impairment occurs in approximately 20% of patients with significant proteinuria.\n\n\n# References\n\n[NHS Guidelines on Henoch ](https://www.nhs.uk/conditions/henoch-schonlein-purpura-hsp/)\n\n[Information from Great Ormond Street Hospital](https://www.gosh.nhs.uk/conditions-and-treatments/conditions-we-treat/henoch-sch-nlein-purpura-hsp)\n \n[East and North Hertfordshire NHS Trust Guidance](https://www.enherts-tr.nhs.uk/wp-content/uploads/2022/10/Management-of-Henoch-Schonlein-purpura-in-Children-and-Young-People-under-16-years.pdf)\n \n[Patient Info Henoch Schonlein Purpura](https://patient.info/doctor/henoch-schonlein-purpura-pro)\n\n[EULAR Criteria for Henoch Schonlein Purpura](https://pubmed.ncbi.nlm.nih.gov/20413568/)",
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"__typename": "Condition",
"id": "310",
"name": "Henoch-Schonlein purpura",
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"__typename": "UkmlaTopic",
"id": "5",
"name": "Child health"
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"learningPoint": "Henoch-Schonlein Purpura is a small vessel vasculitis in children, presenting with a triad of joint pain, abdominal pain, and palpable purpura.",
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"question": "A 9-year-old girl presents to A&E with her mother with a 1 day history of a rash on her lower limbs. She has been recovering from a cold recently. She denies previous similar episodes. She limps whilst walking around the room and is gripping her abdomen in pain. On examination, there are no findings on auscultation of her chest. Her knee is tender but not visibly swollen. Her rash is palpable and purpuric bilaterally on her lower limbs. A urine dipstick reveals protein +++ and ++ haematuria.\n\nWhich of the following is the most likely diagnosis?",
"sbaAnswer": [
"a"
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173,459,035 | false | 93 | null | 6,494,981 | null | false | [] | null | 10,728 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Studies with positive or statistically significant results are more likely to be published in journals, whereas those without statistically significant results are less likely to be published. This may make effect sizes appear better or greater than they actually are. This is not the type of bias represented in this question.",
"id": "53341",
"label": "e",
"name": "Publication bias",
"picture": null,
"votes": 169
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect because time interval bias occurs when a clinical trial is stopped early once the desired conclusion is achieved.",
"id": "53339",
"label": "c",
"name": "Time interval bias",
"picture": null,
"votes": 32
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Recall bias refers to a skew that occurs due to individuals with a certain outcome (or without a certain outcome) being more (or less) likely to recall an exposure, as the outcome has already been achieved. For example, individuals with lung cancer may be more likely to recall even small amounts of smoking history, which may positively skew the data.",
"id": "53340",
"label": "d",
"name": "Recall bias",
"picture": null,
"votes": 159
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Sampling bias describes a skew in the data that occurs when some members of a population are more likely to be selected for inclusion within a study than others. There is no indication of this being an issue within the question, for example an inadequate mix of genders or ethnicities.",
"id": "53338",
"label": "b",
"name": "Sampling bias",
"picture": null,
"votes": 257
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Bias refers to a skew in the data due to a systematic issue at any stage of a study. In this case, participants have dropped out due to unwanted side-effects, which is likely to give a negative skew to the results, as they are not followed up for long enough or included in the final results, to determine if the drug had an impact on their blood pressure or not. This is referred to as attrition bias.",
"id": "53337",
"label": "a",
"name": "Attrition bias",
"picture": null,
"votes": 1198
}
],
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"__typename": "Concept",
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"__typename": "Chapter",
"explanation": "# Definition\n\nSelection bias is the selection of individuals, groups or data for analysis in such a way that proper randomization is not achieved, thereby ensuring that the sample obtained is not representative of the population intended to be analysed.\n\n# Types of Selection Bias \n\nSome of the different types of Selection Bias are:\n\n# Sampling bias\n\nThis is due to a non-random sample of a population, causing some members of the population to be less likely to be included than others, resulting in a biased sample, defined as a statistical sample of a population (or non-human factors) in which all participants are not equally balanced or objectively represented\n\n# Time interval bias\n\nEarly termination of a trial at a time when its results support a desired conclusion\n\n# Susceptibility bias\n\nWhen one disease predisposes for a second disease, and the treatment for the first disease erroneously appears to predispose to the second disease. Partitioning data with knowledge of the contents of the partitions, and then analysing them with tests designed for blindly chosen partitions. Selection of which studies to include in a meta-analysis.\n\n# Attrition bias\n\nIs a kind of selection bias caused by attrition or loss of participants, discounting trial subjects/tests that did not run to completion.\n\n# Intention to treat analysis\n\nIntention to treat analyses are done to avoid the effects of crossover and dropout, which may break the random assignment to the treatment groups in a study",
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"demo": null,
"entitlement": null,
"id": "607",
"name": "Selection Bias",
"status": null,
"topic": {
"__typename": "Topic",
"id": "51",
"name": "Medical Statistics",
"typeId": 2
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"topicId": 51,
"totalCards": null,
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"difficulty": 1,
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"id": "10728",
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"learningPoint": "Attrition bias occurs when participants drop out of a study or trial in a way that affects the validity of the results, leading to a biased sample that may not accurately represent the original population.",
"likes": 2,
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"question": "A clinical trial recruited 1000 participants to evaluate the efficacy of a new anti-hypertensive. 500 participants were randomly assigned to receive amlodipine whilst the other 500 participants were assigned to receive a new anti-hypertensive for 1 year. The primary objective of the study was to evaluate the efficacy of each drug in reducing blood pressure in both groups. However, 21 participants taking amlodipine and 57 participants taking the new anti-hypertensive left the clinical trial before it completed as they experienced unwanted side effects. The study did not include these participants in the final results and concluded that the new anti-hypertensive was not effective at reducing blood pressure compared to amlodipine.\n\nWhich of the following types of bias is this study at risk of?",
"sbaAnswer": [
"a"
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"totalVotes": 1815,
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173,459,036 | false | 94 | null | 6,494,981 | null | false | [] | null | 10,729 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Beta-blockers are used in the management of hypertension after conventional therapies - ACEi, calcium channel blockers, and thiazide-like diuretics - have been considered. It is a 4th line agent, alongside spironolactone and alpha-blockers; spironolactone is used when the potassium is <4.5, and a beta-blocker/alpha-blocker >4.5. Side effects of atenolol include vivid dreams, erectile dysfunction, and fatigue.",
"id": "53345",
"label": "d",
"name": "Prescribe atenolol",
"picture": null,
"votes": 141
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Nifedipine is another dihydropyridine calcium channel blocker like amlodipine. It is unlikely he will respond to this when he has not responded to amlodipine, and the two would not be prescribed together. The next step is therefore to add an ACEi.",
"id": "53346",
"label": "e",
"name": "Prescribe nifedipine",
"picture": null,
"votes": 66
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect because this patient's blood pressure is greater than his target, and so his antihypertensive management requires escalation. He is already on maximum dose amlodipine and continuing this is unlikely to achieve his target.",
"id": "53343",
"label": "b",
"name": "Continue amlodipine",
"picture": null,
"votes": 105
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Anti-hypertensives should only be discontinued if they produce unwanted side effects or if the patient refuses to take them, since adding additional agents is more likely to produce better control than substituting with novel agents. Indapamide is a thiazide-like diuretic which is used after calcium channel blockers and ACEi as a third step. Common side effects of indapamide include hyperuricaemia, postural hypotension, and hypokalaemia.",
"id": "53344",
"label": "c",
"name": "Discontinue amlodipine and prescribe indapamide",
"picture": null,
"votes": 79
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is the correct answer because this patient is already taking amlodipine hence the next step in management is to add an ACE-inhibitor such as ramipril. Step 2 in the management of hypertension involves combining an ACE-inhibitor with a calcium channel blocker. The blood pressure target for this patient (an adult under 80) should be 140/90mmHg in clinic and 135/85mmHg at home. Remember common side effects of ACE-inhibitors such as a dry cough, delayed angioedema, and a dry mouth.",
"id": "53342",
"label": "a",
"name": "Prescribe ramipril",
"picture": null,
"votes": 2958
}
],
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"comment": "isn't add in an ACEi/ARB OR a thiazide-like duiretic on the flowchart?\n",
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"comment": "Yes but the options only allow you to add ACEi",
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"explanation": "# Summary\r\n\r\nPrimary hypertension, accounting for approximately 90-95% of cases of hypertension, is characterised by persistently elevated blood pressure due to age-related pathophysiological changes. It is a major risk factor for cardiovascular disease, cerebrovascular disease, chronic kidney disease, and peripheral vascular disease. Diagnosis is based on ambulatory blood pressure monitoring (ABPM) readings of 135/85mmHg or higher. Classification is determined by the severity of the hypertension. Management depends on the classification of the hypertension and involves lifestyle modifications and pharmacological anithypertensives according to NICE guidelines. Effective management, through lifestyle changes and medications, significantly reduces the associated risks and improves outcomes for individuals with hypertension.\r\n\r\n# Definition \r\n\r\nA 'normal' blood pressure ranges between 90/60mmHg to 140/90mmHg. The definition of hypertension is a 24h ambulatory blood pressure average reading (ABPM) that is more than or equal to 135/85mmHg. \r\n\r\n# Epidemiology\r\n\r\nIn 2015, it was reported that high blood pressure affected more than 1 in 4 adults in England (31% of men; 26% of women). In England, it is estimated that primary hypertension affects around 13.5 million people and contributed to 75,000 deaths.\r\n\r\n# Pathophysiology\r\n\r\nPrimary hypertension is as a result of a series of complex physiological changes as we age. Hypertension often occurs as a result of reduced elasticity of large arteries, age-related and atherosclerosis-related calcification, and degradation of arterial elastin. It may also be present in conditions associated with increased cardiac output, such as anaemia, hyperthyroidism and aortic regurgitation.\r\n\r\nAlthough the risk of cardiovascular disease increases progressively with increasing systolic and diastolic blood pressure, raised systolic pressure is more important than raised diastolic pressure as a risk factor for cardiovascular and renal disease.\r\n\r\n# Classification \r\n\r\nHypertension can be classified according to how high a patient's blood pressure is. \r\n\r\n* Stage 1: Clinic => 140/90mmHg; ABPM => 135/85mmHg \r\n* Stage 2: Clinic => 160/100mmHg; ABPM =>150/95mmHg \r\n* Stage 3: Clinic systolic BP (SBP) => 180 or diastolic BP (DBP) =>120mmHg\r\n\r\n\r\n# Symptoms and Signs\r\n\r\nHypertension, unless malignant, is asymptomatic and does not have any clinical signs. It is diagnosed with ABPM and further investigations should focus on diagnosing end-organ complications of hypertension. \r\n\r\n# Investigations\r\n\r\n[lightgallery]\r\n\r\n* Hypertensive patients are commonly first identified at GP appointments or during hospital admissions. Due to the prominence of 'white coat hypertension', ABPM is now required for the diagnosis of hypertension. \r\n* Hypertension should be suspected in a patient who has a clinic blood pressure of =>140/90mmHg. \r\n* **1st line: ABPM** or home blood pressure monitoring if ABPM is not tolerated or declined. \r\n* Alongside ABPM: assessment for end-organ damage and assessment of cardiovascular risk (QRISK2 scores). \r\n * Urine dip and albumin:creatinine level\r\n * Blood glucose, lipids and renal function\r\n * Fundoscopy for evidence of hypertensive retinopathy\r\n * ECG: look for evidence of LV hypertrophy\r\n\r\n\r\nN.B. if presentation is suspicious for secondary hypertension refer and investigate as appropriate (see section). \r\n\r\nN.B. Referral for same-day specialist assessment should be arranged for people with: \r\n\r\n* Clinic blood pressure of 180/120mmHg and higher with signs of retinal haemorrhage or papilloedema (accelerated hypertension) or life-threatening symptoms (e.g. new onset confusion, chest pain, heart failure signs or AKI). \r\n\r\n# Management\r\n\r\n## Principles of Management \r\n\r\n### Conservative Management \r\n\r\nControlling risk factors for cardiovascular disease:\r\n\r\n* Weight loss\r\n* Healthy diet (reduce salt and saturated fats)\r\n* Reduce alcohol and caffeine\r\n* Reduce stress\r\n* Stop smoking\r\n\r\n### Medical Management\r\n\r\nIndications to start pharmacological management of primary hypertension:\r\n\r\n* Stage 1 hypertensive patients who are <80 years old with end organ damage, CVS disease, renal disease, diabetes or 10-year CVS risk >10% OR\r\n* Anyone with stage 2 hypertension\r\n\r\n### 2019 NICE Guidelines for Pharmacological Management of Primary Hypertension \r\n\r\n[lightgallery1]\r\n\r\n* Step 1: \r\n\t* **ACE-inhibitor** (e.g. Ramipril) if <=55 years old\r\n\t* **DHP-Calcium Channel Blocker** (e.g. Amlodipine) if >55 years old OR African or Caribbean ethnicity\r\n\t* If unable to tolerate ACE-inhibitor then switch to _Angiotensin Receptor Blocker_ (e.g. Candesartan)\r\n* Step 2: \r\n\t* (If maximal dose of Step 1 has failed or not tolerated)\r\n\t* **Combine CCB and ACE-I/ARB**\r\n* Step 3:\r\n\t* (If maximal doses of Step 2 has failed or not tolerated)\r\n\t* **Add thiazide-like diuretic** (e.g. Indapamide)\r\n* Step 4: *Resistant Hypertension*\r\n\t* If blood potassium <4.5mmol/L then add **spironolactone**\r\n\t* If >4.5mmol/L **increase thiazide-like diuretic dose**\r\n\t* Other options at this point if the potassium is >4.5mmol/L include:\r\n\t\t* Alpha blocker (e.g. Doxazosin)\r\n\t\t* Beta blocker (e.g. Atenolol)\r\n\t\t* Referral to cardiology for further advice\r\n\r\n**ABPM Targets:**\r\n \r\n* Age <80 ABPM target <135/85\r\n* Age >80 ABPM target <145/85 (due to risk of postural drop and falls)\r\n* T1DM with end-organ damage <130/80\r\n\r\n# Complications\r\n\r\n* Increased risk of morbidity and mortality from all causes\r\n* Coronary artery disease\r\n* Heart failure\r\n* Renal failure\r\n* Stroke\r\n* Peripheral vascular disease\r\n\r\n# Prognosis \r\n\r\nHypertension remains one of the biggest risk factors for cardiovascular disease and its associated disabilities. Management of hypertension (with lifestyle modifications or pharmacological therapies) has been shown to reduce these risks significantly. \r\n\r\n# NICE Guidelines\r\n> <https://cks.nice.org.uk/topics/hypertension/> \r\n\r\n# References \r\n\r\n<https://patient.info/heart-health/high-blood-pressure-hypertension>\r\n<https://www.ahajournals.org/doi/full/10.1161/01.CIR.101.3.329> ",
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"question": "A 59-year-old male presents to the GP for a follow-up appointment after his hypertension annual review. He is currently asymptomatic and takes amlodipine 10mg once daily. His average blood pressure reading is 151/98mmHg.\n\nWhich of the following is the next best step in the management of this patient?",
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"explanation": "This is correct because patients with oesophageal adenocarcinoma who undergo chemotherapy or radiation therapy as supportive treatment can get painful sores in the mouth and throat. This reduces appetite causing further weight loss. A gastrostomy tube is a feeding tube which can provide nutrition. In the question stem, it states that he is significantly cachectic and not eating well. This feeding tube is placed into the stomach and can be removed when no longer needed. Note that in this context, chemotherapy will be palliative, to relieve symptoms and slow down the growth, rather than to cure the cancer.",
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"explanation": "This is incorrect because palliative radiotherapy, as would be offered in a patient with metastatic cancer, is used to control local, advanced symptoms, such as pain, bleeding, dysphagia, and spinal cord or cerebral metastases. This patient may have palliative radiotherapy needs, but he is going to start chemotherapy soon, and as such his nutrition is the next priority, in the absence of any other red flags necessitating early radiotherapy such as bleeding or cord compression.",
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"explanation": "This is incorrect because dilation is required for areas that are narrowed or blocked to improve difficulty swallowing. A balloon-like device is placed into the throat to stretch the area which can help with symptoms of dysphagia. However, this question stem points towards the main issue as poor nutrition and reduced appetite, leading to cachexia. He reports no dysphagia.",
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"explanation": "This is incorrect because although an oesophageal stent can improve difficulty swallowing, this patient does not report any dysphagia. An oesophageal stent is a hollow tube which is placed in the area of a tumour resulting in oesophageal narrowing to relieve dysphagia.",
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"explanation": "# Summary\n\nOesophageal carcinoma, primarily categorised as adenocarcinoma or squamous cell carcinoma, is a malignancy impacting the oesophagus. Adenocarcinoma is most prevalent in the Western world, typically located in the lower third of the oesophagus and linked to gastro-oesophageal reflux disease. Squamous cell carcinoma is prevalent globally and typically seen in the upper two-thirds of the oesophagus. Smoking is a significant risk factor for both types. Key signs and symptoms include progressive dysphagia, weight loss, and possible hoarseness. The primary investigation method is upper GI endoscopy, with further assessments for staging including CT scans, MRI, endoscopic ultrasound, FDG-PET scan, and occasionally laparoscopy. Management approaches depend on the staging of the disease, but include surgical, endoscopic, and non-surgical options such as radiotherapy and chemotherapy.\n\n# Definition\n\nOesophageal carcinoma is a type of cancer that originates from the epithelial cells lining the oesophagus, primarily categorised into adenocarcinoma or squamous cell carcinoma.\n\n# Epidemiology\n\nSquamous cell carcinoma of the oesophagus is the most prevalent type globally, often seen in the upper two-thirds of the oesophagus. Conversely, adenocarcinoma has become the most common cause of oesophageal carcinoma in the Western world, owing to the increasing prevalence of GORD, and is often seen in the lower one-third of the oeseophagus.\n\n# Aetiology\n\nRisk factors for oesophageal carcinoma include:\n\n- **Smoking**: The most significant risk factor for both adenocarcinoma and squamous cell carcinoma.\n- High alcohol intake\n- Obesity and gastro-oesophageal reflux disease: Linked specifically to adenocarcinoma, as recurrent reflux leads to metaplastic formations of mucin-producing glandular tissue known as Barrett's oesophagus, which can further develop into neoplasia.\n- Achalasia\n- Zenker diverticulum\n- Oesophageal web\n- High intake of hot beverages\n- Dietary intake of:\n - Increased dietary nitrosamines\n - Areca or betel nuts\n\n# Signs and Symptoms\n\nPatients with oesophageal carcinoma often present with the following symptoms:\n\n- Progressive dysphagia: Initially for solids, and later for liquids. Dysphagia typically occurs when there is obstruction of more than two-thirds of the lumen.\n- Weight loss: This symptom, the second most common, results from a combination of anorexia and dysphagia.\n- Odynophagia: Pain on swallowing can occur.\n- Hoarseness: Can develop if there is local invasion of the recurrent laryngeal nerve.\n\n# Differential Diagnosis\n\n- Gastro-oesophageal reflux disease (GORD): GORD also presents with dysphagia and odynophagia, but is often associated with heartburn, regurgitation, and chest pain.\n- Achalasia: Achalasia is characterised by dysphagia for solids and liquids from the start, regurgitation of undigested food, and chest pain.\n- Peptic stricture: Presents with intermittent dysphagia for solid foods, heartburn, and acid regurgitation.\n- Zenker diverticulum: Presents with dysphagia, regurgitation of undigested food, halitosis, and possible aspiration pneumonia.\n- Neurological causes of dysphagia such as motor neuron disease, mysaesthenia gravis\n- Oesophagitis - often due to candidiasis and presents with odynophagia more than dysphagia. May be underlying immunosuppression e.g. HIV.\n\n# Investigations\n\n### NICE 2-week-wait criteria:\n\n- Offer urgent direct access upper gastrointestinal endoscopy (to be performed within 2 weeks) to assess for oesophageal cancer in people with **dysphagia** or those aged 55 years and over with weight loss and any of the following: upper abdominal pain, reflux, or dyspepsia.\n- Consider non-urgent direct access upper gastrointestinal endoscopy to assess for oesophageal cancer in people with haematemesis.\n\nInvestigations for oesophageal carcinoma encompass:\n\n\n\n- Initial investigation: Upper GI endoscopy is performed to visualise and grade the tumour via biopsy.\n- Staging:\n - CT chest, abdomen and pelvis: Assesses the size of the tumour, local and lymph node spread, and any visceral metastases.\n - MRI: Identifies metastatic spread to the liver and advanced local disease.\n - Endoscopic ultrasound: Assesses whether a tumour is amenable for resection.\n - FDG-PET scan: Identifies distant and nodal metastases.\n - Laparoscopy: Used to identify intra-abdominal metastases if all other imaging has been negative.\n\n# Management\n\nManagement of oesophageal carcinoma is based on the stage of the disease and may include:\n\n- Surgical resection: The primary choice for localised disease.\n- Endoscopic therapies: Such as endoscopic mucosal resection or endoscopic submucosal dissection for early-stage disease.\n- Non-surgical options: Such as radiotherapy, chemotherapy or chemoradiotherapy for advanced disease, or as neoadjuvant or adjuvant therapy with surgery.\n\n# NICE Guidelines\n\n[Click here to see the NICE guidelines on oesophageal cancer](https://www.nice.org.uk/guidance/conditions-and-diseases/cancer/oesophageal-cancer)",
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"question": "A 55-year-old man presents to the gastroenterology outpatient clinic with his wife. His wife is very concerned because his voice has changed over the past year and his appetite has reduced, though he reports no dysphagia. He has no significant past medical history. He has been smoking since the age of 16. On examination, he appears significantly cachectic. An endoscopy shows evidence of an oesophageal adenocarcinoma and a CT chest, abdomen, pelvis identifies metastases to the liver. His consultant decides to begin a course of chemotherapy in a few weeks.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Whilst cerebellar dysfunction can cause a bilateral intention tremor (occurs at the end of a purposeful movement e.g. as a finger reaches almost to its target), you would expect other cerebellar signs on examination (remember neumonic DANISH: Disdiadochokinesis, Ataxia, Nystagmus, Intention tremor, Slurred speech, Hypotonia). Again, the family history and jaw involvement make Essential tremor more likely.",
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"explanation": "## Summary\n\nEssential tremor (ET) is a common neurological movement disorder, often characterized by a rhythmic, postural or action tremor primarily affecting the upper extremities. Its prevalence increases with age and can have a significant impact on daily activities and quality of life. It is heritable in about 50% of cases, and while there are treatment options available, they only manage symptoms and don't cure the underlying disorder.\n\n## Definition\n\nEssential tremor (ET) is a chronic neurologic condition that typically manifests as an involuntary shaking or trembling usually on changing posture or performing an action, most commonly in the hands and arms, but can also affect other body parts such as the head, voice, lower limbs, tongue, face, and the trunk.\n\n## Epidemiology\n\nET is one of the most prevalent movement disorders, with the incidence increasing with age. The condition may manifest at any age, from childhood to adulthood. The age of onset tends to be earlier in those with a positive family history.\n\n## Aetiology \n\nThe etiology of ET is complex and not completely understood, but it is believed to be multifactorial, involving both genetic and environmental factors. \n\nIn approximately 50% of the cases, ET is inherited as an autosomal dominant trait, suggesting a significant genetic component.\n\n## Signs and symptoms\n\nThe main clinical feature of ET is a postural or kinetic tremor, which predominantly affects the upper limbs distally. \n\nAdditional symptoms may include:\n\n- Involvement of the head, lower limbs, voice, tongue, face, and the trunk, although less common.\n- Increased tremor amplitude over time, causing difficulty with tasks such as writing, eating, holding objects, dressing, and speaking.\n- Exacerbation of tremor during situations of anxiety, stress, and social interaction.\n- Potential development of severe psychosocial disability, including depression, particularly in patients with head and voice tremors.\n\nClassically, ingestion of alcohol can temporarily improve the tremor.\n\n## Differential diagnosis\n\nET should be distinguished from other types of tremors. Main differentials include:\n\n- **Parkinson's disease**: Resting tremor, bradykinesia, rigidity, postural instability.\n- **Hyperthyroidism-associated tremor**: Palpitations, heat intolerance, weight loss, anxiety.\n- **Dystonic tremor**: Abnormal posturing, muscle contractions, worsened by voluntary movement. \n\n## Investigations\n\nThe diagnosis of ET is mainly clinical. \n\nOnce suspected, a thorough evaluation of functional and psychosocial disabilities should be performed using objective scales to determine the need for pharmacotherapy. \n\nFurther investigations, such as blood tests or neuroimaging, may be warranted to rule out other potential causes of tremor.\n\n## Management\n\nManagement of ET is primarily symptomatic and may include:\n\n- Pharmacological therapy, using agents such as **propranolol** (first line), primidone, topiramate, gabapentin, clonazepam.\n- Surgical intervention for severe cases, including deep brain stimulation, focused ultrasound thalamotomy, and radiosurgical (Gamma Knife) thalamotomy.\n\n## References\n\n[More information on Essential Tremor](https://www.ncbi.nlm.nih.gov/books/NBK499986/)\n\n",
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"question": "A 70 year old man presents to the GP for a routine asthma check-up. He is incidentally noted to have a coarse tremor in his right hand whilst reaching for a pen. On examination, the tremor is present in both hands when outstretched, and also affects his jaw. Neurological examination is otherwise unremarkable. He mentions that several family members also have similar tremors.\n\nWhich condition is the most likely cause of his tremor?",
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"explanation": "Whilst this is a good thought, de-escalation should be the initial management of delirium and part of this assessment would be whether pain is a contributing factor. Paracetamol should therefore only be given in certain circumstances rather than as a first line treatment for every delirious patient.",
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"name": "Give some paracetamol as he may be in pain",
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"explanation": "All sedation is a form of restraint, and carries risk. Sedation can worsen delirium, increase falls risk and have side-effects. It should not be administered before trying non-pharmacological interventions first. Lorazepam is a reasonable sedative option but haloperidol is the only agent recommended (with caution) by NICE.",
"id": "61965",
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"explanation": "# Summary\n\nDelirium, also known as acute confusional state, is a frequent condition, primarily observed among elderly individuals. It manifests through symptoms such as disorientation, hallucinations, inattention, memory problems, mood or personality changes, and disturbed sleep. Comprehensive investigation includes physical examination and infection screen. Management focuses on treating the underlying cause, optimising the patient's environment, and, in severe cases, considering sedative measures.\n\n# Definition\n\nDelirium is an acute and fluctuating disturbance in attention and cognition, often accompanied by a change in consciousness. It is typically reversible and frequently seen in the elderly, particularly in inpatient settings. It manifests in three subtypes:\n\n* **Hyperactive** Delirium: Marked by increased psychomotor activity, restlessness, agitation, and hallucinations.\n* **Hypoactive** Delirium: Characterised by lethargy, reduced responsiveness, and withdrawal.\n* **Mixed** Delirium: Combines features of both hyperactive and hypoactive delirium.\n\n# Epidemiology\n\nDelirium is a common condition, predominantly affecting elderly people, and is seen in up to 30% of elderly inpatients. The incidence increases with age, severity of illness, and the presence of pre-existing cognitive impairment.\n\n# Aetiology\n\nThe causes of delirium can be multifactorial and are remembered using the mnemonic DELIRIUMS:\n\n- D: Drugs and Alcohol (Anti-cholinergics, opiates, anti-convulsants, recreational)\n- E: Eyes, ears and emotional disturbances\n- L: Low Output state (Myocardial Infarction, Acute Respiratory Distress Syndrome, Pulmonary Embolism, Congestive Heart Failure, Chronic Obstructive Pulmonary Disease)\n- I: Infection\n- R: Retention (of urine or stool)\n- I: Ictal (related to seizure activity)\n- U: Under-hydration/Under-nutrition\n- M: Metabolic disorders (Electrolyte imbalance, thyroid disorders, Wernicke's encephalopathy)\n- (S): Subdural hematoma, Sleep deprivation\n\n# Signs and Symptoms\n\nDelirium can present in a number of different ways, including:\n\n- Disorientation\n- Hallucinations - visual or auditory\n- Inattention\n- Memory problems\n- Change in mood or personality. **Sundowning** is agitation and confusion worsening in the late afternoon or evening.\n- Disturbed sleep\n\nPatients may be hypoactive (sedated) or hyperactive (very agitated), and these presentations can fluctuate over time. Hyperactive delirium is easily seen due to the presentation, while hypoactive delirium can be easily missed as patients may appear more withdrawn.\n\n# Differential Diagnosis\n\nDelirium can mimic several other conditions and it's crucial to consider the following in differential diagnosis, each with its key signs and symptoms:\n\n- Dementia: Characterized by gradual onset, stable consciousness level, and progressive decline in cognitive function.\n- Psychosis: May present with hallucinations and delusions, but usually with preserved orientation and memory.\n- Depression: May exhibit poor concentration and slow cognition, but typically with a stable consciousness level and often accompanied by pervasive feelings of sadness or guilt.\n- Stroke: Abrupt onset with focal neurologic signs and specific deficits in speech, motor, or sensory function.\n \n# Investigations\n\n- 4AT and CAM are commonly used tools for delirium assessment.\n\nInitial investigations should include a comprehensive physical examination and infection screen. Additional investigations should be guided by clinical suspicion based on the patient's history and physical examination. These may include:\n\n- Bedside - bladder scan, review medications, ECG (arrhythmias, ischaemic changes that could cause hypoperfusion) urine MC&S - you should not perform urine dipstick if >65 as they are less sensitive in this age group.\n- Bloods: FBC, urea and electrolyes, liver function tests, thyroid function tests, and blood cultures.\n- Imaging: chest X-ray, or ultrasound of the abdomen. Neuroimaging with CT or MRI head is reserved for those without a clear identifiable cause.\n\n\n# Management\n\nManagement of delirium primarily focuses on treating the underlying cause. Non-pharmacological strategies should be the first line, which include:\n\n- Providing an environment with good lighting\n- Maintaining a regular sleep-wake cycle\n- Regular orientation and reassurance\n- Ensuring the patient's glasses and hearing aids are used if needed\n\nFor patients who are extremely agitated and potentially a danger to themselves or others, pharmacological interventions such as small doses of haloperidol or lorazepam. Olanzapine may also be considered however, these should be used with caution, especially in the elderly, due to the risk of side effects. \n\n# NICE Guidelines\n\nFor more information, see [NICE CKS on delirium](https://cks.nice.org.uk/topics/delirium/).",
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"question": "A 79 year old male with a urinary tract infection on the medical ward is acutely agitated and confused. He is shouting, disturbing other patients and the ward nurses are struggling to cope. He is pulling out his lines and trying to climb out of bed. He is 70kg and only past medical history is gout.\n\nWhich of the following is the most appropriate initial management of this situation?",
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"explanation": "De-escalation has already been tried and failed in this case. It is reasonable to also take more restrictive measures i.e. pharmacological intervention.",
"id": "61971",
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"explanation": "Phenobarbital is a long-acting sedative-hypnotic anti-epileptic agent that is not recommended. Haloperidol would usually be first-line treatment but Lewy Body Dementia (and Parkinson's disease) contraindicate its use. Other notable contraindications include recent myocardial infarction, long QTc, hypokalaemia, and decompensated heart failure.",
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"explanation": "While bloods may be useful for identifying underlying causes of his delirium, it would be practically dangerous if the patient is resisting intervention and not useful in the acute setting where rapid de-escalation or sedation is needed in the first instance.",
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"name": "Take some blood tests",
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"explanation": "Lorazepam is a reasonable first-choice benzodiazepine for sedation in this case as it is rapid onset and short acting. Haloperidol would usually be first-line treatment but Lewy Body Dementia (and Parkinson's Disease) contraindicate its use. Other notable contraindications include recent myocardial infarction, long QTc, hypokalaemia, and decompensated heart failure.",
"id": "61968",
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"explanation": "Diazepam is a long-acting benzodiazepine; a short-acting agent like lorazepam would be preferable to minimise restraint and adverse effects. Haloperidol would usually be first-line treatment but Lewy Body Dementia (and Parkinson's disease) contraindicate its use. Other notable contraindications include recent myocardial infarction, long QTc, hypokalaemia, and decompensated heart failure.",
"id": "61970",
"label": "c",
"name": "Diazepam",
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"explanation": "# Summary\n\nDelirium, also known as acute confusional state, is a frequent condition, primarily observed among elderly individuals. It manifests through symptoms such as disorientation, hallucinations, inattention, memory problems, mood or personality changes, and disturbed sleep. Comprehensive investigation includes physical examination and infection screen. Management focuses on treating the underlying cause, optimising the patient's environment, and, in severe cases, considering sedative measures.\n\n# Definition\n\nDelirium is an acute and fluctuating disturbance in attention and cognition, often accompanied by a change in consciousness. It is typically reversible and frequently seen in the elderly, particularly in inpatient settings. It manifests in three subtypes:\n\n* **Hyperactive** Delirium: Marked by increased psychomotor activity, restlessness, agitation, and hallucinations.\n* **Hypoactive** Delirium: Characterised by lethargy, reduced responsiveness, and withdrawal.\n* **Mixed** Delirium: Combines features of both hyperactive and hypoactive delirium.\n\n# Epidemiology\n\nDelirium is a common condition, predominantly affecting elderly people, and is seen in up to 30% of elderly inpatients. The incidence increases with age, severity of illness, and the presence of pre-existing cognitive impairment.\n\n# Aetiology\n\nThe causes of delirium can be multifactorial and are remembered using the mnemonic DELIRIUMS:\n\n- D: Drugs and Alcohol (Anti-cholinergics, opiates, anti-convulsants, recreational)\n- E: Eyes, ears and emotional disturbances\n- L: Low Output state (Myocardial Infarction, Acute Respiratory Distress Syndrome, Pulmonary Embolism, Congestive Heart Failure, Chronic Obstructive Pulmonary Disease)\n- I: Infection\n- R: Retention (of urine or stool)\n- I: Ictal (related to seizure activity)\n- U: Under-hydration/Under-nutrition\n- M: Metabolic disorders (Electrolyte imbalance, thyroid disorders, Wernicke's encephalopathy)\n- (S): Subdural hematoma, Sleep deprivation\n\n# Signs and Symptoms\n\nDelirium can present in a number of different ways, including:\n\n- Disorientation\n- Hallucinations - visual or auditory\n- Inattention\n- Memory problems\n- Change in mood or personality. **Sundowning** is agitation and confusion worsening in the late afternoon or evening.\n- Disturbed sleep\n\nPatients may be hypoactive (sedated) or hyperactive (very agitated), and these presentations can fluctuate over time. Hyperactive delirium is easily seen due to the presentation, while hypoactive delirium can be easily missed as patients may appear more withdrawn.\n\n# Differential Diagnosis\n\nDelirium can mimic several other conditions and it's crucial to consider the following in differential diagnosis, each with its key signs and symptoms:\n\n- Dementia: Characterized by gradual onset, stable consciousness level, and progressive decline in cognitive function.\n- Psychosis: May present with hallucinations and delusions, but usually with preserved orientation and memory.\n- Depression: May exhibit poor concentration and slow cognition, but typically with a stable consciousness level and often accompanied by pervasive feelings of sadness or guilt.\n- Stroke: Abrupt onset with focal neurologic signs and specific deficits in speech, motor, or sensory function.\n \n# Investigations\n\n- 4AT and CAM are commonly used tools for delirium assessment.\n\nInitial investigations should include a comprehensive physical examination and infection screen. Additional investigations should be guided by clinical suspicion based on the patient's history and physical examination. These may include:\n\n- Bedside - bladder scan, review medications, ECG (arrhythmias, ischaemic changes that could cause hypoperfusion) urine MC&S - you should not perform urine dipstick if >65 as they are less sensitive in this age group.\n- Bloods: FBC, urea and electrolyes, liver function tests, thyroid function tests, and blood cultures.\n- Imaging: chest X-ray, or ultrasound of the abdomen. Neuroimaging with CT or MRI head is reserved for those without a clear identifiable cause.\n\n\n# Management\n\nManagement of delirium primarily focuses on treating the underlying cause. Non-pharmacological strategies should be the first line, which include:\n\n- Providing an environment with good lighting\n- Maintaining a regular sleep-wake cycle\n- Regular orientation and reassurance\n- Ensuring the patient's glasses and hearing aids are used if needed\n\nFor patients who are extremely agitated and potentially a danger to themselves or others, pharmacological interventions such as small doses of haloperidol or lorazepam. Olanzapine may also be considered however, these should be used with caution, especially in the elderly, due to the risk of side effects. \n\n# NICE Guidelines\n\nFor more information, see [NICE CKS on delirium](https://cks.nice.org.uk/topics/delirium/).",
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"question": "A 68 year old male is becoming increasingly aggressive and agitated on the ward. He is confused and lashing out at staff members despite several attempts at de-escalation. He has acute pneumonia, a past medical history of metastatic rectal cancer and Lewy Body Dementia.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "The PHQ-9 is a tool for assessment of depression severity in primary care. The acute and fluctuating confusion and clinical context suggests delirium in this case, rather than depression or pseudo-dementia.",
"id": "61977",
"label": "e",
"name": "PHQ-9 (Patient Health Questionnaire-9)",
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"explanation": "NICE recommend the short-CAM to assess and confirm a diagnosis of delirium. The acute and fluctuating course, and clinical context suggest delirium rather than other causes of confusion.",
"id": "61973",
"label": "a",
"name": "Short-CAM (Confusion Assessment Method)",
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"explanation": "The MoCA is used for assessment of cognitive impairment rather than delirium. The acute and fluctuating course suggest delirium rather than worsening dementia. Dementia is a risk factor for delirium.",
"id": "61976",
"label": "d",
"name": "MoCA (Montreal Cognitive Assessment)",
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"explanation": "The MMSE is used for assessment of cognitive impairment rather than delirium. The acute and fluctuating course suggest delirium rather than worsening dementia. Dementia is a risk factor for delirium.",
"id": "61974",
"label": "b",
"name": "MMSE (Mini-Mental Status Exam)",
"picture": null,
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"explanation": "The MSE is a tool for assessment of psychiatric conditions by way of observation and interaction with a patient. The acute and fluctuating confusion and clinical context suggests delirium rather than psychosis or pseudo-dementia.",
"id": "61975",
"label": "c",
"name": "MSE (Mental State Examination)",
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"explanation": "# Summary\n\nDelirium, also known as acute confusional state, is a frequent condition, primarily observed among elderly individuals. It manifests through symptoms such as disorientation, hallucinations, inattention, memory problems, mood or personality changes, and disturbed sleep. Comprehensive investigation includes physical examination and infection screen. Management focuses on treating the underlying cause, optimising the patient's environment, and, in severe cases, considering sedative measures.\n\n# Definition\n\nDelirium is an acute and fluctuating disturbance in attention and cognition, often accompanied by a change in consciousness. It is typically reversible and frequently seen in the elderly, particularly in inpatient settings. It manifests in three subtypes:\n\n* **Hyperactive** Delirium: Marked by increased psychomotor activity, restlessness, agitation, and hallucinations.\n* **Hypoactive** Delirium: Characterised by lethargy, reduced responsiveness, and withdrawal.\n* **Mixed** Delirium: Combines features of both hyperactive and hypoactive delirium.\n\n# Epidemiology\n\nDelirium is a common condition, predominantly affecting elderly people, and is seen in up to 30% of elderly inpatients. The incidence increases with age, severity of illness, and the presence of pre-existing cognitive impairment.\n\n# Aetiology\n\nThe causes of delirium can be multifactorial and are remembered using the mnemonic DELIRIUMS:\n\n- D: Drugs and Alcohol (Anti-cholinergics, opiates, anti-convulsants, recreational)\n- E: Eyes, ears and emotional disturbances\n- L: Low Output state (Myocardial Infarction, Acute Respiratory Distress Syndrome, Pulmonary Embolism, Congestive Heart Failure, Chronic Obstructive Pulmonary Disease)\n- I: Infection\n- R: Retention (of urine or stool)\n- I: Ictal (related to seizure activity)\n- U: Under-hydration/Under-nutrition\n- M: Metabolic disorders (Electrolyte imbalance, thyroid disorders, Wernicke's encephalopathy)\n- (S): Subdural hematoma, Sleep deprivation\n\n# Signs and Symptoms\n\nDelirium can present in a number of different ways, including:\n\n- Disorientation\n- Hallucinations - visual or auditory\n- Inattention\n- Memory problems\n- Change in mood or personality. **Sundowning** is agitation and confusion worsening in the late afternoon or evening.\n- Disturbed sleep\n\nPatients may be hypoactive (sedated) or hyperactive (very agitated), and these presentations can fluctuate over time. Hyperactive delirium is easily seen due to the presentation, while hypoactive delirium can be easily missed as patients may appear more withdrawn.\n\n# Differential Diagnosis\n\nDelirium can mimic several other conditions and it's crucial to consider the following in differential diagnosis, each with its key signs and symptoms:\n\n- Dementia: Characterized by gradual onset, stable consciousness level, and progressive decline in cognitive function.\n- Psychosis: May present with hallucinations and delusions, but usually with preserved orientation and memory.\n- Depression: May exhibit poor concentration and slow cognition, but typically with a stable consciousness level and often accompanied by pervasive feelings of sadness or guilt.\n- Stroke: Abrupt onset with focal neurologic signs and specific deficits in speech, motor, or sensory function.\n \n# Investigations\n\n- 4AT and CAM are commonly used tools for delirium assessment.\n\nInitial investigations should include a comprehensive physical examination and infection screen. Additional investigations should be guided by clinical suspicion based on the patient's history and physical examination. These may include:\n\n- Bedside - bladder scan, review medications, ECG (arrhythmias, ischaemic changes that could cause hypoperfusion) urine MC&S - you should not perform urine dipstick if >65 as they are less sensitive in this age group.\n- Bloods: FBC, urea and electrolyes, liver function tests, thyroid function tests, and blood cultures.\n- Imaging: chest X-ray, or ultrasound of the abdomen. Neuroimaging with CT or MRI head is reserved for those without a clear identifiable cause.\n\n\n# Management\n\nManagement of delirium primarily focuses on treating the underlying cause. Non-pharmacological strategies should be the first line, which include:\n\n- Providing an environment with good lighting\n- Maintaining a regular sleep-wake cycle\n- Regular orientation and reassurance\n- Ensuring the patient's glasses and hearing aids are used if needed\n\nFor patients who are extremely agitated and potentially a danger to themselves or others, pharmacological interventions such as small doses of haloperidol or lorazepam. Olanzapine may also be considered however, these should be used with caution, especially in the elderly, due to the risk of side effects. \n\n# NICE Guidelines\n\nFor more information, see [NICE CKS on delirium](https://cks.nice.org.uk/topics/delirium/).",
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"question": "A 77 year old female with acute constipation and a recent diagnosis of Alzheimer's disease has a 2 day history of worsening confusion. She was highly disorientated this morning however is lucid on review later that afternoon.\n\nWhich of the following tools would be most appropriate to diagnose and assess this patient's new confusion?",
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"explanation": "FTD is classically characterised by behavioural and personality changes, and would be expected to have a progressive rather than step-wise decline.",
"id": "61982",
"label": "e",
"name": "Frontotemporal dementia",
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"explanation": "Lewy Body Dementia (LBD) has a progressive onset and distinguishing features can include Parkinsonism, REM sleep disorder and visual hallucinations.",
"id": "61980",
"label": "c",
"name": "Lewy Body Dementia",
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"explanation": "Vascular dementia tends to have a 'step-wise' decline, with multiple vascular events causing acute on chronic deficits. This patient has risk factors and evidence of vasculopathy.",
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"name": "Vascular dementia",
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"explanation": "Pseudodementia is a term used to describe cognitive impairment associated with psychiatric disorders especially depression in the elderly. There is no suggestion of depression in the question; therefore, dementia is more likely.",
"id": "61981",
"label": "d",
"name": "Pseudodementia",
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"explanation": "While there can be overlap in that vascular dementia can affect any part of the brain and therefore mimic Alzheimer's Disease, AD has a slow and progressive onset.",
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"explanation": "# Summary\n\nVascular dementia (VaD) is a cognitive impairment resulting from cerebrovascular disease, often presenting with progressive stepwise cognitive deterioration over months or years. Typical presentations are stroke-related vascular disease, subcortical vascular dementia, and mixed dementia. Diagnosis is established via comprehensive history, formal cognitive screening, medication review, exclusion of reversible organic causes, and neuroimaging, preferably MRI. Management revolves around symptomatic treatment, detection and control of cardiovascular risk factors, and advanced care planning.\n\n# Definition\n\nVascular dementia is an umbrella term denoting a collection of cognitive impairment syndromes caused by cerebrovascular disease.These include stroke-related vascular disease, subcortical vascular dementia, and mixed dementia —a combination of Alzheimer's disease and vascular dementia.\n\n# Epidemiology\n\nVascular dementia (VaD) is the second most common type of dementia after Alzheimer's disease, accounting for around 15-20% of all dementia cases.\n\nPrevalence of VaD increases with age, being rare before the age of 65 but significantly rising thereafter. \n\nThe incidence of VaD is higher in males than in females, and higher in individuals with cardiovascular risk factors.\n\n# Aetiology\n\nThe primary cause of vascular dementia is ischemic or hemorrhagic cerebrovascular disease, which leads to brain damage. \n\nVarious vascular events or conditions can lead to VaD, including multi-infarct dementia, single-infarct dementia, subcortical vascular dementia (also known as Binswanger's disease), and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).\n\nRisk factors for VaD mirror those for stroke and other cardiovascular diseases: hypertension, diabetes mellitus, hyperlipidemia, smoking, and atrial fibrillation are significant risk factors. \n\nLess common causes include inflammatory and immunological vascular disorders, genetic conditions, and infections that affect the brain's blood vessels.\n\n# Signs and Symptoms\n\nThe hallmark of vascular dementia is a progressive, **stepwise** deterioration in cognition. This typically occurs over a span of several months to years. Patients may present with a history of strokes, which may be accompanied by stepwise cognitive decline or sudden changes in cognitive function, as well as stroke-like symptoms:\n\n- Visual disturbance\n- Sensory or motor symptoms\n- Difficulty with attention and concentration\n- Seizures\n- Memory disturbance\n- Gait/speech/emotional disturbance\n\nTo compare with Alzheimer's dementia, there is less impairment in episodic memory and more in visual skills, semantic memory and executive functioning.\n\n# Differential Diagnosis\n\nThe differential diagnosis for vascular dementia includes, but is not limited to:\n\n- **Alzheimer's disease**: Predominant memory impairment, slower and continuous decline, usually lack of significant vascular risk factors or neuroimaging evidence of cerebrovascular disease.\n- **Lewy body dementia**: Fluctuating cognition, visual hallucinations, Parkinsonism, and REM sleep behavior disorder are the core features.\n- **Frontotemporal dementia**: Prominent changes in personality and behavior or language difficulties with relative sparing of memory.\n- **Normal pressure hydrocephalus**: Gait disturbance, urinary incontinence, and cognitive impairment (triad of Hakim-Adams).\n\n# Investigations\n\nThe investigations for vascular dementia generally include:\n\n- Comprehensive history and examination.\n- Formal cognition screening, such as MMSE (Mini-Mental State Examination) or MoCA (Montreal Cognitive Assessment).\n- Medication review to exclude medication-induced cognitive impairment.\n- Exclusion of reversible organic causes such as vitamin B12 or folic acid deficiency, hypothyroidism, or normal pressure hydrocephalus.\n- MRI Head, to identify vascular changes, infarcts, or white matter hyperintensities indicative of cerebrovascular disease. The hallmark of vascular dementia is extensive white matter change and infarcts evident on MRI imaging.\n\n[lightgallery]\n\n# Management\n\nThe management of vascular dementia involves:\n\n- Detection of and addressing cardiovascular risk factors such as hypertension, diabetes, hyperlipidemia, and smoking to slow disease progression.\n- Cognitive stimulation programmes, music and art therapy, etc. to help with cognitive impairment. \n- Symptomatic treatment, including cognitive enhancers such as cholinesterase inhibitors or memantine - if there is evidence of co-existent AD, Parkinson's dementia, or dementia with Lewy bodies. Management of neuropsychiatric symptoms.\n- Advanced care planning to prepare for progressive cognitive and physical decline.\n\n# NICE Guidelines\n\n[NICE CKS - Dementia](https://cks.nice.org.uk/topics/dementia/)",
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"question": "A 67 year old male is brought to GP by his family over concerns for his memory. He has type 2 diabetes, a previous CABG and COPD. He has had a sudden deterioration in his cognition three weeks ago, with persistent confusion and difficulty with word finding. He had a similar abrupt decline last year and needed additional support ever since.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "Levodopa, also known as L-DOPA, can cross the blood-brain barrier (unlike dopamine), where it is then converted into dopamine by DOPA-decarboxylase to replenish depleted dopamine supplies in the brain.",
"id": "61983",
"label": "a",
"name": "It is a dopamine precursor and therefore acts as a prodrug",
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"explanation": "Dopamine analogues have a similar but different structure to dopamine and therefore can work as dopamine agonists. Example include cabergoline, bromocriptine, pramipexole, ropinirole and rotigotine.",
"id": "61987",
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"name": "It is a dopamine analogue",
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"explanation": "Dopamine re-uptake inhibitors are not commonly used to treat Parkinson's disease. Examples of noradrenaline/dopamine-reuptake inhibitors include buproprion and modafnil.",
"id": "61986",
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"name": "It is a dopamine re-uptake inhibitor",
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"explanation": "Levodopa is a substrate for this enzyme, rather than acting to increase the rate of its metabolism",
"id": "61984",
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"name": "It accelerates DOPA-decarboxylase activity",
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"explanation": "This enzyme converts levodopa to dopamine. Notably, its inhibition it would reduce dopamine production and therefore not be desirable.",
"id": "61985",
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"explanation": "# Summary\n\nParkinson's disease (PD) is a neurodegenerative disorder predominantly affecting adults over 65 years characterised by asymmetric tremor, bradykinesia, and rigidity. The condition results from Lewy body formation and neuronal death in the dopaminergic cells of the substantia nigra. Clinical features include assymetric resting tremor, slow shuffling gait, cogwheel rigidity, bradykinesia, and non-motor features such as autonomic dysfunction and psychiatric disturbances. Diagnosis is primarily clinical, supported by response to treatment trials. Pharmacological treatment with Levodopa remains the first-line therapy, with other agents used for specific symptom control or in later disease stages. Surgical interventions such as deep brain stimulation may be considered in certain cases. Prognosis varies, with little impact on overall life expectancy.\n\n\n# Definition\n\nParkinson's disease (PD) is a neurodegenerative disorder that presents with generalised slowing of movements (bradykinesia), resting tremor and rigidity.\n\n# Epidemiology\n\n- Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease. \n- It affects 0.3% of the UK population.\n- It is estimated that PD affects at least 1% of the population over 60\n\n\n# Aetiology\n\n- The exact cause of Parkinson's disease is unknown. \n- It is believed to result from the accumulation of \"Lewy bodies\", intracellular inclusions primarily composed of misfolded **alpha synuclein**. \n- These bodies form and lead to neuronal death in the dopaminergic cells of the substantia nigra of the basal ganglia, thereby causing the characteristic symptoms. \n- Both dominant and recessive familial variants of Parkinson's disease have been identified.\n\n# Clinical Features \n\nParkinson's disease is characterised by the following core features:\n\n* Bradykinesia\n* Asymmetric 3-5Hz \"pill-rolling\" resting tremor\n* Rigidity\n\t* Often noted to be 'cog-wheeling' which occurs when the tremor coincidees with rigidity\n* Gait Disturbance\n\t * Small, shuffling steps\n\t * Difficult initation and turning 'en bloc turning'\n\nOther features associated with Parkinson's Disease include:\n\n- Hypomimic facies\n- Micrographia (secondary to a combination of bradykinesia and rigidity)\n\nNon-motor features of Parkinson's disease are also common and may precede onset of motor symptoms by many years. These include:\n\n* Autonomic dysfunction, leading to constipation, symptomatic orthostasis (postural hypotension), and erectile dysfunction\n* Olfactory loss\n* Constipation\n* Sleep disorders such as REM behavioural disorder \n* Psychiatric features including depression, anxiety, and hallucinations\n\n\nPostural instability is a late feature of idiopathic Parkinson's disease. This said, very prominent early autonomic dysfunction should raise the suspicion of Multiple System Atrophy.\n\nEarly and prominent cognitive dysfunction should raise the suspicion of dementia with Lewy bodies (DLB).\n\n# Differential diagnosis\n\nKey differentials for Parkinson's disease, along with their signs and symptoms, include:\n\n* **Multiple System Atrophy (MSA):** Very prominent autonomic dysfunction, early postural instability, poor response to levodopa\n* **Dementia with Lewy Bodies (DLB):** Early and prominent cognitive dysfunction, visual hallucinations, fluctuating cognition\n* **Progressive Supranuclear Palsy (PSP):** Early gait instability and falls, vertical gaze palsy, prominent axial rigidity\n* **Corticobasilar Degeneration**: May have predominant apraxia, aphasia and 'alien hand' syndrome\n* **Wilson's Disease:** Secondary to copper deposition in the Basal Ganglia. May be associated with signs of liver disease\n* **Dementia Pugilistica:** Secondary to repeated head trauma\n* **Drug Induced Parkinsonism** Secondary to antipsychotic therapy, usually symmetrical tremor and less responsive to Levodopa\n\n# Investigations\n\nParkinson's disease is primarily a clinical diagnosis, supported by positive response to treatment trials. \n\nAn absolute failure to respond to 1-1.5g of levodopa daily almost excludes a diagnosis of idiopathic Parkinson's disease.\n\nOther investigations such as MRI Head or a Dopamine Transporter Scan (DaT scan) can be considered in atypical cases. \n\n# Management\n\nManagement should by led by a multidisciplinary team of neurologists, nurse specialists, physiotherapists, occupational therapists and other allied healthcare professionals.\n\n## Pharmacological Management\n\n### Levodopa\n\n- Levodopa is the precurser to dopamine\n- It is used as a dopamine replacement agent\n- Should be started in all patients with **significant functional impairment** according to NICE guidelines\n- Typically combined with Carbidopa, which decreases side effects and improves CNS bioavailability), oftern referred to as **Co-careldopa**\n- Absolute failure to respond to 1-1.5g of levodopa daily virtually excludes a diagnosis of idiopathic Parkinson's disease, though a response to levodopa does not confirm the diagnosis (as many primary parkinsonian syndromes may also respond).\n\n\nSide effects can be split into peripheral and central (depending on where the acting dopamine receptor is for the side effect).\n\nPeripheral side effects include:\n\n- Postural hypotension\n- Nausea & vomiting*\n\n\nWith time, and as the underlying disease progresses, levodopa may become a less effective and patients may report end-of-dose effects, where motor activity progressively declines as the previous dose wears off, and on-off phenomena, which manifest as seemingly random fluctuations in drug effect.\n\nOne of the most disabling side effects is **drug-induced dyskinesia**: writhing and uncoordinated movements of the limbs associated with poorly organised dopaminergic control of motor activity.\n\nIt typically takes 2-5 years to develop complete loss of response.\n\n*Domperidone is the anti-emetic of choice in those with Parkinson’s disease which has anti-dopaminergic activity but does NOT cross the blood brain barrier. \n\n### Dopamine agonists\n\n- Examples include: Ropinirole, rotigotine, Apomorphine. Previous ergot derived formulations (eg cabergoline) as now not widely used as are associated with lung fibrosis. \n- Have a longer half life than levodopa but are not as potent\n- Are often used in early disease in those without functional impairment, or late in disease when dyskinesias and motor fluctuations secondary to levodopa is a problem.\n- Increases activity of dopamine via the mesolimbic pathway which may affect reward centres and lead to unwanted risk-taking behaviours such as gambling. \n- Apomorphine is the most potent dopamine agonist and is typically given subcutaneously. It works well against motor fluctuations and dyskinesia. Often used late in disease. \n\n\n### MAO-B Inhibitors\n\n- Examples include: Selegiline, Rasagiline.\n- Reduce dopamine breakdown peripherally & thus increase central update of levodopa. Often used in combination with levodopa later in disease.\n- Initial animal studies suggested a \"neuroprotective effect\" although this has not been seen in human studies.\n- Can cause serotonin syndrome. \n\n### COMT Inhibitors\n\n- COMT inhibitors, or catechol- O -methyltransferase inhibitors include Entacapone and Tolcapone.\n- Extend the use of levodopa. Useful in wearing off effect in levodopa use.\n- Tolcapone is more potent than entacapone and can result in hepatotoxicity. \n\n### Amantadine\n\n- NMDA receptor antagonist that has an unclear action in Parkinson's Disease.\n- Can be used in those suffering from dyskinesia. \n\n\n### Anticholinergic agents\n\n- Examples include: Procyclidine, Trihexyphenidyl\n- Can be used in those with mild tremors. \n- Rarely used in clinical practice \n\n\n## Surgical Management\n\n- Deep Brain Stimulation: typically performed by implanting a stimulating device into a target area of the brain, often the thalamus or the subthalamus.\n\n# Prognosis\n\n- Parkinson's disease is typically slowly progressive, but the rate of progression is variable. \n- The mortality rate for elderly people aged 70-89 years with Parkinson's disease is 2-5 times higher than for age-matched controls in some studies. \n- The risk of dementia is about 2-6 times higher in people with Parkinson's disease than in healthy controls",
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"question": "Which of the following best describes the mechanism of action of Levodopa in the treatment of Parkinson's disease?",
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"explanation": "The change is bowel habit is very acute and there are no other red flags in context. It would not be the most likely diagnosis at this point.",
"id": "61989",
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"name": "Colorectal cancer",
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"explanation": "A good differential, however, hard stool in the rectum and history of constipation would go against this. There are no infective symptoms or vomiting to support this.",
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"explanation": "Common in this age group; however, you would not expect hard stool on per rectum examination, and might expect a more inflammatory history.",
"id": "61991",
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"explanation": "Coeliac disease would classically present younger, more chronically and with general symptoms such as weight loss. There may other auto-immune history.",
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"explanation": "Severe constipation can lead to diarrhoea as liquid stool flows around immovable solid stool in the bowel.",
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"explanation": "# Summary\n\nConstipation is a common gastrointestinal disorder characterised by infrequent bowel movements, hard stools, excessive straining, tenesmus and sometimes necessitating manual evacuation. The disorder can be primary, due to a functional issue, or secondary, due to various causes such as diet, certain medications, and endocrine or neurological disorders. Key investigations include full blood count, electrolytes, thyroid function, blood glucose, and imaging if suspicious of secondary causes. Management is dependent on the underlying cause and may involve lifestyle modifications, a range of laxatives, and referral to a specialist centre for gut motility evaluation if laxatives fail to resolve symptoms.\n\n# Definition\n\nConstipation may involve any or all of the following (Rome IV criteria):\n\n- Fewer than three bowel movements per week\n- Hard stool in more than 25% of bowel movements\n- Tenesmus (sense of incomplete evacuation) in more than 25% of bowel movements\n- Excessive straining in more than 25% of bowel movements\n- A need for manual evacuation of bowel movements\n\nIt can be categorised as:\n\n- Primary constipation: no organic cause, thought to be due to dysregulation of the function of the colon or anorectal muscles\n- Secondary constipation: due to factors such as diet, medications, metabolic, endocrine or neurological disorders or obstruction\n\n# Epidemiology\n\nRisk factors include:\n\n- Advanced age\n- Inactivity\n- Low calorie intake\n- Low fibre diet\n- Certain medications\n- Female sex\n\n# Aetiology\n\nCauses of constipation include:\n\n- Dietary factors, such as inadequate fibre or fluid intake\n- Behavioural factors, like inactivity (common cause of constipation in inpatients) or avoidance of defecation\n- Electrolyte disturbances, like hypercalcaemia\n- Certain drugs, particularly opiates, calcium channel blockers and some antipsychotics\n- Neurological disorders, like spinal cord lesions, Parkinson's disease, and diabetic neuropathy\n- Endocrine disorders, such as hypothyroidism\n- Colon diseases, like strictures or malignancies. Bowel obstruction can also cause complete constipation (obstipation)\n- Anal diseases, like anal fissures or proctitis\n\n# Signs and symptoms\n\nSymptoms and signs of constipation include:\n\n- Infrequent bowel movements (less than 3 per week)\n- Difficulty passing bowel motions\n- Tenesmus\n- Excessive straining\n- Abdominal distension\n- Abdominal mass felt at the left or right lower quadrants (stool)\n- Rectal bleeding\n- Anal fissures\n- Haemorrhoids\n- Presence of hard stool or impaction on digital rectal examination\n\nALARMS features which may indicate gastrointestinal malignancy include: anaemia, weight loss, anorexia, recent onset, melaena/haematemesis/PR bleeding, swallowing difficulties\n\n\n# Investigations\n\n### 2-week-wait criteria\n\n- Constipation (or diarrhoea) with weight loss, 60 and over. Consider an urgent, direct access CT scan, or an urgent ultrasound scan if CT is not available, to rule out **pancreatic cancer**\n\nIf it a patient does not fit the 2-week-wait criteria above, and the cause is thought to be primary, then it is likely that no further investigations are needed.\n\nHowever, if there is suspicion over secondary causes of constipation, investigations may include:\n\nBedside:\n\n- PR exam\n- Stool culture – MC&S, ova,cysts,parasites\n- FIT testing (if accompanied with new rectal bleeding and signs suggestive of colorectal cancer), faecal calprotectin\n\nBloods:\n\n- Full blood count (may show an anaemia), U+Es (including calcium), TFTs\n\nImaging:\n\n- Abdominal x-ray if suspicious of a secondary cause of constipation such as obstruction (may reveal faecal loading)\n- Barium enema if suspicious of impaction or rectal mass\n- Colonoscopy if suspicious of lower GI malignancy\n\n[lightgallery]\n\n# Management\n\nConservative:\n\n- Lifestyle modifications such as dietary improvements and increased exercise\n\nMedical:\n\n**Laxatives** are the mainstay of treatment, please see summary table below.\n\n| Class of Laxative | Drug Name Example | Indication | Mechanism of Action | Side Effects | Contraindications |\n|---------------------|-------------------|--------------------------------------------------------------|---------------------------------------------------------|---------------------------------------|-----------------------------------------------------------|\n| Bulking Agents | Ispaghula Husk | Used for constipation, especially in individuals who need to increase stool bulk. | Increase faecal mass and stimulate peristalsis | Contraindicated in dysphagia, GI obstruction, faecal impaction | Colonic atony, faecal impaction, intestinal obstruction, reduced gut motility, sudden change in bowel habit that has persisted more than two weeks; undiagnosed rectal bleeding |\n| Stimulant | Senna, bisacodyl | Used for short-term relief of constipation. | Increase intestinal motility | Cramps | Contraindicated in acute obstruction or colitis; Prolonged use causes colonic atony (+ melanosis coli) |\n| Stool Softeners | Sodium Docusate, Macrogol | Used to soften stool and make bowel movements easier. | Use in fissures, reduce anticipatory withholding | Flatulence, nausea | Ileus; intestinal obstruction; intestinal perforation; risk of intestinal perforation; severe inflammatory bowel disease; toxic megacolon | \n| Osmotic Laxatives | Lactulose | Used for the treatment of constipation, particularly in cases of hepatic encephalopathy. | Retain fluid in bowel and discourage ammonia-producing microorganisms; First-line for hepatic encephalopathy | Abdominal discomfort, flatulence, diarrhea, electrolyte imbalance | Known hypersensitivity to lactulose, galactosemia, intestinal obstruction |\n| Phosphate Enema | Phosphate Enema | Used for rapid bowel evacuation, often before medical procedures or examinations requiring an empty bowel. | Rapid bowel evacuation, need digital rectal examination (DRE) first | Abdominal cramps, electrolyte imbalance, dehydration | Contraindicated in patients with renal impairment, heart failure, electrolyte abnormalities, and those at risk of phosphate nephropathy |\n\n\nIf laxatives fail to resolve symptoms, referral to a specialist centre for evaluation of gut motility may be necessary. \n\nSurgical:\n\n- If suspicions of colorectal cancer, referral to lower GI/colorectal surgeons\n- If concerns over obstruction these patients need to go to A&E for urgent management and imaging\n\n# NICE Guidelines\n\n[NICE: Treatment Summary: Constipation](https://bnf.nice.org.uk/treatment-summary/constipation.html)\n\n# References\n\n[World Gastroenterology Organisation: Constipation](https://www.worldgastroenterology.org/guidelines/global-guidelines/constipation)\n",
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"question": "A 65 year old male presents to GP with 2 day history of diarrhoea and soiling. He denies fevers; he feels nauseous but is otherwise well with no vomiting. Previously he has tended towards constipation and opens his bowels on average three times per week. He denies weight loss or bleeding per rectum.\nOn examination he has diffuse mild abdominal tenderness, and hard stool in his rectum but no blood.\n\nWhich of the following is the most likely diagnosis?",
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"explanation": "Levomepromazine is a typical antipsychotic drug that affects multiple receptor types (adrenergic, dopaminergic, histamine, muscarinic and serotonin receptors). It is used primarily for its anti-emetic and sedative properties in palliative care.",
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"explanation": "Midazolam is a rapid acting benzodiazepine used to treat terminal agitation at the end of life.",
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"explanation": "Betahistine is used as a treatment for vertigo in menieres disease",
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"explanation": "Glycopyrronium is an anti-cholinergic (anti-muscarinic) agent used to reduce excessive secretions at the end of life.",
"id": "61994",
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"name": "Glycopyrronium",
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"__typename": "QuestionChoice",
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"explanation": "Hyoscine Butylbromide (commonly referred to by a brand name, Buscopan) is an anti-spasmodic, not used as an anti-emetic.",
"id": "61996",
"label": "d",
"name": "Hyoscine Butylbromide",
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"explanation": "# Summary\n\nMedications in end-of-life care focus on alleviating distressing symptoms in patients nearing death. A holistic approach is vital, considering physical, emotional, and social aspects of symptoms, often involving a multidisciplinary team. For pain management, the WHO pain ladder guides pharmacological strategies, with morphine as the primary strong opioid. Specific treatments for other symptoms depend on the underlying cause and it is important to consider reversible causes and non-pharmacological measures.\n\n\n\n# Definition\n\nMedications used in end of life care aim to relieve distressing symptoms which may appear in the last days, weeks, or months of life. They are commonly prescribed as 'anticipatory' or 'just in case' medications for a patient known to be nearing the end of life.\n\n\nThey can be administered:\n\n\n- Orally - if the patient is safely able to swallow\n- Subcutaneously - via single dose or continuous syringe pump\n- Transdermally - especially for stable symptoms and if available\n- Intramuscularly - less common\n- Intravenously - less common, but may be helpful if a patient already has access\n\n## A note on holistic care\n\nIn palliative care, and in medicine, it is important to consider all symptoms in context. There are many different aspects to symptoms. These include the physical cause, the patient's beliefs about their illness and symptoms, social contributors and impacts, their emotional and behavioural responses. Holistic assessment and management are crucial, which is why the multidisciplinary team is so important. \n\nFor example, a patient may have been prescribed very effective analgesia but is unable to administer medicines themselves. They may also have a very strong emotional response to pain or believe that they deserve their symptoms. They may benefit from a package of care or financial support for terminal illness which a social worker could help with, or an occupational therapist to help with activities of daily living. Counselling may give the patient a space to explore their feelings around their symptoms and their illness, while spiritual support could alleviate some existential distress. These additional interventions work alongside pharmacological therapy to optimise a person's quality of life through their illness.\n\nThis chapter focuses on medications for symptoms towards the end of life, but it is crucial to remember that each patient has a different combination of needs which requires an individual assessment and management plan, often with input from a range of health and social care professionals.\n\n# Pain\n\n\nInitial pharmacological management of pain should follow the WHO pain ladder. Once patients have reached the top of this ladder (requiring regular strong opioids), careful optimisation is necessary to ensure the right level of pain relief while minimising side effects.\n\n- Morphine is the first-line strong opioid analgesic. This can be given as a modified release or immediate release form. \n- Generally, patients would have a regular 'background' dose based on their 24-hour requirements, plus a PRN dose available for **breakthrough pain.** PRN doses are usually 1/6-1/10 of the 24 hour dose. Analgesia requirements should be reviewed regularly, for example every 24 hours.\n- Alternatives to morphine may be necessary for patients with poor renal function. These include oxycodone, alfentanyl or buprenorphine.\n- When prescribing opioid analgesia consider co-prescribing a regular laxative and an as-required anti-emetic. Monitor for signs of opioid toxicity (respiratory depression, sedation, myoclonus) and switch to alternatives or dose reduce as necessary.\n\nWhen switching analgesia, it is helpful to convert the dose first to oral morphine before converting to the desired medication. Please note that different routes also have different equivalent doses, so it is always safest to check guidelines.\n\n\nThe following table shows dose equivalents of 10mg oral morphine\n\n\n| Analgesic/Route | Dose | Conversion Factor |\n| ----------------------------- | ------- | ----------------- |\n| Codeine/tramadol/dihydrocodeine oral | 100mg | x10 |\n| Diamorphine IM/IV/Subcut | 3mg | x3.3 |\n| Morphine IM/IV/Subcut | 5mg | x2 |\n| Oxycodone oral\\* | 5mg\\* | x2\\* |\n| Oxycodone Subcut\\* | 2.5mg\\* | x4\\* |\n| Alfentanil Subcut | 0.3mg | x30 |\n\n\n*NB - oral oxycodone potency is between 1.3-2x that of oral morphine. Different trusts will adopt different guidance on which you should use. If in doubt, always opt for the lower dose and titrate up.\n\n\n# Breathlessness\n\nConsider non-pharmacological measures for breathlessness first. For example, sitting the patient up, opening a window or setting up a fan can all help.\n\nPharmacological management may involve low-dose opioids, benzodiazepines or therapeutic oxygen, and should be tailored to the patient.\n\n\n# Nausea and vomiting\n\nIt is important to consider the likely cause of nausea and vomiting, as medications target different parts of the vomiting pathway. Perform a full assessment to determine the likely cause of the nausea and vomiting. Consider parenteral routes of administration - patients may have severe gastrointestinal disturbance or at least may not be able to keep down oral antiemetics long enough to be effective.\n\nThe following table shows the primary site of activity and side effects of commonly used antiemetics:\n\n| Antiemetic | Receptor activity | Side effects & cautions | Useful for |\n|---|---|---|---|\n| Metoclopramide | Dopamine antagonist | Extrapyramidal symptoms, drowsiness, restlessness, diarrhoea. Do not give with antimuscarinics or in mechanical bowel obstruction | Gastric stasis, functional bowel obstruction |\n| Cyclizine | Histamine, acetylcholine antagonist | Drowsiness, antimuscarinic | Raised intracranial pressure, vestibular dysfunction |\n| Hyoscine | Acetylcholine antagonist | Antimuscarinic | Motion sickness |\n| Haloperidol | Dopamine antagonist | Less common in palliative care doses | Chemical |\n| Levomepromazine | Dopamine, histamine, acetylcholine, 5HT2 antagonist | Sedation, postural hypotension, antimuscarinic |Broad range |\n| Ondansetron | 5HT3 antagonist | Constipation, arrhythmias, movement disorder | Cytotoxic-related |\n\n- For chemically-mediated symptoms (for example medications, metabolic derangemenet), aim to treat the underlying cause. Antiemetics that may be helpful include haloperidol, metoclopramide or levomepromazine.\n- For nausea and vomiting due to raised intracranial pressure, cyclizine is usually used first-line. Dexamethasone or radiotherapy may be helpful to reduce the pressure-associated symptoms.\n- For patients with vestibular disturbance (for example symptoms associated with movement), cyclizine usually used first-line. Alternatives include hyoscine hydrobromide.\n- For patients with bowel obstruction, seek specialist advice. If due to peristaltic failure, review medications and consider starting metoclopramide (providing there is no colic). Likewise for gastric stasis, consider metoclopramide. For patients with mechanical obstruction and/or colic, do not give metoclopramide. Exclude constipation, give cyclizine for nausea and treat colic with hyoscine butylbromide.\n- If nausea and vomiting is due to compression from an abdominal or pelvic tumour, cyclizine should be used first-line.\n- For anxiety-related nausea and vomiting, begin with non-pharmacological measures for anxiety, such as CBT. A benzodiazepine or levomepromazine would be first-line pharmacological options.\n\n# Agitation\n\nAs with other symptoms, aim to manage reversible causes of agitation and possible delirium first. Consider non-pharmacological measures such as environmental modification. For patients in their last days of life, haloperidol or low-dose midazolam may be prescribed. Often, this is done as part of anticipatory prescribing.\n\n\n# Respiratory tract secretions\n\nRespiratory tract secretions often occur in the last days of life as a person becomes less able to clear their airways. They are rarely a cause of distress to the patient, but may be upsetting for family members or those close to the patient. An antimuscarinic such as hyoscine butylbromide or glycopyrronium bromide may be prescribed for noisy respiratory secretions.\n\n\n# NICE guidelines\n\n\n[NICE Guidance: Care of dying adults in the last days of life](https://www.nice.org.uk/guidance/ng31)\n\n[NICE CKS: Palliative care - general issues](https://cks.nice.org.uk/topics/palliative-care-general-issues/)\n\n[NICE CKS: Palliative care - dyspnoea](https://cks.nice.org.uk/topics/palliative-care-dyspnoea/)\n\n[NICE CKS: Palliative care - nausea and vomiting](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative care - secretions](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative cancer care - pain](https://cks.nice.org.uk/topics/)\n\n# References\n\n[Pallcare.info](https://www.pallcare.info/book.php)\n\n[BNF: Ondansetron](https://bnf.nice.org.uk/drugs/ondansetron/#drug-action)\n\n[BNF: Nausea and labyrinth disorders](https://bnf.nice.org.uk/treatment-summaries/nausea-and-labyrinth-disorders/)\n\n[BNF: Prescribing in palliative care](https://bnf.nice.org.uk/medicines-guidance/prescribing-in-palliative-care/)",
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"question": "Which of the following is most commonly used as an end of life 'anticipatory' medication to treat symptoms of nausea and vomiting?",
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"__typename": "QuestionChoice",
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"explanation": "Statins are unlikely to confer much prognostic benefit at his age. Primary prevention dose statins are prescribed usually on the basis of QRISK score >10% (risk of a cardiac event within next 10 years). The QRISK tool cannot be used for people >84 years old, but NICE suggests using holistic clinical judgement as to whether to prescribe in this case, taking into account comorbidities, polypharmacy, general frailty, and life expectancy.",
"id": "61998",
"label": "a",
"name": "Atorvastatin 20mg OD",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is for BPH and therefore likely to be offering symptomatic benefit",
"id": "62002",
"label": "e",
"name": "Finasteride 5mg OD",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This patient may still have an active sex life despite his age and therefore may be important to continue. Also, as this is a PRN medication, if he is not taking it, stopping it would not significantly reduce polypharmacy.",
"id": "61999",
"label": "b",
"name": "Sildenafil 50mg PRN",
"picture": null,
"votes": 539
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is for pain likely related to his arthritis, and is therefore likely to be of symptomatic benefit",
"id": "62001",
"label": "d",
"name": "Paracetamol 1g QDS",
"picture": null,
"votes": 192
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is for hypertension and should be continued in this case",
"id": "62000",
"label": "c",
"name": "Amlodipine 5mg OD",
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"votes": 52
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"explanation": "# Definition\n\nHypercholesterolaemia is the term used to denote raised serum levels of one or more of total cholesterol.\n\n# Causes\n\nCauses can primary or secondary.\n\nSecondary causes include:\n\n- Familial dyslipidaemias\n- Familial hypercholesterolaemia\n- Apoprotein disorders\n- Medical conditions\n\t- Hypothyroidism\n\t- Obstructive jaundice\n\t- Cushings syndrome\n\t- Nephrotic syndrome\n\t- Chronic Kidney Disease\n- Drugs e.g. thiazide diuretics, glucocorticoids, ciclosporin\n- Pregnancy\n- Obesity \n- Alcohol abuse\n\n\n# Physicial signs\n\nDiagnosis is usually biochemical. \n\nThere are two key physical signs which may indicate familial hypercholesterolaemia\n\n - Premature arcus senilis\n - Tendon xanthomata\n\n# Investigations\n\n- Lipid profile \n- Fasting blood glucose\n- Renal function\n- Liver function tests\n- Thyroid function tests\n\n# Management\n\n\n## Statins\n\n- Statins are the first line treatment of high cholesterol. \n- They are HMG-CoA reductase inhibitors. \n- This enzyme plays a key role in the production of cholesterol, so inhibiting it reduces the cholesterol in the body.\n- In patients with high cholesterol, the QRISK score is used to see if they would benefit from statins as primary prevention against cardiovascular disease. \n- If an adult is under 80 years old and their QRISK is greater than 10% then a statin should be offered. \n- For primary prevention of CVD aim for a greater than 40% reduction in non-HDL cholesterol\n- For secondary prevention of CVD, aim for low-density lipoprotein (LDL) cholesterol levels of 2.0 mmol per litre or less, or non-HDL cholesterol levels of 2.6 mmol per litre or less.\n\n## Doses\n\n- Atorvastatin 20mg is the usual starting dose for primary prevention.\n- For patients who need a statin as secondary prevention, e.g following a stroke, heart attack, peripheral arterial disease or angina, atorvastatin at 80mg starting dose should be used.\n\n## Side effects of statins\n\n\nCommon side effects of statins include muscle pain, abdominal pain, constipation and headache.\n\nIf a patient is struggling with significant myalgia, this may indeed indicate a myositis. Creatinine Kinase can be measured and if it is 5-10 times the upper limit of normal, the statin should be stopped. \n\nStatins can also cause abnormal liver function so this should be monitored with a repeat blood test in 4-6 weeks time. If the transaminases (ALT, AST) are 3 times the upper limit the statin should be stopped.\n\nOffer ezetimibe instead of a statin to people for whom statins are contraindicated/cause abnormal blood test results.\n\n# NICE Guidelines\n\n[NICE Guidelines - Cardiovascular disease: risk assessment and reduction, including lipid modification ](https://www.nice.org.uk/guidance/ng238/chapter/Recommendations)",
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"question": "A 92 year old male is undergoing a medication review at the GP surgery. He is frail, has a past medical history of hypertension, chronic kidney disease 3, osteoarthritis, osteoporosis, erectile dysfuction, and benign prostatic hyperplasia. His conditions and symptoms are well controlled.\n\nWhich of the following medications would be reasonable to discontinue due to lack of clinical benefit?",
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"explanation": "Correct. The bleeding occurs from bridging veins between the dura and arachnoid layers just outside the cortex. This is a low pressure potential space and so blood diffuses around the curve of the brain.",
"id": "62003",
"label": "a",
"name": "Crescent-shaped hyperdense (i.e. appears bright) extra-axial collection that spreads diffusely over the affected hemisphere",
"picture": null,
"votes": 1103
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is an extradural haemorrhage, between the dura and the skull, which usually are tightly adherent, so the blood forces the layers apart like a balloon.",
"id": "62005",
"label": "c",
"name": "A peripheral, hyperdense (i.e. appears bright), bi-convex (lentiform) collection",
"picture": null,
"votes": 152
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "The collection would be expected to be hyperdense (bright) in the acute phase. The appearance is otherwise correct.",
"id": "62004",
"label": "b",
"name": "Crescent-shaped hypodense (i.e. appears dark) extra-axial collection that spreads diffusely over the affected hemisphere",
"picture": null,
"votes": 251
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is a extradural haemmorrhage as above. The collection would also be expected to be hyperdense (bright) in the acute phase.",
"id": "62006",
"label": "d",
"name": "A peripheral, hypodense (i.e. appears dark), bi-convex (lentiform) collection",
"picture": null,
"votes": 44
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is an intracerebral haemmorhage: a bleed in the brain itself. This can be related to chronic hypertension or underlying abnormal vasculature or lesions such as tumour or infarct. There is often surrounding hypodense (darker) oedema.",
"id": "62007",
"label": "e",
"name": "A hyperdense (i.e. appears bright) collection of blood within the parenchyma of the brain",
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"explanation": "\n### Summary\n\nA subdural haematoma (SDH) is a neurological condition characterized by the accumulation of venous blood between the dura mater and arachnoid mater, often following minor trauma in elderly patients. It can present with a reduced Glasgow Coma Scale (GCS), and is commonly seen in patients with fluctuating GCS. Diagnosis is typically established through a CT scan, with the appearance of the clot varying based on its age. Management strategies largely depend on the stage of the haematoma, with craniotomy indicated for acute haemorrhages, and burr holes recommended for chronic haemorrhages.\n\n### Definition\n\nA subdural haematoma is characterised by the accumulation of venous blood in the potential space between the dura mater and arachnoid mater of the brain.\n\n### Epidemiology\n\nSubdural haematomas typically occur in elderly individuals, particularly those over 65 years of age. It is often a consequence of minor trauma, leading to shearing forces that tear bridging veins between the cortex and dura mater. Risk factors include:\n\n- Advancing age (>65 years old)\n- Bleeding disorders or anticoagulant therapy\n- Chronic alcohol use\n- Trauma.\n\n### Aetiology\n\nThe haematoma results from shearing forces that tear the bridging veins between the cortex and dura mater. These forces commonly arise from minor head traumas but can also occur spontaneously in patients with bleeding disorders, anticoagulant therapy, or chronic alcohol use.\n\n### Signs and Symptoms\n\nClinical presentation of a subdural haematoma varies but may include:\n\n- Headache\n- Nausea or vomiting\n- Confusion\n- Fluctuating GCS\n- Behavioural change.\n\n\n### Differential Diagnosis\n\nDifferential diagnoses for subdural haematoma include:\n\n- Epidural haematoma: Characterized by a brief loss of consciousness, followed by a \"lucid interval\" and then rapid neurological deterioration.\n- Traumatic brain injury: Symptoms may include headache, confusion, lightheadedness, dizziness, blurred vision, or tired eyes.\n- Stroke: Presents with sudden numbness or weakness, especially on one side of the body, confusion, trouble speaking or understanding, trouble seeing in one or both eyes, and trouble walking, dizziness, or loss of balance or coordination.\n- Dementia: Gradual cognitive decline without fluctuating GCS.\n- Migraine: Recurrent headaches that might be accompanied by nausea, vomiting, and sensitivity to light and sound.\n\n### Investigations\n\nDiagnosis of a subdural haematoma is primarily established through a CT scan. \n\nThe appearance of the clot varies based on its age:\n\n- Hyperacute phase (<1 hour): The clot may appear isodense, with underlying cerebral oedema.\n- Acute phase (<3 days): The clot appears as a crescent-shaped hyperdense extra-axial collection over the affected hemisphere.\n- Sub-acute phase (3 days to 3 weeks): The clot appears more isodense compared to the adjacent cortex, making identification more difficult. Contrast-enhanced CT or MRI can aid identification. There may be associated mass effect causing midline shift and sulcal effacement.\n- Chronic phase (>3 weeks): The haematoma appears hypodense relative to the adjacent cortex.\n\n[lightgallery]\n\n[lightgallery1]\n\nFurther investigations may include:\n\n- Routine blood tests including FBC, Renal Profile, Liver Function Tests\n- Clotting profile (to assess for coagulopathy)\n\n### Management\n\nManagement of a subdural haematoma depends on the stage, patient’s premorbid baseline, and functional status. Many cases are managed conservatively, especially if there is no midline shift or cerebral oedema. However, for more severe cases, neurosurgical referral is required.\n\n- **Conservative management**: If no significant midline shift or cerebral oedema.\n\t- For patients taking the DOAC dabigatran, Idarucizumab is a licensed NICE-approval reversal agent which can be given.\n- **Surgical management**: In cases where intervention is necessary, options include:\n - **Craniotomy**: Typically for acute haemorrhages.\n - **Burr holes**: Typically for chronic haemorrhages.\n",
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"question": "A 79 year old male presents to A&E after a fall 2 days ago. He was initially fine but has been increasingly confused since. He complains of mild headache and has vomited twice. CT head shows a subdural haemmorhage.\n\nWhich of the following describes the classical appearance of acute SDH on imaging?",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "Frontotemporal dementia (FTD) is characterised by changes in behaviour, personality, and language. The patient in this scenario presents with symptoms that are consistent with FTD, due to degeneration of neurons in the frontal and temporal lobes. MCA is not a specific tool to diagnose FTD, it only indicates the patient's cognitive function which is normal in this case. The anterior temporal lobes are particularly affected in FTD, and this is reflected in the MRI finding of temporal lobe atrophy.",
"id": "62008",
"label": "a",
"name": "Frontotemporal dementia",
"picture": null,
"votes": 2187
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Parkinson's dementia occurs more than one year after the diagnosis of Parkinson's disease, which is not the case here. On top of that, it is characterised by three cardinal features: parkinsonism in extremities, visual hallucinations, and fluctuations in lucidity. MRI findings in Parkinson's dementia are atrophy of the hippocampus and the amygdala, and decreased gray matter volume in the frontal and temporal lobes.",
"id": "62012",
"label": "e",
"name": "Parkinson's dementia",
"picture": null,
"votes": 23
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Alzheimer's disease is characterised by a gradual onset (over several years) of memory impairment, which is followed by difficulties in language and executive function. It should be suspected in adults who demonstrate long-lasting problems with spatial navigation and visual awareness, and usually manifests as wandering or becoming lost.",
"id": "62010",
"label": "c",
"name": "Alzheimer's disease",
"picture": null,
"votes": 72
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Dementia with Lewy bodies (DLB) is characterised by initial cognitive deterioration, prominent deficits in attention, visual hallucinations, fluctuating cognitive function, followed by extrapyramidal symptoms such as rigidity, bradykinesia, gait instability, and autonomic dysfunction which develop within one year of onset.",
"id": "62009",
"label": "b",
"name": "Lewy-body dementia",
"picture": null,
"votes": 45
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Vascular dementia usually presents in patients with history of multiple cerebrovascular events, either transient ischaemic attacks or strokes. Typically there is a step-wise deterioration of cerebral function with each event. It should be considered in those with a history of cerebrovascular disease with global impairment of cognition.",
"id": "62011",
"label": "d",
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"explanation": "# Summary\n\nFrontotemporal dementia (FTD) is a neurodegenerative disorder primarily affecting the frontal and temporal lobes of the brain. It characteristically presents at a younger age compared to other forms of dementia, with early personality changes and language impairments being key signs and symptoms. Investigations often involve neuroimaging and genetic testing, particularly in cases of suspected hereditary conditions. The management of FTD includes symptom-targeted strategies, with behavioural and psychological interventions playing a crucial role. One specific cause of FTD is Pick's disease, characterised by the accumulation of TAU proteins in neurons, identified post-mortem.\n\n# Definition\n\nFrontotemporal dementia (FTD) is a heterogeneous group of neurodegenerative disorders characterised by progressive atrophy of the frontal and/or temporal lobes of the brain, leading to impairments in behaviour, personality, language, and motor functions.\n\n# Epidemiology\n\nFTD is one of the most common forms of early-onset dementia, with the age of onset typically occurring during the sixth or seventh decade of life. The prevalence and incidence rates of FTD vary globally due to genetic and environmental factors.\n\n# Aetiology\n\nThe precise aetiology of FTD is unknown; however, the condition is thought to result from the atrophy of the frontal and temporal lobes of the brain. Genetic mutations can play a role, particularly in familial cases. One specific cause is Pick's disease, characterised by the presence of \"Pick's bodies\" - accumulations of TAU protein within neurons. FTD is associated with ALS - 40% of people with FTD carry same genetic mutation which is commonest cause of ALS.\n\n# Signs and Symptoms\n\nFTD typically presents with:\n\n- Personality changes: Patients often exhibit disinhibited behaviour and apathy early on.\n- Language impairments: Early language difficulties can be present, varying from mild problems with word finding to severe aphasia.\n- Cognitive decline: Although memory may be relatively preserved in the early stages, executive function is frequently impaired.\n- Motor abnormalities: Some patients may develop features of motor neuron disease, including muscle weakness and dysarthria.\n\n# Differential Diagnosis\n\nThe differential diagnosis for FTD includes other forms of dementia and neurological disorders, such as:\n\n- Alzheimer's disease: Characterised by memory loss, confusion, trouble handling money and paying bills, and mood changes. Pathology is defined by the presence of beta-amyloid plaques and neurofibrillary tangles.\n- Vascular dementia: Presents with step-wise cognitive decline, focal neurological signs, and evidence of cerebrovascular disease on neuroimaging.\n- Creutzfeldt-Jakob disease: Rapidly progressive dementia with neurological signs such as myoclonus, ataxia, and visual disturbances. Periodic sharp wave complexes on EEG are suggestive.\n- Primary progressive aphasia: Characterised by gradual, insidious decline in language abilities with relative preservation of other cognitive functions, at least in the early stages.\n\n# Investigations\n\nDiagnosis of FTD often involves:\n\n- Neuroimaging: Structural imaging (MRI or CT) can show atrophy of the frontal and/or temporal lobes. Specifically, MRI can show focal gyral atrophy and knife-blade appearance.\n- Genetic testing: This may be used in cases where an inherited form of FTD is suspected, especially if there is a strong family history.\n\n# Management\n\nThere is currently no cure for FTD; management focuses on alleviating symptoms and providing support. Strategies include:\n\n- Behavioural interventions: Counselling, behaviour modification strategies, and caregiver support can help manage behavioural symptoms.\n- Pharmacotherapy: Selective serotonin reuptake inhibitors (SSRIs) and antipsychotics can help control behavioural symptoms, though their use must be carefully balanced against side effects.\n- There is no good evidence that the cholinesterase inhibitors or memantine help people with FTD, including Pick's disease. In some people they may make symptoms worse.\n- Supportive care: Speech and language therapy, physiotherapy, and occupational therapy can help manage the impacts of the disease on daily functioning.\n \n# NICE Guidelines\n\n[Click here to see information on NICE\nCKS on dementia](https://cks.nice.org.uk/topics/dementia/)",
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"question": "A 65-year-old man presents to the GP clinic with his wife, complaining of binge eating, impulsiveness, and increased sexual activity. His wife states that people have a hard time understanding his speech, and he often forgets the names of his close friends. Otherwise, there are no other memory problems. He can care for himself, manage his accounts, and mingle well. His past and family history are insignificant.\n\nVital signs and physical and neurological examination are unremarkable. The Montreal Cognitive Assessment (MCA) score is 26/30, and a recent brain MRI shows asymmetrical anterior left temporal atrophy.\n\nWhat is the most likely diagnosis?",
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"explanation": "Alzheimer's dementia is characterised by a gradual onset (over several years) of memory impairment, which is followed by difficulties in language and executive function. The patient's history of recurrent visual hallucinations and sleep disturbances are not typical features of Alzheimer's dementia. It should be suspected in adults who demonstrate long-lasting problems with spatial navigation and visual awareness, and usually manifests as wandering or becoming lost.",
"id": "62015",
"label": "c",
"name": "Alzheimer's dementia",
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"votes": 102
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Multiple sclerosis (MS) is a chronic autoimmune disorder that affects the brain, spinal cord, and optic nerves. MS is more common in females under the age of 50 years, often presents as muscle (sensory) weakness, spasticity, loss of balance, and visual disturbances. The patient's wife mentions that he tends to hallucinate and become restless quite often, which are not typical symptoms of MS.",
"id": "62017",
"label": "e",
"name": "Multiple sclerosis",
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"explanation": "Vascular dementia usually presents in patients with history of multiple cerebrovascular events, either transient ischaemic attacks or strokes. Typically there is a step-wise deterioration of cerebral function with each event. It should be considered in those with a history of cerebrovascular disease with global impairment of cognition.",
"id": "62014",
"label": "b",
"name": "Vascular dementia",
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"explanation": "Pseudo-dementia is a functional psychiatric illness (or rarely a deliberate simulation) that can mimic the apparent cognitive decline of true dementia. It is believed that pseudo-dementia is triggered by intense stress and head injuries, and linked to depression. It will characteristically ameliorate once the depression has been treated.",
"id": "62016",
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"explanation": "The most likely diagnosis in this scenario is Lewy-body dementia (LBD). It is a progressive degenerative dementia that is characterised by a decline in cognitive function, and symptoms such as visual hallucinations, sleep disturbances, and behavioural changes. The patient has difficulty maintaining attention and is easily distracted and disinterested, however, he is able to recall vivid details about his early life. This is an example of **fluctuating cognitive function** which is a common feature of LBD. Additionally, his examination findings (features of parkinsonism) further supports the diagnosis. Lewy-body dementia is characterised by the presence of Lewy bodies in the brainstem and cortex with a myriad of features of dementia and Parkinsonism.",
"id": "62013",
"label": "a",
"name": "Lewy-body dementia",
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"explanation": "# Summary\n\nDementia with Lewy bodies (DLB) is a progressive, complex condition, accounting for approximately 10-15% of dementia cases. DLB is characterised by the presence of Lewy bodies, abnormal protein deposits, within brain cells, particularly in the substantia nigra, paralimbic, and neocortical areas. The clinical picture is often characterised by fluctuating cognition, Parkinsonism, and visual hallucinations. A diagnosis is primarily clinical, although dopamine uptake scanning can provide supplementary data. Patients with DLB are highly sensitive to neuroleptics, potentially exacerbating Parkinsonism. \n\n# Definition\n\nDementia with Lewy bodies (DLB) is a type of progressive dementia caused by deposits of an abnormal protein, alpha-synuclein, forming cytoplasmic inclusions known as Lewy bodies within brain cells. These aggregates disrupt normal cell functioning and eventually lead to neuronal death.\n\n# Epidemiology\n\nDLB is the third most common type of dementia, following Alzheimer's disease and vascular dementia. It represents around 10-15% of all dementia cases.\n\n# Aetiology\n\nThe primary pathological feature of DLB is the presence of Lewy bodies in the brain's substantia nigra, paralimbic, and neocortical areas. However, the exact cause of this accumulation remains unknown. An association with Parkinson's disease has been noted, with many patients exhibiting overlapping symptoms. \n\nNew research suggests that LBD and Parkinson’s disease have much more overlap than originally thought. Parkinson’s disease starts in the basal ganglia/brainstem and then progresses upwards towards cerebral cortex (hence dementia is late), whereas in LBD the process progresses downwards from the cerebral cortex.\n\n# Clinical Features\n\nThe clinical features of DLB include:\n\n- Fluctuating cognition: Changes in attention and alertness may occur\n- Parkinsonism: Rigidity, bradykinesia, and postural instability are common\n- Visual hallucinations: Patients often experience complex and recurrent visual hallucinations\n\t- Classically, patients complain of seeing small mammals around them \n- High sensitivity to neuroleptics: These drugs can induce or worsen parkinsonism\n\nA general rule of thumb that can help with distinguishing LBD form Parkinson's disease (PD) is if cognitive impairment and parkinsonism develop <1 year of each other, it is likely LBD. If diagnosed with PD and dementia develops >1 year later this is Parkinson’s disease.\n\n# Differential Diagnosis\n\nDifferential diagnoses for DLB include:\n\n- Alzheimer's disease: Characterised by gradual memory loss, difficulties with problem-solving, and changes in mood or behaviour. However, Alzheimer's patients do not typically exhibit the severe sensitivity to neuroleptics seen in DLB.\n- Parkinson's disease dementia: While it shares many symptoms with DLB, Parkinson's disease dementia typically starts with motor symptoms before cognitive decline. \n- Vascular dementia: This condition features stepwise cognitive decline and evidence of cerebrovascular disease. Parkinsonism and hallucinations are less common.\n\n# Investigations\n\nDiagnosis is primarily clinical, involving a careful medical history and physical examination. However, some additional investigations may be useful, such as:\n\n- Dopamine transporter (DaT) scan: This can help distinguish DLB from other types of dementia.\n- Neuropsychological testing: To assess cognitive functioning and fluctuations.\n- Electroencephalography (EEG): Although not diagnostic, a slowing background rhythm may be seen in DLB.\n\n\n# Management\n\nManagement of DLB includes should follow the biopsychosocial model - please see our Dementia section for holistic management principles.\n\n- Non-pharmacological interventions: These include cognitive stimulation, physical therapy, and occupational therapy.\n- Supportive care: As DLB is a progressive disorder, palliative and end-of-life care considerations are essential.\n- Medications: Cholinesterase inhibitors can help manage cognitive symptoms. However, caution is required with antipsychotic medications due to neuroleptic sensitivity.\n\n\n# NICE Guidelines\n\n[Click here to see information on NICE CKS on dementia](https://cks.nice.org.uk/topics/dementia/)",
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"question": "A 70-year-old man is brought to the emergency department after falling and breaking his hip. When questioned further, it becomes apparent that he is confused, has trouble maintaining attention and easily distracted and disinterested. However, when asked about his childhood memories, he is able to recall vivid details about his early life. His wife mentions that he tends to hallucinate and become restless quite often. On Mini-Mental State Examination, he scores 21 and exhibits bradykinesia, a shuffling gait, and a tremor in his left hand.\n\nWhat is the most likely diagnosis?",
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"explanation": "Lithium is commonly used to treat bipolar disorder. There is a high chance of developing delirium following exposure to it. Therefore, it is avoided.",
"id": "62022",
"label": "e",
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"explanation": "Trimipramine is a tricyclic antidepressant medication that is commonly used to treat depression. It is avoided due to the fear of drug-induced delirium.",
"id": "62020",
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"explanation": "Nortriptyline is commonly used to treat depression, anxiety, and chronic pain. Tricyclic antidepressants are avoided as they cause drug-induced delirium.",
"id": "62021",
"label": "d",
"name": "Nortriptyline",
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"explanation": "Risperidone is an atypical antipsychotic medication that is commonly used to treat a wide range of psychiatric disorders, including psychosis, bipolar disorder, and schizophrenia.",
"id": "62019",
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"explanation": "Delirium is an acute confusional state characterised by severe changes in behaviour and cognition. It is often triggered by an illness, medication, or withdrawal from a substance. Patients with delirium may present with visual hallucinations, delusions, and frank psychosis. The lowest possible dose of olanzapine or haloperidol is preferred if supportive management fails.",
"id": "62018",
"label": "a",
"name": "Olanzapine",
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"comment": "why olanzapine and not risperideone?",
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"comment": "Hello, I did some quick searching and found that olanzapine has a faster onset of action compared to Risperidone. In addition, Risperidone also has higher incidence of extra-pyramidal side effects and should be used with caution in elderly patients. Happy to be corrected if anyone else has any further information",
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"comment": "Why not haloperidol?",
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"comment": "because its not an option in the question",
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"explanation": "# Summary\n\nDelirium, also known as acute confusional state, is a frequent condition, primarily observed among elderly individuals. It manifests through symptoms such as disorientation, hallucinations, inattention, memory problems, mood or personality changes, and disturbed sleep. Comprehensive investigation includes physical examination and infection screen. Management focuses on treating the underlying cause, optimising the patient's environment, and, in severe cases, considering sedative measures.\n\n# Definition\n\nDelirium is an acute and fluctuating disturbance in attention and cognition, often accompanied by a change in consciousness. It is typically reversible and frequently seen in the elderly, particularly in inpatient settings. It manifests in three subtypes:\n\n* **Hyperactive** Delirium: Marked by increased psychomotor activity, restlessness, agitation, and hallucinations.\n* **Hypoactive** Delirium: Characterised by lethargy, reduced responsiveness, and withdrawal.\n* **Mixed** Delirium: Combines features of both hyperactive and hypoactive delirium.\n\n# Epidemiology\n\nDelirium is a common condition, predominantly affecting elderly people, and is seen in up to 30% of elderly inpatients. The incidence increases with age, severity of illness, and the presence of pre-existing cognitive impairment.\n\n# Aetiology\n\nThe causes of delirium can be multifactorial and are remembered using the mnemonic DELIRIUMS:\n\n- D: Drugs and Alcohol (Anti-cholinergics, opiates, anti-convulsants, recreational)\n- E: Eyes, ears and emotional disturbances\n- L: Low Output state (Myocardial Infarction, Acute Respiratory Distress Syndrome, Pulmonary Embolism, Congestive Heart Failure, Chronic Obstructive Pulmonary Disease)\n- I: Infection\n- R: Retention (of urine or stool)\n- I: Ictal (related to seizure activity)\n- U: Under-hydration/Under-nutrition\n- M: Metabolic disorders (Electrolyte imbalance, thyroid disorders, Wernicke's encephalopathy)\n- (S): Subdural hematoma, Sleep deprivation\n\n# Signs and Symptoms\n\nDelirium can present in a number of different ways, including:\n\n- Disorientation\n- Hallucinations - visual or auditory\n- Inattention\n- Memory problems\n- Change in mood or personality. **Sundowning** is agitation and confusion worsening in the late afternoon or evening.\n- Disturbed sleep\n\nPatients may be hypoactive (sedated) or hyperactive (very agitated), and these presentations can fluctuate over time. Hyperactive delirium is easily seen due to the presentation, while hypoactive delirium can be easily missed as patients may appear more withdrawn.\n\n# Differential Diagnosis\n\nDelirium can mimic several other conditions and it's crucial to consider the following in differential diagnosis, each with its key signs and symptoms:\n\n- Dementia: Characterized by gradual onset, stable consciousness level, and progressive decline in cognitive function.\n- Psychosis: May present with hallucinations and delusions, but usually with preserved orientation and memory.\n- Depression: May exhibit poor concentration and slow cognition, but typically with a stable consciousness level and often accompanied by pervasive feelings of sadness or guilt.\n- Stroke: Abrupt onset with focal neurologic signs and specific deficits in speech, motor, or sensory function.\n \n# Investigations\n\n- 4AT and CAM are commonly used tools for delirium assessment.\n\nInitial investigations should include a comprehensive physical examination and infection screen. Additional investigations should be guided by clinical suspicion based on the patient's history and physical examination. These may include:\n\n- Bedside - bladder scan, review medications, ECG (arrhythmias, ischaemic changes that could cause hypoperfusion) urine MC&S - you should not perform urine dipstick if >65 as they are less sensitive in this age group.\n- Bloods: FBC, urea and electrolyes, liver function tests, thyroid function tests, and blood cultures.\n- Imaging: chest X-ray, or ultrasound of the abdomen. Neuroimaging with CT or MRI head is reserved for those without a clear identifiable cause.\n\n\n# Management\n\nManagement of delirium primarily focuses on treating the underlying cause. Non-pharmacological strategies should be the first line, which include:\n\n- Providing an environment with good lighting\n- Maintaining a regular sleep-wake cycle\n- Regular orientation and reassurance\n- Ensuring the patient's glasses and hearing aids are used if needed\n\nFor patients who are extremely agitated and potentially a danger to themselves or others, pharmacological interventions such as small doses of haloperidol or lorazepam. Olanzapine may also be considered however, these should be used with caution, especially in the elderly, due to the risk of side effects. \n\n# NICE Guidelines\n\nFor more information, see [NICE CKS on delirium](https://cks.nice.org.uk/topics/delirium/).",
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"question": "A 78-year-old woman in long-term residential care has recently become confused, disoriented and hallucinating following a chest infection. She has already been prescribed antibiotics for the chest infection, which she started taking a day ago. The staff are concerned that she is a risk to herself. They have attempted verbal and non-verbal de-escalation techniques; however, she continues to be agitated and restless.\n\nWhat is the single most appropriate short-term medication?",
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"explanation": "While it is important to address the patient's emotional distress, a referral to a psychiatrist may not be necessary in this case. The patient's symptoms are consistent with normal grief reactions and do not suggest the presence of a mental health disorder.",
"id": "62024",
"label": "b",
"name": "Refer to a psychiatrist",
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"explanation": "In this case, the patient is experiencing **normal grief reaction** after the loss of his wife. Grief can be a difficult and emotionally overwhelming experience, and it is important to provide support and reassurance to the patient. Offering social support, such as connecting the patient with a support group or community resources, can also help promote healing and coping with his grief.",
"id": "62023",
"label": "a",
"name": "Reassure and offer social support",
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"explanation": "As this patient's symptoms are related to a precipitating event, a diagnosis of depression should not be made until after a normal grieving period, usually for about six months or more. Therefore, SSRIs are not offered immediately.",
"id": "62025",
"label": "c",
"name": "Prescribe selective serotonin reuptake inhibitor (SSRI)",
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"explanation": "Risperidone is an antipsychotic medication and is not typically used to treat a normal grief reaction. Illusions and hallucinations of the deceased person are not uncommon, which resolve spontaneously after a few weeks to months. Therefore, it is not an appropriate intervention in this case.",
"id": "62026",
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"explanation": "ECT is considered for treating severe depression in cases where a rapid response is necessary (life-threatening) or if other treatments have been unsuccessful.",
"id": "62027",
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"name": "Electroconvulsive therapy (ECT)",
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"explanation": "# Summary\n\nDepression is a common mental health disorder typified by low mood, anhedonia, significant weight change, sleep and activity changes, fatigue, feelings of guilt or worthlessness, or poor concentration. It is defined by the DSM as the presence of 5 out of 8 symptoms for at least 2 weeks. It is more prevalent in females. Key investigations include FBC, TFT, U+E, LFT, Glucose, B12/folate, cortisol, toxicology screen, and CNS imaging to rule out organic causes. Management strategies encompass low to high intensity psychological interventions, pharmacotherapy including anti-depressants, and in severe cases, lithium or ECT.\n\n# Definition\n\nDepression is a mental health disorder characterised by:\n\n- **ICD-11 Criteria:**\n - Depressive Episode: Depressed mood, loss of interest (anhedonia), and reduced energy (fatigue) persisting for at least two weeks.\n\n- **DSM-V Criteria:**\n - Major Depressive Disorder (MDD): Presence of a major depressive episode lasting at least two weeks, with specific criteria regarding mood, cognitive, and physical symptoms.\n - Persistent Depressive Disorder (Dysthymia): A chronic form of depression lasting for at least two years. \n\nThis consists of the presence of at least five out of a possible eight defining symptoms, during the same two-week period, where at least one of the symptoms is depressed mood or loss of interest or pleasure\n\n**Severity:**\n\n- Mild: Few, if any, symptoms in excess of those required to make the diagnosis (associated symptoms, see below), and the symptoms result in minor functional impairment.\n- Moderate: Symptoms or functional impairment between \"mild\" and \"severe.\"\n- Severe: The number of symptoms, intensity, and impairment are all greatly increased.\n\n\n# Epidemiology\n\nDepression is a highly prevalent mental health disorder. It represents the third most common reason for consulting a general practitioner in the UK. Depression demonstrates a higher prevalence in females.\n\n# Aetiology\n\nThe aetiology of depression involves a complex interplay of genetic and environmental factors. History of previous mental health issues, physical illnesses, and social challenges like divorce, poverty, and unemployment can all contribute to its development.\n\n# Clinical Features\n\nDepression is defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM) as the presence of 5 out of the following 9 symptoms, occurring nearly every day for at least 2 weeks:\n\n1. **Depressed mood or irritability** for most of the day, indicated by either subjective report (feels sad or empty) or observation by others (appears tearful).\n2. **Anhedonia:** Decreased interest or pleasure in most activities, most of the day.\n3. Significant **weight change** (5%) or change in appetite.\n4. **Sleep alterations:** Insomnia or hypersomnia.\n5. **Activity changes:** Psychomotor agitation or retardation.\n6. **Fatigue** or loss of energy.\n7. **Guilt or feelings of worthlessness:** Excessive or inappropriate guilt or feelings of worthlessness.\n8. **Cognitive issues:** Diminished ability to think or concentrate, or increased indecisiveness.\n9. **Suicidality:** Thoughts of death or suicide, or formulation of a suicide plan.\n\n### Additional Features (Severe Depression)\n- **Psychotic Features:** Delusions (e.g. nihilistic delusions, Cotard's syndrome) and hallucinations.\n- **Depressive Stupor:** Profound immobility, mutism, and refusal to eat or drink, sometimes necessitating electroconvulsive therapy (ECT).\n\n# Differential Diagnosis\n\nThe main differentials and their key signs and symptoms include:\n\n- **Bipolar Disorder:** Characterised by periods of mania/hypomania (elevated mood, inflated self-esteem, decreased need for sleep, increased talkativeness, distractibility, increased goal-directed activity) alternating with depressive episodes.\n- **Anxiety Disorders:** Persistent and excessive worry, restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and sleep disturbance.\n- **Psychotic Disorders:** Hallucinations, delusions, disorganised speech, grossly disorganised or catatonic behaviour.\n- **Substance/Medication-Induced Mood Disorder:** Mood disturbance associated with intoxication or withdrawal from substances or side effects of medications.\n- **Adjustment Disorders:** Development of emotional or behavioural symptoms in response to identifiable stressors.\n\n\nVarious organic causes should be considered and ruled out through careful history-taking, physical examination, and relevant investigations. These include:\n\n- Neurological disorders such as Parkinson's disease, dementia, and multiple sclerosis.\n- Endocrine disorders, especially thyroid dysfunction and hypo/hyperadrenalism (e.g., Cushing's and Addison's disease).\n- Substance use or medication side effects (e.g., steroids, isotretinoin, alcohol, beta-blockers, benzodiazepines, and methyldopa).\n- Chronic conditions such as diabetes and obstructive sleep apnea.\n- Long-standing infections, such as mononucleosis.\n- Neoplasms and cancers - low mood can theoretically be a presenting complaint in any cancer, with pancreatic cancer being a notable example.\n\n\n# Investigations\n\n- Standard investigations for depression may include Full Blood Count (FBC), Thyroid Function Test (TFT), Urea and Electrolytes (U&E), Liver Function Test (LFT), Glucose, B12/folate levels, cortisol levels, toxicology screen, and imaging of the Central Nervous System (CNS).\n- These help rule out organic causes (listed above) such as endocrine disorders (e.g. thyroid disorders).\n- There are several questionnaires that can also be used to help assess depressive symptoms, such as the Hospital Anxiety and Depression (HAD) Scale and Patient Health Questionnaire (PHQ-9).\n\n# Management\n\nDepression is usually managed in primary care. GPs can refer to secondary care (Psychiatry) if there is a high-suicide risk, symptoms of bipolar disorder, symptoms of psychosis, or if there is evidence of severe depression unresponsive to initial treatment.\n\r\n**Persistent subthreshold depressive symptoms or mild-to-moderate depression:**\n\n- 1st line = Low-intensity psychological interventions (individual self-help, computerised CBT). \r\n- 2nd line = High-intensity psychological interventions (individual CBT, interpersonal therapy) \r\n- 3rd line = Consider antidepressants \r\n\r\n**Mild depression unresponsive to treatment and moderate-to-severe depression:**\n\n- 1st line = High-intensity psychological interventions + antidepressants (1st line = SSRI)\r\n- 2nd line (Treatment-resistant depression) – switch antidepressants and then use adjuncts \r\n\r\n**Severe depression and poor oral intake/psychosis/stupor:**\n\n- 1st line = ECT \n- Although the exact mechanism remains elusive, it is thought that the induced seizure, rather than the ECT procedure itself, has therapeutic benefits. Short-term side effects of ECT include headache, muscle aches, nausea, temporary memory loss, and confusion, while long-term side effects can include persistent memory loss. Due to the induced seizure, there is a risk of oral damage, and due to the general anaesthetic, a small risk of death.\r\n\n**Recurrent depression:** \n\n- Treated with antidepressant + lithium \r\n\n\nMedical management of depression - additional notes:\n\n- First-line pharmacological treatment typically involves a Selective Serotonin Reuptake Inhibitor (SSRI) such as sertraline. SNRIs such as venlafaxine can also be used first-line, but are less preferable due to the risk of damage from overdose, which is less likely with SSRIs.\n- In people aged 18-25 there is an increased risk of impulsivity and suicidal risk upon commencing antidepressant medication and so they should have a follow-up appointment arranged after one week to monitor progress. Initial reviews can otherwise be arranged 2-4 weeks after starting medication in patients >25.\n- Continuation of antidepressants for at least six months post-remission is recommended to mitigate relapse risk. Tapering should be done gradually over a four-week period when discontinuing antidepressants.\n\n\n\n# NICE Guidelines\n\n[NICE Guidance on the Management of Depression](https://www.nice.org.uk/guidance/cg90)",
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"question": "A 76-year-old man presents to the GP clinic with chest pain. On further questioning, he breaks into tears and feels emotional about the loss of his wife six weeks ago. She passed away due to terminal-stage breast cancer metastasising to the brain. He now feels guilty for not taking care of her properly. He also mentions that he hears his wife's voice intermittently while cooking in the kitchen. His vital signs, serum troponin and ECG, are all normal. He has no past medical history.\n\nWhat is the most appropriate next step in management?",
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"explanation": "In rare cases, aggression, violence, or agitation may pose a safety risk and require urgent treatment with benzodiazepines or antipsychotics after other measures have been unsuccessful. However, it is not the case here.",
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"explanation": "Antidepressants may be helpful if there are symptoms of depression simultaneously with Alzheimer's disease. However, they are not helpful here and are not the most appropriate option.",
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"explanation": "The patient has already tried donepezil and could not tolerate it due to gastrointestinal side effects. Continuing treatment with an increased dose of donepezil would not be an appropriate management plan as well as the next step.",
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"explanation": "**Memantine is the second-line medication**, and it is effective in slowing the progression of cognitive symptoms in patients with moderate to severe Alzheimer's disease. It is a preferred medication for patients who cannot tolerate donepezil.",
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"explanation": "# Summary\n\nAlzheimer's disease, the most common form of dementia, is a progressive neurodegenerative disorder that leads to cognitive decline, memory impairment, and a range of behavioural and psychological symptoms. Its impact extends beyond the individual, affecting families and healthcare systems worldwide. This comprehensive guide explores the key aspects of Alzheimer's disease, from its definition and pathophysiology to clinical features, diagnostic considerations, management approaches, and prognosis. Adherence to NICE guidelines ensures evidence-based care for patients with this challenging condition.\n\n# Definition\n\nAlzheimer's disease is a chronic, neurodegenerative disorder characterized by the progressive accumulation of abnormal protein deposits, primarily amyloid plaques and tau tangles, in the brain. This leads to the deterioration of cognitive function, memory loss, and various behavioural and psychological symptoms.\n\n\n# Epidemiology\n\nAlzheimer's disease is a global health concern, with an increasing prevalence as the population ages. It is estimated that millions of individuals worldwide are affected, with higher incidence rates in older age groups. Women are more commonly affected than men, and several genetic and environmental factors influence disease risk.\n\n\n# Pathophysiology\n\n\nAlzheimer's disease is a complex and progressive neurodegenerative disorder characterized by distinct pathophysiological hallmarks. These hallmarks are responsible for the gradual decline in cognitive function and the characteristic clinical features observed in affected individuals.\n\n1. **Amyloid Plaques:** The accumulation of beta-amyloid protein fragments outside nerve cells in the form of plaques is a hallmark feature. These abnormal protein deposits are believed to disrupt neuronal communication, trigger inflammation, and ultimately lead to cell death.\n\n2. **Tau Tangles:** Inside nerve cells, abnormal tau protein accumulates, forming neurofibrillary tangles. These tangles interfere with the transport of essential nutrients within neurons, contributing to their dysfunction and eventual demise.\n\n3. **Neuronal Loss and Brain Atrophy:** As the disease progresses, significant neuronal loss occurs, particularly in brain regions responsible for memory and cognitive function, such as the hippocampus and the cerebral cortex. This loss is associated with brain atrophy, visible on imaging studies.\n\n4. **Neurotransmitter Imbalance:** Alzheimer's disease disrupts the balance of neurotransmitters, particularly acetylcholine, which plays a crucial role in memory and learning. Reduced acetylcholine levels further contribute to cognitive decline.\n\n5. **Inflammatory Response:** Chronic neuroinflammation, characterized by the activation of microglia and astrocytes, is a prominent feature in Alzheimer's disease. Inflammation may exacerbate neuronal damage and contribute to the progression of the disease.\n\n# Risk Factors\n\nSeveral factors influence an individual's risk of developing Alzheimer's disease. These include:\n\n- **Age:** Advanced age is the most significant risk factor, with the incidence of Alzheimer's disease increasing exponentially after the age of 65.\n\n- **Genetic Predisposition:** Mutations in specific genes, such as the apolipoprotein E (APOE) gene, increase the risk of developing Alzheimer's disease. Additionally, individuals with Down's syndrome are at a higher risk due to a triplication of chromosome 21, which carries the amyloid precursor protein (APP) gene.\n\n- **Family History:** Having a first-degree relative with Alzheimer's disease can increase one's susceptibility.\n\n- **Cardiovascular Risk Factors:** Conditions like hypertension, diabetes, obesity, and hypercholesterolemia have been associated with an elevated risk of Alzheimer's disease.\n\n- **Lifestyle Factors:** Physical inactivity, smoking, and a diet high in saturated fats may contribute to increased risk.\n\n- **Traumatic Brain Injury:** A history of head injuries, particularly repeated concussions, has been linked to a higher risk of developing Alzheimer's disease.\n\n- **Low Educational Attainment:** Lower levels of education may be associated with an increased risk.\n\nUnderstanding these risk factors and their relationship to the disease's pathophysiology is crucial for early identification, prevention, and management of Alzheimer's disease.\n\n# Clinical Features\n\nAlzheimer's disease is characterized by a constellation of cognitive and behavioural symptoms, which may include:\n\n* **Memory Impairment:** Early in the disease, individuals often experience difficulties in recalling recent events and conversations.\n* **Language Impairment:** This may manifest as difficulty finding words, struggling to express oneself, and, in later stages, aphasia.\n* **Executive Dysfunction:** Impaired ability to plan, organize, and carry out tasks, leading to difficulties in activities of daily living.\n* **Behavioural Changes:** Individuals may exhibit agitation, aggression, or apathy, sometimes accompanied by mood swings and irritability.\n* **Psychological Symptoms:** Hallucinations, delusions, and paranoia can occur, particularly in later stages of the disease.\n* **Disorientation:** Affected individuals may become disoriented in familiar surroundings, unable to recognize places or people.\n* **Loss of Motor Skills:** In advanced stages, motor skills decline, leading to difficulties with mobility and self-care.\n\n# Differential Diagnosis\n\n\n1. **Vascular Dementia:** Cognitive impairment in vascular dementia often presents suddenly and is associated with a history of cerebrovascular events.\n\n2. **Lewy Body Dementia:** Visual hallucinations and fluctuating cognitive impairment are more common in Lewy body dementia.\n\n3. **Frontotemporal Dementia:** This condition typically presents with profound behavioural and personality changes, often affecting social conduct.\n\n4. **Mild Cognitive Impairment (MCI):** MCI is a transitional state between normal cognitive aging and dementia. Unlike Alzheimer's, MCI may not significantly impact daily functioning.\n\n5. **Normal Age-Related Cognitive Decline:** Age-related cognitive changes are common but do not interfere significantly with daily activities.\n\n# Investigations\n\nDiagnosing Alzheimer's disease may involve a series of assessments, including:\n\n- **History** - including a functional history, which may be informed using a structured instrument such as the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) or the Functional Activities Questionnaire (FAQ). A collateral history may be necessary, and a risk assessment should also be taken.\n- Assess cognitive decline using an approved scoring tool such as MMSE, MOCA, 10-point Cognitive Screener (10-CS), 6-item Cognitive Impairment Test (6-CIT), 6-item Screener, Memory Impairment Screen (MIS), Mini-Cog, Test Your Memory (TYM) \n- **Examination** - physical examination including a full neurological examination looking for abnormaliities in coordination, gait, sensation and motor signs.\n- **Blood tests** - to rule out reversible causes, this is known as a confusion screen and is often done in primary care. It includes FBC, U&E, LFTs, CRP/ESR, Ca2+, TFTs, B12, folate, syphilis, HIV. If there is an acute onset of symptoms delirium should be considered as this is a different pathway.\n- Once reversible causes are ruled out and a diagnosis of dementia is still suspected, refer to a specialist dementia diagnostic service (such as a memory clinic or community old age psychiatry service. Here, a full functional assessment is carried out and the patient will be referred for **neuroimaging**, such as CT or MRI.\n\t- **Brain Imaging:** Magnetic resonance imaging (MRI) and positron emission tomography (PET) scans can reveal brain atrophy and the presence of amyloid plaques.\n\t- **Cerebrospinal Fluid Analysis:** May be used to detect specific biomarkers associated with Alzheimer's disease.\n\n# Management\n\n- **Non-Pharmacological Approaches:** Psychological interventions, cognitive stimulation therapy, and occupational therapy can help manage behavioural and psychological symptoms.\n\n- **Support for Caregivers:** Education and support for family members and caregivers are vital to help them navigate the challenges of providing care.\n\n- **Patient-Centered Care:** Tailoring interventions to the individual's needs and preferences, while ensuring their safety and well-being.\n- **Pharmacological Intervention:** Medications, such as cholinesterase inhibitors (e.g. donepezil) and N-methyl-D-aspartate (NMDA) receptor antagonists (e.g. memantine), may be prescribed to manage cognitive symptoms.\n\t- Pharmacological treatments may have modest benefits, and include the cholinesterase inhibitors rivastigamine, galantamine, and donpezil in mild-moderate dementia, and the NMDA inhibitor memantine in severe dementia (as classified using the MMSE score: severe: <10; moderate: 10-20; mild: 21-26/30. \n\t- If there is evidence of behavioral and psychological symptoms of dementia (BPSD), low-dose risperidone may be started\n\n\n# NICE Guidelines\n\n[NICE CKS - Dementia](https://cks.nice.org.uk/topics/dementia/)\n\n# References\n\n[NHS UK - Alzheimer's Disease](https://www.nhs.uk/conditions/alzheimers-disease/)\n\n[Alzheimer's Association](https://www.alz.org/alzheimers-dementia/what-is-alzheimers)\n\n\n\n\n\n",
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"question": "A 78-year-old woman was brought to the clinic by her daughter due to confusion and memory impairment. She had been exhibiting behaviours such as starting tasks, forgetting to finish them, and having difficulty naming objects. A diagnosis of Alzheimer's disease was confirmed, and the patient was started on donepezil.\n\nHowever, she has since experienced significant gastrointestinal side effects and multiple episodes of syncope. Additionally, her daughter reports that the patient has been wandering randomly on the streets and hearing voices claiming to be aliens from the moon.\n\nOn examination, the patient is agitated and disoriented and keeps asking the same questions during the interview. Which of the following medication is the most appropriate next step in management for this patient?",
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"explanation": "Cardiac arrhythmias are abnormal heart rhythms that can cause dizziness, fainting, and even sudden cardiac arrest. However, the patient's vital signs are within normal limits, there is no evidence of cardiac injury or dysfunction, and a normal ECG makes a cardiac arrhythmia less likely in this case.",
"id": "62036",
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"name": "Cardiac arrhythmia",
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"explanation": "Orthostatic hypotension is characterised by a drop in blood pressure upon standing up from a sitting posture, which can cause dizziness, light-headedness, and fainting. It is often caused by low blood volume, medications, or underlying medical conditions that affect blood pressure regulation. However, there is no variation in blood pressure from sitting to standing posture, which suggests that his fall was not due to orthostatic hypotension.",
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"name": "Orthostatic hypotension",
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"explanation": "Epilepsy is characterised by recurrent seizures due to abnormal electrical activity in the brain. Seizures typically involve convulsions or twitching and may be accompanied by altered consciousness or behaviour. In this case, the patient did not have any post-ictal state, which suggests that the fall was not due to a seizure.",
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"name": "Epilepsy",
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"explanation": "Vasovagal syncope occurs due to a sudden drop in blood pressure and heart rate, usually triggered by a physiological stimulus such as standing for a long time, emotional distress, or pain. It is characterised by a feeling of light-headedness or dizziness, followed by loss of consciousness, and often involves incontinence due to the relaxation of the sphincter muscles.",
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"explanation": "Alcohol intoxication can cause dizziness, light-headedness, and loss of consciousness, as well as impair judgment and coordination. However, the patient did not report consuming alcohol, and there are no other indications of alcohol use, such as slurred speech or the smell of alcohol on the breath.",
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"explanation": "# Summary\n \nSyncope means a transient loss of consciousness and is a common emergency presentation. There are many causes with important differentials being reflex syncope, orthostatic hypotension and cardiac syncope. The term \"blackouts\" is commonly used to refer to a loss of consciousness, and includes differentials such as seizures. A thorough history (including a collateral if available) is important to help to differentiate the above, followed by examination including a lying-standing blood pressure. Initial investigations include an ECG, a blood glucose and consideration of a basic set of bloods to screen for abnormalities such as hyponatraemia that could trigger seizures. Emergency management encompasses ruling out serious causes, treating any injuries sustained during the episode and referral on for specialist investigations and management as appropriate.\n\n# Definition \n\nBlackouts refer to episodes of transient loss of consciousness, which occur for a variety of reasons. Syncope refers to a transient loss of consciousness secondary to cerebral hypoperfusion, with syncopal presentations making up the majority of cases of blackouts.\n \n# Epidemiology \n \nBlackouts are common, with an estimated 50% of the population experiencing at least one in their lifetime. 3% of emergency department presentations and 1% of hospital admissions in the UK are due to blackouts.\n \n# Aetiology\n \n**Causes of cardiac syncope:**\n\n- Structural\n - Acute myocardial infarction \n - Aortic stenosis \n - Ischaemic cardiomyopathy\n - Hypertrophic obstructive cardiomyopathy\n - Cardiac tamponade\n- Electrical \n - Tachyarrhythmias e.g. superventricular tachycarcia (SVT), ventricular tachycardia (VT), ventricular fibrillation (VF)\n - Bradyarrhythmias e.g. sick sinus syndrome, heart block\n - Inherited channelopathies e.g. Brugada syndrome\n\n**Causes of reflex syncope:**\n \n - Vasovagal syncope (\"fainting\")\n - Situational syncope e.g. following defecation, post-exercise, or straining to pass urine\n - Carotid sinus syndrome - occurs due to hypersensitivity of the carotid sinus baroreceptor\n\n**Other causes of syncope:**\n \n - Orthostatic hypotension\n - Pulmonary embolism\n - Occult haemorrhage e.g. subarachnoid haemorrhage, GI bleeding, ruptured aortic aneurysm\n - Head trauma\n - Hypoglycaemia\n\n **Non-syncopal causes of blackouts:**\n \n - Seizures\n - Psychogenic pseudosyncope\n - Psychogenic non-epileptic seizures\n\n# Symptoms and Signs\n \nWhen taking a history and examining a patient after a blackout, there are several additional symptoms and signs to elicit that can help identify the likely cause. If the blackout was witnessed, take a collateral history also. \n\n**Questions to ask about before the blackout:**\n\n- What were they doing/any triggers?\n - Exertional syncope (cardiac)\n - After exercise (vasovagal/orthostatic hypotension)\n - Head movements/pressure on neck (carotid sinus syndrome)\n - Prolonged standing (orthostatic hypotension)\n - Pain (vasovagal)\n - Repeated episodes after defecation/micturition/swallowing/coughing (situational syncope)\n - After a meal (vasovagal or orthostatic hypotension)\n- Prodromal symptoms?\n - Feeling warm/hot, sweating, nausea (vasovagal)\n - Déjà vu or jamais vu (epilepsy)\n- Intercurrent illness?\n - e.g. diarrhoea and vomiting leading to dehydration and hypotension\n- Associated symptoms?\n - Palpitations/chest pain/shortness of breath (cardiac/PE)\n - Headache (subarachnoid haemorrhage)\n - Visual disturbance (if worse on standing may be orthostatic hypotension/vasovagal)\n - Lightheadedness (orthostatic hypotension/vasovagal)\n \n**Questions to ask about during the blackout:**\n \n- Any protective measures taken?\n - e.g. hands outstretched to break fall \n - It can be difficult to ascertain whether the patient lost consciousness\n - If protective measures were observed may be a fall rather than a blackout\n - Patients having a vasovagal may lower themselves to the floor\n- Tongue biting?\n - Lateral tongue typical in epilepsy\n - Tip of tongue typical in vasovagal\n- Incontinence of bowels or bladder? (epilepsy)\n- Duration of loss of consciousness\n - Less than 30 seconds (suggests syncope)\n - Over 1 minute (suggests epilepsy)\n - Over 5 minutes (psychogenic causes more likely)\n- Seizure activity observed?\n - Myoclonic jerks are common in vasovagal syncope\n - Prolonged limb jerking and abnormal posturing suggests a seizure\n- Appearance during blackout e.g. pallor, eyes closed or open? \n \n\n**Questions to ask about after the blackout:**\n\n- Any injuries sustained during the blackout?\n - Ask about site and severity\n- Confusion or amnesia after conciousness regained?\n - If lasts minutes may indicate post-ictal state after a seizure\n- Focal neurological signs (e.g. weakness down one side)\n\n**Other important questions:**\n\n- Any previous blackouts/similar events?\n- Past medical history e.g. any heart disease?\n- Medications (may contribute to orthostatic hypotension)\n- Family history including sudden cardiac or unexplained death in young relatives\n- Recreational drug and alcohol use (alcohol may exacerbate orthostatic hypotension)\n\n**On examination:**\n\n- Do a full set of observations including a lying standing blood pressure to assess for a postural drop\n - A fall in systolic blood pressure by 20mmHg or more or diastolic by 10mmHg or more, or a fall in the systolic to <90mmHg with symptoms indicates orthostatic hypotension\n- Full systems examination focusing on the heart (e.g. any murmurs or abnormalities of the pulse?)\n- Neurological examination including cognitive function (may be abnormal in the post-ictal state)\n \n# Investigations\n \nInitial investigations as follows should be carried out in the emergency setting; patients should also be referred for further specialist investigations (e.g. EEG for epilepsy, Holter monitoring for suspected arrhythmias) as appropriate.\n\n- **Blood glucose** for hypoglycaemia\n- **ECG** looking for arrhythmias, ischaemic changes or evidence of structural abnormalities (e.g. left ventricular hypertrophy in severe aortic stenosis)\n- **Blood tests** looking for electrolyte abnormalities that could trigger seizures or arrhythmias, anaemia in haemorrhage, raised inflammatory markers in intercurrent illness, AKI in dehydration\n- **Transthoracic Echocardiography** should be done in suspected structural heart disease (e.g. aortic stenosis)\n- **24 hour ambulatory blood pressure monitoring** with an activity diary may be useful to assess for e.g. post-prandial hypotension\n \n# Management\n \n- Specific emergency management may be required for any serious cause identified (e.g. head injury, ruptured aortic aneurysm).\n- Investigate for and treat any injuries resulting from the collapse and provide analgesia.\n- Some patients can be discharged with reassurance and advice e.g. uncomplicated vasovagal episode, situational syncope.\n- Patients with suspected epilepsy should be referred to a first fit clinic.\n- Patients with suspected psychogenic causes of blackouts should also be referred for neurology assessment as these can be difficult to differentiate from epilepsy\n- Patients with suspected cardiac syncope (e.g. abnormal ECG, exercise-induced syncope, heart murmur, heart failure, new/unexplained breathlessness or family history of sudden cardiac death in the young/inherited cardiac condition) should be referred for specialist review within 24 hours.\n- Consider urgent referral for cardiovascular review in all patients over 65 with syncope and no prodromal symptoms.\n- All patients with syncope of unclear cause should be referred for specialist cardiovascular review (with urgency based on the clinical picture)\n\n **Driving advice for patients with syncope:**\n\n- Patients with unexplained syncope must inform the DVLA and their licence will be revoked for 6 months (12 months if Group 2) \n- Patients with a vasovagal whilst standing can drive and need not inform the DVLA if they are Group 1 drivers (Group 2 drivers must not drive and should inform the DVLA)\n- Patients with cardiac syncope must not drive and should inform the DVLA - group 1 drivers may be allowed to drive after 4 weeks if a cause is identified and treated\n- Full guidance including for seizures can be found in the references section\n \n# NICE Guidelines\n \n[NICE CKS Guidance on Blackouts](https://cks.nice.org.uk/topics/blackouts/)\n\n[NICE: Transient loss of consciousness ('blackouts') in over 16s](https://www.nice.org.uk/guidance/cg109)\n \n# References \n \n[DVLA guidance on transient loss of consciousness](https://www.gov.uk/guidance/neurological-disorders-assessing-fitness-to-drive#transient-loss-of-consciousness-blackouts--or-lostaltered-awareness)",
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"question": "A 45-year-old chef presents to the emergency department following a fall in the kitchen after cooking for many hours. He reports feeling lightheaded and dizzy before losing consciousness. He has no memory of the fall and did not experience any convulsions or twitching, or tongue biting. He further mentions that he had soiled his pants unconsciously. Past medical and family history is unremarkable. His vital signs are within normal limits, there is no significant change in BP from sitting to standing, and there are no apparent injuries from the fall. ECG is unremarkable.\n\nWhich of the following is the most likely diagnosis in this patient?",
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"explanation": "Doing nothing and not transfusing blood is also incorrect because it could further deteriorate the patient's condition and potentially harm or even death. If the patient is unconscious, the healthcare professional is deemed to act in the best interest of the patient's health.",
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"label": "b",
"name": "Do not transfuse blood, as there is no patient consent",
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"explanation": "Requesting the husband to sign a disclaimer is also incorrect because it does not address the patient's lack of capacity to make decisions and the need for urgent medical intervention.",
"id": "62042",
"label": "e",
"name": "Request the husband to sign a disclaimer",
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"answer": false,
"explanation": "Waiting for a second opinion from another consultant is an incorrect answer because time is of the essence in this situation and the patient's condition is critical.",
"id": "62040",
"label": "c",
"name": "Wait for a second opinion from another consultant",
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"explanation": "In this case, the patient lacks the capacity to make an informed decision about blood transfusion due to her unconscious state. There is no indication that the patient has an advance directive that allows her husband to make this decision on her behalf. While most Jehovah's Witnesses may carry a blood refusal card, it is not mentioned in this case. Therefore, the appropriate course of action is to **treat the patient as you would any other unconscious patient who presents to the emergency department** until she regains the capacity to make an informed decision.",
"id": "62038",
"label": "a",
"name": "Transfuse blood without consent",
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"explanation": "Seeking judicial review instructions and contacting the Jehovah's Witnesses council is also an incorrect answer because it would take too long, and the patient's condition is not stable enough to wait. This might have been the best choice if the patient was relatively stable and conscious in a non-emergency scenario.",
"id": "62041",
"label": "d",
"name": "Seek judicial review instructions and contact Jehovah's witness council",
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"explanation": "# What are Best Interests? \n\nIf someone lacks capacity to make a specific decision, a decision may have to be made in their _best interests_. This means that a decision will be made on their behalf, having been considered from their point of view. The decision should be one that health and social care professionals believe is the right decision for _that individual patient themselves_ (and not the decision that the professionals desire without taking the patients interests into account).\n\n# Best Interests Criteria\n\nWhen making a best interests decision on behalf of someone who lacks capacity, five factors must be considered:\n\n1. Equal consideration and non-discrimination\n2. All relevant circumstances\n3. Regaining Capcity\n4. Participation\n5. Wishes, Feelings, Beliefs and Values\n\n# What are Equal Consideration and Non-discrimination? \n\nThe person making the decision about what is in the patient's best interests must not make assumptions based on _age, appearance, condition or behaviour_.\n\n# What are All Relevant Circumstances? \n\nIn order to determine what is in the patient's best interests, all the things that the patient would take into account if they were making the decision themselves should be identified .\n\n# Regaining Capacity \n\nIt must be considered whether the patient is likely to regain capacity. If so, the professional(s) need to consider whether or not the decision can be delayed until then.\n\n# Participation \n\nAll practicable steps should be taken in order to encourage and enable participation by the patient in the decision making process.\n\n# Wishes, Feelings, Beliefs and Values \n\nThe wishes, feelings, beliefs and values of the patient should be found out and taken into consideration. This includes views they have expressed in the past, religious or moral opinions, or other factors that might influence the decision they would make themselves.",
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"question": "A 28-year-old unconscious woman is brought to the Emergency Department after a road traffic accident, exhibiting signs of shock and drifting in and out of consciousness. A FAST scan reveals a large collection of free fluid in the peritoneal cavity, requiring immediate blood transfusion. However, her husband objects to the transfusion, citing their devotion to the Jehovah's Witnesses and their opposition to blood transfusion.\n\nWhat is the most appropriate next step in management?",
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"explanation": "It is not appropriate for family members to be responsible for disclosing the results of medical investigations or aspects of care to the patient without a doctor disclosing and discussing it with the patient directly in the first place.",
"id": "62047",
"label": "e",
"name": "Suggest that the family inform the patient of the diagnosis at a later time that they deem appropriate",
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"__typename": "QuestionChoice",
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"explanation": "The patient should be given all relevant information about their health and treatment options, regardless of whether they specifically ask about it.",
"id": "62045",
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"name": "Only reveal the diagnosis to the patient if she specifically asks about it",
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"explanation": "It is not appropriate to delegate the task of disclosing a diagnosis to another healthcare provider, especially one who was not involved in ordering the diagnostic test and treatment of the patient.",
"id": "62046",
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"name": "Wait until the patient has finished grieving and have her GP break the news to her once she is out of the hospital",
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"explanation": "It is essential to respect the patient's right to be fully informed about their health and treatment options. In this case, the patient has the right to know about her cancer diagnosis, regardless of the family's concerns about how they may handle the news. It is important to have an **open and honest conversation with the patient about their diagnosis and treatment options** while also being sensitive to their emotional state and providing support and resources as needed. It is inappropriate to withhold this information from the patient or present the results as inconclusive, as this could affect their ability to make informed decisions about their care.",
"id": "62043",
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"name": "Acknowledge the family's concerns but still inform the patient of her diagnosis, as she has the right to know",
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"explanation": "By withholding the diagnosis from the patient, the healthcare professional would be denying the patient the opportunity to make informed decisions about their treatment and care. Additionally, it could have serious negative consequences for their well-being, as they would not be aware of the true nature of their condition. Therefore, it is paramount to inform the patient of their diagnosis, regardless of their mental state or the potential emotional impact it may have.",
"id": "62044",
"label": "b",
"name": "Agree to keep the patient's cancer diagnosis a secret out of compassion for her mental state",
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"explanation": "# Duties of Care: Legal and Professional\n\nLegal:\n\n1. General Practitioners\n2. Hospitals and their Doctors\n3. All Doctors (GP and Hospital)\n\nProfessional:\n\n1. The GMC\n\n# General Practitioners(GPs)\n\nGPs have a _legal_ duty of care to all persons registered on the General Practice's list, and to anyone who needs emergency help in the practice area.\n\n# Hospitals and their Doctors\n\nIt is the NHS Trusts and Health Authorities who owe a legal duty of care to patients being treated by their employees, not the hospital doctors themselves. This is called _vicarious liability_, and means it is the Trusts, not the Doctors who are held responsible for their actions.\n\n_e.g. If a negligence claim is made following negligence from a doctor working in University College London Hospital's A&E department, the claim will be against University College London Hospitals NHS Foundation Trust, not the doctor._\n\n# All Doctors (GP and Hospital)\n\nAll doctors owe a legal duty of care to anyone they _offer help to_ (assuming this help is accepted). For example, a hospital doctor doesn't owe a legal duty of care to a woman he finds collapsed in the street, until she accepts his offer of help.\n\n# The GMC \n\nThe General Medical Council (GMC) sets out a professional duty (which applies to all doctors) to offer assistance in an emergency.\n\nNB: this is a professional, not legal, obligation.",
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"question": "An 80-year-old woman is admitted to the hospital for shortness of breath and coughing up blood-stained sputum. Imaging studies show a mass in her lung that is likely to be cancer. A biopsy confirms the diagnosis. The patient's family requests the doctor not to tell her about the cancer diagnosis because they believe it will be too much for her to handle, given that her husband recently died of prostate cancer. The family asks for the results to be presented as inconclusive instead.\n\nWhat is the most appropriate course of action?",
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"explanation": "While diuretics can be used to treat swelling, it would not be appropriate to add another diuretic without first reviewing the patient's medication regimen and considering all potential causes.",
"id": "62049",
"label": "b",
"name": "Add another diuretic",
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"explanation": "While it may be appropriate to provide reassurance to the patient, it is important to also take action to address the underlying cause of the patient's symptoms.",
"id": "62051",
"label": "d",
"name": "Reassure",
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"explanation": "It is important for the healthcare professional to carefully review the patient's medication regimen to identify any potential causes of the patient's symptoms, particularly in **elderly patients who may be at an increased risk for drug interactions and adverse side effects due to polypharmacy**. Her complaints are probably related to intolerance to the calcium channel blocker (amlodipine). Additionally, the diuretic (furosemide) may have contributed to the progression of oedema. The most appropriate next step would be to stop amlodipine and furosemide and switch to another antihypertensive medication, such as ACE inhibitors.",
"id": "62048",
"label": "a",
"name": "Review medication",
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"explanation": "While limb elevation may help to reduce swelling in some cases, it would not address the underlying cause of the patient's symptoms.",
"id": "62050",
"label": "c",
"name": "Limb elevation",
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"__typename": "QuestionChoice",
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"explanation": "It is important to review the patient's medication regimen as soon as possible to identify any potential causes of the patient's symptoms and determine the most appropriate course of action. Reviewing after some time would only worsen her condition.",
"id": "62052",
"label": "e",
"name": "Review after six weeks",
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"comment": "Can someone explain to me - why in the explanation does it say that furosemide may have contributed to the oedema?",
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"comment": "what a weird Q and accompanying answer...1: why's she on furose for HTN and 2...why's the furose contributing to oedema. I'm lost. I basically got the right answer because it was the least WRONG out of all the answers haha",
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"explanation": "# Summary\r\n\r\nPrimary hypertension, accounting for approximately 90-95% of cases of hypertension, is characterised by persistently elevated blood pressure due to age-related pathophysiological changes. It is a major risk factor for cardiovascular disease, cerebrovascular disease, chronic kidney disease, and peripheral vascular disease. Diagnosis is based on ambulatory blood pressure monitoring (ABPM) readings of 135/85mmHg or higher. Classification is determined by the severity of the hypertension. Management depends on the classification of the hypertension and involves lifestyle modifications and pharmacological anithypertensives according to NICE guidelines. Effective management, through lifestyle changes and medications, significantly reduces the associated risks and improves outcomes for individuals with hypertension.\r\n\r\n# Definition \r\n\r\nA 'normal' blood pressure ranges between 90/60mmHg to 140/90mmHg. The definition of hypertension is a 24h ambulatory blood pressure average reading (ABPM) that is more than or equal to 135/85mmHg. \r\n\r\n# Epidemiology\r\n\r\nIn 2015, it was reported that high blood pressure affected more than 1 in 4 adults in England (31% of men; 26% of women). In England, it is estimated that primary hypertension affects around 13.5 million people and contributed to 75,000 deaths.\r\n\r\n# Pathophysiology\r\n\r\nPrimary hypertension is as a result of a series of complex physiological changes as we age. Hypertension often occurs as a result of reduced elasticity of large arteries, age-related and atherosclerosis-related calcification, and degradation of arterial elastin. It may also be present in conditions associated with increased cardiac output, such as anaemia, hyperthyroidism and aortic regurgitation.\r\n\r\nAlthough the risk of cardiovascular disease increases progressively with increasing systolic and diastolic blood pressure, raised systolic pressure is more important than raised diastolic pressure as a risk factor for cardiovascular and renal disease.\r\n\r\n# Classification \r\n\r\nHypertension can be classified according to how high a patient's blood pressure is. \r\n\r\n* Stage 1: Clinic => 140/90mmHg; ABPM => 135/85mmHg \r\n* Stage 2: Clinic => 160/100mmHg; ABPM =>150/95mmHg \r\n* Stage 3: Clinic systolic BP (SBP) => 180 or diastolic BP (DBP) =>120mmHg\r\n\r\n\r\n# Symptoms and Signs\r\n\r\nHypertension, unless malignant, is asymptomatic and does not have any clinical signs. It is diagnosed with ABPM and further investigations should focus on diagnosing end-organ complications of hypertension. \r\n\r\n# Investigations\r\n\r\n[lightgallery]\r\n\r\n* Hypertensive patients are commonly first identified at GP appointments or during hospital admissions. Due to the prominence of 'white coat hypertension', ABPM is now required for the diagnosis of hypertension. \r\n* Hypertension should be suspected in a patient who has a clinic blood pressure of =>140/90mmHg. \r\n* **1st line: ABPM** or home blood pressure monitoring if ABPM is not tolerated or declined. \r\n* Alongside ABPM: assessment for end-organ damage and assessment of cardiovascular risk (QRISK2 scores). \r\n * Urine dip and albumin:creatinine level\r\n * Blood glucose, lipids and renal function\r\n * Fundoscopy for evidence of hypertensive retinopathy\r\n * ECG: look for evidence of LV hypertrophy\r\n\r\n\r\nN.B. if presentation is suspicious for secondary hypertension refer and investigate as appropriate (see section). \r\n\r\nN.B. Referral for same-day specialist assessment should be arranged for people with: \r\n\r\n* Clinic blood pressure of 180/120mmHg and higher with signs of retinal haemorrhage or papilloedema (accelerated hypertension) or life-threatening symptoms (e.g. new onset confusion, chest pain, heart failure signs or AKI). \r\n\r\n# Management\r\n\r\n## Principles of Management \r\n\r\n### Conservative Management \r\n\r\nControlling risk factors for cardiovascular disease:\r\n\r\n* Weight loss\r\n* Healthy diet (reduce salt and saturated fats)\r\n* Reduce alcohol and caffeine\r\n* Reduce stress\r\n* Stop smoking\r\n\r\n### Medical Management\r\n\r\nIndications to start pharmacological management of primary hypertension:\r\n\r\n* Stage 1 hypertensive patients who are <80 years old with end organ damage, CVS disease, renal disease, diabetes or 10-year CVS risk >10% OR\r\n* Anyone with stage 2 hypertension\r\n\r\n### 2019 NICE Guidelines for Pharmacological Management of Primary Hypertension \r\n\r\n[lightgallery1]\r\n\r\n* Step 1: \r\n\t* **ACE-inhibitor** (e.g. Ramipril) if <=55 years old\r\n\t* **DHP-Calcium Channel Blocker** (e.g. Amlodipine) if >55 years old OR African or Caribbean ethnicity\r\n\t* If unable to tolerate ACE-inhibitor then switch to _Angiotensin Receptor Blocker_ (e.g. Candesartan)\r\n* Step 2: \r\n\t* (If maximal dose of Step 1 has failed or not tolerated)\r\n\t* **Combine CCB and ACE-I/ARB**\r\n* Step 3:\r\n\t* (If maximal doses of Step 2 has failed or not tolerated)\r\n\t* **Add thiazide-like diuretic** (e.g. Indapamide)\r\n* Step 4: *Resistant Hypertension*\r\n\t* If blood potassium <4.5mmol/L then add **spironolactone**\r\n\t* If >4.5mmol/L **increase thiazide-like diuretic dose**\r\n\t* Other options at this point if the potassium is >4.5mmol/L include:\r\n\t\t* Alpha blocker (e.g. Doxazosin)\r\n\t\t* Beta blocker (e.g. Atenolol)\r\n\t\t* Referral to cardiology for further advice\r\n\r\n**ABPM Targets:**\r\n \r\n* Age <80 ABPM target <135/85\r\n* Age >80 ABPM target <145/85 (due to risk of postural drop and falls)\r\n* T1DM with end-organ damage <130/80\r\n\r\n# Complications\r\n\r\n* Increased risk of morbidity and mortality from all causes\r\n* Coronary artery disease\r\n* Heart failure\r\n* Renal failure\r\n* Stroke\r\n* Peripheral vascular disease\r\n\r\n# Prognosis \r\n\r\nHypertension remains one of the biggest risk factors for cardiovascular disease and its associated disabilities. 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"question": "A 60-year-old Caribbean-origin woman with a history of asthma, hypertension, hyperlipidaemia, and osteoporosis presents to the clinic with swelling in both ankles and shortness of breath. Her current medication regimen includes albuterol and fluticasone for asthma, metformin for diabetes, amlodipine and furosemide for hypertension, atorvastatin for hyperlipidaemia and alendronate for osteoporosis.\n\nWhat is the most appropriate course of action?",
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"explanation": "# Summary\r\n\r\nPrimary hypertension, accounting for approximately 90-95% of cases of hypertension, is characterised by persistently elevated blood pressure due to age-related pathophysiological changes. It is a major risk factor for cardiovascular disease, cerebrovascular disease, chronic kidney disease, and peripheral vascular disease. Diagnosis is based on ambulatory blood pressure monitoring (ABPM) readings of 135/85mmHg or higher. Classification is determined by the severity of the hypertension. Management depends on the classification of the hypertension and involves lifestyle modifications and pharmacological anithypertensives according to NICE guidelines. Effective management, through lifestyle changes and medications, significantly reduces the associated risks and improves outcomes for individuals with hypertension.\r\n\r\n# Definition \r\n\r\nA 'normal' blood pressure ranges between 90/60mmHg to 140/90mmHg. The definition of hypertension is a 24h ambulatory blood pressure average reading (ABPM) that is more than or equal to 135/85mmHg. \r\n\r\n# Epidemiology\r\n\r\nIn 2015, it was reported that high blood pressure affected more than 1 in 4 adults in England (31% of men; 26% of women). In England, it is estimated that primary hypertension affects around 13.5 million people and contributed to 75,000 deaths.\r\n\r\n# Pathophysiology\r\n\r\nPrimary hypertension is as a result of a series of complex physiological changes as we age. Hypertension often occurs as a result of reduced elasticity of large arteries, age-related and atherosclerosis-related calcification, and degradation of arterial elastin. It may also be present in conditions associated with increased cardiac output, such as anaemia, hyperthyroidism and aortic regurgitation.\r\n\r\nAlthough the risk of cardiovascular disease increases progressively with increasing systolic and diastolic blood pressure, raised systolic pressure is more important than raised diastolic pressure as a risk factor for cardiovascular and renal disease.\r\n\r\n# Classification \r\n\r\nHypertension can be classified according to how high a patient's blood pressure is. \r\n\r\n* Stage 1: Clinic => 140/90mmHg; ABPM => 135/85mmHg \r\n* Stage 2: Clinic => 160/100mmHg; ABPM =>150/95mmHg \r\n* Stage 3: Clinic systolic BP (SBP) => 180 or diastolic BP (DBP) =>120mmHg\r\n\r\n\r\n# Symptoms and Signs\r\n\r\nHypertension, unless malignant, is asymptomatic and does not have any clinical signs. It is diagnosed with ABPM and further investigations should focus on diagnosing end-organ complications of hypertension. \r\n\r\n# Investigations\r\n\r\n[lightgallery]\r\n\r\n* Hypertensive patients are commonly first identified at GP appointments or during hospital admissions. Due to the prominence of 'white coat hypertension', ABPM is now required for the diagnosis of hypertension. \r\n* Hypertension should be suspected in a patient who has a clinic blood pressure of =>140/90mmHg. \r\n* **1st line: ABPM** or home blood pressure monitoring if ABPM is not tolerated or declined. \r\n* Alongside ABPM: assessment for end-organ damage and assessment of cardiovascular risk (QRISK2 scores). \r\n * Urine dip and albumin:creatinine level\r\n * Blood glucose, lipids and renal function\r\n * Fundoscopy for evidence of hypertensive retinopathy\r\n * ECG: look for evidence of LV hypertrophy\r\n\r\n\r\nN.B. if presentation is suspicious for secondary hypertension refer and investigate as appropriate (see section). \r\n\r\nN.B. Referral for same-day specialist assessment should be arranged for people with: \r\n\r\n* Clinic blood pressure of 180/120mmHg and higher with signs of retinal haemorrhage or papilloedema (accelerated hypertension) or life-threatening symptoms (e.g. new onset confusion, chest pain, heart failure signs or AKI). \r\n\r\n# Management\r\n\r\n## Principles of Management \r\n\r\n### Conservative Management \r\n\r\nControlling risk factors for cardiovascular disease:\r\n\r\n* Weight loss\r\n* Healthy diet (reduce salt and saturated fats)\r\n* Reduce alcohol and caffeine\r\n* Reduce stress\r\n* Stop smoking\r\n\r\n### Medical Management\r\n\r\nIndications to start pharmacological management of primary hypertension:\r\n\r\n* Stage 1 hypertensive patients who are <80 years old with end organ damage, CVS disease, renal disease, diabetes or 10-year CVS risk >10% OR\r\n* Anyone with stage 2 hypertension\r\n\r\n### 2019 NICE Guidelines for Pharmacological Management of Primary Hypertension \r\n\r\n[lightgallery1]\r\n\r\n* Step 1: \r\n\t* **ACE-inhibitor** (e.g. Ramipril) if <=55 years old\r\n\t* **DHP-Calcium Channel Blocker** (e.g. Amlodipine) if >55 years old OR African or Caribbean ethnicity\r\n\t* If unable to tolerate ACE-inhibitor then switch to _Angiotensin Receptor Blocker_ (e.g. Candesartan)\r\n* Step 2: \r\n\t* (If maximal dose of Step 1 has failed or not tolerated)\r\n\t* **Combine CCB and ACE-I/ARB**\r\n* Step 3:\r\n\t* (If maximal doses of Step 2 has failed or not tolerated)\r\n\t* **Add thiazide-like diuretic** (e.g. Indapamide)\r\n* Step 4: *Resistant Hypertension*\r\n\t* If blood potassium <4.5mmol/L then add **spironolactone**\r\n\t* If >4.5mmol/L **increase thiazide-like diuretic dose**\r\n\t* Other options at this point if the potassium is >4.5mmol/L include:\r\n\t\t* Alpha blocker (e.g. Doxazosin)\r\n\t\t* Beta blocker (e.g. Atenolol)\r\n\t\t* Referral to cardiology for further advice\r\n\r\n**ABPM Targets:**\r\n \r\n* Age <80 ABPM target <135/85\r\n* Age >80 ABPM target <145/85 (due to risk of postural drop and falls)\r\n* T1DM with end-organ damage <130/80\r\n\r\n# Complications\r\n\r\n* Increased risk of morbidity and mortality from all causes\r\n* Coronary artery disease\r\n* Heart failure\r\n* Renal failure\r\n* Stroke\r\n* Peripheral vascular disease\r\n\r\n# Prognosis \r\n\r\nHypertension remains one of the biggest risk factors for cardiovascular disease and its associated disabilities. Management of hypertension (with lifestyle modifications or pharmacological therapies) has been shown to reduce these risks significantly. \r\n\r\n# NICE Guidelines\r\n> <https://cks.nice.org.uk/topics/hypertension/> \r\n\r\n# References \r\n\r\n<https://patient.info/heart-health/high-blood-pressure-hypertension>\r\n<https://www.ahajournals.org/doi/full/10.1161/01.CIR.101.3.329> ",
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"comment": "I think abx shouldn't be delayed as culture takes quite long time, you can start empirically then adjust once culture results come back.",
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"explanation": "# Summary \n\nLower urinary tract infections (LUTIs), often manifesting as cystitis, typically involve the infection of the bladder. Primarily caused by transurethral ascent of colonic commensals like E. coli, symptoms include urinary frequency, dysuria, urgency, foul-smelling urine, and suprapubic pain. Investigations are generally limited to a urine dipstick test for leucocytes and nitrites, while management involves oral nitrofurantoin or trimethoprim, and conservative measures. A key differential diagnosis is pyelonephritis, a urinary tract infection affecting the kidneys. Pyelonephritis exhibits more severe symptoms like fever, malaise, loin pain, and vomiting, and requires hospital admission and intravenous antibiotics.\n\n# Definition \n\nA lower urinary tract infection (LUTI) is generally defined as an infection of the bladder, often manifesting as cystitis.\n\n# Aetiology \n\nLUTIs are caused by the transurethral ascent of colonic commensals, most commonly **E. coli**.\n\n# Signs and symptoms\n\nPatients with LUTIs generally present with:\n\n- Urinary frequency\n- Dysuria\n- Urgency\n- Foul-smelling urine\n- Suprapubic pain\n- Clinical examination may be normal or reveal suprapubic tenderness.\n\nRed flag symptoms such as haematuria, loin pain, rigors, nausea, vomiting, and altered mental state may indicate more serious infection, and these patients may have/are at risk of developing pyelonephritis (see below) and likely need referral to A&E.\n\n\n# Investigations\n\nFor LUTIs:\n\n- Urine dipstick is positive for leucocytes and nitrites in most cases.\n- In uncomplicated cases, no further investigations are required.\n- In children, men, and pregnant women a mid-stream urine sample should be sent.\n\nNB: Urine dipstick is unreliable in women aged older than 65 years and those who are catheterised.\n\nIf being managed in secondary care due to red flag symptoms consider:\n\n- If there are signs of systemic upset consider routine blood tests such as FBC, U+E, and CRP.\n- For uncomplicated UTIs, imaging is rarely required, but if there are concerns over antecedents/complications such as urinary retention/obstruction, an USS bladder/kidney scan would be the first port of call.\n\n# Management \n\n[lightgallery]\n\n[lightgallery1]\n\nFor LUTIs:\n\n- First line management is with oral nitrofurantoin or trimethoprim. Antibiotic duration can vary (see below) however in women the standard course length is 3 days.\n- The patient should be advised on conservative measures to reduce the risk of further infection e.g. regular fluid intake, post-coital voiding.\n\n## Specific situations\n\n**UTI in Men:**\n\n- Empirical antibiotic drug treatment (if no cultures with sensitivities) with trimethoprim or nitrofurantoin for **7 days.**\n- Refer to urology if there are ongoing symptoms despite treatment, if there is an underlying risk factor for UTIs (e.g. urinary calculi, suspected obstruction, previous GU surgery), or if there are recurrent episodes of UTI.\n\n**UTI during Pregnancy (with no haematuria):**\n\n- First-line antibiotics are nitrofurantoin (but *avoid at term),* for **7 days.**\n- If nitrofurantoin is not suitable due to e.g. renal function, or there is no improvement in symptoms, consider second-choice antibiotics such as amoxicillin/cefalexin for 7 days.\n\n\n# NICE Guidelines\n\n[Click here for NICE CKS on urinary tract infection (lower) - women](https://cks.nice.org.uk/topics/urinary-tract-infection-lower-women/)\n\n[Click here for NICE CKS on pyelonephritis - acute](https://cks.nice.org.uk/topics/pyelonephritis-acute/)\n",
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"question": "A 70-year-old woman presents to a GP clinic complaining of dysuria, suprapubic pain, and urgency for the past week. Her past medical and surgical history is unremarkable. Her vital signs are:\n\n - Temperature: 37.1 °C\n - Pulse rate: 80/min\n - Blood pressure: 120/80 mmHg\n - Respiratory rate: 18/min\n\nWhat is the most appropriate next course of action?",
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"explanation": "Gabapentin is a medication that can effectively relieve neuropathic pain when combined with other pain medications. However, the dosage of gabapentin must be gradually increased to avoid side effects, so it may not be a suitable choice for a patient who needs rapid pain relief.",
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"explanation": "Morphine is a common opioid medication, but its active by-products can build up in the body when the kidneys are not functioning properly, which increases the risk of harmful neuroexcitatory effects if the medication is rapidly increased in dosage. Moreover, it is contraindicated in chronic kidney disease.",
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"explanation": "Oxycodone is a powerful opioid medication preferred in palliative care patients with severe renal impairment. It is often the **preferred opioid for treating cancer-related pain in patients with chronic kidney disease**. When managing end-of-life care for renal failure or disease patients, oxycodone 1.25 – 2.5 mg is prescribed to alleviate pain. However, it is important to exercise caution as there is a higher potential for opioid toxicity. Therefore, increasing the dosing intervals with the lowest possible dose is necessary to ensure safety.",
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"explanation": "A transdermal fentanyl patch is an effective pain medication for patients who are already taking opioids regularly. It does not produce any active by-products that can accumulate in the body and cause problems in patients with end-stage kidney disease. However, it should only be used in patients who are already tolerant to opioids.",
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"comment": "Oxycodone is NOT recommended for end-stage renal failure, only in mild-moderate CKD. In end-stage/severe CKD, analgesics such as fentanyl, alfentanil and buprenorphine should be used.",
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"comment": "Acetaminophen?? Why don't you go the whole way and call it Tylenol",
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"explanation": "# Summary\n\nMedications in end-of-life care focus on alleviating distressing symptoms in patients nearing death. A holistic approach is vital, considering physical, emotional, and social aspects of symptoms, often involving a multidisciplinary team. For pain management, the WHO pain ladder guides pharmacological strategies, with morphine as the primary strong opioid. Specific treatments for other symptoms depend on the underlying cause and it is important to consider reversible causes and non-pharmacological measures.\n\n\n\n# Definition\n\nMedications used in end of life care aim to relieve distressing symptoms which may appear in the last days, weeks, or months of life. They are commonly prescribed as 'anticipatory' or 'just in case' medications for a patient known to be nearing the end of life.\n\n\nThey can be administered:\n\n\n- Orally - if the patient is safely able to swallow\n- Subcutaneously - via single dose or continuous syringe pump\n- Transdermally - especially for stable symptoms and if available\n- Intramuscularly - less common\n- Intravenously - less common, but may be helpful if a patient already has access\n\n## A note on holistic care\n\nIn palliative care, and in medicine, it is important to consider all symptoms in context. There are many different aspects to symptoms. These include the physical cause, the patient's beliefs about their illness and symptoms, social contributors and impacts, their emotional and behavioural responses. Holistic assessment and management are crucial, which is why the multidisciplinary team is so important. \n\nFor example, a patient may have been prescribed very effective analgesia but is unable to administer medicines themselves. They may also have a very strong emotional response to pain or believe that they deserve their symptoms. They may benefit from a package of care or financial support for terminal illness which a social worker could help with, or an occupational therapist to help with activities of daily living. Counselling may give the patient a space to explore their feelings around their symptoms and their illness, while spiritual support could alleviate some existential distress. These additional interventions work alongside pharmacological therapy to optimise a person's quality of life through their illness.\n\nThis chapter focuses on medications for symptoms towards the end of life, but it is crucial to remember that each patient has a different combination of needs which requires an individual assessment and management plan, often with input from a range of health and social care professionals.\n\n# Pain\n\n\nInitial pharmacological management of pain should follow the WHO pain ladder. Once patients have reached the top of this ladder (requiring regular strong opioids), careful optimisation is necessary to ensure the right level of pain relief while minimising side effects.\n\n- Morphine is the first-line strong opioid analgesic. This can be given as a modified release or immediate release form. \n- Generally, patients would have a regular 'background' dose based on their 24-hour requirements, plus a PRN dose available for **breakthrough pain.** PRN doses are usually 1/6-1/10 of the 24 hour dose. Analgesia requirements should be reviewed regularly, for example every 24 hours.\n- Alternatives to morphine may be necessary for patients with poor renal function. These include oxycodone, alfentanyl or buprenorphine.\n- When prescribing opioid analgesia consider co-prescribing a regular laxative and an as-required anti-emetic. Monitor for signs of opioid toxicity (respiratory depression, sedation, myoclonus) and switch to alternatives or dose reduce as necessary.\n\nWhen switching analgesia, it is helpful to convert the dose first to oral morphine before converting to the desired medication. Please note that different routes also have different equivalent doses, so it is always safest to check guidelines.\n\n\nThe following table shows dose equivalents of 10mg oral morphine\n\n\n| Analgesic/Route | Dose | Conversion Factor |\n| ----------------------------- | ------- | ----------------- |\n| Codeine/tramadol/dihydrocodeine oral | 100mg | x10 |\n| Diamorphine IM/IV/Subcut | 3mg | x3.3 |\n| Morphine IM/IV/Subcut | 5mg | x2 |\n| Oxycodone oral\\* | 5mg\\* | x2\\* |\n| Oxycodone Subcut\\* | 2.5mg\\* | x4\\* |\n| Alfentanil Subcut | 0.3mg | x30 |\n\n\n*NB - oral oxycodone potency is between 1.3-2x that of oral morphine. Different trusts will adopt different guidance on which you should use. If in doubt, always opt for the lower dose and titrate up.\n\n\n# Breathlessness\n\nConsider non-pharmacological measures for breathlessness first. For example, sitting the patient up, opening a window or setting up a fan can all help.\n\nPharmacological management may involve low-dose opioids, benzodiazepines or therapeutic oxygen, and should be tailored to the patient.\n\n\n# Nausea and vomiting\n\nIt is important to consider the likely cause of nausea and vomiting, as medications target different parts of the vomiting pathway. Perform a full assessment to determine the likely cause of the nausea and vomiting. Consider parenteral routes of administration - patients may have severe gastrointestinal disturbance or at least may not be able to keep down oral antiemetics long enough to be effective.\n\nThe following table shows the primary site of activity and side effects of commonly used antiemetics:\n\n| Antiemetic | Receptor activity | Side effects & cautions | Useful for |\n|---|---|---|---|\n| Metoclopramide | Dopamine antagonist | Extrapyramidal symptoms, drowsiness, restlessness, diarrhoea. Do not give with antimuscarinics or in mechanical bowel obstruction | Gastric stasis, functional bowel obstruction |\n| Cyclizine | Histamine, acetylcholine antagonist | Drowsiness, antimuscarinic | Raised intracranial pressure, vestibular dysfunction |\n| Hyoscine | Acetylcholine antagonist | Antimuscarinic | Motion sickness |\n| Haloperidol | Dopamine antagonist | Less common in palliative care doses | Chemical |\n| Levomepromazine | Dopamine, histamine, acetylcholine, 5HT2 antagonist | Sedation, postural hypotension, antimuscarinic |Broad range |\n| Ondansetron | 5HT3 antagonist | Constipation, arrhythmias, movement disorder | Cytotoxic-related |\n\n- For chemically-mediated symptoms (for example medications, metabolic derangemenet), aim to treat the underlying cause. Antiemetics that may be helpful include haloperidol, metoclopramide or levomepromazine.\n- For nausea and vomiting due to raised intracranial pressure, cyclizine is usually used first-line. Dexamethasone or radiotherapy may be helpful to reduce the pressure-associated symptoms.\n- For patients with vestibular disturbance (for example symptoms associated with movement), cyclizine usually used first-line. Alternatives include hyoscine hydrobromide.\n- For patients with bowel obstruction, seek specialist advice. If due to peristaltic failure, review medications and consider starting metoclopramide (providing there is no colic). Likewise for gastric stasis, consider metoclopramide. For patients with mechanical obstruction and/or colic, do not give metoclopramide. Exclude constipation, give cyclizine for nausea and treat colic with hyoscine butylbromide.\n- If nausea and vomiting is due to compression from an abdominal or pelvic tumour, cyclizine should be used first-line.\n- For anxiety-related nausea and vomiting, begin with non-pharmacological measures for anxiety, such as CBT. A benzodiazepine or levomepromazine would be first-line pharmacological options.\n\n# Agitation\n\nAs with other symptoms, aim to manage reversible causes of agitation and possible delirium first. Consider non-pharmacological measures such as environmental modification. For patients in their last days of life, haloperidol or low-dose midazolam may be prescribed. Often, this is done as part of anticipatory prescribing.\n\n\n# Respiratory tract secretions\n\nRespiratory tract secretions often occur in the last days of life as a person becomes less able to clear their airways. They are rarely a cause of distress to the patient, but may be upsetting for family members or those close to the patient. An antimuscarinic such as hyoscine butylbromide or glycopyrronium bromide may be prescribed for noisy respiratory secretions.\n\n\n# NICE guidelines\n\n\n[NICE Guidance: Care of dying adults in the last days of life](https://www.nice.org.uk/guidance/ng31)\n\n[NICE CKS: Palliative care - general issues](https://cks.nice.org.uk/topics/palliative-care-general-issues/)\n\n[NICE CKS: Palliative care - dyspnoea](https://cks.nice.org.uk/topics/palliative-care-dyspnoea/)\n\n[NICE CKS: Palliative care - nausea and vomiting](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative care - secretions](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative cancer care - pain](https://cks.nice.org.uk/topics/)\n\n# References\n\n[Pallcare.info](https://www.pallcare.info/book.php)\n\n[BNF: Ondansetron](https://bnf.nice.org.uk/drugs/ondansetron/#drug-action)\n\n[BNF: Nausea and labyrinth disorders](https://bnf.nice.org.uk/treatment-summaries/nausea-and-labyrinth-disorders/)\n\n[BNF: Prescribing in palliative care](https://bnf.nice.org.uk/medicines-guidance/prescribing-in-palliative-care/)",
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"question": "A 60-year-old man presents to the GP with severe lower back pain for the past few days. He has a history of end-stage renal disease on haemodialysis, diabetes mellitus type 2, hypertension, and was recently diagnosed with prostate cancer. He further mentions that the pain (8/10) is severe in the lumbar region and has significant paraspinal muscle spasms. It does not radiate and denies any recent changes in bladder or bowel habits. His current medications include lisinopril, atenolol, insulin, and as needed, acetaminophen.\n\nPhysical examination is normal except for tenderness over the lumbar spine and an AV fistula in the left forearm. Vital signs are normal. A CT scan shows lytic lesions in the lumbar spine.\n\nWhat is the most appropriate treatment for his pain?",
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"explanation": "According to the radiographic findings, which show a **Garden stage III hip fracture**, this patient requires immediate surgical intervention to repair the fracture and stabilise the joint. A hemiarthroplasty would be the safest choice due to her age and comorbidities, as it carries a relatively lower risk compared to a total hip replacement.",
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"explanation": "Intramedullary nailing is the \"gold standard\" treatment for managing femoral shaft fractures.",
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"explanation": "Due to her current medical conditions, which are currently impairing her mobility, it would not be advisable for her to undergo a total hip replacement at this age.",
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"explanation": "A Dynamic hip screw is regarded as the 'gold standard' implant for application in all extracapsular fractures. This is an intra-capsular fracture.",
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"explanation": "The clinical scenario is a surgical emergency that requires prompt intervention to stabilise the fracture and restore function to the hip joint. While physiotherapy may be an important part of the patient's rehabilitation after the surgery, it is not an appropriate treatment for the fracture itself.",
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"explanation": "# Summary\n\nA fracture of the neck of the femur is a break occurring in the upper part of the femur, just below the ball-and-socket hip joint. This fracture is common among the elderly population, particularly those with osteoporosis. Notable symptoms include severe hip or groin pain, an inability to bear weight on the affected leg, and external rotation and shortening of the affected leg. Diagnosis typically involves X-rays, though CT scans or MRI may be employed for more complex cases. Management is primarily surgical, with options including cannulated screw fixation, dynamic hip screw, hemiarthroplasty, and total hip arthroplasty, chosen based on factors such as the patient's age, health, and the type of fracture. Complications can include non-union, avascular necrosis, deep vein thrombosis, and pulmonary embolism.\n\n# Definition\n\nA fracture of the neck of the femur is a type of hip fracture that specifically involves the upper part of the femur, just below the ball of the hip's ball-and-socket joint.\n\n# Types of Neck of Femur Fracture\n\nFractures of the neck of the femur are generally classified into two types based on their location in relation to the hip joint capsule:\n\n- **Intracapsular Fractures**: These fractures occur within the joint capsule. They are further subdivided into displaced and non-displaced fractures. Displaced fractures carry a high risk of avascular necrosis due to possible disruption of the blood supply to the femoral head.\n \n- **Extracapsular Fractures**: These fractures occur outside the joint capsule and include intertrochanteric and subtrochanteric fractures. They have a better prognosis due to a lower risk of avascular necrosis.\n\n# Epidemiology\n\nFractures of the neck of the femur are a common injury, particularly in older individuals. This is largely attributed to the increased prevalence of osteoporosis in this population, which makes the bones more susceptible to fractures.\n\n# Aetiology\n\nThe main cause of a fracture to the neck of the femur is a fall, often in the elderly and those with weakened bones due to osteoporosis. Other potential causes can include high-energy trauma such as car accidents, especially in younger individuals.\n\n# Signs and Symptoms\n\nPatients with a fractured neck of femur commonly present with:\n\n- Severe pain in the hip or groin\n- Inability to bear weight on the affected leg\n- Shortening and external rotation of the affected leg\n- Swelling or bruising over the hip area\n\n# Differential Diagnosis\n\nThe differential diagnosis for a fractured neck of femur should include other injuries that could present with similar symptoms:\n\n- **Intertrochanteric Fracture**: Another type of hip fracture, characterised by pain in the hip or groin, inability to bear weight, and often shortening and external rotation of the affected leg.\n- **Pelvic Fracture**: Can be caused by falls or high-energy trauma. Symptoms can include severe pain in the hip or groin, inability to bear weight, and possible signs of internal bleeding.\n- **Hip Dislocation**: Usually a result of high-energy trauma, symptoms include severe hip pain, inability to move the leg, and a visibly deformed hip.\n\n# Investigations\n\nThe primary investigation for a suspected fractured neck of femur is a hip X-ray, which typically reveals the fracture and its severity. In cases where the fracture is not clear on X-ray, a CT scan or MRI may be necessary.\n\n[lightgallery]\n\n# Management\n\nManagement of a fractured neck of the femur is primarily surgical. The choice of surgical intervention depends on several factors, including the type of fracture, the patient's age, general health, and mobility prior to the injury.\n\n- **Cannulated Screw Fixation**: This is often used for non-displaced intracapsular fractures. The procedure involves the insertion of screws across the fracture line to stabilise it.\n \n- **Dynamic Hip Screw (DHS)**: This technique is usually used for stable, extracapsular fractures. It involves the insertion of a single large screw into the femoral head, combined with a side plate fixed to the femoral shaft.\n \n- **Hemiarthroplasty**: This involves replacing the femoral head and neck with a prosthesis. It is typically performed for displaced intracapsular fractures in older patients with lower activity levels, as these fractures have a high risk of non-union and avascular necrosis.\n \n- **Total Hip Arthroplasty (THA)**: This procedure involves the replacement of both the femoral head and the acetabulum with prosthetic components. It is typically used for displaced intracapsular fractures in younger, more active patients or older patients with pre-existing osteoarthritis.\n \n\n# Complications\n\nPotential complications from a fracture of the neck of the femur include:\n\n- Non-union of the fracture\n- Avascular necrosis due to interruption of blood supply to the femoral head\n- Deep vein thrombosis (DVT)\n- Pulmonary embolism (PE)\n- Infection\n- Dislocation of the hip prosthesis, in cases where arthroplasty has been performed\n\n# References\n\n[Click here to read more about fractures of the neck of femur](https://teachmesurgery.com/orthopaedic/hip/femoral-neck-fractures/)",
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"question": "A 85-year-old woman presents to the emergency department with severe pain in her left hip and difficulty walking and bearing weight on the left leg. She reports falling on her left side while getting out of bed this morning. She recently had a stroke a few months ago that left her with paralysis on the left side, and she is using a frame while walking. Past medical history includes hypothyroidism, osteoporosis, hypercholesterolaemia and heart failure.\n\nExamination reveals a shortened and externally rotated left lower limb. X-ray shows a complete and partially displaced subcapital fracture of the neck of the femur.\n\nWhich of the following management option is the most appropriate choice?",
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"explanation": "# Pathophysiology\n\nTrimethoprim can lead to a transient rise in creatinine levels by reducing the creatinine excretion of the kidneys. \n\nThis does NOT reflect the actual GFR and therefore this phenomenon is not reflective of an Acute kidney injury but rather the calculated eGFR due to a transient rise in Creatinine.",
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"question": "A 70-year-old woman has been seen at the GP clinic for a review of her bloods. A week ago, she complained of burning micturition, dysuria, and lower pelvic pain. She was diagnosed with urinary tract infection and was started on trimethoprim. Past medical history includes chronic obstructive pulmonary disease, coronary artery disease, rheumatoid arthritis, and type 2 diabetes mellitus. She takes ipratropium bromide and salbuterol inhalers, aspirin, clopidogrel, atorvastatin, ciclosporin, and metformin.\n\n\nHer vital signs and physical examination are unremarkable. A week ago,\nCreatinine: 89 µmol/L (60-120 µmol/L)\nUrinalysis: 0-1 RBCs, 0-2 WBCs, 5-10 hyaline casts.\n\n\nHer recent blood tests reveal:\nCreatinine: 140 µmol/L (60-120 µmol/L)\n\n\nGiven the blood results, what is the best course of action?",
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"explanation": "Oxybutynin is a medication used to treat **urge incontinence**, or 'overactive bladder'. It works by relaxing the muscles of the bladder and preventing involuntary contractions. If the patient's symptoms persist despite bladder training and frequency being a significant issue, encourage her to continue with bladder training and consider adding oxybutynin as a first-line treatment option.",
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"explanation": "Duloxetine is a selective serotonin and norepinephrine reuptake inhibitor (SSNRI) that is also used to treat **stress incontinence**. It works by inhibiting the reuptake of serotonin and norepinephrine in the brain, which can improve muscle tone in the pelvic floor and reduce leakage. However, pelvic floor exercises are generally the first line of treatment for stress incontinence, and duloxetine is typically reserved for patients who have not responded to pelvic floor muscle training. Therefore, duloxetine is considered a second-line treatment option for the patient, but only if she prefers medication to surgery or is not a suitable candidate for surgery.",
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"explanation": "Pelvic floor exercises, also known as 'Kegel exercises', involve contracting and relaxing the pelvic floor muscles to improve muscle strength and tone. They are an effective treatment for **stress incontinence**, characterised by urine leakage during activities that increase intra-abdominal pressure, such as coughing, sneezing, or lifting heavy objects. Refer the patient to an appropriate specialist for supervised pelvic floor muscle training (PFMT) for a minimum of 3 months. The patient should perform **a minimum of 8 pelvic floor muscle contractions at least three times daily**.",
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"explanation": "Bladder training (at least six weeks) involves retraining the bladder to hold more urine for extended periods and emptying it at scheduled intervals. It is often used to treat urinary incontinence caused by **urge incontinence**, characterised by a strong, sudden urge to urinate and frequent urination. However, in this case, the patient's symptoms are consistent with stress incontinence rather than urge incontinence (or 'overactive bladder'), and bladder training is not the most appropriate initial step in her management.",
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"explanation": "# Summary\n\nUrinary incontinence refers to the involuntary loss of urine and can be categorised into stress, urge, overflow, functional, and mixed types. Key signs and symptoms vary, ranging from involuntary urine leakage when intra-abdominal pressure is raised in stress incontinence, to an abrupt and uncontrollable urge to urinate in urge incontinence. Essential investigations encompass physical examination, questionnaires, bladder diaries, urinalysis, and occasionally cystometry or cystograms. Management strategies depend on the type and severity of incontinence, encompassing conservative methods (like lifestyle modifications), medical treatment (such as Duloxetine, anticholinergics), and surgical options (for example, incontinence pessaries, mid-urethral slings). Generally, stress incontinence is managed with pelvic floor exercises, whereas urge incontinence is initially managed with bladder re-training exercises.\n\n# Types \n\nUrinary incontinence can be categorised into:\n\n1. Stress incontinence\n2. Urge incontinence\n3. Overflow incontinence\n3. Functional incontinence\n4. Mixed incontinence \n\nReversible causes of urinary incontinence can be remembered using the mneumonic **'DIAPPERS':**\n\nD - Delirium\n\nI - Infection\n\nA - Atrophic vaginitis or urethritis\n\nP - Pharmaceutical (medications)\n\nP - Psychiatric disorders\n\nE - Endocrine disorders (e.g. diabetes)\n\nR - Restricted mobility\n\nS - Stool impaction\n\n\n# Approach to Incontinence\n\nOne of the keys is to rule out reversible causes and then try to work out which type of urinary incontinence is. A framework or approach to this is below:\n\n- Physical examination\n\n - An examination will identify features of pelvic organ prolapse as well as the ability to contract pelvic floor muscles.\n\n- Questionnaires\n\n - These are recommended in order to quantify the symptoms and assess the severity on patients quality of life which may help when deciding if a patient would benefit from more invasive treatment\n\n- Bladder diary\n\n - These are also useful for quantifying symptoms and documenting the number and type of episodes of incontinence. They may potentially show a relationship between causes and symptoms.\n\n- Urinalysis\n\n - This will help to rule out infection as an acute cause\n\n- Cystometry\n\n - This is an investigation which measures bladder pressure whilst voiding. It is not recommended in patients with clear histories where the diagnosis is clear.\n\n- Cystogram\n\n - If a fistula is suspected, contrast is instilled into the bladder and a radiological image is obtained in order to see if the contrast travels anywhere else.\n\n\n# Stress incontinence\n\nThis involves leaking of urine when intra-abdominal pressure is raised, putting pressure on the bladder. The pressure of the urine overcomes the mechanisms designed to maintain continence.\n\n## Risk factors \n\n- Childbirth (especially vaginal).This may be due to a combination of injury to the pelvic floor musculature and connective tissue (for example leading to prolapse), as well as nerve damage as a result of pregnancy and labor.\n- Hysterectomy\n\n\n## Triggers\n\nActs such as coughing, laughing, sneezing or exercising can increase abdominal pressure sufficiently.\n\n## Causes\n\nAny abnormality in the anatomy of the bladder, sphincters and urethra can result in stress incontinence.\n\n\n## Conservative management\n\nGeneral lifestyle advice such as avoiding caffeine, fizzy and sugary drinks, as well as avoiding excessive fluid intake, can go far in helping incontinence.\n\nPelvic floor exercises when done with good technique and consistently strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment.\n\n## Medical management\n\nDuloxetine can help with stress incontinence, but it's only recommended if conservative measures fail and the patient is not a surgical candidate.\n\n## Surgical management \n\n- Incontinence pessaries are placed transvaginally and apply pressure to the anterior vaginal wall. This helps to support the urethra and sphincters. However, the evidence for them is poor in individuals without prolapse and isn't recommended by NICE. It would be worth trying if there was a clinical prolapse.\n- Bulking agents are injectable materials placed at the bladder neck to improve continence. This procedure is typically reserved for patients who are poor surgical candidates and isn't as efficacious as other methods\n- Colposuspension and fascial slings involve suspending the anterior vaginal wall to the iliopectineal ligament of Cooper.\n- Mid-urethral slings are the gold standard surgical treatment of stress incontinence. It compresses the urethra against a supportive layer and assists in the closure of the urethra during increased intra-abdominal pressures. It's minimally invasive and can be performed in the outpatient setting.\n\n\n# Urge incontinence\n\n## Definition \n\nThis involves the sudden and involuntary loss of urine associated with urgency.\n\n## Risk factors \n\nRisk factors for urgency include:\n\n- Recurrent urinary tract infections\n- High BMI\n- Advancing age\n- Smoking\n- Caffeine\n\n\n## Conservative management \n\nGeneral lifestyle advice such as avoiding caffeine, fizzy and sugary drinks as well as avoiding excessive fluid intake can go far in helping incontinence. Chemicals contained in these drinks can irritate the bladder, contributing to urge symptoms.\n\nPelvic floor exercises when done with good technique and consistently, strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment. In urge incontinence, contraction of the pelvic floor relaxes the detrusor. Bladder training is also helpful.\n\n## Medical/surgical management\n\n- Pharmacological management\n\t- Anticholinergic medications can help reduce the symptoms of urge and overactive bladder by inhibiting the parasympathetic action on the detrusor muscle.\n\t\t- Examples include: **Oxybutynin, Tolterodine, Fesoterodine, Solifenacin**. If one agent has limited impact, it can be combined with another. Use with caution in elderly however due to increased risk of delirium (side-effect).\n\t- Mirabegron (beta-3 receptor agonist) can be used in older people, but should be used with caution in patients with hypertension.\n\n- Bladder instillation\n\n - Intravesical injection of Botox can be used to paralyse the detrusor muscle and reduce the symptoms of urge and overactive bladder.\n\n- Sacral neuromodulation\n\n - Sacral nerve stimulation has been shown to control symptoms of an overactive bladder. This is only done in tertiary centres for patient who have failed or are unsuitable for all other treatments.\n\n\n# Functional incontinence\n\n## Definition \n\nThis involves an individual having the urge to pass urine, but for whatever reason they're unable to access the necessary facilities and as a result are incontinent.\n\n## Causes \n\nFunctional incontinence associated with:\n\n- Sedating medications\n- Alcohol\n- Dementias\n\n# Overflow incontinence\n\n## Definition \n\nThis occurs when small amounts of urine leak without warning. When the pressure within the bladder overcomes the pressures of the outlet structures urine leaks.\n\n## Causes \n\nThis occurs either due to underactivity of the detrusor muscle such as from neurological damage, or if the urinary outlet pressures are too high, as in constipation or prostatism.\n\n\n\n# NICE Guidelines\n\n[NICE Guidance - Urinary incontinence and pelvic organ prolapse in women: management](https://www.nice.org.uk/guidance/ng123)",
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"explanation": "Frontotemporal dementia is a type of neurodegenerative disorder that affects intellectual functions such as abstract thinking, reasoning, and executive function, leading to difficulties with activities of daily living. It is characterised by changes in behaviour, dietary habits, empathy, apathy, and executive function and may initially present with intact memory.",
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"explanation": "Normal pressure hydrocephalus causes a classical triad of symptoms: urinary incontinence, dementia and Parkinsonian-like gait abnormality. This is secondary to reduced CSf absorption and is reversible. Whilst this patient has dementia, and is in the right demographic category for this condition, she does not exihibit the other features.",
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"explanation": "Pseudodementia (depressive dementia) is often **short and abrupt in onset**, while dementia is more often gradual. Suspect pseudodementia in older people with predominantly cognitive symptoms (memory loss, prominent slowing of movement, and slowed speech) with a relatively acute onset in whom a major life event has occurred as they are more likely to be suffering from a simultaneous major depressive episode as opposed to true dementia.",
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"explanation": "Vascular dementia tends to affect executive function earlier and cause memory loss later. It tends to progress in steps, with each episode causing intellectual decline that may be followed by modest recovery. Cognitive loss may be focal, making them more aware of their deficits and more prone to depression.",
"id": "62085",
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"explanation": "# Summary\n\nPseudodementia, a significant differential for dementia, is primarily associated with cognitive deficits in older patients battling depression. Key signs and symptoms include a short duration of dementia and equal effects on both long and short-term memory, with patients often demonstrating amnesia for specific, emotionally charged events. The condition is characterised by early loss of social skills and an overall lack of effort in performing tasks. Investigations focus on comprehensive cognitive assessments and psychiatric evaluations to distinguish it from dementia. Management primarily involves treating the underlying depression and providing cognitive-behavioural therapy.\n\n# Definition\n\nPseudodementia is a condition primarily associated with cognitive deficits in older patients suffering from depression. It is an important differential of dementia, characterised by cognitive and memory impairments that mimic those of dementia but with an underlying psychiatric cause.\n\n\n# Aetiology\nWhile the exact cause of pseudodementia is unknown, it is primarily associated with **depression** in older adults. Other psychiatric conditions, such as anxiety disorders, can also contribute to its development.\n\n# Signs and Symptoms\n\n* Short duration of symptoms mimicking dementia\n* Equal impact on long-term and short-term memory\n* Amnesia concerning specific, often emotionally charged, events\n* Detailed complaints about memory disturbances\n* Highlighted failures in responses to memory-related questions\n* Early loss of social skills in the disease progression\n* Common responses of “don't know” to questions, rather than attempting to guess\n* Minimal effort in task performance\n\n\n# Investigations\n\nInvestigations into pseudodementia focus on comprehensive cognitive assessments and psychiatric evaluations to differentiate it from dementia. Neuroimaging studies can help rule out organic causes.\n\n# Management\n\nThe management of pseudodementia primarily involves treating the underlying depressive disorder, often with a combination of antidepressant medication and cognitive-behavioural therapy. With appropriate treatment, cognitive symptoms usually improve or resolve. In contrast, dementia is a progressive condition with, to date, no curative treatment.",
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"question": "An 80-year-old woman presents with a complaint of forgetfulness for the past three months. She used to live with her husband but has been living alone since his passing two years ago. Recently, she has become increasingly forgetful and socially withdrawn. She contacts her children less frequently than she used to and has been late paying her bills. She blames her recent memory impairment on tiredness. Her medical history includes being treated for depression as a teenager. Her physical examination is unremarkable, and the Mini-Mental State Examination score is 27/30, but she declines to answer some questions and needs to be urged to participate in the assessment.\n\nWhat is the single most likely diagnosis?",
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"explanation": "# Summary\n\nPostural or orthostatic hypotension is a condition characterised by a significant drop in blood pressure upon standing. Key signs and symptoms include dizziness, syncope, falls, fractures, and more frequent occurrences following meals, exercise, and in warm environments. Key investigations involve identifying a fall of 20mmHg or more in systolic blood pressure, or a fall of 10mmHg or more in diastolic pressure. Management strategies largely depend on the cause and can range from ensuring adequate hydration to evaluating polypharmacy to pharmacotherapy.\n\n# Definition\n\nOrthostatic hypotension is characterised by a decrease in systolic blood pressure of 20 mmHg or a decrease in diastolic blood pressure of 10 mmHg within three minutes of standing when compared with blood pressure from the sitting or supine position.\n\n# Epidemiology\n\nOrthostatic hypotension is common in the elderly population, with approximately 50% of elderly individuals living in residential institutions being affected. \n\n# Aetiology\n\nThe causes of orthostatic hypotension include:\n\n- Medications, particularly vasodilators, diuretics, negative inotropes, antidepressants, and opiates\n- Chronic hypertension due to the loss of baroreceptor reflexes\n- Dehydration\n- Sepsis\n- Autonomic nervous system dysfunction, such as Parkinson's disease\n- Adrenal insufficiency\n\n# Signs and symptoms\n\nPatients with orthostatic hypotension may present with:\n\n- Dizziness\n- Syncope\n- Falls\n- Fractures\n- More frequent occurrences after meals or exercise\n- More frequent occurrences in warm environments\n- Sometimes precipitated by coughing or defecating\n- Symptoms can occur several minutes after standing up\n\n# Differential diagnosis\n\nWhen diagnosing orthostatic hypotension, it is essential to rule out other conditions that may cause similar symptoms. These can include:\n\n- Vertigo: Characterized by a spinning sensation and loss of balance\n- Hypoglycemia: Presents with signs such as shakiness, hunger, confusion, and sweating\n- Cardiac arrhythmias: Symptoms may include palpitations, chest pain, and shortness of breath\n\n# Investigations\n\nThe diagnosis of orthostatic hypotension is confirmed by a significant fall of 20mmHg or more in systolic blood pressure, or a fall of 10mmHg or more in diastolic pressure upon standing.\n\n# Management\n\nManagement of orthostatic hypotension depends on the underlying cause and may include:\n\n- Ensuring adequate hydration\n- Evaluating polypharmacy to identify medication-related causes\n- Implementing strategies to reduce adverse outcomes from falls (e.g., fall alarm, soft flooring)\n- Advising behavioral changes such as rising from sitting slowly, maintaining adequate hydration\n- Recommending the use of compression stockings\n- Employing pharmacotherapy, including fludrocortisone and midodrine, although the evidence base for fludrocortisone is weak\n\n# References\n\n- [NICE Guideline: Orthostatic hypotension due to autonomic dysfunction: midodrine](https://www.nice.org.uk/advice/esnm61/chapter/)",
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"question": "A 70-year-old man presents with dizziness, headache, light-headedness, and frequent falls over the past month, often feeling faint after standing up from sitting for long periods. His past medical history is significant for depression and hypertension, and he has been taking sertraline and amlodipine for the past two years without any reported side effects. Recently, chlorthalidone was added for hypertension six months ago. \n\nThe patient's blood pressure is 160/90 mmHg while sitting, 130/69 mmHg after standing for 3 minutes, with a pulse rate of 78 beats per minute.\nOn examination, no other significant findings are noted. Laboratory investigations of complete blood count and serum electrolytes are unremarkable.\n\n\nWhich among the following is the next best step in managing his complaints?",
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"explanation": "Osteoporosis is fairly common in post-menopausal women, primarily due to diminished oestrogen levels in the body, which is critical for maintaining bone homeostasis.\n - **Receptor activator of nuclear factor-kappa B (RANK)** is expressed on the surface of osteoclast precursors, which are cells responsible for bone resorption.\n - **RANK ligand (RANKL)** is expressed on the surface of osteoblast precursors, which are cells responsible for bone formation, and activates RANK on osteoclast precursors.\nIn normal bone homeostasis, the balance between RANKL and its inhibitor, osteoprotegerin is essential for maintaining bone mass. However, in osteoporosis, there is an imbalance in favour of RANKL, resulting in increased RANK activation and bone resorption. This leads to decreased bone density and an increased risk of fractures.",
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"explanation": "# Summary \r\n\r\nOsteoporosis is a chronic condition characterised by low bone density and increased propensity to sustain fragility fractures. It is diagnosed with a dual-energy X-ray absorptiometry (DEXA) scan if a patient's T-score is less than -2.5. It is very common in older patients, especially post-menopausal women, with other risk factors including long-term corticosteroid use, low body weight and immobility. Other key investigations include checking calcium and vitamin D levels as these may require supplementation if low. Treatment is with bone-sparing treatment, with bisphosphonates being the first-line option in the majority of patients. Lifestyle changes such as smoking cessation, taking regular exercise and maintaining a healthy diet are important. Falls risk assessment is also key to reducing the risk of fragility fractures, especially in older patients. \r\n\r\n# Definition\r\n\r\nOsteoporosis refers to a state of low bone density with structural deterioration of bones. This causes bones to weaken, increasing the risk of fragility fractures (defined as a fracture sustained due to a fall from standing or without any trauma). \r\n\r\nPatients are defined as having osteoporosis if their bone mineral density (BMD) is at least 2.5 standard deviations below the mean peak mass of young healthy adults. This is measured with a dual-energy X-ray absorptiometry (DEXA) scan which gives BMD for the lumbar vertebrae and the femur. \r\n\r\n# Epidemiology\r\n\r\n- In the UK, around 2 million people are estimated to have osteoporosis\r\n- Post-menopausal women are particularly at risk due to accelerated bone loss secondary to decreased oestrogen production\r\n- Prevalence also increases significantly with age\r\n- Almost 50% of 80 year old women have osteoporosis\r\n- White ethnicity is also a risk factor\r\n- There are approximately 300,000 fragility fractures per year in the UK, with osteoporosis often being undiagnosed at the time of presentation\r\n\r\n# Aetiology\r\n\r\nRisk of fragility fractures increases as bone density declined, however there are many other factors that increase fracture risk:\r\n\r\n| Risk factors reducing bone density | Risk factors that do not reduce bone density |\r\n|----------|----------|\r\n| Low body weight | Older age |\r\n| Menopause | Inflammatory arthritis (e.g. rheumatoid arthritis) |\r\n| Immobility | Prolonged use of oral corticosteroids |\r\n| Chronic disease e.g. chronic kidney disease, chronic obstructive pulmonary disease, chronic liver disease | Smoking |\r\n| Malabsorption e.g. coeliac disease, inflammatory bowel disease, pancreatic insufficiency | Alcohol excess |\r\n| Endocrine disease e.g. hyperparathyroidism, hyperthyroidism | History of fragility fracture |\r\n| Certain medications (proton pump inhibitors, selective serotonin reuptake inhibitors, carbamazepine) - mixed evidence | Parental hip fracture |\r\n\r\n# Signs and Symptoms\r\n\r\nOsteoporosis itself is asymptomatic and so is usually diagnosed either with screening of people at high risk (e.g. those on long-term corticosteroids) or when someone presents with a fragility fracture.\r\n\r\nThe most common fragility fractures seen are:\r\n\r\n- Vertebral body\r\n- Neck of femur (hip)\r\n- Distal radius\r\n- Proximal humerus\r\n- Pelvis\r\n\r\nSome osteoporotic fractures (e.g. vertebral fractures) may also be asymptomatic acutely. Loss of height and kyphosis may occur due to multiple vertebral fractures, with severe kyphosis leading to reduced mobility and function.\r\n\r\nOther common symptoms of fragility fractures include acute severe pain, difficulty weight-bearing (e.g. for a hip fracture) and mobilising. \r\n\r\nSigns include deformities, such as a shortened and externally rotated leg due to a hip fracture or a \"dinner fork\" deformity in a Colles' wrist fracture.\r\n\r\nThe area around the fracture may be bruised, swollen and tender to touch. \r\n\r\n# Differential Diagnosis\r\n\r\n- **Bone metastases** may lead to pathological fractures, either in patients with known malignancies or as a first presentation of cancer (especially lung, prostate, breast, kidney and thyroid)\r\n- **Osteomalacia** usually occurs secondary to severe vitamin D deficiency and increases fracture risk due to bone weakening; other symptoms include bone pain, muscle pain and proximal weakness with a waddling gait\r\n- **Multiple myeloma** also is associated with pathological fractures, as well as hypercalcaemia, renal impairment, anaemia and bone pain\r\n- **Paget's disease** increases the risk of fracture due to abnormal bone remodelling, leading to features of bone pain and bowing of the long bones\r\n- **Osteogenesis imperfecta** is a genetic condition that commonly presents in childhood with fragility fractures, bowing of the long bones, short stature and blue sclera\r\n- **Avascular necrosis** may mimic a spontaneous fracture with severe pain after no or minimal trauma, commonly affecting the femoral head\r\n\r\n# Investigations\r\n\r\n- The diagnostic investigation for osteoporosis is a **dual-energy X-ray absorptiometry scan (DEXA)**\r\n- This measures **bone mineral density (BMD)**\r\n- A T-score of -2.5 or less is considered diagnostic of osteoporosis\r\n- If the T-score is between -1 and -2.5 this is referred to as osteopenia\r\n- Z-score is also reported (this compares bone density to a age, sex and ethnicity matched population rather than healthy young adults) - below -2 is low for their age\r\n- The following patients should be offered a DEXA scan as the initial step in assessment\r\n- Aged over 50 presenting with a fragility fracture\r\n- Aged under 40 with a major risk factor for fragility fracture (e.g. long-term steroids) \r\n- Those about to start treatment that will rapidly decrease bone density (e.g. hormone deprivation in breast cancer) - consider\r\n- All other patients with risk factors should have their fracture risk assessed as the initial step\r\n- **QFracture** and **FRAX** are the two online assessment tools used\r\n- These both predict a patient's 10-year risk of hip and major osteoporotic fractures\r\n- QFracture is interpreted based on whether the risk score is greater or less than 10%\r\n- FRAX plots fracture risk versus age on a graph that stratifies people into low/intermediate/high risk\r\n- With QFracture, those at approximately 10% risk or more at 10 years should have a DEXA scan \r\n- With FRAX, patients at intermediate or high risk of fracture should have a DEXA\r\n- In women over the age of 75 with a history of fragility fractures, a clinical diagnosis of osteoporosis may be appropriate (if a DEXA is unfeasible)\r\n\r\nOther investigations required in all patients include:\r\n\r\n- **Vitamin D** to check for deficiency; this is needed prior to starting bisphosphonate treatment\r\n- **Bone profile** to check serum calcium as this may also require supplementation\r\n- **X-rays** or other imaging modalities (e.g. CT or MRI) may be required to diagnose and assess fragility fractures\r\n\r\nIf an underlying cause is suspected, the following investigations may be appropriate:\r\n\r\n- **Full blood count** which may show anaemia in malabsorption or malignancy, and leukocytosis in malignancy or inflammatory disease\r\n- **Liver function tests** for chronic liver disease\r\n- **U&Es** for chronic kidney disease\r\n- **ESR** or **CRP** which may be raised in inflammatory disease or malignancy\r\n- **Thyroid function tests** if hyperthyroidism is suspected\r\n- **Testosterone** and **sex hormone-binding globulin** if hypogonadism is suspected in men\r\n- **Anti-TTG antibodies** for coeliac disease if there is evidence of malabsorption\r\n\r\n# Management\r\n\r\n**Conservative management:**\r\n\r\n- Identification and treatment of any underlying condition contributing to osteoporosis\r\n- Optimisation of risk factors e.g. smoking cessation, alcohol reduction\r\n- Advise patients to take regular weight-bearing exercise to improve muscle strength, including walking, strength training and balance and flexibility training\r\n- Advise patients to eat a balanced diet and assess their calcium intake\r\n- Assess falls risk and consider measures to reduce this, including referral to multidisciplinary falls teams \r\n- Referral to specialist services for patients with very high fracture risk (e.g. T score less than -3.5, multiple vertebral fractures)\r\n\r\n**Medical management:**\r\n\r\n- Prescribing vitamin D supplementation for patients not exposed to adequate sunlight\r\n- Prescribing calcium supplements to patients with an inadequate dietary calcium intake\r\n- For patients at high risk of fragility fracture, prescribe bone-sparing treatment\r\n- Treatment should be started promptly after a fragility fracture to reduce the risk of another fracture\r\n- Oral bisphosphonates are the first-line treatment in the majority of patients \r\n- Options include alendronate and risedronate, which can be given either daily or weekly\r\n\t- These must be taken on an empty stomach, at least 30 minutes before food or other medications\r\n\t- Tablets need to be swallowed whole with a glass of water whilst the patient is upright; they should stay upright for at least 30 minutes after this\r\n\t- Common side effects include nausea, dyspepsia, gastritis, abdominal pain and musculoskeletal pains\r\n\t- Rarer side effects include oesophagitis or ulceration, stricturing or erosions, osteonecrosis of the jaw or external auditory canal and atypical stress fractures\r\n\t- To minimise risk of osteonecrosis of the jaw, patients with poor dentition or malignancy should have a dental check-up (and any work required performed) before starting bisphosphonates\r\n\t- They should also continue to have routine dental checks and maintain good oral hygiene during treatment \r\n\t- Contraindications include severe chronic kidney disease, hypocalcaemia or vitamin D deficiency, and oesophageal abnormalities such as stricture or achalasia \r\n\t- Patients with recent peptic ulceration, upper gastrointestinal bleeding or surgery, dysphagia, gastritis or duodenitis should be prescribed bisphosphonates with caution\r\n- If oral bisphosphonates are not tolerated or unsuitable, options for bone-sparing treatment include:\r\n\t- Parenteral bisphosphonates (e.g. zoledronate)\r\n\t- Denosumab\r\n\t- Raloxifene hydrochloride\r\n\t- Strontium ranelate\r\n\t- Hormone replacement therapy should be considered for younger women experiencing menopausal symptoms as this will also reduce their fragility fracture risk\r\n\t- Teriparatide and romosozumab are other bone-sparing treatments that may be recommended first-line in women with severe osteoporosis - these are then followed by bisphosphonate treatment\r\n\r\n**Surgical management:**\r\n\r\n- Fragility fractures may require surgical fixation or joint replacement (e.g. hip arthroplasty for a fractured neck of femur)\r\n\r\n# Complications\r\n\r\n- Hip fractures are high-consequence injuries and lead to permanent disability in 50% and death in 20% of patients \r\n- Vertebral fractures may lead to disabling and painful kyphosis which may in turn cause difficulty breathing and gastrointestinal problems such as dyspepsia\r\n- Wrist fractures can significantly affect independence and functional ability\r\n- Many patients experience a \"fracture cascade\" where further fractures occur in the years following the initial one\r\n- Pain from fractures can lead to poor sleep, low mood and reduced quality of life\r\n- Complications of treatment may be significant (e.g. osteonecrosis of the jaw or oesophageal ulceration with bisphosphonates)\r\n\r\n# Prognosis\r\n\r\n- There is no cure for osteoporosis\r\n- In general however, prognosis is good with effective treatment\r\n- Bisphosphonate treatment should be reviewed after 3-5 years\r\n- If patients remain at high risk of fracture it may be continued for up to 7-10 years\r\n- Patients with previous hip or vertebral fractures, those aged 70 or older or those who sustain another fragility fracture whilst on bone protection often require longer durations of treatment\r\n- Repeat DEXA may be appropriate to aid decision making\r\n- If bone protection is stopped, fracture risk should be reassessed 18 months to 3 years later\r\n\r\n# NICE Guidelines\r\n\r\n[NICE CKS: Osteoporosis - prevention of fragility fractures](https://cks.nice.org.uk/topics/osteoporosis-prevention-of-fragility-fractures/)\r\n\r\n[NICE - Osteoporosis: assessing the risk of fragility fracture](https://www.nice.org.uk/guidance/cg146)\r\n\r\n# References\r\n\r\n[National Osteoporosis Guideline Group - Prevention and Treatment of Osteoporosis](https://www.nogg.org.uk/full-guideline)\r\n\r\n[BNF Treatment Summary - Osteoporosis](https://bnf.nice.org.uk/treatment-summaries/osteoporosis/)\r\n\r\n[Radiopaedia - Dual-energy x-ray absorptiometry](https://radiopaedia.org/articles/dual-energy-x-ray-absorptiometry-1?lang=gb)\r\n\r\n[WHO - Fragility fractures](https://www.who.int/news-room/fact-sheets/detail/fragility-fractures)\r\n\r\n[International Longevity Centre UK report on Osteoporosis](https://ilcuk.org.uk/wp-content/uploads/2018/10/OsteoporosisUK.pdf)\r\n\r\n\r\n",
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"question": "A 60-year-old woman has presented with severe low back pain for the past three months. She has been a chronic smoker since childhood and had premature menopause at the age of 38 years. A dual-energy x-ray absorptiometry (DXA) scan, which assesses her bone density, revealed a T-score below −2.5.\n\nGiven the likely diagnosis, what receptor is overactive at the molecular level in the patient's condition?",
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"explanation": "A T-score of less than -1 indicates that the patient has low bone mass, also known as osteopenia. While this level of bone loss does not meet the criteria for osteoporosis, it does put the patient at increased risk for fractures and may warrant further evaluation and preventive measures.",
"id": "62099",
"label": "b",
"name": "T-score <−1",
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"explanation": "This option is incorrect. A T-score of less than -3.5 would indicate very severe osteoporosis, a more advanced stage of bone loss. However, it is not the threshold for initiating bisphosphonate therapy.",
"id": "62102",
"label": "e",
"name": "T-score <−3.5",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "Treatment with bisphosphonates (such as alendronate) is typically started if the T-score is −2.5 standard deviations below the mean. T-score is defined as the bone mineral density (BMD) at the site when compared to the young normal reference mean (healthy 30-year-old).",
"id": "62098",
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"name": "T-score <−2.5",
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"explanation": "This option is incorrect. A T-score of less than -3 would also indicate osteoporosis, however it is not the threshold for initiating bisphosphonate therapy.",
"id": "62101",
"label": "d",
"name": "T-score <−3",
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"explanation": "This option is incorrect. A T-score of less than -1.5 would fall within the range of osteopenia and would not meet the criteria for initiating bisphosphonate therapy.",
"id": "62100",
"label": "c",
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"explanation": "# Summary \r\n\r\nOsteoporosis is a chronic condition characterised by low bone density and increased propensity to sustain fragility fractures. It is diagnosed with a dual-energy X-ray absorptiometry (DEXA) scan if a patient's T-score is less than -2.5. It is very common in older patients, especially post-menopausal women, with other risk factors including long-term corticosteroid use, low body weight and immobility. Other key investigations include checking calcium and vitamin D levels as these may require supplementation if low. Treatment is with bone-sparing treatment, with bisphosphonates being the first-line option in the majority of patients. Lifestyle changes such as smoking cessation, taking regular exercise and maintaining a healthy diet are important. Falls risk assessment is also key to reducing the risk of fragility fractures, especially in older patients. \r\n\r\n# Definition\r\n\r\nOsteoporosis refers to a state of low bone density with structural deterioration of bones. This causes bones to weaken, increasing the risk of fragility fractures (defined as a fracture sustained due to a fall from standing or without any trauma). \r\n\r\nPatients are defined as having osteoporosis if their bone mineral density (BMD) is at least 2.5 standard deviations below the mean peak mass of young healthy adults. This is measured with a dual-energy X-ray absorptiometry (DEXA) scan which gives BMD for the lumbar vertebrae and the femur. \r\n\r\n# Epidemiology\r\n\r\n- In the UK, around 2 million people are estimated to have osteoporosis\r\n- Post-menopausal women are particularly at risk due to accelerated bone loss secondary to decreased oestrogen production\r\n- Prevalence also increases significantly with age\r\n- Almost 50% of 80 year old women have osteoporosis\r\n- White ethnicity is also a risk factor\r\n- There are approximately 300,000 fragility fractures per year in the UK, with osteoporosis often being undiagnosed at the time of presentation\r\n\r\n# Aetiology\r\n\r\nRisk of fragility fractures increases as bone density declined, however there are many other factors that increase fracture risk:\r\n\r\n| Risk factors reducing bone density | Risk factors that do not reduce bone density |\r\n|----------|----------|\r\n| Low body weight | Older age |\r\n| Menopause | Inflammatory arthritis (e.g. rheumatoid arthritis) |\r\n| Immobility | Prolonged use of oral corticosteroids |\r\n| Chronic disease e.g. chronic kidney disease, chronic obstructive pulmonary disease, chronic liver disease | Smoking |\r\n| Malabsorption e.g. coeliac disease, inflammatory bowel disease, pancreatic insufficiency | Alcohol excess |\r\n| Endocrine disease e.g. hyperparathyroidism, hyperthyroidism | History of fragility fracture |\r\n| Certain medications (proton pump inhibitors, selective serotonin reuptake inhibitors, carbamazepine) - mixed evidence | Parental hip fracture |\r\n\r\n# Signs and Symptoms\r\n\r\nOsteoporosis itself is asymptomatic and so is usually diagnosed either with screening of people at high risk (e.g. those on long-term corticosteroids) or when someone presents with a fragility fracture.\r\n\r\nThe most common fragility fractures seen are:\r\n\r\n- Vertebral body\r\n- Neck of femur (hip)\r\n- Distal radius\r\n- Proximal humerus\r\n- Pelvis\r\n\r\nSome osteoporotic fractures (e.g. vertebral fractures) may also be asymptomatic acutely. Loss of height and kyphosis may occur due to multiple vertebral fractures, with severe kyphosis leading to reduced mobility and function.\r\n\r\nOther common symptoms of fragility fractures include acute severe pain, difficulty weight-bearing (e.g. for a hip fracture) and mobilising. \r\n\r\nSigns include deformities, such as a shortened and externally rotated leg due to a hip fracture or a \"dinner fork\" deformity in a Colles' wrist fracture.\r\n\r\nThe area around the fracture may be bruised, swollen and tender to touch. \r\n\r\n# Differential Diagnosis\r\n\r\n- **Bone metastases** may lead to pathological fractures, either in patients with known malignancies or as a first presentation of cancer (especially lung, prostate, breast, kidney and thyroid)\r\n- **Osteomalacia** usually occurs secondary to severe vitamin D deficiency and increases fracture risk due to bone weakening; other symptoms include bone pain, muscle pain and proximal weakness with a waddling gait\r\n- **Multiple myeloma** also is associated with pathological fractures, as well as hypercalcaemia, renal impairment, anaemia and bone pain\r\n- **Paget's disease** increases the risk of fracture due to abnormal bone remodelling, leading to features of bone pain and bowing of the long bones\r\n- **Osteogenesis imperfecta** is a genetic condition that commonly presents in childhood with fragility fractures, bowing of the long bones, short stature and blue sclera\r\n- **Avascular necrosis** may mimic a spontaneous fracture with severe pain after no or minimal trauma, commonly affecting the femoral head\r\n\r\n# Investigations\r\n\r\n- The diagnostic investigation for osteoporosis is a **dual-energy X-ray absorptiometry scan (DEXA)**\r\n- This measures **bone mineral density (BMD)**\r\n- A T-score of -2.5 or less is considered diagnostic of osteoporosis\r\n- If the T-score is between -1 and -2.5 this is referred to as osteopenia\r\n- Z-score is also reported (this compares bone density to a age, sex and ethnicity matched population rather than healthy young adults) - below -2 is low for their age\r\n- The following patients should be offered a DEXA scan as the initial step in assessment\r\n- Aged over 50 presenting with a fragility fracture\r\n- Aged under 40 with a major risk factor for fragility fracture (e.g. long-term steroids) \r\n- Those about to start treatment that will rapidly decrease bone density (e.g. hormone deprivation in breast cancer) - consider\r\n- All other patients with risk factors should have their fracture risk assessed as the initial step\r\n- **QFracture** and **FRAX** are the two online assessment tools used\r\n- These both predict a patient's 10-year risk of hip and major osteoporotic fractures\r\n- QFracture is interpreted based on whether the risk score is greater or less than 10%\r\n- FRAX plots fracture risk versus age on a graph that stratifies people into low/intermediate/high risk\r\n- With QFracture, those at approximately 10% risk or more at 10 years should have a DEXA scan \r\n- With FRAX, patients at intermediate or high risk of fracture should have a DEXA\r\n- In women over the age of 75 with a history of fragility fractures, a clinical diagnosis of osteoporosis may be appropriate (if a DEXA is unfeasible)\r\n\r\nOther investigations required in all patients include:\r\n\r\n- **Vitamin D** to check for deficiency; this is needed prior to starting bisphosphonate treatment\r\n- **Bone profile** to check serum calcium as this may also require supplementation\r\n- **X-rays** or other imaging modalities (e.g. CT or MRI) may be required to diagnose and assess fragility fractures\r\n\r\nIf an underlying cause is suspected, the following investigations may be appropriate:\r\n\r\n- **Full blood count** which may show anaemia in malabsorption or malignancy, and leukocytosis in malignancy or inflammatory disease\r\n- **Liver function tests** for chronic liver disease\r\n- **U&Es** for chronic kidney disease\r\n- **ESR** or **CRP** which may be raised in inflammatory disease or malignancy\r\n- **Thyroid function tests** if hyperthyroidism is suspected\r\n- **Testosterone** and **sex hormone-binding globulin** if hypogonadism is suspected in men\r\n- **Anti-TTG antibodies** for coeliac disease if there is evidence of malabsorption\r\n\r\n# Management\r\n\r\n**Conservative management:**\r\n\r\n- Identification and treatment of any underlying condition contributing to osteoporosis\r\n- Optimisation of risk factors e.g. smoking cessation, alcohol reduction\r\n- Advise patients to take regular weight-bearing exercise to improve muscle strength, including walking, strength training and balance and flexibility training\r\n- Advise patients to eat a balanced diet and assess their calcium intake\r\n- Assess falls risk and consider measures to reduce this, including referral to multidisciplinary falls teams \r\n- Referral to specialist services for patients with very high fracture risk (e.g. T score less than -3.5, multiple vertebral fractures)\r\n\r\n**Medical management:**\r\n\r\n- Prescribing vitamin D supplementation for patients not exposed to adequate sunlight\r\n- Prescribing calcium supplements to patients with an inadequate dietary calcium intake\r\n- For patients at high risk of fragility fracture, prescribe bone-sparing treatment\r\n- Treatment should be started promptly after a fragility fracture to reduce the risk of another fracture\r\n- Oral bisphosphonates are the first-line treatment in the majority of patients \r\n- Options include alendronate and risedronate, which can be given either daily or weekly\r\n\t- These must be taken on an empty stomach, at least 30 minutes before food or other medications\r\n\t- Tablets need to be swallowed whole with a glass of water whilst the patient is upright; they should stay upright for at least 30 minutes after this\r\n\t- Common side effects include nausea, dyspepsia, gastritis, abdominal pain and musculoskeletal pains\r\n\t- Rarer side effects include oesophagitis or ulceration, stricturing or erosions, osteonecrosis of the jaw or external auditory canal and atypical stress fractures\r\n\t- To minimise risk of osteonecrosis of the jaw, patients with poor dentition or malignancy should have a dental check-up (and any work required performed) before starting bisphosphonates\r\n\t- They should also continue to have routine dental checks and maintain good oral hygiene during treatment \r\n\t- Contraindications include severe chronic kidney disease, hypocalcaemia or vitamin D deficiency, and oesophageal abnormalities such as stricture or achalasia \r\n\t- Patients with recent peptic ulceration, upper gastrointestinal bleeding or surgery, dysphagia, gastritis or duodenitis should be prescribed bisphosphonates with caution\r\n- If oral bisphosphonates are not tolerated or unsuitable, options for bone-sparing treatment include:\r\n\t- Parenteral bisphosphonates (e.g. zoledronate)\r\n\t- Denosumab\r\n\t- Raloxifene hydrochloride\r\n\t- Strontium ranelate\r\n\t- Hormone replacement therapy should be considered for younger women experiencing menopausal symptoms as this will also reduce their fragility fracture risk\r\n\t- Teriparatide and romosozumab are other bone-sparing treatments that may be recommended first-line in women with severe osteoporosis - these are then followed by bisphosphonate treatment\r\n\r\n**Surgical management:**\r\n\r\n- Fragility fractures may require surgical fixation or joint replacement (e.g. hip arthroplasty for a fractured neck of femur)\r\n\r\n# Complications\r\n\r\n- Hip fractures are high-consequence injuries and lead to permanent disability in 50% and death in 20% of patients \r\n- Vertebral fractures may lead to disabling and painful kyphosis which may in turn cause difficulty breathing and gastrointestinal problems such as dyspepsia\r\n- Wrist fractures can significantly affect independence and functional ability\r\n- Many patients experience a \"fracture cascade\" where further fractures occur in the years following the initial one\r\n- Pain from fractures can lead to poor sleep, low mood and reduced quality of life\r\n- Complications of treatment may be significant (e.g. osteonecrosis of the jaw or oesophageal ulceration with bisphosphonates)\r\n\r\n# Prognosis\r\n\r\n- There is no cure for osteoporosis\r\n- In general however, prognosis is good with effective treatment\r\n- Bisphosphonate treatment should be reviewed after 3-5 years\r\n- If patients remain at high risk of fracture it may be continued for up to 7-10 years\r\n- Patients with previous hip or vertebral fractures, those aged 70 or older or those who sustain another fragility fracture whilst on bone protection often require longer durations of treatment\r\n- Repeat DEXA may be appropriate to aid decision making\r\n- If bone protection is stopped, fracture risk should be reassessed 18 months to 3 years later\r\n\r\n# NICE Guidelines\r\n\r\n[NICE CKS: Osteoporosis - prevention of fragility fractures](https://cks.nice.org.uk/topics/osteoporosis-prevention-of-fragility-fractures/)\r\n\r\n[NICE - Osteoporosis: assessing the risk of fragility fracture](https://www.nice.org.uk/guidance/cg146)\r\n\r\n# References\r\n\r\n[National Osteoporosis Guideline Group - Prevention and Treatment of Osteoporosis](https://www.nogg.org.uk/full-guideline)\r\n\r\n[BNF Treatment Summary - Osteoporosis](https://bnf.nice.org.uk/treatment-summaries/osteoporosis/)\r\n\r\n[Radiopaedia - Dual-energy x-ray absorptiometry](https://radiopaedia.org/articles/dual-energy-x-ray-absorptiometry-1?lang=gb)\r\n\r\n[WHO - Fragility fractures](https://www.who.int/news-room/fact-sheets/detail/fragility-fractures)\r\n\r\n[International Longevity Centre UK report on Osteoporosis](https://ilcuk.org.uk/wp-content/uploads/2018/10/OsteoporosisUK.pdf)\r\n\r\n\r\n",
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"question": "A 55-year-old woman, a baker by profession, was brought to the emergency department after falling while at work, resulting in a hip fracture. Her past medical history is significant for anorexia nervosa, and a family history of osteoporosis in a second-degree relative. She is a chronic smoker and alcoholic. Her BMI is 17.9 kg/m2. A complete physical examination, including the systems, is unremarkable.\n\nGiven the likely diagnosis, what is the standard deviation threshold for commencing bisphosphonate therapy?",
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"explanation": "This would correspond to a patient who is fully active, able to carry out all pre-disease performance without restriction. This does not match the description of the patient, as she is confined to bed, unable to perform any self-care activities or walk around her house, and requires assistance with dressing.",
"id": "62107",
"label": "e",
"name": "Status 0",
"picture": null,
"votes": 26
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"__typename": "QuestionChoice",
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"explanation": "This would correspond to a patient who is able to walk and do light work, but is unable to do heavy work. This does not match the description of the patient, as she is unable to perform any self-care activities or walk around her house and is confined to bed.",
"id": "62106",
"label": "d",
"name": "Status 1",
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"__typename": "QuestionChoice",
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"explanation": "This would correspond to a patient who is restricted in self-care and is unable to carry out any work activities. This does not match the description of the patient, as she is confined to bed, unable to perform any self-care activities or walk around her house, and requires assistance with dressing.",
"id": "62104",
"label": "b",
"name": "Status 3",
"picture": null,
"votes": 325
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"explanation": "This would correspond to a patient who is restricted in physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature. This does not match the description of the patient, as she is confined to bed, unable to perform any self-care activities or walk around her house, and requires assistance with dressing.",
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"name": "Status 2",
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"explanation": "The patient is confined to bed, unable to perform any self-care activities or walk around her house, and requires assistance with dressing. This corresponds to a WHO Performance Status of 4 (completely disabled, bedridden, and requiring active nursing care).",
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"explanation": "# Summary\n\n\nWHO Performance status classification categorises patients into different groups dependent on their physical fitness, measured by their ability to perform activities of daily living. It is used to assess their suitability for chemotherapy, and has some prognostic significance. \n\n\nChemotherapy as a treatment is not without its side effects, which can limit quality of life and have negative impacts on other comorbidities. Treatment decisions involve a risk-benefit analysis, and as such a patients' performance status has a significant bearing on what treatment options are most appropriate.\n\n\n# Classification\n\n\nThe WHO performance status classification categorises patients as:\n\n\n- 0: able to carry out all normal activity without restriction\n- 1: restricted in strenuous activity but ambulatory and able to carry out light work\n- 2: ambulatory and capable of all self-care but unable to carry out any work activities; up and about more than 50% of waking hours\n- 3: symptomatic and in a chair or in bed for greater than 50% of the day but not bedridden\n- 4: completely disabled; cannot carry out any self-care; totally confined to bed or chair.\n\n\n# References\n\n[NICE Appendix C: WHO performance status classification](https://www.nice.org.uk/guidance/ta121/chapter/appendix-c-who-performance-status-classification#:~:text=The%20WHO%20performance%20status%20classification,to%20carry%20out%20light%20work)\n\n[JAMA Oncology: Performance status in patients with cancer](https://jamanetwork.com/journals/jamaoncology/fullarticle/2432463)",
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"question": "A 67-year-old woman with a history of advanced breast cancer presents to the oncology clinic for her follow-up appointment. She has been receiving palliative chemotherapy for the past nine months and reports having significant symptom control. Her past medical history is significant for diabetes and obesity.\n\nOn physical examination, the patient appears tired and anxious. She is able to speak in short sentences and is short of breath with any activity. She has difficulty with personal hygiene and requires assistance with dressing. She is unable to prepare meals or walk around her house and is confined to bed. You are writing a letter to her oncologist and want to include her WHO Performance Status.\n\nWhat is the patient's WHO Performance Status?",
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"explanation": "Correct. This is the mechanism of action of osmotic laxatives such as macrogols (e.g. MOVICOL) or lactulose.",
"id": "62108",
"label": "a",
"name": "Causes increased water retention in the lumen of the large bowel. This can in turn lead to distention which can stimulate peristalsis",
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"__typename": "QuestionChoice",
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"explanation": "This describes the mechanism of action of stimulant laxatives such as Senna.",
"id": "62109",
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"name": "Stimulation of colonic nerves to cause peristalsis",
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"explanation": "This is the mechanism of action of Docusate, often described as a stool-softener",
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"name": "It acts as a surfactant, which causes reduction in surface tension and allows fat and water into the faeces to soften the stool",
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"explanation": "This is the mechanism of action of Prucalopride",
"id": "62111",
"label": "d",
"name": "By stimulation of serotonin (5HT4) receptors, which stimulates intestinal motility",
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"__typename": "QuestionChoice",
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"explanation": "This is the mechanism of action of bulk-forming laxatives such as isphagula husk",
"id": "62112",
"label": "e",
"name": "It increases the soluable fibre content of the stool thereby increasing water and stool mass in the bowel lumen. This in turn stimulates peristalsis",
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"explanation": "# Summary\n\nConstipation is a common gastrointestinal disorder characterised by infrequent bowel movements, hard stools, excessive straining, tenesmus and sometimes necessitating manual evacuation. The disorder can be primary, due to a functional issue, or secondary, due to various causes such as diet, certain medications, and endocrine or neurological disorders. Key investigations include full blood count, electrolytes, thyroid function, blood glucose, and imaging if suspicious of secondary causes. Management is dependent on the underlying cause and may involve lifestyle modifications, a range of laxatives, and referral to a specialist centre for gut motility evaluation if laxatives fail to resolve symptoms.\n\n# Definition\n\nConstipation may involve any or all of the following (Rome IV criteria):\n\n- Fewer than three bowel movements per week\n- Hard stool in more than 25% of bowel movements\n- Tenesmus (sense of incomplete evacuation) in more than 25% of bowel movements\n- Excessive straining in more than 25% of bowel movements\n- A need for manual evacuation of bowel movements\n\nIt can be categorised as:\n\n- Primary constipation: no organic cause, thought to be due to dysregulation of the function of the colon or anorectal muscles\n- Secondary constipation: due to factors such as diet, medications, metabolic, endocrine or neurological disorders or obstruction\n\n# Epidemiology\n\nRisk factors include:\n\n- Advanced age\n- Inactivity\n- Low calorie intake\n- Low fibre diet\n- Certain medications\n- Female sex\n\n# Aetiology\n\nCauses of constipation include:\n\n- Dietary factors, such as inadequate fibre or fluid intake\n- Behavioural factors, like inactivity (common cause of constipation in inpatients) or avoidance of defecation\n- Electrolyte disturbances, like hypercalcaemia\n- Certain drugs, particularly opiates, calcium channel blockers and some antipsychotics\n- Neurological disorders, like spinal cord lesions, Parkinson's disease, and diabetic neuropathy\n- Endocrine disorders, such as hypothyroidism\n- Colon diseases, like strictures or malignancies. Bowel obstruction can also cause complete constipation (obstipation)\n- Anal diseases, like anal fissures or proctitis\n\n# Signs and symptoms\n\nSymptoms and signs of constipation include:\n\n- Infrequent bowel movements (less than 3 per week)\n- Difficulty passing bowel motions\n- Tenesmus\n- Excessive straining\n- Abdominal distension\n- Abdominal mass felt at the left or right lower quadrants (stool)\n- Rectal bleeding\n- Anal fissures\n- Haemorrhoids\n- Presence of hard stool or impaction on digital rectal examination\n\nALARMS features which may indicate gastrointestinal malignancy include: anaemia, weight loss, anorexia, recent onset, melaena/haematemesis/PR bleeding, swallowing difficulties\n\n\n# Investigations\n\n### 2-week-wait criteria\n\n- Constipation (or diarrhoea) with weight loss, 60 and over. Consider an urgent, direct access CT scan, or an urgent ultrasound scan if CT is not available, to rule out **pancreatic cancer**\n\nIf it a patient does not fit the 2-week-wait criteria above, and the cause is thought to be primary, then it is likely that no further investigations are needed.\n\nHowever, if there is suspicion over secondary causes of constipation, investigations may include:\n\nBedside:\n\n- PR exam\n- Stool culture – MC&S, ova,cysts,parasites\n- FIT testing (if accompanied with new rectal bleeding and signs suggestive of colorectal cancer), faecal calprotectin\n\nBloods:\n\n- Full blood count (may show an anaemia), U+Es (including calcium), TFTs\n\nImaging:\n\n- Abdominal x-ray if suspicious of a secondary cause of constipation such as obstruction (may reveal faecal loading)\n- Barium enema if suspicious of impaction or rectal mass\n- Colonoscopy if suspicious of lower GI malignancy\n\n[lightgallery]\n\n# Management\n\nConservative:\n\n- Lifestyle modifications such as dietary improvements and increased exercise\n\nMedical:\n\n**Laxatives** are the mainstay of treatment, please see summary table below.\n\n| Class of Laxative | Drug Name Example | Indication | Mechanism of Action | Side Effects | Contraindications |\n|---------------------|-------------------|--------------------------------------------------------------|---------------------------------------------------------|---------------------------------------|-----------------------------------------------------------|\n| Bulking Agents | Ispaghula Husk | Used for constipation, especially in individuals who need to increase stool bulk. | Increase faecal mass and stimulate peristalsis | Contraindicated in dysphagia, GI obstruction, faecal impaction | Colonic atony, faecal impaction, intestinal obstruction, reduced gut motility, sudden change in bowel habit that has persisted more than two weeks; undiagnosed rectal bleeding |\n| Stimulant | Senna, bisacodyl | Used for short-term relief of constipation. | Increase intestinal motility | Cramps | Contraindicated in acute obstruction or colitis; Prolonged use causes colonic atony (+ melanosis coli) |\n| Stool Softeners | Sodium Docusate, Macrogol | Used to soften stool and make bowel movements easier. | Use in fissures, reduce anticipatory withholding | Flatulence, nausea | Ileus; intestinal obstruction; intestinal perforation; risk of intestinal perforation; severe inflammatory bowel disease; toxic megacolon | \n| Osmotic Laxatives | Lactulose | Used for the treatment of constipation, particularly in cases of hepatic encephalopathy. | Retain fluid in bowel and discourage ammonia-producing microorganisms; First-line for hepatic encephalopathy | Abdominal discomfort, flatulence, diarrhea, electrolyte imbalance | Known hypersensitivity to lactulose, galactosemia, intestinal obstruction |\n| Phosphate Enema | Phosphate Enema | Used for rapid bowel evacuation, often before medical procedures or examinations requiring an empty bowel. | Rapid bowel evacuation, need digital rectal examination (DRE) first | Abdominal cramps, electrolyte imbalance, dehydration | Contraindicated in patients with renal impairment, heart failure, electrolyte abnormalities, and those at risk of phosphate nephropathy |\n\n\nIf laxatives fail to resolve symptoms, referral to a specialist centre for evaluation of gut motility may be necessary. \n\nSurgical:\n\n- If suspicions of colorectal cancer, referral to lower GI/colorectal surgeons\n- If concerns over obstruction these patients need to go to A&E for urgent management and imaging\n\n# NICE Guidelines\n\n[NICE: Treatment Summary: Constipation](https://bnf.nice.org.uk/treatment-summary/constipation.html)\n\n# References\n\n[World Gastroenterology Organisation: Constipation](https://www.worldgastroenterology.org/guidelines/global-guidelines/constipation)\n",
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"explanation": "# Summary\n\nUrinary incontinence refers to the involuntary loss of urine and can be categorised into stress, urge, overflow, functional, and mixed types. Key signs and symptoms vary, ranging from involuntary urine leakage when intra-abdominal pressure is raised in stress incontinence, to an abrupt and uncontrollable urge to urinate in urge incontinence. Essential investigations encompass physical examination, questionnaires, bladder diaries, urinalysis, and occasionally cystometry or cystograms. Management strategies depend on the type and severity of incontinence, encompassing conservative methods (like lifestyle modifications), medical treatment (such as Duloxetine, anticholinergics), and surgical options (for example, incontinence pessaries, mid-urethral slings). Generally, stress incontinence is managed with pelvic floor exercises, whereas urge incontinence is initially managed with bladder re-training exercises.\n\n# Types \n\nUrinary incontinence can be categorised into:\n\n1. Stress incontinence\n2. Urge incontinence\n3. Overflow incontinence\n3. Functional incontinence\n4. Mixed incontinence \n\nReversible causes of urinary incontinence can be remembered using the mneumonic **'DIAPPERS':**\n\nD - Delirium\n\nI - Infection\n\nA - Atrophic vaginitis or urethritis\n\nP - Pharmaceutical (medications)\n\nP - Psychiatric disorders\n\nE - Endocrine disorders (e.g. diabetes)\n\nR - Restricted mobility\n\nS - Stool impaction\n\n\n# Approach to Incontinence\n\nOne of the keys is to rule out reversible causes and then try to work out which type of urinary incontinence is. A framework or approach to this is below:\n\n- Physical examination\n\n - An examination will identify features of pelvic organ prolapse as well as the ability to contract pelvic floor muscles.\n\n- Questionnaires\n\n - These are recommended in order to quantify the symptoms and assess the severity on patients quality of life which may help when deciding if a patient would benefit from more invasive treatment\n\n- Bladder diary\n\n - These are also useful for quantifying symptoms and documenting the number and type of episodes of incontinence. They may potentially show a relationship between causes and symptoms.\n\n- Urinalysis\n\n - This will help to rule out infection as an acute cause\n\n- Cystometry\n\n - This is an investigation which measures bladder pressure whilst voiding. It is not recommended in patients with clear histories where the diagnosis is clear.\n\n- Cystogram\n\n - If a fistula is suspected, contrast is instilled into the bladder and a radiological image is obtained in order to see if the contrast travels anywhere else.\n\n\n# Stress incontinence\n\nThis involves leaking of urine when intra-abdominal pressure is raised, putting pressure on the bladder. The pressure of the urine overcomes the mechanisms designed to maintain continence.\n\n## Risk factors \n\n- Childbirth (especially vaginal).This may be due to a combination of injury to the pelvic floor musculature and connective tissue (for example leading to prolapse), as well as nerve damage as a result of pregnancy and labor.\n- Hysterectomy\n\n\n## Triggers\n\nActs such as coughing, laughing, sneezing or exercising can increase abdominal pressure sufficiently.\n\n## Causes\n\nAny abnormality in the anatomy of the bladder, sphincters and urethra can result in stress incontinence.\n\n\n## Conservative management\n\nGeneral lifestyle advice such as avoiding caffeine, fizzy and sugary drinks, as well as avoiding excessive fluid intake, can go far in helping incontinence.\n\nPelvic floor exercises when done with good technique and consistently strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment.\n\n## Medical management\n\nDuloxetine can help with stress incontinence, but it's only recommended if conservative measures fail and the patient is not a surgical candidate.\n\n## Surgical management \n\n- Incontinence pessaries are placed transvaginally and apply pressure to the anterior vaginal wall. This helps to support the urethra and sphincters. However, the evidence for them is poor in individuals without prolapse and isn't recommended by NICE. It would be worth trying if there was a clinical prolapse.\n- Bulking agents are injectable materials placed at the bladder neck to improve continence. This procedure is typically reserved for patients who are poor surgical candidates and isn't as efficacious as other methods\n- Colposuspension and fascial slings involve suspending the anterior vaginal wall to the iliopectineal ligament of Cooper.\n- Mid-urethral slings are the gold standard surgical treatment of stress incontinence. It compresses the urethra against a supportive layer and assists in the closure of the urethra during increased intra-abdominal pressures. It's minimally invasive and can be performed in the outpatient setting.\n\n\n# Urge incontinence\n\n## Definition \n\nThis involves the sudden and involuntary loss of urine associated with urgency.\n\n## Risk factors \n\nRisk factors for urgency include:\n\n- Recurrent urinary tract infections\n- High BMI\n- Advancing age\n- Smoking\n- Caffeine\n\n\n## Conservative management \n\nGeneral lifestyle advice such as avoiding caffeine, fizzy and sugary drinks as well as avoiding excessive fluid intake can go far in helping incontinence. Chemicals contained in these drinks can irritate the bladder, contributing to urge symptoms.\n\nPelvic floor exercises when done with good technique and consistently, strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment. In urge incontinence, contraction of the pelvic floor relaxes the detrusor. Bladder training is also helpful.\n\n## Medical/surgical management\n\n- Pharmacological management\n\t- Anticholinergic medications can help reduce the symptoms of urge and overactive bladder by inhibiting the parasympathetic action on the detrusor muscle.\n\t\t- Examples include: **Oxybutynin, Tolterodine, Fesoterodine, Solifenacin**. If one agent has limited impact, it can be combined with another. Use with caution in elderly however due to increased risk of delirium (side-effect).\n\t- Mirabegron (beta-3 receptor agonist) can be used in older people, but should be used with caution in patients with hypertension.\n\n- Bladder instillation\n\n - Intravesical injection of Botox can be used to paralyse the detrusor muscle and reduce the symptoms of urge and overactive bladder.\n\n- Sacral neuromodulation\n\n - Sacral nerve stimulation has been shown to control symptoms of an overactive bladder. This is only done in tertiary centres for patient who have failed or are unsuitable for all other treatments.\n\n\n# Functional incontinence\n\n## Definition \n\nThis involves an individual having the urge to pass urine, but for whatever reason they're unable to access the necessary facilities and as a result are incontinent.\n\n## Causes \n\nFunctional incontinence associated with:\n\n- Sedating medications\n- Alcohol\n- Dementias\n\n# Overflow incontinence\n\n## Definition \n\nThis occurs when small amounts of urine leak without warning. When the pressure within the bladder overcomes the pressures of the outlet structures urine leaks.\n\n## Causes \n\nThis occurs either due to underactivity of the detrusor muscle such as from neurological damage, or if the urinary outlet pressures are too high, as in constipation or prostatism.\n\n\n\n# NICE Guidelines\n\n[NICE Guidance - Urinary incontinence and pelvic organ prolapse in women: management](https://www.nice.org.uk/guidance/ng123)",
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"explanation": "# Summary\n\nUrinary incontinence refers to the involuntary loss of urine and can be categorised into stress, urge, overflow, functional, and mixed types. Key signs and symptoms vary, ranging from involuntary urine leakage when intra-abdominal pressure is raised in stress incontinence, to an abrupt and uncontrollable urge to urinate in urge incontinence. Essential investigations encompass physical examination, questionnaires, bladder diaries, urinalysis, and occasionally cystometry or cystograms. Management strategies depend on the type and severity of incontinence, encompassing conservative methods (like lifestyle modifications), medical treatment (such as Duloxetine, anticholinergics), and surgical options (for example, incontinence pessaries, mid-urethral slings). Generally, stress incontinence is managed with pelvic floor exercises, whereas urge incontinence is initially managed with bladder re-training exercises.\n\n# Types \n\nUrinary incontinence can be categorised into:\n\n1. Stress incontinence\n2. Urge incontinence\n3. Overflow incontinence\n3. Functional incontinence\n4. Mixed incontinence \n\nReversible causes of urinary incontinence can be remembered using the mneumonic **'DIAPPERS':**\n\nD - Delirium\n\nI - Infection\n\nA - Atrophic vaginitis or urethritis\n\nP - Pharmaceutical (medications)\n\nP - Psychiatric disorders\n\nE - Endocrine disorders (e.g. diabetes)\n\nR - Restricted mobility\n\nS - Stool impaction\n\n\n# Approach to Incontinence\n\nOne of the keys is to rule out reversible causes and then try to work out which type of urinary incontinence is. A framework or approach to this is below:\n\n- Physical examination\n\n - An examination will identify features of pelvic organ prolapse as well as the ability to contract pelvic floor muscles.\n\n- Questionnaires\n\n - These are recommended in order to quantify the symptoms and assess the severity on patients quality of life which may help when deciding if a patient would benefit from more invasive treatment\n\n- Bladder diary\n\n - These are also useful for quantifying symptoms and documenting the number and type of episodes of incontinence. They may potentially show a relationship between causes and symptoms.\n\n- Urinalysis\n\n - This will help to rule out infection as an acute cause\n\n- Cystometry\n\n - This is an investigation which measures bladder pressure whilst voiding. It is not recommended in patients with clear histories where the diagnosis is clear.\n\n- Cystogram\n\n - If a fistula is suspected, contrast is instilled into the bladder and a radiological image is obtained in order to see if the contrast travels anywhere else.\n\n\n# Stress incontinence\n\nThis involves leaking of urine when intra-abdominal pressure is raised, putting pressure on the bladder. The pressure of the urine overcomes the mechanisms designed to maintain continence.\n\n## Risk factors \n\n- Childbirth (especially vaginal).This may be due to a combination of injury to the pelvic floor musculature and connective tissue (for example leading to prolapse), as well as nerve damage as a result of pregnancy and labor.\n- Hysterectomy\n\n\n## Triggers\n\nActs such as coughing, laughing, sneezing or exercising can increase abdominal pressure sufficiently.\n\n## Causes\n\nAny abnormality in the anatomy of the bladder, sphincters and urethra can result in stress incontinence.\n\n\n## Conservative management\n\nGeneral lifestyle advice such as avoiding caffeine, fizzy and sugary drinks, as well as avoiding excessive fluid intake, can go far in helping incontinence.\n\nPelvic floor exercises when done with good technique and consistently strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment.\n\n## Medical management\n\nDuloxetine can help with stress incontinence, but it's only recommended if conservative measures fail and the patient is not a surgical candidate.\n\n## Surgical management \n\n- Incontinence pessaries are placed transvaginally and apply pressure to the anterior vaginal wall. This helps to support the urethra and sphincters. However, the evidence for them is poor in individuals without prolapse and isn't recommended by NICE. It would be worth trying if there was a clinical prolapse.\n- Bulking agents are injectable materials placed at the bladder neck to improve continence. This procedure is typically reserved for patients who are poor surgical candidates and isn't as efficacious as other methods\n- Colposuspension and fascial slings involve suspending the anterior vaginal wall to the iliopectineal ligament of Cooper.\n- Mid-urethral slings are the gold standard surgical treatment of stress incontinence. It compresses the urethra against a supportive layer and assists in the closure of the urethra during increased intra-abdominal pressures. It's minimally invasive and can be performed in the outpatient setting.\n\n\n# Urge incontinence\n\n## Definition \n\nThis involves the sudden and involuntary loss of urine associated with urgency.\n\n## Risk factors \n\nRisk factors for urgency include:\n\n- Recurrent urinary tract infections\n- High BMI\n- Advancing age\n- Smoking\n- Caffeine\n\n\n## Conservative management \n\nGeneral lifestyle advice such as avoiding caffeine, fizzy and sugary drinks as well as avoiding excessive fluid intake can go far in helping incontinence. Chemicals contained in these drinks can irritate the bladder, contributing to urge symptoms.\n\nPelvic floor exercises when done with good technique and consistently, strengthen the muscles of the pelvic floor. It can help both stress and urge incontinence and can be more effective than drug treatment. In urge incontinence, contraction of the pelvic floor relaxes the detrusor. Bladder training is also helpful.\n\n## Medical/surgical management\n\n- Pharmacological management\n\t- Anticholinergic medications can help reduce the symptoms of urge and overactive bladder by inhibiting the parasympathetic action on the detrusor muscle.\n\t\t- Examples include: **Oxybutynin, Tolterodine, Fesoterodine, Solifenacin**. If one agent has limited impact, it can be combined with another. Use with caution in elderly however due to increased risk of delirium (side-effect).\n\t- Mirabegron (beta-3 receptor agonist) can be used in older people, but should be used with caution in patients with hypertension.\n\n- Bladder instillation\n\n - Intravesical injection of Botox can be used to paralyse the detrusor muscle and reduce the symptoms of urge and overactive bladder.\n\n- Sacral neuromodulation\n\n - Sacral nerve stimulation has been shown to control symptoms of an overactive bladder. This is only done in tertiary centres for patient who have failed or are unsuitable for all other treatments.\n\n\n# Functional incontinence\n\n## Definition \n\nThis involves an individual having the urge to pass urine, but for whatever reason they're unable to access the necessary facilities and as a result are incontinent.\n\n## Causes \n\nFunctional incontinence associated with:\n\n- Sedating medications\n- Alcohol\n- Dementias\n\n# Overflow incontinence\n\n## Definition \n\nThis occurs when small amounts of urine leak without warning. When the pressure within the bladder overcomes the pressures of the outlet structures urine leaks.\n\n## Causes \n\nThis occurs either due to underactivity of the detrusor muscle such as from neurological damage, or if the urinary outlet pressures are too high, as in constipation or prostatism.\n\n\n\n# NICE Guidelines\n\n[NICE Guidance - Urinary incontinence and pelvic organ prolapse in women: management](https://www.nice.org.uk/guidance/ng123)",
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"question": "Which of the following best describes the mechanism of action of oxybutynin in treatment of urge incontinence?",
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"explanation": "Aspirin is a COX-1 and COX-2 inhibitor. It does not commonly cause postural hypotension.",
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"explanation": "This is an anti-spasmodic agent commonly used in treatment of irritable bowel syndrome. It would not commonly cause postural drop.",
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"explanation": "# Summary\n\nPostural or orthostatic hypotension is a condition characterised by a significant drop in blood pressure upon standing. Key signs and symptoms include dizziness, syncope, falls, fractures, and more frequent occurrences following meals, exercise, and in warm environments. Key investigations involve identifying a fall of 20mmHg or more in systolic blood pressure, or a fall of 10mmHg or more in diastolic pressure. Management strategies largely depend on the cause and can range from ensuring adequate hydration to evaluating polypharmacy to pharmacotherapy.\n\n# Definition\n\nOrthostatic hypotension is characterised by a decrease in systolic blood pressure of 20 mmHg or a decrease in diastolic blood pressure of 10 mmHg within three minutes of standing when compared with blood pressure from the sitting or supine position.\n\n# Epidemiology\n\nOrthostatic hypotension is common in the elderly population, with approximately 50% of elderly individuals living in residential institutions being affected. \n\n# Aetiology\n\nThe causes of orthostatic hypotension include:\n\n- Medications, particularly vasodilators, diuretics, negative inotropes, antidepressants, and opiates\n- Chronic hypertension due to the loss of baroreceptor reflexes\n- Dehydration\n- Sepsis\n- Autonomic nervous system dysfunction, such as Parkinson's disease\n- Adrenal insufficiency\n\n# Signs and symptoms\n\nPatients with orthostatic hypotension may present with:\n\n- Dizziness\n- Syncope\n- Falls\n- Fractures\n- More frequent occurrences after meals or exercise\n- More frequent occurrences in warm environments\n- Sometimes precipitated by coughing or defecating\n- Symptoms can occur several minutes after standing up\n\n# Differential diagnosis\n\nWhen diagnosing orthostatic hypotension, it is essential to rule out other conditions that may cause similar symptoms. These can include:\n\n- Vertigo: Characterized by a spinning sensation and loss of balance\n- Hypoglycemia: Presents with signs such as shakiness, hunger, confusion, and sweating\n- Cardiac arrhythmias: Symptoms may include palpitations, chest pain, and shortness of breath\n\n# Investigations\n\nThe diagnosis of orthostatic hypotension is confirmed by a significant fall of 20mmHg or more in systolic blood pressure, or a fall of 10mmHg or more in diastolic pressure upon standing.\n\n# Management\n\nManagement of orthostatic hypotension depends on the underlying cause and may include:\n\n- Ensuring adequate hydration\n- Evaluating polypharmacy to identify medication-related causes\n- Implementing strategies to reduce adverse outcomes from falls (e.g., fall alarm, soft flooring)\n- Advising behavioral changes such as rising from sitting slowly, maintaining adequate hydration\n- Recommending the use of compression stockings\n- Employing pharmacotherapy, including fludrocortisone and midodrine, although the evidence base for fludrocortisone is weak\n\n# References\n\n- [NICE Guideline: Orthostatic hypotension due to autonomic dysfunction: midodrine](https://www.nice.org.uk/advice/esnm61/chapter/)",
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"question": "A 76 year old male presents to the emergency department after multiple falls. He has a past medical history of irritable bowel syndrome, heart failure, chronic obstructive pulmonary disease and benign prostatic hypertrophy. His heart rate is 76bpm, and his blood pressure is 146/82 on lying and 124/79 upon standing (at 3 minutes). He is euvolaemic on examination.\n\nWhich of the following medication is most likely to be responsible for this presentation?",
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"explanation": "These are both nitrates and therefore concurrent use would increase risk of side effects including hypotension, howvever GTN is often required for acute angina attacks; there is no contraindication.",
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"label": "b",
"name": "Glyceryl Trinitrate (GTN)",
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"explanation": "Diltiazem is a calcium channel blocker. Concurrent use can increase risk of hypotension but is not a severe interaction.",
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"explanation": "Concurrent use increases the risk of hypotension and represents a severe interaction and manufacturer advises to avoid co-prescribing.",
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"label": "a",
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"explanation": "Bisoprolol is a beta-blocker commonly used alongside ISMN in treatment of ischaemic heart disease. Concurrent use can increase risk of hypotension but is not a severe interaction and can usually be continued.",
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"explanation": "# Indication\n\nSildenafil is used to treat erectile dysfunction. \n\n# Mechanism\n\nIt is a phosphodiesterase 5 (PDE5) inhibitor which enhances the effect of nitric oxide causing smooth muscle relaxation and subsequent penile erection due to inflow of blood.\n\n# Side effects\n\nSildenafil citrate is contra-indicated in patients taking organic nitrates due to risk of hypotension.\n\nSide effects include flushing, headache, dyspepsia, nasal congestion, dizziness, diarrhoea, rashes and UTIs.",
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"question": "A 67 year old male is suffering from worsening stable angina. The next step in management is to commence Isosorbide mononitrate.\n\nWhich of the following medications constitutes a severe interaction with isosorbide mononitrate (ISMN)?",
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"explanation": "Although close to the calculated 15mg, dosing should align with standard prescribing practices, and 15mg is the more appropriate, rounded dose.",
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"explanation": "While closer to 1/6th of the individual dose (45mg), it is not calculated based on the total daily dose (90mg), which is the correct basis for breakthrough dosing.",
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"explanation": "An appropriate breakthrough dose is 1/6th to 1/10th of the total daily dose of morphine. In this case she takes total 90mg/day, so 1/6th dose is 15mg of morphine for rapid analgesia control. ",
"id": "62138",
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"explanation": "This dose is too low to provide effective breakthrough analgesia for a patient on a daily morphine dose of 90mg. It would likely be insufficient to manage acute pain episodes.",
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"explanation": "Modified-release morphine is inappropriate for breakthrough pain due to its delayed onset of action. Immediate-release formulations are preferred for rapid pain relief.",
"id": "62141",
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"explanation": "# Summary\n\nMedications in end-of-life care focus on alleviating distressing symptoms in patients nearing death. A holistic approach is vital, considering physical, emotional, and social aspects of symptoms, often involving a multidisciplinary team. For pain management, the WHO pain ladder guides pharmacological strategies, with morphine as the primary strong opioid. Specific treatments for other symptoms depend on the underlying cause and it is important to consider reversible causes and non-pharmacological measures.\n\n\n\n# Definition\n\nMedications used in end of life care aim to relieve distressing symptoms which may appear in the last days, weeks, or months of life. They are commonly prescribed as 'anticipatory' or 'just in case' medications for a patient known to be nearing the end of life.\n\n\nThey can be administered:\n\n\n- Orally - if the patient is safely able to swallow\n- Subcutaneously - via single dose or continuous syringe pump\n- Transdermally - especially for stable symptoms and if available\n- Intramuscularly - less common\n- Intravenously - less common, but may be helpful if a patient already has access\n\n## A note on holistic care\n\nIn palliative care, and in medicine, it is important to consider all symptoms in context. There are many different aspects to symptoms. These include the physical cause, the patient's beliefs about their illness and symptoms, social contributors and impacts, their emotional and behavioural responses. Holistic assessment and management are crucial, which is why the multidisciplinary team is so important. \n\nFor example, a patient may have been prescribed very effective analgesia but is unable to administer medicines themselves. They may also have a very strong emotional response to pain or believe that they deserve their symptoms. They may benefit from a package of care or financial support for terminal illness which a social worker could help with, or an occupational therapist to help with activities of daily living. Counselling may give the patient a space to explore their feelings around their symptoms and their illness, while spiritual support could alleviate some existential distress. These additional interventions work alongside pharmacological therapy to optimise a person's quality of life through their illness.\n\nThis chapter focuses on medications for symptoms towards the end of life, but it is crucial to remember that each patient has a different combination of needs which requires an individual assessment and management plan, often with input from a range of health and social care professionals.\n\n# Pain\n\n\nInitial pharmacological management of pain should follow the WHO pain ladder. Once patients have reached the top of this ladder (requiring regular strong opioids), careful optimisation is necessary to ensure the right level of pain relief while minimising side effects.\n\n- Morphine is the first-line strong opioid analgesic. This can be given as a modified release or immediate release form. \n- Generally, patients would have a regular 'background' dose based on their 24-hour requirements, plus a PRN dose available for **breakthrough pain.** PRN doses are usually 1/6-1/10 of the 24 hour dose. Analgesia requirements should be reviewed regularly, for example every 24 hours.\n- Alternatives to morphine may be necessary for patients with poor renal function. These include oxycodone, alfentanyl or buprenorphine.\n- When prescribing opioid analgesia consider co-prescribing a regular laxative and an as-required anti-emetic. Monitor for signs of opioid toxicity (respiratory depression, sedation, myoclonus) and switch to alternatives or dose reduce as necessary.\n\nWhen switching analgesia, it is helpful to convert the dose first to oral morphine before converting to the desired medication. Please note that different routes also have different equivalent doses, so it is always safest to check guidelines.\n\n\nThe following table shows dose equivalents of 10mg oral morphine\n\n\n| Analgesic/Route | Dose | Conversion Factor |\n| ----------------------------- | ------- | ----------------- |\n| Codeine/tramadol/dihydrocodeine oral | 100mg | x10 |\n| Diamorphine IM/IV/Subcut | 3mg | x3.3 |\n| Morphine IM/IV/Subcut | 5mg | x2 |\n| Oxycodone oral\\* | 5mg\\* | x2\\* |\n| Oxycodone Subcut\\* | 2.5mg\\* | x4\\* |\n| Alfentanil Subcut | 0.3mg | x30 |\n\n\n*NB - oral oxycodone potency is between 1.3-2x that of oral morphine. Different trusts will adopt different guidance on which you should use. If in doubt, always opt for the lower dose and titrate up.\n\n\n# Breathlessness\n\nConsider non-pharmacological measures for breathlessness first. For example, sitting the patient up, opening a window or setting up a fan can all help.\n\nPharmacological management may involve low-dose opioids, benzodiazepines or therapeutic oxygen, and should be tailored to the patient.\n\n\n# Nausea and vomiting\n\nIt is important to consider the likely cause of nausea and vomiting, as medications target different parts of the vomiting pathway. Perform a full assessment to determine the likely cause of the nausea and vomiting. Consider parenteral routes of administration - patients may have severe gastrointestinal disturbance or at least may not be able to keep down oral antiemetics long enough to be effective.\n\nThe following table shows the primary site of activity and side effects of commonly used antiemetics:\n\n| Antiemetic | Receptor activity | Side effects & cautions | Useful for |\n|---|---|---|---|\n| Metoclopramide | Dopamine antagonist | Extrapyramidal symptoms, drowsiness, restlessness, diarrhoea. Do not give with antimuscarinics or in mechanical bowel obstruction | Gastric stasis, functional bowel obstruction |\n| Cyclizine | Histamine, acetylcholine antagonist | Drowsiness, antimuscarinic | Raised intracranial pressure, vestibular dysfunction |\n| Hyoscine | Acetylcholine antagonist | Antimuscarinic | Motion sickness |\n| Haloperidol | Dopamine antagonist | Less common in palliative care doses | Chemical |\n| Levomepromazine | Dopamine, histamine, acetylcholine, 5HT2 antagonist | Sedation, postural hypotension, antimuscarinic |Broad range |\n| Ondansetron | 5HT3 antagonist | Constipation, arrhythmias, movement disorder | Cytotoxic-related |\n\n- For chemically-mediated symptoms (for example medications, metabolic derangemenet), aim to treat the underlying cause. Antiemetics that may be helpful include haloperidol, metoclopramide or levomepromazine.\n- For nausea and vomiting due to raised intracranial pressure, cyclizine is usually used first-line. Dexamethasone or radiotherapy may be helpful to reduce the pressure-associated symptoms.\n- For patients with vestibular disturbance (for example symptoms associated with movement), cyclizine usually used first-line. Alternatives include hyoscine hydrobromide.\n- For patients with bowel obstruction, seek specialist advice. If due to peristaltic failure, review medications and consider starting metoclopramide (providing there is no colic). Likewise for gastric stasis, consider metoclopramide. For patients with mechanical obstruction and/or colic, do not give metoclopramide. Exclude constipation, give cyclizine for nausea and treat colic with hyoscine butylbromide.\n- If nausea and vomiting is due to compression from an abdominal or pelvic tumour, cyclizine should be used first-line.\n- For anxiety-related nausea and vomiting, begin with non-pharmacological measures for anxiety, such as CBT. A benzodiazepine or levomepromazine would be first-line pharmacological options.\n\n# Agitation\n\nAs with other symptoms, aim to manage reversible causes of agitation and possible delirium first. Consider non-pharmacological measures such as environmental modification. For patients in their last days of life, haloperidol or low-dose midazolam may be prescribed. Often, this is done as part of anticipatory prescribing.\n\n\n# Respiratory tract secretions\n\nRespiratory tract secretions often occur in the last days of life as a person becomes less able to clear their airways. They are rarely a cause of distress to the patient, but may be upsetting for family members or those close to the patient. An antimuscarinic such as hyoscine butylbromide or glycopyrronium bromide may be prescribed for noisy respiratory secretions.\n\n\n# NICE guidelines\n\n\n[NICE Guidance: Care of dying adults in the last days of life](https://www.nice.org.uk/guidance/ng31)\n\n[NICE CKS: Palliative care - general issues](https://cks.nice.org.uk/topics/palliative-care-general-issues/)\n\n[NICE CKS: Palliative care - dyspnoea](https://cks.nice.org.uk/topics/palliative-care-dyspnoea/)\n\n[NICE CKS: Palliative care - nausea and vomiting](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative care - secretions](https://cks.nice.org.uk/topics/)\n\n[NICE CKS: Palliative cancer care - pain](https://cks.nice.org.uk/topics/)\n\n# References\n\n[Pallcare.info](https://www.pallcare.info/book.php)\n\n[BNF: Ondansetron](https://bnf.nice.org.uk/drugs/ondansetron/#drug-action)\n\n[BNF: Nausea and labyrinth disorders](https://bnf.nice.org.uk/treatment-summaries/nausea-and-labyrinth-disorders/)\n\n[BNF: Prescribing in palliative care](https://bnf.nice.org.uk/medicines-guidance/prescribing-in-palliative-care/)",
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"question": "A 65 year old female with pancreatic cancer is reviewed by the palliative care team. She currently takes 45mg of modified release morphine twice daily, with no other opioids currently prescribed. It is agreed that some additional analgaesia should be prescribed as required for acute episodes of pain during the day.\n\nShe has normal renal function.\n\nWhich of the following would be an appropriate additional morphine prescription in this case?",
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"explanation": "Storage symptoms such as urinary urgency, frequency and nocturia are more commonly associated with PD",
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"name": "Acute Urinary retention???",
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"explanation": "Freezing is a mid to late motor sign commonly experienced by people with PD, when they find they are transiently unable to move.",
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"explanation": "Reduction in sense of smell is a common non-motor symptom of PD that often precedes motor symptom onset.",
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"comment": "????",
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"comment": "according to my geri consultant anosmia is actually a very rare symptom and he's never seen it any of his parkinsons patients so quesmed i think you are wrong ",
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"comment": "skill issue",
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"comment": "he needs to spend more time on the wards",
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"explanation": "# Summary\n\nParkinson's disease (PD) is a neurodegenerative disorder predominantly affecting adults over 65 years characterised by asymmetric tremor, bradykinesia, and rigidity. The condition results from Lewy body formation and neuronal death in the dopaminergic cells of the substantia nigra. Clinical features include assymetric resting tremor, slow shuffling gait, cogwheel rigidity, bradykinesia, and non-motor features such as autonomic dysfunction and psychiatric disturbances. Diagnosis is primarily clinical, supported by response to treatment trials. Pharmacological treatment with Levodopa remains the first-line therapy, with other agents used for specific symptom control or in later disease stages. Surgical interventions such as deep brain stimulation may be considered in certain cases. Prognosis varies, with little impact on overall life expectancy.\n\n\n# Definition\n\nParkinson's disease (PD) is a neurodegenerative disorder that presents with generalised slowing of movements (bradykinesia), resting tremor and rigidity.\n\n# Epidemiology\n\n- Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease. \n- It affects 0.3% of the UK population.\n- It is estimated that PD affects at least 1% of the population over 60\n\n\n# Aetiology\n\n- The exact cause of Parkinson's disease is unknown. \n- It is believed to result from the accumulation of \"Lewy bodies\", intracellular inclusions primarily composed of misfolded **alpha synuclein**. \n- These bodies form and lead to neuronal death in the dopaminergic cells of the substantia nigra of the basal ganglia, thereby causing the characteristic symptoms. \n- Both dominant and recessive familial variants of Parkinson's disease have been identified.\n\n# Clinical Features \n\nParkinson's disease is characterised by the following core features:\n\n* Bradykinesia\n* Asymmetric 3-5Hz \"pill-rolling\" resting tremor\n* Rigidity\n\t* Often noted to be 'cog-wheeling' which occurs when the tremor coincidees with rigidity\n* Gait Disturbance\n\t * Small, shuffling steps\n\t * Difficult initation and turning 'en bloc turning'\n\nOther features associated with Parkinson's Disease include:\n\n- Hypomimic facies\n- Micrographia (secondary to a combination of bradykinesia and rigidity)\n\nNon-motor features of Parkinson's disease are also common and may precede onset of motor symptoms by many years. These include:\n\n* Autonomic dysfunction, leading to constipation, symptomatic orthostasis (postural hypotension), and erectile dysfunction\n* Olfactory loss\n* Constipation\n* Sleep disorders such as REM behavioural disorder \n* Psychiatric features including depression, anxiety, and hallucinations\n\n\nPostural instability is a late feature of idiopathic Parkinson's disease. This said, very prominent early autonomic dysfunction should raise the suspicion of Multiple System Atrophy.\n\nEarly and prominent cognitive dysfunction should raise the suspicion of dementia with Lewy bodies (DLB).\n\n# Differential diagnosis\n\nKey differentials for Parkinson's disease, along with their signs and symptoms, include:\n\n* **Multiple System Atrophy (MSA):** Very prominent autonomic dysfunction, early postural instability, poor response to levodopa\n* **Dementia with Lewy Bodies (DLB):** Early and prominent cognitive dysfunction, visual hallucinations, fluctuating cognition\n* **Progressive Supranuclear Palsy (PSP):** Early gait instability and falls, vertical gaze palsy, prominent axial rigidity\n* **Corticobasilar Degeneration**: May have predominant apraxia, aphasia and 'alien hand' syndrome\n* **Wilson's Disease:** Secondary to copper deposition in the Basal Ganglia. May be associated with signs of liver disease\n* **Dementia Pugilistica:** Secondary to repeated head trauma\n* **Drug Induced Parkinsonism** Secondary to antipsychotic therapy, usually symmetrical tremor and less responsive to Levodopa\n\n# Investigations\n\nParkinson's disease is primarily a clinical diagnosis, supported by positive response to treatment trials. \n\nAn absolute failure to respond to 1-1.5g of levodopa daily almost excludes a diagnosis of idiopathic Parkinson's disease.\n\nOther investigations such as MRI Head or a Dopamine Transporter Scan (DaT scan) can be considered in atypical cases. \n\n# Management\n\nManagement should by led by a multidisciplinary team of neurologists, nurse specialists, physiotherapists, occupational therapists and other allied healthcare professionals.\n\n## Pharmacological Management\n\n### Levodopa\n\n- Levodopa is the precurser to dopamine\n- It is used as a dopamine replacement agent\n- Should be started in all patients with **significant functional impairment** according to NICE guidelines\n- Typically combined with Carbidopa, which decreases side effects and improves CNS bioavailability), oftern referred to as **Co-careldopa**\n- Absolute failure to respond to 1-1.5g of levodopa daily virtually excludes a diagnosis of idiopathic Parkinson's disease, though a response to levodopa does not confirm the diagnosis (as many primary parkinsonian syndromes may also respond).\n\n\nSide effects can be split into peripheral and central (depending on where the acting dopamine receptor is for the side effect).\n\nPeripheral side effects include:\n\n- Postural hypotension\n- Nausea & vomiting*\n\n\nWith time, and as the underlying disease progresses, levodopa may become a less effective and patients may report end-of-dose effects, where motor activity progressively declines as the previous dose wears off, and on-off phenomena, which manifest as seemingly random fluctuations in drug effect.\n\nOne of the most disabling side effects is **drug-induced dyskinesia**: writhing and uncoordinated movements of the limbs associated with poorly organised dopaminergic control of motor activity.\n\nIt typically takes 2-5 years to develop complete loss of response.\n\n*Domperidone is the anti-emetic of choice in those with Parkinson’s disease which has anti-dopaminergic activity but does NOT cross the blood brain barrier. \n\n### Dopamine agonists\n\n- Examples include: Ropinirole, rotigotine, Apomorphine. Previous ergot derived formulations (eg cabergoline) as now not widely used as are associated with lung fibrosis. \n- Have a longer half life than levodopa but are not as potent\n- Are often used in early disease in those without functional impairment, or late in disease when dyskinesias and motor fluctuations secondary to levodopa is a problem.\n- Increases activity of dopamine via the mesolimbic pathway which may affect reward centres and lead to unwanted risk-taking behaviours such as gambling. \n- Apomorphine is the most potent dopamine agonist and is typically given subcutaneously. It works well against motor fluctuations and dyskinesia. Often used late in disease. \n\n\n### MAO-B Inhibitors\n\n- Examples include: Selegiline, Rasagiline.\n- Reduce dopamine breakdown peripherally & thus increase central update of levodopa. Often used in combination with levodopa later in disease.\n- Initial animal studies suggested a \"neuroprotective effect\" although this has not been seen in human studies.\n- Can cause serotonin syndrome. \n\n### COMT Inhibitors\n\n- COMT inhibitors, or catechol- O -methyltransferase inhibitors include Entacapone and Tolcapone.\n- Extend the use of levodopa. Useful in wearing off effect in levodopa use.\n- Tolcapone is more potent than entacapone and can result in hepatotoxicity. \n\n### Amantadine\n\n- NMDA receptor antagonist that has an unclear action in Parkinson's Disease.\n- Can be used in those suffering from dyskinesia. \n\n\n### Anticholinergic agents\n\n- Examples include: Procyclidine, Trihexyphenidyl\n- Can be used in those with mild tremors. \n- Rarely used in clinical practice \n\n\n## Surgical Management\n\n- Deep Brain Stimulation: typically performed by implanting a stimulating device into a target area of the brain, often the thalamus or the subthalamus.\n\n# Prognosis\n\n- Parkinson's disease is typically slowly progressive, but the rate of progression is variable. \n- The mortality rate for elderly people aged 70-89 years with Parkinson's disease is 2-5 times higher than for age-matched controls in some studies. \n- The risk of dementia is about 2-6 times higher in people with Parkinson's disease than in healthy controls",
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"explanation": "This patient is at high risk of malnutrition and action should be taken.",
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"explanation": "# Summary\n\nConstipation is a common gastrointestinal disorder characterised by infrequent bowel movements, hard stools, excessive straining, tenesmus and sometimes necessitating manual evacuation. The disorder can be primary, due to a functional issue, or secondary, due to various causes such as diet, certain medications, and endocrine or neurological disorders. Key investigations include full blood count, electrolytes, thyroid function, blood glucose, and imaging if suspicious of secondary causes. Management is dependent on the underlying cause and may involve lifestyle modifications, a range of laxatives, and referral to a specialist centre for gut motility evaluation if laxatives fail to resolve symptoms.\n\n# Definition\n\nConstipation may involve any or all of the following (Rome IV criteria):\n\n- Fewer than three bowel movements per week\n- Hard stool in more than 25% of bowel movements\n- Tenesmus (sense of incomplete evacuation) in more than 25% of bowel movements\n- Excessive straining in more than 25% of bowel movements\n- A need for manual evacuation of bowel movements\n\nIt can be categorised as:\n\n- Primary constipation: no organic cause, thought to be due to dysregulation of the function of the colon or anorectal muscles\n- Secondary constipation: due to factors such as diet, medications, metabolic, endocrine or neurological disorders or obstruction\n\n# Epidemiology\n\nRisk factors include:\n\n- Advanced age\n- Inactivity\n- Low calorie intake\n- Low fibre diet\n- Certain medications\n- Female sex\n\n# Aetiology\n\nCauses of constipation include:\n\n- Dietary factors, such as inadequate fibre or fluid intake\n- Behavioural factors, like inactivity (common cause of constipation in inpatients) or avoidance of defecation\n- Electrolyte disturbances, like hypercalcaemia\n- Certain drugs, particularly opiates, calcium channel blockers and some antipsychotics\n- Neurological disorders, like spinal cord lesions, Parkinson's disease, and diabetic neuropathy\n- Endocrine disorders, such as hypothyroidism\n- Colon diseases, like strictures or malignancies. Bowel obstruction can also cause complete constipation (obstipation)\n- Anal diseases, like anal fissures or proctitis\n\n# Signs and symptoms\n\nSymptoms and signs of constipation include:\n\n- Infrequent bowel movements (less than 3 per week)\n- Difficulty passing bowel motions\n- Tenesmus\n- Excessive straining\n- Abdominal distension\n- Abdominal mass felt at the left or right lower quadrants (stool)\n- Rectal bleeding\n- Anal fissures\n- Haemorrhoids\n- Presence of hard stool or impaction on digital rectal examination\n\nALARMS features which may indicate gastrointestinal malignancy include: anaemia, weight loss, anorexia, recent onset, melaena/haematemesis/PR bleeding, swallowing difficulties\n\n\n# Investigations\n\n### 2-week-wait criteria\n\n- Constipation (or diarrhoea) with weight loss, 60 and over. Consider an urgent, direct access CT scan, or an urgent ultrasound scan if CT is not available, to rule out **pancreatic cancer**\n\nIf it a patient does not fit the 2-week-wait criteria above, and the cause is thought to be primary, then it is likely that no further investigations are needed.\n\nHowever, if there is suspicion over secondary causes of constipation, investigations may include:\n\nBedside:\n\n- PR exam\n- Stool culture – MC&S, ova,cysts,parasites\n- FIT testing (if accompanied with new rectal bleeding and signs suggestive of colorectal cancer), faecal calprotectin\n\nBloods:\n\n- Full blood count (may show an anaemia), U+Es (including calcium), TFTs\n\nImaging:\n\n- Abdominal x-ray if suspicious of a secondary cause of constipation such as obstruction (may reveal faecal loading)\n- Barium enema if suspicious of impaction or rectal mass\n- Colonoscopy if suspicious of lower GI malignancy\n\n[lightgallery]\n\n# Management\n\nConservative:\n\n- Lifestyle modifications such as dietary improvements and increased exercise\n\nMedical:\n\n**Laxatives** are the mainstay of treatment, please see summary table below.\n\n| Class of Laxative | Drug Name Example | Indication | Mechanism of Action | Side Effects | Contraindications |\n|---------------------|-------------------|--------------------------------------------------------------|---------------------------------------------------------|---------------------------------------|-----------------------------------------------------------|\n| Bulking Agents | Ispaghula Husk | Used for constipation, especially in individuals who need to increase stool bulk. | Increase faecal mass and stimulate peristalsis | Contraindicated in dysphagia, GI obstruction, faecal impaction | Colonic atony, faecal impaction, intestinal obstruction, reduced gut motility, sudden change in bowel habit that has persisted more than two weeks; undiagnosed rectal bleeding |\n| Stimulant | Senna, bisacodyl | Used for short-term relief of constipation. | Increase intestinal motility | Cramps | Contraindicated in acute obstruction or colitis; Prolonged use causes colonic atony (+ melanosis coli) |\n| Stool Softeners | Sodium Docusate, Macrogol | Used to soften stool and make bowel movements easier. | Use in fissures, reduce anticipatory withholding | Flatulence, nausea | Ileus; intestinal obstruction; intestinal perforation; risk of intestinal perforation; severe inflammatory bowel disease; toxic megacolon | \n| Osmotic Laxatives | Lactulose | Used for the treatment of constipation, particularly in cases of hepatic encephalopathy. | Retain fluid in bowel and discourage ammonia-producing microorganisms; First-line for hepatic encephalopathy | Abdominal discomfort, flatulence, diarrhea, electrolyte imbalance | Known hypersensitivity to lactulose, galactosemia, intestinal obstruction |\n| Phosphate Enema | Phosphate Enema | Used for rapid bowel evacuation, often before medical procedures or examinations requiring an empty bowel. | Rapid bowel evacuation, need digital rectal examination (DRE) first | Abdominal cramps, electrolyte imbalance, dehydration | Contraindicated in patients with renal impairment, heart failure, electrolyte abnormalities, and those at risk of phosphate nephropathy |\n\n\nIf laxatives fail to resolve symptoms, referral to a specialist centre for evaluation of gut motility may be necessary. \n\nSurgical:\n\n- If suspicions of colorectal cancer, referral to lower GI/colorectal surgeons\n- If concerns over obstruction these patients need to go to A&E for urgent management and imaging\n\n# NICE Guidelines\n\n[NICE: Treatment Summary: Constipation](https://bnf.nice.org.uk/treatment-summary/constipation.html)\n\n# References\n\n[World Gastroenterology Organisation: Constipation](https://www.worldgastroenterology.org/guidelines/global-guidelines/constipation)\n",
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"question": "An 80 year old female is brought into hospital by her neighbour, who discovered she has been self-neglecting at home. She has had a poor diet for several months, related to Alzheimer's dementia and poor mobility.\nToday, she is 167cm tall, 52kg. Her previous recorded weight was 60kg 5 months ago.\nBMI = 18.6\nShe is otherwise well and happily accepts lunch on the ward.\n\n\n **STEP 1: BMI score**\n - Greater than 20kg/m2= 0 points\n - 18.5 - 20kg/m2 = +1 point\n - <18.5kg/m2 = +2 points\n\n\nN.B. BMI = weight (kg)/(height)^2 (m)\n\n\n **STEP 2: Unintentional weight loss score**\n\n\n - <5% = 0 points\n - 5-10% = +1 point\n - Greater than 10% = +2 points\n\n\n **STEP 3: Patient is acutely ill and there has been or is likely to be no nutritional intake for >5 days**\n - No = 0 points\n - Yes = +2 points\n\n\nTotal MUST score:\n - Low risk = 0\n - Medium Risk = 1\n - High risk = 2+\n\n\nBased on this patient's MUST score, which of the following represents the best nutritional management plan?",
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"explanation": "It would be inappropriate for a family member to break bad news, especially without an appropriate clinician present to ensure accurate information sharing. It is also doubtful whether the daughter would tell the patient at all.",
"id": "62155",
"label": "c",
"name": "Agree to let the daughter tell the patient once she has recovered and is at home in her own environment",
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"explanation": "LPA is only applicable in patients who have lost capacity. Therefore the patient currently has full power to decide regarding her care, provided she has capacity to do so.",
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"label": "d",
"name": "You cannot disclose, as the daughter has Legal Power of Attorney and therefore has the right to decide on the patient's behalf",
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"__typename": "QuestionChoice",
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"explanation": "You must assess capacity before deciding whether to follow or override the daughter's wishes. Secondly, even if there is capacity the patient herself has 'the right not to know'- ask first.",
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"label": "b",
"name": "Tell the patient everything",
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"explanation": "LPA is only applicable in patients who have lost capacity. Therefore the capacitous patient can currently override the daughter's wishes. If the patient does/does not want to know, that is her decision to make.",
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"name": "Assess capacity: if the patient has capacity, tell her whatever she would like to know",
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"explanation": "A best interests meeting would not be appropriate if the patient has capacity to make her own decisions.",
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"name": "Call a Best Interests Meeting, with other healthcare professionals and Next of Kin",
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"explanation": "# Overview\n\nBuilt into the Mental Capacity Act (2005) are provisions designed to aid decision making on behalf of vulnerable individuals who lack capacity. Three of them are making a Lasting Power of Attorney, Independent Mental Capacity Advocates, and the Court of Protection. Each have different roles but all aim to ensure that all decisions made on behalf of an individual are in their best interests.\n\n# Lasting Power of Attorney (LPA) \n\nIf an individual wants to legally appoint someone they trust to make decisions on their behalf in the future if they lose capacity, they can do this by making a lasting power of attorney (LPA). Usually an individual chooses a close relative or friend to be their \"attorney\", who is given legal power to make decisions about their health and care if they lose capacity at some point in the future.\n\nAn individual's attorney can make decisions about health and care decisions, including:\n\n_Where an individual should live, what care or treatment they should receive, decisions about their daily routine (food, activities, etc.). If special permission has been given, an attorney can also make decisions about life-saving treatment._\n\n# Independent Mental Capacity Advocates (IMCAs) \n\nIMCAs are used when an individual lacks the capacity to make a specific important decision, when there is no-one independent of services (e.g. a family member or friend) appropriate to represent the individual lacking capacity.\n\nIMCAs support and represent the individual who lacks capacity, ensuring the Mental Capacity Act, 2005 is followed.\n\n# Court of Protection \n\nThe Court of Protection is a court that if applied to, can make decisions about an individual's health, welfare, finances and property under the Mental Capacity Act 2005.\n\nThe types of decisions the court can rule on include:\n_Whether an individual has capacity to make a decision, whether a decision is in an individual's best interests, removing an attorney under a lasting power of attorney._\n\nThe Court of Protection always makes decisions in an individual's best interests.",
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"question": "A 92 year old female is admitted after feeling generally unwell, with a one day history of left iliac fossa pain and bloody diarrhoea. A computed topography (CT) scan of her abdomen shows evidence of acute diverticulitis. However, it also shows a thickening of the ascending colon which is highly suspicious for malignancy.\n\nThe patient's daughter has Lasting Power of Attorney (LPA). She believes it is not in the patient's best interests to be told about the possible cancer diagnosis as it would cause too much distress. She asks you not to reveal the full scan result to the patient.\nThe patient had shown evidence of capacity at the time of your initial review.\n\nWhich of the following would be the most appropriate next course of action?",
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"__typename": "QuestionSBA",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Advance Statements are not a legally binding document, wheras Advance DIrectives are.",
"id": "62161",
"label": "d",
"name": "An Advance Statement is a legally binding document outlining specific treatments a patient would and would not wish to receive in their future care",
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"answer": true,
"explanation": "This is the definition of an advance statement",
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"name": "An Advance Statement is a document outlining general wishes, feelings, beliefs and values surrounding a patient's future care, to which decision-makers can refer when making best-interests decisions in the event of loss of capacity",
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"answer": false,
"explanation": "This is a Do Not Attempt CPR form. Advance Statements are not standardised and cover more than just wishes regarding CPR, although this could be included in an Advance Statement.",
"id": "62162",
"label": "e",
"name": "An Advance Statement is a standardised document that indicates that the patient is not for cardiopulmonary resuscitation (CPR) in the event of cardiac arrest",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "They are two disctinct documents.",
"id": "62159",
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"name": "An Advance Statement is another interchangable term for an Advance Decision",
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"explanation": "Advance Statements are not a legally binding document, wheras Advance DIrectives are.",
"id": "62160",
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"explanation": "# Overview\n\nThe Mental Capacity Act (MCA) includes provisions that allow people to plan for their care in advance, for a situation in the future where they do not have the capacity to make decisions. Two of these are Advanced Statements and Advanced Decisions. An individual can make both an Advanced Statement and an Advance Decision.\n\n# Definition of Advanced Decisions\n\nAn Advanced Decision, short for Advanced Decision to Refuse Treatment, is a legally binding document. Its purpose is to ensure that an individual can refuse a specific treatment(s) that they do not want to have in the future.\n\n# Advanced Decision Criteria\n\nIn order for an Advanced Decision to be legally binding, it must meet certain criteria:\n\n _It must be valid (this means it must have been made at a time when the individual had capacity to make that decision)._\n\n _It must be applicable (this means the wording must be specific to the medical circumstances, and not vague or unclear)._\n\n _It must have been made when the individual was over 18, and fully informed about their decision._\n\n _It must not have been made under the influence or duress of other people_\n\n _It must be written down, be signed and witnessed (if it concerns a refusal of life-saving treatment)_\n\n# What Can Advanced Decisions Cover?\n\nTreatments that can be refused include life-sustaining treatments. It cannot refuse basic care (such as washing), food or drink by mouth, measures designed purely for comfort (e.g. painkillers), or treatment for a mental health condition if the individual is sectioned under the Mental Health Act. It can also not demand specific treatment or something that is illegal (e.g. assisted dying).\n\n# Definition of Advanced Statement\n\nAn Advance Statement is sometimes called a \"Statement of Wishes and Care Preferences\". It allows an individual to make general statements about their wishes, beliefs, feelings and values and how these influence their preferences for their future care and treatment.\n\nAn Advance Statement is not by itself legally binding, but legally must be taken into consideration when making a \"best interests\" decision on someone's behalf under the Mental Capacity Act (MCA), 2005. This is because one of the criteria of the MCA is that a patient's \"wishes, feelings, beliefs and values\" must be taken into consideration; an Advanced Statement provides evidence of this.\n\n# Advanced Statement information included\n\nInformation that can be included in an Advanced Statement can be anything that is important to the individual. This might include:\n\n _Religious or spiritual views, and those that might relate to care_\n\n _Food preferences_\n\n _Information about your daily routine_\n _Where you would like to be cared for (in hospital, at home, in a care home etc.)_\n\n _Any people who you would like to be consulted when best interests decisions are being made on your behalf (however this does not give the same legal power as creating a Lasting Power of Attorney)_\n\n# What Can Advanced Statement Cover?\n\nAn Advanced Statement can be made verbally, but it is better to write it down so there is clear documented evidence of an individual's wishes and views. Copies of the Advanced Statement can be given to anyone the individual wishes to have a copy (e.g. their GP, carers and relatives).",
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"question": "A 87 year old female presents to A&E with confusion and sepsis. She is critically unwell. She has an Advance Statement document by her bedside.\n\nWhich of the following answers best describes an Advance Statement?",
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"explanation": "The patient's next of kin's advice should always be sought and considered. However, if the patient does not have capacity, we must act in their best interest. In this case it would be to prevent the patient from leaving hospital.",
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"label": "d",
"name": "Ask the next of kin if they will allow the patient to leave",
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"explanation": "The Mental Health Act (MHA) is used to detain patients in their best interest if they **have a mental health disorder**, and are at **risk to themselves or others**.\n\nSection 2 of the MHA is for assessment and treatment, and lasts 28 days.\n\nThis patient has acute, organic, lack of capacity secondary to delirium. He does not have a mental health disorder and therefore it would be inappropriate to detain him under the MHA.",
"id": "62164",
"label": "b",
"name": "Detain the patient under the Mental Health Act Section 2",
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"explanation": "The Mental Health Act (MHA) is used to detain patients in their best interest if they **have a mental health disorder**, and are at **risk to themselves or others**.\n\nSection 3 of the MHA is for treatment, and can last up to 3 months.\n\nThis patient has acute, organic, lack of capacity secondary to delirium. He does not have a mental health disorder and therefore it would be inappropriate to detain him under the MHA.",
"id": "62165",
"label": "c",
"name": "Detain the patient under the Mental Health Act Section 3",
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"explanation": "A patient with capacity is allowed to make an 'unwise' decision. If a patient is deemed to have capacity they can of course leave hospital, but we asked them to sign s form declaring that they are doing so against medical advice - a 'self-discharge' form. This patient does not have capacity and it would be in his best interest to prevent him leaving hospital.",
"id": "62167",
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"name": "Allow the patient to leave after signing a self-discharge form",
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"explanation": "Correct! The Deprivation of Liberty Safeguards is the procedure in law used where it is necessary to deprive a patient or resident of their liberty as they lack capacity to consent to treatment or care to keep them safe from harm. This patient lacks capacity so can be detained for their best interest. Mental capacity is guided by the principles of the Mental Capacity Act.",
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"comment": "Not what DoLS is for - you detain them under the mental capacity act and DoLS protects the patient from us",
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"explanation": "# Deprivation of Liberty\n\nArticle 5 of the Human Rights Act states that 'everyone has the right to liberty and security of person. No one shall be deprived of his or her liberty [unless] in accordance with a procedure prescribed in law'.\n\nThere is likely a deprivation of liberty if:\n\n- The person is subject to continuous supervision and control _and_\n- The person is not free to leave\n\n# The Deprivation of Liberty Safeguards \n\nThe Deprivation of Liberty Safeguards is the procedure in law used where it is necessary to deprive a patient or resident of their liberty as they lack capacity to consent to treatment or care to keep them safe from harm.\n\nThese procedures must be authorised by a supervisory authority e.g. local authority.\n\nThe following conditions must be met to allow a person to be deprived of their liberty under the safeguards:\n\n- The person must be 18 or over.\n- The person must be suffering from a mental disorder.\n- The person must be a patient in hospital or a resident in a care home.\n- The person lacks capacity to decide for themselves about the restrictions which are proposed so they can receive the necessary care and treatment.\n- The proposed restrictions would deprive the person of their liberty.\n- The proposed restrictions would be in the person's best interests.\n- Whether the person should instead be considered for detention under the Mental Health Act.\n- There is no valid advance decision to refuse treatment or support that would be overridden by any DoLS process.\n\n# Capacity \n\n- All patients are initially assumed to have capacity\n- Capacity is decision-specific e.g. a patient may be able to decide which clothes to wear, but not where is safest to live\n- Capacity can be impaired permanently, temporarily, or can fluctuate\n- Patients deemed to have capacity are freely able to make decisions that the healthcare provider thinks unwise or dangerous\n\n# The Mental Capacity Act \n\nThe mental capacity act haas five key principles:\n\n1. Every adult is assumed to have capacity unless proved otherwise\n2. A person must be given all practicable help to make their own decisions before they are deemed to lack capacity\n3. Unwise, unsafe or dangerous decisions does not mean that person does not have capacity.\n4. All treatment given to a person who lacks capacity must be in the patients best interests\n5. Anything done for a person who lacks capacity must be done in the least restrictive way possible\n\n# Power of attorney \n\nThis is a legal document drawn up by a competent adult that nominates another person to make decisions on their behalf. This can be related to financial and property, or health and welfare. It can only be used when that adult has lost capacity.\n\n# Advance directives \n\nAn advance directive is a medical decision made by a patient with capacity, regarding their future wishes for treatment. It only comes into force if a patient subsequently lacks capacity.\n\n# References \n\n- [Social Care Institute for Excellence: Deprivation of Liberty Safeguards (DoLS)](https://www.scie.org.uk/mca/dols)\n- [NICE Guidance: Decision-making and mental capacity](https://www.nice.org.uk/guidance/ng108)\n",
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"question": "A 76-year-old man is admitted to the geriatrics ward with a urinary tract infection. He past medical history includes only COPD and hypertension. He has delirium but no background of cognitive impairment. He remains on IV antibiotics and requires further management.\n\nHe appears confused and states that he would like to be discharged and is planning to leave. He does is not able to understand the risks of leaving hospital and make an informed decision.\n\nWhich of the following is the best course of action?",
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"explanation": "The Garden classification is a simple categorisation of intracapsular neck of femur fractures, which dictates the most appropriate management option. This patient has a Garden classification 3 fracture, as it is complete, and partially displaced. The following table describes the four classifications.\n\n| Garden classification | Description |\n| ------------- |:-------------:|\n| 1 | Incomplete fracture, undisplaced|\n| 2 | Complete fracture, undisplaced |\n| 3| Complete fracture, partially displaced |\n| 4| Complete fracture, fully displaced |",
"id": "62169",
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"explanation": "The Garden classification is a simple categorisation of intracapsular neck of femur fractures, which dictates the most appropriate management option. **There are only 4 classifications in this scale\n**. This patient has a Garden classification 3 fracture, as it is complete, and partially displaced. The following table describes the four classifications.\n\n| Garden classification | Description |\n| ------------- |:-------------:|\n| 1 | Incomplete fracture, undisplaced|\n| 2 | Complete fracture, undisplaced |\n| 3| Complete fracture, partially displaced |\n| 4| Complete fracture, fully displaced |",
"id": "62172",
"label": "e",
"name": "Garden Classification 5",
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"__typename": "QuestionChoice",
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"explanation": "The Garden classification is a simple categorisation of intracapsular neck of femur fractures, which dictates the most appropriate management option. This patient has a Garden classification 3 fracture, as it is complete, and partially displaced. The following table describes the four classifications.\n\n| Garden classification | Description |\n| ------------- |:-------------:|\n| 1 | Incomplete fracture, undisplaced|\n| 2 | Complete fracture, undisplaced |\n| 3| Complete fracture, partially displaced |\n| 4| Complete fracture, fully displaced |",
"id": "62170",
"label": "c",
"name": "Garden Classification 2",
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"__typename": "QuestionChoice",
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"explanation": "The Garden classification is a simple categorisation of intracapsular neck of femur fractures, which dictates the most appropriate management option. This patient has a Garden classification 3 fracture, as it is complete, and partially displaced. The following table describes the four classifications.\n\n| Garden classification | Description |\n| ------------- |:-------------:|\n| 1 | Incomplete fracture, undisplaced|\n| 2 | Complete fracture, undisplaced |\n| 3| Complete fracture, partially displaced |\n| 4| Complete fracture, fully displaced |",
"id": "62168",
"label": "a",
"name": "Garden Classification 3",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "The Garden classification is a simple categorisation of intracapsular neck of femur fractures, which dictates the most appropriate management option. This patient has a Garden classification 3 fracture, as it is complete, and partially displaced. The following table describes the four classifications.\n\n| Garden classification | Description |\n| ------------- |:-------------:|\n| 1 | Incomplete fracture, undisplaced|\n| 2 | Complete fracture, undisplaced |\n| 3| Complete fracture, partially displaced |\n| 4| Complete fracture, fully displaced |",
"id": "62171",
"label": "d",
"name": "Garden Classification 4",
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"comment": "1,2 - use a screw (dynamic hip screw)\n3,4 - displaced, replace (hip replacement)",
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"comment": "Aren't dynamic hip screws used for extrascapular fractures not intrascapular??",
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"comment": "I think they mean ORIF with cancellous screws",
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"explanation": "# Summary\n\nA fracture of the neck of the femur is a break occurring in the upper part of the femur, just below the ball-and-socket hip joint. This fracture is common among the elderly population, particularly those with osteoporosis. Notable symptoms include severe hip or groin pain, an inability to bear weight on the affected leg, and external rotation and shortening of the affected leg. Diagnosis typically involves X-rays, though CT scans or MRI may be employed for more complex cases. Management is primarily surgical, with options including cannulated screw fixation, dynamic hip screw, hemiarthroplasty, and total hip arthroplasty, chosen based on factors such as the patient's age, health, and the type of fracture. Complications can include non-union, avascular necrosis, deep vein thrombosis, and pulmonary embolism.\n\n# Definition\n\nA fracture of the neck of the femur is a type of hip fracture that specifically involves the upper part of the femur, just below the ball of the hip's ball-and-socket joint.\n\n# Types of Neck of Femur Fracture\n\nFractures of the neck of the femur are generally classified into two types based on their location in relation to the hip joint capsule:\n\n- **Intracapsular Fractures**: These fractures occur within the joint capsule. They are further subdivided into displaced and non-displaced fractures. Displaced fractures carry a high risk of avascular necrosis due to possible disruption of the blood supply to the femoral head.\n \n- **Extracapsular Fractures**: These fractures occur outside the joint capsule and include intertrochanteric and subtrochanteric fractures. They have a better prognosis due to a lower risk of avascular necrosis.\n\n# Epidemiology\n\nFractures of the neck of the femur are a common injury, particularly in older individuals. This is largely attributed to the increased prevalence of osteoporosis in this population, which makes the bones more susceptible to fractures.\n\n# Aetiology\n\nThe main cause of a fracture to the neck of the femur is a fall, often in the elderly and those with weakened bones due to osteoporosis. Other potential causes can include high-energy trauma such as car accidents, especially in younger individuals.\n\n# Signs and Symptoms\n\nPatients with a fractured neck of femur commonly present with:\n\n- Severe pain in the hip or groin\n- Inability to bear weight on the affected leg\n- Shortening and external rotation of the affected leg\n- Swelling or bruising over the hip area\n\n# Differential Diagnosis\n\nThe differential diagnosis for a fractured neck of femur should include other injuries that could present with similar symptoms:\n\n- **Intertrochanteric Fracture**: Another type of hip fracture, characterised by pain in the hip or groin, inability to bear weight, and often shortening and external rotation of the affected leg.\n- **Pelvic Fracture**: Can be caused by falls or high-energy trauma. Symptoms can include severe pain in the hip or groin, inability to bear weight, and possible signs of internal bleeding.\n- **Hip Dislocation**: Usually a result of high-energy trauma, symptoms include severe hip pain, inability to move the leg, and a visibly deformed hip.\n\n# Investigations\n\nThe primary investigation for a suspected fractured neck of femur is a hip X-ray, which typically reveals the fracture and its severity. In cases where the fracture is not clear on X-ray, a CT scan or MRI may be necessary.\n\n[lightgallery]\n\n# Management\n\nManagement of a fractured neck of the femur is primarily surgical. The choice of surgical intervention depends on several factors, including the type of fracture, the patient's age, general health, and mobility prior to the injury.\n\n- **Cannulated Screw Fixation**: This is often used for non-displaced intracapsular fractures. The procedure involves the insertion of screws across the fracture line to stabilise it.\n \n- **Dynamic Hip Screw (DHS)**: This technique is usually used for stable, extracapsular fractures. It involves the insertion of a single large screw into the femoral head, combined with a side plate fixed to the femoral shaft.\n \n- **Hemiarthroplasty**: This involves replacing the femoral head and neck with a prosthesis. It is typically performed for displaced intracapsular fractures in older patients with lower activity levels, as these fractures have a high risk of non-union and avascular necrosis.\n \n- **Total Hip Arthroplasty (THA)**: This procedure involves the replacement of both the femoral head and the acetabulum with prosthetic components. It is typically used for displaced intracapsular fractures in younger, more active patients or older patients with pre-existing osteoarthritis.\n \n\n# Complications\n\nPotential complications from a fracture of the neck of the femur include:\n\n- Non-union of the fracture\n- Avascular necrosis due to interruption of blood supply to the femoral head\n- Deep vein thrombosis (DVT)\n- Pulmonary embolism (PE)\n- Infection\n- Dislocation of the hip prosthesis, in cases where arthroplasty has been performed\n\n# References\n\n[Click here to read more about fractures of the neck of femur](https://teachmesurgery.com/orthopaedic/hip/femoral-neck-fractures/)",
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"question": "An 87-year-old woman is admitted through the emergency department following a fall at home. She fell onto her left side and is complaining of left hip pain. On examination, her left leg is shortened and externally rotated. She is in significant pain on any movement and she will not allow you to examine her any further due to the pain.\n\nLeft hip X-ray report: Complete intracapsular neck of femur fracture, that is partially displaced. Marked soft tissue injury noted.\n\nWhich of the following best describes the abnormality identified on the X-ray?",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "Patients have a legal right to confidentiality (under both Common Law and Human Rights Law), and doctors have the corresponding legal duty to provide this right to confidentiality. As the patient has capacity, you must gain their consent before discussing their case with the patient's relative.",
"id": "62173",
"label": "a",
"name": "Ask the patient if they allow you to discuss her case with her daughter",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Patients have a legal right to confidentiality (under both Common Law and Human Rights Law), and doctors have the corresponding legal duty to provide this right to confidentiality. As the patient has capacity, you must gain **their** **consent** before discussing their case with the patient's relative. The consultant may offer valuable guidance, but it is the patient's decision to give permission or not.",
"id": "62176",
"label": "d",
"name": "Ask the consultant if you can discuss the patient's case with her daughter",
"picture": null,
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Patient's have a legal right to confidentiality. However, you may take steps to obtain consent (asking the patient!). Family discussions may often be helpful in providing best care to your patients.",
"id": "62175",
"label": "c",
"name": "Refuse to disclose details with the daughter over the phone",
"picture": null,
"votes": 95
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Patients have a legal right to confidentiality (under both Common Law and Human Rights Law), and doctors have the corresponding legal duty to provide this right to confidentiality. As the patient has capacity, you must gain their consent before discussing their case with the patient's relative.",
"id": "62174",
"label": "b",
"name": "Discuss the details with the daughter as her Mother will need more care at home",
"picture": null,
"votes": 2
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Patients have a legal right to confidentiality (under both Common Law and Human Rights Law), and doctors have the corresponding legal duty to provide this right to confidentiality. As the patient has capacity, you must gain their **consent** before discussing their case with the patient's relative, not just to inform them. This patient has capacity and can therefore refuse this.",
"id": "62177",
"label": "e",
"name": "Inform the patient that you will update her daughter",
"picture": null,
"votes": 5
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"explanation": "# Overview\n\nPatients have a legal right to confidentiality (under both Common Law and Human Rights Law), and doctors have the corresponding legal duty to provide this right to confidentiality.\n\nHowever, this right to confidentiality is not absolute. There are a number of situations in which the law obliges doctors to breach confidentiality, i.e. there is a legal duty to breach confidentiality. There are also some situations where a doctor has a legal defence to breach confidentiality.\n\n# Legal Duties to Breach Confidentiality\n\n1. If ordered to by a court or judge\n2. To satisfy statutory requirements\n\n _e.g. to inform the local authority about notifiable diseases under the Public Health Act 1984_\n\n _e.g. under the Road Traffic Act, must provide identifying information to the police on request_\n\n _e.g. under the Terrorism Act 2000, must report any suspicions of terrorism_",
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"question": "A 76-year-old patient is on the geriatrics ward following a fall at home. They have a 75 pack year smoking history and a recent diagnosis of lung cancer. Investigations identify multiple bony metastases. The patient is not for active management and is being reviewed by the palliative care team.\n\nShe is not confused and clearly has capacity to make decisions about her care. She is aware of her condition and poor prognosis. She currently lives alone, but will require support at home on discharge. She tells you she has one daughter who lives abroad, who does not know about her diagnosis.\n\nHer daughter calls the ward and asks to know all of the details of her Mother's condition.\n\nWhich of the following is the next best step?",
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"explanation": "A cataract is an opacity in the lens. They are more common in the elderly, but they would not cause drusen on fundoscopy. Classic presenting symptoms include 'haloes around lights', and there will be a loss of the red reflex on examination",
"id": "62182",
"label": "e",
"name": "Cataract",
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"explanation": "This patient has dry age related macular degeneration (ARMD). In wet ARMD, one would see neovascularisation, bleeding and fluid leakage on fundoscopy. This presents more rapidly and has a poorer prognosis than dry ARMD.",
"id": "62179",
"label": "b",
"name": "Wet age related macular degeneration",
"picture": null,
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"explanation": "Central retinal vein occlusion (CRVO) typically causes **sudden** painless visual loss, whilst this patient's presentation is far more insidious in onset. Fundoscopy in CRVO will show: haemorrhages, cotton wool spots, retunal oedema and tortuous retinal veins. None of these are present here.",
"id": "62181",
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"explanation": "Correct! This patient has dry age related macular degeneration (ARMD). The 'yellow deposits' on fundoscopy are drusen which are seen in the condition. Dry ARMD accounts for the vast majority of cases. All patients with ARMD should be encouraged to stop smoking.",
"id": "62178",
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"name": "Dry age related macular degeneration",
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"explanation": "Whilst this patient has known hypertension, this is well controlled (with normal BP on assessment) with one anti-hypertensive medication. Signs on fundoscopy of hypertensive retinopathy include: narrowing of the retinal arteries, retinal haemorrhages, hard exudates and cotton wool spots.",
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"label": "c",
"name": "Hypertensive retinopathy",
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"explanation": "# Summary\n\nAge-related macular degeneration (ARMD) is the most prevalent cause of blindness in the UK, characterized by the degeneration of photoreceptors in the central retina leading to drusen formation. There are two types: dry (most common, characterised by drusen deposition), and wet (exudative, caused by neovascularisation and carries worse prognosis). Key symptoms include subacute loss of and/or distortion of the central visual field, reduced visual acuity, night blindness, and photopsia. The primary investigation methods include slit-lamp biomicroscopy, colour fundus photography, fluorescein angiography, and ocular coherence tomography (OCT). Management generally involves smoking cessation, and depending on the type of ARMD, zinc and antioxidant supplements (dry ARMD) or anti-vascular endothelial growth factor (anti-VEGF) injections (wet ARMD).\n\n# Definition\n\nAge-related macular degeneration (ARMD) is the leading cause of blindness in the UK. Patients present with subacute loss of and/or distortion of the central visual field.\n\nARMD describes degeneration of photoreceptors in the central retina (macula) that leads to the formation of drusen, which are visible on slit-lamp biomicroscopy.\n\n# Risk factors\n\n- Age – the biggest risk factor for developing ARMD\n- Male sex\n- Smoking (doubles the likelihood of ARMD-related vision loss) – a smoking history should always be taken in patients with ARMD\n- Family history \n- Cardiovascular risk factors: hypertension, diabetes mellitus, coagulopathy, dyslipidaemia\n\n# Dry vs Wet ARMD\n\n| | Dry ARMD | Wet ARMD |\n| ------------- |:-------------:| :-----:|\n| **Prevalence** | 85–90% of cases | 10–15% of cases|\n| **Features** |Drusen, macular thinning (geographic atrophy) | Neovascularisation, bleeding, leakage of fluid|\n| **Prognosis**| Slow progression over decades | Rapid progression over months, with poor prognosis |\n\n# Signs and Symptoms\n\n**Symptoms**:\n\n* Reduced visual acuity, worse for near vision and central vision (patients may say they struggle seeing faces)\n* Variability in visual disturbance from day to day is characteristic\n* Poor vision at night\n* Photopsia – perceived flickering of lights\n* Glare\n\n**Signs**:\n\n* Visual distortion – particularly line perception when tested with Amsler grids. This is known as metamorphopsia.\n* **Dr**usen in **dr**y ARMD – yellow pigmented spots on the retina that are collected around the macula\n* Subretinal or intraretinal haemorrhages in wet ARMD – seen as red patches on the retina around the macula\n\n[lightgallery]\n\n# Differential Diagnosis\n\n\n2. **Diabetic Macular Oedema (DME):**\n - **Diabetic Retinopathy:** Patients with diabetic retinopathy can experience macular oedema, which may lead to similar symptoms as neovascular AMD, such as visual distortion or blurred central vision.\n\n3. **Retinal Vein Occlusion (RVO):**\n - **Central or Branch RVO:** A blockage of retinal veins can lead to macular oedema, haemorrhages, and vision changes similar to those in neovascular AMD.\n\n4. **Central Serous Chorioretinopathy (CSC):**\n - **CSC:** This condition often presents with central serous retinal detachment, leading to vision disturbances. It can mimic wet AMD, but CSC is characterised by serous fluid accumulation rather than CNV.\n\n\nA comprehensive eye examination, including optical coherence tomography (OCT), fluorescein angiography, and fundus photography, is often necessary to differentiate AMD from these conditions and guide appropriate management and treatment decisions.\n\n# Investigations\n\n\n| Technique | Notes |\n|-----------|------|\n| **Slit-lamp biomicroscopy**| Allows identification of exudative, pigmentary or haemorrhagic changes in the retina to allow diagnosis of ARMD |\n| **Colour fundus photography** | Done at each assessment to monitor progression|\n| **Fluorescein angiography** | Used to identify neovascular ARMD to guide anti-VEGF therapy |\n| **Ocular coherence tomography (OCT)** | Allows assessment of all layers of the retina and identification of disease not visible by slit-lamp biomicroscopy |\n\n# Management\n\nSmoking cessation is important for all patients with ARMD.\n\n## Dry ARMD\n\nZinc and antioxidant vitamin A, C and E supplements have been shown to reduce progression by up to 30%.\n\n## Wet ARMD\n\nAnti-vascular endothelial growth factor (anti-VEGF) injections limit progression and can even reverse vision loss – typically administered in monthly injections.\n\n# NICE Guidelines\n\n[Click here for NICE CKS on ARMD](https://cks.nice.org.uk/topics/macular-degeneration-age-related/)\n\n# References\n\n[Click here for more detailed Eye Wiki notes on ARMD](https://eyewiki.aao.org/Age-Related_Macular_Degeneration#Management)",
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"question": "A 79-year-old presents with progressively worsening vision. He reports that he struggles to drive at night, but cannot pinpoint when this all began. He has a past medical history of hypertension and hypercholesterolaemia. He takes amlodipine and atorvastatin, and has no allergies. He smokes 10 cigarrettes per day and drinks 10 units of alcohol a week.\n\nHis observations are within normal limits. Fundoscopy identifies yellow deposits.",
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"explanation": "Dementia symptoms can precede motor symptoms, but if motor symptoms are rapidly followed by dementia onset (within 1 year) this would indicate LBD.",
"id": "62133",
"label": "a",
"name": "Emergence of dementia 6 months after parkinsonian motor symptom onset",
"picture": null,
"votes": 138
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Lewy bodies are protein aggregates (primarily alpha-synuclein) which are characteristic of both Parkinson's Disease and LBD and therefore not a distinguishing feature.",
"id": "62137",
"label": "e",
"name": "Histological finding of 'Lewy Bodies' in the brain on autopsy",
"picture": null,
"votes": 101
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is a motor sign suggestive of Progressive Supranuclear Palsy, a Parkinson's plus syndrome. It is not a feature of LBD.",
"id": "62136",
"label": "d",
"name": "Vertical gaze palsy",
"picture": null,
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Visual hallucinations are found in both LBD and PDD.",
"id": "62134",
"label": "b",
"name": "Visual hallucinations",
"picture": null,
"votes": 369
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "REM sleep behaviour disorder (acting out dreams) is found in both LBD and PDD",
"id": "62135",
"label": "c",
"name": "REM (rapid eye movement) sleep behaviour disorder",
"picture": null,
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"comment": "In LBD don't you get emergence of dementia BEFORE parkinsonian motor symptoms",
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"explanation": "# Summary\n\nParkinson's disease (PD) is a neurodegenerative disorder predominantly affecting adults over 65 years characterised by asymmetric tremor, bradykinesia, and rigidity. The condition results from Lewy body formation and neuronal death in the dopaminergic cells of the substantia nigra. Clinical features include assymetric resting tremor, slow shuffling gait, cogwheel rigidity, bradykinesia, and non-motor features such as autonomic dysfunction and psychiatric disturbances. Diagnosis is primarily clinical, supported by response to treatment trials. Pharmacological treatment with Levodopa remains the first-line therapy, with other agents used for specific symptom control or in later disease stages. Surgical interventions such as deep brain stimulation may be considered in certain cases. Prognosis varies, with little impact on overall life expectancy.\n\n\n# Definition\n\nParkinson's disease (PD) is a neurodegenerative disorder that presents with generalised slowing of movements (bradykinesia), resting tremor and rigidity.\n\n# Epidemiology\n\n- Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease. \n- It affects 0.3% of the UK population.\n- It is estimated that PD affects at least 1% of the population over 60\n\n\n# Aetiology\n\n- The exact cause of Parkinson's disease is unknown. \n- It is believed to result from the accumulation of \"Lewy bodies\", intracellular inclusions primarily composed of misfolded **alpha synuclein**. \n- These bodies form and lead to neuronal death in the dopaminergic cells of the substantia nigra of the basal ganglia, thereby causing the characteristic symptoms. \n- Both dominant and recessive familial variants of Parkinson's disease have been identified.\n\n# Clinical Features \n\nParkinson's disease is characterised by the following core features:\n\n* Bradykinesia\n* Asymmetric 3-5Hz \"pill-rolling\" resting tremor\n* Rigidity\n\t* Often noted to be 'cog-wheeling' which occurs when the tremor coincidees with rigidity\n* Gait Disturbance\n\t * Small, shuffling steps\n\t * Difficult initation and turning 'en bloc turning'\n\nOther features associated with Parkinson's Disease include:\n\n- Hypomimic facies\n- Micrographia (secondary to a combination of bradykinesia and rigidity)\n\nNon-motor features of Parkinson's disease are also common and may precede onset of motor symptoms by many years. These include:\n\n* Autonomic dysfunction, leading to constipation, symptomatic orthostasis (postural hypotension), and erectile dysfunction\n* Olfactory loss\n* Constipation\n* Sleep disorders such as REM behavioural disorder \n* Psychiatric features including depression, anxiety, and hallucinations\n\n\nPostural instability is a late feature of idiopathic Parkinson's disease. This said, very prominent early autonomic dysfunction should raise the suspicion of Multiple System Atrophy.\n\nEarly and prominent cognitive dysfunction should raise the suspicion of dementia with Lewy bodies (DLB).\n\n# Differential diagnosis\n\nKey differentials for Parkinson's disease, along with their signs and symptoms, include:\n\n* **Multiple System Atrophy (MSA):** Very prominent autonomic dysfunction, early postural instability, poor response to levodopa\n* **Dementia with Lewy Bodies (DLB):** Early and prominent cognitive dysfunction, visual hallucinations, fluctuating cognition\n* **Progressive Supranuclear Palsy (PSP):** Early gait instability and falls, vertical gaze palsy, prominent axial rigidity\n* **Corticobasilar Degeneration**: May have predominant apraxia, aphasia and 'alien hand' syndrome\n* **Wilson's Disease:** Secondary to copper deposition in the Basal Ganglia. May be associated with signs of liver disease\n* **Dementia Pugilistica:** Secondary to repeated head trauma\n* **Drug Induced Parkinsonism** Secondary to antipsychotic therapy, usually symmetrical tremor and less responsive to Levodopa\n\n# Investigations\n\nParkinson's disease is primarily a clinical diagnosis, supported by positive response to treatment trials. \n\nAn absolute failure to respond to 1-1.5g of levodopa daily almost excludes a diagnosis of idiopathic Parkinson's disease.\n\nOther investigations such as MRI Head or a Dopamine Transporter Scan (DaT scan) can be considered in atypical cases. \n\n# Management\n\nManagement should by led by a multidisciplinary team of neurologists, nurse specialists, physiotherapists, occupational therapists and other allied healthcare professionals.\n\n## Pharmacological Management\n\n### Levodopa\n\n- Levodopa is the precurser to dopamine\n- It is used as a dopamine replacement agent\n- Should be started in all patients with **significant functional impairment** according to NICE guidelines\n- Typically combined with Carbidopa, which decreases side effects and improves CNS bioavailability), oftern referred to as **Co-careldopa**\n- Absolute failure to respond to 1-1.5g of levodopa daily virtually excludes a diagnosis of idiopathic Parkinson's disease, though a response to levodopa does not confirm the diagnosis (as many primary parkinsonian syndromes may also respond).\n\n\nSide effects can be split into peripheral and central (depending on where the acting dopamine receptor is for the side effect).\n\nPeripheral side effects include:\n\n- Postural hypotension\n- Nausea & vomiting*\n\n\nWith time, and as the underlying disease progresses, levodopa may become a less effective and patients may report end-of-dose effects, where motor activity progressively declines as the previous dose wears off, and on-off phenomena, which manifest as seemingly random fluctuations in drug effect.\n\nOne of the most disabling side effects is **drug-induced dyskinesia**: writhing and uncoordinated movements of the limbs associated with poorly organised dopaminergic control of motor activity.\n\nIt typically takes 2-5 years to develop complete loss of response.\n\n*Domperidone is the anti-emetic of choice in those with Parkinson’s disease which has anti-dopaminergic activity but does NOT cross the blood brain barrier. \n\n### Dopamine agonists\n\n- Examples include: Ropinirole, rotigotine, Apomorphine. Previous ergot derived formulations (eg cabergoline) as now not widely used as are associated with lung fibrosis. \n- Have a longer half life than levodopa but are not as potent\n- Are often used in early disease in those without functional impairment, or late in disease when dyskinesias and motor fluctuations secondary to levodopa is a problem.\n- Increases activity of dopamine via the mesolimbic pathway which may affect reward centres and lead to unwanted risk-taking behaviours such as gambling. \n- Apomorphine is the most potent dopamine agonist and is typically given subcutaneously. It works well against motor fluctuations and dyskinesia. Often used late in disease. \n\n\n### MAO-B Inhibitors\n\n- Examples include: Selegiline, Rasagiline.\n- Reduce dopamine breakdown peripherally & thus increase central update of levodopa. Often used in combination with levodopa later in disease.\n- Initial animal studies suggested a \"neuroprotective effect\" although this has not been seen in human studies.\n- Can cause serotonin syndrome. \n\n### COMT Inhibitors\n\n- COMT inhibitors, or catechol- O -methyltransferase inhibitors include Entacapone and Tolcapone.\n- Extend the use of levodopa. Useful in wearing off effect in levodopa use.\n- Tolcapone is more potent than entacapone and can result in hepatotoxicity. \n\n### Amantadine\n\n- NMDA receptor antagonist that has an unclear action in Parkinson's Disease.\n- Can be used in those suffering from dyskinesia. \n\n\n### Anticholinergic agents\n\n- Examples include: Procyclidine, Trihexyphenidyl\n- Can be used in those with mild tremors. \n- Rarely used in clinical practice \n\n\n## Surgical Management\n\n- Deep Brain Stimulation: typically performed by implanting a stimulating device into a target area of the brain, often the thalamus or the subthalamus.\n\n# Prognosis\n\n- Parkinson's disease is typically slowly progressive, but the rate of progression is variable. \n- The mortality rate for elderly people aged 70-89 years with Parkinson's disease is 2-5 times higher than for age-matched controls in some studies. \n- The risk of dementia is about 2-6 times higher in people with Parkinson's disease than in healthy controls",
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"question": "Which of the following characteristics support diagnosis of Lewy Body Dementia (LBD) rather than Parkinson's disease dementia (PDD)?",
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"explanation": "Those with a lorry, bus or coach driving liscence who suffer a stroke must report this to the DVLA regardless of their ongoing symptoms or neurological defecit. Therefore, a neurological examination would not change the outcome of the consultation.",
"id": "62191",
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"name": "Conduct a full neurological examination to determine if he is safe to drive",
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"explanation": "As the patient is a bus driver, it is therefore in the public's best interest to report the issue to the DVLA without the patient's consent. However, it is important to inform the patient of your intention to disclose this to the DVLA and explain your legal responsibility to do so.",
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"name": "Contact the DVLA and inform the patient",
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"explanation": "This would only be acceptable if the patient agrees to stop driving in the meantime whilst they consider reporting to the DVLA. If they do not agree to this then it is the doctor's responsibility to report it.",
"id": "62192",
"label": "e",
"name": "Review the patient again in 2 weeks to see if he has changed his mind",
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"explanation": "This would be the case for a car or motorbike liscence, however, the patient is a bus driver and therefore there is a legal responsibility for the patient to inform the DVLA that they have had a stroke.",
"id": "62190",
"label": "c",
"name": "The patient only needs to inform the DVLA if he is still having problems 1 month after the stroke",
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"explanation": "Whilst the patient may have capacity there is a legal responsibility for doctors to report to the DVLA in this situation if they have not been able to persuade the patient to stop driving.",
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"name": "Nothing as the patient has capacity",
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"explanation": "# Legal Duties \n\nWhen considering ethical scenarios, various things can guide decisions that healthcare professionals make. One of these is the law. The law can not only provide details of what _cannot_ be done (i.e. what is illegal), it can also set out certain things that have to be done; these are called legal duties.\n\nExamples of legal duties include:\n\n**Confidentiality**\n\nA legal duty to breach confidentiality, if: ordered to by a court or judge, a patient is diagnosed with a notifiable disease (notify the local authority), the police request information on a road traffic accident, or grounds are met under the Terrorism Act 2000.\n\n**General Practitioners**\n\nGeneral Practitioners have a legal duty of care to all persons registered on their practice list or anyone who needs help in the practice area.\n\nAny doctor who offers help to someone, where the **help is accepted**, then owes that person a legal duty of care.\n\n# Legal Defences \n\nA doctor may have a professional duty (or moral duty) to do something that breaks the law. For example, breaching confidentiality where none of the above conditions are met. In some of these circumstances, a **legal defence** may exist, which allows the doctor to fulfil their professional/moral duty without facing criminal proceedings.\n\n**Legal defences** are established defences for breaking the law, which negate the criminality of the offence. In these situations, the law _allows_ the action to the taken, but does not _oblige_ it.\n\nFor example, the _public interest defence_ is an established legal defence. This means doctors are able to breach confidentiality if they know there is a risk of harm to the public by not doing so, e.g. may have to break confidentiality if a patient with mental illness poses harm to others.\n\n# Examples of Legal Defences \n\nLegal defence to breach confidentiality if: the public interest defence applies, it relates to serious crime or it relates to serious Sexually Transmitted Diseases\n\nNB: Serious Crime - gunshot and knife wounds have special consideration. Doctors have a duty to inform the police when patients present with these injuries, but what information they choose to disclose is left up to professional decision. Doctors can choose and then justify what information they disclose as a public interest defence (i.e. by giving the patient's name and address, the police might be able to prevent further harm to others).",
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"question": "A 53 year old male bus driver attends his GP practice, he has recently been discharged from hospital after having a stroke. He has attend to discuss his new medication. He mentions that he has not told the DVLA about the stroke as he is keen to return to work and does not want to lose his liscense. After discussing why he needs to inform the DVLA he continues to refuse.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Given the patient's age he needs exclusion of malignancy before looking at a dietary cause for his iron-deficiency anaemia.",
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"label": "c",
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"explanation": "Whilst tiredness can be multi-factorial and social stressors or care needs may be a factor, the most important first step is ruling out malignancy",
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"explanation": "Whilst a blood film can be helpful in determining the type of anaemia (eg hypochromic or microcytic), with the above results including the haematinics it is likely an iron deficiency anaemia. If there was a suspicion of a haematological malignancy or the blood results were suggestive of bone marrow failure, then a blood film would be helpful.",
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"explanation": "NICE guidance advises referral on the 2 week wait suspected cancer pathway for patients over the age of 60 with iron deficiency anaemia.",
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"name": "Urgent 2 week wait referral for lower gastrointestinal tract cancers",
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"explanation": "Whilst the patient is pre-diabetic and may benefit from some lifestyle modifications, given his age and iron deficiency anaemia the most important step is 2 week wait referral for suspected lower gastrointestinal cancer.",
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"explanation": "# Summary\n\nIron deficiency anaemia (IDA) is a common haematological disorder characterized by a shortage of iron in the body, leading to diminished red blood cell production and subsequent oxygen transport. Typical symptoms include fatigue, paleness, shortness of breath, and cognitive impairment. In older adults, it is imperative to consider the possibility of colorectal malignancy, as IDA may result from gastrointestinal bleeding. Thorough investigations, including endoscopic procedures, are often necessary. Management involves iron supplementation, dietary adjustments, and addressing underlying causes. \n\n# Definition\n\nIron deficiency anaemia is a haematological disorder stemming from an insufficient supply of iron, which is vital for the synthesis of haemoglobin—a crucial component of red blood cells. Without adequate iron, the body struggles to produce a sufficient quantity of healthy red blood cells, leading to a reduction in oxygen-carrying capacity and subsequent symptoms of anaemia.\n\n# Epidemiology\n\nIron deficiency anaemia is a global health concern, affecting individuals of all age groups. The prevalence is particularly high among young children, women of childbearing age, and elderly individuals. Geographical variations in prevalence exist, with a higher burden in regions with limited access to diverse diets and iron-rich foods.\n\n\n# Aetiology \n\nThe causes of iron deficiency anaemia are multifactorial and can be attributed to several factors:\n\n- **Dietary Insufficiency:** Inadequate iron intake, especially in individuals with restrictive diets or limited access to iron-rich foods.\n- **Chronic Blood Loss:** Gastrointestinal bleeding, heavy menstrual periods, and other sources of chronic blood loss (e.g. angiodysplasia) can deplete iron stores.\n- **Malabsorption Disorders:** Conditions like coeliac disease, inflammatory bowel disease and atrophic gastritis can hinder iron absorption in the gut. Hookworms are a more prominent cause in tropical setting.\n- **Increased Demand:** During pregnancy and rapid growth phases, the body's iron requirements can surpass the available supply. This can also occur if there is chronic haemolysis\n\n# Signs and Symptoms\n\nThe symptoms of iron deficiency anaemia include: \n\n- Tiredness\n- Lethargy\n- Weakness\n- Palpitations: An increased heart rate may be noticeable, especially when at rest.\n- Cognitive Impairment: Some patients may exhibit difficulty concentrating or memory issues.\n- Cold Intolerance\n- Headaches and dizziness\n- Brittle Nails: Changes in the nails, such as brittleness and spoon-shaped deformities **(koilonychia)**, can be observed.\n- Angular stomatitis\n- Atrophic glossitis\n- Pica: Iron-deficiency anaemia may manifest as pica, with cravings for non-food substances like ice (pagophagia) or clay (geophagia). This is more common in children.\n\n\n# Differential Diagnosis\n\nDistinguishing IDA from other forms of anaemia (such as anaemia of chronic disease) and underlying conditions is crucial. \n\n- **Colorectal Malignancy:** In older adults, it is imperative to rule out colorectal malignancies, especially when IDA is detected. Gastrointestinal bleeding, often occult, can be a sign of an underlying tumour.\n- **Thalassaemias:** Thalasasemias, a group of genetic disorders affecting haemoglobin production, may present with microcytic anaemia. Hemoglobin electrophoresis can help differentiate thalassaemias from IDA.\n- **Chronic Inflammatory Conditions:** Chronic diseases like rheumatoid arthritis or inflammatory bowel disease can lead to anaemia of chronic disease, which must be considered in the evaluation.\n\n# Investigations\n\nTogether with classical symptoms, full blood count (FBC) and blood film will show the presence of: \n\n- **Hypochromic, microcytic red cells** \n- Additional **pencil cells** \n- Occasional **target cells**\n\nReticulocyte counts will be low for the degree of anaemia; red cell count will also be low.\n\n**Further tests** may be performed to confirm the diagnosis of iron deficiency anaemia including:\n\n- **Total iron binding capacity** (TIBC) – Will typically be high as the body mobilises available iron stores owing to the iron deficiency\n\n- **Ferritin** – will be low as available iron stores in the body are mobilised to counteract the iron deficiency\n\n - Note: Ferritin should be measured alongside B<sub>12</sub> and folate to assess possible coexisting haematinic deficiency\n\n - A low ferritin is diagnostic of iron deficiency; however, a normal or high ferritin does not exclude iron deficiency\n\n - Ferritin is an acute phase protein so levels can be masked/influenced by other conditions, particularly inflammation \n – It is good to check a C-reactive protein (CRP) at the same time\n\nIron deficiency anaemia in patients >60y should prompt suspicion **colonic malignancy until proven otherwise** and prompt FIT testing and subsequent 2 week wait referral if indicated according to NICE guidelines. \n\n# Management\n\n* **Iron Supplementation:** Oral or intravenous iron supplements are administered to correct iron deficiency. Intravenous iron is preferred in cases of severe deficiency or malabsorption. Important considerations of oral iron supplementation (usually a 3 month course) include:\n\t* Side effects - diarrhoea, constipation, black stools, abdominal pain, nausea\n\t* If it is not tolerated due to SEs, reduce the dose to one tablet on alternate days, or consider alternative oral preparations.\n\t* Iron supplements should be taken on an empty stomach (preferably one hour before a meal) with a drink containing vitamin C, such as a glass of orange juice or another juice drink with added vitamin C. This aids absorption.\n\t* Oral iron decreases the absorption of oral Levothyroxine. Therefore if both are prescribed, advise patients to take at least 4 hours apart.\n\t* Monitoring - recheck FBC within 4 weeks of starting treatment (haemoglobin concentration should rise by about 20 g/L over 3–4 weeks). Then check the FBC again at 2–4 months to ensure that the haemoglobin level has returned to normal. Once Hb is normal can continue supplementation for 3 further months, and then monitor at 3/6/12-monthly intervals.\n* **Dietary Modifications:** Encouraging a diet rich in iron sources, such as red meat, leafy greens, and fortified cereals, can help maintain iron levels.\n* **Treatment of Contributing Conditions:** If the cause of IDA is chronic blood loss or malabsorption, addressing the underlying condition is essential.\n* **Endoscopic Procedures:** In cases where gastrointestinal bleeding is suspected, endoscopy and colonoscopy may be necessary to locate and treat the bleeding source.\n\n\n# NICE Guidelines\n\n[NICE CKS - Iron-deficiency anaemia](https://cks.nice.org.uk/topics/anaemia-iron-deficiency/)",
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"question": "A 70 year old man presented to his GP with several months of increasing tiredness. His examination was unremarkable. The GP carried out some blood tests which are as follows:\n\n\n||||\n|--------------|:-------:|---------------|\n|Haemoglobin|87 g/L|(M) 130 - 170, (F) 115 - 155|\n|White Cell Count|10x10<sup>9</sup>/L|3.0 - 10.0|\n|Platelets|140x10<sup>9</sup>/L|150 - 400|\n|Mean Cell Volume (MCV)|78 fL|80 - 96|\n|Serum Vitamin B12|532 ng/L|160 - 925|\n|Serum Folate|3.0 μg/L|3 - 15|\n|HbA1c (Glycated Haemoglobin)|47 mmol/mol or %|20 - 42 or 4-6%|\n\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "The patient's presentation is classic of croup, caused by parainfluenza virus. Croup is also known as laryngotracheobronchitis, is an infection of the upper airway. It commonly occurs in children under the age of three, with a harsh 'barking' or 'seal-like' cough, increased work of breathing and fevers. Whilst parainfluenza is the primary cause for croup, other viruses can also cause croup e.g. adenovirus, influenza and RSV.",
"id": "62198",
"label": "a",
"name": "Parainfluenza virus",
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"explanation": "Respiratory syncytial virus (RSV) can also cause croup, but this is less common. RSV is the most common pathogen causing bronchiolitis. Bronchiolitis occurs most commonly in under 1 year-olds, and it also presents with respiratory distress but not the bark like cough seen in croup.",
"id": "62199",
"label": "b",
"name": "Respiratory syncytial virus",
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"explanation": "This pathogen can cause Scarlet fever, which presents with a course ('sandpaper') red rash on the cheeks, a bright red inflamed tongue with fevers and a sore throat.",
"id": "62201",
"label": "d",
"name": "Streptococcus pyogenes",
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"explanation": "Adenovirus can also cause croup, however it is not the most common causative pathogen. Adenovirus is the most common pathogen to cause bronchiolitis obliterans- a rare condition of airway obstruction due to scarring of the bronchioles from recurrent infections",
"id": "62202",
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"name": "Adenovirus",
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"__typename": "QuestionChoice",
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"explanation": "This bacteria can cause bacterial tracheitis in children, which is a rare but very serious condition. It can present similarly to croup but with a quickly progressive airway obstruction and thick airway secretions",
"id": "62200",
"label": "c",
"name": "Staphylococcus aureus",
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"explanation": "# Summary\n \n\nCroup (also known as acute laryngotracheobronchitis) is a common childhood infection characterised by a harsh barking cough and inspiratory stridor. It is usually mild and self-limiting, however, some cases may cause severe respiratory distress requiring hospitalisation and supportive treatment. Parainfluenza viruses are the commonest causes, but the diagnosis is a clinical one and as symptoms such as stridor can worsen if the child is distressed, investigations should only be done if necessary. Oral steroids should be given to all children; in moderate to severe cases nebulised adrenaline, supplementary oxygen and airway support may be indicated.\n \n\n# Definition\n \n\nCroup, or acute laryngotracheobronchitis, is an upper respiratory tract infection that in most cases has a viral aetiology. Key symptoms include a barking cough, hoarse voice and inspiratory stridor. \n\n# Epidemiology\n \n\nCroup commonly affects children aged from 6 months old to 3 years old, with the peak incidence at 2 years. It is uncommon after the age of 6.\n\nSimilar to other viral infections, it is commonest in the autumn and winter months and is linked to parainfluenza epidemics. \n\n# Aetiology\n \nThe commonest cause is the parainfluenza virus. Other viral causes include adenovirus, respiratory syncytial virus (RSV), rhinovirus and influenza.\nRarely, bacteria can cause croup (e.g. Mycoplasma pneumoniae).\n\nThe pathophysiology involves infection and resulting inflammation of the subglottic and laryngeal mucosa which causes partial obstruction of the airways leading to respiratory distress and stridor.\n\n# Signs and Symptoms\n\n- The prodromal phase of coryzal symptoms, fever and a non-specific cough usually lasts 12-72 hours.\n- Characteristic symptoms of croup such as the harsh barking cough, hoarse voice or cry and inspiratory stridor then develop - these tend to be worse at night.\n- In severe cases, children may become drowsy and lethargic, or conversely more agitated.\n- The usual course of disease is resolution of symptoms within 48 hours (up to a week at most).\n\nOn examination, look for the following red flags that may indicate impending respiratory failure:\n\n- Signs of respiratory distress e.g. intercostal recessions, accessory muscle usage, tachypnoea\n- Cyanosis\n- Decreased level of consciousness\n- Stridor may decrease due to worsening airway obstruction\n- Decreased air entry on auscultation of the chest\n- Tachycardia\n\n# Differential Diagnosis\n \n\n- **Epiglottitis**: Sudden onset high fever, drooling, and dysphagia are seen without the barking cough of croup. Usually secondary to Haemophilus influenzae B and so significantly rarer since routine immunisation against this.\n- **Bacterial tracheitis**: Suspect if acute deterioration following initial viral symptoms, with high fevers, stridor and respiratory distress.\n- **Foreign body aspiration**: No prodrome or fever, usually sudden onset of choking, cough or wheeze after eating or playing with small objects.\n- **Anaphylaxis**: Rapid onset stridor, possible urticarial rash and facial swelling; suspect if history of previous episodes with allergens or family history of atopy.\n \n\n# Investigations\n \nDiagnosis is clinical, and investigations need to be carefully considered as distressing the child may lead to worsening of symptoms due to agitation.\n\nFurther investigation may include: \n\n- Pulse oximetry should be done to determine if supplementary oxygen is required.\n- Chest X-ray may be of use if a differential diagnosis such as an inhaled foreign body is suspected. \n - In croup, an X-ray may show a steeple sign, where the upper trachea is seen to taper.\n \n\n# Management\n\nClassifying the severity of croup is key to determining appropriate management:\n\n| Severity | Description |\n|------------------------------|---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|\n| Mild | Seal-like barking cough but no stridor or sternal/intercostal recession at rest. |\n| Moderate | Seal-like barking cough with stridor and sternal recession at rest; no (or little) agitation or lethargy. |\n| Severe | Seal-like barking cough with stridor and sternal/intercostal recession associated with agitation or lethargy. |\n| Impending respiratory failure | Minimal barking cough, stridor may become harder to hear. Increasing upper airway obstruction, sternal/intercostal recession, asynchronous chest wall and abdominal movement, fatigue, pallor or cyanosis, decreased level of consciousness or tachycardia. The degree of chest wall recession may diminish with the onset of respiratory failure as the child tires. A respiratory rate of over 70 breaths/minute is also indicative of severe respiratory distress. |\n\nMild cases with no stridor or chest wall recessions at rest may be treated at home with a single dose of oral dexamethasone (0.15mg/kg). In children treated at home, families should be safety-netted on signs of deterioration and advised to check on the child regularly and encourage fluids. Paracetamol or ibuprofen can be used for fever and pain.\n\nChildren with any of the following should be considered for hospital admission:\n\n* Stridor and/or sternal recession at rest\n* High fever\n* Respiratory rate > 60\n* Cyanosis\n* Lethargy or agitation\n* Fluid intake < 75% of normal or no wet nappies for 12 hours\n* Aged under 3 months\n* Chronic conditions such as immunodeficiency, chronic lung disease or neuromuscular disorders\n\nManagement is supportive as there is no treatment indicated for the usual causative viruses, and may include:\n\n- Supplementary oxygen if low saturations - consider how best to deliver this so as not to distress the child (e.g. a parent holding an oxygen mask to the face)\n- Steroids for all - if unable to swallow oral dexamethasone or prednisolone can give nebulised budesonide\n- Nebulised adrenaline for temporary symptom relief\n- Anaesthetics +/- ENT input if concerns regarding airway or respiratory failure\n\n# Complications\n\n- Dehydration secondary to poor fluid intake during illness\n- Pneumonia due to secondary bacterial infection \n- Respiratory failure \n- Death is very rare (1 in every 30,000 cases)\n\n# Prognosis\n\nUsually, symptoms resolve within 48 hours but may last longer. Occasionally, severe upper airway obstruction can occur, causing respiratory failure and arrest.\n\n# NICE Guidelines\n\n[NICE CKS: Croup](https://cks.nice.org.uk/topics/croup/)\n\n# References\n \n[BNF Treatment summaries: Croup](https://bnf.nice.org.uk/treatment-summaries/croup/)\n\n[Patient.info: Croup](https://patient.info/doctor/croup-pro)",
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"question": "A 2 year old presents to the GP surgery with her mother. She has had 2 days of a harsh cough, a low grade temperature and decreased oral intake.\nOn examination she has mild stridor, a bark like cough and subcostal recession.\n\nWhich organism is the most likely cause of her presentation?",
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"explanation": "A levonorgestrel-releasing intrauterine system (IUS) such as Mirena® is a coil that elutes levongesterel. It is used as contraception as well as a treatment for menorrhagia when dysfunctional intrauterine bleeding has been diagnosed. NICE guidance suggests initiating treatment for heavy menstrual bleeding without further investigation when the patient is low risk for fibroids or uterine cavity abnormalities, such as this patient.\nThe coil should be offered first line and disucssed with the patient to see if it aligns with their wishes in terms of contraception. The patient should also be counselled on the IUS causing menstrual irregularities for the first 6 months.",
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"explanation": "An intrauterine device (IUD) is also known as the copper coil. It is a form of contraception. It is not recommended in menorrhagia as the IUD can cause periods to be heavier.",
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"explanation": "An ultrasound is recommended if there is a suspicion of fibroids eg a mass felt on examination, age of over 30 or dysmenorrhea.",
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"explanation": "Whilst this can be used as a treatment option for menorrhagia secondary to dysfunctional uterine bleeding, it is contraindicated for this patient due to her history of migraines with aura.",
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"explanation": "Tranexamic acid can be offered to treat menorrhagia for those who find the IUS unsuitable. It can also be beneficial to those who are suspected to have fibroids as it can be used in the interim before investigations have been arranged.",
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"explanation": "# Summary\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive containing synthetic oestrogen and progestogen. It works by inhibiting ovulation, thickening cervical mucus, and altering the endometrium to prevent fertilisation and implantation. Indications for COCP use include contraception, menstrual cycle regulation, and treatment of dysmenorrhea, menorrhagia, acne, and hirsutism. Contraindications are categorised by UKMEC criteria, detailed in this chapter. \n \n# Definition\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive. It contains synthetic versions of the female hormones oestrogen and progestogen. \n \n\n# Mechanism of Action\n \n\n* **Inhibition of Ovulation:** The COCP contains synthetic versions of the hormones oestrogen and progestogen. These hormones together suppress the release of gonadotrophins (LH and FSH) from the pituitary gland, preventing the maturation and release of an egg from the ovaries.\n \n\n* **Thickening of Cervical Mucus:** The progestogen component of the COCP increases the viscosity of cervical mucus, making it more difficult for sperm to enter the uterus and fertilise an egg.\n \n\n * **Alteration of the Endometrium:** The COCP induces changes in the lining of the uterus (endometrium), making it less suitable for the implantation of a fertilised egg.\n \n\n# Indications\n \n\nThere are a range of reasons for women to be recommended the oral combined contraceptive pill. For example:\n \n\n* **Contraception:** The COCP works as a long-term contraception. It is taken orally once a day, at around the same time each day. \n * **Menstrual Cycle Regulation:** The COCP can help regulate irregular menstrual cycles. \n * **Dysmenorrhea:** The COCP may be used to reduce menstrual cramps. \n * **Menorrhagia:** The COCP can decrease heavy menstrual bleeding.\n * **Acne and Hirsutism:** The COCP helps in the treatment of acne and excessive hirsutism in women, which may happen in conditions such as polycystic ovary syndrome (PCOS) or other androgen excess conditions.\n * **Premenstrual Syndrome (PMHS**: The COCP can alleviate symptoms of PMS, such as mood swings, bloating, and irritability.\n \n# Contraindications \n \nThere are numerous contra-indications to the Combined Oral Contraceptive Pill. These can be divided into absolute contraindications, known as ''UKMEC 4'', a situation where the disadvantages outweigh the advantages (UKMEC 3), a situation where the advantages outweigh the disadvantages (UKMEC 2), and a situation whereby there is no limit on that choice of contraception (UKMEC 1).\n \n\n## Absolute Contraindications to Contraception (UKMEC 4)\n \n \n * Known or suspected pregnancy\n * Hypertension with SBP ≥160 mmHg or DBP ≥100 mmHg\n * Smoker over the age of 35 who smokes >15 cigarettes a day \n * Current and history of ischaemic heart disease\n * History of stroke (including TIA) \n * Vascular disease\n * History or current VTE\n * Major surgery with prolonged immobilisation\n * Breastfeeding <6 weeks postpartum\n * Not breastfeeding and <3 weeks postpartum with other risk factors for VTE\n * Known thrombogenic mutations \n * Complicated valvular and congenital heart disease\n * Cardiomyopathy with impaired cardiac function\n * Atrial fibrillation \n * Migraine with aura (any age)\n * Current breast cancer \n * Severe (decompensated) cirrhosis \n * Hepatocellular adenoma and hepatocellular carcinoma\n * Positive antiphospholipid antibodies \n \n \n \n## Disadvantages of a contraceptive outweigh the advantages (UKMEC 3)\n \n * Obesity (BMI ≥35 kg/m2)\n * Multiple risk factors for cardiovascular disease (e.g. smoking, diabetes mellitus, hypertension, obesity, dyslipidaemia) \n * Well controlled hypertension, and hypertension with SBP >140-159 mmHg or DBP <90-99 mmHg\n * Smoker over age of 35 who smokes <15 cigarettes a day, or anyone over age of 35 who stopped smoking <1 year ago\n * Family history of thrombosis before 45 years old\n * Not breastfeeding and <3 weeks postpartum without other risk factors for VTE\n * Not breastfeeding and between 3-6 weeks postpartum with other risk factors for VTE\n * Organ transplant with complications (e.g. graft failure, rejection) \n * Immobility (unrelated to surgery)\n * Migraine without aura (any age) [applies to *continuation* of COCP]\n * History (≥5 years ago) of migraine\nwith aura (any age) \n * Undiagnosed breast mass or symptoms [applies to *initiation* of COCP] \n * Carriers of known gene mutations associated with breast cancer\n * Past breat cancer \n * Diabetes mellitus with nephropathy, retinopathy, neuropathy or other vascular complications \n * Symptomatic gall bladder disease treated medically or currently active \n * Past COCP associated cholestasis \n * Acute viral hepatitis [applies to *initiation* of COCP]\n \n \n \n## Advantages of a contraceptive outweigh the disadvantages (UKMEC 2)\n \n * Smokers under the age of 35, and people aged over 35 who stopped smoking over 1 year ago \n * Obesity (BMI ≥30–34 kg/m2) \n * Family history of VTE in first-degree relative aged ≥45 years\n * History of raised blood pressure in pregnancy \n * Breast feeding between 6 weeks-6 months postpartum\n * Not breastfeeding and between 3-6 weeks postpartum without other risk factors for VTE\n * Uncomplicated organ transplant \n * Known dyslipidaemia \n * Major surgery without prolonged immobilisation \n * Superficial venous thrombosis \n * Uncomplicated valvular and congenital heart disease\n * Cardiomyopathy with normal cardiac function \n * Long QT syndrome \n * Non-migrainous headaches [applies to *continuation* of COCP]\n * Migraine without aura [applies to *initiation* of COCP] \n * Idiopathic intracranial hypertension \n * Unexplained vaginal bleeding\n * Cervical cancer \n * Undiagnosed breast mass or symptoms [applies to *continuation* of COCP]\n * Insulin-dependent diabetes mellitus without vascular disease \n * Symptomatic gall bladder disease treated through cholecystectomy, or asymptomatic gall bladder disease, or history of pregnancy-related cholestasis \n * Acute viral hepatitis [applies to *continuation* of COCP]\n * Inflammatory bowel disease \n * Sickle cell disease \n * Rheumatoid arthritis\n * SLE without antiphospholipid antibodies \n \n\n \n\n# Side-effects and Complications\n \n**Common Side-Effects:**\n \n\n * Breast tenderness \n * Abdominal discomfort, nausea diarrhoea \n * Headaches\n * Mood changes\n * Reduced libido \n \n\n**Rare but Serious Side-Effects:**\n \n\n * Embolism or thrombus, including: DVT and PE, stroke, myocardial infarction\n * Increased risk of breast cancer\n * Increased risk of cervical cancer \n \n\n \n\n# Follow-up\n\nArrange follow up 3 months following initial prescription of a COCP, and annually thereafter.\n \n\nAt follow-up, ensure to: \n \n\n * Check blood pressure and BMI. \n * Ask about headaches (including migraine). \n * Check for risk factors that may be contraindicators to COCP (as per UKMEC criteria). \n * Enquire about side-effects. \n * Enquire about how woman is taking the COCP (i.e. adherence). \n \n\n \n\n# Missed Pill Rules\n \n\n**Missed One Pill:**\n \n\n* Advise patient to take the pill as soon as possible, even if it means taking two pills in one day.\n* * Continue taking the rest of the pack as usual.\nNo additional contraception needed if this is the only pill missed in the pack.\n \n\n**Missed Two or More Pills in Week 1 (Days 1-7):**\n \n\n * Advise patient to take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * Use additional contraception for the next 7 days.\n * If they had unprotected sex during this week, seek emergency contraception.\n \n\n**Missed Two or More Pills in Week 2 (Days 8-14):**\n \n\n * Take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n\n**Missed Two or More Pills in Week 3 (Days 15-21):**\n \n\n* Finish the active pills in the current pack, then start a new pack immediately without taking the usual 7-day break.\n* No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n# NICE Guidelines \n \n\n[Click here to view NICE Guidelines on COCP](https://cks.nice.org.uk/topics/contraception-combined-hormonal-methods/management/combined-oral-contraceptive/)\n \n \n# References\n \n[Click here to see the UKMEC summary sheet on contraception](https://www.fsrh.org/standards-and-guidance/documents/ukmec-2016-summary-sheets/)",
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"question": "A 25 year old female attends her GP surgery with heavy periods for the past 6 months. Due to this she is struggling to go to work when menstruating. Her periods are regular with no intermenstrual bleeding.\nShe has a past medical history of migraines with aura for which she takes sumitriptain.\n\nAn examination reveals no abnormalities. Blood tests are carried out which show a mild anaemia and a normal clotting screen.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "Combined hormonal contraceptive patches such as Evra are contraindicated when less than 6 weeks post partum and breastfeeding. This is because of the increased risk for VTE post natally which would be increased further with the use of a combined hormonal contraceptive patch.",
"id": "62212",
"label": "e",
"name": "Combined hormonal contraceptive patch",
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"explanation": "Contraception is not required for the first 21 days post partum, however, beyond that contraception is recommended even if still breastfeeding. Lactational amenorrhea is a temporary lack of fertility whilst breast feeding. Lactational amenorrhea method (LAM) is sometimes used as a form of 'natural' contraception. If used correctly it is effective with only 2 in 100 people becoming pregnant in the first 6 months post partum. However, it requires consistent and exclusive breast feeding and amenorrhoea. It is only effective for the first 6 months post-partum. It is therefore recommended by the Faculty of Sexual and Reproductive Healthcare to implement contraception before 21 days.",
"id": "62209",
"label": "b",
"name": "Reassure her that no contraception is needed when breastfeeding",
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"explanation": "The IUD, also known as the copper coil, can commonly cause periods to be heavier. As this patient has a history of menorrhagia it is not a suitable option for her.",
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"label": "d",
"name": "Intrauterine device (IUD)",
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"answer": true,
"explanation": "The POP has no adverse affects on lactation or infant outcomes such as growth and development. Very small amounts of progesterone can be found in breast milk of those taking the POP.",
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"label": "a",
"name": "Progesterone only pill (POP)",
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"explanation": "The COCP is contraindicated less than 6 weeks post partum and breast feeding. There is an increased risk for VTE post-natally, this would be increased by use of COCP.",
"id": "62210",
"label": "c",
"name": "Restart the COCP",
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"explanation": "# Summary\n \n \nMenorrhagia is defined as excessive menstrual bleeding that significantly impacts a woman's quality of life. It is often characterised by heavy or prolonged menstrual periods and may result in iron deficiency anaemia. There is no set cut-off when defining menorrhagia: it is the patient who determines if bleeding is heavy to them or not. However, thorough clinical evaluation, including a full blood count, clotting studies, and possibly a transvaginal ultrasound, is necessary to identify potential underlying causes. Management strategies largely depend on the cause and may involve medical treatments like the Mirena® coil, mefenamic acid, tranexamic acid, hormonal contraceptives, or surgical interventions in refractory cases.\n \n \n# Definition\n \n \nMenorrhagia is a clinical condition defined as excessive blood loss during a menstrual period to an extent that it substantially affects a woman's quality of life.\n \n \n# Epidemiology\n \n \nMenorrhagia is a common gynaecological complaint. In about half of cases, no underlying pathology is found, and the condition is referred to as dysfunctional uterine bleeding.\n \n \n# Aetiology\n \n \nThe aetiology of menorrhagia can be categorised into two groups: local and systemic. \n \nLocal causes include:\n \n - Fibroids\n - Adenomyosis\n - Endometrial polyps\n - Endometriosis\n - Pelvic inflammatory disease\n - Endometrial cancer (be highly suspicious of this if there is postmenopausal bleeding)\n \n \nSystemic causes encompass:\n \n \n - Bleeding disorders\n - Hypothyroidism\n - Liver and kidney disease\n - Obesity\n \n \n# Signs and Symptoms\n \n \nThe primary symptom of menorrhagia is **heavy or prolonged menstrual bleeding**. \n\nHowever, other associated signs and symptoms may be present, depending on the underlying cause (see differential diagnosis). If severe enough, menorrhagia can also cause anaemia, which would present with **fatigue, weakness, shortness of breath and palpitations.**\n\n\n \n \n# Differential Diagnosis\n \n \nThe differential diagnosis for menorrhagia includes conditions that cause abnormal uterine bleeding. These may include:\n \n \n - **Fibroids:** Often asymptomatic, but can cause heavy or prolonged periods, pelvic pain or pressure, and frequent urination.\n - **Adenomyosis:** Symptoms can include prolonged, heavy menstrual bleeding, severe menstrual cramps, and pain during intercourse.\n - Endometrial polyps: Can cause irregular menstrual bleeding, bleeding between periods, excessively heavy periods, or postmenopausal bleeding.\n - **Endometrial cancer:** Symptoms include abnormal vaginal bleeding, pelvic pain, and pain during intercourse.\n- **Hypothyroidism:** Causes fatigue, weight gain and constipation.\n- **Clotting disorders:** Leads to excessive bleeding from minor injuries. \n \n \n# Investigations\n \n \nThe investigation of menorrhagia should include:\n \n**Bedside:**\n\n- Speculum and bimanual examination: This helps rule out causes such as cervical ectropion, or to investigate fibroids by feeling pelvic masses. \n\n**Bloods:**\n\n- FBC and iron studies: To rule out anaemia. \n- LFTs and clotting screen: To rule out liver and clotting disorders. \n- TFTs, if clinically indicated: To rule out hypothyroidism. \n\n**Imaging:**\n\n- Transvaginal ultrasound: To identify underlying causes such as fibroids or endometrial polyps.\n\n \n# Management\n \n \nThe management of menorrhagia largely depends on the underlying cause. If an underyling cause is found, the primary management involves treatment of that cause. \nOtherwise, if the cause is dysfunctional uterine bleeding, potential treatments include:\n \n**Medical:**\n\n - Mirena® coil: This is first line and most effective treatment option for menorrhagia. \n\nOtherwise:\n \n - Mefenamic acid: NSAID that prevents bleeding and helps relieve pain. \n - Tranexamic acid: Reduces bleeding but no effect on pain. \n - Combined oral contraceptive pill: Reduces bleeding, particularly helpful if the patient also requires contraception. \n\n**Surgical:**\n\n- Endometrial ablation (will require ongoing contraception)\n- Hysterectomy \n \nThese options are only applicable in rare cases refractory to medical management. \n \n\n# Complications\n\n- Anaemia: Occurs if bleeding is sufficiently severe.\n- Low mood, including depression and anxiety: The welfare and social complications (e.g. interference with work and social life) can have significant mental health impacts. \n\n# NICE Guidelines\n \n \n[Click here for more information on menorrhagia](https://cks.nice.org.uk/topics/menorrhagia/)\n \n# References\n\n[BMJ Best Practice](https://bestpractice.bmj.com/topics/en-gb/171)\n\n[Patient Info](https://patient.info/doctor/menorrhagia)",
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"question": "A 36 year old female attends her GP practice to discuss contraception. She is 4 weeks post partum and is currently breast feeding. She is on day 2 of her first period since giving birth.\nShe has a past medical history of menorrhagia, she does not take any regular medication.\nShe previously took a combined oral contraceptive pill (COCP).\n\nWhich of the following is most appropriate next step in managing this patient?",
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"explanation": "Amlodopine is a calcium channel blocker, it is first line pharmacological treatment for hypertension in those over the of 55 years old. It is therefore appropriate for this patient after diagnosis of hypertension, which first requires ambulatory blood pressure monitoring to confirm the diagnosis.",
"id": "62216",
"label": "d",
"name": "Commence amlodopine",
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"explanation": "Whilst these measures are helpful in treating hypertension and should be recommended alongside pharmacological treatment, a diagnosis of hypertension first needs to be made with ambulatory blood pressure monitoring.",
"id": "62214",
"label": "b",
"name": "Advise lifestyle changes such as weight loss and increase exercise",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Ramipril is an ACE-inhibitor, it is first line for primary hypertension in those under 55 years of age. The patient is 69 years old, therefore ramipril would not be first line.",
"id": "62215",
"label": "c",
"name": "Commence ramipril",
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"explanation": "Patients with two measured blood pressures >140/90 mmHg should be offered either ABPM or home blood pressure monitoring. ABPM involves wearing a device that checks the blood pressure regularly over a 24 hour period. Patients are instructed to continue their usual activities throughout the day. This also help eliminate any 'white coat hypertension' which is when a patient's blood pressure increases due to the anxiety of being in a health care setting.",
"id": "62213",
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"name": "Ambulatory blood pressure monitoring (ABPM)",
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"explanation": "Whilst it is important to get multiple blood pressure readings, it is recommended to arrange ambulatory blood pressure monitoring and diagnose hypertension from an average of those readings.",
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"name": "Recheck the blood pressure in 2 weeks time",
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"comment": "I thought if they had stage 2 HTN, you could skip to treatment immediately?",
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"explanation": "# Summary\r\n\r\nPrimary hypertension, accounting for approximately 90-95% of cases of hypertension, is characterised by persistently elevated blood pressure due to age-related pathophysiological changes. It is a major risk factor for cardiovascular disease, cerebrovascular disease, chronic kidney disease, and peripheral vascular disease. Diagnosis is based on ambulatory blood pressure monitoring (ABPM) readings of 135/85mmHg or higher. Classification is determined by the severity of the hypertension. Management depends on the classification of the hypertension and involves lifestyle modifications and pharmacological anithypertensives according to NICE guidelines. Effective management, through lifestyle changes and medications, significantly reduces the associated risks and improves outcomes for individuals with hypertension.\r\n\r\n# Definition \r\n\r\nA 'normal' blood pressure ranges between 90/60mmHg to 140/90mmHg. The definition of hypertension is a 24h ambulatory blood pressure average reading (ABPM) that is more than or equal to 135/85mmHg. \r\n\r\n# Epidemiology\r\n\r\nIn 2015, it was reported that high blood pressure affected more than 1 in 4 adults in England (31% of men; 26% of women). In England, it is estimated that primary hypertension affects around 13.5 million people and contributed to 75,000 deaths.\r\n\r\n# Pathophysiology\r\n\r\nPrimary hypertension is as a result of a series of complex physiological changes as we age. Hypertension often occurs as a result of reduced elasticity of large arteries, age-related and atherosclerosis-related calcification, and degradation of arterial elastin. It may also be present in conditions associated with increased cardiac output, such as anaemia, hyperthyroidism and aortic regurgitation.\r\n\r\nAlthough the risk of cardiovascular disease increases progressively with increasing systolic and diastolic blood pressure, raised systolic pressure is more important than raised diastolic pressure as a risk factor for cardiovascular and renal disease.\r\n\r\n# Classification \r\n\r\nHypertension can be classified according to how high a patient's blood pressure is. \r\n\r\n* Stage 1: Clinic => 140/90mmHg; ABPM => 135/85mmHg \r\n* Stage 2: Clinic => 160/100mmHg; ABPM =>150/95mmHg \r\n* Stage 3: Clinic systolic BP (SBP) => 180 or diastolic BP (DBP) =>120mmHg\r\n\r\n\r\n# Symptoms and Signs\r\n\r\nHypertension, unless malignant, is asymptomatic and does not have any clinical signs. It is diagnosed with ABPM and further investigations should focus on diagnosing end-organ complications of hypertension. \r\n\r\n# Investigations\r\n\r\n[lightgallery]\r\n\r\n* Hypertensive patients are commonly first identified at GP appointments or during hospital admissions. Due to the prominence of 'white coat hypertension', ABPM is now required for the diagnosis of hypertension. \r\n* Hypertension should be suspected in a patient who has a clinic blood pressure of =>140/90mmHg. \r\n* **1st line: ABPM** or home blood pressure monitoring if ABPM is not tolerated or declined. \r\n* Alongside ABPM: assessment for end-organ damage and assessment of cardiovascular risk (QRISK2 scores). \r\n * Urine dip and albumin:creatinine level\r\n * Blood glucose, lipids and renal function\r\n * Fundoscopy for evidence of hypertensive retinopathy\r\n * ECG: look for evidence of LV hypertrophy\r\n\r\n\r\nN.B. if presentation is suspicious for secondary hypertension refer and investigate as appropriate (see section). \r\n\r\nN.B. Referral for same-day specialist assessment should be arranged for people with: \r\n\r\n* Clinic blood pressure of 180/120mmHg and higher with signs of retinal haemorrhage or papilloedema (accelerated hypertension) or life-threatening symptoms (e.g. new onset confusion, chest pain, heart failure signs or AKI). \r\n\r\n# Management\r\n\r\n## Principles of Management \r\n\r\n### Conservative Management \r\n\r\nControlling risk factors for cardiovascular disease:\r\n\r\n* Weight loss\r\n* Healthy diet (reduce salt and saturated fats)\r\n* Reduce alcohol and caffeine\r\n* Reduce stress\r\n* Stop smoking\r\n\r\n### Medical Management\r\n\r\nIndications to start pharmacological management of primary hypertension:\r\n\r\n* Stage 1 hypertensive patients who are <80 years old with end organ damage, CVS disease, renal disease, diabetes or 10-year CVS risk >10% OR\r\n* Anyone with stage 2 hypertension\r\n\r\n### 2019 NICE Guidelines for Pharmacological Management of Primary Hypertension \r\n\r\n[lightgallery1]\r\n\r\n* Step 1: \r\n\t* **ACE-inhibitor** (e.g. Ramipril) if <=55 years old\r\n\t* **DHP-Calcium Channel Blocker** (e.g. Amlodipine) if >55 years old OR African or Caribbean ethnicity\r\n\t* If unable to tolerate ACE-inhibitor then switch to _Angiotensin Receptor Blocker_ (e.g. Candesartan)\r\n* Step 2: \r\n\t* (If maximal dose of Step 1 has failed or not tolerated)\r\n\t* **Combine CCB and ACE-I/ARB**\r\n* Step 3:\r\n\t* (If maximal doses of Step 2 has failed or not tolerated)\r\n\t* **Add thiazide-like diuretic** (e.g. Indapamide)\r\n* Step 4: *Resistant Hypertension*\r\n\t* If blood potassium <4.5mmol/L then add **spironolactone**\r\n\t* If >4.5mmol/L **increase thiazide-like diuretic dose**\r\n\t* Other options at this point if the potassium is >4.5mmol/L include:\r\n\t\t* Alpha blocker (e.g. Doxazosin)\r\n\t\t* Beta blocker (e.g. Atenolol)\r\n\t\t* Referral to cardiology for further advice\r\n\r\n**ABPM Targets:**\r\n \r\n* Age <80 ABPM target <135/85\r\n* Age >80 ABPM target <145/85 (due to risk of postural drop and falls)\r\n* T1DM with end-organ damage <130/80\r\n\r\n# Complications\r\n\r\n* Increased risk of morbidity and mortality from all causes\r\n* Coronary artery disease\r\n* Heart failure\r\n* Renal failure\r\n* Stroke\r\n* Peripheral vascular disease\r\n\r\n# Prognosis \r\n\r\nHypertension remains one of the biggest risk factors for cardiovascular disease and its associated disabilities. Management of hypertension (with lifestyle modifications or pharmacological therapies) has been shown to reduce these risks significantly. \r\n\r\n# NICE Guidelines\r\n> <https://cks.nice.org.uk/topics/hypertension/> \r\n\r\n# References \r\n\r\n<https://patient.info/heart-health/high-blood-pressure-hypertension>\r\n<https://www.ahajournals.org/doi/full/10.1161/01.CIR.101.3.329> ",
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"explanation": "Topical preparations of adapalene (a retinoid) and benzoyl peroxide (an anti-septic) is a first line option for any severity of acne. A 12 week course is recommended. It should be discussed that this medication can cause skin irritation and photosensitivity.\nThere are other topical combinations that can be used first-line, including topical tretinoin with topical clindamycin.",
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"explanation": "# Summary\n\nAcne vulgaris is a common chronic disorder of the pilo-sebaceous unit, resulting in blockage of the follicle, formation of comedones and inflammation. Key signs and symptoms include open/closed comedones, inflammatory papules and pustules, and in severe cases, nodules and cysts. The disorder predominantly affects the face, neck, chest, and back, and has a significant psychological impact due to altered physical appearance. Acne is primarily diagnosed clinically, with further investigations necessary only in uncertain cases or prior to commencing certain treatments like isotretinoin. Treatment is guided by severity and may involve topical or systemic therapy based on the NICE guidelines. Potential complications include post-inflammatory hyperpigmentation, hypopigmentation, erythema, psycho/social/sexual dysfunction, and scarring.\n\n\n# Definition\n\n- A a chronic disorder of the skin affecting the pilo-sebaceous unit, in which there is blockage of the follicle leading to comedones and inflammation. \n- Vulgaris translates as \"common\", which is true as this condition affects over 80% of adolescents.\n\n# Epidemiology\n\n* It is one of the most common dermatological conditions globally, affecting individuals of all ethnicities and ages.\n* Prevalence is highest in adolescents and young adults, with up to 80% of individuals experiencing some degree of acne during their lifetime.\n* While most common in adolescents, adult-onset acne can occur, affecting people well into their 30s and beyond.\n* Acne affects both males and females, but the prevalence and severity may vary between genders.\n* The psychological impact of acne can be significant, affecting self-esteem and overall quality of life.\n\n# Risk Factors\n\nSeveral factors contribute to the development and exacerbation of acne, including:\n\n* Hormonal changes (e.g. during puberty, menstrual cycle, polycystic ovary syndrome)\n* Increased sebum (oil) production\n* Blockage of hair follicles and sebaceous glands by keratin and sebum\n* Bacterial colonization (Propionibacterium acnes)\n* Family history of acne\n* Certain medications (e.g. corticosteroids, hormonal treatments)\n\n# Pathophysiology\n\n- In normal skin, skin cells in the stratum corneum of the epidermis (corneocytes) desquamate successfully without blocking pilo-sebaceous units.\n- In acne, the corneocytes are excessively cohesive. They do not detach successfully.\n- Because of this, the keratin rich corneocytes accumulate and block off hair follicles causing follicular hyperkeratinisation.\n- Sebum is trapped in the hair follicle since it cannot be drained away. Androgens may also contribute to this causing sebaceous gland hyperplasia and increased sebum production. \n- This combination of sebum and keratin forms micro-comedones - the earliest feature of acne vulgaris. This is only visible under a microscope.\n- Gradually, the follicle becomes more distended with keratin and sebum, and the micro-comedone enlarges to become a comedone. \n- Initially, these are closed comedones, referred to as whiteheads. The contents are not exposed to the skin surface or oxygen, and therefore appear as fleshy/white papules. \n- Eventually, closed comedones become open comedones. As their contents become exposed to oxygen, they oxidise which causes black discolouration. Open comedones are therefore referred to as blackheads.\n- Comedones are then colonised with a gram positive bacillus called Propionibacterium (Cutibacterium) acnes. This is a commensal organism (part of the normal skin flora) but leads to an inflammatory response in the right conditions of the comedone, in a predisposed patient. \n- The comedone is subsequently transformed into an inflammatory papule, which is now associated with erythema. A papule is a solid, raised lesion less than 0.5cm in diameter. \n- As things progress and more neutrophils accumulate, the inflammatory papule becomes a pustule; this is a lesion less than 0.5cm in diameter that contains pus. \n- Eventually, the inflammatory papule or pustule becomes so distended that it ruptures into the dermis, triggering a marked and deep seated inflammatory response. \n- This leads to the formation of nodules/cysts, which are painful and red. A nodule is a solid lesion larger than 0.5cm, and cysts are walled off fluid containing structures. \n\n[lightgallery]\n\n# Classification\n\n- Non-inflammatory: blackheads and whiteheads.\n- Inflammatory: inflammatory papules, pustules, and nodules (cysts.)\n- Mild acne: predominantly non-inflammatory lesions. \n- Moderate acne: predominantly inflammatory papules and pustules. \n- Severe acne: nodules (cysts), scarring, acne fulminans, and acne conglobata. \n\n# Clinical Features\n\n- Open/closed Comedones, inflammatory papules and pustules, nodules, and cysts may be present.\n- The face is most often affected. The neck, chest and back may also be affected.\n- Psychological dysfunction due to changes physical appearance\n- Scarring: associated with inflammatory acne. Hypertrophic and keloid scars are more common in darker skin tones. \n\t- Atrophic: flat or indented, such as ice-pick, box-car, or rolling scars.\n\t- Hypertrophic: raised scars.\n\t- Keloid: raised scars that extend beyond the initial boundaries of the injury. \n- Post-inflammatory hyperpigmentation and hypopigmentation: associated with inflammatory acne. \n- Post inflammatory erythema: associated with inflammatory acne.\n- Acne fulminans: an uncommon but severe, serious acne presentation. \n\t- Inflammatory nodules/cysts that are painful, ulcerating, and haemorrhagic appear, with associated systemic upset (raised white cell count, joint pain, fever, fatigue.) \n\t- These patients should be reviewed urgently within 24 hours. It usually affects teenage male patients.\n- Acne conglobata: another uncommon presentation of severe nodular/cystic acne with interconnecting sinus tracts and extensive scaring. \n\n[lightgallery1]\n\n[lightgallery2]\n\n# Investigations\n\n- Acne is a clinical diagnosis and investigations are not usually needed. \n- Swabs may be indicated if the diagnosis is uncertain (e.g. if ruling out infectious pustules.)\n- Investigations will be required prior to commencing isotretinoin if indicated.\n- In some particular presentations where an endocrine cause is suspected, there may be endocrinological investigations (hyperandrogenic states such as PCOS or androgen secreting tumours.)\n\n# Treatment\n\nManagement of acne is multifaceted including education, topical/oral treatments and lifestyle modifications. \n\n- Each treatment combination is given as a 12 week course. \n- Combination therapies help reduce antimicrobial resistance. \n- Antibiotics are used predominantly since they have anti-inflammatory effects, rather than for their antimicrobial effects.\n- **Mild-moderate acne** is treated with any 2 of the following in combination:\n\t- Topical benzoyl peroxide.\n\t- Topical antibiotics (clindamycin)\n\t- Topical retinoids (tretinoin/adapalene)\n- **Moderate-severe acne** is treated with a 12-week coures of the following first line options:\n\t- Topical retinoids (tretinoin/adapelene) + topical benzoyl peroxide.\n\t- Topical retinoids + topical antibiotics (clindamycin)\n\t- Topical benzoyl peroxide + topical retinoid (tretinoin/adapelene) + oral antibiotic (lymecycline/doxycycline.) \n\t- Topical azelaic acid + oral antibiotic (lymecycline/doxycycline) \n\t- Second line oral antibiotics: trimethoprim and erythromycin e.g. in pregnant/breast-feeding women where tetracyclines are contra-indicated. \n\t- Combined oral contraceptives (COCPs) (if not contraindicated) in combination with topical agents can be considered as an alternative to systemic antibiotics in women\n\nNB: topical retinoids and oral tetracyclines are contraindicated during pregnancy and when planning a pregnancy, and so women of childbearing potential will need to use effective contraception, or choose an alternative treatment to these options.\n\t\n- As per NICE guidelines, referral to specialist Dermatology is indicated in the case of:\n\t- Acne fulminans.\n\t- Mild-moderate acne not responding to two 12 week courses of treatment as above.\n\t- Moderate-severe acne not responding to one 12 week course of treatment as above, including an oral antibiotic.\n\t- Psychological distress/mental health disorder contributed to by acne.\n\t- Acne with persistent pigmentary changes.\n\t- Acne with scarring.\n- Other available agents:\n\t- Co-cyprindiol: anti-androgenic contraceptive agent - may be trialled in primary care on female patients, but usually second line COCP due to increased risk of venous thromboembolism, and can only be given for 3 months. \n\t- Spironolactone: anti-androgenic - not often used. Not for male patients. \n\t- **Isotretinoin (oral retinoid):** the usual next step if the standard treatment fails and is prescribed by a dermatologist. \n\t\t* Notable adverse effects: dry skin/mouth/eyes/lips (most common), teratogenecity, photosensitivity, low mood, nose bleeds, hair thinning, raised triglycerides, intracranial hypertension \n\t\t* Isotretinoin is a well established teratogen that results in miscarriages and severe birth defects. As a result, the manufacturer recommends that all female patients taking isotretinoin are also using two forms of contraception from one month before until one month after use. For this reason a pregnancy test should also be done before initiating treatment\n\t\t* There is a controversial association between isotretinoin and depression/suicide. Recent research has shown that concerns about links between isotretinoin and depression or suicide are not established. This has now been included into the NICE guidelines. However it is still important to screen for depression/suicidal ideation before prescribing and during treatment.\n\t\n\t\n# Complications\n\n- Post-inflammatory erythema\n- Post-inflammatory hyper- and hypo- pigmentation\n- Psycho/social/sexual dysfunction \n- Scars (atrophic, hypertrophic, keloid)\n\t- Keloid scars: over-proliferating scar tissue/collagen extending beyond the boundaries of the lesion. Takes 3-4 weeks typically to develop after injury. They can cause itch and pain. It is fleshy, smooth, firm, and does not regress with time. The original injury may be minor, for example piercing or insect bite. Treatment is usually with intralesional steroids (triamcinolone). Cryotherapy and laser may also be used. Surgical resection is unlikely to be successful due to further scarring. Risk factors include:\n\t\t- Darker skin/Chinese/Hispanic origin \n\t\t- Less than 30 years of age\n\t\t- Previous keloid scarring \n\t- These are distinct from hypetrophic scars, which are thick and raised but remain within the injured boundary and tend to improve over time. \n\n# NICE Guidelines\n\n[NICE CKS for Acne Vulgaris](https://cks.nice.org.uk/topics/acne-vulgaris/)",
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"question": "A 17 year old male presents to the GP with acne vulgaris.\nOn examination he has open and closed comedones with a few cystic lesions on his face, back and chest.\n\nWhich of the following is the best next step in the management of this patient?",
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"a"
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173,459,366 | false | 8 | null | 6,494,991 | null | false | [] | null | 12,506 | {
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "As this patient does not present with post menopausal bleeding she does not require a 2 week wait referral.",
"id": "62225",
"label": "c",
"name": "Two week wait referral for endometrial cancer",
"picture": null,
"votes": 89
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"__typename": "QuestionChoice",
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"explanation": "Whilst chemical irritants found in some washing poweders, soaps, panty liners or condoms may cause vulva or vaginal irritation which could present with similar symptoms, atrophic vaginitis is the most likely cause given the patient's age. Therefore, these may be helpful changes to make but topical oestrogen would be the first-line choice.",
"id": "62226",
"label": "d",
"name": "Recommend changing washing powder and soap",
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"explanation": "Whilst systemic HRT would be helpful in treating atrophic vaginitis due to the affects of oestrogen, it is not first line treatment to those presenting solely with atrophic vaginitis. It would be appropriate if the patient presents with other menopausal symptoms. 10-25% of those recieving HRT will still have symptoms of atrophic vaginitis which require additional topical oestrogen.",
"id": "62227",
"label": "e",
"name": "Systemic hormone replacement therapy (HRT)",
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"explanation": "The history is more suggestive of atrophic vaginitis rather than a UTI. However, having atrophic vaginitis can predispose to UTIs, therefore it is important to screen for symptoms of one such as dysuria or increased urinary frequency.",
"id": "62224",
"label": "b",
"name": "Antibiotics for a urinary tract infection (UTI)",
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"explanation": "Atrophic vaginitis is caused by a fall in oestrogen, it is therefore most common in post-menopausal people. Common symptoms include vaginal dryness, pain and itching. It can also cause urinary symptoms and UTIs. Topical oestrogen is a first line treatment option.",
"id": "62223",
"label": "a",
"name": "Topical oestrogen",
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"explanation": "# Summary\n \n \nAtrophic vaginitis, also known as vulvovaginal atrophy, is a condition characterised by inflammation and thinning of genital tissues due to reduced oestrogen levels, most commonly seen after menopause. Key signs and symptoms include thinning of vaginal mucosa, loss of pubic hair, narrowed introitus, and vaginal dryness, among others. Key investigations include clinical examination, transvaginal ultrasound, endometrial biopsy if required, and an infection screen. Management strategies primarily involve hormonal treatments, non-hormonal treatments, and in some cases, transvaginal laser therapy.\n \n \n# Definition\n \n \nAtrophic vaginitis, also known as vulvovaginal atrophy, is characterised by inflammation and thinning of the genital tissues due to a decrease in oestrogen levels. This condition is most common after menopause.\n \n \n \n\n# Aetiology\n \n \nThe primary cause of atrophic vaginitis is a decline in oestrogen levels, which typically occurs post-menopause.\n \n \n# Signs and Symptoms\n \n \n - Thinning of the vaginal mucosa\n - Loss of pubic hair\n - Narrowed introitus\n - Loss of vaginal rugae (folds)\n - Vaginal dryness and itching\n - Dyspareunia\n - Post-coital bleeding\n - Vaginal discharge from inflammation\n - Urinary symptoms such as dysuria and recurrent UTI\n \n \n# Differential Diagnosis\n \n \n- **Endometrial cancer and endometrial hyperplasia:** presents with post-menopausal bleeding. Ruled out with transvaginal USS and possible biopsy.\n- **Sexually transmitted infection:** presents with itching and abnormal discharge. Would have cervical tenderness on bimanual examination and can be diagnosed using vaginal swabs. \n- **Lichen planus:** can cause itchiness and dyspareunia. Would present with pale, dry patches which may be cracked and cause bleeding. \n- **Vaginismus:** also presents with dyspareunia but would not show signs of atrophy on speculum examination. \n\n \n \n# Investigations\n \n **Bedside:**\n \n* Clinical examination, including speculum examination if tolerated, to look for vaginal signs of atrophy. This is usually enough for diagnosis. \n* Vaginal swabs for infection screening if itching of discharge is present. \n \nNo bloods, imaging or invasive tests are required. \n \n\n# Management\n \n \nHormonal treatment:\n \n - Topical oestrogen preparations\n - Systemic hormone-replacement therapy (oral or transdermal)\n\n \nNon-hormonal treatments:\n\n - Lubricants, which provide short-term improvement to vaginal dryness, alleviating symptoms such as dyspareunia\n - Moisturisers, which should be used regularly\n\n \n \n# References\n \n \n [Patient Info](https://patient.info/doctor/atrophic-vaginitis)",
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"question": "A 68 year old female attends her GP practice with symptoms of vaginal dryness associated with itching.\nOn speculum examination it is noted that the vaginal skin is thin.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "The AQ-10 is the autism spectrum quotient, used to screen adults for autism. The patient is presenting with symptoms of depression. Autistic spectrum disorders (ASDs) are characterised by a spectrum of social, language and behavioural deficits. Whilst the history mentions loss of interest in social activities like hobbies or work it has been over a 4 week period, it is therefore less suggestive of autism.",
"id": "62231",
"label": "d",
"name": "AQ-10",
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"explanation": "CIWA (clinical institute withdrawal assessment) is used to monitor symptoms of alcohol withdrawal. As the patient is presenting with symptoms of depression the most helpful tool would be the PHQ-9 to measure the severity of depression. Alcohol use is important to discuss with the patient as well.",
"id": "62230",
"label": "c",
"name": "CIWA score",
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"votes": 45
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"explanation": "AUDIT-test (Alcohol use disorders indentification test) is used as a screening tool for alcohol harm. Discussing alcohol use with the patient is helpful, but they are presenting with symptoms of depression, therefore the PHQ-9 would be the most useful.",
"id": "62229",
"label": "b",
"name": "AUDIT-test",
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"votes": 60
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "The mini-mental state examination is a 30 point test used to assess cognitive function. It can be used as a screening tool for dementia, however it is not a diagnostic test. Whilst this patient presents with poor concetration, dementia is very unlikely due to his age as well as low mood being a presenting complaint, this is more suggestive of depression.",
"id": "62232",
"label": "e",
"name": "MMSE",
"picture": null,
"votes": 151
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"__typename": "QuestionChoice",
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"explanation": "The PHQ-9 is a self tested questionnaire that examines the nine DSM-5 criteria for depression (depressed mood, loss of interest or pleasure, weight change, change in sleep, change in activity, fatigue, concentration and suicidality) which the patient has presented with. It can be used to measure the severity of depression and monitor treatment response.",
"id": "62228",
"label": "a",
"name": "PHQ-9",
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"explanation": "# Summary\n\nDepression is a common mental health disorder typified by low mood, anhedonia, significant weight change, sleep and activity changes, fatigue, feelings of guilt or worthlessness, or poor concentration. It is defined by the DSM as the presence of 5 out of 8 symptoms for at least 2 weeks. It is more prevalent in females. Key investigations include FBC, TFT, U+E, LFT, Glucose, B12/folate, cortisol, toxicology screen, and CNS imaging to rule out organic causes. Management strategies encompass low to high intensity psychological interventions, pharmacotherapy including anti-depressants, and in severe cases, lithium or ECT.\n\n# Definition\n\nDepression is a mental health disorder characterised by:\n\n- **ICD-11 Criteria:**\n - Depressive Episode: Depressed mood, loss of interest (anhedonia), and reduced energy (fatigue) persisting for at least two weeks.\n\n- **DSM-V Criteria:**\n - Major Depressive Disorder (MDD): Presence of a major depressive episode lasting at least two weeks, with specific criteria regarding mood, cognitive, and physical symptoms.\n - Persistent Depressive Disorder (Dysthymia): A chronic form of depression lasting for at least two years. \n\nThis consists of the presence of at least five out of a possible eight defining symptoms, during the same two-week period, where at least one of the symptoms is depressed mood or loss of interest or pleasure\n\n**Severity:**\n\n- Mild: Few, if any, symptoms in excess of those required to make the diagnosis (associated symptoms, see below), and the symptoms result in minor functional impairment.\n- Moderate: Symptoms or functional impairment between \"mild\" and \"severe.\"\n- Severe: The number of symptoms, intensity, and impairment are all greatly increased.\n\n\n# Epidemiology\n\nDepression is a highly prevalent mental health disorder. It represents the third most common reason for consulting a general practitioner in the UK. Depression demonstrates a higher prevalence in females.\n\n# Aetiology\n\nThe aetiology of depression involves a complex interplay of genetic and environmental factors. History of previous mental health issues, physical illnesses, and social challenges like divorce, poverty, and unemployment can all contribute to its development.\n\n# Clinical Features\n\nDepression is defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM) as the presence of 5 out of the following 9 symptoms, occurring nearly every day for at least 2 weeks:\n\n1. **Depressed mood or irritability** for most of the day, indicated by either subjective report (feels sad or empty) or observation by others (appears tearful).\n2. **Anhedonia:** Decreased interest or pleasure in most activities, most of the day.\n3. Significant **weight change** (5%) or change in appetite.\n4. **Sleep alterations:** Insomnia or hypersomnia.\n5. **Activity changes:** Psychomotor agitation or retardation.\n6. **Fatigue** or loss of energy.\n7. **Guilt or feelings of worthlessness:** Excessive or inappropriate guilt or feelings of worthlessness.\n8. **Cognitive issues:** Diminished ability to think or concentrate, or increased indecisiveness.\n9. **Suicidality:** Thoughts of death or suicide, or formulation of a suicide plan.\n\n### Additional Features (Severe Depression)\n- **Psychotic Features:** Delusions (e.g. nihilistic delusions, Cotard's syndrome) and hallucinations.\n- **Depressive Stupor:** Profound immobility, mutism, and refusal to eat or drink, sometimes necessitating electroconvulsive therapy (ECT).\n\n# Differential Diagnosis\n\nThe main differentials and their key signs and symptoms include:\n\n- **Bipolar Disorder:** Characterised by periods of mania/hypomania (elevated mood, inflated self-esteem, decreased need for sleep, increased talkativeness, distractibility, increased goal-directed activity) alternating with depressive episodes.\n- **Anxiety Disorders:** Persistent and excessive worry, restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and sleep disturbance.\n- **Psychotic Disorders:** Hallucinations, delusions, disorganised speech, grossly disorganised or catatonic behaviour.\n- **Substance/Medication-Induced Mood Disorder:** Mood disturbance associated with intoxication or withdrawal from substances or side effects of medications.\n- **Adjustment Disorders:** Development of emotional or behavioural symptoms in response to identifiable stressors.\n\n\nVarious organic causes should be considered and ruled out through careful history-taking, physical examination, and relevant investigations. These include:\n\n- Neurological disorders such as Parkinson's disease, dementia, and multiple sclerosis.\n- Endocrine disorders, especially thyroid dysfunction and hypo/hyperadrenalism (e.g., Cushing's and Addison's disease).\n- Substance use or medication side effects (e.g., steroids, isotretinoin, alcohol, beta-blockers, benzodiazepines, and methyldopa).\n- Chronic conditions such as diabetes and obstructive sleep apnea.\n- Long-standing infections, such as mononucleosis.\n- Neoplasms and cancers - low mood can theoretically be a presenting complaint in any cancer, with pancreatic cancer being a notable example.\n\n\n# Investigations\n\n- Standard investigations for depression may include Full Blood Count (FBC), Thyroid Function Test (TFT), Urea and Electrolytes (U&E), Liver Function Test (LFT), Glucose, B12/folate levels, cortisol levels, toxicology screen, and imaging of the Central Nervous System (CNS).\n- These help rule out organic causes (listed above) such as endocrine disorders (e.g. thyroid disorders).\n- There are several questionnaires that can also be used to help assess depressive symptoms, such as the Hospital Anxiety and Depression (HAD) Scale and Patient Health Questionnaire (PHQ-9).\n\n# Management\n\nDepression is usually managed in primary care. GPs can refer to secondary care (Psychiatry) if there is a high-suicide risk, symptoms of bipolar disorder, symptoms of psychosis, or if there is evidence of severe depression unresponsive to initial treatment.\n\r\n**Persistent subthreshold depressive symptoms or mild-to-moderate depression:**\n\n- 1st line = Low-intensity psychological interventions (individual self-help, computerised CBT). \r\n- 2nd line = High-intensity psychological interventions (individual CBT, interpersonal therapy) \r\n- 3rd line = Consider antidepressants \r\n\r\n**Mild depression unresponsive to treatment and moderate-to-severe depression:**\n\n- 1st line = High-intensity psychological interventions + antidepressants (1st line = SSRI)\r\n- 2nd line (Treatment-resistant depression) – switch antidepressants and then use adjuncts \r\n\r\n**Severe depression and poor oral intake/psychosis/stupor:**\n\n- 1st line = ECT \n- Although the exact mechanism remains elusive, it is thought that the induced seizure, rather than the ECT procedure itself, has therapeutic benefits. Short-term side effects of ECT include headache, muscle aches, nausea, temporary memory loss, and confusion, while long-term side effects can include persistent memory loss. Due to the induced seizure, there is a risk of oral damage, and due to the general anaesthetic, a small risk of death.\r\n\n**Recurrent depression:** \n\n- Treated with antidepressant + lithium \r\n\n\nMedical management of depression - additional notes:\n\n- First-line pharmacological treatment typically involves a Selective Serotonin Reuptake Inhibitor (SSRI) such as sertraline. SNRIs such as venlafaxine can also be used first-line, but are less preferable due to the risk of damage from overdose, which is less likely with SSRIs.\n- In people aged 18-25 there is an increased risk of impulsivity and suicidal risk upon commencing antidepressant medication and so they should have a follow-up appointment arranged after one week to monitor progress. Initial reviews can otherwise be arranged 2-4 weeks after starting medication in patients >25.\n- Continuation of antidepressants for at least six months post-remission is recommended to mitigate relapse risk. Tapering should be done gradually over a four-week period when discontinuing antidepressants.\n\n\n\n# NICE Guidelines\n\n[NICE Guidance on the Management of Depression](https://www.nice.org.uk/guidance/cg90)",
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"question": "A 24 year old male attends his GP practice with 4 weeks of low mood. He has been struggling to sleep, has lost interest in his hobbies and is struggling to concentrate at work.\n\nWhich of the following tools is most appropriate to use in aiding the diagnosis?",
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173,459,368 | false | 10 | null | 6,494,991 | null | false | [] | null | 12,508 | {
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"__typename": "QuestionChoice",
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"explanation": "Lisinopril is an angiotensin-converting enzyme inhibitor (ACEi) which would be the first choice medication in newly diagnosed hypertensive individuals with type 2 diabetes mellitus and in those who are less than 55 years of age and not of black African or African–Caribbean family origin.",
"id": "62235",
"label": "c",
"name": "Lisinopril",
"picture": null,
"votes": 239
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"__typename": "QuestionChoice",
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"explanation": "Metoprolol is a beta-blocker, usually prescribed following a specialist referral if resistant hypertension is unresponsive to maximum tolerable doses of ACEi/ARB + CCB + thiazide-like diuretic (step-3 treatment).",
"id": "62236",
"label": "d",
"name": "Metoprolol",
"picture": null,
"votes": 22
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Indapamide, a thiazide-like diuretic, is added in step 2 management of hypertension if it is not controlled with step 1 treatment with either ACEi or ARB; or CCB.",
"id": "62237",
"label": "e",
"name": "Indapamide",
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"explanation": "**Calcium channel blockers (CCB) are the preferred step-1 medication for newly diagnosed hypertension in black African or African-Caribbean ethnicities**, irrespective of age. They tend to develop low renin, salt-sensitive type hypertension for which monotherapy with beta-blockers or ACE inhibitors is less effective than calcium channel blockers in this particular ethnicity.",
"id": "62233",
"label": "a",
"name": "Amlodipine",
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"__typename": "QuestionChoice",
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"explanation": "Telmisartan is an angiotensin receptor blocker (ARB) which would be the first choice medication in newly diagnosed hypertensive individuals of any age with type 2 diabetes mellitus. Moreover, an ARB is preferred over an ACE inhibitor in black African or African-Caribbean family origin.",
"id": "62234",
"label": "b",
"name": "Telmisartan",
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"explanation": "# Summary\r\n\r\nPrimary hypertension, accounting for approximately 90-95% of cases of hypertension, is characterised by persistently elevated blood pressure due to age-related pathophysiological changes. It is a major risk factor for cardiovascular disease, cerebrovascular disease, chronic kidney disease, and peripheral vascular disease. Diagnosis is based on ambulatory blood pressure monitoring (ABPM) readings of 135/85mmHg or higher. Classification is determined by the severity of the hypertension. Management depends on the classification of the hypertension and involves lifestyle modifications and pharmacological anithypertensives according to NICE guidelines. Effective management, through lifestyle changes and medications, significantly reduces the associated risks and improves outcomes for individuals with hypertension.\r\n\r\n# Definition \r\n\r\nA 'normal' blood pressure ranges between 90/60mmHg to 140/90mmHg. The definition of hypertension is a 24h ambulatory blood pressure average reading (ABPM) that is more than or equal to 135/85mmHg. \r\n\r\n# Epidemiology\r\n\r\nIn 2015, it was reported that high blood pressure affected more than 1 in 4 adults in England (31% of men; 26% of women). In England, it is estimated that primary hypertension affects around 13.5 million people and contributed to 75,000 deaths.\r\n\r\n# Pathophysiology\r\n\r\nPrimary hypertension is as a result of a series of complex physiological changes as we age. Hypertension often occurs as a result of reduced elasticity of large arteries, age-related and atherosclerosis-related calcification, and degradation of arterial elastin. It may also be present in conditions associated with increased cardiac output, such as anaemia, hyperthyroidism and aortic regurgitation.\r\n\r\nAlthough the risk of cardiovascular disease increases progressively with increasing systolic and diastolic blood pressure, raised systolic pressure is more important than raised diastolic pressure as a risk factor for cardiovascular and renal disease.\r\n\r\n# Classification \r\n\r\nHypertension can be classified according to how high a patient's blood pressure is. \r\n\r\n* Stage 1: Clinic => 140/90mmHg; ABPM => 135/85mmHg \r\n* Stage 2: Clinic => 160/100mmHg; ABPM =>150/95mmHg \r\n* Stage 3: Clinic systolic BP (SBP) => 180 or diastolic BP (DBP) =>120mmHg\r\n\r\n\r\n# Symptoms and Signs\r\n\r\nHypertension, unless malignant, is asymptomatic and does not have any clinical signs. It is diagnosed with ABPM and further investigations should focus on diagnosing end-organ complications of hypertension. \r\n\r\n# Investigations\r\n\r\n[lightgallery]\r\n\r\n* Hypertensive patients are commonly first identified at GP appointments or during hospital admissions. Due to the prominence of 'white coat hypertension', ABPM is now required for the diagnosis of hypertension. \r\n* Hypertension should be suspected in a patient who has a clinic blood pressure of =>140/90mmHg. \r\n* **1st line: ABPM** or home blood pressure monitoring if ABPM is not tolerated or declined. \r\n* Alongside ABPM: assessment for end-organ damage and assessment of cardiovascular risk (QRISK2 scores). \r\n * Urine dip and albumin:creatinine level\r\n * Blood glucose, lipids and renal function\r\n * Fundoscopy for evidence of hypertensive retinopathy\r\n * ECG: look for evidence of LV hypertrophy\r\n\r\n\r\nN.B. if presentation is suspicious for secondary hypertension refer and investigate as appropriate (see section). \r\n\r\nN.B. Referral for same-day specialist assessment should be arranged for people with: \r\n\r\n* Clinic blood pressure of 180/120mmHg and higher with signs of retinal haemorrhage or papilloedema (accelerated hypertension) or life-threatening symptoms (e.g. new onset confusion, chest pain, heart failure signs or AKI). \r\n\r\n# Management\r\n\r\n## Principles of Management \r\n\r\n### Conservative Management \r\n\r\nControlling risk factors for cardiovascular disease:\r\n\r\n* Weight loss\r\n* Healthy diet (reduce salt and saturated fats)\r\n* Reduce alcohol and caffeine\r\n* Reduce stress\r\n* Stop smoking\r\n\r\n### Medical Management\r\n\r\nIndications to start pharmacological management of primary hypertension:\r\n\r\n* Stage 1 hypertensive patients who are <80 years old with end organ damage, CVS disease, renal disease, diabetes or 10-year CVS risk >10% OR\r\n* Anyone with stage 2 hypertension\r\n\r\n### 2019 NICE Guidelines for Pharmacological Management of Primary Hypertension \r\n\r\n[lightgallery1]\r\n\r\n* Step 1: \r\n\t* **ACE-inhibitor** (e.g. Ramipril) if <=55 years old\r\n\t* **DHP-Calcium Channel Blocker** (e.g. Amlodipine) if >55 years old OR African or Caribbean ethnicity\r\n\t* If unable to tolerate ACE-inhibitor then switch to _Angiotensin Receptor Blocker_ (e.g. Candesartan)\r\n* Step 2: \r\n\t* (If maximal dose of Step 1 has failed or not tolerated)\r\n\t* **Combine CCB and ACE-I/ARB**\r\n* Step 3:\r\n\t* (If maximal doses of Step 2 has failed or not tolerated)\r\n\t* **Add thiazide-like diuretic** (e.g. Indapamide)\r\n* Step 4: *Resistant Hypertension*\r\n\t* If blood potassium <4.5mmol/L then add **spironolactone**\r\n\t* If >4.5mmol/L **increase thiazide-like diuretic dose**\r\n\t* Other options at this point if the potassium is >4.5mmol/L include:\r\n\t\t* Alpha blocker (e.g. Doxazosin)\r\n\t\t* Beta blocker (e.g. Atenolol)\r\n\t\t* Referral to cardiology for further advice\r\n\r\n**ABPM Targets:**\r\n \r\n* Age <80 ABPM target <135/85\r\n* Age >80 ABPM target <145/85 (due to risk of postural drop and falls)\r\n* T1DM with end-organ damage <130/80\r\n\r\n# Complications\r\n\r\n* Increased risk of morbidity and mortality from all causes\r\n* Coronary artery disease\r\n* Heart failure\r\n* Renal failure\r\n* Stroke\r\n* Peripheral vascular disease\r\n\r\n# Prognosis \r\n\r\nHypertension remains one of the biggest risk factors for cardiovascular disease and its associated disabilities. Management of hypertension (with lifestyle modifications or pharmacological therapies) has been shown to reduce these risks significantly. \r\n\r\n# NICE Guidelines\r\n> <https://cks.nice.org.uk/topics/hypertension/> \r\n\r\n# References \r\n\r\n<https://patient.info/heart-health/high-blood-pressure-hypertension>\r\n<https://www.ahajournals.org/doi/full/10.1161/01.CIR.101.3.329> ",
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"question": "A 45-year-old Nigerian man presents to the GP clinic complaining of persistent headaches and fatigue. He has no significant medical history and has never been diagnosed with hypertension before. On physical examination, his clinic blood pressure is 170/110 mmHg. A diagnosis of hypertension is confirmed as his ambulatory blood pressure monitoring reveals similar BP reading of 168/112 mmHg.\n\nWhat is the first-line management of his condition?",
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"explanation": "He can resume driving a week after successful coronary intervention if there is no other urgent revascularization planned (within four weeks), the left ventricular ejection fraction (LVEF) is at least 40% before hospital discharge, and there are no other disqualifying conditions. He meets all of these criteria, and it has already been four weeks since the procedure. Therefore, **he can start driving immediately and does not need to notify the Driver and Vehicle Licensing Agency (DVLA)** about this.",
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"explanation": "# Summary\r\n\r\nAcute coronary syndrome (ACS) refers to a set of symptoms and signs that occur due to reduced blood flow to the heart at rest. It encompasses 3 distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). In the case of infarction, this is a medical emergency requiring urgent treatment. ACS is most commonly caused by the rupture of atherosclerotic plaques in coronary arteries leading to further narrowing, and potentially complete occlusion, of these critical blood vessels. Diagnosis involves clinical evaluation, ECGs, and troponin levels. Treatment strategies differ for STEMI and NSTEMI/unstable angina but include oxygen therapy if hypoxic, antiplatelet medication, glyceryl trinitrates, morphine, and percutaneous coronary intervention (PCI). Post-MI management includes aspirin, dual antiplatelet therapy, beta-blockers, ACE inhibitors, high-dose statins, and cardiac rehabilitation. There are many complications to be aware of post-ACS and these include arrhythmias, heart failure, and cardiac tamponade, and others.\r\n\r\n# Definition \r\n\r\nAcute coronary syndrome is a set of symptoms and signs that occur due to decreased blood flow to the heart at rest. It broadly refers to three distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI). \r\n\r\n# Epidemiology \r\n\r\nIn the UK, there are over 80,000 hospital admissions due to ACS every year. Coronary artery disease remains the largest cause of death in the UK. \r\n\r\n# Pathophysiology\r\n\r\nCoronary artery disease refers to the narrowing of coronary arteries by atherosclerosis and plaque formation. In stable angina, when the demand for myocardial oxygen increases with exertion, narrowed coronary arteries cannot meet this increased demand leading to myocardial ischaemia and pain. Conversely, in ACS, the symptoms occur at rest. This is because there is sudden plaque rupture and clot formation in the narrowed coronary arteries. If there is partial occlusion of the coronary artery this leads to ischaemia and chest pain at rest (unstable angina). If the coronary artery becomes more occluded or fully occluded this leads to significant hypoperfusion of the myocardium and ultimately leads to infarction (death) of the myocardial tissue (NSTEMI or STEMI). \r\n\r\n# Risk Factors\r\n\r\nCoronary artery disease and the development of plaques can be attributed to non-modifiable and modifiable risk factors. Modifiable risk factors must be addressed in the management of IHD. \r\n\r\n* Non-modifiable:\r\n * Age\r\n * Male sex\r\n * Family history\r\n * Ethnicity (particularly South Asians)\r\n* Modifiable:\r\n * Smoking\r\n * Hypertension\r\n * Hyperlipidaemia\r\n * Hypercholesterolaemia\r\n * Obesity\r\n * Diabetes\r\n * Stress\r\n * High fat diets\r\n * Physical inactivity\r\n\r\n# Classification \r\n\r\nAcute coronary syndrome can be split up into three distinct diagnoses: \r\n\r\n1. **Unstable angina**: caused by partial occlusion of a coronary artery. Troponin negative chest pain with normal/abnormal ECG signs. \r\n2. **Non-ST Elevation Myocardial Infarction**: caused by severe but incomplete occlusion of a coronary artery. Troponin positive chest pain without ST elevation. \r\n3. **ST-Elevation Myocardial Infarction**: caused by complete occlusion of a coronary artery. Troponin positive chest pain with ST elevation on ECG. \r\n\r\n*Myocardial Ischaemia vs. Myocardial Infarction and the Release of Troponin*\r\n\r\nIt is important at this stage to distinguish between angina (stable angina is on exertion and unstable angina is at rest) and myocardial infarction. Angina refers to myocardial ischaemia that causes chest pain but does not lead to the death of myocardial tissue and does not lead to a troponin rise. In myocardial infarction, the hypoperfusion of the myocardium is so profound that it leads to the death of myocardial tissue. It is when there is myocardial tissue death that troponin is released into the bloodstream and a troponin rise is found on blood tests.\r\n\r\n*Type 2 Myocardial Infarction* \r\n\r\nIt is also important to mention that some patient may have myocardial infarctions due to cardiac hypoperfusion for other reasons (e.g. severe sepsis, hypotension, hypovolaemia or coronary artery spasm). These are usually termed type 2 myocardial infarctions and may not require the conventional treatment outlined below. \r\n\r\n# Symptoms and Signs\r\n\r\n* Chest pain - the classical presentation can be considered in terms of the SOCRATES mnemonic:\r\n * Site - Central/left sided\r\n * Onset - Sudden\r\n * Character - Crushing ('like someone is sitting on your chest')\r\n * Radiation - Left arm, neck and jaw\r\n * Associated symptoms - Nausea, sweating, clamminess, shortness of breath, sometimes vomiting or syncope\r\n * Timing - Constant\r\n * Exacerbating/relieving factors - Worsened by exercise/exertion and may be improved by GTN\r\n * Severity - Often extremely severe\r\n* Atypical presentations may include:\r\n * Epigastric pain\r\n * No pain (more common in elderly and **patients with diabetes**):\r\n * Acute breathlessness\r\n * Palpitations\r\n * Acute confusion\r\n * Diabetic hyperglycaemic crises\r\n * Syncope\r\n\r\n# Differential Diagnoses\r\n\r\nIt is important to remember that there are non-MI causes of chest pain and these should be considered when making a diagnosis:\r\n\r\n* Cardiac\r\n * Myocarditis\r\n * Pericarditis\r\n * Cardiomyopathy\r\n * Valvular disease\r\n * Cardiac trauma\r\n* Pulmonary\r\n * PE\r\n * Pneumonia\r\n * Pneumothorax\r\n* Vascular\r\n * Aortic dissection\r\n* GI\r\n * Oesophageal spasm\r\n * Oesophagitis\r\n * Peptic ulcer\r\n * Pancreatitis\r\n * Cholecystitis\r\n* MSK\r\n * Rib fracture\r\n * Costochondritis\r\n * Muscle injury\r\n * Herpes zoster\r\n\r\n# Diagnosis of ACS \r\n\r\nDiagnosis depends on a combination of clinical, ECG and biochemical findings which helps distinguish between the various types of ACS.\r\n\r\n* Unstable angina - cardiac chest pain at rest + abnormal/normal ECG + **normal troponin**.\r\n* NSTEMI - cardiac chest pain at rest + abnormal/normal ECG (but not ST-elevation) + **raised troponin**\r\n* STEMI - cardiac chest pain at rest + **persistent ST-elevation/new LBBB** (note that there is no need for a troponin in this case).\r\n\r\n## Diagnosis of STEMI\r\n\r\n* ST segment elevation **>2mm** in adjacent chest leads\r\n* ST segment elevation **>1mm** in adjacent limb leads\r\n* New left bundle branch block (LBBB) with chest pain or suspicion of MI\r\n\r\n## Diagnosis of NSTEMI\r\n\r\nDiagnosis of NSTEMI requires two of the following:\r\n\r\n* Cardiac chest pain\r\n* Newly abnormal ECG which does not demonstrate ST-elevation e.g. ST depression, T wave inversion or non-specific changes. \r\n* Raised troponin (with no other reasonable explanation)\r\n\r\n# Investigations\r\n\r\n## Bedside \r\n\r\n* ECG \r\n\t* Looking for ST-elevation, LBBB or other ST abnormalities\r\n\t* This is the most important investigation and should not be delayed for other investigations (e.g. bloods) because this will define immediate management.\r\n\t* If an ECG shows STEMI then troponin is essentially irrelevant and the patient requires immediate treatment.\r\n\r\n## Bloods \r\n\r\n* Troponin: performed **at least 3 hours** after pain starts. It will also need to be repeated (usually 6 hours after the first level) in order to demonstrate a dynamic troponin rise. \r\n* Renal function: good renal function is required for coronary angiogram +/- PCI due to the use of contrast. \r\n* HbA1c and lipid profile: looking for modifiable risk factors for coronary artery disease. \r\n* FBC and CRP - rule out infectious causes of chest pain\r\n* D-dimer - may be used in _appropriate_ patients to rule out PE. *Be very careful about who you do a D-dimer on!*\r\n\r\n## Imaging \r\n\r\n* CXR: should be completed in all those presenting with a chest symptoms. It will help to rule out other causes of chest pain (e.g. pneumothorax) and look for complications of a large MI (e.g. pulmonary oedema in acute heart failure). \r\n\r\n# ECG Interpretation - Cardiac Territories and Affected Vessels\r\n\r\nThe importance of a 12-lead ECG is that it allows one to view electrical activity of the heart from different \"views\". In MI (particularly STEMI) this allows you to understand which territory (and therefore which vessel) is being affected.\r\n\r\n| Location of ST elevation | Area of myocardium | Coronary artery |\r\n| -------------------------- | ------------------ | -------------------- |\r\n| II, III, aVF | Inferior | RCA |\r\n| V1-2 | Septal | Proximal LAD |\r\n| V3-4 | Anterior | LAD |\r\n| V5-6 | Apex | Distal LAD/ LCx/ RCA |\r\n| I, aVL | Lateral | Lcx |\r\n| V7-V9 (ST depression V1-3) | Posterolateral | RCA/ LCx |\r\n\r\n\r\nRCA: right coronary artery, LAD: left anterior descending, LCx: Left circumflex\r\n\r\n[lightgallery]\r\n\r\n[lightgallery2]\r\n\r\n[lightgallery3]\r\n\r\n[lightgallery4]\r\n\r\n\r\nNSTEMIs may also show T wave abnormalities (such as ST depression and T wave inversions) in vascular territories as above. However, changes can also often not include all the specific leads of that territory in an NSTEMI.\r\n\r\n# Troponin Interpretation\r\n\r\nTroponin is a myocardial protein that is released into the bloodstream when cardiac myocytes are damaged. Serum levels typically rise **3 hours** after myocardial infarction begins.\r\n\r\nDifferent hospitals have differing guidelines (and assays) for interpretations of results. In general there are three groups of troponin levels:\r\n\r\n* Low - definitely no myocardial cell death. The patient is not having an MI although they may be experiencing unstable angina.\r\n* Mildly raised - This is an equivocal result and may be due to other non-MI related factors (see below). These patients usually need a <u>6-12 hour repeat test</u>.\r\n * If repeat troponin is raised on the repeat they are having an MI.\r\n * If repeat troponin is stable or falling then they are unlikely to be having an MI.\r\n* Definitely raised with sequential dynamic troponin rises - MI confirmed (be aware of the possibility of a Type 2 MI)\r\n\r\n## Non-ACS causes of a raised troponin\r\n\r\nAlthough troponin is often used diagnose myocardial infarction, there are in fact many causes of a raised troponin:\r\n\r\n* Myocardial infarction\r\n* Pericarditis\r\n* Myocarditis\r\n* Arrythmias\r\n* Defibrillation\r\n* Acute heart failure\r\n* Pulmonary embolus\r\n* Type A aortic dissection\r\n* Chronic kidney disease\r\n* Prolonged strenuous exercise\r\n* Sepsis\r\n\r\nIt is therefore critical to have good clinical grounds to test a troponin in order to avoid unnecessary treatments and investigations.\r\n\r\n# Management\r\n\r\nAcute management depends on the type of acute coronary syndrome. It is broadly split into the management of STEMI and the management of NSTEMI/unstable angina. \r\n\r\n# Management of STEMI\r\n\r\n[lightgallery5]\r\n\r\nFor emergencies, always follow A-E structure. \r\n\r\n1. Targeted oxygen therapy (aiming for sats >90%)\r\n2. Loading dose of **PO aspirin 300mg**\r\n - Note that some hospital protocols will also call for a loading dose of a second anti-platelet agent such as clopidogrel (300mg) or ticagrelor (180mg)\r\n - For those going on to have PCI, NICE guidance suggests adding prasugrel (if not on anti-coagulation) or clopidogrel (if on anti-coagulation)\r\n3. **Sublingual GTN spray** - for symptom relief\r\n4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart\r\n5. Primary percutaneous coronary intervention (PPCI) for those who:\r\n - Present **within 12 hours of onset of pain** AND\r\n - Are **<2 hours** since <u>first medical contact</u>\r\n\r\nRemember that (particularly in STEMI) _time is heart_ therefore urgent treatment, escalation, and delivery of PPCI is critical to good outcomes.\r\n\r\n# Management of NSTEMI/Unstable Angina\r\n\r\n[lightgallery6]\r\n\r\nFor emergencies, always follow A-E structure. \r\n\r\n1. Targeted oxygen therapy (aiming for sats >90%)\r\n2. Loading dose of **PO aspirin 300mg** and fondaparinux\r\n * Patients should have their 6 month mortality score (often the GRACE score) calculated as early as possible - all those who are anything other than lowest risk should also be given **prasugrel or ticagrelor** unless they have a high risk of bleeding where **PO clopidogrel 300mg** is more appropriate.\r\n3. **Sublingual GTN spray** - for symptom relief\r\n4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart\r\n5. Start antithrombin therapy such as **treatment dose low molecular weight heparin** or **fondaparinux** if they are for an immediate angiogram\r\n6. Patients with <u>high 6 month risk of mortality</u> should be offered an angiogram within 96 hours of symptom onset.\r\n\r\nNote that management of unstable angina is similar to that of NSTEMI with aspirin for all patients and fondaparinux and early angiography for those at high risk.\r\n\r\n# Post-MI management\r\n\r\n[lightgallery7]\r\n\r\n* ALL patients post-MI patients should be started on the following 5 drugs:\r\n 1. **Aspirin 75mg OM** + second anti-platelet (**clopidogrel 75mg OD** or **ticagrelor 90mg OD**)\r\n 2. **Beta blocker (normally bisoprolol)**\r\n 3. **ACE-inhibitor (normally ramipril)**\r\n 4. **High dose statin (e.g. Atorvastatin 80mg ON)**\r\n* All patients should have an **ECHO** performed to assess systolic function and any evidence of heart failure should be treated.\r\n* All patients should be referred to **cardiac rehabilitation**.\r\n* Patients who have been treated without angiography should be considered for ischaemia testing to assess for inducible ischaemia. \r\n\r\n# Complications\r\n\r\n* Ventricular arrhythmia\r\n* Recurrent ischaemia/infarction/angina\r\n* Acute mitral regurgitation\r\n* Congestive heart failure\r\n* 2nd, 3rd degree heart block\r\n* Cardiogenic shock\r\n* Cardiac tamponade\r\n* Ventricular septal defects\r\n* Left ventricular thrombus/aneurysm\r\n* Left/right ventricular free wall rupture\r\n* Dressler's Syndrome\r\n* Acute pericarditis\r\n\r\n## Ventricular Arrhythmias\r\n\r\n* Ventricular arrhythmias can occur as a consequence of MI, during cardiac catheterisation, or after reperfusion.\r\n* Most post-MI ventricular arrhythmias are short lived and self-resolve.\r\n* However if sustained VT or VF occurs they should be treated as per the Advanced Life Support protocols.\r\n\r\n## Recurrent Ischaemia/Infarction/Angina\r\n\r\n* Occasionally inserted stents can thrombose requiring reintervention.\r\n* New infarcts can occur in different vascular territories - this is less likely in the age of PCI where all territory are imaged during the procedure.\r\n* Angina and chest pain can continue for some time after an MI and is more common in NSTEMI patients.\r\n\r\n## Congestive Heart Failure\r\n\r\n* Heart failure can occur as a consequence of impairment heart muscle function secondary to ischaemia.\r\n* It should be treated as any other acute heart failure.\r\n* Ventricular function may improve over months as the heart muscle recovers.\r\n\r\n## Heart Block\r\n\r\n* Various levels of heart block are common - particularly following **inferior** infarcts (because the right coronary artery supplies the SAN).\r\n* These may be treated with:\r\n * Simple observation (as many will revert back to sinus rhythm)\r\n * Transcutaneous/venous pacing (if symptomatic)\r\n * Permanent pacing (if failing to resolve)\r\n\r\n## Left Ventricular Thrombus/Aneurysm\r\n\r\n* Aneurysm can occur following an anterior MI where the myocardium can be susceptible to wall stress leading to an aneurysm.\r\n* It may be silent, cause arrhythmias or embolic events.\r\n* It is definitely diagnosed on ECHO but ECG may show persisting ST elevation.\r\n* Thrombus can form either within an above described aneurysm or around hypokinetic regions of the myocardium.\r\n* Thrombi can embolise causing complications such as stroke, acute limb ischaemia and mesenteric ischaemia.\r\n\r\n## Left/Right Ventricular Free Wall Rupture\r\n\r\n* Necrosis of the free walls of either ventricle can lead to rupture allowing blood into the pericardial space.\r\n* This leads to a rapid tamponade and normally leads to cardiac arrest/death within seconds.\r\n* Treatment includes pericardiocentesis and surgery but prognosis is extremely poor.\r\n\r\n## Acute Mitral Regurgitation\r\n\r\n* This can occur because of papillary muscle rupture and carries a poor prognosis. Occurs commonly due to infero-osterior MI. \r\n* This presents with:\r\n * Pansystolic murmur heard best at the apex\r\n * Severe and sudden heart failure\r\n* It is diagnosed on echocardiogram and may require surgical correction.\r\n\r\n## Ventricular Septal Defect\r\n\r\n* Interventricular septal rupture is a short-term complications of myocardial infarction.\r\n* Rupture caused by an anterior infarct is generally apical and simple.\r\n* Rupture caused by an inferior infarct is generally basal and more complex.\r\n* Without reperfusion, septal rupture typically occurs within the first week after the infarction.\r\n* Features of septal rupture include:\r\n * Shortness of breath\r\n * Chest pain\r\n * Heart failure\r\n * Hypotension\r\n * Harsh, loud pan-systolic murmur along the left sternal border.\r\n * Palpable parasternal thrill.\r\n* Diagnosis is with echocardiogram.\r\n* Patients are managed with emergency cardiac surgery.\r\n\r\n## Dressler's syndrome\r\n\r\n* Dressler's syndrome or post-infarction pericarditis typically presents with persistent fever and pleuritic chest pain **2-3 weeks** or up to a few months after an MI.\r\n* Note that patients can get pericarditis immediately following MI which is NOT considered Dressler's syndrome.\r\n* Symptoms usually resolve after several days.\r\n* Occasionally it can also present with features of pericardial effusion and has become relatively uncommon since the introduction of PCI.\r\n* Management: **high dose aspirin**\r\n\r\n# Prognosis \r\n\r\nDue to the development of PPCI and post-MI care (cardiac rehabilitation) the mortality rates following myocardial infarction continue to decline. Those patients who go on to develop heart failure after myocardial infarction have a significantly worse prognosis than those who do not. \r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines for Unstable Angina and NSTEMI](https://www.nice.org.uk/guidance/cg94)\r\n\n[NICE Guidelines for STEMI](https://www.nice.org.uk/guidance/cg167)\r\n\r\n# References\r\n\r\n[Patient UK Information on Acute Coronary Syndrome](<https://patient.info/doctor/acute-coronary-syndrome-pro>)",
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"explanation": "In the UK, there are services available to help individuals diagnosed with sexually transmitted infections (STIs) or HIV inform their sexual partners of their diagnosis. These services aim to protect the public by informing partners of the possibility of infection and encouraging them to seek medical care. In most cases, patients are given a choice to inform their partners themselves or to provide details to a healthcare worker to contact them anonymously. If the patient is unable to inform their partners within a specific time frame, the healthcare worker may step in to do so. In the case described, the man refuses to disclose to the wife of his HIV diagnosis, despite mulitple consultations. As HIV is a communicable disease, it is essential for the wife to be informed so that she can be tested and take steps to protect her health. Therefore, the healthcare provider would contact the wife through the partner notification program's protocols. The patient would be informed that this disclosure will occur, as long as it is safe to do so.",
"id": "62248",
"label": "a",
"name": "Notify wife via partner notification programme",
"picture": null,
"votes": 965
}
],
"comments": [
{
"__typename": "QuestionComment",
"comment": "wont her partner know it was him so doesnt help??",
"createdAt": 1715021967,
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"comment": "You can't assume that the patient in having UPSI with his wife, you cant assume the wife is at risk of serious harm and therefore do not have any legal obligation to breech confidentiality via a partner notification programme.",
"createdAt": 1738757828,
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"explanation": "# Overview\n\nOne legal defence to breaching confidentiality is the **public interest** defence. This was established by Common Law.\n\n# W v Egdell 1990 \n\n_W v Egdell 1990_: A doctor breached confidentiality to prevent a prisoner getting a transfer while he still posed a risk to others.\n\n# Criteria to fulfil when breaching confidentiality under a public interest defence\n\n1. A risk of harm needs to be identified\n2. Patient consent should be gained if possible\n\n _You do not need to attempt to gain consent if doing so would put you at risk of serious harm, or would prejudice the prevention, detection or prosecution of crime._\n\n3. The patient should be warned that disclosure will be made\n4. Disclosure should be made on a need-to-know basis (i.e. only to the relevant people)\n5. The disclosures made should be kept to a minimum (i.e. only disclosing relevant information)\n6. The information should be anonymised, if possible.",
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"question": "A 25-year-old man presents to the sexual health clinic for HIV testing after a recent high-risk sexual exposure during a holiday. The test returns positive, and he is advised to start antiretroviral therapy as soon as possible to prevent the progression of the infection. He is also advised to inform his wife about his HIV status, however, he is reluctant to do so. He asks the doctor to keep it confidential. You re-visit this topic on multiple occasions but the patient still refuses to disclose this to his wife.\n\nWhat is the single most appropriate action in this situation?",
"sbaAnswer": [
"a"
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173,459,371 | false | 13 | null | 6,494,991 | null | false | [] | null | 12,512 | {
"__typename": "QuestionSBA",
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{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is not an appropriate action to take as it goes against the patient's autonomy and confidentiality. In the United Kingdom, abortion is legal and whilst doctors are allowed to **conscientiously object**, it is not against our law and thus should not be referred to the police.",
"id": "62254",
"label": "b",
"name": "Refuse termination of pregnancy and inform the police",
"picture": null,
"votes": 9
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The patient, in this case, is an 18-year-old female, which means she is a legal adult according to UK law and has the right to make her own healthcare decisions and provide consent for medical treatment. Informing her parents or seeking their consent is unnecessary in this situation, as the patient can understand the risks and benefits of the procedure and has clearly expressed her desire for an abortion. It is important for healthcare providers to respect the patient's autonomy and confidentiality in this situation, even if it goes against their personal beliefs or values.",
"id": "62255",
"label": "c",
"name": "Refuse termination of pregnancy and inform her parents",
"picture": null,
"votes": 2
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Whilst termination of pregnancy is legal in the UK, doctors are allowed to refuse to offer this treatment if it goes agaist their personal values or belief. They **must** however refer patients seeking such interventions onto another doctor who can facilitate this. This is termed 'conscientious objecting'.",
"id": "62257",
"label": "e",
"name": "Perform surgical termination of pregnancy",
"picture": null,
"votes": 57
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is the most appropriate action to take in this situation as it respects the patient's autonomy and allows her to receive the care she desires while also acknowledging and respecting the healthcare provider's *conscientious objection*. **It is important to ensure that the patient's needs are met while also taking into consideration the healthcare provider's beliefs and values.** However, doctors are **obliged** to refer the patient on to an appropriate alternative, and cannot deny the care to this patient.",
"id": "62253",
"label": "a",
"name": "Refuse termination of pregnancy and refer to your colleague to carry out the procedure",
"picture": null,
"votes": 1542
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Whilst termination of pregnancy is legal in the UK, doctors are allowed to refuse to offer this treatment if it goes agaist their personal values or belief. They **must** however refer patients seeking such interventions onto another doctor who can facilitate this. This is termed 'conscientious objecting'.",
"id": "62256",
"label": "d",
"name": "Perform medical termination of pregnancy",
"picture": null,
"votes": 127
}
],
"comments": [],
"concept": {
"__typename": "Concept",
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"__typename": "Chapter",
"explanation": "# Summary \n\nTermination of pregnancy refers to deliberate process of ending a pregnancy. It may be legally performed for a number of reasons under the Abortion Act 1967, either medically or surgically. \n\n# Definition \n\nTermination of pregnancy refers to the deliberate medical process of ending a pregnancy so that it does not result in the birth of a baby. This can be achieved through medical or surgical means. \n\n# Legal Categorisation\n\nIn the UK, termination of pregnancy (TOP) is governed by the The Abortion Act of 1967. **There are five 'categories' for performing a TOP:**\n\nA: An abortion is permissible if continuing the pregnancy would involve a greater risk to the life of the pregnant person than terminating the pregnancy.\n\nB: An abortion is allowed if continuing the pregnancy would involve a greater risk of grave permanent injury to the physical or mental health of the pregnant person.\n\nC: Termination is allowed if continuing the pregnancy would involve a greater risk to the physical or mental health of the pregnant person or any existing children of their family than terminating the pregnancy. This ground is most often used and is applicable up to 24 weeks of pregnancy.\n\nD: An abortion is permissible if there is a substantial risk that the existing children of the family would suffer if the pregnancy were continued. This ground is applicable up to 24 weeks of pregnancy.\n\nE: An abortion is permissible if there is a substantial risk that the fetus would be born with serious physical or mental disabilities. There is no time limit for abortions under this ground.\n\n\n\nAdditionally, there are two important sections for **emergencies**:\n\nF: An abortion can be performed in an emergency if it is necessary to save the life of the pregnant person. This can be done without the need for approval by two doctors.\n\nG: An abortion can be performed in an emergency if it is necessary to prevent grave permanent injury to the physical or mental health of the pregnant person. Similar to ground F, this can be done without the need for approval by two doctors.\n\n\n**Important considerations:**\n\n* Certification: Except in emergencies (grounds F and G), two doctors must agree and certify that at least one of the grounds for abortion (A-E) is met.\n* Time Limits: Grounds C and D are only applicable up to 24 weeks of pregnancy, while grounds A, B, and E have no time limit.\n* Consent: The pregnant person's consent is required, and they must be fully informed about the procedure and its implications.\n* Location: Abortions must be carried out in an approved hospital or clinic.\n\n\n# Medical Termination of Pregnancy (MTOP)\n\nUsually facilitated with the use of :\n\n* Mifepristone, a progesterone antagonist, blocks the progesterone required for continuation of the pregnancy. This is administered first (orally). \n* Misoprostol, a prostaglandin analogue. This causes smooth muscle contractions of the myometrium, resulting in expulsion of uterine contents. Misoprostol is administered 24-48h after mifepristone (also oral), and may be repeated 3-hourly (max 5 doses) until expulsion). \n\nNote: \n\n* For early pregnancies (0-9 weeks) this can be performed at home.\n* For pregnancies around 9-24 weeks, perform in clinic.\n* For later pregnancies (from around 22 weeks) may require feticide (intracardiac KCl injection) \n\n\n**Side effects and Complications:**\n\n* Severe nausea\n* Cramps \n* Diarrhoea\n* Vaginal bleeding\n* Incomplete termination of pregnancy: these cases then must be managed surgically\n\n# Surgical Termination of Pregnancy (STOP)\n\nSurgical management is the more effective option for larger pregnancies that may be further along in gestation. Surgical management may include: \n\n* Suction termination\n* Dilatation and evacuation/curettage 'D&C'\n\n\n\n**Side effects and Complications:**\n\n* Retained products of conception\n* Haemorrhage \n* Infection \n* Perforation \n\n\n# NICE Guidelines\n\n[Click here for NICE Guidelines: Termination of Pregnancy](https://www.nice.org.uk/guidance/ng140/documents/draft-guideline)\n\n# References\n\n[British Pregnancy Advisory Service: Abortion Treatments](https://www.bpas.org/abortion-care/abortion-treatments/)\n\n[The Abortion Act 1967](https://www.legislation.gov.uk/ukpga/1967/87/section/1)",
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"name": "Termination of pregnancy",
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"id": "26",
"name": "Gynaecology",
"typeId": 2
},
"topicId": 26,
"totalCards": 2,
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"question": "An 18-year-old female who is 14 weeks pregnant has requested a termination of pregnancy as she is an emotionally abusive relationship and this is significantly affecting her mental health. She does not feel she would be able to raise this child. However, your religious belief does not align with the patient's intentions, and you do not wish to arrange the abortion.\n\nWhat is the most appropriate action to take in this situation?",
"sbaAnswer": [
"a"
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173,459,372 | false | 14 | null | 6,494,991 | null | false | [] | null | 12,513 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Referring the woman to a domestic abuse support group may be a useful resource for her, but it does not address the key issue here, which is **child safeguarding**.",
"id": "62260",
"label": "c",
"name": "Refer her to a domestic abuse support group",
"picture": null,
"votes": 158
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "In this situation, the patient has disclosed that she is experiencing domestic abuse and that there are children present in the home. This raises safeguarding concern for both the adult and children. Capacitous adults can refuse referral for themselves, but they cannot refuse referrals for child safeguarding concerns. Therefore, the most appropriate course of action would be a child safeguarding referral.",
"id": "62258",
"label": "a",
"name": "Refer to child safeguarding service",
"picture": null,
"votes": 937
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "While the woman may benefit from mental health support due to the domestic abuse she has experienced, it is important to also consider the issue of child safeguarding and take appropriate action. Referring to a mental health service alone is not sufficient in this situation.",
"id": "62262",
"label": "e",
"name": "Refer to mental health service",
"picture": null,
"votes": 6
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "While it is important to respect the woman's autonomy and decision-making capacity, it is also essential to consider the safety and well-being of the children in this situation. Failing to refer to social services for child safeguarding could put the children at risk of harm. Capacitous adults can refuse referral for themselves, but they cannot refuse referrals for child safeguarding concerns. Therefore, the most appropriate course of action would be a child safeguarding referral.",
"id": "62261",
"label": "d",
"name": "Respect her decision and do not refer",
"picture": null,
"votes": 129
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "While providing pain medication may be appropriate to address the woman's physical injuries, it is important to also address the issue of domestic abuse and consider the potential ongoing risk to the woman and her children.",
"id": "62259",
"label": "b",
"name": "Prescribe her analgesia and discharge her",
"picture": null,
"votes": 10
}
],
"comments": [],
"concept": {
"__typename": "Concept",
"chapter": {
"__typename": "Chapter",
"explanation": "# Overview\n\nOne legal defence to breaching confidentiality is the **public interest** defence. This was established by Common Law.\n\n# W v Egdell 1990 \n\n_W v Egdell 1990_: A doctor breached confidentiality to prevent a prisoner getting a transfer while he still posed a risk to others.\n\n# Criteria to fulfil when breaching confidentiality under a public interest defence\n\n1. A risk of harm needs to be identified\n2. Patient consent should be gained if possible\n\n _You do not need to attempt to gain consent if doing so would put you at risk of serious harm, or would prejudice the prevention, detection or prosecution of crime._\n\n3. The patient should be warned that disclosure will be made\n4. Disclosure should be made on a need-to-know basis (i.e. only to the relevant people)\n5. The disclosures made should be kept to a minimum (i.e. only disclosing relevant information)\n6. The information should be anonymised, if possible.",
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"id": "30",
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"question": "A 26-year-old woman presents to the GP clinic with pain and multiple bruises on her arms and face. She tells the GP that she has been suffering from domestic abuse at the hands of her partner for the past year. She has two children, ages 5 and 7, who are currently at home with her. She has the capacity and understands the risks and benefits of seeking help and support. However, she declines a referral to social services or any other support services, saying that she fears what her partner might do if she seeks help.\n\nWhat is the single most appropriate action in this situation?",
"sbaAnswer": [
"a"
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173,459,373 | false | 15 | null | 6,494,991 | null | false | [] | null | 12,514 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Dementia might have contributed to her death, but it is not the direct cause. Hence, it is not stated as the cause of death.",
"id": "62264",
"label": "b",
"name": "Dementia",
"picture": null,
"votes": 77
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Cardiac, respiratory, liver, or kidney failure should not be included as causes of death on a death certificate. Instead, the underlying cause, such as ischemic heart disease, should be stated.",
"id": "62265",
"label": "c",
"name": "Heart failure",
"picture": null,
"votes": 89
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Cardiac, respiratory, liver, or kidney failure should not be included as causes of death on a death certificate. Instead, the underlying cause, such as ischemic heart disease, should be stated.",
"id": "62266",
"label": "d",
"name": "Cardiac arrest",
"picture": null,
"votes": 1064
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "In very limited circumstances, old age should only be given as the sole cause of death. A death certificate that lists \"old age\" or \"senility\" as the cause of death will usually be referred to the coroner unless the deceased is 80 years or older, only if the cause of death cannot be identified.",
"id": "62267",
"label": "e",
"name": "Old age",
"picture": null,
"votes": 75
},
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "In death certificates, it is appropriate to list the pathological cause, like ischemic heart disease, rather than modes of dying, like liver, heart, or respiratory failure.",
"id": "62263",
"label": "a",
"name": "Ischaemic heart disease",
"picture": null,
"votes": 429
}
],
"comments": [
{
"__typename": "QuestionComment",
"comment": "come again?",
"createdAt": 1685320568,
"dislikes": 1,
"id": "26931",
"isLikedByMe": 0,
"likes": 8,
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"displayName": "Malignant Serotonin",
"id": 3366
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"__typename": "QuestionComment",
"comment": "Doesn't say anywhere that she has IHD???",
"createdAt": 1686307924,
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"displayName": "Transplant Pudendal",
"id": 17013
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"__typename": "QuestionComment",
"comment": "how do we know its IHD? ",
"createdAt": 1715022240,
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"__typename": "QuestionComment",
"comment": "Lol i think its coz its SBA everything else is not a probable answer",
"createdAt": 1715022263,
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"__typename": "Concept",
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"__typename": "Chapter",
"explanation": "# Overview\n\nConfirming, or verifying, death is a common request in hospital and in primary care.\n\nLegally in the UK, verifying death does not require a doctor to confirm that death has occurred. It is however a doctor's legal duty to notify the cause of death by issuing a death certificate. \n\n# Steps\n\nThere is also no legal definition to confirm death in the UK.\n\nHowever, it is generally accepted that confirming death consists of:\n\n- Confirming the patients identity\n- Checking for any obvious signs of life\n- Checking response to verbal and painful stimuli\n- Assessing pupils - they should be fixed and dilated\n- Feeling a central pulse\n- Listening for heart sounds and respiratory sounds for a total of 5 minutes.",
"files": null,
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"name": "Death Confirmation",
"status": null,
"topic": {
"__typename": "Topic",
"id": "57",
"name": "Geriatrics",
"typeId": 2
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"question": "An 87-year-old woman with a past medical history of dementia dies at home. Two days prior, her GP had visited her and noted that her blood glucose levels were deteriorating. On the day of her death, the patient's daughter witnessed her last moments as she complained of chest pain and breathlessness and then suddenly collapsed and died. The daughter called for an ambulance, but the patient passed away before it arrived. She was not resuscitated as she wished not to attempt cardiopulmonary resuscitation.\n\nWhich of the following is the most likely cause of death to be included on the death certificate?",
"sbaAnswer": [
"a"
],
"totalVotes": 1734,
"typeId": 1,
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173,459,374 | false | 16 | null | 6,494,991 | null | false | [] | null | 12,515 | {
"__typename": "QuestionSBA",
"choices": [
{
"__typename": "QuestionChoice",
"answer": true,
"explanation": "Nicotine is a commonly used medication for smoking cessation and is available in various strengths. The recommended starting dose for **nicotine replacement therapy is 4 mg for people who smoke more than 20 cigarettes a day**, which is the case for this patient.",
"id": "62268",
"label": "a",
"name": "Nicotine 4 mg",
"picture": null,
"votes": 634
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Currently, e-cigarettes are not a treatment option that smoking cessation clinics can prescribe. However, they can be suggested to individuals who have not successfully quit with medication, but this should be done on a case-by-case basis and with clinical judgement.",
"id": "62272",
"label": "e",
"name": "E-cigarettes",
"picture": null,
"votes": 85
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Varenicline is usually not preferred in this patient as he has a history of severe depression, which can exacerbate his depression.",
"id": "62270",
"label": "c",
"name": "Varenicline 500 micrograms",
"picture": null,
"votes": 253
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "It is incorrect because it is a lower dose than what is recommended for this patient based on the number of cigarettes he smokes per day. It would have been the right choice if he had smoked less than 20 cigarettes each day.",
"id": "62269",
"label": "b",
"name": "Nicotine 2 mg",
"picture": null,
"votes": 314
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Bupropion is usually not preferred in this patient as he has a history of binge eating disorder, which can further worsen his mental health.",
"id": "62271",
"label": "d",
"name": "Bupropion 150 mg",
"picture": null,
"votes": 487
}
],
"comments": [],
"concept": {
"__typename": "Concept",
"chapter": {
"__typename": "Chapter",
"explanation": "# Summary\n\nSmoking is a major public health issue, leading to premature death and multiple health conditions including cancers, COPD and cardiovascular diseases. Encouraging smoking cessation is therefore an important aspect of health promotion. The main strategies include behavioural therapies and pharmacotherapies, which include nicotine replacement therapy (NRT), bupropion, and varenicline. E-cigarettes and vaping are popular aids to smoking cessation and may be offered alongside behavioural support.\n\n# Epidemiology\n\nSmoking is the single biggest cause of premature death in the UK. There are around 10 million active smokers and approximately 50% will eventually die from smoking related conditions (on average 10 years earlier than non-smokers).\n\nConditions associated with smoking include:\n\n- Cancer - smoking is the commonest cause of lung cancer, and contributes to the development of many other tumour types\n- COPD\n- Cardiovascular disease - including stroke, ischaemic heart disease and peripheral vascular disease\n- Peptic ulcers\n- Pregnancy complications (e.g. stillbirth, birth defects, low birth weight)\n- Infertility\n- Osteoporosis\n- Dementia\n- Dental disease\n\nPassive smoking (exposure to second-hand smoke) is also associated with increased risk of lung cancer and heart disease as well as asthma, chest infections and otitis media in children.\n\n# Nicotine Withdrawal Symptoms\n\nWhen attempting to stop smoking, people may experience a variety of unpleasant symptoms due to both physical and psychological dependence on smoking and nicotine. \n\nMost people find they improve within 2-3 weeks of stopping smoking although some may last longer.\n\nSymptoms include:\n\n- Mood changes (irritability, frustration, anger, anxiety, depression)\n- Insomnia\n- Poor concentration\n- Increased appetite and weight gain\n- Restlessness\n- Cravings for cigarettes\n\n# Management\n\n- Patients should be asked if they smoke at every opportunity\n- Those who do smoke should be offered Very Brief Advice (VBA), also known as the 3 As:\n- **Ask** patients if they smoke\n- **Advise** those who smoke that the best way to quit is with specialist support\n- **Act** refer to smoking cessation services if they wish to quit\n- Those who do not want to quit smoking should be offered advice about harm reduction and encouraged to seek support if they are considering quitting\n- Harm reduction strategies include:\n- Cutting down with or without NRT \n- Temporarily stopping smoking with or without NRT\n- Using an e-cigarette\n\n## Behavioural Advice\n\n- Abrupt quitting is the most effective way to stop smoking\n- Encourage patients to set a quit date\n- After this date they should commit to not smoking at all (\"not a puff\" rule)\n- Think about ways to avoid other people smoking and situations in which they would usually smoke\n- Discuss individual barriers to stopping smoking\n- Signpost to resources e.g. free helplines, phone apps\n- Individual and group support services are also available \n- Offer follow up and ongoing support\n\n## Medical Management\n\nOnly one of the following should be prescribed at any time.\n\n- **Nicotine replacement therapy (NRT)**\n\t- Reduces cravings and nicotine withdrawal symptoms\n\t- Multiple formulations are available including patches, gums, sprays and lozenges\n\t- Should be started on the day of quitting\n\t- Common side-effects include nausea, dizziness, vivid dreams and palpitations\n\t- Combination NRT is the most effective - this involves using a patch for 'background' cravings and a short-acting preparation (e.g. a mouth spray) for 'breakthrough' cravings\n- **Bupropion**\n\t- Acts by inhibiting reuptake of dopamine and noradrenaline\n\t- Tablet taken once a day for 6 days then twice a day for 7-9 weeks\n\t- Should be started 7-14 days before the quit date\n\t- Contraindicated in:\n\t- Epilepsy (decreases seizure threshold)\n\t- Eating disorders\n\t- Bipolar disorder\n\t- Brain tumours\n\t- Current benzodiazepine or alcohol withdrawal\n\t- Pregnancy and breast-feeding\n\t- Important side-effects include insomnia, hypersensitivity reactions and rarely seizures\n- **Varenicline**\n\t- Works as a partial nicotinic receptor agonist\n\t- Taken as an oral medication which is uptitrated in dose over the first week\n\t- Start 7-14 days before the quit date, usually continued for 12 weeks\n\t- Contraindicated in pregnancy and end-stage renal disease\n\t- Important side-effects include psychiatric effects (e.g. suicidal thoughts, depression and hallucinations), nausea and headaches\n- **E-cigarettes**\n\t- These are not licensed medications and are not available on the NHS currently but patients may wish to buy them \n\t- Patients should be advised that there is not enough evidence to know whether there are long-term harms of vaping\n\t- However, available evidence suggests that vaping is significantly less harmful than smoking and can help people stop smoking\n\t- Advise patients using e-cigarettes to stop smoking tobacco completely\n\n# Prognosis\n\nAround half of people using NHS Stop Smoking services are successful in quitting at four weeks, with evidence suggesting that people who stop smoking for a month are five times more likely to quit long term. \n\nStopping smoking before the age of 50 halves the risk of dying of smoking-related disease.\n\n\n# NICE Guidelines\n\n[NICE - Tobacco dependence](https://www.nice.org.uk/guidance/ng92)\n\n[NICE CKS - Smoking Cessation](https://cks.nice.org.uk/topics/smoking-cessation/)\n\n# References\n\n[Action on Smoking and Health](https://ash.org.uk/)\n\n[NHS advice on e-cigarettes](https://www.nhs.uk/live-well/quit-smoking/using-e-cigarettes-to-stop-smoking/)\n\n[National Centre for Smoking Cessation and Training](https://www.ncsct.co.uk/)",
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"question": "A 45-year-old man presents to the smoking cessation clinic requesting medication to help him quit smoking. He has tried behavioural therapy and counselling at his GP clinic, but they did not work for him. He is also under treatment for severe depression and binge eating disorder for the past few years. Otherwise, there is no other significant medical history. He currently smokes 25 cigarettes daily and has been smoking for the past 25 years.\n\nWhich of the following is the most appropriate next step?",
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"explanation": "The most common side effect of amlodipine is swelling of the ankles and feet (peripheral oedema).",
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"explanation": "Sertraline is a selective serotonin reuptake inhibitor used to treat depression and anxiety disorders. It is the most likely cause of his gastrointestinal symptoms, as nausea, vomiting, and diarrhoea are common side effects of SSRIs. Non-pharmacologic methods should be tried first in appropriate circumstances when treating the elderly. Behavioural therapy, relaxation techniques, and counselling should be tried first in a grief reaction.",
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"explanation": "# Summary\n\nAntidepressants encompass a variety of classes of drugs which despite the name, are used to treat multiple conditions other than depression, such as anxiety, panic disorder, obsessive-compulsive disorder, post-traumatic stress disorder, and phobic states such as social anxiety disorder. Tricyclic antidepressants and monoamine oxidase inhibitors are older classes though are sometimes still used today, with selective serotonin reuptake inhibitors (SSRIs) becoming popular over the last decade due to their more favourable side effect profiles and lower risk of toxicity. Important considerations of these drugs include their side effects, monitoring, \n\n\n# Selective serotonin reuptake inhibitors (SSRIs)\n\n## Mechanism of action\n\nSSRIs selectively inhibit serotonin reuptake, increasing its availability and enhancing mood regulation.\n\n## Indications\n\n- SSRIs are first line for medical management of depression, generalised anxiety disorder (GAD), panic disorder, obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD), and phobic states such as social anxiety disorder. \n\nCautions: \n- Should be omitted in mania\n- Should be used with caution in children and adolescents\n- Sertraline is best for patients with ischaemic heart disease\n- Should be avoided in patients taking warfarin, due to increased risk of bleeding\n\n## Side effects\n\nSSRIs have a number of recognised side effects. These include:\n\n- GI upset\n- Anxiety and agitation\n- QT interval prolongation (especially associated with citalopram)\n- Sexual dysfunction\n- Hyponatraemia\n- Gastric Ulcer\n\n## Monitoring\n\n- In people aged 18-25 there is an increased risk of impulsivity and suicidal risk upon commencing antidepressant medication and so they should have a follow-up appointment arranged after one week to monitor progress. Initial reviews can otherwise be arranged 2-4 weeks after starting medication in patients >25.\n- Continuation of antidepressants for at least six months post-remission is recommended to mitigate relapse risk. Tapering should be done gradually over a four-week period when discontinuing antidepressants.\n\n## Serotonin syndrome\n\nSerotonin syndrome, also known as serotonin toxicity, is a potentially life-threatening condition linked with increased serotoninergic activity in the central nervous system. It typically presents within the first few months of starting a Selective Serotonin Reuptake Inhibitor (SSRI) or due to drug interactions (SSRI + tramadol). The syndrome is characterised by a triad of mental status changes, autonomic hyperactivity, and neuromuscular abnormalities. It is a clinical diagnosis, and management strategies include discontinuation of the offending drug and supportive care. Please see separate section in Emergency Medicine section for more information.\n\n\n# Serotonin and norepinephrine reuptake inhibitors (SNRIs)\n\n## Mechanism of action\n\nSNRIs work by increasing serotonin and norepinephrine levels, improving mood and anxiety.\n\n\n## Indications\n\n- SNRIs such as venlafaxine can also be used as first line pharmacological treatment of depression if SSRIs are not indicated or have been unsuccessful.\n- Venlafaxine and duloxetine are also licensed for treatment of generalised anxiety disorder (GAD) and panic disorder.\n- Contraindicated in those with a history of heart disease and high\nblood pressure\n\n## Side effects\n\nCommon side effects include:\n\n* Nausea\n* Insomnia\n* Increased heart rate\n* Agitation\n\n\n# Noradrenergic and specific serotonergic antidepressant (NaSSA)\n\n\n## Mechanism of action\n\nNaSSAs such as mirtazepine also work by modulating norepinephrine and serotonin levels in the brain.\n\n## Indications\n\n- Mirtazepine is a second line choice of medication for management of depression, though may be preferred if in particular there are concerns over weight loss, as one of it's side effects is increased appetite. It may also be preferred if there are issues with getting to sleep as it is a light sedative and so it is usually taken in the evening.\n\n## Side effects\n\n* Sedation\n* Increased appetite\n* Weight gain\n* Constipation/diarrhoea\n\n# Tricyclic antidepressants (TCAs)\n\n## Mechanism of action\n\nTricyclic and related antidepressants block the re-uptake of both serotonin and noradrenaline, and examples include amitriptyline, clomipramine and imipramine. They are also antimuscarinic (see contraindications and side effects below).\n\n## Indications\n\nThey are another example of second line choices for treatment of depression, and are sometimes. used in the management of panic and other anxiety disorders.\n\nCautions:\n\n- Contraindicated in those with previous heart disease\n- Can exacerbate schizophrenia\n- May exacerbate long QT syndrome\n- Use with caution in pregnancy and breastfeeding\n- May alter blood sugar in T1 and T2 diabetes mellitus\n- May precipitate urinary retention, so avoid in men with enlarged prostates\n- Uses the Cytochrome P450 metabolic pathway, so avoid in those on other CP450 medications or those with liver damage\n\n## Side effects\n\nTricyclic anti-depressants are a second line medication for depression. They are strongly associated with anti-cholinergic activity. Consequently, the common side effects include:\n\n- Urinary retention\n- Drowsiness\n- Blurred vision\n- Constipation\n- Dry mouth\n\n## Toxicity\n\nKey signs and symptoms include drowsiness, confusion, arrhythmias, seizures, vomiting, headache, flushing, and dilated pupils. Essential investigations include blood tests (FBC, UE, CRP, LFTs), Venous Blood Gas, and an ECG to check for QT interval prolongation. The management primarily involves supportive care based on patient symptoms, with considerations for activated charcoal within 2-4 hours of the overdose and intensive care review in severe cases.\n\n# Monoamine oxidase inhibitors (MAO-Is)\n\n\n## Mechanism of action\n\nMonoamine oxidase (MAO) normally metabolises serotonin and noradrenaline in the presynaptic cell. MAO inhibitors inhibit monoamine oxidase which leads to an elevation in brain levels of catecholamines and serotonin. It has a similar structure to amphetamine so this also affects the uptake and release of dopamine, noradrenaline, and serotonin.\n\nExamples include moclobemide (MAO-B inhibitor), phenelzine (MAO-A inhibitor).\n\n## Indications\n\nThey were historically used to treat depression but are used less frequently now.\n\nCautions:\n\n* Cerebrovascular disease\n* Manic phase of bipolar disorder\n* Phaeochromocytoma\n* Severe cardiovascular disease\n\n## Side effects\n\n* Hypertensive reactions ('cheese reaction') with tyramine-containing foods (so patients need to avoid pickled herring, Bovril, Oxo, Marmite, cheese, salami).\n* Should also avoid broad bean pods as these contain dopa.\n\n# References\n\n[Click here to see the BNF summary for antidepressants](https://bnf.nice.org.uk/treatment-summary/antidepressant-drugs.html)",
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"question": "A 54-year-old man with a history of hypertension, osteoporosis, benign prostatic hyperplasia, and constipation comes to the clinic ten months after the death of his spouse. He reports decreased appetite and difficulty sleeping and performing daily activities. He is currently taking amlodipine, terazosin, alendronate, and over-the-counter fibre supplements and recently started sertraline for depression. He is now complaining of diarrhoea, nausea and vomiting.\n\nWhich of the following drugs would have led to his complaints?",
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"explanation": "Milk and milk products, orange juice, and meals can reduce oral bisphosphonate absorption, so they must only be taken on an empty stomach.",
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"explanation": "Bisphosphonates cause adverse upper gastrointestinal effects such as nausea, reflux, oesophagitis, oesophageal ulcers, and gastritis. They are avoided at bedtime or before getting up in the morning.",
"id": "62285",
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"explanation": "Due to the risk of oropharyngeal ulcers, the tablet should be swallowed whole with plain water (200 mL); it should not be sucked or chewed.",
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"explanation": "Patients should receive supplemental calcium and vitamin D if dietary intake is inadequate. However, taking both at the same time impairs bisphosphonate absorption. Between taking bisphosphonate and calcium supplements or antacids, a minimum interval of 30 minutes is advised.",
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"explanation": "One of the extra-intestinal complications of Crohn's disease is secondary osteoporosis. On top of that, steroid therapy further increases its risk. Therefore, bisphosphonates are simultaneously started in elderly postmenopausal women to enhance bone mineral density. Oesophagal irritation or ulceration are adverse effects of bisphosphotes, so patients are instructed to stay upright and not lie down for at least 30 minutes or until the first meal of the day.",
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"explanation": "# Summary \r\n\r\nOsteoporosis is a chronic condition characterised by low bone density and increased propensity to sustain fragility fractures. It is diagnosed with a dual-energy X-ray absorptiometry (DEXA) scan if a patient's T-score is less than -2.5. It is very common in older patients, especially post-menopausal women, with other risk factors including long-term corticosteroid use, low body weight and immobility. Other key investigations include checking calcium and vitamin D levels as these may require supplementation if low. Treatment is with bone-sparing treatment, with bisphosphonates being the first-line option in the majority of patients. Lifestyle changes such as smoking cessation, taking regular exercise and maintaining a healthy diet are important. Falls risk assessment is also key to reducing the risk of fragility fractures, especially in older patients. \r\n\r\n# Definition\r\n\r\nOsteoporosis refers to a state of low bone density with structural deterioration of bones. This causes bones to weaken, increasing the risk of fragility fractures (defined as a fracture sustained due to a fall from standing or without any trauma). \r\n\r\nPatients are defined as having osteoporosis if their bone mineral density (BMD) is at least 2.5 standard deviations below the mean peak mass of young healthy adults. This is measured with a dual-energy X-ray absorptiometry (DEXA) scan which gives BMD for the lumbar vertebrae and the femur. \r\n\r\n# Epidemiology\r\n\r\n- In the UK, around 2 million people are estimated to have osteoporosis\r\n- Post-menopausal women are particularly at risk due to accelerated bone loss secondary to decreased oestrogen production\r\n- Prevalence also increases significantly with age\r\n- Almost 50% of 80 year old women have osteoporosis\r\n- White ethnicity is also a risk factor\r\n- There are approximately 300,000 fragility fractures per year in the UK, with osteoporosis often being undiagnosed at the time of presentation\r\n\r\n# Aetiology\r\n\r\nRisk of fragility fractures increases as bone density declined, however there are many other factors that increase fracture risk:\r\n\r\n| Risk factors reducing bone density | Risk factors that do not reduce bone density |\r\n|----------|----------|\r\n| Low body weight | Older age |\r\n| Menopause | Inflammatory arthritis (e.g. rheumatoid arthritis) |\r\n| Immobility | Prolonged use of oral corticosteroids |\r\n| Chronic disease e.g. chronic kidney disease, chronic obstructive pulmonary disease, chronic liver disease | Smoking |\r\n| Malabsorption e.g. coeliac disease, inflammatory bowel disease, pancreatic insufficiency | Alcohol excess |\r\n| Endocrine disease e.g. hyperparathyroidism, hyperthyroidism | History of fragility fracture |\r\n| Certain medications (proton pump inhibitors, selective serotonin reuptake inhibitors, carbamazepine) - mixed evidence | Parental hip fracture |\r\n\r\n# Signs and Symptoms\r\n\r\nOsteoporosis itself is asymptomatic and so is usually diagnosed either with screening of people at high risk (e.g. those on long-term corticosteroids) or when someone presents with a fragility fracture.\r\n\r\nThe most common fragility fractures seen are:\r\n\r\n- Vertebral body\r\n- Neck of femur (hip)\r\n- Distal radius\r\n- Proximal humerus\r\n- Pelvis\r\n\r\nSome osteoporotic fractures (e.g. vertebral fractures) may also be asymptomatic acutely. Loss of height and kyphosis may occur due to multiple vertebral fractures, with severe kyphosis leading to reduced mobility and function.\r\n\r\nOther common symptoms of fragility fractures include acute severe pain, difficulty weight-bearing (e.g. for a hip fracture) and mobilising. \r\n\r\nSigns include deformities, such as a shortened and externally rotated leg due to a hip fracture or a \"dinner fork\" deformity in a Colles' wrist fracture.\r\n\r\nThe area around the fracture may be bruised, swollen and tender to touch. \r\n\r\n# Differential Diagnosis\r\n\r\n- **Bone metastases** may lead to pathological fractures, either in patients with known malignancies or as a first presentation of cancer (especially lung, prostate, breast, kidney and thyroid)\r\n- **Osteomalacia** usually occurs secondary to severe vitamin D deficiency and increases fracture risk due to bone weakening; other symptoms include bone pain, muscle pain and proximal weakness with a waddling gait\r\n- **Multiple myeloma** also is associated with pathological fractures, as well as hypercalcaemia, renal impairment, anaemia and bone pain\r\n- **Paget's disease** increases the risk of fracture due to abnormal bone remodelling, leading to features of bone pain and bowing of the long bones\r\n- **Osteogenesis imperfecta** is a genetic condition that commonly presents in childhood with fragility fractures, bowing of the long bones, short stature and blue sclera\r\n- **Avascular necrosis** may mimic a spontaneous fracture with severe pain after no or minimal trauma, commonly affecting the femoral head\r\n\r\n# Investigations\r\n\r\n- The diagnostic investigation for osteoporosis is a **dual-energy X-ray absorptiometry scan (DEXA)**\r\n- This measures **bone mineral density (BMD)**\r\n- A T-score of -2.5 or less is considered diagnostic of osteoporosis\r\n- If the T-score is between -1 and -2.5 this is referred to as osteopenia\r\n- Z-score is also reported (this compares bone density to a age, sex and ethnicity matched population rather than healthy young adults) - below -2 is low for their age\r\n- The following patients should be offered a DEXA scan as the initial step in assessment\r\n- Aged over 50 presenting with a fragility fracture\r\n- Aged under 40 with a major risk factor for fragility fracture (e.g. long-term steroids) \r\n- Those about to start treatment that will rapidly decrease bone density (e.g. hormone deprivation in breast cancer) - consider\r\n- All other patients with risk factors should have their fracture risk assessed as the initial step\r\n- **QFracture** and **FRAX** are the two online assessment tools used\r\n- These both predict a patient's 10-year risk of hip and major osteoporotic fractures\r\n- QFracture is interpreted based on whether the risk score is greater or less than 10%\r\n- FRAX plots fracture risk versus age on a graph that stratifies people into low/intermediate/high risk\r\n- With QFracture, those at approximately 10% risk or more at 10 years should have a DEXA scan \r\n- With FRAX, patients at intermediate or high risk of fracture should have a DEXA\r\n- In women over the age of 75 with a history of fragility fractures, a clinical diagnosis of osteoporosis may be appropriate (if a DEXA is unfeasible)\r\n\r\nOther investigations required in all patients include:\r\n\r\n- **Vitamin D** to check for deficiency; this is needed prior to starting bisphosphonate treatment\r\n- **Bone profile** to check serum calcium as this may also require supplementation\r\n- **X-rays** or other imaging modalities (e.g. CT or MRI) may be required to diagnose and assess fragility fractures\r\n\r\nIf an underlying cause is suspected, the following investigations may be appropriate:\r\n\r\n- **Full blood count** which may show anaemia in malabsorption or malignancy, and leukocytosis in malignancy or inflammatory disease\r\n- **Liver function tests** for chronic liver disease\r\n- **U&Es** for chronic kidney disease\r\n- **ESR** or **CRP** which may be raised in inflammatory disease or malignancy\r\n- **Thyroid function tests** if hyperthyroidism is suspected\r\n- **Testosterone** and **sex hormone-binding globulin** if hypogonadism is suspected in men\r\n- **Anti-TTG antibodies** for coeliac disease if there is evidence of malabsorption\r\n\r\n# Management\r\n\r\n**Conservative management:**\r\n\r\n- Identification and treatment of any underlying condition contributing to osteoporosis\r\n- Optimisation of risk factors e.g. smoking cessation, alcohol reduction\r\n- Advise patients to take regular weight-bearing exercise to improve muscle strength, including walking, strength training and balance and flexibility training\r\n- Advise patients to eat a balanced diet and assess their calcium intake\r\n- Assess falls risk and consider measures to reduce this, including referral to multidisciplinary falls teams \r\n- Referral to specialist services for patients with very high fracture risk (e.g. T score less than -3.5, multiple vertebral fractures)\r\n\r\n**Medical management:**\r\n\r\n- Prescribing vitamin D supplementation for patients not exposed to adequate sunlight\r\n- Prescribing calcium supplements to patients with an inadequate dietary calcium intake\r\n- For patients at high risk of fragility fracture, prescribe bone-sparing treatment\r\n- Treatment should be started promptly after a fragility fracture to reduce the risk of another fracture\r\n- Oral bisphosphonates are the first-line treatment in the majority of patients \r\n- Options include alendronate and risedronate, which can be given either daily or weekly\r\n\t- These must be taken on an empty stomach, at least 30 minutes before food or other medications\r\n\t- Tablets need to be swallowed whole with a glass of water whilst the patient is upright; they should stay upright for at least 30 minutes after this\r\n\t- Common side effects include nausea, dyspepsia, gastritis, abdominal pain and musculoskeletal pains\r\n\t- Rarer side effects include oesophagitis or ulceration, stricturing or erosions, osteonecrosis of the jaw or external auditory canal and atypical stress fractures\r\n\t- To minimise risk of osteonecrosis of the jaw, patients with poor dentition or malignancy should have a dental check-up (and any work required performed) before starting bisphosphonates\r\n\t- They should also continue to have routine dental checks and maintain good oral hygiene during treatment \r\n\t- Contraindications include severe chronic kidney disease, hypocalcaemia or vitamin D deficiency, and oesophageal abnormalities such as stricture or achalasia \r\n\t- Patients with recent peptic ulceration, upper gastrointestinal bleeding or surgery, dysphagia, gastritis or duodenitis should be prescribed bisphosphonates with caution\r\n- If oral bisphosphonates are not tolerated or unsuitable, options for bone-sparing treatment include:\r\n\t- Parenteral bisphosphonates (e.g. zoledronate)\r\n\t- Denosumab\r\n\t- Raloxifene hydrochloride\r\n\t- Strontium ranelate\r\n\t- Hormone replacement therapy should be considered for younger women experiencing menopausal symptoms as this will also reduce their fragility fracture risk\r\n\t- Teriparatide and romosozumab are other bone-sparing treatments that may be recommended first-line in women with severe osteoporosis - these are then followed by bisphosphonate treatment\r\n\r\n**Surgical management:**\r\n\r\n- Fragility fractures may require surgical fixation or joint replacement (e.g. hip arthroplasty for a fractured neck of femur)\r\n\r\n# Complications\r\n\r\n- Hip fractures are high-consequence injuries and lead to permanent disability in 50% and death in 20% of patients \r\n- Vertebral fractures may lead to disabling and painful kyphosis which may in turn cause difficulty breathing and gastrointestinal problems such as dyspepsia\r\n- Wrist fractures can significantly affect independence and functional ability\r\n- Many patients experience a \"fracture cascade\" where further fractures occur in the years following the initial one\r\n- Pain from fractures can lead to poor sleep, low mood and reduced quality of life\r\n- Complications of treatment may be significant (e.g. osteonecrosis of the jaw or oesophageal ulceration with bisphosphonates)\r\n\r\n# Prognosis\r\n\r\n- There is no cure for osteoporosis\r\n- In general however, prognosis is good with effective treatment\r\n- Bisphosphonate treatment should be reviewed after 3-5 years\r\n- If patients remain at high risk of fracture it may be continued for up to 7-10 years\r\n- Patients with previous hip or vertebral fractures, those aged 70 or older or those who sustain another fragility fracture whilst on bone protection often require longer durations of treatment\r\n- Repeat DEXA may be appropriate to aid decision making\r\n- If bone protection is stopped, fracture risk should be reassessed 18 months to 3 years later\r\n\r\n# NICE Guidelines\r\n\r\n[NICE CKS: Osteoporosis - prevention of fragility fractures](https://cks.nice.org.uk/topics/osteoporosis-prevention-of-fragility-fractures/)\r\n\r\n[NICE - Osteoporosis: assessing the risk of fragility fracture](https://www.nice.org.uk/guidance/cg146)\r\n\r\n# References\r\n\r\n[National Osteoporosis Guideline Group - Prevention and Treatment of Osteoporosis](https://www.nogg.org.uk/full-guideline)\r\n\r\n[BNF Treatment Summary - Osteoporosis](https://bnf.nice.org.uk/treatment-summaries/osteoporosis/)\r\n\r\n[Radiopaedia - Dual-energy x-ray absorptiometry](https://radiopaedia.org/articles/dual-energy-x-ray-absorptiometry-1?lang=gb)\r\n\r\n[WHO - Fragility fractures](https://www.who.int/news-room/fact-sheets/detail/fragility-fractures)\r\n\r\n[International Longevity Centre UK report on Osteoporosis](https://ilcuk.org.uk/wp-content/uploads/2018/10/OsteoporosisUK.pdf)\r\n\r\n\r\n",
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"explanation": "# Summary\r\n\r\nPrimary hypertension, accounting for approximately 90-95% of cases of hypertension, is characterised by persistently elevated blood pressure due to age-related pathophysiological changes. It is a major risk factor for cardiovascular disease, cerebrovascular disease, chronic kidney disease, and peripheral vascular disease. Diagnosis is based on ambulatory blood pressure monitoring (ABPM) readings of 135/85mmHg or higher. Classification is determined by the severity of the hypertension. Management depends on the classification of the hypertension and involves lifestyle modifications and pharmacological anithypertensives according to NICE guidelines. Effective management, through lifestyle changes and medications, significantly reduces the associated risks and improves outcomes for individuals with hypertension.\r\n\r\n# Definition \r\n\r\nA 'normal' blood pressure ranges between 90/60mmHg to 140/90mmHg. The definition of hypertension is a 24h ambulatory blood pressure average reading (ABPM) that is more than or equal to 135/85mmHg. \r\n\r\n# Epidemiology\r\n\r\nIn 2015, it was reported that high blood pressure affected more than 1 in 4 adults in England (31% of men; 26% of women). In England, it is estimated that primary hypertension affects around 13.5 million people and contributed to 75,000 deaths.\r\n\r\n# Pathophysiology\r\n\r\nPrimary hypertension is as a result of a series of complex physiological changes as we age. Hypertension often occurs as a result of reduced elasticity of large arteries, age-related and atherosclerosis-related calcification, and degradation of arterial elastin. It may also be present in conditions associated with increased cardiac output, such as anaemia, hyperthyroidism and aortic regurgitation.\r\n\r\nAlthough the risk of cardiovascular disease increases progressively with increasing systolic and diastolic blood pressure, raised systolic pressure is more important than raised diastolic pressure as a risk factor for cardiovascular and renal disease.\r\n\r\n# Classification \r\n\r\nHypertension can be classified according to how high a patient's blood pressure is. \r\n\r\n* Stage 1: Clinic => 140/90mmHg; ABPM => 135/85mmHg \r\n* Stage 2: Clinic => 160/100mmHg; ABPM =>150/95mmHg \r\n* Stage 3: Clinic systolic BP (SBP) => 180 or diastolic BP (DBP) =>120mmHg\r\n\r\n\r\n# Symptoms and Signs\r\n\r\nHypertension, unless malignant, is asymptomatic and does not have any clinical signs. It is diagnosed with ABPM and further investigations should focus on diagnosing end-organ complications of hypertension. \r\n\r\n# Investigations\r\n\r\n[lightgallery]\r\n\r\n* Hypertensive patients are commonly first identified at GP appointments or during hospital admissions. Due to the prominence of 'white coat hypertension', ABPM is now required for the diagnosis of hypertension. \r\n* Hypertension should be suspected in a patient who has a clinic blood pressure of =>140/90mmHg. \r\n* **1st line: ABPM** or home blood pressure monitoring if ABPM is not tolerated or declined. \r\n* Alongside ABPM: assessment for end-organ damage and assessment of cardiovascular risk (QRISK2 scores). \r\n * Urine dip and albumin:creatinine level\r\n * Blood glucose, lipids and renal function\r\n * Fundoscopy for evidence of hypertensive retinopathy\r\n * ECG: look for evidence of LV hypertrophy\r\n\r\n\r\nN.B. if presentation is suspicious for secondary hypertension refer and investigate as appropriate (see section). \r\n\r\nN.B. Referral for same-day specialist assessment should be arranged for people with: \r\n\r\n* Clinic blood pressure of 180/120mmHg and higher with signs of retinal haemorrhage or papilloedema (accelerated hypertension) or life-threatening symptoms (e.g. new onset confusion, chest pain, heart failure signs or AKI). \r\n\r\n# Management\r\n\r\n## Principles of Management \r\n\r\n### Conservative Management \r\n\r\nControlling risk factors for cardiovascular disease:\r\n\r\n* Weight loss\r\n* Healthy diet (reduce salt and saturated fats)\r\n* Reduce alcohol and caffeine\r\n* Reduce stress\r\n* Stop smoking\r\n\r\n### Medical Management\r\n\r\nIndications to start pharmacological management of primary hypertension:\r\n\r\n* Stage 1 hypertensive patients who are <80 years old with end organ damage, CVS disease, renal disease, diabetes or 10-year CVS risk >10% OR\r\n* Anyone with stage 2 hypertension\r\n\r\n### 2019 NICE Guidelines for Pharmacological Management of Primary Hypertension \r\n\r\n[lightgallery1]\r\n\r\n* Step 1: \r\n\t* **ACE-inhibitor** (e.g. Ramipril) if <=55 years old\r\n\t* **DHP-Calcium Channel Blocker** (e.g. Amlodipine) if >55 years old OR African or Caribbean ethnicity\r\n\t* If unable to tolerate ACE-inhibitor then switch to _Angiotensin Receptor Blocker_ (e.g. Candesartan)\r\n* Step 2: \r\n\t* (If maximal dose of Step 1 has failed or not tolerated)\r\n\t* **Combine CCB and ACE-I/ARB**\r\n* Step 3:\r\n\t* (If maximal doses of Step 2 has failed or not tolerated)\r\n\t* **Add thiazide-like diuretic** (e.g. Indapamide)\r\n* Step 4: *Resistant Hypertension*\r\n\t* If blood potassium <4.5mmol/L then add **spironolactone**\r\n\t* If >4.5mmol/L **increase thiazide-like diuretic dose**\r\n\t* Other options at this point if the potassium is >4.5mmol/L include:\r\n\t\t* Alpha blocker (e.g. Doxazosin)\r\n\t\t* Beta blocker (e.g. Atenolol)\r\n\t\t* Referral to cardiology for further advice\r\n\r\n**ABPM Targets:**\r\n \r\n* Age <80 ABPM target <135/85\r\n* Age >80 ABPM target <145/85 (due to risk of postural drop and falls)\r\n* T1DM with end-organ damage <130/80\r\n\r\n# Complications\r\n\r\n* Increased risk of morbidity and mortality from all causes\r\n* Coronary artery disease\r\n* Heart failure\r\n* Renal failure\r\n* Stroke\r\n* Peripheral vascular disease\r\n\r\n# Prognosis \r\n\r\nHypertension remains one of the biggest risk factors for cardiovascular disease and its associated disabilities. Management of hypertension (with lifestyle modifications or pharmacological therapies) has been shown to reduce these risks significantly. \r\n\r\n# NICE Guidelines\r\n> <https://cks.nice.org.uk/topics/hypertension/> \r\n\r\n# References \r\n\r\n<https://patient.info/heart-health/high-blood-pressure-hypertension>\r\n<https://www.ahajournals.org/doi/full/10.1161/01.CIR.101.3.329> ",
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"explanation": "# Summary\n\nHyperlipidaemia is an umbrella term used to describe high serum levels of cholesterol and/or triglycerides. It is an important cardiovascular risk factor and is commonly targeted with lipid-lowering treatment either as primary or secondary prevention. It is often asymptomatic but may present with tendon xanthomata, corneal arcus and xanthelasmata. Investigations include a lipid profile, liver function tests, HbA1c and renal function. The QRISK calculator is used to estimate a patient's 10 year risk of having a stroke or heart attack and guides who should be recommended primary prevention (typically those with a score of 10% or higher). Management is typically with statins in the first instance, alongside lifestyle advice, addressing any secondary causes of hyperlipidaemia and considering other cardiovascular risk factors.\n\n# Definition\n\nHyperlipidaemia refers to raised levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C), triglycerides or a combination of these. Dyslipidaemia includes hyperlipidaemia but also encompasses low levels of high-density lipoprotein cholesterol (HDL-C) which is also a cardiovascular risk factor. \n\nHyperlipidaemia is associated with atherosclerosis, where fibrofatty plaques form in the walls of arteries. These lead to narrowing and hardening of the vessels, reducing blood flow to target organs. If plaques rupture, this leads to thrombosis with subsequent obstruction of the artery (either partial or complete), which may manifest clinically for example as a stroke or myocardial infarction.\n\n# Epidemiology\n\n- Hyperlipidaemia is very common - 59% of adults had raised total cholesterol in the 2021 Health Survey for England\n- This rose to 72% of adults aged 45 to 64\n- Risk factors include:\n- Older age\n- Male sex\n- Being overweight or obese\n- Eating a diet high in saturated fats and trans-fatty acids\n- Sedentary lifestyle\n- Smoking\n- Alcohol excess\n- Medical conditions (e.g. diabetes, chronic kidney disease)\n- A small proportion of cases are due to familial hypercholesterolaemia (FH)\n- Approximately 1 in 500 of the UK population have heterozygous FH \n- Homozygous FH is more severe but rarer, affecting around 1 in every 300,000 people\n- FH is significantly underdiagnosed, with only around 4% of cases identified\n\n# Aetiology\n\n**Causes of hypercholesterolaemia without hypertriglyceridaemia:**\n\n- Familial hypercholesterolaemia\n- Nephrotic syndrome\n- Hypothyroidism\n- Cholestatic liver disease e.g. primary biliary cirrhosis\n- Cushing's syndrome\n- Anorexia nervosa\n- Medications e.g. ciclosporin\n\n**Causes of hypertriglyceridaemia +/- hypercholesterolaemia:**\n\n- Diabetes\n- Pregnancy\n- End-stage renal disease\n- HIV \n- Alcohol excess\n- Metabolic syndrome\n- Monoclonal gammopathy\n- Medications e.g. steroids, isotretinoin, antiretrovirals\n- Familial combined hyperlipidaemia\n\n# Signs and Symptoms\n\nPatients are often asymptomatic and detected incidentally with a lipid profile - those with a family history of an inherited hyperlipidaemia or premature coronary heart disease may be screened.\n\nAll patients with established cardiovascular disease (e.g. ischaemic heart disease, stroke, peripheral vascular disease) should have their lipid levels checked and secondary prevention treatment offered.\n\nClinical signs may also be seen:\n\n- Tendon xanthomata (hard painless nodules on the knuckles and Achilles tendons, typically seen in FH)\n- Xanthelasma (yellow cholesterol deposits on the eyelids)\n- Corneal arcus (blue/grey rim surrounding the iris) - these are normal in older people but may indicate hyperlipidaemia under the age of 40\n\n# Investigations\n\n**Bedside:**\n\n- **Urine dip** to screen for proteinuria if chronic kidney disease (CKD) or nephrotic syndrome is suspected\n- **Blood glucose** to screen for diabetes\n- **ECG** may show ischaemic changes due to coronary artery disease\n- **Pregnancy test** in women of childbearing age (statins are contraindicated in pregnancy and breastfeeding)\n\n**Blood tests:**\n\n- **Lipid profile** to diagnose hyperlipidaemia - a total cholesterol of > 9 mmol/L or non-HDL of > 7.5 mmol/L warrants specialist assessment for FH\n- **U&Es** to screen for renal failure\n- **LFTs** may be deranged in cholestatic liver disease and albumin will be low in nephrotic syndrome; patients with significantly abnormal LFTs should not be started on statins\n- **HbA1c** to screen for diabetes\n- **Thyroid function tests** if there are clinical signs of thyroid disease\n- **Creatine kinase** in patients with a history of persistent generalised unexplained muscle symptoms (e.g. myalgia)\n\n**Special tests:**\n\n- **Genetic testing** if a primary hyperlipidaemia is suspected\n\n# Management\n\n**Conservative:**\n\n- Advise all patients on lifestyle changes to reduce their cardiovascular risk:\n- Smoking cessation\n- Weight loss advice if overweight or obese\n- For obese patients, also assess for sleep apnoea and treat if appropriate\n- Eat a diet high in fruit, vegetables, fibre and increase mono-unsaturated fat intake (e.g. olive oil)\n- Reduce intake of sugar, saturated fat and salt\n- Drink in moderation (less than 14 units per week spread over 3-5 days)\n- Take at least 150 minutes of moderate intensity or 75 minutes of vigorous intensity exercise per week\n- Do muscle-strengthening exercises on at least 2 days per week\n- Offer referral to support services to help patients achieve the above changes as necessary, for example:\n\t- Smoking cessation services\n\t- Weight management services\n\t- Alcohol support services in patients dependent on alcohol\n\t- Exercise referral schemes\n\t- Perform a cardiovascular risk assessment\n- QRISK3 is the recommended tool that calculates a patient's risk of having a heart attack or stroke over the next 10 years\n\t- It takes into account a range of risk factors including age, sex, comorbidities (e.g. diabetes, CKD, severe mental illness), smoking status, cholesterol/HDL ratio, blood pressure and body mass index\n\t- A QRISK3 score of 10% or more is an indication for primary prevention\n\t- In some cases, lifestyle change alone may be an appropriate first-line management step \n\t- Cardiovascular risk should be reassessed after the person has tried to change their lifestyle\n\nTreatment targets are as follows:\n\n- Primary prevention - at least 40% reduction in non-HDL cholesterol\n- Secondary prevention - LDL cholesterol ≤ 2 mmol/L or non-HDL cholesterol ≤ 2.6 mmol/L\n- Consider referring patients with suspected FH or another inherited dyslipidaemia to specialist lipid management services\n- Dietician input should be considered for patients with FH\n\n**Medical:**\n\n- Statin treatment should be offered to people with:\n\t- A QRISK3 of 10% or higher\n\t- Familial hypercholesterolemia \n\t- CKD\n\t- Type 1 diabetes in people aged 40 years+/have had diabetes for 10 years+/with nephropathy/other cardiovascular risk factors\n\t- Statin treatment should be considered in:\n\t- People aged 85 and older, especially if they smoke or have hypertension\n\t- Anyone aged 18–40 with type 1 diabetes\n- First line for **primary prevention** is 20 mg of atorvastatin - this can be uptitrated to a maximum of 80 mg per day if required\n- For **secondary prevention,** 80 mg of atorvastatin should be started in the first instance (lower doses may be considered in patients with CKD or those at higher risk of adverse effects)\n- If statins are not tolerated or contraindicated (e.g. active liver disease or unexplained persistent transaminitis), ezetimibe is the usual second-line option\n- Patients should be counselled before starting statins (see patient decision aid in references section) and safety netted for side effects of muscle symptoms including rhabdomyolysis\n- Patients started on statins should be monitored with a full lipid profile and liver function tests 2-3 months into treatment; liver function should be repeated again at 1 year\n- Other lipid-lowering drugs may be considered if statins and/or ezetimibe are not effective or tolerated - these include:\n\t- Icosapent ethyl - an omega−3 fish-oil based medication with multiple mechanisms of action\n\t- Bempedoic acid - an inhibitor of adenosine triphosphate citrate lyase which reduces hepatic cholesterol synthesis\n\t- Inclisiran - an inhibitor of PCSK9 production \n\t- Alirocumab and evolocumab - these are both monoclonal antibodies that inhibit PCSK9\n\t- Fenofibrate - reduces triglycerides with variable effects on cholesterol\n\t- Colestyramine - bile acid sequestrant\n\n# Complications\n\n- Ischaemic heart disease \n- Acute coronary syndrome\n- Stroke and transient ischaemic attack\n- Peripheral vascular disease\n- Erectile dysfunction\n- Aortic disease\n\n# NICE Guidelines\n\n[NICE CKS - Lipid modification - CVD prevention](https://cks.nice.org.uk/topics/lipid-modification-cvd-prevention/)\n\n[NICE CKS - Familial hypercholesterolaemia](https://cks.nice.org.uk/topics/hypercholesterolaemia-familial/)\n\n[NICE CKS - CVD risk assessment and management](https://cks.nice.org.uk/topics/cvd-risk-assessment-management/)\n\n[NICE Decision Aid - Should I take a statin?](https://www.nice.org.uk/guidance/ng238/resources/patient-decision-aid-on-should-i-take-a-statin-pdf-243780159)\n\n# References\n\n[https://patient.info/doctor/hyperlipidaemia-pro](https://patient.info/doctor/hyperlipidaemia-pro)\n\n[BNF Treatment Summaries - Dysplipidaemias](https://bnf.nice.org.uk/treatment-summaries/dyslipidaemias/)\n\n[NHS Digital - Health Survey for England 2021](https://digital.nhs.uk/data-and-information/publications/statistical/health-survey-for-england/2021-part-2/adult-health-cholesterol)\n\n[QRISK3 calculator](https://qrisk.org/)",
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"question": "A 50-year-old woman visits the GP for a routine health checkup. She was diagnosed with type 2 diabetes a few months ago (well-controlled on oral hypoglycemics). Examination is unremarkable, with normal vital signs. Blood tests reveal very high serum cholesterol and low-density lipoprotein levels. She is advised to take Simvastatin 20mg once daily.\n\nWhich of the following are patients told to avoid whilst taking statins?",
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"explanation": "Linaclotide is a guanylate cyclase-C agonist that stimulates peristalsis by increasing fluid secretion and reducing visceral hypersensitivity. It is mainly used in irritable bowel syndrome associated with constipation.",
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"explanation": "Lactulose is an osmotic laxative which increases the volume of water in the large intestine by either drawing fluid from the body or retaining the liquid with which they are consumed at the time of administration.",
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"explanation": "# Summary\n\nConstipation is a common gastrointestinal disorder characterised by infrequent bowel movements, hard stools, excessive straining, tenesmus and sometimes necessitating manual evacuation. The disorder can be primary, due to a functional issue, or secondary, due to various causes such as diet, certain medications, and endocrine or neurological disorders. Key investigations include full blood count, electrolytes, thyroid function, blood glucose, and imaging if suspicious of secondary causes. Management is dependent on the underlying cause and may involve lifestyle modifications, a range of laxatives, and referral to a specialist centre for gut motility evaluation if laxatives fail to resolve symptoms.\n\n# Definition\n\nConstipation may involve any or all of the following (Rome IV criteria):\n\n- Fewer than three bowel movements per week\n- Hard stool in more than 25% of bowel movements\n- Tenesmus (sense of incomplete evacuation) in more than 25% of bowel movements\n- Excessive straining in more than 25% of bowel movements\n- A need for manual evacuation of bowel movements\n\nIt can be categorised as:\n\n- Primary constipation: no organic cause, thought to be due to dysregulation of the function of the colon or anorectal muscles\n- Secondary constipation: due to factors such as diet, medications, metabolic, endocrine or neurological disorders or obstruction\n\n# Epidemiology\n\nRisk factors include:\n\n- Advanced age\n- Inactivity\n- Low calorie intake\n- Low fibre diet\n- Certain medications\n- Female sex\n\n# Aetiology\n\nCauses of constipation include:\n\n- Dietary factors, such as inadequate fibre or fluid intake\n- Behavioural factors, like inactivity (common cause of constipation in inpatients) or avoidance of defecation\n- Electrolyte disturbances, like hypercalcaemia\n- Certain drugs, particularly opiates, calcium channel blockers and some antipsychotics\n- Neurological disorders, like spinal cord lesions, Parkinson's disease, and diabetic neuropathy\n- Endocrine disorders, such as hypothyroidism\n- Colon diseases, like strictures or malignancies. Bowel obstruction can also cause complete constipation (obstipation)\n- Anal diseases, like anal fissures or proctitis\n\n# Signs and symptoms\n\nSymptoms and signs of constipation include:\n\n- Infrequent bowel movements (less than 3 per week)\n- Difficulty passing bowel motions\n- Tenesmus\n- Excessive straining\n- Abdominal distension\n- Abdominal mass felt at the left or right lower quadrants (stool)\n- Rectal bleeding\n- Anal fissures\n- Haemorrhoids\n- Presence of hard stool or impaction on digital rectal examination\n\nALARMS features which may indicate gastrointestinal malignancy include: anaemia, weight loss, anorexia, recent onset, melaena/haematemesis/PR bleeding, swallowing difficulties\n\n\n# Investigations\n\n### 2-week-wait criteria\n\n- Constipation (or diarrhoea) with weight loss, 60 and over. Consider an urgent, direct access CT scan, or an urgent ultrasound scan if CT is not available, to rule out **pancreatic cancer**\n\nIf it a patient does not fit the 2-week-wait criteria above, and the cause is thought to be primary, then it is likely that no further investigations are needed.\n\nHowever, if there is suspicion over secondary causes of constipation, investigations may include:\n\nBedside:\n\n- PR exam\n- Stool culture – MC&S, ova,cysts,parasites\n- FIT testing (if accompanied with new rectal bleeding and signs suggestive of colorectal cancer), faecal calprotectin\n\nBloods:\n\n- Full blood count (may show an anaemia), U+Es (including calcium), TFTs\n\nImaging:\n\n- Abdominal x-ray if suspicious of a secondary cause of constipation such as obstruction (may reveal faecal loading)\n- Barium enema if suspicious of impaction or rectal mass\n- Colonoscopy if suspicious of lower GI malignancy\n\n[lightgallery]\n\n# Management\n\nConservative:\n\n- Lifestyle modifications such as dietary improvements and increased exercise\n\nMedical:\n\n**Laxatives** are the mainstay of treatment, please see summary table below.\n\n| Class of Laxative | Drug Name Example | Indication | Mechanism of Action | Side Effects | Contraindications |\n|---------------------|-------------------|--------------------------------------------------------------|---------------------------------------------------------|---------------------------------------|-----------------------------------------------------------|\n| Bulking Agents | Ispaghula Husk | Used for constipation, especially in individuals who need to increase stool bulk. | Increase faecal mass and stimulate peristalsis | Contraindicated in dysphagia, GI obstruction, faecal impaction | Colonic atony, faecal impaction, intestinal obstruction, reduced gut motility, sudden change in bowel habit that has persisted more than two weeks; undiagnosed rectal bleeding |\n| Stimulant | Senna, bisacodyl | Used for short-term relief of constipation. | Increase intestinal motility | Cramps | Contraindicated in acute obstruction or colitis; Prolonged use causes colonic atony (+ melanosis coli) |\n| Stool Softeners | Sodium Docusate, Macrogol | Used to soften stool and make bowel movements easier. | Use in fissures, reduce anticipatory withholding | Flatulence, nausea | Ileus; intestinal obstruction; intestinal perforation; risk of intestinal perforation; severe inflammatory bowel disease; toxic megacolon | \n| Osmotic Laxatives | Lactulose | Used for the treatment of constipation, particularly in cases of hepatic encephalopathy. | Retain fluid in bowel and discourage ammonia-producing microorganisms; First-line for hepatic encephalopathy | Abdominal discomfort, flatulence, diarrhea, electrolyte imbalance | Known hypersensitivity to lactulose, galactosemia, intestinal obstruction |\n| Phosphate Enema | Phosphate Enema | Used for rapid bowel evacuation, often before medical procedures or examinations requiring an empty bowel. | Rapid bowel evacuation, need digital rectal examination (DRE) first | Abdominal cramps, electrolyte imbalance, dehydration | Contraindicated in patients with renal impairment, heart failure, electrolyte abnormalities, and those at risk of phosphate nephropathy |\n\n\nIf laxatives fail to resolve symptoms, referral to a specialist centre for evaluation of gut motility may be necessary. \n\nSurgical:\n\n- If suspicions of colorectal cancer, referral to lower GI/colorectal surgeons\n- If concerns over obstruction these patients need to go to A&E for urgent management and imaging\n\n# NICE Guidelines\n\n[NICE: Treatment Summary: Constipation](https://bnf.nice.org.uk/treatment-summary/constipation.html)\n\n# References\n\n[World Gastroenterology Organisation: Constipation](https://www.worldgastroenterology.org/guidelines/global-guidelines/constipation)\n",
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"question": "A 75-year-old woman was started on oral morphine following a pathological fracture. After a week, she returns complaining of constipation. She has been straining, and her stools are rock-hard. Moreover, she mentions the feeling of incomplete evacuation of stools. A diagnosis of opioid-induced constipation is suspected. She is advised to take an over-the-counter laxative to soften her stool.\n\nWhich laxative acts by this mechanism?",
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"explanation": "A history of recent trauma with unusual limitation of both active and passive movements on examination is most likely due to a fracture of the olecranon process.",
"id": "62312",
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"name": "Fracture of the olecranon process",
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"explanation": "Olecranon bursitis (student's elbow) is usually caused by constant friction and irritation of the elbow while repetitively leaning and working on the table for various reasons. In this clinical vignette, her occupation raises suspicion of this condition.",
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"explanation": "In rheumatoid arthritis, the whole joint is inflamed instead of localised, fluctuant swelling. Characteristic rheumatic nodules, which are firm without fluctuation, can cause swelling over the olecranon region.",
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"name": "Rheumatoid arthritis",
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"explanation": "Septic arthritis presents with fever, severe excruciating pain and swelling of the whole joint rather than the bursa. A painful and limited range of movements on examination characterises it.",
"id": "62310",
"label": "c",
"name": "Septic arthritis",
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"explanation": "Lateral epicondylitis (tennis elbow) is due to micro-tearing of the fibres and resultant inflammation of the extensor tendons in the forearm. It can be differentiated from olecranon bursitis by the presence of tenderness to palpation over the origin of the extensor carpi radialis brevis tendon.",
"id": "62311",
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"comment": "sounds like a funny desk job to me",
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"comment": "crawling for a promotion huh",
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"explanation": "# Definition \n\nOlecranon bursitis is inflammation of the olecranon bursa. \n\n# Aetiology \n\nIt will classically occur after repetitive damage, such as leaning on the elbow.\n\n# Examination \n\nExamination reveals a swelling directly over the olecranon which is fluctuant with no signs of infection.\n\n# Management \n\n\nManagement is generally conservative with the use of ice, anti inflammatory medications and an elbow support. If this does not improve the condition and it is affecting the patients activities of daily living a steroid injection can be considered.",
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"question": "A 43-year-old woman presents to the GP with painful swelling on her right elbow. Her past medical history includes psoriatic arthritis. She denies any trauma but mentions she is often crawling and leaning on her elbow while doing her desk job as a clerk. On examination, there is a fluctuant swelling the size of a golf ball, tenderness, and erythema over the posterior aspect of the elbow.\n\nWhat is the most likely diagnosis?",
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"explanation": "DPP-4 inhibitors such as Sitagliptin would be the most appropriate second line therapy as they are not known to cause weight gain",
"id": "62315",
"label": "c",
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"explanation": "The main side effect of thiazolidinediones (rosiglitazone and pioglitazone) is water retention, leading to oedema and weight gain. Hence, they are not the best choice as an additional drug.",
"id": "62316",
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"explanation": "Insulin will help improve glycaemic control but is associated with weight gain and hypoglycaemia. Moreover, insulin is usually commenced if a trial of multiple oral hypoglycaemic agents fails to control his condition.",
"id": "62317",
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"name": "Insulin",
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"explanation": "Although sulfonylureas such as glipizide and glimepiride are the most preferred options as an add-on medication to metformin. However, their side effects (weight gain and hypoglycaemia) make them less likely a suitable choice in this scenario.",
"id": "62314",
"label": "b",
"name": "Glimepiride",
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"explanation": "Glucagon-like peptide-1 (GLP-1) receptor agonists such as exenatide can be used as fourth line agents. In patients with BMI >= 35 kg/m² they have been known to cause weight loss.",
"id": "62313",
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"explanation": "# Summary\n\nType 2 Diabetes Mellitus is a chronic metabolic disorder characterized by pancreatic beta-cell insufficiency and insulin resistance. The primary signs and symptoms include hyperglycaemia and associated sequelae. Key investigations include random and fasting blood glucose, 2-hour glucose tolerance, and HbA1C tests. Management of type 2 diabetes primarily revolves around lifestyle modifications, hypoglycaemic agents, and insulin therapy when necessary. Major complications involve the gastrointestinal system, nervous system, peripheral arteries, foot infections, sexual dysfunction, and cardiac system. \n\n# Definition\n\nType 2 Diabetes Mellitus (T2DM) is a chronic metabolic condition characterized by inadequate insulin production from pancreatic beta cells, resulting in insulin resistance. This leads to an elevation in blood glucose levels, causing hyperglycaemia.\n\n# Epidemiology\n\nT2DM generally manifests in adults, and it is often associated with a strong familial predisposition. It accounts for approximately 90-95% of all diagnosed cases of diabetes.\n\n# Aetiology\n\nT2DM results from a combination of genetic and environmental factors. Known contributors include:\n\n- Poor dietary habits\n- Lack of physical activity\n- Obesity\n\n# Signs and symptoms\n\nIndividuals with T2DM may initially be asymptomatic, but over time, they may develop:\n\n- Polyuria\n- Polydipsia\n- Unexplained weight loss\n- Blurry vision\n- Fatigue\n\n# Differential diagnosis\n\nThe primary differentials for T2DM include Type 1 Diabetes Mellitus, Maturity Onset Diabetes of the Young (MODY), and Secondary Diabetes Mellitus. The main distinguishing features of these differentials are:\n\n- Type 1 Diabetes Mellitus: Early onset (typically in childhood or adolescence), often presents with ketoacidosis, and requires insulin therapy from diagnosis.\n- MODY: Early onset (typically before 25 years), non-insulin dependent, and often has a strong family history.\n- Secondary Diabetes Mellitus: Often presents with other signs of pancreatic disease (e.g., pancreatitis, cystic fibrosis), or due to certain medications (e.g., glucocorticoids, antipsychotics).\n\n# Investigations\n\nIf symptomatic, one of the following results is sufficient for diagnosis:\n\n- Random blood glucose ≥ 11.1mmol/l\n- Fasting plasma glucose ≥ 7mmol/l\n- 2-hour glucose tolerance ≥ 11.1mmol/l\n- HbA1C ≥ 48mmol/mol (6.5%)\n\nIf the patient is asymptomatic, two results are required from different days.\n\n# Management\n\nManagement of T2DM involves patient education, lifestyle modifications, pharmacological interventions, and close monitoring of glucose levels:\n\n- Lifestyle modifications: Advice on diet, regular physical activity, and smoking cessation\n- Pharmacological interventions: \n\t- Initial drug treatment is usually metformin, with consideration of other agents like Pioglitazone, DPP‑4 inhibitors, sulphonylureas, or SGLT-2 inhibitors for those who cannot take metformin.\n\t- Following initial management, consider dual therapy with metformin, pioglitazone, a DPP‑4 inhibitor or a sulphonylurea (such as gliclizide).\n\t- If dual therapy has not controlled drug glucose, triple therapy using the above medications can be considered. Otherwise, starting insulin may be necessary.\n- Close Monitoring: Measure HbA1c levels at 3-6 month intervals. If the patient is on insulin or is at risk of hypoglycaemia, self-monitoring of glucose at home is necessary.\n\n[lightgallery]\n\n[lightgallery1]\n\n[lightgallery2]\n\n[lightgallery3]\n\n[lightgallery4]\n\n\n**Insulin Therapy**\n\nNICE guidance recommends basal insulin therapy with isophane (NPH) insulin as the first type to be used as it is most cost effective eg. Insulatard. Quick acting insulin analogues eg. Humalog, Novorapid, may be added in with meals if there is a big post meal glucose excursion.\n\nLong acting insulin analogues include Levemir, Lantus, Insulin Degludec and Abasaglar (a biosimilar insulin).\n\nMixed insulin combination which contain varying proportions of short and intermediate acting insulin such as Novomix 30 (30% short acting, 70% intermediate acting insulin) are more convenient because of fewer injections per day but may not be as successful.\n\n**Blood Pressure targets in Diabetes**\n\n- Blood pressure control needs to be strict in diabetes because these patients are at higher risk of macro- and microvascular complications.\n- NICE Hypertension Guidance [CG136] sets the same blood pressure targets as those who do not have diabetes.\n\n# Complications\n\nComplications of T2DM are diverse, affecting multiple systems:\n\n1. **Gastrointestinal Complications: Gastroparesis** - a result of poor glycaemic control leading to nerve damage of the autonomic nervous system. Characterized by delayed gastric emptying, early satiety, abnormal stomach wall movements, and morning nausea.\n2. **Neurological Complications: Autonomic Neuropathy** - may lead to postural hypotension and associated symptoms like dizziness, falls, and loss of consciousness.\n3. **Vascular Complications: Peripheral Arterial Disease (PAD)** - patients present with foot discolouration, gangrene, intermittent claudication, rest pain, night pain and absent peripheral pulses (confirmed on doppler).\n4. **Foot Complications: Diabetic Foot Infections** - patients with vascular and neuropathic complications are at high risk for diabetic foot ulceration and subsequent infection.\n5. **Sexual Dysfunction** - caused by a combination of factors including poor glycaemic control, neuropathy, microvascular complications, obesity, hypertension, depression, medication side effects, etc.\n6. **Cardiac Complications** - diabetes significantly increases the risk of cardiovascular disease, contributing to major morbidity and mortality.\n\n# References\n\n[Click here for NICE CKS on diabetes type 2](https://cks.nice.org.uk/topics/diabetes-type-2/)\n",
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"question": "A 45-year-old man with a history of type 2 diabetes mellitus presents to the GP for an annual review. He has been on metformin for the past year and mentions being compliant with it. He has recently noticed consistently high blood sugars ranging between 11-14 mmol/L before meals (normal range 3.5-5.5 mmol/L). His physical examination is notable for a body mass index (BMI) of 38 kg/m2 and acanthosis nigricans. His current HbA1c is 60 mmol/mol (normal range 20-42 mmol/mol).\n\nWhich of the following medication is the most appropriate option?",
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"explanation": "This is an incorrect answer. In persons with classic diabetic symptoms such as fatigue, polydipsia, polyuria, and blurred vision, a single abnormal blood test result, either HbA1c or fasting plasma glucose, is reliable. However, as this patient is asymptomatic, a second abnormal test on another day is required to confirm the diagnosis.",
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"explanation": "This is an incorrect answer. Diagnosing T2DM based on a single abnormal test result in an asymptomatic patient is inappropriate as it depends on various other factors. Although metformin is considered the first-line agent, a confirmed diagnosis is mandatory first.",
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"explanation": "This is an incorrect answer. Diagnosing T2DM based on a single abnormal test result is inappropriate as it depends on various other factors. Insulin therapy is initiated if either oral hypoglycaemics are unsuitable or fail to control blood sugar levels despite maximum doses or there is an immediate risk of hyperglycaemia-associated complications.",
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"comment": "The abnormal test is random plasma glucose and \"all blood test results\" doesn't specify including HbA1C, so a repeat blood test finding an abnormal HbA1C would fulfill the \"two abnormal separate tests\". That's confusing because assuming the first bloods were result 1/2, it implies \"Confirm diagnosis of T2DM after an abnormal HbA1c result\" is the answer (it being results 2/2), not \"Confirm diagnosis of T2DM after an abnormal HbA1c result on two different days\"",
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This leads to an elevation in blood glucose levels, causing hyperglycaemia.\n\n# Epidemiology\n\nT2DM generally manifests in adults, and it is often associated with a strong familial predisposition. It accounts for approximately 90-95% of all diagnosed cases of diabetes.\n\n# Aetiology\n\nT2DM results from a combination of genetic and environmental factors. Known contributors include:\n\n- Poor dietary habits\n- Lack of physical activity\n- Obesity\n\n# Signs and symptoms\n\nIndividuals with T2DM may initially be asymptomatic, but over time, they may develop:\n\n- Polyuria\n- Polydipsia\n- Unexplained weight loss\n- Blurry vision\n- Fatigue\n\n# Differential diagnosis\n\nThe primary differentials for T2DM include Type 1 Diabetes Mellitus, Maturity Onset Diabetes of the Young (MODY), and Secondary Diabetes Mellitus. The main distinguishing features of these differentials are:\n\n- Type 1 Diabetes Mellitus: Early onset (typically in childhood or adolescence), often presents with ketoacidosis, and requires insulin therapy from diagnosis.\n- MODY: Early onset (typically before 25 years), non-insulin dependent, and often has a strong family history.\n- Secondary Diabetes Mellitus: Often presents with other signs of pancreatic disease (e.g., pancreatitis, cystic fibrosis), or due to certain medications (e.g., glucocorticoids, antipsychotics).\n\n# Investigations\n\nIf symptomatic, one of the following results is sufficient for diagnosis:\n\n- Random blood glucose ≥ 11.1mmol/l\n- Fasting plasma glucose ≥ 7mmol/l\n- 2-hour glucose tolerance ≥ 11.1mmol/l\n- HbA1C ≥ 48mmol/mol (6.5%)\n\nIf the patient is asymptomatic, two results are required from different days.\n\n# Management\n\nManagement of T2DM involves patient education, lifestyle modifications, pharmacological interventions, and close monitoring of glucose levels:\n\n- Lifestyle modifications: Advice on diet, regular physical activity, and smoking cessation\n- Pharmacological interventions: \n\t- Initial drug treatment is usually metformin, with consideration of other agents like Pioglitazone, DPP‑4 inhibitors, sulphonylureas, or SGLT-2 inhibitors for those who cannot take metformin.\n\t- Following initial management, consider dual therapy with metformin, pioglitazone, a DPP‑4 inhibitor or a sulphonylurea (such as gliclizide).\n\t- If dual therapy has not controlled drug glucose, triple therapy using the above medications can be considered. 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"explanation": "The evaluation of patients with tonsillitis involves using the CENTOR score, a scoring system that includes:\n\n- Fever\n- Tonsillar exudate\n- Tender cervical lymphadenopathy\n- Abscence of cough\n\nEach of these factors is assigned one point, and the total score is used to determine the likelihood of *streptococcal* *pharyngitis* or 'strep throat'. NICE guidelines advise commencing antibiotics immediately if the **CENTOR score is 3 or 4**. As her score is 3, and she is allergic to penicillins, clarithromycin is the most appropriate medication.",
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"explanation": "If the patient has a CENTOR score of 1 or 2, they are unlikely to benefit from an antibiotic, and an antibiotic prescription should not be offered. However, they may consider using the antibiotic if their sore throat has not started to improve within 3-5 days or if their symptoms worsen. They should be given the option of returning for reassessment and be advised to do so if their symptoms continue to worsen despite using the antibiotic prescription.",
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"comment": "Another question of a similar presentation indicated hospital admission...",
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"explanation": "# Summary\n \n \nTonsillitis is a condition characterised by the inflammation of the tonsils due to infection. The main signs and symptoms include sore throat, headache, fever, and lymphadenopathy. Investigation methods such as throat swabs are not routinely performed, and blood tests are reserved for patients with immunodeficiency. Management strategies primarily include treatment with paracetamol and ibuprofen, with antibiotics prescribed in certain cases.\n \n \n# Definition\n \n \nTonsillitis is a medical condition that is characterised by the inflammation of the tonsils, which are the masses of lymphoid tissue located at the back of the throat. This inflammation is primarily due to an infection.\n \n \n# Epidemiology\n \n \nSore throat is a very common presenting complaint. Cases are highest in children during the winter months.\n \n# Aetiology\n \n \nThe aetiology of tonsillitis is usually due to a viral or bacterial infection. Common viruses include the Epstein-Barr virus, influenza virus, adenovirus, and rhinovirus. Bacterial tonsillitis can be caused by Group A streptococcus, which is also responsible for strep throat.\n \n \n# Signs and Symptoms\n \n \nPatients with tonsillitis typically present with the following symptoms:\n \n \n - Sore throat\n - Headache\n - Fever (pyrexia)\n - Enlarged and tender lymph nodes (lymphadenopathy)\n - Enlarged & erythematous tonsils\n - Tonsillar exudate\n - Some people may also experience abdominal pain, and nausea & vomiting\n - There may be signs of dehydration\n \n \n# Differential Diagnosis\n \n \nWhen diagnosing tonsillitis, it's important to differentiate it from other conditions with similar symptoms such as: \n \n - **Pharyngitis:** Symptoms include sore throat, fever, and headache. Unlike tonsillitis, patients do not usually present with lymphadenopathy.\n - **Infectious mononucleosis:** Characterised by fatigue, sore throat, fever, and swollen lymph nodes. A key difference is the presence of severe fatigue and splenomegaly.\n \n \n# Investigations\n \n \nInvestigations for tonsillitis typically involve clinical examination and patient history. Additional tests such as throat swabs are only used when an alternative bacterial cause is suspected. Blood tests are primarily reserved for those with suspected immunodeficiency.\n \n## Scoring systems to predict the need of antibiotic treatment:\n \n \n### Centor Criteria\n \n \nThe Centor Criteria is a set of clinical predictors used to identify patients with Group A streptococcal pharyngitis:\n \n \n - History of fever\n - Presence of tonsillar exudates\n - Absence of cough\n - Tender anterior cervical lymphadenopathy\n \n \nPatients presenting with three or four of these criteria should be considered for antibiotic treatment.\n \nFeverPAIN criteria:\n \n - Fever\n - Purulence (exudate)\n - Attended within 3 days of symptom onset\n - Inflamed tonsils\n - No cough or coryza (suggests viral origin)\n \nA score of four or five indicates a high probability of streptococcal infection and hence the need for antibiotics.\n \n \n# Management\n \n \nManagement strategies for tonsillitis include:\n \n \n - Symptomatic treatment with paracetamol and ibuprofen\n - Antibiotic therapy in cases featuring (phenoxymethylpenicillin is first-line):\n - Marked systemic upset\n - Three or more Centor criteria, or four or more FeverPAIN criteria\n - Underlying immunodeficiency\n - Increased risk of complications \n - Clarithromycin can be used if there is penicillin allergy \n - In some cases a delayed antibiotic prescription may be indicated\n \nIf a patient appears severely unwell, dehydrated or presents with complications, refer urgently to hospital or for specialist assessment.\n \nPatients may be referred to ENT for tonsillitis if they have recurrent episodes of tonsillitis. The criteria for this is:\n \n - 7+ episodes in one year\n - 5+ episodes per year for two years\n - 3+ episodes per year for three years\n \n# Complications\n \n \nPotential complications of tonsillitis include:\n \n \n - Recurrent Tonsillitis: This is the most common complication. The evidence base for tonsillectomies as a treatment is poor, leading to stricter referral criteria.\n - Retropharyngeal Abscess: A rare complication characterised by soft tissue swelling, more common in young children. Symptoms include a stiff and extended neck and refusal to eat or drink.\n - Peritonsillar Abscess (Quinsy): Presents with sore throat, difficulty swallowing, peritonsillar bulge, uvular deviation, trismus, and muffled voice. Treatment has shifted from surgical drainage to antibiotics and aspiration.\n - Lemierre's Syndrome: In this rare complication, inflammation leads to pharyngotonsilitis, inflammation within the internal jugular vein, and septic emboli. Treatment may require high-dose benzylpenicillin and debridement.\n \n \nComplications of streptococcal tonsillitis include:\n \n - Scarlet fever\n - Acute rheumatic fever\n - Post-streptococcal glomerulonephritis\n - Reactive arthritis\n \n# NICE Guidelines \n \n[Click here for NICE CKS on sore throat - acute](https://cks.nice.org.uk/topics/sore-throat-acute/)",
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"question": "A 10-year-old girl is brought to the GP clinic complaining of a sore throat, neck pain, headache and high-grade fever for the past five days. There are no similar complaints among her family or peers. Her vaccinations are up to date, and she is allergic to penicillin. Her vital signs are normal except for an elevated temperature (39.3°C). On examination, both tonsils are enlarged, hyperaemic tonsils with pus, and tender lymph nodes in the neck.\n\nWhat is the most appropriate next step in management?",
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"explanation": "Intra-articular corticosteroid injections are used to deliver a high dose of corticosteroids directly to the joint to reduce inflammation and provide short-term pain relief. They are used in managing acute flares of joint pain rather than the initial treatment of osteoarthritis.",
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"explanation": "Diclofenac is tyically given topically and is the most appropriate initial management option for this patient's knee pain. Osteoarthritis (OA) is the most likely diagnosis, based on her clinical presentation and examination findings. OA is a degenerative joint disease that results in the erosion of cartilage in the intra-articular joints, causing joint pain and stiffness. Topical NSAIDs are the the first-line treatment for mild to moderate OA. It is effective in reducing pain and improving function in people with OA.",
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"explanation": "Allopurinol is used in gout prophylaxis. It decreases the production of uric acid and reduces the risk of kidney damage caused by high uric acid levels in the blood. Allopurinol is not used in the treatment of osteoarthritis.",
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"explanation": "Naproxen is a non-steroidal anti-inflammatory drug (NSAID) that is highly effective in treating osteoarthritis. However, oral NSAIDs are considered second-line agents in OA if both paracetamol and topical NSAIDs are ineffective.",
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"explanation": "There is no role for oral corticosteroids in the management of osteoarthritis. Corticosteroids are potent anti-inflammatory medications that are used to treat a variety of autoimmune conditions, but they are not recommended for the treatment of OA due to the potential for serious side effects and the limited effectiveness in relieving OA symptoms.",
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"comment": "literally says in the notes that NSAIDs are preffered over paracetamol in knee OA",
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"explanation": "# Summary\n\nOsteoarthritis (OA) is a chronic, degenerative joint disease characterised by loss of articular cartilage, remodelling of bone with osteophyte formation and mild synovitis. The main risk factor is older age, although obesity, joint injury and genetics also contribute. Presentation is with gradual onset pain that is worse with activity, with associated functional limitations. The most commonly affected joints are the knees, hips and small joints of the hands. Diagnosis is clinical, and severity of disease on X-ray does not correlate well with severity of symptoms. Management should be individualised, with important components being exercise, simple analgesia and optimisation of risk factors (such as maintaining a healthy weight). Where there is ongoing pain and disability, options include intra-articular steroid injections and surgical intervention (such as joint replacement).\n\n# Definition\n\nOsteoarthritis (OA) is the commonest form of arthritis, which is characterised by degenerative changes affecting the entirety of joints affected. Cartilage is lost, the subchondral bone becomes sclerosed with formation of osteophytes and subchondral cysts and there is inflammation of the synovial membrane lining the joint capsule (synovitis). \n\n# Epidemiology\n\n- Approximately 10 million people in the UK have osteoarthritis\n- More women than men are affected\n- Average age of onset is 55 \n- The commonest joint affected is the knee, followed by the hip then the hand\n\n# Aetiology\n\nOsteoarthritis develops due to a combination of factors, with important contributors including:\n\n- Older age\n- Female sex\n- Overweight or obesity\n- Family history of OA\n- Previous joint injury\n- Joint damage due to inflammation (e.g. in patients with inflammatory arthritis)\n- Physical inactivity and reduced muscle strength\n- Low bone density \n- Deformities such as development dysplasia of the hip or leg length discrepancy\n- Stresses on joints due to occupational factors (e.g. repetitive squatting or kneeling) or exercise\n\n# Signs and Symptoms\n\nKey symptoms include:\n\n- Pain in the affected joint exacerbated by use\n- Pain may radiate e.g to the thigh, knee and ankle in hip OA, or to the wrist in hand OA\n- Joints may feel stiff (although prolonged morning stiffness is suggestive of inflammatory arthritis)\n- Functional limitations such as difficulty opening jars (hand OA) or mobilising (knee or hip OA)\n- Locking or giving way of the knee\n\nExamination findings include:\n\n- Restricted and painful range of motion (e.g. in hip OA internal rotation with the hip flexed is particularly painful)\n- Crepitus (friction between bone and cartilage) \n- Affected joints may appear swollen or enlarged\n- A small effusion may form, especially when the knee is affected\n- Synovitis may present with mild soft tissue swelling, tenderness and warmth\n- Muscle wasting and weakness can result from disuse atrophy\n- Joint instability\n- An antalgic gait (\"limping\") in knee OA\n- Trendelenburg gait in hip OA (due to weak abductors patients lurch towards the affected hip)\n- Deformities, including:\n- Heberden's nodes (bony nodules over the distal interphalangeal joints) \n- Bouchard's nodes (bony nodules over the proximal interphalangeal joints) \n- Fixed flexion of the first carpometacarpal joint with hyperextension of the distal joints\n- This may lead to squaring of the joint with subluxation and remodelling\n- Ulnar or radial deviation of joints in the hand may occur\n- In severe hip OA the leg may be shortened due to fixed flexion and external rotation\n- Varus (most commonly) or valgus deformities of the knees \n\n# Differential Diagnosis\n\n- **Inflammatory arthritis** such as rheumatoid arthritis, ankylosing spondylitis; pain that improves with activity and morning stiffness lasting over 30 minutes are differentiating factors, systemic symptoms such as malaise and weight loss may be present\n- **Septic arthritis** is an important differential for all patients presenting with an acutely painful swollen joint (which may occur in an acute flare of osteoarthritis); patients may be systemically unwell with fevers\n- **Fracture** e.g. of the tibial plateau may mimic OA symptoms of pain and limited mobility; usually the patient is unable to weight bear with swelling of the affected area; a history of trauma should be elicited\n- **Malignancy** including bone metastases, multiple myeloma or sarcoma may cause mechanical pain leading to functional limitations; red flags include weight loss, night sweats, persistent pain not relieved by rest and night pain\n- **Greater trochanteric pain syndrome** most commonly occurs in middle-aged women and causes lateral hip pain and tenderness worsened by activity; it may also radiate to the lateral knee\n- **Iliotibial band syndrome** presents with lateral knee pain worse with activity, which is often accompanied by clicking or clunking sounds when the knee is moved; occurs most commonly due to repetitive knee flexion e.g. cyclists or runners \n- **Meniscal tear** may occur after an injury involving a twisting or pivoting movement; similar symptoms of pain, swelling, locking and giving way of the knee and range of motion may be limited on examination\n- **Trigger thumb** may mimic OA of the hand with pain, clicking and catching when the thumb is flexed; a nodule may be palpable in the tendon\n- **Ganglion cysts** occur more commonly in people with OA and present as soft tissue swellings e.g. at the base of the thumb; often asymptomatic but may cause pain and limit movement of the joint\n\n# Investigations\n\nDiagnosis of OA is clinical and can be made without any investigations in a patient of 45 or older if there are no features suggesting another underlying cause of symptoms.\n\nIf there is diagnostic uncertainty or a rapid deterioration in symptoms, **X-rays** of affected joints may be of use. Typical findings can be remembered with the mnemonic \"LOSS\":\n\n- **L**oss or narrowing of joint space due to thinning of cartilage\n- **O**steophytes i.e. formation of new bony spurs at the joint margins\n- **S**ubchondral sclerosis i.e. increased bone density beneath the cartilage\n- **S**ubchondral cysts which are fluid-filled sacs in the subchondral bone\n\n[lightgallery]\n\nHowever, severity of OA features on X-ray may not correlate well with severity of clinical disease.\n\nOther investigations if the diagnosis is in doubt should be targeted to the differential suspected, and may include:\n\n- Further imaging such as MRI to look for ligament or cartilage damage (e.g. a meniscal tear)\n- Joint aspiration with synovial fluid analysis to exclude septic arthritis or crystal arthritis\n- Blood tests for inflammatory markers, rheumatoid factor and anti-CCP (for example) if rheumatoid arthritis is suspected\n\nBaseline bloods for renal function and full blood count should be considered in all patients starting NSAID treatment, especially older patients who are at higher risk of adverse effects.\n\n# Management\n\n**Conservative management:**\n\n- Patient education and advice on self-care e.g. appropriate footwear\n- Weight loss advice and signposting to services in patients with excess body weight\n- Exercise has many benefits including strengthening muscles, improving fitness, reducing pain and improving function\n- Options include online fitness programmes designed for people with arthritis, physiotherapy and supervised exercise sessions\n- Physiotherapy services may also be able to offer manual therapies and joint supports such as braces or splints to reduce load and improve instability\n- Occupational health input may be needed in patients with functional impairment to assess their working environment and suggest adaptations\n- Patients should be asked about psychosocial stressors and support offered e.g. for associated depression and anxiety\n- Occupational therapy input may be helpful to advise on aids and devices to assist with activities of daily living (e.g. walking sticks, sock aids, grab rails, tap turners)\n- Podiatry input may be useful to assess the biomechanics of joint pain and advise on orthotic devices such as insoles\n- Referral to a pain management service may be appropriate for patients who have not responded to maximal medical (and if appropriate, surgical) management of OA\n- Assess falls risk and consider referral to specialist services for patients at risk (e.g. those with abnormal gait or balance, or who have had a fall in the last year)\n\n**Medical management:**\n\n- First-line analgesia is with topical NSAIDs (such as ibuprofen gel) - patients should be made aware that some systemic absorption may occur\n- If this is ineffective or unsuitable, oral NSAIDs should be considered (with a PPI for gastroprotection if there are risk factors for gastrointestinal side effects)\n- Paracetamol or weak opioids (e.g. codeine) may also be used in the short-term\n- Topical capsaicin is another option, especially for knee OA\n- Intra-articular steroid injections may be considered if other treatments are not effective, and/or to enable therapeutic exercise\n\n**Surgical management:**\n\n- Patients with OA of the hip, knee or shoulder who have symptoms significantly impacting quality of life despite optimal medical management should be considered for orthopaedic referral\n- The usual operation offered is an arthroplasty (joint replacement)\n- Rehabilitation before and after surgery is key to optimising outcomes\n\n# Complications\n\n- Joint deformities (as above)\n- Increased risk of falls\n- Functional limitations, e.g. hand OA may making writing, turning keys or fasting buttons challenging\n- Reduced mobility \n- Sleep difficulties\n- Low mood and anxiety\n- Chronic pain\n\n# Prognosis\n\n- Not all cases of OA are progressive and the disease course is variable\n- OA of the hands generally has a good prognosis, especially interphalangeal joint involvement\n- Hip OA has a poorer prognosis with many patients requiring arthroplasty\n- Knee arthroplasties for OA are also common however many patients' symptoms improve or remain stable with time \n- Intermittent flares of OA may occur, where symptoms increase in intensity suddenly\n- Flares tend to last for a few days before improving\n\n# NICE Guidelines\n\n[NICE CKS - Osteoarthritis](https://cks.nice.org.uk/topics/osteoarthritis)\n\n[NICE - Osteoarthritis in over 16s: diagnosis and management](https://www.nice.org.uk/guidance/ng226/)\n\n# References\n\n[WHO fact sheet - Osteoarthritis](https://www.who.int/news-room/fact-sheets/detail/osteoarthritis)\n\n[BNF Treatment Summaries - Osteoarthritis](https://bnf.nice.org.uk/treatment-summaries/osteoarthritis/)\n\n[Patient UK - Osteoarthritis](https://patient.info/doctor/osteoarthritis-pro)",
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"question": "A 60-year-old woman with a history of type 2 diabetes mellitus and hyperlipidaemia presents to the GP with worsening pain in both knees over the past year. The pain is exacerbated by walking and relieved by rest, and warm compresses have provided temporary relief in the past. On examination, a \"crepitus\" is heard while palpating over the knee joints bilaterally. Her body mass index is 32kgm<sup>2</sup>.\n\nWhat is the most appropriate initial treatment for her condition?",
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"explanation": "While psoriasis may also present with scaly, itchy patches on the skin, it is typically more persistent and chronic than pityriasis rosea. It is also more likely to affect other areas of the body, such as the scalp, nails, and joints. In addition, psoriasis is typically accompanied by other physical findings, such as thickened, pitted nails and red, swollen joints.",
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"explanation": "Eczema, also known as atopic dermatitis, is a chronic skin condition that typically presents with red, itchy patches on the skin. However, eczema tends to affect areas of the body that are more prone to irritation, such as the face, neck, and inner elbow, rather than the chest and abdomen. Eczema is also more likely to be chronic and persists over time rather than resolving on its own within a few weeks as pityriasis rosea does.",
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"explanation": "Tinea corporis is a dermatophyte infection of the face, trunk, and extremities. It is often confused with the herald patch of pityriasis rosea. The distinguishing features of tinea corporis are a less severe involvement of the centre of the lesion, a more active edge and itching. In contrast, circular patches of scaling and erythema are clues to pityriasis rosea.",
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"explanation": "The symptoms described in the clinical scenario are consistent with pityriasis rosea, a skin condition probably due to human Herpesviruses 6 and 7. It typically starts with a single patch (herald patch) on the trunk or neck, which is oval, 2-5cm in size, and has a central, salmon-coloured area and a dark-red peripheral zone separated by fine scales. A secondary rash of smaller patches follows, with a \"Christmas tree\" distribution on the trunk, neck, and upper limbs.",
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"explanation": "# Summary\n\nPityriasis rosea is a common rash that is characterized by a preceding **herald patch** - a single, large, discoid (coin-shaped), erythematous patch. This patch classically has a 'collarette' of scale just inside the edge of the lesion. A few days later a widespread rash appears across the trunk consisting of multiple small, erythematous, scaly patches (similar but smaller than the herald patch). These lesions are classically distributed across the trunk in a **'christmas tree' pattern**. There are associations with viral infections and drugs. The condition is self-limiting and resolves without any treatment.\n\n# Definition\n\nA self-limiting rash that resolves after 10 weeks characterised by a herald patch and subsequent fir-tree pattern eruption\n\n# Pathophysiology\n\nTriggers of pityriasis rosea:\n\n- Viruses: such as HHV6/7, COVID-19, and Flu\n- Drugs: such as gold, ACEi, penicillamine, and biologics. \n- Many vaccines: BCG, hepatitis B, and pneumococcal. \n\t\n# Clinical Features\n\n- Usually, a few days after a viral infection e.g. an URTI, the patient presents with a 'herald patch.'\n- This is a red-pink oval/discoid plaque with a peripheral colarette of scale on the trunk or upper arm/thigh. It may be misdiagnosed as ringworm.\n- 1-20 days later, a similar widespread eruption (but the individual lesions may be smaller) occurs on the body that follows a fir tree (Christmas tree) pattern appears, with the long axis of the lesions sweeping from back to front as if following Langer's lines.\n- In most cases, there are virtually no symptoms except for the rash.\n\n[lightgallery]\n[lightgallery1]\n[lightgallery2]\n\n\n# Treatment\n\n- 25% patients may have intense pruritus. Antihistamines, emollients, and topical steroids may be of use in these patients. It is self-limiting and will resolve on its own. \n\n# NICE Guidelines\n\n[Click here for NICE CKS on pityriasis rosea](https://cks.nice.org.uk/topics/pityriasis-rosea/)",
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"question": "A 30-year-old woman presents to the GP clinic with a mildly itchy rash on her chest and abdomen, which consists of pink scaly patches. The patient reports that the rash appeared suddenly about a week ago and has not improved since. On examination, the rash is salmon-coloured, oval, and has a surrounding ring of scale. It has a characteristic \"Christmas tree\" distribution.\n\nWhat is the most likely diagnosis?",
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"explanation": "Watchful waiting may be suitable for men with slowly progressing tumours or significant comorbidities who are likely to die of other causes and not suffer significant morbidity from prostate cancer. However, it is not the appropriate choice as the diagnosis of prostate carcinoma is not yet confirmed.",
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"explanation": "PSA test is offered in individuals whose DRE findings are inconclusive. It is not an effective screening tool for prostate cancer because it is not sensitive or specific enough. Moreover, it is an inaccurate marker for prostate cancer as it is elevated in several non-cancerous conditions.",
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"explanation": "TURP is primarily indicated for treating benign prostatic hyperplasia (BPH), a non-malignant condition characterised by overgrowth of the prostate gland. TURP is not indicated for the treatment of prostate cancer due to its limited extent and inability to eradicate malignant cells.",
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"explanation": "Advanced age and a positive family history increase the likelihood of developing prostate cancer. The abnormal findings on the DRE are consistent with prostate carcinoma. **NICE guidelines suggest referring the person for further evaluation through a suspected cancer pathway referral (within two weeks) if there are signs of malignancy on DRE.**",
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"explanation": "Transrectal ultrasonography can evaluate the prostate gland for abnormalities, such as cancer. However, transrectal ultrasonography has a high false-positive rate which makes it unsuitable as a screening tool for prostate cancer, as it would generate too many false positives and lead to unnecessary follow-up tests and treatment. It may still be helpful in directing prostatic biopsy.",
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"explanation": "# Summary\n\nProstate cancer is a common malignancy affecting males, particularly in Western societies. It is characterised by abnormal growth of cells in the prostate gland and can be asymptomatic in early stages. Advanced disease may manifest as urinary issues, pelvic discomfort, bone pain, and erectile dysfunction. The primary investigations are digital rectal examination and a urine dip, with PSA (Prostate Specific Antigen) testing, which carries issues of sensitivity and specificity. MRI is a key tool for assessment, alongside a Gleason score for grading biopsy samples. Management ranges from active surveillance for low-grade disease to hormonal therapy and surgery for more advanced cases.\n\n# Definition\n\nProstate cancer is a malignant tumour that arises from the cells of the prostate, a small walnut-sized gland that produces seminal fluid in men. This condition varies greatly in its presentation, with some cases growing slowly and requiring minimal treatment, while others are aggressive and can spread quickly.\n\nThe majority of prostate cancers are adenocarcinomas, and they usually primarily affect the peripheral prostate. They spread lymphatically first via the obturator nodes.\n\n\n# Epidemiology\n\nProstate cancer is responsible for approximately 48,000 new diagnoses each year in the UK, accounting for 13% of all cancer cases. It is the second most prevalent cancer among men globally, preceded only by lung cancer.\n\n\n# Aetiology\n\n### Non-modifiable risk factors\n\n- African ethnicity\n- BRCA gene mutations\n- Family history of prostate cancer\n- Age (risk increases with advancing age)\n\n### Modifiable risk factors\n\nResearch into modifiable risk factors is ongoing. Some potential factors are:\n\n- Obesity\n- Smoking\n- Diet rich in animal fats and dairy products\n\n# Signs and Symptoms\n\nIn its early stages, prostate cancer often produces no symptoms as it affects the peripheral prostate. However, as the disease progresses with local advancement (which can cause compression of the urethra), symptoms may include:\n\n- Urinary symptoms, including difficulty initiating or stopping urination\n- Poor urine stream\n- Haematospermia (blood in semen)\n- Pelvic discomfort\n- Bone pain, potentially indicating metastatic disease\n- Erectile dysfunction\n\n# Differential Diagnosis\n\nSeveral conditions can mimic the symptoms of prostate cancer and should be considered during evaluation:\n\n- Benign Prostatic Hyperplasia (BPH): Characterised by difficulty in urination, increased frequency of urination, nocturia, and potentially, haematuria.\n- Prostatitis: Acute or chronic inflammation of the prostate that can cause pelvic pain, urinary symptoms, and potentially, systemic symptoms such as fever and malaise.\n- Urinary Tract Infection (UTI): Can cause dysuria, urinary frequency, urgency, and potentially, systemic signs of infection.\n- Bladder cancer: May present with haematuria, dysuria, and urinary frequency.\n\n# Investigations\n\n* Initial examination should include a digital rectal examination and a urine dip.\n\t* An asymmetrical hard/craggy/nodular prostate with loss median sulcus is suspicious for malignancy.\n* A PSA blood test may be considered, despite its lack of sensitivity and specificity. This necessitates patient counselling about the potential for over-investigation and over-treatment. Causes of a falsely raised PSA include:\n\t* An active urinary infection or within previous 6 weeks.\n\t* Ejaculation in previous 48 hours.\n\t* Vigorous exercise, for example cycling, in the previous 48 hours.\n\t* Urological intervention such as prostate biopsy in previous 6 weeks.\n\nInterpretation of PSA results:\n\n| Age (years) | Prostate-specific antigen threshold (micrograms/L) |\n|-------------|--------------------------------------------------|\n| Below 40 | Use clinical judgement |\n| 40–49 | More than 2.5 |\n| 50–59 | More than 3.5 |\n| 60–69 | More than 4.5 |\n| 70–79 | More than 6.5 |\n| Above 79 | Use clinical judgement |\n\n\n* **Multi-parametric MRI** is the gold standard radiological investigation, and can show specific areas which can be targetted for biopsy. If metastatic disease is suspected, additional imaging such as CT scans (can show e.g. sclerotic bony lesions) and bone isotope scans may be required.\n* The Gleason grading system is used to assess prostate cancer severity on initial biopsy. It involves analysing the morphological features of prostatic tissue and assigning a score from 1 (normal tissue) to 5 (very poorly differentiated cells). The sum of the two most common scores represents the Gleason score, which has prognostic value.\n\n### 2 week wait referral criteria\n\n- Refer if their prostate feels malignant on DRE.\n- Consider referring a person with possible symptoms of prostate cancer using a suspected cancer pathway referral (for an appointment within 2 weeks) if their PSA level is above the threshold for their age (see above)\n\n# Classification\n\nThe TNM staging system for prostate cancer provides a standardised way to describe the extent of the disease based on three key parameters: tumour size and extent (T), involvement of regional lymph nodes (N), and the presence of distant metastasis (M).\n\n- **T (Tumour):**\n - **T1:** The tumour is not palpable or visible by imaging.\n - T1a: Tumour found incidentally in less than 5% of tissue removed.\n - T1b: Tumour found incidentally in more than 5% of tissue removed.\n - T1c: Identified by needle biopsy due to elevated PSA (prostate-specific antigen) levels.\n - **T2:** The tumour is confined to the prostate.\n - T2a: Tumour involves half or less of one side of the prostate.\n - T2b: Tumour involves more than half of one side but not both sides.\n - T2c: Tumour involves both sides.\n - **T3:** The tumour extends beyond the prostate.\n - T3a: Tumour extends through the prostate capsule.\n - T3b: Tumor invades seminal vesicle(s).\n - **T4:** The tumour invades adjacent structures other than seminal vesicles (e.g., bladder, rectum).\n\n- **N (Lymph Nodes):**\n - **N0:** No regional lymph node involvement.\n - **N1:** Regional lymph node involvement.\n\n- **M (Metastasis):**\n - **M0:** No distant metastasis.\n - **M1:** Distant metastasis present.\n - M1a: Non-regional lymph nodes.\n - M1b: Bones.\n - M1c: Other sites or multiple sites.\n\n\n# Management\n\nHere is a summary table demonstrating management approaches according to TNM staging:\n\n| TNM Stage | Management Options |\n|--------------------------|--------------------------------------------------------|\n| T1 (T1a, T1b, T1c) | Active surveillance (for low-risk cases) |\n| | Watchful waiting |\n| | Radical prostatectomy (for selected cases) |\n| T2 (T2a, T2b, T2c) | Radical prostatectomy (standard treatment) |\n| | External beam radiation therapy |\n| | Brachytherapy (seed implantation) |\n| | Active surveillance (for low-risk cases) |\n| T3 (T3a, T3b) | Hormonal therapy (to delay progression) |\n| | Radical prostatectomy (selected cases) |\n| | External beam radiation therapy |\n| T4 | Hormonal therapy (palliative, delays progression) |\n| | Radiation therapy (palliative) |\n| | Symptomatic management |\n| Not Fit for Radical Prostatectomy | Hormonal therapy (palliative) |\n| Metastatic (M1) | Hormonal therapy (androgen deprivation) |\n| | Chemotherapy (docetaxel, cabazitaxel) |\n| | Targeted therapy (abiraterone, enzalutamide) |\n| | Immunotherapy (sipuleucel-T) |\n\n\n## Active Surveillance\n\nThis approach is suitable for patients with low-grade prostate cancer and involves repeating investigations periodically to monitor disease progression.\n\n## Radiotherapy\n\nRadiotherapy can be used either as a curative measure or for palliation to reduce tumour bulk and associated pain.\n\n## Surgical Management\n\nSurgical removal of the prostate and any affected organs is an option for patients without metastatic disease. Minimally invasive techniques such as robotically assisted laparoscopic prostatectomy (RALP) are becoming more common.\n\n## Hormonal Management\n\nHormonal therapies aim to reduce testosterone levels, slowing the progression of metastatic prostate cancer. This can be achieved with GnRH analogues, androgen antagonists, or GnRH antagonists. \n\nHormonal therapies may cause sexual side effects, including decreased libido, impotence, infertility, and gynecomastia. Metabolic side effects include weight gain, osteoporosis, diabetes, and ischemic heart disease. Haematological side effects include anaemia.\n\n# NICE Guidelines\n\n[Click here for the NICE Guidelines](https://www.nice.org.uk/guidance/ng131)",
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"question": "A 79-year-old man without any active complaints visits his GP because he worries about prostate cancer. His father was diagnosed with prostate cancer at the same age. His vital signs, blood tests and previous colonoscopy results are all normal. A digital rectal examination (DRE) reveals an asymmetrically enlarged, immobile, hard and indurated prostate gland.\n\nWhat is the most appropriate next step in management?",
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"explanation": "The patient is experiencing recurrent vaginal bleeding after many years of attaining menopause, which can be a sign of endometrial cancer. **NICE guidelines recommend a 2 week wait suspected cancer pathway referral for women aged 55 years and over with postmenopausal bleeding (unexplained vaginal bleeding more than 12 months after menstruation has stopped because of the menopause).**",
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"explanation": "This patient's cervical smear was already performed three years ago and was unremarkable, which makes the possibility of cervical cancer less likely. Therefore, repeating the cervical smear would not be an appropriate next step in management.",
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"explanation": "Although HRT helps with her postmenopausal symptoms (such as hot flushes, vaginal dryness, reduced sex drive, etc.,) which she might be currently experiencing, there isn't any evidence stating that it increases the chance of endometrial cancer, or otherwise causes post-menopausal bleeding. Hence, it is not the appropriate choice.",
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"explanation": "The patient is experiencing bleeding after intercourse, which is not a typical symptom of menopause and can be a sign of a more serious underlying condition such as endometrial cancer. Delaying the referral and treatment for six months would not be appropriate and could potentially allow the condition to progress.",
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"explanation": "Tranexamic acid is a medication that is used to treat heavy menstrual bleeding (menorrhagia). However, in this case, the patient is experiencing bleeding after intercourse, which is not a typical symptom of menorrhagia. Additionally, the patient is postmenopausal and has not had a period in nine years. Therefore, prescribing tranexamic acid would not be an appropriate next step in management.",
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"explanation": "# Summary\n \n \nPostmenopausal bleeding is an important symptom that requires thorough investigation due to the potential for serious underlying pathology, such as endometrial cancer. The primary investigations include referral to gynaecology, transvaginal ultrasound, and biopsy of the endometrium. Management strategies will be determined based on the underlying cause of the bleeding. \n \n \n# Definition\n \nPostmenopausal bleeding is any vaginal bleeding that occurs after a patient has not experienced periods for 12 months or more, and who are not receiving hormone therapy. If a woman is receiving hormone replacement therapy (HRT), bleeding is considered postmenopausal if it occurs more than 6 months after menstruation has stopped.\n \n \n# Aetiology\n \nThe most common causes of postmenopausal bleeding include:\n\n* Endometrial atrophy\n* Vaginal atrophy\n* Endometrial polyps\n* Uterine fibroids\n* Endometrial cancer. \n\nOther less common causes include cervical cancer, ovarian tumours and certain medications, such as hormone replacement therapy (HRT) and anticoagulants.\n \n \n# Signs and symptoms\n \n \nFurther symptoms to postmenopausal bleeding will depend on the underlying cause, but may include pelvic pain, weight loss, and systemic symptoms of malignancy.\n \n \n# Differential Diagnosis\n \n \n - **Endometrial cancer:** Often the only symptom is postmenopausal bleeding.\n - **Vaginal atrophy:** Can also cause pruritus, dyspareunia, and vaginal discharge.\n - **Cyclical combined HRT:** Causes regular vaginal bleeding. With continuous HRT, it is common to experience breakthrough bleeding in the first 6 months.\n - **Bleeding disorders:** May be suggested if there is frequent bleeding elsewhere (e.g. recurrent epistaxis) or a family history of a bleeding disorder.\n \n \n# Investigations\n \nAll cases of postmenopausal bleeding should be referral to gynaecology under the 2-week wait pathway. \n\nThe gynaecologist will likely consider the following investigations: \n\n**Bedside:**\n\n- Bimanual and speculum examination\n\n**No blood tests** are required for diagnosis in the first instance, though if underlying bleeding/clotting disorders are suspected a clotting screen would be indicated. \n\n**Imaging:**\n\n - Transvaginal ultrasound to look for abnormal thickening of the endometrium\n - CT CAP: performed following diagnosis of endometrial cancer, for FIGO staging \n\n**Special tests:**\n\n - Biopsy of the endometrium, obtained via hysteroscopy or pipelle\n\n**2 Week Wait Criteria**\n\n- All cases of postmenopausal bleeding in women aged 55 or older should be referred to gynaecology under a 2-week wait. \n\n- In women aged under 55, a 2-week wait referral should also be considered.\n\n- For those not referred in the immediate instance who have a TV USS performed, refer under 2-week wait if endometrial thickness is >4mm, or if otherwise high clinical suspicion of endometrial cancer remains. \n\n \n# Management\n \n \nThe management of postmenopausal bleeding is guided by the underlying cause. This may include hormonal therapy for conditions such as endometrial atrophy, surgical interventions for polyps or cancers, or supportive care for symptoms related to vaginal atrophy. In all cases, ongoing monitoring is essential to ensure that treatment is effective and to detect any changes in the patient's condition.\n\n\n# NICE Guidelines\n\n[Click here for NICE guidelines on Gynaecological Cancers](https://cks.nice.org.uk/topics/gynaecological-cancers-recognition-referral/)\n\n# References\n\n[Patient Info: Postmenopausal bleeding](https://patient.info/doctor/postmenopausal-bleeding)",
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"question": "A 58-year-old woman presents to the GP complaining of bleeding after having intercourse for the past year. She has had ten episodes of mild vaginal bleeding in the past six months. She had regular periods until nine years ago and has not had bleeding in the last six years. She is currently on hormone replacement therapy (HRT). Otherwise, her past medical history is insignificant. Her cervical smear was unremarkable three years ago. A speculum examination shows a normal cervix and vagina.\n\nWhat is the most appropriate next step in management?",
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"explanation": "Staphylococcal skin infections are not a notifiable disease.",
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"explanation": "Food poisoning of any cause is a notifiable disease. It is a statutory obligation to notify UK Health Security Agency (formerly Public Health England). In the UK, notifiable diseases are a list of infectious and non-infectious conditions that healthcare professionals and laboratories are required to report. The purpose of this reporting system is to monitor the occurrence and spread of these diseases in the population and to take appropriate public health action to prevent and control their transmission.",
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"explanation": "# Summary\n \nGastroenteritis is an enteric infection causing acute-onset diarrhoea, sometimes with additional symptoms. Food poisoning results from consuming contaminated substances, while acute diarrhoea involves three or more liquid or semi-liquid stools in 24 hours, lasting less than 14 days. Prolonged diarrhoea lasts over 14 days, and dysentery is acute infectious diarrhoea with blood and mucus. Infectious diarrhoea is commonly spread via the faeco-oral route and often caused by viruses like norovirus, rotavirus, and adenovirus. Bacterial causes include Campylobacter, E. coli, Salmonella, Cholera, Shigella, and Yersinia. Parasites like Cryptosporidium, Entamoeba histolytica, and Giardia can also cause prolonged diarrhoea. Symptoms include sudden-onset diarrhoea, nausea, vomiting, fever, and abdominal pain. Diagnosis often involves assessing hydration status and may require stool cultures or blood tests. Treatment includes rehydration and, in some cases, antimicrobials. Preventative measures include proper food hygiene and handwashing. Certain infections must be reported to health authorities. High-risk groups include young children, the elderly, immunocompromised individuals, and pregnant women, who may face complications such as dehydration, haemorrhagic colitis, and sepsis.\n \n# Definition\n \n **Gastroenteritis:** an enteric infection causing acute-onset diarrhoea, with or without associated symptoms\n \n **Food poisoning:** illness caused by eating or drinking substances contaminated with disease-causing pathogens, toxins or chemicals.\n \n **Acute diarrhoea:** 3+ episodes liquid/semi-liquid stools in in a 24h period, lasting less than 14 days\n \n **Prolonged diarrhoea:** acute-onset diarrhoea lasting over 14 days\n \n **Dysentery:** is acute infectious diarrhoea with blood & mucus, often with associated symptoms\n \n# Aetiology\n \nMost cases of infectious diarrhoea are spread by the faeco-oral route and are caused by viruses. These include:\n \n - **Norovirus:** **most common** cause in the population, and often causes outbreaks. Typically causes projectile vomiting and non-bloody diarrhoea.\n - **Rotavirus:** the most common cause of gastroenteritis in children.\n - **Adenovirus:** typically causes respiratory tract infections but may cause gastrointestinal symptoms in children.\n \nBacteria causing infectious diarrhoea include:\n \n - **Campylobacter**: often associated with contaminated food & drink (in exams: a recent barbeque!), this is the most common cause of bacterial gastroenteritis in the UK. On microscopy, gram-negative rods are seen with characteristic 'seagull' shape, which release enterotoxin in the gut and invade the mucosa. Incubation period is 1 - 5 days and may cause bloody diarrhoea, though vomiting is rare.\n - **E. coli**: the most common cause of traveller's diarrhoea. In the UK, O157:H7 is the most common type and may cause bloody diarrhoea. Sources include improperly cooked meat. Associated complications include haemolytic uraemic syndrome, which typically affects the very young are old and can be fatal.\n - **Salmonella** is associated with consumption of contaminated foods, particularly poultry, eggs and milk. These are gram negative bacteria with an incubation of 16-48 hours. *Salmonella* can cause bloody diarrhoea and is associated with complications such as sepsis, endocarditis, mycotic aneurysm and osteomyelitis.\n - **Cholera** is associated with contaminated water supplies and causes very watery diarrhoea associated with dehydration.\n - **Shigella** and *Yersinia* tend to occur in children. The former can cause severe, bloody diarrhoea.\n - **Bacillus cereus** are gram-positive rods that produce two toxins causing diarrhoea and vomiting within hours of eating contaminated food (in exams, this is usually reheated rice).\n - **Staphylococcus aureus** produces a heat-stable enterotoxin that causes profuse vomiting with mild diarrhoea and abdominal pain. The incubation period is short (under 6 hours) after eating contaminated foods. The bacteria are usually introduced from the skin of the person preparing the food. Foods which do not require cooking carry greater risk.\n \nParasites can be spread by ingestion of contaminated food/drink or from person to person, and often associated with recent travel.\n \n - **Cryptosporidium**: a protozoal infection which may cause prolonged symptoms\n - **Entamoeba histolytica**: most cases are mild but severe cases cause dysentery\n - **Giardia**: causing diarrhoea, constitutional symptoms and bloating which may be prolonged\n \n# Signs and Symptoms\n \nSymptoms include:\n \n - Sudden-onset diarrhoea, with or without blood\n - Faecal urgency\n - Nausea & vomiting\n - Fever, malaise\n - Abdominal pain\n - Associated symptoms specific to the cause\n \n \n# Differential Diagnosis\n \n - ***Clostridium difficile*** infection, causing antibiotic-associated (in particular, cephalosporins) diarrhoea. Patients usually have predisposing risk factors such as recent antibiotics, immunocompromise or PPI use. Typically causes foul-smelling diarrhoea and can cause severe systemic upset and GI complications.\n - Other causes of **diarrhoea**, including irritable bowel syndrome, inflammatory bowel disease, malignancy, endocrine conditions such as thyrotoxicosis. These usually have a more prolonged history and may be associated with other systemic symptoms (except IBS).\n - Other causes of **abdominal pain**, such as appendicitis, intestinal obstruction, diverticulitis, pancreatitis. These are associated with other symptoms such as absolute constipation and vomiting (obstruction) or pain relieved on leaning forward (pancreatitis). Often, there is also more systemic upset and deranged blood tests.\n \n# Investigations\n \n - Often, infectious diarrhoea is a clinical diagnosis and, providing the patient is not systemically unwell, may not need further investigation. \n - It is important to assess hydration status and consider whether the person can tolerate oral fluids.\n - A stool culture may be needed if there are any higher risk features. These include if the person is systemically unwell, is immunocompromised, presents with dysentery or prolonged diarrhoea, there is increased risk of transmission, food poisoning is suspected or symptoms are associated with recent travel.\n - If a person is unwell presenting to secondary care, consider performing blood tests to include FBC, U&Es, CRP, LFTs and TFTs. \n - Consider a VBG, blood cultures and monitoring urine output if they appear septic.\n \n \n# Management\n \n - If a person is systemically unwell, or severely dehydrated, adopt an A-E approach and consider initiating the sepsis six. Admit the patient and seek senior help early. They may need IV fluids, antiemetics or antibiotics.\n - Conservative: advise regular fluids, with or without rehydration salts, and safetynet for signs of dehydration. Antidiarrhoeal drugs are not routinely used, and should be avoided if the patient has symptoms of dysentery or suspected *E. coli 0157*.\n - Medical: antimicrobials are not routinely indicated, but clinical suspicion or positive cultures of the following may prompt initiation of antibiotics:\n \n - *Campylobacter*: macrolide e.g. clarithromycin\n - *Amoeba, Giardia*: anti-protozoal e.g. metronidazole\n - *Cholera*: tetracycline\n \n - If a patient is systemically unwell, immunosuppressed or elderly, consider empirical antibiotics following local pathways and microbiology advice.\n \n - Infectious diarrhoea can be prevented by avoiding foods that are undercooked or prepared in unsanitary conditions, and handwashing at appropriate times and hygiene measures. \n - Enhanced precautions such as isolation and barrier nursing along with handwashing can prevent spread in clinical settings. People should not return to work until 48 hours after their symptoms have resolved.\n \nThe following are notifiable diseases, and should be reported to the local health protection scheme:\n \n - Food poisoning\n - Haemolytic uraemic syndrome\n - Dysentery\n - Enteric fever\n - Cholera\n \n# Complications\n \nYoung children, elderly, people with comorbidities or immunocompromised and pregnant women are at highest risk of complications. These include:\n \n - Dehydration, electrolyte disturbance, acute kidney injury\n - Haemorrhagic colitis, haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura\n - Reactive arthritis\n - Toxic megacolon\n - Sepsis\n \nLonger-term complications include: faltering growth, irritable bowel syndrome and lactose intolerance.\n \nSpecific complications may occur depending on the causative organism.\n \n# NICE Guidelines\n [NICE CKS: Gastroenteritis](https://cks.nice.org.uk/topics/gastroenteritis/)",
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"question": "You have just reviewed five different patients presenting with a primary complaint of diarrhoea and subsequently diagnosed them with the following conditions: *Amoebiasis, Norovirus, Cystoisosporiasis*, *Campylobacter* (food poisoning), and *Giardiasis*.\n\nWhich one of the following would have to be notified to the consultant responsible for infectious disease control?",
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"explanation": "The QRISK2 is an online calculation to estimate the patient's chance of having a cardiovascular event in the next 10 years. If the risk is 10% or higher then the patient can be offered a statin to decrease the risk, known as primary prevention of cardiovascular events.\n\nThe amount the risk would fall by would be dependent on the effectiveness of the statin with the aim being a 40% reduction in non-HDL-C levels. A higher dose statin may be required as well as lifestyle modification to reduce this risk.",
"id": "62361",
"label": "d",
"name": "The patient's risk of having a cardiovascular event can be decreased by 20% by treatment with a statin",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "The QRISK score specifically looks at the risk of cardiovascular events occuring for an individual over 10 years.",
"id": "62359",
"label": "b",
"name": "There is a 20% chance of this patient having a cardiovascular event in the next 20 years",
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"explanation": "The QRISK score is used to predict the likelihood of someone having a cardiovascular event over the next 10 years, it does not predicit morbidity or mortality.",
"id": "62362",
"label": "e",
"name": "The patient an 80% of chance of surviving a cardiovascular event in the next 10 years",
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"explanation": "The QRISK2 is an online calculation to estimate the patient's chance of having a cardiovascular event in the next 10 years. It is used for those under the age of 85 years, and who do not have type 1 diabetes, familial hypercholesterolaemia or chronic kidney disease as these are already considered higher risk for cardiovascular events.\nPatients with a QRISK score of 10% or more should be offered lifestyle advice such as weight loss, smoking cessation and increased exercise. A statin (atorvastatin 20mg is first line) should be offered for primary prevention of cardiovascular disease if lifestyle modification is unsuccessful or inappropriate to offer.",
"id": "62358",
"label": "a",
"name": "There is a 20% chance of this patient having a cardiovascular event in the next 10 years",
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"explanation": "The QRISK score is used to predict the likelihood of someone having a cardiovascular event over the next 10 years, it does not predicit morbidity or mortality.",
"id": "62360",
"label": "c",
"name": "There is a 20% chance mortality risk in the next 10 years from a cardiovascular event",
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"explanation": "# Definition\n\nHypercholesterolaemia is the term used to denote raised serum levels of one or more of total cholesterol.\n\n# Causes\n\nCauses can primary or secondary.\n\nSecondary causes include:\n\n- Familial dyslipidaemias\n- Familial hypercholesterolaemia\n- Apoprotein disorders\n- Medical conditions\n\t- Hypothyroidism\n\t- Obstructive jaundice\n\t- Cushings syndrome\n\t- Nephrotic syndrome\n\t- Chronic Kidney Disease\n- Drugs e.g. thiazide diuretics, glucocorticoids, ciclosporin\n- Pregnancy\n- Obesity \n- Alcohol abuse\n\n\n# Physicial signs\n\nDiagnosis is usually biochemical. \n\nThere are two key physical signs which may indicate familial hypercholesterolaemia\n\n - Premature arcus senilis\n - Tendon xanthomata\n\n# Investigations\n\n- Lipid profile \n- Fasting blood glucose\n- Renal function\n- Liver function tests\n- Thyroid function tests\n\n# Management\n\n\n## Statins\n\n- Statins are the first line treatment of high cholesterol. \n- They are HMG-CoA reductase inhibitors. \n- This enzyme plays a key role in the production of cholesterol, so inhibiting it reduces the cholesterol in the body.\n- In patients with high cholesterol, the QRISK score is used to see if they would benefit from statins as primary prevention against cardiovascular disease. \n- If an adult is under 80 years old and their QRISK is greater than 10% then a statin should be offered. \n- For primary prevention of CVD aim for a greater than 40% reduction in non-HDL cholesterol\n- For secondary prevention of CVD, aim for low-density lipoprotein (LDL) cholesterol levels of 2.0 mmol per litre or less, or non-HDL cholesterol levels of 2.6 mmol per litre or less.\n\n## Doses\n\n- Atorvastatin 20mg is the usual starting dose for primary prevention.\n- For patients who need a statin as secondary prevention, e.g following a stroke, heart attack, peripheral arterial disease or angina, atorvastatin at 80mg starting dose should be used.\n\n## Side effects of statins\n\n\nCommon side effects of statins include muscle pain, abdominal pain, constipation and headache.\n\nIf a patient is struggling with significant myalgia, this may indeed indicate a myositis. Creatinine Kinase can be measured and if it is 5-10 times the upper limit of normal, the statin should be stopped. \n\nStatins can also cause abnormal liver function so this should be monitored with a repeat blood test in 4-6 weeks time. If the transaminases (ALT, AST) are 3 times the upper limit the statin should be stopped.\n\nOffer ezetimibe instead of a statin to people for whom statins are contraindicated/cause abnormal blood test results.\n\n# NICE Guidelines\n\n[NICE Guidelines - Cardiovascular disease: risk assessment and reduction, including lipid modification ](https://www.nice.org.uk/guidance/ng238/chapter/Recommendations)",
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"question": "A 52 year old male attends his GP surgery for a general review. As part of this his assessent, his QRISK2 score is calculated which is 20%.\n\nThe patient wants to know what this means.\n\nWhich of the following is the best description of the patient's QRISK2 score?",
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"explanation": "Statins inhibit of HMG-CoA reductase, the enzyme responsible for cholesterol synthesis as well as lipid and low density lipoprotein (LDL) metabolism and transport.",
"id": "62365",
"label": "c",
"name": "Activation of HMG-CoA reductase",
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"explanation": "HMG-CoA reductase is the key enzyme in cholesterol production in the liver, as well as lipid and low density lipoprotein (LDL) metabolism and transport.\nHyperlipidaemia is associated with increased risk of cardiovasculardisease.",
"id": "62363",
"label": "a",
"name": "Inhibition of HMG-CoA reductase",
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"explanation": "A statin lowers cholesterol by inhibiting HMG-CoA reductase, the key enzyme in cholesterol production in the liver, as well as lipid and low density lipoprotein (LDL) metabolism and transport.\nLipase inhibitors such as Orlistat can be used in weight loss management. It is an inhibitor of gastrointestinal lipase, therefore inhibiting the hydrolysis of triglycerides, therefore prevening their absorption and helping weight loss.",
"id": "62367",
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"id": "62366",
"label": "d",
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"explanation": "ACE inhibitors such as ramipril are used in the treatment of hypertension.\nStatins are HMG-CoA reductase inhibitors.",
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"explanation": "# Definition\n\nHypercholesterolaemia is the term used to denote raised serum levels of one or more of total cholesterol.\n\n# Causes\n\nCauses can primary or secondary.\n\nSecondary causes include:\n\n- Familial dyslipidaemias\n- Familial hypercholesterolaemia\n- Apoprotein disorders\n- Medical conditions\n\t- Hypothyroidism\n\t- Obstructive jaundice\n\t- Cushings syndrome\n\t- Nephrotic syndrome\n\t- Chronic Kidney Disease\n- Drugs e.g. thiazide diuretics, glucocorticoids, ciclosporin\n- Pregnancy\n- Obesity \n- Alcohol abuse\n\n\n# Physicial signs\n\nDiagnosis is usually biochemical. \n\nThere are two key physical signs which may indicate familial hypercholesterolaemia\n\n - Premature arcus senilis\n - Tendon xanthomata\n\n# Investigations\n\n- Lipid profile \n- Fasting blood glucose\n- Renal function\n- Liver function tests\n- Thyroid function tests\n\n# Management\n\n\n## Statins\n\n- Statins are the first line treatment of high cholesterol. \n- They are HMG-CoA reductase inhibitors. \n- This enzyme plays a key role in the production of cholesterol, so inhibiting it reduces the cholesterol in the body.\n- In patients with high cholesterol, the QRISK score is used to see if they would benefit from statins as primary prevention against cardiovascular disease. \n- If an adult is under 80 years old and their QRISK is greater than 10% then a statin should be offered. \n- For primary prevention of CVD aim for a greater than 40% reduction in non-HDL cholesterol\n- For secondary prevention of CVD, aim for low-density lipoprotein (LDL) cholesterol levels of 2.0 mmol per litre or less, or non-HDL cholesterol levels of 2.6 mmol per litre or less.\n\n## Doses\n\n- Atorvastatin 20mg is the usual starting dose for primary prevention.\n- For patients who need a statin as secondary prevention, e.g following a stroke, heart attack, peripheral arterial disease or angina, atorvastatin at 80mg starting dose should be used.\n\n## Side effects of statins\n\n\nCommon side effects of statins include muscle pain, abdominal pain, constipation and headache.\n\nIf a patient is struggling with significant myalgia, this may indeed indicate a myositis. Creatinine Kinase can be measured and if it is 5-10 times the upper limit of normal, the statin should be stopped. \n\nStatins can also cause abnormal liver function so this should be monitored with a repeat blood test in 4-6 weeks time. If the transaminases (ALT, AST) are 3 times the upper limit the statin should be stopped.\n\nOffer ezetimibe instead of a statin to people for whom statins are contraindicated/cause abnormal blood test results.\n\n# NICE Guidelines\n\n[NICE Guidelines - Cardiovascular disease: risk assessment and reduction, including lipid modification ](https://www.nice.org.uk/guidance/ng238/chapter/Recommendations)",
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"question": "A 62 year old female is prescribed a statin for primary prevention of cardiovascular disease.\n\nWhich of the following describes the main mechanism of action of statins?",
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"explanation": "Type 2 diabetics on drug therapy that is not associated with hypoglycaemia (such as metformin, like in this case) should aim for an HbA1c of 48mmol/mol.",
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"explanation": "Type 2 diabetics on drug therapy that is not associated with hypoglycaemia (such as metformin) should aim for an HbA1c of 48mmol/mol.\n\nIn this case, the patient should be offered further diet and lifestyle support, as well as an increase in their medication; an increase in the dose of metformin or the addition of another drug.",
"id": "62368",
"label": "a",
"name": "48mmol/mol",
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"explanation": "Whilst targets should be discussed and agreed with the patient to form an individualised target, in general the HbA1c should be 48mmol/mol for those on drug therapy not associated with hypoglycaemia, and 53 mmol/mol for those on drug therapy which is associated with hypoglycaemia.",
"id": "62370",
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"explanation": "HbA1c should be measured every 3 to 6 months until stable on established therapy, and then every 6 months after that.",
"id": "62372",
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"name": "HbA1c does not need to be monitored after diagnosis",
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"explanation": "Type 2 diabetics who are on treatment associated with hypoglycaemia (such as insulin and solfonylureas) should be aiming for 53 mmol/mol, however, this patient is taking metformin only, therefore their aim should be 48mmol/mol.",
"id": "62369",
"label": "b",
"name": "53 mmol/mol",
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"explanation": "# Summary\n\nType 2 Diabetes Mellitus is a chronic metabolic disorder characterised by pancreatic beta-cell insufficiency and insulin resistance. The resulting hyperglycaemia leads to symptoms such as polyuria, polydipsia and if chronic can have microvascular and macrovascular complications. Key investigations include random and fasting blood glucose, 2-hour glucose tolerance, and HbA1C tests, and diagnosis is based on the results of these +/- symptoms. Management of type 2 diabetes primarily revolves around lifestyle modifications, hypoglycaemic agents, and insulin therapy when necessary, as well as reducing risks for serious complications such as cardiovascular and cerebrovascular disease. Other complications from chronic hyperglycaemia involve the gastrointestinal system, nervous system, peripheral arteries, foot infections, sexual dysfunction, and cardiac system. \n\n# Definition\n\nType 2 Diabetes Mellitus (T2DM) is a chronic metabolic condition characterized by inadequate insulin production from pancreatic beta cells, resulting in insulin resistance. This leads to an elevation in blood glucose levels, causing hyperglycaemia.\n\n# Epidemiology\n\nT2DM generally manifests in adults, and it is often associated with a strong familial predisposition. It accounts for approximately 90-95% of all diagnosed cases of diabetes.\n\n# Aetiology\n\nT2DM results from a combination of genetic and environmental factors. Known contributors include:\n\n- Poor dietary habits\n- Lack of physical activity\n- Obesity\n\n# Signs and symptoms\n\nIndividuals with T2DM may initially be asymptomatic, but over time, they may develop:\n\n- Polyuria\n- Polydipsia\n- Unexplained weight loss\n- Blurry vision\n- Fatigue\n\n# Differential diagnosis\n\nThe primary differentials for T2DM include Type 1 Diabetes Mellitus, Maturity Onset Diabetes of the Young (MODY), and Secondary Diabetes Mellitus. The main distinguishing features of these differentials are:\n\n- Type 1 Diabetes Mellitus: Early onset (typically in childhood or adolescence), often presents with ketoacidosis, and requires insulin therapy from diagnosis.\n- MODY (Maturity Onset Diabetes of the Young):\n\t- MODY 3 is the commonest cause, occurring due to a mutation in HNF1A. It is characterised by a very high blood sugar (10-20), and is very sensitive to sulphonylureas (e.g. gliclazide.) Insulin is the next line of treatment if it doesn't respond.\n\t- MODY 2 is the second commonest cause, occurring due to a glucokinase mutation. Blood sugars rarely rise above 7-8, over many years. Patients are generally well with few complications and the diabetes often responds to diet alone.\n\t- MODY 5 is associated with HNF1 beta mutation, and is associated with pancreatic atrophy, renal cycsts (causing palpable kidneys), epidydymal cysts, a bicornuate uterus, and abnormal LFTs\n- Secondary Diabetes Mellitus: Often presents with other signs of pancreatic disease (e.g., pancreatitis, cystic fibrosis), or due to certain medications (e.g., glucocorticoids, antipsychotics).\n\n# Investigations\n\nIf symptomatic, one of the following results is sufficient for diagnosis:\n\n- Random blood glucose ≥ 11.1mmol/l\n- Fasting plasma glucose ≥ 7mmol/l\n- 2-hour glucose tolerance ≥ 11.1mmol/l\n- HbA1C ≥ 48mmol/mol (6.5%)\n\nIf the patient is asymptomatic, two results are required from different days.\n\n# Management\n\nManagement of T2DM involves patient education, lifestyle modifications, pharmacological interventions, and close monitoring of glucose levels:\n\n- Lifestyle modifications: Advice on diet, regular physical activity, and smoking cessation\n- Pharmacological interventions: \n\t- Initial drug treatment is usually metformin, with consideration of other agents like Pioglitazone, DPP‑4 inhibitors, sulphonylureas, or SGLT-2 inhibitors for those who cannot take metformin.\n\t- If on monotherapy HbA1c >58mmol/mol consider dual therapy with metformin, pioglitazone, a DPP‑4 inhibitor or a sulphonylurea (such as gliclizide).\n\t- If dual therapy has not controlled drug glucose, triple therapy using the above medications can be considered. Otherwise, starting insulin may be necessary.\n- Close Monitoring: Measure HbA1c levels at 3-6 month intervals. If the patient is on insulin or is at risk of hypoglycaemia, self-monitoring of glucose at home is necessary.\n\n\n**Insulin Therapy**\n\nNICE guidance recommends basal insulin therapy with isophane (NPH) insulin as the first type to be used as it is most cost effective eg. Insulatard. Quick acting insulin analogues eg. Humalog, Novorapid, may be added in with meals if there is a big post meal glucose excursion.\n\nLong acting insulin analogues include Levemir, Lantus, Insulin Degludec and Abasaglar (a biosimilar insulin).\n\nMixed insulin combination which contain varying proportions of short and intermediate acting insulin such as Novomix 30 (30% short acting, 70% intermediate acting insulin) are more convenient because of fewer injections per day but may not be as successful.\n\n**Blood Pressure targets in Diabetes**\n\n- Blood pressure control needs to be strict in diabetes because these patients are at higher risk of macro- and microvascular complications.\n- NICE Hypertension Guidance [CG136] sets the same blood pressure targets as those who do not have diabetes, however in diabetics with HTN, ACE-inhibitors are first line as they are reno-protective\n\n# Complications\n\nComplications of diabetes are diverse, affecting multiple systems:\n\n### Macrovascular:\n\n* **Cardiac Complications** - diabetes significantly increases the risk of cardiovascular disease, contributing to major morbidity and mortality.\n* **Peripheral Arterial Disease (PAD)** - patients present with foot discolouration, gangrene, intermittent claudication, rest pain, night pain and absent peripheral pulses (confirmed on doppler).\n* **Cerebrovascular disease** - patients with diabetes are at significantly increased risk of TIAs and stroke and as such it is paramount to address the main risk factors (lipids, BP, smoking, obesity) for these as a broader part of management\n\n\n### Microvascular:\n\n* **Diabetic retinopathy** - characterised by vascular occlusion and leakage in the retinal capillaries, leading to potential sight loss if unmanaged, it is the leading cause of visual loss in adults. See separate section.\n* **Diabetic nephropathy** - a leading cause of chronic kidney disease, it is characterised by proteinuria. Prevention of this complication is achieved with ACE inhibitors/ARBs (by managing blood pressure) and SGLT-2 inhibitors.\n\t* Histological changes include Kimmelstiel-Wilson nodules which are the spherical, eosinophilic, sclerotic nodules characteristic of nodular diabetic glomerulosclerosis \n* **Diabetic neuropathy** - the primary causative factor is chronic hyperglycaemia, which leads to several distinct types neuropathy. See separate section.\n\t* **Autonomic Neuropathy** - may lead to postural hypotension and associated symptoms like dizziness, falls, and loss of consciousness.\n\t* **Gastrointestinal Complications: Gastroparesis** - a result of poor glycaemic control leading to nerve damage of the autonomic nervous system. Characterized by delayed gastric emptying, early satiety, abnormal stomach wall movements, and morning nausea.\n\t* **Foot Complications: Diabetic Foot Infections** - patients with vascular and neuropathic complications are at high risk for diabetic foot ulceration and subsequent infection.\n* **Sexual Dysfunction** - caused by a combination of factors including poor glycaemic control, neuropathy, microvascular complications, obesity, hypertension, depression, medication side effects, etc.\n\n# 'Sick day' rules\n\n1. **Temporary Medication Adjustments**: During acute illness, consider temporarily stopping certain medications until the person is eating and drinking normally for 24–48 hours. \n\t- **Angiotensin-Converting Enzyme Inhibitors (ACEIs), Diuretics, and NSAIDs**: Stop treatment if there is a risk of dehydration to reduce the likelihood of acute kidney injury (AKI).\n\n3. **Metformin**: Stop treatment if there is a risk of dehydration to lower the risk of lactic acidosis.\n\n4. **Sulfonylureas**: Be cautious, as they may increase the risk of hypoglycemia, especially if dietary intake is reduced.\n\n5. **SGLT-2 Inhibitors**: Check for ketones and stop treatment if acutely unwell and/or at risk of dehydration due to the risk of euglycemic diabetic ketoacidosis (DKA).\n\n6. **GLP-1 Receptor Agonists**: Stop treatment if there is a risk of dehydration to reduce the risk of AKI.\n\n7. **Insulin Therapy**: Do not stop insulin treatment; instead, consider adjusting the dose with guidance from the specialist diabetes team.\n\n8. **Blood Glucose Monitoring (if indicated)**: \n - Increase monitoring frequency to at least every 3–4 hours, including overnight.\n - Adjust insulin doses based on results.\n - Continue careful monitoring until blood glucose levels return to baseline.\n - Seek urgent medical advice if blood glucose remains uncontrolled.\n\n9. **Ketone Monitoring (Blood or Urinary)**: \n - Check ketone levels regularly (at least every 3–4 hours, including overnight).\n - Seek immediate medical advice if urine ketone level is greater than 2+ or blood ketone level is greater than 3 mmol/L.\n\n10. **Maintain Normal Meal Pattern**: Encourage maintaining regular meals and fluids, including carbohydrates, if appetite is reduced.\n\n11. **Fluid and Carbohydrate Replacement**:\n - If unable to eat or vomiting, replace meals with carbohydrate-containing drinks (e.g. fruit juices, sugary drinks).\n - Adjust fluid intake based on blood glucose levels (sugar-free fluids for high levels, sugary fluids for low levels).\n\n\n\n# NICE Guidelines\n\n[Click here for NICE CKS on T2DM](https://cks.nice.org.uk/topics/diabetes-type-2/)\n",
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"question": "A 58 year old female attends her GP surgery for a diabetic review. She has had type 2 diabetes for 2 years and takes metformin. She has no other past medical history.\n\nHer most recent HbA1c is 53 mmol/mol.\n\nWhat should her target HbA1c be?",
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"explanation": "This is the recommended upper normal limit of weekly alcohol intake for males and females.",
"id": "62374",
"label": "b",
"name": "14 units",
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"votes": 47
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"__typename": "QuestionChoice",
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"explanation": "Alcohol units are calculated multiplying the total volume of a drink (in ml) by its ABV (measured as a percentage) and dividing the result by 1,000. In this case, 4 x 125 = 500ml, 500ml x 13 (% of ABV) divided by 1000 = 6.5 units, rounded to 7. ",
"id": "62375",
"label": "c",
"name": "2 units",
"picture": null,
"votes": 85
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"__typename": "QuestionChoice",
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"explanation": "Alcohol units are calculated multiplying the total volume of a drink (in ml) by its ABV (measured as a percentage) and dividing the result by 1,000. In this case, 4 x 125 = 500ml, 500ml x 13 (% of ABV) divided by 1000 = 6.5 units, rounded to 7. ",
"id": "62373",
"label": "a",
"name": "7 units",
"picture": null,
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"__typename": "QuestionChoice",
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"explanation": "Alcohol units are calculated multiplying the total volume of a drink (in ml) by its ABV (measured as a percentage) and dividing the result by 1,000. In this case, 4 x 125 = 500ml, 500ml x 13 (% of ABV) divided by 1000 = 6.5 units, rounded to 7. ",
"id": "62376",
"label": "d",
"name": "5 units",
"picture": null,
"votes": 41
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"__typename": "QuestionChoice",
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"explanation": "Alcohol units are calculated multiplying the total volume of a drink (in ml) by its ABV (measured as a percentage) and dividing the result by 1,000. In this case, 4 x 125 = 500ml, 500ml x 13 (% of ABV) divided by 1000 = 6.5 units, rounded to 7. ",
"id": "62377",
"label": "e",
"name": "65 units",
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"explanation": "# Recommended Alcohol Intake\n\nExcessive alcohol consumption is increasing in the UK and has a significant burden of disease.\n\nThe recommended alcohol intake in the UK is 14 units per week for both men and women. NICE guidelines recommend that these units should be spread throughout the week.\n\n# Calculating units\n\nYou can work out how many units there are in an alcoholic drink by multiplying the total volume of the drink in ml by its ABV (percentage alcohol by volume) and dividing the result by 1,000:\n\nUnits = strength (ABV) x volume (ml) ÷ 1000",
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"question": "A 57 year old male attends his GP surgery to discuss his alcohol intake.\nHe drinks four 125ml glasses of 13% red wine a week.\nHow many units, to the nearest whole unit, of alcohol per week does this patient drink?",
"sbaAnswer": [
"a"
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"__typename": "QuestionSBA",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Both patients are drinking over the recommended 14 units with no alcohol free days per week. Therefore they should both be recommended to decrease their alcohol consumption.",
"id": "62380",
"label": "c",
"name": "Advise the patients that their alcohol intake is within current NHS guidelines and no further action is required",
"picture": null,
"votes": 12
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Previous guidance suggested different limits for men and women, for men it was suggested 21 units per week maximum and women 14 units. However, this was changed in 2016 to the current maximum of 14 units for everyone.\nTherefore both patients should be advised to cut down their alcohol intake to a maximum of 14 units per week.",
"id": "62379",
"label": "b",
"name": "Only advise the female patient to decrease her alcohol intake to 14 units",
"picture": null,
"votes": 21
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "The AUDIT questionnaire is used to measure the severity of chronic alcohol misuse. Whilst that may be helpful to assess the patients, most importantly is to recommend that they cut down their units to the recommeneded 14 units per week each.",
"id": "62382",
"label": "e",
"name": "Provide the patients with the AUDIT questionnaire",
"picture": null,
"votes": 245
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "It is recommended to drink no more than 14 units per week for men and women.\nPrevious guidance suggested different limits for men and women, for men it was suggested 21 units per week maximum and women 14 units. However, this was changed in 2016 to the current maximum of 14 units for everyone.",
"id": "62378",
"label": "a",
"name": "Advise both patients to limit alcohol to 14 units per week each with several alcohol free days per week",
"picture": null,
"votes": 1328
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Indications for inpatient withdrawal are:\n\n- Patients drinking >30 units per day\n- Scoring over 30 on the SADQ score\n- High risk of alcohol withdrawal seizures (previous alcohol withdrawal seizures or delirium tremens, or history of epilepsy)\n- Concurrent withdrawal from benzodiazepines\n- Significant medical or psychiatric comorbidity\n- Vulnerable patients\n- Patients under 18\n\nTherefore these patients do not require admission for alcohol detoxification. They should be advised to decrease their alcohol intake to the recommended 14 units per week.",
"id": "62381",
"label": "d",
"name": "Arrange for inpatient alcohol detoxification for both patients",
"picture": null,
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"comment": "\"NICE guidelines recommend that these units should be spread throughout the week.\" The answer says, several alcohol free days of the week.",
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"comment": "Spread out i.e. they shouldn't be consecutive days ",
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"comment": "Only 18 units a week? That's a night down the pub with the boys",
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"explanation": "# Recommended Alcohol Intake\n\nExcessive alcohol consumption is increasing in the UK and has a significant burden of disease.\n\nThe recommended alcohol intake in the UK is 14 units per week for both men and women. NICE guidelines recommend that these units should be spread throughout the week.\n\n# Calculating units\n\nYou can work out how many units there are in an alcoholic drink by multiplying the total volume of the drink in ml by its ABV (percentage alcohol by volume) and dividing the result by 1,000:\n\nUnits = strength (ABV) x volume (ml) ÷ 1000",
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"question": "A male and female couple in their 60's attend their GP surgery to discuss their alcohol intake. They both drink 18 units per week; one 175ml glass of red one each per night during the week and two each on a Saturday and Sunday.\n\nWhich of the following is the best next step in the management of these patients?",
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"explanation": "Mastitis does cause breast pain, however, examination would reveal inflammatory changes such as erythema and warmth. Mastitis is common among those breastfeeding, but it can also occur in smokers.",
"id": "62384",
"label": "b",
"name": "Mastitis",
"picture": null,
"votes": 85
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "A patient under the age of 30 with bilateral breast pain and normal examination is unlikely to have breast cancer.\nThe guidance for urgent referral on the suspected cancer pathway is:\n\n* 30 years or over with unexplained breast lump with or without pain, or\n* 50 years and over with unilateral nipple changes such as discharge or retraction\n\nA referral can be considered for those with skin changes to the breast or those 30 years and over with an unexplained lump in the axilla.\n[Click here for NICE CKS on Breast cancer - recognition and referral] (https://cks.nice.org.uk/topics/breast-cancer-recognition-referral/)",
"id": "62385",
"label": "c",
"name": "Breast malignancy",
"picture": null,
"votes": 8
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Fat necrosis often occurs after trauma to the breast tissue. A lump with overlying bruising would be found on examination.",
"id": "62386",
"label": "d",
"name": "Fat necrosis of the breat",
"picture": null,
"votes": 19
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Fibroadenomas are benign tumours of the breast originating from fibrous and epithelial tissue. Whilst this patient is a typical age for fibroadenomas, she does not present with a lump. Fibroadenomas present with a firm, non tender lump which is highly mobile.",
"id": "62387",
"label": "e",
"name": "Fibroadenoma of the breast",
"picture": null,
"votes": 71
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "Breast tenderness is a common side effect of the combined oral contraceptive pill. This can often be managed with simple analgesia such as paracetamol, however, alternative contraception can be offered if symptoms continue.",
"id": "62383",
"label": "a",
"name": "Side effect of the combined oral contraceptive pill",
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"explanation": "# Summary\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive containing synthetic oestrogen and progestogen. It works by inhibiting ovulation, thickening cervical mucus, and altering the endometrium to prevent fertilisation and implantation. Indications for COCP use include contraception, menstrual cycle regulation, and treatment of dysmenorrhea, menorrhagia, acne, and hirsutism. Contraindications are categorised by UKMEC criteria, detailed in this chapter. \n \n# Definition\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive. It contains synthetic versions of the female hormones oestrogen and progestogen. \n \n\n# Mechanism of Action\n \n\n* **Inhibition of Ovulation:** The COCP contains synthetic versions of the hormones oestrogen and progestogen. These hormones together suppress the release of gonadotrophins (LH and FSH) from the pituitary gland, preventing the maturation and release of an egg from the ovaries.\n \n\n* **Thickening of Cervical Mucus:** The progestogen component of the COCP increases the viscosity of cervical mucus, making it more difficult for sperm to enter the uterus and fertilise an egg.\n \n\n * **Alteration of the Endometrium:** The COCP induces changes in the lining of the uterus (endometrium), making it less suitable for the implantation of a fertilised egg.\n \n\n# Indications\n \n\nThere are a range of reasons for women to be recommended the oral combined contraceptive pill. For example:\n \n\n* **Contraception:** The COCP works as a long-term contraception. It is taken orally once a day, at around the same time each day. \n * **Menstrual Cycle Regulation:** The COCP can help regulate irregular menstrual cycles. \n * **Dysmenorrhea:** The COCP may be used to reduce menstrual cramps. \n * **Menorrhagia:** The COCP can decrease heavy menstrual bleeding.\n * **Acne and Hirsutism:** The COCP helps in the treatment of acne and excessive hirsutism in women, which may happen in conditions such as polycystic ovary syndrome (PCOS) or other androgen excess conditions.\n * **Premenstrual Syndrome (PMHS**: The COCP can alleviate symptoms of PMS, such as mood swings, bloating, and irritability.\n \n# Contraindications \n \nThere are numerous contra-indications to the Combined Oral Contraceptive Pill. These can be divided into absolute contraindications, known as ''UKMEC 4'', a situation where the disadvantages outweigh the advantages (UKMEC 3), a situation where the advantages outweigh the disadvantages (UKMEC 2), and a situation whereby there is no limit on that choice of contraception (UKMEC 1).\n \n\n## Absolute Contraindications to Contraception (UKMEC 4)\n \n \n * Known or suspected pregnancy\n * Hypertension with SBP ≥160 mmHg or DBP ≥100 mmHg\n * Smoker over the age of 35 who smokes >15 cigarettes a day \n * Current and history of ischaemic heart disease\n * History of stroke (including TIA) \n * Vascular disease\n * History or current VTE\n * Major surgery with prolonged immobilisation\n * Breastfeeding <6 weeks postpartum\n * Not breastfeeding and <3 weeks postpartum with other risk factors for VTE\n * Known thrombogenic mutations \n * Complicated valvular and congenital heart disease\n * Cardiomyopathy with impaired cardiac function\n * Atrial fibrillation \n * Migraine with aura (any age)\n * Current breast cancer \n * Severe (decompensated) cirrhosis \n * Hepatocellular adenoma and hepatocellular carcinoma\n * Positive antiphospholipid antibodies \n \n \n \n## Disadvantages of a contraceptive outweigh the advantages (UKMEC 3)\n \n * Obesity (BMI ≥35 kg/m2)\n * Multiple risk factors for cardiovascular disease (e.g. smoking, diabetes mellitus, hypertension, obesity, dyslipidaemia) \n * Well controlled hypertension, and hypertension with SBP >140-159 mmHg or DBP <90-99 mmHg\n * Smoker over age of 35 who smokes <15 cigarettes a day, or anyone over age of 35 who stopped smoking <1 year ago\n * Family history of thrombosis before 45 years old\n * Not breastfeeding and <3 weeks postpartum without other risk factors for VTE\n * Not breastfeeding and between 3-6 weeks postpartum with other risk factors for VTE\n * Organ transplant with complications (e.g. graft failure, rejection) \n * Immobility (unrelated to surgery)\n * Migraine without aura (any age) [applies to *continuation* of COCP]\n * History (≥5 years ago) of migraine\nwith aura (any age) \n * Undiagnosed breast mass or symptoms [applies to *initiation* of COCP] \n * Carriers of known gene mutations associated with breast cancer\n * Past breat cancer \n * Diabetes mellitus with nephropathy, retinopathy, neuropathy or other vascular complications \n * Symptomatic gall bladder disease treated medically or currently active \n * Past COCP associated cholestasis \n * Acute viral hepatitis [applies to *initiation* of COCP]\n \n \n \n## Advantages of a contraceptive outweigh the disadvantages (UKMEC 2)\n \n * Smokers under the age of 35, and people aged over 35 who stopped smoking over 1 year ago \n * Obesity (BMI ≥30–34 kg/m2) \n * Family history of VTE in first-degree relative aged ≥45 years\n * History of raised blood pressure in pregnancy \n * Breast feeding between 6 weeks-6 months postpartum\n * Not breastfeeding and between 3-6 weeks postpartum without other risk factors for VTE\n * Uncomplicated organ transplant \n * Known dyslipidaemia \n * Major surgery without prolonged immobilisation \n * Superficial venous thrombosis \n * Uncomplicated valvular and congenital heart disease\n * Cardiomyopathy with normal cardiac function \n * Long QT syndrome \n * Non-migrainous headaches [applies to *continuation* of COCP]\n * Migraine without aura [applies to *initiation* of COCP] \n * Idiopathic intracranial hypertension \n * Unexplained vaginal bleeding\n * Cervical cancer \n * Undiagnosed breast mass or symptoms [applies to *continuation* of COCP]\n * Insulin-dependent diabetes mellitus without vascular disease \n * Symptomatic gall bladder disease treated through cholecystectomy, or asymptomatic gall bladder disease, or history of pregnancy-related cholestasis \n * Acute viral hepatitis [applies to *continuation* of COCP]\n * Inflammatory bowel disease \n * Sickle cell disease \n * Rheumatoid arthritis\n * SLE without antiphospholipid antibodies \n \n\n \n\n# Side-effects and Complications\n \n**Common Side-Effects:**\n \n\n * Breast tenderness \n * Abdominal discomfort, nausea diarrhoea \n * Headaches\n * Mood changes\n * Reduced libido \n \n\n**Rare but Serious Side-Effects:**\n \n\n * Embolism or thrombus, including: DVT and PE, stroke, myocardial infarction\n * Increased risk of breast cancer\n * Increased risk of cervical cancer \n \n\n \n\n# Follow-up\n\nArrange follow up 3 months following initial prescription of a COCP, and annually thereafter.\n \n\nAt follow-up, ensure to: \n \n\n * Check blood pressure and BMI. \n * Ask about headaches (including migraine). \n * Check for risk factors that may be contraindicators to COCP (as per UKMEC criteria). \n * Enquire about side-effects. \n * Enquire about how woman is taking the COCP (i.e. adherence). \n \n\n \n\n# Missed Pill Rules\n \n\n**Missed One Pill:**\n \n\n* Advise patient to take the pill as soon as possible, even if it means taking two pills in one day.\n* * Continue taking the rest of the pack as usual.\nNo additional contraception needed if this is the only pill missed in the pack.\n \n\n**Missed Two or More Pills in Week 1 (Days 1-7):**\n \n\n * Advise patient to take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * Use additional contraception for the next 7 days.\n * If they had unprotected sex during this week, seek emergency contraception.\n \n\n**Missed Two or More Pills in Week 2 (Days 8-14):**\n \n\n * Take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n\n**Missed Two or More Pills in Week 3 (Days 15-21):**\n \n\n* Finish the active pills in the current pack, then start a new pack immediately without taking the usual 7-day break.\n* No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n# NICE Guidelines \n \n\n[Click here to view NICE Guidelines on COCP](https://cks.nice.org.uk/topics/contraception-combined-hormonal-methods/management/combined-oral-contraceptive/)\n \n \n# References\n \n[Click here to see the UKMEC summary sheet on contraception](https://www.fsrh.org/standards-and-guidance/documents/ukmec-2016-summary-sheets/)",
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"question": "A 24 year old female attends her GP surgery with bilateral breast tenderness for the past two weeks. Examination of the breasts shows no abnormalities.\n\nHer past medical history includes asthma.\n\nShe currently takes a salbutamol inhaler and the combined oral contraceptive pill.\n\nWhich of the following is the most likely explanation for this patient’s symptoms?",
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"explanation": "To avoid pregnancy the patient should be advised to take the missed pill as soon as possible and the next pill at the usual time. This may mean taking two pills in 24 hours. No emergency contraception or extra contraceptive measures are needed if adherence has been good in the 7 days previously. Therefore, there is no extra indication to test for pregnancy.",
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"name": "Stop taking the pill and take a home urinary pregnancy test in two weeks",
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"explanation": "As long as there has been consistent adherence for the 7 days prior, there is no need for emergency contraception if in week 3 of the cycle.\nThe missed pill should be taken as soon as possible and the next pill taken at the usual time. This may mean taking two pills in 24 hours.\n\nIf the patient is struggling with adherence, alternative forms of contraception can be offered such as the IUS.",
"id": "62391",
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"name": "Offer the intraunterine system",
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"explanation": "As long as there has been consistent adherence for the 7 days prior, there is no need for emergency contraception if in week 3 of the cycle.\nThe missed pill should be taken as soon as possible and the next pill taken at the usual time. This may mean taking two pills in 24 hours.",
"id": "62389",
"label": "b",
"name": "Offer emergency contraception",
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"votes": 125
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"explanation": "As long as there has been consistent adherence for the 7 days prior, there is no need for extra precautions. The missed pill should be taken as soon as possible and the next pill taken at the usual time. This may mean taking two pills in 24 hours.",
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"label": "c",
"name": "Abstain from sexual intercorse for the next 7 days",
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"explanation": "In week three (counted as the third week after the hormone-free interval) if one pill is missed (up to 48 hours since the last pill was taken) then the missed pill should be taken as soon as possible and the next pill taken at the usual time. This may mean taking two pills in 24 hours. No additional contraception is required if there has been consistent adherence for the 7 days prior.\n\n[Click here for NICE guidance on contraceptive pills] (https://cks.nice.org.uk/topics/contraception-combined-hormonal-methods/management/combined-oral-contraceptive/)",
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"name": "Take the last pill that was missed, finish the current pack and start the next pack immediately after",
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"comment": "if any 1 pill is missed at any time, there is no need for contraception or anything.. just take the missed pill.. if she were to have missed 2 then this would have been the case",
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"comment": "does she still need to skip the pill free interval if only one pill is missed in week 3?",
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"explanation": "# Summary\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive containing synthetic oestrogen and progestogen. It works by inhibiting ovulation, thickening cervical mucus, and altering the endometrium to prevent fertilisation and implantation. Indications for COCP use include contraception, menstrual cycle regulation, and treatment of dysmenorrhea, menorrhagia, acne, and hirsutism. Contraindications are categorised by UKMEC criteria, detailed in this chapter. \n \n# Definition\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive. It contains synthetic versions of the female hormones oestrogen and progestogen. \n \n\n# Mechanism of Action\n \n\n* **Inhibition of Ovulation:** The COCP contains synthetic versions of the hormones oestrogen and progestogen. These hormones together suppress the release of gonadotrophins (LH and FSH) from the pituitary gland, preventing the maturation and release of an egg from the ovaries.\n \n\n* **Thickening of Cervical Mucus:** The progestogen component of the COCP increases the viscosity of cervical mucus, making it more difficult for sperm to enter the uterus and fertilise an egg.\n \n\n * **Alteration of the Endometrium:** The COCP induces changes in the lining of the uterus (endometrium), making it less suitable for the implantation of a fertilised egg.\n \n\n# Indications\n \n\nThere are a range of reasons for women to be recommended the oral combined contraceptive pill. For example:\n \n\n* **Contraception:** The COCP works as a long-term contraception. It is taken orally once a day, at around the same time each day. \n * **Menstrual Cycle Regulation:** The COCP can help regulate irregular menstrual cycles. \n * **Dysmenorrhea:** The COCP may be used to reduce menstrual cramps. \n * **Menorrhagia:** The COCP can decrease heavy menstrual bleeding.\n * **Acne and Hirsutism:** The COCP helps in the treatment of acne and excessive hirsutism in women, which may happen in conditions such as polycystic ovary syndrome (PCOS) or other androgen excess conditions.\n * **Premenstrual Syndrome (PMHS**: The COCP can alleviate symptoms of PMS, such as mood swings, bloating, and irritability.\n \n# Contraindications \n \nThere are numerous contra-indications to the Combined Oral Contraceptive Pill. These can be divided into absolute contraindications, known as ''UKMEC 4'', a situation where the disadvantages outweigh the advantages (UKMEC 3), a situation where the advantages outweigh the disadvantages (UKMEC 2), and a situation whereby there is no limit on that choice of contraception (UKMEC 1).\n \n\n## Absolute Contraindications to Contraception (UKMEC 4)\n \n \n * Known or suspected pregnancy\n * Hypertension with SBP ≥160 mmHg or DBP ≥100 mmHg\n * Smoker over the age of 35 who smokes >15 cigarettes a day \n * Current and history of ischaemic heart disease\n * History of stroke (including TIA) \n * Vascular disease\n * History or current VTE\n * Major surgery with prolonged immobilisation\n * Breastfeeding <6 weeks postpartum\n * Not breastfeeding and <3 weeks postpartum with other risk factors for VTE\n * Known thrombogenic mutations \n * Complicated valvular and congenital heart disease\n * Cardiomyopathy with impaired cardiac function\n * Atrial fibrillation \n * Migraine with aura (any age)\n * Current breast cancer \n * Severe (decompensated) cirrhosis \n * Hepatocellular adenoma and hepatocellular carcinoma\n * Positive antiphospholipid antibodies \n \n \n \n## Disadvantages of a contraceptive outweigh the advantages (UKMEC 3)\n \n * Obesity (BMI ≥35 kg/m2)\n * Multiple risk factors for cardiovascular disease (e.g. smoking, diabetes mellitus, hypertension, obesity, dyslipidaemia) \n * Well controlled hypertension, and hypertension with SBP >140-159 mmHg or DBP <90-99 mmHg\n * Smoker over age of 35 who smokes <15 cigarettes a day, or anyone over age of 35 who stopped smoking <1 year ago\n * Family history of thrombosis before 45 years old\n * Not breastfeeding and <3 weeks postpartum without other risk factors for VTE\n * Not breastfeeding and between 3-6 weeks postpartum with other risk factors for VTE\n * Organ transplant with complications (e.g. graft failure, rejection) \n * Immobility (unrelated to surgery)\n * Migraine without aura (any age) [applies to *continuation* of COCP]\n * History (≥5 years ago) of migraine\nwith aura (any age) \n * Undiagnosed breast mass or symptoms [applies to *initiation* of COCP] \n * Carriers of known gene mutations associated with breast cancer\n * Past breat cancer \n * Diabetes mellitus with nephropathy, retinopathy, neuropathy or other vascular complications \n * Symptomatic gall bladder disease treated medically or currently active \n * Past COCP associated cholestasis \n * Acute viral hepatitis [applies to *initiation* of COCP]\n \n \n \n## Advantages of a contraceptive outweigh the disadvantages (UKMEC 2)\n \n * Smokers under the age of 35, and people aged over 35 who stopped smoking over 1 year ago \n * Obesity (BMI ≥30–34 kg/m2) \n * Family history of VTE in first-degree relative aged ≥45 years\n * History of raised blood pressure in pregnancy \n * Breast feeding between 6 weeks-6 months postpartum\n * Not breastfeeding and between 3-6 weeks postpartum without other risk factors for VTE\n * Uncomplicated organ transplant \n * Known dyslipidaemia \n * Major surgery without prolonged immobilisation \n * Superficial venous thrombosis \n * Uncomplicated valvular and congenital heart disease\n * Cardiomyopathy with normal cardiac function \n * Long QT syndrome \n * Non-migrainous headaches [applies to *continuation* of COCP]\n * Migraine without aura [applies to *initiation* of COCP] \n * Idiopathic intracranial hypertension \n * Unexplained vaginal bleeding\n * Cervical cancer \n * Undiagnosed breast mass or symptoms [applies to *continuation* of COCP]\n * Insulin-dependent diabetes mellitus without vascular disease \n * Symptomatic gall bladder disease treated through cholecystectomy, or asymptomatic gall bladder disease, or history of pregnancy-related cholestasis \n * Acute viral hepatitis [applies to *continuation* of COCP]\n * Inflammatory bowel disease \n * Sickle cell disease \n * Rheumatoid arthritis\n * SLE without antiphospholipid antibodies \n \n\n \n\n# Side-effects and Complications\n \n**Common Side-Effects:**\n \n\n * Breast tenderness \n * Abdominal discomfort, nausea diarrhoea \n * Headaches\n * Mood changes\n * Reduced libido \n \n\n**Rare but Serious Side-Effects:**\n \n\n * Embolism or thrombus, including: DVT and PE, stroke, myocardial infarction\n * Increased risk of breast cancer\n * Increased risk of cervical cancer \n \n\n \n\n# Follow-up\n\nArrange follow up 3 months following initial prescription of a COCP, and annually thereafter.\n \n\nAt follow-up, ensure to: \n \n\n * Check blood pressure and BMI. \n * Ask about headaches (including migraine). \n * Check for risk factors that may be contraindicators to COCP (as per UKMEC criteria). \n * Enquire about side-effects. \n * Enquire about how woman is taking the COCP (i.e. adherence). \n \n\n \n\n# Missed Pill Rules\n \n\n**Missed One Pill:**\n \n\n* Advise patient to take the pill as soon as possible, even if it means taking two pills in one day.\n* * Continue taking the rest of the pack as usual.\nNo additional contraception needed if this is the only pill missed in the pack.\n \n\n**Missed Two or More Pills in Week 1 (Days 1-7):**\n \n\n * Advise patient to take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * Use additional contraception for the next 7 days.\n * If they had unprotected sex during this week, seek emergency contraception.\n \n\n**Missed Two or More Pills in Week 2 (Days 8-14):**\n \n\n * Take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n\n**Missed Two or More Pills in Week 3 (Days 15-21):**\n \n\n* Finish the active pills in the current pack, then start a new pack immediately without taking the usual 7-day break.\n* No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n# NICE Guidelines \n \n\n[Click here to view NICE Guidelines on COCP](https://cks.nice.org.uk/topics/contraception-combined-hormonal-methods/management/combined-oral-contraceptive/)\n \n \n# References\n \n[Click here to see the UKMEC summary sheet on contraception](https://www.fsrh.org/standards-and-guidance/documents/ukmec-2016-summary-sheets/)",
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"question": "A 32 year old female attends her GP practice. She is sexually active and takes the combined oral contraceptive pill (COCP), however she had forgotten to take her pill last night. Prior to this she has had good adherence. She is currently in week three of her cycle.\n\nWhich of the following is the best next step in the management of this patients?",
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"explanation": "Ullipristal acetate is a selective progesterone-receptor modulator.\nIt is liscensed as a form of emergency contraception when taken within 120 hours of UPSI.\nIt prevents the LH surge preventing ovulation for 5 days.",
"id": "62393",
"label": "a",
"name": "Ullipristal acetate (ellaOne®)",
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"explanation": "The copper IUD is the most effective emergency contraception, it can be utilised 5 days after UPSI. It prevents fertilisation, and also has anti-implantation effects by causing inflammation in the endometrial lining.\nWhilst this would be an appropriate option, however, the patient has menorrhagia. The IUD is not a suitable option as it often increases symptoms of menorrhagia.",
"id": "62397",
"label": "e",
"name": "The copper intrauterine device (IUD)",
"picture": null,
"votes": 314
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Ullipristal acetate should be offered, it is liscenced as emergency contraception for up to 120 hours after UPSI.",
"id": "62395",
"label": "c",
"name": "Advise her to take a pregnancy test in a weeks time as it is too late to take emergency contraception",
"picture": null,
"votes": 32
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Levonorgestrel it is progesterone-only emergency contraception.\nLevonorgestrel can be used as emergency contraception if the UPSI took place within 72 hours.\nIt delays ovulation by 5 days and thickens the cervical mucus.\nFor this patient, as it has been over 72 hours since UPSI, Levonorgestrel is not effective emergency contraception.",
"id": "62394",
"label": "b",
"name": "Levonorgestrel (Levonelle)",
"picture": null,
"votes": 111
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{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is called the Yuzpe regimen, it is when a high dose of a combined oral contraceptive pill is used as emergency contraception. Taken within 72 hours of UPSI it has a 75% reduction in the risk of pregnancy. However, this method is no longer used in the UK as it was demonstrated to be far less effective than levonorgestrel.",
"id": "62396",
"label": "d",
"name": "Two doses of the combined oral contraceptive pill",
"picture": null,
"votes": 8
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"explanation": "# Overview\n\nEmergency contraception is indicated where unprotected sexual intercourse (UPSI) has occured, or where a contraceptive method has been used incorrectly.\n\n# Copper intrauterine device (Cu-IUD)\n\n- Gold standard emergency contraception\n- Can be used 120 hours after the first episode of UPSI in a cycle, or within 120 hours of the earliest expected date of ovulation\n- Inhibits fertilization by its toxic effect on sperm and ova.\n- If fertilization does occur, the Cu-IUD has an anti-implantation effect.\n- Contraindications include uterine fibroids with distortion of uterine cavity, documented/suspected pelvic inflammatory disease (PID) and documented/suspected sexually transmitted infection, especially chlamydia or gonorrhoea\n\n\n# Ulipristal acetate (\"Ella One\")\n\n- Selective progesterone receptor modulator\n- Binds to human progesterone receptors, suppressing the LH surge and delays ovulation for at least 5 days, until sperm from the UPSI are no longer viable\n- It delays ovulation even after the start of the LH surge\n- Can be used within 120 hours of UPSI\n- Guidance is to wait 5 days before starting ongoing hormonal contraception\n- Can only be used once per cycle\n- Contraindications:\n - Diseases of malabsorption e.g. Crohn’s\n - Hypersensitivity to Ulipristal Acetate\n - Severe hepatic dysfunction\n - Enzyme inducing drugs e.g. rifampicin\n - Give 3mg levonorgestrel if the patient refuses an IUD, ulipristal acetate is **absolutely** contraindicated here\n - Breast feeding – avoid breastfeeding for 7 days after taking UPA\n - Asthma insufficiently controlled by corticosteroids\n - Drugs increasing gastric pH e.g. omeprazole, ranitidine\n\n\n# Levonorgestrel (\"Levonelle\")\n\n- Can be used within 72 hours of UPSI\n- Inhibits or delays ovulation for a period of approximately 5 days, until sperm from the UPSI are no longer viable\n- Also thickens cervical mucus\n- Can quick start hormonal contraception\n- Can take more than once in the same cycle if further UPSI\n- Ineffective after the LH surge\n- Contraindications: no absolute contraindications, however, efficacy may be reduced by: diseases of malabsorption, e.g. Crohn's disease, BMI > 26 or weight >70kg and enzyme inducing drugs e.g. rifampicin\n - If patient refuses IUD, then double dose i.e. 3mg **at once** may be taken\n\n\n\n### External links \n\n- [FPA: Your guide to emergency contraception](https://www.fpa.org.uk/download/your-guide-to-emergency-contraception/)\n- [NICE: Clinical Knowledge Summary: Emergency Contraception](https://cks.nice.org.uk/topics/contraception-emergency/)\n- [BMJ Best Practice: Contraception](https://bestpractice.bmj.com/topics/en-gb/418)\n- [World Health Organization. Family planning - a global handbook for providers](http://apps.who.int/iris/bitstream/handle/10665/260156/9780999203705-eng.pdf?sequence=1)",
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"question": "A 21 year old female attends her GP surgery to discuss emergency contraception after having unprotected sexual intercourse (UPSI) 4 days ago. She does not currently use any method of contraception.\n\nHer past medical history is of menorrhagia secondary to dysfunctional uterine bleeding.\n\nWhich of the following is the best next step in the management of this patients?",
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"explanation": "This would unnecessarily delay contraception. The COCP can be started at any time during the menstrual cycle, provided additional precautions are taken if started after day 5.",
"id": "62400",
"label": "c",
"name": "To wait until day 1 of her next cycle to start the COCP",
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"explanation": "Immediate protection only applies if the COCP is started within the first 5 days of the menstrual cycle. Since the patient is on day 4 and sexually active, additional precautions are required for 7 days to ensure she is protected.",
"id": "62399",
"label": "b",
"name": "Start the COCP immediately, with no further precautions needed",
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"explanation": "When the COCP is started between day 1-5, FSRH states that no further precautions are required.",
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"explanation": "This does not align with FSRH guidelines, which recommend 7 days of additional contraception for maximum protection when starting the COCP outside the first 5 days of the menstrual cycle.",
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"name": "Start the COCP and advise the use of additional precautions for the next 3 days",
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"explanation": "This is not a standard recommendation for starting the COCP and would not address the need for additional contraception during the initial 7-day window when the COCP is not yet effective.",
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"name": "Start the COCP immediately but omit the hormone free week of this cycle",
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"comment": "how are you supposed to learn this off by heart?\n",
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"comment": "Directly from the notes:\n\nStarting combined hormonal contraception\n\nIf the patient starts her pill on the first day of a natural period, she will be protected from pregnancy immediately\nIf the patient starts at any other time in her cycle, she will need to use additional precautions (e.g. condoms) for 7 days\nNew mothers can begin to take the pill 21 days after giving birth, providing they are not breastfeeding\n",
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"explanation": "# Summary\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive containing synthetic oestrogen and progestogen. It works by inhibiting ovulation, thickening cervical mucus, and altering the endometrium to prevent fertilisation and implantation. Indications for COCP use include contraception, menstrual cycle regulation, and treatment of dysmenorrhea, menorrhagia, acne, and hirsutism. Contraindications are categorised by UKMEC criteria, detailed in this chapter. \n \n# Definition\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive. It contains synthetic versions of the female hormones oestrogen and progestogen. \n \n\n# Mechanism of Action\n \n\n* **Inhibition of Ovulation:** The COCP contains synthetic versions of the hormones oestrogen and progestogen. These hormones together suppress the release of gonadotrophins (LH and FSH) from the pituitary gland, preventing the maturation and release of an egg from the ovaries.\n \n\n* **Thickening of Cervical Mucus:** The progestogen component of the COCP increases the viscosity of cervical mucus, making it more difficult for sperm to enter the uterus and fertilise an egg.\n \n\n * **Alteration of the Endometrium:** The COCP induces changes in the lining of the uterus (endometrium), making it less suitable for the implantation of a fertilised egg.\n \n\n# Indications\n \n\nThere are a range of reasons for women to be recommended the oral combined contraceptive pill. For example:\n \n\n* **Contraception:** The COCP works as a long-term contraception. It is taken orally once a day, at around the same time each day. \n * **Menstrual Cycle Regulation:** The COCP can help regulate irregular menstrual cycles. \n * **Dysmenorrhea:** The COCP may be used to reduce menstrual cramps. \n * **Menorrhagia:** The COCP can decrease heavy menstrual bleeding.\n * **Acne and Hirsutism:** The COCP helps in the treatment of acne and excessive hirsutism in women, which may happen in conditions such as polycystic ovary syndrome (PCOS) or other androgen excess conditions.\n * **Premenstrual Syndrome (PMHS**: The COCP can alleviate symptoms of PMS, such as mood swings, bloating, and irritability.\n \n# Contraindications \n \nThere are numerous contra-indications to the Combined Oral Contraceptive Pill. These can be divided into absolute contraindications, known as ''UKMEC 4'', a situation where the disadvantages outweigh the advantages (UKMEC 3), a situation where the advantages outweigh the disadvantages (UKMEC 2), and a situation whereby there is no limit on that choice of contraception (UKMEC 1).\n \n\n## Absolute Contraindications to Contraception (UKMEC 4)\n \n \n * Known or suspected pregnancy\n * Hypertension with SBP ≥160 mmHg or DBP ≥100 mmHg\n * Smoker over the age of 35 who smokes >15 cigarettes a day \n * Current and history of ischaemic heart disease\n * History of stroke (including TIA) \n * Vascular disease\n * History or current VTE\n * Major surgery with prolonged immobilisation\n * Breastfeeding <6 weeks postpartum\n * Not breastfeeding and <3 weeks postpartum with other risk factors for VTE\n * Known thrombogenic mutations \n * Complicated valvular and congenital heart disease\n * Cardiomyopathy with impaired cardiac function\n * Atrial fibrillation \n * Migraine with aura (any age)\n * Current breast cancer \n * Severe (decompensated) cirrhosis \n * Hepatocellular adenoma and hepatocellular carcinoma\n * Positive antiphospholipid antibodies \n \n \n \n## Disadvantages of a contraceptive outweigh the advantages (UKMEC 3)\n \n * Obesity (BMI ≥35 kg/m2)\n * Multiple risk factors for cardiovascular disease (e.g. smoking, diabetes mellitus, hypertension, obesity, dyslipidaemia) \n * Well controlled hypertension, and hypertension with SBP >140-159 mmHg or DBP <90-99 mmHg\n * Smoker over age of 35 who smokes <15 cigarettes a day, or anyone over age of 35 who stopped smoking <1 year ago\n * Family history of thrombosis before 45 years old\n * Not breastfeeding and <3 weeks postpartum without other risk factors for VTE\n * Not breastfeeding and between 3-6 weeks postpartum with other risk factors for VTE\n * Organ transplant with complications (e.g. graft failure, rejection) \n * Immobility (unrelated to surgery)\n * Migraine without aura (any age) [applies to *continuation* of COCP]\n * History (≥5 years ago) of migraine\nwith aura (any age) \n * Undiagnosed breast mass or symptoms [applies to *initiation* of COCP] \n * Carriers of known gene mutations associated with breast cancer\n * Past breat cancer \n * Diabetes mellitus with nephropathy, retinopathy, neuropathy or other vascular complications \n * Symptomatic gall bladder disease treated medically or currently active \n * Past COCP associated cholestasis \n * Acute viral hepatitis [applies to *initiation* of COCP]\n \n \n \n## Advantages of a contraceptive outweigh the disadvantages (UKMEC 2)\n \n * Smokers under the age of 35, and people aged over 35 who stopped smoking over 1 year ago \n * Obesity (BMI ≥30–34 kg/m2) \n * Family history of VTE in first-degree relative aged ≥45 years\n * History of raised blood pressure in pregnancy \n * Breast feeding between 6 weeks-6 months postpartum\n * Not breastfeeding and between 3-6 weeks postpartum without other risk factors for VTE\n * Uncomplicated organ transplant \n * Known dyslipidaemia \n * Major surgery without prolonged immobilisation \n * Superficial venous thrombosis \n * Uncomplicated valvular and congenital heart disease\n * Cardiomyopathy with normal cardiac function \n * Long QT syndrome \n * Non-migrainous headaches [applies to *continuation* of COCP]\n * Migraine without aura [applies to *initiation* of COCP] \n * Idiopathic intracranial hypertension \n * Unexplained vaginal bleeding\n * Cervical cancer \n * Undiagnosed breast mass or symptoms [applies to *continuation* of COCP]\n * Insulin-dependent diabetes mellitus without vascular disease \n * Symptomatic gall bladder disease treated through cholecystectomy, or asymptomatic gall bladder disease, or history of pregnancy-related cholestasis \n * Acute viral hepatitis [applies to *continuation* of COCP]\n * Inflammatory bowel disease \n * Sickle cell disease \n * Rheumatoid arthritis\n * SLE without antiphospholipid antibodies \n \n\n \n\n# Side-effects and Complications\n \n**Common Side-Effects:**\n \n\n * Breast tenderness \n * Abdominal discomfort, nausea diarrhoea \n * Headaches\n * Mood changes\n * Reduced libido \n \n\n**Rare but Serious Side-Effects:**\n \n\n * Embolism or thrombus, including: DVT and PE, stroke, myocardial infarction\n * Increased risk of breast cancer\n * Increased risk of cervical cancer \n \n\n \n\n# Follow-up\n\nArrange follow up 3 months following initial prescription of a COCP, and annually thereafter.\n \n\nAt follow-up, ensure to: \n \n\n * Check blood pressure and BMI. \n * Ask about headaches (including migraine). \n * Check for risk factors that may be contraindicators to COCP (as per UKMEC criteria). \n * Enquire about side-effects. \n * Enquire about how woman is taking the COCP (i.e. adherence). \n \n\n \n\n# Missed Pill Rules\n \n\n**Missed One Pill:**\n \n\n* Advise patient to take the pill as soon as possible, even if it means taking two pills in one day.\n* * Continue taking the rest of the pack as usual.\nNo additional contraception needed if this is the only pill missed in the pack.\n \n\n**Missed Two or More Pills in Week 1 (Days 1-7):**\n \n\n * Advise patient to take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * Use additional contraception for the next 7 days.\n * If they had unprotected sex during this week, seek emergency contraception.\n \n\n**Missed Two or More Pills in Week 2 (Days 8-14):**\n \n\n * Take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n\n**Missed Two or More Pills in Week 3 (Days 15-21):**\n \n\n* Finish the active pills in the current pack, then start a new pack immediately without taking the usual 7-day break.\n* No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n# NICE Guidelines \n \n\n[Click here to view NICE Guidelines on COCP](https://cks.nice.org.uk/topics/contraception-combined-hormonal-methods/management/combined-oral-contraceptive/)\n \n \n# References\n \n[Click here to see the UKMEC summary sheet on contraception](https://www.fsrh.org/standards-and-guidance/documents/ukmec-2016-summary-sheets/)",
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"question": "A 22 year old female attends her GP surgery to discuss contraception. She decides to try a combined oral contraceptive pill (COCP).\nShe is currently menstruating and is on day 4 of her cycle. She is sexually active.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "This would not be a suitable form of contraception for this patient. She has already reported to struggle with adherence to her current COCP, therefore is likely to have the same problem with the POP. Furthermore, the POP is not currently recommended as treatment for menorrhagia.",
"id": "62407",
"label": "e",
"name": "Progesterone only pill (POP)",
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"explanation": "Patients with menorrhagia who want contraception can be offered the IUS, e.g. Mirena coil. The IUS is Levonorgestrel-releasing, it prevents fertilisation, thickens cervical mucus and thins the endometrial lining. It can cause irregular vaginal bleeding or spotting for the first few months, however, it decreases the amount of menstrual blood loss and therefore is first line treatment for menorrhagia.",
"id": "62403",
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"name": "The intrauterine system (IUS)",
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"explanation": "The SDI is a progesterone-only form of contraception.\nWhilst the SDI may be a good option for patients who struggle to remember to take a pill everyday, it is not a currently recommended treatment of menorrhagia.",
"id": "62405",
"label": "c",
"name": "Subdermal implant (SDI)",
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"explanation": "The IUD, also known as the copper coil, would not be an appropriate choice of contraception for this patient as she had menorrhagia which the IUD is likely to make worse.",
"id": "62404",
"label": "b",
"name": "The intrauterine device (IUD)",
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"explanation": "The IUS should be offered first line, especially to a patient wanting contraception. However, non-hormonal treatment options for menorrhagia imclude the use of tranexamic acid.",
"id": "62406",
"label": "d",
"name": "Barrier method contraception and tranexamic acid",
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"explanation": "# Summary\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive containing synthetic oestrogen and progestogen. It works by inhibiting ovulation, thickening cervical mucus, and altering the endometrium to prevent fertilisation and implantation. Indications for COCP use include contraception, menstrual cycle regulation, and treatment of dysmenorrhea, menorrhagia, acne, and hirsutism. Contraindications are categorised by UKMEC criteria, detailed in this chapter. \n \n# Definition\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive. It contains synthetic versions of the female hormones oestrogen and progestogen. \n \n\n# Mechanism of Action\n \n\n* **Inhibition of Ovulation:** The COCP contains synthetic versions of the hormones oestrogen and progestogen. These hormones together suppress the release of gonadotrophins (LH and FSH) from the pituitary gland, preventing the maturation and release of an egg from the ovaries.\n \n\n* **Thickening of Cervical Mucus:** The progestogen component of the COCP increases the viscosity of cervical mucus, making it more difficult for sperm to enter the uterus and fertilise an egg.\n \n\n * **Alteration of the Endometrium:** The COCP induces changes in the lining of the uterus (endometrium), making it less suitable for the implantation of a fertilised egg.\n \n\n# Indications\n \n\nThere are a range of reasons for women to be recommended the oral combined contraceptive pill. For example:\n \n\n* **Contraception:** The COCP works as a long-term contraception. It is taken orally once a day, at around the same time each day. \n * **Menstrual Cycle Regulation:** The COCP can help regulate irregular menstrual cycles. \n * **Dysmenorrhea:** The COCP may be used to reduce menstrual cramps. \n * **Menorrhagia:** The COCP can decrease heavy menstrual bleeding.\n * **Acne and Hirsutism:** The COCP helps in the treatment of acne and excessive hirsutism in women, which may happen in conditions such as polycystic ovary syndrome (PCOS) or other androgen excess conditions.\n * **Premenstrual Syndrome (PMHS**: The COCP can alleviate symptoms of PMS, such as mood swings, bloating, and irritability.\n \n# Contraindications \n \nThere are numerous contra-indications to the Combined Oral Contraceptive Pill. These can be divided into absolute contraindications, known as ''UKMEC 4'', a situation where the disadvantages outweigh the advantages (UKMEC 3), a situation where the advantages outweigh the disadvantages (UKMEC 2), and a situation whereby there is no limit on that choice of contraception (UKMEC 1).\n \n\n## Absolute Contraindications to Contraception (UKMEC 4)\n \n \n * Known or suspected pregnancy\n * Hypertension with SBP ≥160 mmHg or DBP ≥100 mmHg\n * Smoker over the age of 35 who smokes >15 cigarettes a day \n * Current and history of ischaemic heart disease\n * History of stroke (including TIA) \n * Vascular disease\n * History or current VTE\n * Major surgery with prolonged immobilisation\n * Breastfeeding <6 weeks postpartum\n * Not breastfeeding and <3 weeks postpartum with other risk factors for VTE\n * Known thrombogenic mutations \n * Complicated valvular and congenital heart disease\n * Cardiomyopathy with impaired cardiac function\n * Atrial fibrillation \n * Migraine with aura (any age)\n * Current breast cancer \n * Severe (decompensated) cirrhosis \n * Hepatocellular adenoma and hepatocellular carcinoma\n * Positive antiphospholipid antibodies \n \n \n \n## Disadvantages of a contraceptive outweigh the advantages (UKMEC 3)\n \n * Obesity (BMI ≥35 kg/m2)\n * Multiple risk factors for cardiovascular disease (e.g. smoking, diabetes mellitus, hypertension, obesity, dyslipidaemia) \n * Well controlled hypertension, and hypertension with SBP >140-159 mmHg or DBP <90-99 mmHg\n * Smoker over age of 35 who smokes <15 cigarettes a day, or anyone over age of 35 who stopped smoking <1 year ago\n * Family history of thrombosis before 45 years old\n * Not breastfeeding and <3 weeks postpartum without other risk factors for VTE\n * Not breastfeeding and between 3-6 weeks postpartum with other risk factors for VTE\n * Organ transplant with complications (e.g. graft failure, rejection) \n * Immobility (unrelated to surgery)\n * Migraine without aura (any age) [applies to *continuation* of COCP]\n * History (≥5 years ago) of migraine\nwith aura (any age) \n * Undiagnosed breast mass or symptoms [applies to *initiation* of COCP] \n * Carriers of known gene mutations associated with breast cancer\n * Past breat cancer \n * Diabetes mellitus with nephropathy, retinopathy, neuropathy or other vascular complications \n * Symptomatic gall bladder disease treated medically or currently active \n * Past COCP associated cholestasis \n * Acute viral hepatitis [applies to *initiation* of COCP]\n \n \n \n## Advantages of a contraceptive outweigh the disadvantages (UKMEC 2)\n \n * Smokers under the age of 35, and people aged over 35 who stopped smoking over 1 year ago \n * Obesity (BMI ≥30–34 kg/m2) \n * Family history of VTE in first-degree relative aged ≥45 years\n * History of raised blood pressure in pregnancy \n * Breast feeding between 6 weeks-6 months postpartum\n * Not breastfeeding and between 3-6 weeks postpartum without other risk factors for VTE\n * Uncomplicated organ transplant \n * Known dyslipidaemia \n * Major surgery without prolonged immobilisation \n * Superficial venous thrombosis \n * Uncomplicated valvular and congenital heart disease\n * Cardiomyopathy with normal cardiac function \n * Long QT syndrome \n * Non-migrainous headaches [applies to *continuation* of COCP]\n * Migraine without aura [applies to *initiation* of COCP] \n * Idiopathic intracranial hypertension \n * Unexplained vaginal bleeding\n * Cervical cancer \n * Undiagnosed breast mass or symptoms [applies to *continuation* of COCP]\n * Insulin-dependent diabetes mellitus without vascular disease \n * Symptomatic gall bladder disease treated through cholecystectomy, or asymptomatic gall bladder disease, or history of pregnancy-related cholestasis \n * Acute viral hepatitis [applies to *continuation* of COCP]\n * Inflammatory bowel disease \n * Sickle cell disease \n * Rheumatoid arthritis\n * SLE without antiphospholipid antibodies \n \n\n \n\n# Side-effects and Complications\n \n**Common Side-Effects:**\n \n\n * Breast tenderness \n * Abdominal discomfort, nausea diarrhoea \n * Headaches\n * Mood changes\n * Reduced libido \n \n\n**Rare but Serious Side-Effects:**\n \n\n * Embolism or thrombus, including: DVT and PE, stroke, myocardial infarction\n * Increased risk of breast cancer\n * Increased risk of cervical cancer \n \n\n \n\n# Follow-up\n\nArrange follow up 3 months following initial prescription of a COCP, and annually thereafter.\n \n\nAt follow-up, ensure to: \n \n\n * Check blood pressure and BMI. \n * Ask about headaches (including migraine). \n * Check for risk factors that may be contraindicators to COCP (as per UKMEC criteria). \n * Enquire about side-effects. \n * Enquire about how woman is taking the COCP (i.e. adherence). \n \n\n \n\n# Missed Pill Rules\n \n\n**Missed One Pill:**\n \n\n* Advise patient to take the pill as soon as possible, even if it means taking two pills in one day.\n* * Continue taking the rest of the pack as usual.\nNo additional contraception needed if this is the only pill missed in the pack.\n \n\n**Missed Two or More Pills in Week 1 (Days 1-7):**\n \n\n * Advise patient to take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * Use additional contraception for the next 7 days.\n * If they had unprotected sex during this week, seek emergency contraception.\n \n\n**Missed Two or More Pills in Week 2 (Days 8-14):**\n \n\n * Take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n\n**Missed Two or More Pills in Week 3 (Days 15-21):**\n \n\n* Finish the active pills in the current pack, then start a new pack immediately without taking the usual 7-day break.\n* No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n# NICE Guidelines \n \n\n[Click here to view NICE Guidelines on COCP](https://cks.nice.org.uk/topics/contraception-combined-hormonal-methods/management/combined-oral-contraceptive/)\n \n \n# References\n \n[Click here to see the UKMEC summary sheet on contraception](https://www.fsrh.org/standards-and-guidance/documents/ukmec-2016-summary-sheets/)",
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"question": "A 24 year old attends her GP surgery to discuss contraception. She currently takes a combined oral contraceptive pill (COCP). She has had to take emergency contraception twice this year due to forgetting to take the pill multiple days in a row. She wants to discuss alterantive methods of contraception.\n\nHer past medical history includes menorrhagia, which was previously investigated and is secondry to dysfunctional uterine bleeding.\n\nWhich of the following is the best next step in the management of this patient?",
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"explanation": "The POP thins the lining of the endometrium to prevent implantation into the endometrium. It also thickens the cervical mucus to prevent sperm reaching the egg.",
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"explanation": "Whilst some POPs do inhibit ovulation, the primary mechanism of action is by thickening of the cervical mucus and thinning of the endometrium. The progesterone only implant's primary mechanism of action is by preventing ovulation.\nThis is, however, the primary mechanism of action of the combined contraceptive pill.",
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"explanation": "The POP thins the endometrium, preventing implantation. It also thickens cervical mucus to prevent sperm reaching the egg.",
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"explanation": "This is the mechanism of action of the copper intrauterine device (IUD), which releases copper ions which is toxic to sperm, preventing fertilisation.\nThe POP's mechanism of action to prevent pregnancy is primrily thickening of the cervical mucus and thinning of the endometrium. Some POPs also prevent ovulation.\nThe thickening of the cervical mucus prevents sperm reaching the egg, the thinning of the endometrium prevents implantation.",
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"explanation": "# Summary\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive containing synthetic oestrogen and progestogen. It works by inhibiting ovulation, thickening cervical mucus, and altering the endometrium to prevent fertilisation and implantation. Indications for COCP use include contraception, menstrual cycle regulation, and treatment of dysmenorrhea, menorrhagia, acne, and hirsutism. Contraindications are categorised by UKMEC criteria, detailed in this chapter. \n \n# Definition\n \n\nThe combined oral contraceptive pill (COCP) is a long-term contraceptive. It contains synthetic versions of the female hormones oestrogen and progestogen. \n \n\n# Mechanism of Action\n \n\n* **Inhibition of Ovulation:** The COCP contains synthetic versions of the hormones oestrogen and progestogen. These hormones together suppress the release of gonadotrophins (LH and FSH) from the pituitary gland, preventing the maturation and release of an egg from the ovaries.\n \n\n* **Thickening of Cervical Mucus:** The progestogen component of the COCP increases the viscosity of cervical mucus, making it more difficult for sperm to enter the uterus and fertilise an egg.\n \n\n * **Alteration of the Endometrium:** The COCP induces changes in the lining of the uterus (endometrium), making it less suitable for the implantation of a fertilised egg.\n \n\n# Indications\n \n\nThere are a range of reasons for women to be recommended the oral combined contraceptive pill. For example:\n \n\n* **Contraception:** The COCP works as a long-term contraception. It is taken orally once a day, at around the same time each day. \n * **Menstrual Cycle Regulation:** The COCP can help regulate irregular menstrual cycles. \n * **Dysmenorrhea:** The COCP may be used to reduce menstrual cramps. \n * **Menorrhagia:** The COCP can decrease heavy menstrual bleeding.\n * **Acne and Hirsutism:** The COCP helps in the treatment of acne and excessive hirsutism in women, which may happen in conditions such as polycystic ovary syndrome (PCOS) or other androgen excess conditions.\n * **Premenstrual Syndrome (PMHS**: The COCP can alleviate symptoms of PMS, such as mood swings, bloating, and irritability.\n \n# Contraindications \n \nThere are numerous contra-indications to the Combined Oral Contraceptive Pill. These can be divided into absolute contraindications, known as ''UKMEC 4'', a situation where the disadvantages outweigh the advantages (UKMEC 3), a situation where the advantages outweigh the disadvantages (UKMEC 2), and a situation whereby there is no limit on that choice of contraception (UKMEC 1).\n \n\n## Absolute Contraindications to Contraception (UKMEC 4)\n \n \n * Known or suspected pregnancy\n * Hypertension with SBP ≥160 mmHg or DBP ≥100 mmHg\n * Smoker over the age of 35 who smokes >15 cigarettes a day \n * Current and history of ischaemic heart disease\n * History of stroke (including TIA) \n * Vascular disease\n * History or current VTE\n * Major surgery with prolonged immobilisation\n * Breastfeeding <6 weeks postpartum\n * Not breastfeeding and <3 weeks postpartum with other risk factors for VTE\n * Known thrombogenic mutations \n * Complicated valvular and congenital heart disease\n * Cardiomyopathy with impaired cardiac function\n * Atrial fibrillation \n * Migraine with aura (any age)\n * Current breast cancer \n * Severe (decompensated) cirrhosis \n * Hepatocellular adenoma and hepatocellular carcinoma\n * Positive antiphospholipid antibodies \n \n \n \n## Disadvantages of a contraceptive outweigh the advantages (UKMEC 3)\n \n * Obesity (BMI ≥35 kg/m2)\n * Multiple risk factors for cardiovascular disease (e.g. smoking, diabetes mellitus, hypertension, obesity, dyslipidaemia) \n * Well controlled hypertension, and hypertension with SBP >140-159 mmHg or DBP <90-99 mmHg\n * Smoker over age of 35 who smokes <15 cigarettes a day, or anyone over age of 35 who stopped smoking <1 year ago\n * Family history of thrombosis before 45 years old\n * Not breastfeeding and <3 weeks postpartum without other risk factors for VTE\n * Not breastfeeding and between 3-6 weeks postpartum with other risk factors for VTE\n * Organ transplant with complications (e.g. graft failure, rejection) \n * Immobility (unrelated to surgery)\n * Migraine without aura (any age) [applies to *continuation* of COCP]\n * History (≥5 years ago) of migraine\nwith aura (any age) \n * Undiagnosed breast mass or symptoms [applies to *initiation* of COCP] \n * Carriers of known gene mutations associated with breast cancer\n * Past breat cancer \n * Diabetes mellitus with nephropathy, retinopathy, neuropathy or other vascular complications \n * Symptomatic gall bladder disease treated medically or currently active \n * Past COCP associated cholestasis \n * Acute viral hepatitis [applies to *initiation* of COCP]\n \n \n \n## Advantages of a contraceptive outweigh the disadvantages (UKMEC 2)\n \n * Smokers under the age of 35, and people aged over 35 who stopped smoking over 1 year ago \n * Obesity (BMI ≥30–34 kg/m2) \n * Family history of VTE in first-degree relative aged ≥45 years\n * History of raised blood pressure in pregnancy \n * Breast feeding between 6 weeks-6 months postpartum\n * Not breastfeeding and between 3-6 weeks postpartum without other risk factors for VTE\n * Uncomplicated organ transplant \n * Known dyslipidaemia \n * Major surgery without prolonged immobilisation \n * Superficial venous thrombosis \n * Uncomplicated valvular and congenital heart disease\n * Cardiomyopathy with normal cardiac function \n * Long QT syndrome \n * Non-migrainous headaches [applies to *continuation* of COCP]\n * Migraine without aura [applies to *initiation* of COCP] \n * Idiopathic intracranial hypertension \n * Unexplained vaginal bleeding\n * Cervical cancer \n * Undiagnosed breast mass or symptoms [applies to *continuation* of COCP]\n * Insulin-dependent diabetes mellitus without vascular disease \n * Symptomatic gall bladder disease treated through cholecystectomy, or asymptomatic gall bladder disease, or history of pregnancy-related cholestasis \n * Acute viral hepatitis [applies to *continuation* of COCP]\n * Inflammatory bowel disease \n * Sickle cell disease \n * Rheumatoid arthritis\n * SLE without antiphospholipid antibodies \n \n\n \n\n# Side-effects and Complications\n \n**Common Side-Effects:**\n \n\n * Breast tenderness \n * Abdominal discomfort, nausea diarrhoea \n * Headaches\n * Mood changes\n * Reduced libido \n \n\n**Rare but Serious Side-Effects:**\n \n\n * Embolism or thrombus, including: DVT and PE, stroke, myocardial infarction\n * Increased risk of breast cancer\n * Increased risk of cervical cancer \n \n\n \n\n# Follow-up\n\nArrange follow up 3 months following initial prescription of a COCP, and annually thereafter.\n \n\nAt follow-up, ensure to: \n \n\n * Check blood pressure and BMI. \n * Ask about headaches (including migraine). \n * Check for risk factors that may be contraindicators to COCP (as per UKMEC criteria). \n * Enquire about side-effects. \n * Enquire about how woman is taking the COCP (i.e. adherence). \n \n\n \n\n# Missed Pill Rules\n \n\n**Missed One Pill:**\n \n\n* Advise patient to take the pill as soon as possible, even if it means taking two pills in one day.\n* * Continue taking the rest of the pack as usual.\nNo additional contraception needed if this is the only pill missed in the pack.\n \n\n**Missed Two or More Pills in Week 1 (Days 1-7):**\n \n\n * Advise patient to take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * Use additional contraception for the next 7 days.\n * If they had unprotected sex during this week, seek emergency contraception.\n \n\n**Missed Two or More Pills in Week 2 (Days 8-14):**\n \n\n * Take the last pill they missed as soon as possible. \n * Continue taking the rest of the pack as usual.\n * No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n\n**Missed Two or More Pills in Week 3 (Days 15-21):**\n \n\n* Finish the active pills in the current pack, then start a new pack immediately without taking the usual 7-day break.\n* No additional contraception needed if they have taken pills correctly for the 7 days prior to the missed pill.\n \n# NICE Guidelines \n \n\n[Click here to view NICE Guidelines on COCP](https://cks.nice.org.uk/topics/contraception-combined-hormonal-methods/management/combined-oral-contraceptive/)\n \n \n# References\n \n[Click here to see the UKMEC summary sheet on contraception](https://www.fsrh.org/standards-and-guidance/documents/ukmec-2016-summary-sheets/)",
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"question": "A 26 year old female attends her GP surgery to discuss contraception. She decides to try the progesterone only pill (POP).\n\nWhich of the following is the primary mechanism of action of this medication?",
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