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{ "__typename": "QuestionSBA", "choices": [ { "__typename": "QuestionChoice", "answer": false, "explanation": "Anticoagulation is indicated if her CHA₂DS₂-VASc score is 2 or more. She only has a score of 1 for being female", "id": "31755", "label": "c", "name": "Long term anticoagulation", "picture": null, "votes": 649 }, { "__typename": "QuestionChoice", "answer": true, "explanation": "We can be fairly certain that this woman's onset of atrial fibrillation is less than 48 hours, and since she's presented to an acute medical unit, DC cardioversion would be the most appropriate management. Factors favouring rhythm control over rate control in this case include being symptomatic, the first presentation of atrial fibrillation, and her age. She may require anticoagulation prior to cardioversion.\n\nHad this patient presented to the GP, management in primary care could also be considered, depending on patient preferences and clinical judgement", "id": "31753", "label": "a", "name": "Direct current (DC) cardioversion", "picture": null, "votes": 4825 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Bisoprolol may be used to rate control atrial fibrillation (AF). However, as this is her first presentation of AF, she is young and symptomatic, and she has presented to the emergency department, rhythm control would be more favourable in the first instance.\n\nIn primary care, rate control may be initiated rather than cardioversion, depending on patient preference and clinical judgement", "id": "31757", "label": "e", "name": "Bisoprolol", "picture": null, "votes": 3152 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "TOEs may sometimes be used to exclude a left atrial appendage thrombus before cardioversion if the onset of AF was more than 48 hours prior to the planned cardioversion, as an alternative to anticoagulation", "id": "31754", "label": "b", "name": "Transoesophageal Echocardiogram (TOE)", "picture": null, "votes": 708 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Digoxin may be used second line for rate control of atrial fibrillation if a beta blocker or rate limiting calcium channel blocker is not sufficient in the first instance", "id": "31756", "label": "d", "name": "Digoxin", "picture": null, "votes": 530 } ], "comments": [ { "__typename": "QuestionComment", "comment": "hello everyone - good luck for all your exams xoxo", "createdAt": 1655059775, "dislikes": 0, "id": "12061", "isLikedByMe": 0, "likes": 30, "parentId": null, "questionId": 6351, "replies": [ { "__typename": "QuestionComment", "comment": "you too!! good luck :)", "createdAt": 1655663385, "dislikes": 0, "id": "12300", "isLikedByMe": 0, "likes": 3, "parentId": 12061, "questionId": 6351, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Abigail ", "id": 23295 } }, { "__typename": "QuestionComment", "comment": "Thank you!", "createdAt": 1682170430, "dislikes": 0, "id": "22440", "isLikedByMe": 0, "likes": 1, "parentId": 12061, "questionId": 6351, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Camiodarone", "id": 27328 } } ], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Versicolor Sclerosis", "id": 10483 } }, { "__typename": "QuestionComment", "comment": "Would you not rate control and DC cardiovert as OP? She's 95bpm and no other evidence of haemodynamic compromise? Or is this because it's her first presentation you hit her with DCCV??", "createdAt": 1669122966, "dislikes": 0, "id": "14687", "isLikedByMe": 0, "likes": 2, "parentId": null, "questionId": 6351, "replies": [ { "__typename": "QuestionComment", "comment": "If presenting with very recently started AF you cardiovert, if it is longer standing or there is doubt about onset then either rate control or delayed cardioversion with anticoagulation", "createdAt": 1682170491, "dislikes": 0, "id": "22441", "isLikedByMe": 0, "likes": 2, "parentId": 14687, "questionId": 6351, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Camiodarone", "id": 27328 } } ], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "BenWhiteside", "id": 25369 } }, { "__typename": "QuestionComment", "comment": "There is no evidence that she is symptomatic or haemodynamically unstable. She has presented <48 hours and so rhythm or rate control can be used. Does this question require re-writing?", "createdAt": 1682832997, "dislikes": 5, "id": "22986", "isLikedByMe": 0, "likes": 9, "parentId": null, "questionId": 6351, "replies": [ { "__typename": "QuestionComment", "comment": "She IS symptomatic, she's come in to A&E with palpitations. Since the history is <48 hours, her risk of clots is low so she can be cardioverted straight away, as is preferred.", "createdAt": 1684410406, "dislikes": 1, "id": "25125", "isLikedByMe": 0, "likes": 0, "parentId": 22986, "questionId": 6351, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Amnesia Defibrillator", "id": 21454 } }, { "__typename": "QuestionComment", "comment": "in what world is she asymptomatic with palpitations? ", "createdAt": 1708949814, "dislikes": 1, "id": "42877", "isLikedByMe": 0, "likes": 0, "parentId": 22986, "questionId": 6351, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Ale", "id": 20565 } } ], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "PagingDr", "id": 30418 } }, { "__typename": "QuestionComment", "comment": "What would be mx if she presented to GP?", "createdAt": 1704143563, "dislikes": 0, "id": "37410", "isLikedByMe": 0, "likes": 1, "parentId": null, "questionId": 6351, "replies": [ { "__typename": "QuestionComment", "comment": "“ In primary care, rate control may be initiated rather than cardioversion, depending on patient preference and clinical judgement”", "createdAt": 1723715753, "dislikes": 0, "id": "54680", "isLikedByMe": 0, "likes": 0, "parentId": 37410, "questionId": 6351, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Lo", "id": 13055 } } ], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "RNA Gastro", "id": 13210 } } ], "concept": { "__typename": "Concept", "chapter": { "__typename": "Chapter", "explanation": "# Summary \r\n\r\nAtrial fibrillation (AF) is the most common arrhythmia characterised by irregular and uncoordinated atrial contraction at a rate of 300-600 beats per minute. Its prevalence increases with age, and it can be caused by various cardiac and non-cardiac factors. Symptoms of AF include palpitations, chest pain, shortness of breath, lightheadedness, and syncope. Diagnosis is confirmed by an ECG showing the absence of p waves and an irregularly irregular rhythm. Management depends on the acute or chronic nature of the AF and involves rate or rhythm control strategies. Anticoagulation is essential to mitigate the risk of stroke in chronic AF. Complications include heart failure, embolism, and bleeding. With appropriate management, AF has a favourable prognosis.\r\n\r\n# Definition \r\n\r\nAtrial fibrillation (AF) is characterised by irregular, uncoordinated atrial contraction usually at a rate of 300-600 beats per minute. Delay at the AVN means that only some of the atrial impulses are conducted to the ventricles, resulting in an irregular ventricular response.\r\n\r\n# Epidemiology \r\n\r\nAF is the commonest sustained cardiac arrhythmia. The prevalence of AF roughly doubles with each advancing decade of age, from 0.5% at age 50 years to almost 9% at age 80 years.\r\n\r\n# Pathophysiology\r\n\r\nThe exact pathophysiology of AF is unclear, but factors that cause atrial dilatation through inflammation and fibrosis leads to disorganised electrical impulses (which originate near the pulmonary veins) that overwhelm the SAN. These disorganised electrical impulses are usually at a rate of 300-600 beats per minute and are intermittently conducted through the AVN leading to irregular activation of the ventricles. \r\n\r\n# Classification \r\n\r\n* Acute: lasts <48 hours\r\n* Paroxysmal: lasts <7 days and is intermittent\r\n* Persistent: lasts >7 days but is amenable to cardioversion\r\n* Permanent: lasts >7 days and is not amenable to cardioversion\r\n\r\nAtrial fibrillation can also be classified as to whether it is 'fast' or 'slow'. Fast AF refers to AF that is at a rate of =>100bpm. Slow AF refers to AF that is at a rate of <=60bpm. \r\n\r\n# Causes \r\n\r\nCardiac:\r\n\r\n* Ischaemic heart disease: most common cause in the UK. \r\n* Hypertension\r\n* Rheumatic heart disease (typically affecting the mitral valve): most common cause in less developed countries.\r\n* Peri-/myocarditis\r\n\r\nNon-cardiac:\r\n\r\n* Dehydration\r\n* Endocrine causes e.g. hyperthyroidism\r\n* Infective causes e.g. sepsis \r\n* Pulmonary causes e.g. pneumonia or pulmonary embolism\r\n* Environmental toxins e.g. alcohol abuse\r\n* Electrolyte disturbances e.g. hypokalaemia, hypomagnesaemia \r\n\r\n# Symptoms\r\n\r\n* Palpitations\r\n* Chest pain\r\n* Shortness of breath\r\n* Lightheadedness\r\n* Syncope\r\n\r\n# Signs\r\n\r\n* Irregularly irregular pulse rate with a variable volume pulse.\r\n* A single waveform on the jugular venous pressure (due to loss of the a wave - this normally represents atrial contraction).\r\n* An apical to radial pulse deficit (as not all atrial impulses are mechanically conducted to the ventricles).\r\n* On auscultation there may be a variable intensity first heart sound.\r\n* Features suggestive of the underlying cause e.g. hyperthyroidism, alcohol excess, sepsis\r\n* Features suggestive of complications resulting from the AF e.g. heart failure.\r\n\r\n# Differential Diagnoses \r\n\r\nImportant differentials for atrial fibrillation include other common causes of narrow and broad complex tachycardias. Tachycardias may present with palpitations, shortness of breath, and dyspnoea. \r\n\r\n* **Atrial Flutter** \r\n\t* **Similarities**: atrial flutter may have a regular peripheral pulse or may be irregularly irregular if the flutter has variable block. Atrial fibrillation leads to an irregularly irregular peripheral pulse on palpation.\r\n\t* **Differences**: distinguishing between the two requires an ECG. Atrial fibrillation on ECG shows a fibrillating baseline with no visible p waves. Atrial flutter characteristically has a sawtooth baseline. \r\n\r\n* **Supraventricular Tachycardia**\r\n\t* **Similarities**: atrial flutter is a type of SVT, and other types including AVNRT and AVRT may present identically. \r\n\t* **Differences**: distinguishing between different types of SVT requires an ECG. \r\n\r\n* **Ventricular Tachycardia**\r\n\t* **Similarities**:both may present similarly. \r\n\t* **Differences**: the ECG patterns differ tremendously. \r\n\r\nFor palpitation histories, it is also important to consider whether the presentation is being driven by anxiety. However, it is important as a rule of thumb to rule out organic causes first. \r\n\r\n# Investigations\r\n\r\n## Bedside\r\n\r\n**Definitive diagnosis: 12-lead ECG** shows absence of p waves with an irregularly irregular rhythmn. \r\n\r\n[lightgallery]\n\n- If a person has a suspected diagnosis of paroxysmal AF which is not detected on standard ECG, arrange ambulatory electrocardiography or cardiology referral, depending on the frequency and duration of symptoms and local referral pathways\r\n\r\n## Bloods \r\n\r\nRoutine bloods: to look for reversible causes including infection (raised WCC or CRP), hyperthyroidism (raised T3/T4) or alcohol use (raised MCV and GGT).\r\n\r\n## Imaging\r\n\r\nEchocardiogram: can be used to see if there is a cardiac cause of the AF e.g. left atrial dilatation secondary to mitral valve disease. \r\n\r\n# Management\n\nConsider emergency admission or Cardiology referral if a patient presents with:\n\n- New-onset AF within the past 48 hours and is haemodynamically unstable\n- Severe symptoms of AF due to rapid (bpm > 150 ) or very slow (bpm < 40) ventricular rate\n- Concomitant acute decompensated heart failure\n- Complications of AF, such as TIA/stroke\n- An acute, potentially reversible trigger such as pneumonia/sepsis or thyrotoxicosis\n\nIf they do not require acute management or emergency admission, they can be considered for anticoagulation and rate-control treatment in primary care.\r\n\r\n## Management of Acute or New-onset Atrial Fibrillation\r\n\r\nFor emergencies, always follow an A-E structure. Identify reversible causes (dyselectrolytaemias, drugs, cardiac causes etc.) \r\n\r\n*If there are adverse signs (e.g. shock, syncope, heart failure, myocardial ischaemia):* \r\n\r\n* **1st line** = **synchronised DC cardioversion +/- amiodarone.**\r\n\r\n*If there are no adverse signs:* and the rhythm is irregular it is likely atrial fibrillation. \r\n\r\n* **If the patient is stable and onset of AF <48 hours**: \r\n\t* Rate or rhythmn control.\r\n\t* Rhythm control with DC cardioversion (+ sedation) or pharmacological anti-arrhythmics (fleicanide if no structural heart disease, amiodarone if history of structural heart disease). \r\n\t* If DC cardioversion is delayed then heparin will be required to anticoagulate the patient. \r\n\r\n* **If the patient is stable and onset of AF >48 hours/unclear time of onset**: \r\n\t* Rate control only. \r\n\t* Rate control with beta-blockers, diltiazem or digoxin. \r\n\t* Need to anticoagulate for 3/52 prior to attempting cardioversion due to the risk of throwing off a clot. You can also perform a TOE to exclude a mural thrombus. \r\n\r\nIf AF persists or reversible causes are not present then decisions should be made about rate control, rhythm control or electrical cardioversion.\r\n\r\n## Management of Chronic AF \r\n\r\nThe cornerstones of managing chronic AF are related to symptom control and mitigating stroke risk. \r\n\r\n## Symptom Management of Chronic AF \r\n\r\n### Rate vs. Rhythm Control \r\n\r\n#### Rate-Control\r\n\r\nThe aim of rate control is to reduce a patient's heart rate in order to reduce symptoms.\r\n \r\n* First line in most patients. See below for patients who should undergo rhythm control. \r\n* **1st line medications:** beta-blocker (bisoprolol) or rate-limiting calcium channel blocker (diltiazem). \r\n* **2nd line medications**: dual therapy (under specialist guidance) \r\n* Digoxin monotherapy may be considered in those with non-paroxysmal AF who are sedentary. \r\n \r\n#### Rhythm Control\r\n\r\nThe aim of rhythm control is to revert a patient back into sinus rhythm. \r\n \r\nRhythm control should be offered to patients who have: \r\n\r\n* AF secondary to a reversible cause\r\n* Heart failure thought to be caused by AF\r\n* New-onset AF\r\n* Or those for whom a rhythm control strategy would be more suitable based on clinical judgement. \r\n\r\nRhythm control can be achieved via two methods:\r\n\r\n* Electrical cardioversion\r\n* Pharmacological cardioversion: amiodarone, fleicanide or sotalol. \r\n\r\nThe moment of return to sinus rhythm poses the highest stroke risk. Therefore, rhythm control should only be attempted if the onset of AF <48 hours, a patient has undergone 3/52 of anticoagulation or has had a TOE to exclude a mural thrombus. \r\n\r\nNote that patients in chronic AF or those who have failed cardioversion before are unlikely to be successfully cardioverted so this would not be considered in most of these cases.\r\n\r\n#### Catheter Ablation \r\n\r\nA final option for rhythm control is catheter ablation of the arrhythmogenic focus between the pulmonary veins and left atrium. Even if teh foci is ablated, this does not reduce stroke risk and the patient must be anticoagulated. There is a high risk of recurrence (50% have recurrent AF). \r\n\r\n## Medications used for Rate Control \r\n\r\n### Beta-blockers\r\n\r\n* The most commonly used beta-blocker in AF is bisoprolol.\r\n* Commonly used medication for acute treatment and chronic management.\r\n* Technically it is contraindicated in COPD and asthma (in reality unless the conditions are considered _brittle_ it is not a problem). \r\n* Cannot be used in hypotension because it will drop blood pressure.\r\n* Note that sotalol CANNOT be used as a rate control agent because of its rhythm control action.\r\n\r\n### Non-dihydropyridine calcium channel blockers\r\n\r\n* Calcium channel blockers used in AF are diltiazem or verapamil.\r\n* They are not frequently used in hospital settings because they are negatively ionotropic and therefore they are contraindicated in heart failure.\r\n\r\n### Digoxin\r\n\r\n* Usual for patients who are hypotensive or who have co-existent heart failure.\r\n* Should be avoided in younger patients because it increases cardiac mortality.\r\n* Often used second-line in conjunction with beta-blockers if fast AF remains refractory.\r\n\r\n## Medications used for Rhythm Control\r\n\r\n* Flecainide\r\n * Can be either given regularly or as a \"pill in the pocket\" when symptoms come on.\r\n * Is preferred in _young patients_ who have _structurally normal hearts_ because it can induce fatal arrhythmias in those with structural heart disease.\r\n\r\n* Amiodarone\r\n * Extremely effective drug in controlling both rate and rhythm.\r\n * However it comes with a massive list of significant side-effects so should normally only be given to _older, sedentary patients_.\r\n\r\n* Sotalol\r\n * This is a beta blocker with additional K channel blocker action.\r\n * Used for those that don't meet the demographics for either flecainide or amiodarone.\r\n\r\n## Mitigating Stroke Risk in Chronic AF \r\n\r\nIn atrial fibrillation, the lack of organised atrial contraction can lead to blood stasis in the left atrium. Due to the left atrial appendage, blood clots easily here and if part of this clot embolises it can lead to a stroke. Therefore, if a patient has any history of atrial fibrillation or atrial flutter the need for anticoagulation must be considered. \r\n\r\nPatients need to be considered according to their stroke risk (CHADS2VASc score) and their bleeding risk (ORBIT score) to determine whether anticoagulation is appropriate. \r\n\r\n### CHADS2VASc Score\r\n\r\nPatients should be risk stratified using the CHADS2VASc score:\r\n\r\n* C: 1 point for congestive cardiac failure.\r\n* H: 1 point for hypertension.\r\n* A2: 2 points if the patient is aged 75 or over.\r\n* D: 1 point if the patient has diabetes mellitus.\r\n* S2: 2 points if the patient has previously had a stroke or transient ischaemic attack (TIA).\r\n* V: 1 point if the patient has known vascular disease.\r\n* A: 1 point if the patient is aged 65-74.\r\n* Sc: 1 point if the patient is female.\r\n\r\n#### Interpretation of the CHADS2VASc score\r\n\r\nThe minimum score is 0 (associated with 0% annual stroke risk) and maximum score is 9 (15% annual stroke risk).\r\nMales who score 1 or more or females who score 2 or more should be anticoagulated (as long as the risk of stroke outweighs the risk of bleeding). \r\n\r\n#### ORBIT Score\r\n\r\nRisks of anticoagulation also need to be considered. Historically the HASBLED score stratified bleeding risk:\r\n\r\n* H: Hypertension 1 point\r\n* A: Abnormal renal or liver function 2 points if both are present\r\n* S: Stroke (previous) 1 point\r\n* B: Major bleed (previous) 1 point\r\n* L: Labile INR 1 point\r\n* E: Elderly (>65) 1 point\r\n* D: Drugs/alcohol 1 point for drug or alcohol use (2 points if both are present)\r\n\r\nIn their 2021 AF guidelines NICE suggested the use of the ORBIT score which takes into account:\r\n\r\n* Sex\r\n* Haemoglobin (<13mg/Dl in males, <12mg<dL in females) 2 points\r\n* Age (>74) 1 point\r\n* Bleeding history 2 points\r\n* Renal function (eGFR <60) 1 point\r\n* Concomitant use of anti-platelets 1 point\r\n\r\n#### Interpretation of the HASBLED and ORBIT scores\r\n\r\nIn reality very little guidance exists about how to weigh up the stroke and bleeding risks when making a decision on anticoagulation. Choice of long term anticoagulation is generally a decision led by patient choice and clinical judgement.\r\n\r\n### Anticoagulation options in AF\r\n\r\n* **Direct oral anticoagulants (DOACs)**:\r\n * Considered first line for anticoagulation in AF. \r\n * Examples of DOACs are edoxaban, apixaban, rivaroxaban & dabigatran\r\n * **Do not** require monitoring\r\n * Generally associated with fewer bleeding risks compared to warfarin.\r\n * Most have approximately 12 hour half-lives therefore if a patient misses a dose they are not covered.\r\n\r\n* **Warfarin**:\r\n * Requires cover with LMWH for 5 days when initiating treatment (because warfarin is initially _prothrombotic_).\r\n * Requires regular INR monitoring.\r\n * INR can be affected by a whole host of drugs and foods.\r\n * Has 40 hour half-life therefore anticoagulant effect lasts days.\r\n * Is the only oral anticoagulant licenced for **valvular AF**.\r\n* **Low Molecular Weight Heparin (LMWH)**:\r\n * An example of a LMWH is enoxaparin.\r\n * A rare option in patients who cannot tolerate oral treatment.\r\n * Involves daily _treatment dose_ injections.\r\n\r\n# Complications\r\n\r\nMost complications are either from uncontrolled heart rate, embolism or from anticoagulation. They include:\r\n\r\n* Heart failure\r\n* Systemic emboli:\r\n * Ischaemic Stroke\r\n * Mesenteric ischaemia\r\n * Acute limb ischaemia\r\n* Bleeding:\r\n * GI\r\n * Intracranial\r\n \r\n# Prognosis \r\n\r\nIf patients are anticoagulated and are on either rhythm or rate control AF can remain a benign cardiac arrhythmia. \r\n\r\n# NICE Guidelines\r\n\n[Click here to see information on NICE CKS guidance for AF](https://cks.nice.org.uk/topics/atrial-fibrillation/)\r\n\r\n# References\r\n \r\n[Live Life in the Fast Lane AF ECG Summary](https://litfl.com/atrial-fibrillation-ecg-library/)", "files": null, "highlights": [], "id": "620", "pictures": [ { "__typename": "Picture", "caption": "An ECG showing an irregularly irregular heart rate and absent p waves, these are characteristic signs of atrial fibrillation.", "createdAt": 1665036193, "id": "761", "index": 0, "name": "AF.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/pum5vnoi1665036171705.jpg", "path256": "images/pum5vnoi1665036171705_256.jpg", "path512": "images/pum5vnoi1665036171705_512.jpg", "thumbhash": "OSgCA4CWoKSOh/hWJ4WQcAg=", "topic": null, "topicId": null, "updatedAt": 1708373886 } ], "typeId": 2 }, "chapterId": 620, "demo": null, "entitlement": null, "id": "632", "name": "Atrial fibrillation", "status": null, "topic": { "__typename": "Topic", "id": "35", "name": "Cardiology", "typeId": 2 }, "topicId": 35, "totalCards": 34, "typeId": null, "userChapter": null, "userNote": null, "videos": [ { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "632", "name": "Atrial fibrillation" } ], "demo": false, "description": null, "duration": 826.2, "endTime": null, "files": null, "id": "672", "live": false, "museId": "KmBA8iR", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/cardiology.png", "title": "Atrial fibrillation 2", "userViewed": false, "views": 129, "viewsToday": 23 }, { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "632", "name": "Atrial fibrillation" } ], "demo": false, "description": null, "duration": 302.06, "endTime": null, "files": null, "id": "41", "live": false, "museId": "nTGanPL", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/cardiology.png", "title": "Atrial fibrillation ", "userViewed": false, "views": 468, "viewsToday": 48 }, { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "632", "name": "Atrial fibrillation" } ], "demo": false, "description": null, "duration": 423.66, "endTime": null, "files": null, "id": "178", "live": false, "museId": "53f9EFj", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/hematology.png", "title": "High INR 2", "userViewed": false, "views": 135, "viewsToday": 15 }, { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "632", "name": "Atrial fibrillation" } ], "demo": false, "description": null, "duration": 4294.36, "endTime": null, "files": null, "id": "610", "live": false, "museId": "8JoZgLE", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/cardiology.png", "title": "Quesmed Tutorial: Arrhythmias", "userViewed": false, "views": 591, "viewsToday": 35 }, { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "632", "name": "Atrial fibrillation" } ], "demo": false, "description": null, "duration": 4459.69, "endTime": null, "files": null, "id": "330", "live": false, "museId": "1QTvHhh", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/respiratory.png", "title": "Quesmed Tutorial: PE and DVT", "userViewed": false, "views": 110, "viewsToday": 11 }, { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "632", "name": "Atrial fibrillation" } ], "demo": false, "description": null, "duration": 4692.22, "endTime": null, "files": null, "id": "306", "live": false, "museId": "AdKRmxV", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/cardiology.png", "title": "Quesmed Tutorial: Cardiology", "userViewed": false, "views": 2232, "viewsToday": 47 } ] }, "conceptId": 632, "conditions": [], "difficulty": 3, "dislikes": 16, "explanation": null, "highlights": [], "id": "6351", "isLikedByMe": 0, "learningPoint": "In acute atrial fibrillation onset within 48 hours, direct current (DC) cardioversion is often the preferred management approach to quickly restore normal sinus rhythm and reduce the risk of complications.", "likes": 9, "multiAnswer": null, "pictures": [], "prescribeAnswer": null, "presentations": [], "psaSectionId": null, "qaAnswer": null, "question": "A 62-year-old woman presents to the Accident and Emergency department with a sudden onset of palpitations 6 hours earlier. In the department, her ECG shows atrial fibrillation at a rate of 95 beats per minute. She has a past medical history of asthma, and had an NHS Health Check the day before, where she was noted to be in sinus rhythm.\n\nWhich of the following is the most suitable next step in the management of this patient?", "sbaAnswer": [ "a" ], "totalVotes": 9864, "typeId": 1, "userPoint": null }

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{ "__typename": "QuestionSBA", "choices": [ { "__typename": "QuestionChoice", "answer": false, "explanation": "There is no indication of ST-elevation on this ECG. A STEMI will cause ST elevation acutely, but it is important to note that the ECG changes will evolve over time", "id": "31759", "label": "b", "name": "ST-elevation myocardial infarction (STEMI)", "picture": null, "votes": 637 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Acute pericarditis is associated with global concave ST elevation and PR depression, which is not seen on this ECG", "id": "31760", "label": "c", "name": "Acute pericarditis", "picture": null, "votes": 910 }, { "__typename": "QuestionChoice", "answer": true, "explanation": "This ECG shows left ventricular hypertrophy (increased amplitude of the QRS complex, particularly noticeable in V1-V4) and non-specific T-wave inversion. In an otherwise young, healthy person, the most likely cause of left ventricular hypertrophy is HCM. This would also explain his symptoms of chest pain and shortness of breath on exertion. He should be referred for an urgent cardiology review for consideration of an implantable cardioverter-defibrillator (ICD)", "id": "31758", "label": "a", "name": "Hypertrophic cardiomyopathy (HCM)", "picture": null, "votes": 6650 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Hyperkalaemia is classically associated with \"tall tented T waves\" on an ECG, which are not seen on this ECG", "id": "31761", "label": "d", "name": "Hyperkalaemia", "picture": null, "votes": 662 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "RBBB is associated with a QRS duration of >120ms and an RSR' pattern in V1-V3 (\"M-shaped\" as in \"WiLLiaM MaRRoW\"), which is not seen on this ECG", "id": "31762", "label": "e", "name": "Right bundle branch block (RBBB)", "picture": null, "votes": 633 } ], "comments": [ { "__typename": "QuestionComment", "comment": "can't see all of the ecg\n", "createdAt": 1656151211, "dislikes": 0, "id": "12476", "isLikedByMe": 0, "likes": 4, "parentId": null, "questionId": 6352, "replies": [], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Bonello's Bad Boys", "id": 23088 } }, { "__typename": "QuestionComment", "comment": "Doesnt seem like an LVH on ecg", "createdAt": 1718970296, "dislikes": 0, "id": "53414", "isLikedByMe": 0, "likes": 2, "parentId": null, "questionId": 6352, "replies": [ { "__typename": "QuestionComment", "comment": "agreed - should be deep S waves in V1/V2 and tall R waves in V5/V6", "createdAt": 1719053356, "dislikes": 0, "id": "53492", "isLikedByMe": 0, "likes": 3, "parentId": 53414, "questionId": 6352, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Lymph Neoplasia", "id": 8652 } } ], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Supine Bladder", "id": 35998 } } ], "concept": { "__typename": "Concept", "chapter": { "__typename": "Chapter", "explanation": "# Summary\r\n\r\nHypertrophic cardiomyopathy (HCM) is an autosomal dominant condition characterised by left ventricular hypertrophy without an apparent cause. It is a common inherited cardiac condition and a significant cause of sudden cardiac death in young adults. HCM is attributed to mutations in genes encoding sarcomere proteins leading to chaotic and disorganized myocytes. HCM may be asymptomatic but can also lead to exertional syncope, dyspnoea, chest pain and heart failure. Definitive diagnosis is made via echocardiogram. Management involves lifestyle modifications, medication for symptom control, surgical or interventional procedures for severe cases, and consideration of implantable cardioverter-defibrillators in those at risk of sudden cardiac death. Prognosis varies, with an annual mortality rate of 1.1%, and a 20-year survival rate estimated at 81% after diagnosis.\r\n\r\n# Definition \r\n\r\nHypetrophic cardiomyopathy (HCM) is an autosomal dominant condition characterised by asymmetrical septal hypertrophy leading to left ventricular hypetrophy and diastolic dysfunction in the absence of an obvious cause (e.g. hypertension). \r\n\r\n# Epidemiology \r\n\r\nHCM is estimated to impact 1 in 500 people. It is the most common inherited cardiac condition. Inheritance of HCM is in an autosomal dominant fashion. However, 50% of cases result due to sporadic mutations. Most of the hypertrophy develops during childhood and adolescent, however, genetic variation means late-onset disease can occur.\r\n\r\n# Pathophysiology\r\n\r\nHCM is attributed to mutations in one or a number of genes that encode for sarcomere proteins. A common mutation is in the beta-myosin heavy chain gene leading to myocyte hypetrophy with chaotic and disorganised myocytes. \r\n\r\n# Symptoms\r\n\r\n* May be asymptomatic \r\n* Or can present with symptoms of left ventricular outflow obstruction, pulmonary congestion or heart failure: \r\n\t* Exertional syncope \r\n\t* Pre-syncope/syncope\r\n\t* Sudden cardiac death \r\n\t* Exertional dyspnoea \r\n\t* Fatigue\r\n\t* Chest pain: may be anginal (due to decreased blood flow through the coronary arteries) or atypical. \r\n\r\n# Signs\r\n\r\nPhysical examination can often be normal or non-specific, however typical findings may include:\r\n\r\n* \"Jerky\" pulse\r\n* Double apex beat\r\n* Harsh ejection systolic murmur\r\n* Apical thrill\r\n* A wave in JVP \r\n\r\n# Differential Diagnoses\r\n\r\n* Aortic Stenosis \r\n\t* Similarities: both may have an ejection systolic murmur and present similarly with chest pain, exertional syncope and dyspnoea. \r\n\t* Differences: can be difficult to delineate clinically, but demographics may be very different. Aortic stenosis tends to affect older patients, whilst HOCM is likely to be found in younger patients. \r\n\r\n* Hypertensive Disease \r\n\t* Similarities: chronic high blood pressure can lead to left ventricular hypertrophy. \r\n\t* Differences: echocardiogram reveals asymmetrical left ventricular hypertrophy in HOCM. Family history and patient demographics may also suggest HOCM over hypertensive disease. \r\n\r\n* Supravalvular Aortic Stenosis: \r\n\t* Similarities: both may have an ejection systolic murmur. \r\n\t* Differences: supravalvular aortic stenosis is a congenital cardiac condition whereas HOCM tends to develop over time. Supravalvular stenosis can be distinguished from HOCM on echocardiography due to the level of obstruction either above or below the aortic valve respectively. \r\n\r\n# Investigations\r\n\r\n**ECG** typically demonstrates: \r\n\r\n* Abnormal Q waves\r\n* Deep T wave inversion \r\n* LVH \r\n\r\n**Echocardiogram: definitive diagnosis** \r\n\r\n* HCM is reliably diagnosed on echocardiogram. \r\n* Findings of HOCM on echocardiogram can be remembered with the mnemonic 'MR SAM ASH'. \r\n\t* **M**itral **R**egurgitation\r\n\t* **S**ystolic **A**nterior **M**otion of the mitral valve leaflets \r\n\t* **A**symmetrical **S**eptal **H**ypertrophy. \r\n\r\n**Genetic testing:** there is a role for genetic testing in HCM in families where there are known cases of HCM. \r\n\r\n# Management\r\n\r\n## Conservative \r\n\r\nMany patients with HCM do not have any symptoms and have a normal life expectancy. They are often counselled on not undertaking particularly stressful exercise or competitive athletics. \r\n\r\n## Medical \r\n\r\nMedical treatment of HCM remains symptoms control. \r\n**1st line: beta-blockers** to reduce palpitations symptoms, ectopic beats and are anti-anginal. \r\n\r\nOther medications that can be used are: non-dihydropyridine calcium channel blockers (verapamil), anti-arrhythmics (amiodarone) and anticoagulation (for AF). \r\n\r\n## Surgical and Interventional\r\n\r\nManagement of the septal hypetrophy in those with severe left ventricular outflow tract obstruction (LVOTO) or symptoms that are refractory to medical management. \r\n\r\n* Surgical septal myectomy\r\n* Alcohol septal ablation\r\n\r\nFor those at significant risk of sudden cardiac death an ICD may be inserted to mitigate this risk. \r\n\r\n# Complications\r\n\r\nThe abnormal morphology of the left ventricle can cause severe consequences for heart function: \r\n\r\n* Left ventricular outflow tract obstruction (LVOTO)\r\n* Diastolic dysfunction: HFpEF\r\n* Ischaemia \r\n* Mitral regurgitation: MR SAM ASH on echocardiogram \r\n\r\n# Prognosis \r\n\r\nThe annual mortality rate for HCM is 1.1% of people per year and the HCM survival rate is estimated to be 81% at 20 years after diagnosis. \r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines on Non-Surgical Reduction of the Myocardium in HCM](<https://www.nice.org.uk/guidance/ipg40>)\r\n\r\n# References\r\n\r\n[Patient UK HCM Summary](<https://patient.info/doctor/hypertrophic-cardiomyopathy-pro>)\n\r\n[American Heart Association Article on HCM](<https://www.ahajournals.org/doi/full/10.1161/circresaha.116.309348>)", "files": null, "highlights": [], "id": "626", "pictures": [], "typeId": 2 }, "chapterId": 626, "demo": null, "entitlement": null, "id": "640", "name": "Hypertrophic cardiomyopathy", "status": null, "topic": { "__typename": "Topic", "id": "35", "name": "Cardiology", "typeId": 2 }, "topicId": 35, "totalCards": 11, "typeId": null, "userChapter": null, "userNote": null, "videos": [] }, "conceptId": 640, "conditions": [], "difficulty": 2, "dislikes": 1, "explanation": null, "highlights": [], "id": "6352", "isLikedByMe": 0, "learningPoint": "Hypertrophic obstructive cardiomyopathy (HOCM) often presents on ECG with left ventricular hypertrophy (increased amplitude of the QRS complex, especially in leads V1-V4) and non-specific T-wave inversion, indicating the presence of abnormal heart muscle.", "likes": 10, "multiAnswer": null, "pictures": [ { "__typename": "Picture", "caption": null, "createdAt": 1639016489, "id": "355", "index": 0, "name": "HOCM ECG.jpg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/nk5ppkwa1639016481198.jpg", "path256": "images/nk5ppkwa1639016481198_256.jpg", "path512": "images/nk5ppkwa1639016481198_512.jpg", "thumbhash": "dkgCBICUh3eIh3iAh4mahc+H+A==", "topic": { "__typename": "Topic", "id": "35", "name": "Cardiology", "typeId": 2 }, "topicId": 35, "updatedAt": 1708373886 } ], "prescribeAnswer": null, "presentations": [], "psaSectionId": null, "qaAnswer": null, "question": "An 18 year old man attends to his GP with chest pain and shortness of breath on exertion. He has no significant past medical history. An ECG is performed:\n\n[lightgallery]\n\nWhich of the following is the most likely to account for the ECG findings?", "sbaAnswer": [ "a" ], "totalVotes": 9492, "typeId": 1, "userPoint": null }

[]

{ "__typename": "QuestionSBA", "choices": [ { "__typename": "QuestionChoice", "answer": false, "explanation": "Unstable angina does not produce ST elevation on an ECG. Much like NSTEMI, unstable angina can produce ECG changes such as ST-segment depression and T wave flattening or inversion. Unstable angina can be differentiated from NSTEMIs as unstable angina does not cause a rise in cardiac enzymes 8-12 after the onset of symptoms", "id": "31765", "label": "c", "name": "Unstable angina", "picture": null, "votes": 143 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "An NSTEMI, by definition, does not produce ST elevation on an ECG. ECG changes in an NSTEMI include ST-segment depression and T wave flattening or inversion, and can be differentiated from unstable angina by raised cardiac enzymes 8-12 after the onset of symptoms", "id": "31764", "label": "b", "name": "Non-ST elevation myocardial infarction (NSTEMI)", "picture": null, "votes": 602 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "GORD will not produce ECG changes, however, does manifest as burning chest pain", "id": "31766", "label": "d", "name": "Gastro-oesophageal reflux disease (GORD)", "picture": null, "votes": 32 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Musculoskeletal chest pain will not produce ECG changes", "id": "31767", "label": "e", "name": "Musculoskeletal chest pain", "picture": null, "votes": 52 }, { "__typename": "QuestionChoice", "answer": true, "explanation": "The ECG demonstrates ST elevation (>0.1mV) in the inferior leads (II, III and aVF) as well as reciprocal depression in the anterior leads. Central crushing chest pain is the classical symptom associated with a STEMI", "id": "31763", "label": "a", "name": "ST-elevation myocardial infarction (STEMI)", "picture": null, "votes": 9275 } ], "comments": [ { "__typename": "QuestionComment", "comment": "Because being Polish and not being able to speak English are both essential factors to determine the ongoing pathology and definitely not reinforcement of a stereotype", "createdAt": 1686763660, "dislikes": 6, "id": "28768", "isLikedByMe": 0, "likes": 4, "parentId": null, "questionId": 6353, "replies": [], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Supine Kawasaki", "id": 19785 } } ], "concept": { "__typename": "Concept", "chapter": { "__typename": "Chapter", "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>)", "files": null, "highlights": [], "id": "641", "pictures": [ { "__typename": "Picture", "caption": null, "createdAt": 1672906680, "id": "1422", "index": 6, "name": "NSTEMI (NICE).png", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/8zcda6v21672906675511.jpg", "path256": "images/8zcda6v21672906675511_256.jpg", "path512": "images/8zcda6v21672906675511_512.jpg", "thumbhash": "qvcJDYZrpbpdiHh+qQhpZXtffngI", "topic": null, "topicId": null, "updatedAt": 1708373886 }, { "__typename": "Picture", "caption": "A posterior STEMI.", "createdAt": 1665036193, "id": "798", "index": 4, "name": "Posterior STEMI.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/8fmhcpq11665036171703.jpg", "path256": "images/8fmhcpq11665036171703_256.jpg", "path512": "images/8fmhcpq11665036171703_512.jpg", "thumbhash": "eDgCBILYt6iDeXh/lYVojIDGCA==", "topic": null, "topicId": null, "updatedAt": 1708373886 }, { "__typename": "Picture", "caption": null, "createdAt": 1672906681, "id": "1437", "index": 7, "name": "Secondary prevention post MI (NICE).png", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/jdniw1l11672906675510.jpg", "path256": "images/jdniw1l11672906675510_256.jpg", "path512": "images/jdniw1l11672906675510_512.jpg", "thumbhash": "ZOcJBYJY2Vd+dnd/mtd5d0le/1Qj", "topic": null, "topicId": null, "updatedAt": 1708373886 }, { "__typename": "Picture", "caption": "An anterolateral STEMI.", "createdAt": 1665036193, "id": "753", "index": 2, "name": "Anterolateral STEMI.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/6b6d62x21665036171702.jpg", "path256": "images/6b6d62x21665036171702_256.jpg", "path512": "images/6b6d62x21665036171702_512.jpg", "thumbhash": "JwgKA4A/d3drh2iHB3q181U=", "topic": null, "topicId": null, "updatedAt": 1708373886 }, { "__typename": "Picture", "caption": "An anterior STEMI.", "createdAt": 1665036193, "id": "767", "index": 1, "name": "Anterior STEMI.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/cdi2n93z1665036171703.jpg", "path256": "images/cdi2n93z1665036171703_256.jpg", "path512": "images/cdi2n93z1665036171703_512.jpg", "thumbhash": "ORgCBIBYRmafp3eCp3x3hHA4CA==", "topic": null, "topicId": null, "updatedAt": 1708373886 }, { "__typename": "Picture", "caption": "A left bundle branch block.", "createdAt": 1665036198, "id": "1081", "index": 3, "name": "LBBB.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/75p0c58h1665036171701.jpg", "path256": "images/75p0c58h1665036171701_256.jpg", "path512": "images/75p0c58h1665036171701_512.jpg", "thumbhash": "MRgGBIBleXiPiIiGiIlvTorAaA==", "topic": null, "topicId": null, "updatedAt": 1708373886 }, { "__typename": "Picture", "caption": null, "createdAt": 1672906680, "id": "1426", "index": 5, "name": "STEMI (NICE).png", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/lkv1opvv1672906675512.jpg", "path256": "images/lkv1opvv1672906675512_256.jpg", "path512": "images/lkv1opvv1672906675512_512.jpg", "thumbhash": "aPcJDYTpioeOZnh/d2mXZ+l/n2UG", "topic": null, "topicId": null, "updatedAt": 1708373886 }, { "__typename": "Picture", "caption": "An inferior STEMI.", "createdAt": 1665036192, "id": "741", "index": 0, "name": "Inferior STEMI.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/82faisu41665036171703.jpg", 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5, "multiAnswer": null, "pictures": [ { "__typename": "Picture", "caption": null, "createdAt": 1639016492, "id": "356", "index": 0, "name": "ECG - STEMI.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/ufyrz1qv1639016491099.jpg", "path256": "images/ufyrz1qv1639016491099_256.jpg", "path512": "images/ufyrz1qv1639016491099_512.jpg", "thumbhash": "IhgCA4ADZnmMd3d4pY8lsDg=", "topic": { "__typename": "Topic", "id": "35", "name": "Cardiology", "typeId": 2 }, "topicId": 35, "updatedAt": 1708373886 } ], "prescribeAnswer": null, "presentations": [], "psaSectionId": null, "qaAnswer": null, "question": "A 52-year-old Polish man is brought to the accident and emergency department by ambulance. He speaks no English, but he points to his chest to suggest that he is in pain. Blood tests have not yet returned. His ECG is as follows:\n\n[lightgallery]\n\nWhich of the following is the most likely cause for this man's presentation?", "sbaAnswer": [ "a" ], "totalVotes": 10104, "typeId": 1, "userPoint": null }

[]

{ "__typename": "QuestionSBA", "choices": [ { "__typename": "QuestionChoice", "answer": false, "explanation": "Flecainide can be used to treat VT, but is not as effective as amiodarone", "id": "31771", "label": "d", "name": "Flecainide", "picture": null, "votes": 349 }, { "__typename": "QuestionChoice", "answer": true, "explanation": "According to NICE guidelines, amiodarone is the preferred drug to manage VT", "id": "31768", "label": "a", "name": "Amiodarone", "picture": null, "votes": 5467 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Although this patient does have signs of heart failure (an \"adverse feature\"), this is chronic and long standing and doesn't appear to be secondary to her arrhythmia. Therefore, cardioversion is not indicated in this instance", "id": "31769", "label": "b", "name": "Direct current (DC) cardioversion: one shock only", "picture": null, "votes": 840 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Her heart failure is chronic and not secondary to her arrhythmia so this is not an indication for cardioversion. She has no other indications for cardioversion such as shock, syncope or myocardial ischaemia. If she did have any of these symptoms then up to 3 synchronised DC shocks can be given in attempt to cardiovert", "id": "31770", "label": "c", "name": "Direct current (DC) cardioversion: up to 3 shocks", "picture": null, "votes": 1531 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "IV furosemide would not treat this patient's ventricular tachycardia", "id": "31772", "label": "e", "name": "Bolus of IV furosemide", "picture": null, "votes": 192 } ], "comments": [ { "__typename": "QuestionComment", "comment": "The question does not clarify whether the VT is mono- or polymorphic. Although IV mag sulph isn't an answer, it does make the question more confusing", "createdAt": 1684248587, "dislikes": 3, "id": "24806", "isLikedByMe": 0, "likes": 1, "parentId": null, "questionId": 6354, "replies": [ { "__typename": "QuestionComment", "comment": "don't introduce what ifs. If the VT was polymorphic they would have to say so. ", "createdAt": 1708950060, "dislikes": 0, "id": "42879", "isLikedByMe": 0, "likes": 2, "parentId": 24806, "questionId": 6354, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Ale", "id": 20565 } } ], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Supine Body", "id": 1961 } }, { "__typename": "QuestionComment", "comment": "She has acute exacerbation of heart failure does this not mean DC cardioversion?", "createdAt": 1684353527, "dislikes": 0, "id": "25055", "isLikedByMe": 0, "likes": 3, "parentId": null, "questionId": 6354, "replies": [ { "__typename": "QuestionComment", "comment": "however she is haemodynamically stable\n", "createdAt": 1684681508, "dislikes": 1, "id": "25551", "isLikedByMe": 0, "likes": 0, "parentId": 25055, "questionId": 6354, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Kawasaki Gland", "id": 3673 } }, { "__typename": "QuestionComment", "comment": "no because heat failure is a long standing problem that is not caused by the arrhythmia ", "createdAt": 1708950022, "dislikes": 0, "id": "42878", "isLikedByMe": 0, "likes": 0, "parentId": 25055, "questionId": 6354, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Ale", "id": 20565 } } ], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Abscess Sclerosis", "id": 28476 } }, { "__typename": "QuestionComment", "comment": "How do we know this is Broad Complex? ", "createdAt": 1684582515, "dislikes": 1, "id": "25390", "isLikedByMe": 0, "likes": 0, "parentId": null, "questionId": 6354, "replies": [ { "__typename": "QuestionComment", "comment": "VT is broad complex", "createdAt": 1684871616, "dislikes": 0, "id": "25919", "isLikedByMe": 0, "likes": 5, "parentId": 25390, "questionId": 6354, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Acute Body", "id": 10999 } } ], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Embolism Hypertension", "id": 5138 } } ], "concept": { "__typename": "Concept", "chapter": { "__typename": "Chapter", "explanation": "# Summary \n\nVentricular Tachycardia (VT) is a regular broad complex tachycardia that originates from the ventricles of the heart. The patient may have a pulse or not - if VT is pulseless it is one of the shockable cardiac arrest rhythms. Emergency management involves identification of VT on an ECG or heart monitor, then treating patients with a pulse and no adverse features with IV amiodarone. Patients who do not respond to this or have adverse features should be treated with synchronised DC cardioversion. Patients in cardiac arrest with VT should be treated as per the Advanced Life Support (ALS) algorithm with cardiopulmonary resuscitation (CPR), adrenaline and amiodarone as well as unsynchronised shocks. \n\n# Definition\n \nVentricular Tachycardia (VT) is a type of broad complex tachycardia characterised by a heart rate of more than 100 bpm and a QRS width of more than 120ms. Other types of broad complex tachycardias include Torsades de Pointes (which is a type of ventricular tachycardia described as polymorphic, where there are multiple ventricular foci) and Supraventricular Tachycardia with aberrant conduction.\n \n[lightgallery]\n \n\n# Aetiology\n \nFactors that increase the risk of VT include:\n \n- Electrolyte abnormalities such as hypokalaemia and hypomagnesaemia\n- Structural heart disease including previous myocardial infarction and cardiomyopathies\n- Drugs that cause QT prolongation e.g. clarithromycin, erythromycin (for Torsades de Pointes) \n- Inherited channelopathies e.g. Romano-Ward syndrome (for Torsades de Pointes)\n\n# Management\n \n**Pulseless VT:**\n\nPulseless VT is one of the four cardiac arrest rhythms, as so is managed as per Advanced Life Support guidelines:\n\n- CPR will be in progress\n- 120-360 J unsynchronised shock should be administered as early as possible, then every 2 minutes\n- IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock\n- Adrenaline should be administered every 3-5 minutes thereafter\n- A further dose of amiodarone 150 mg IV should be given after 5 shocks\n\n**Pulsed VT with adverse features:**\n\nIf a patient has a pulse, management is determined by whether they have any of the following adverse features:\n\n - Heart failure\n - Myocardial ischaemia (chest pain)\n - Shock\n - Syncope\n\nIf one or more of these are present, attempt to cardiovert the patient using synchronised DC shocks (up to 3 attempts). If the patient is conscious this will require sedation or anaesthesia.\n\nIf this is not effective, an amiodarone infusion would be the next step under expert guidance (300mg IV over 10-20 minutes followed by 900mg infusion over 24 hours).\n\n**Pulsed VT with no adverse features:**\n\nFirst line treatment is amiodarone 300mg IV over 10-60 minutes.\n\nIf this is ineffective then attempt to cardiovert using synchronised DC shocks (up to 3 attempts) with sedation or anaesthesia.\n\n**Torsades de Pointes:**\n\nThis is a special situation which is managed differently to monomorphic VT - Torsades de Pointes often self-terminates but the risk is that it deteriorates into ventricular fibrillation (causing cardiac arrest).\n\nIV Magnesium is the mainstay of treatment, along with treatment of any underlying cause identified (e.g. correcting electrolyte imbalance, stopping QT-prolonging medications).\n\n# References\n \n[Resuscitation Council UK - Adult advanced life support Guidelines](https://www.resus.org.uk/library/2021-resuscitation-guidelines/adult-advanced-life-support-guidelines)\n\n[Resuscitation Council UK - Adult Tachycardia Algorithm](https://www.resus.org.uk/sites/default/files/2021-04/Tachycardia%20Algorithm%202021.pdf)\n\n[Patient UK - Torsades de Pointes](https://patient.info/doctor/torsades-de-pointes)", "files": null, "highlights": [], "id": "669", "pictures": [ { "__typename": "Picture", "caption": "Ventricular tachycardia seen on an ECG.", "createdAt": 1665036184, "id": "714", "index": 0, "name": "VT.png", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/fua0u2q41665036171705.jpg", "path256": "images/fua0u2q41665036171705_256.jpg", "path512": "images/fua0u2q41665036171705_512.jpg", "thumbhash": "NQgCBICvh4eJiHiGh3YAAAAAAA==", "topic": null, "topicId": null, "updatedAt": 1708373886 } ], "typeId": 2 }, "chapterId": 669, "demo": null, "entitlement": null, "id": "694", "name": "Emergency Management of Ventricular Tachycardia", "status": null, "topic": { "__typename": "Topic", "id": "39", "name": "Emergency Medicine", "typeId": 2 }, "topicId": 39, "totalCards": 5, "typeId": null, "userChapter": null, "userNote": null, "videos": [ { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "694", "name": "Emergency Management of Ventricular Tachycardia" } ], "demo": false, "description": null, "duration": 4294.36, "endTime": null, "files": null, "id": "610", "live": false, "museId": "8JoZgLE", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/cardiology.png", "title": "Quesmed Tutorial: Arrhythmias", "userViewed": false, "views": 591, "viewsToday": 35 } ] }, "conceptId": 694, "conditions": [], "difficulty": 2, "dislikes": 7, "explanation": null, "highlights": [], "id": "6354", "isLikedByMe": 0, "learningPoint": "Amiodarone is the first-line treatment for stable ventricular tachycardia in patients with heart failure.", "likes": 9, "multiAnswer": null, "pictures": [], "prescribeAnswer": null, "presentations": [], "psaSectionId": null, "qaAnswer": null, "question": "A medical emergency call is put out for a 70-year-old female patient on a medical ward. Ventricular tachycardia (VT) is present on her ECG. She is haemodynamically stable. On examination, she is well perfused, has a GCS of 15, and has pitting oedema to her knees bilaterally.\n\nShe was admitted to hospital three days prior for an exacerbation of heart failure and was being treated with intravenous furosemide.\n\nWhich of the following treatments is most appropriate to manage VT in this patient?", "sbaAnswer": [ "a" ], "totalVotes": 8379, "typeId": 1, "userPoint": null }

[]

{ "__typename": "QuestionSBA", "choices": [ { "__typename": "QuestionChoice", "answer": false, "explanation": "This is the management for hyperkalaemia. There are no signs of hyperkalaemia on this ECG", "id": "31774", "label": "b", "name": "Insulin and dextrose infusion", "picture": null, "votes": 131 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "As this patient is symptomatic, he should have treatment. Patients with 2:1 heart block who are asymptomatic will not necessarily need treatment", "id": "31777", "label": "e", "name": "Watch and wait", "picture": null, "votes": 370 }, { "__typename": "QuestionChoice", "answer": true, "explanation": "The ECG shows a 2:1 heart block (second degree atrioventricular block). As this patient is symptomatic, he may benefit from the placement of a temporary or permanent pacemaker", "id": "31773", "label": "a", "name": "Cardiac pacemaker", "picture": null, "votes": 6018 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "There is no indication for DC cardioversion in second degree atrioventricular block", "id": "31775", "label": "c", "name": "Direct current (DC) cardioversion", "picture": null, "votes": 448 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "This is the management for rate control in atrial fibrillation. The ECG demonstrates that the patient is in 2:1 atrioventricular block", "id": "31776", "label": "d", "name": "Bisoprolol", "picture": null, "votes": 148 } ], "comments": [ { "__typename": "QuestionComment", "comment": "how do you know this is 2:1 heart block and not U waves?", "createdAt": 1657202776, "dislikes": 1, "id": "12826", "isLikedByMe": 0, "likes": 0, "parentId": null, "questionId": 6355, "replies": [ { "__typename": "QuestionComment", "comment": "Two p waves : One QRS complex\nThe reason its not a U wave is because you can tell there is a QRS complex missing between both p waves in the middle of the rhythm strip ", "createdAt": 1683738800, "dislikes": 0, "id": "24001", "isLikedByMe": 0, "likes": 1, "parentId": 12826, "questionId": 6355, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "NattyMedic", "id": 27604 } } ], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Dani Dean", "id": 19688 } } ], "concept": { "__typename": "Concept", "chapter": { "__typename": "Chapter", "explanation": "# Summary\r\n\r\nHeart block refers to an obstruction in the electrical conduction system of the heart. This obstruction can occur at various points in the conduction system, including the sinoatrial node, atrioventricular node, Bundle of His, or bundle branches. Atrioventricular heart block specifically affects the conduction between the atria and ventricles. The severity of heart block can range from first degree, which is generally benign, to second degree (Mobitz Type I and II), to complete (third degree) heart block, which requires immediate management with a permanent pacemaker due to the risk of asystole. The underlying causes and management strategies differ for each type of heart block.\r\n\r\n# Definition \r\n\r\nHeart block occurs due to an obstruction in the electrical conduction system of the heart. It can occur anywhere along the conduction system of the heart from the sinoatrial node to the atrioventricular node to the Bundle of His or within the bundle branches themselves. \r\n\r\nSinoatrial node block rarely leads to symptoms as the atrioventricular node acts as a secondary pacemaker. Bundle branch blocks are a form of heart block but they are discussed in a separate section. The rest of this section will discuss atrioventricular block in more detail. \r\n\r\nPatients with atrioventricular heart block may be asymptomatic or may present with fatigue, lightheadeness, syncope, shortness of breath and most seriously in cardiac arrest or with sudden death. \r\n\r\n# First Degree Heart Block\r\n\r\n## Definition\r\n\r\nThis is caused by prolonged conduction of electrical activity through the AV node. It can be identified on ECG by finding a PR interval >200ms.\r\n\r\n[lightgallery]\r\n\r\n## Causes\r\n\r\n* High vagal tone: e.g. athletes\r\n* Acute inferior MI\r\n* Electrolyte abnormalities: e.g. hyperkalaemia\r\n* Drugs: e.g. NHP-CCBs, beta-blockers, digoxin, cholinesterase inhibitors\r\n\r\n## Management\r\n\r\nFirst degree heart block itself is benign and does not need treating. However, any pathological underlying cause should be reversed.\r\n\r\n# Second Degree Heart Block \r\n\r\nSecond degree heart block is split into Mobitz Type I and Mobitz Type II heart block. \r\n\r\n# Mobitz Type I\r\n\r\n## Definition\r\n\r\nWenckebach phenomenon or Mobitz type I is a type of second degree heart block that is usually due to reversible conduction block at the AV node. It is characterised by progressive lengthening of the PR interval which results in a P wave that fails to conduct a QRS.\r\n\r\n[lightgallery1]\r\n\r\n## Causes\r\n\r\n* MI (mainly inferior)\r\n* Drugs such as beta/calcium channel blockers, digoxin\r\n* Professional athletes due to high vagal tone\r\n* Myocarditis\r\n* Cardiac surgery\r\n\r\n## Management\r\n\r\nIt is generally asymptomatic and does not require any specific management as the risk of high AV block/complete heart block is low. If symptoms do arise, ECG monitoring may be required, precipitating drugs must be stopped and if they are bradycardic with adverse features they should be treated with atropine.\r\n\r\n# Mobitz Type II\r\n\r\n## Definition\r\n\r\nMobitz type II block is a type of second degree AV block where there are intermittent non-conducted P waves. The _PR interval is constant_ (may be normal or prolonged) and there may no pattern or fixed ratios such as 2:1 or 3:1 block. It is usually caused by conduction system failure, especially at the His-Purkinje system.\r\n\r\nIn most cases there is a broad QRS indicating a distal block in the His-Purkinje system and many patients have pre-existing left bundle branch block/bifascicular block.\r\n\r\n[lightgallery2]\r\n\r\n## Causes\r\n\r\n* Infarction: particularly anterior MI which damages the bundle branches\r\n* Surgery: mitral valve repair or septal ablation\r\n* Inflammatory/autoimmune: rheumatic heart disease, SLE, systemic sclerosis, myocarditis\r\n* Fibrosis: Lenegre's disease\r\n* Infiltration: sarcoidosis, haemochromatosis, amyloidosis\r\n* Medication: beta-blockers, calcium channel blockers, Digoxin, amiodarone\r\n\r\n## Management\r\n\r\nDefinitive management is with a permanent pacemaker as these <u>_patients are at risk of complete heart block_</u> and at risk of becoming haemodynamically unstable.\r\n\r\n# Complete (Third degree) Heart Block\r\n\r\n## Definition\r\n\r\nComplete heart block occurs when atrial impulses fail to be conducted to the ventricles. Sufficient cardiac output may be secondary to a ventricular or junctional escape rhythm.\r\n\r\nECG shows severe bradycardia and complete dissociation between the P waves and the QRS complexes. These patients are at high risk of asystole, ventricular tachycardia and cardiac arrest. \r\n\r\n[lightgallery3]\r\n\r\n## Causes\r\n\r\n* Myocardial infarction: especially inferior\r\n* Drugs acting at the AVN: beta blockers, dihydropyridine calcium channel blockers, or adenosine\r\n* Idiopathic fibrosis\r\n\r\n## Management\r\n\r\nManagement of complete (third degree) heart block is via the acute bradycardia guideline (see below). Permanent pacemaker insertion is eventually required due to the risk of sudden death.\n\nAcute management:\n\nFor emergencies, always follow an A-E structure. Identify reversible causes (dyselectrolytaemias, drugs, cardiac causes etc.) \r\n\r\n*If there are adverse signs (e.g. shock, syncope, heart failure, myocardial ischaemia):* \r\n\r\n* **1st line** = **500 micrograms atropine IV**\r\n * Atropine blocks the vagal nerve which increases firing rate of the SAN. \r\n* **2nd line** = if the first dose of atropine is not working can consider giving additional doses of atropine 500mcg up to 3mg until response. Alternatively, **transcutaenous pacing** or **isoprenaline** or **adrenaline** or **alternative drugs** including aminophylline, adrenaline, glucagon (in beta-blocker or calcium channel blocker overdose). \r\n\r\n*If there are no adverse signs but a risk of asystole, or a satisfactory response to 500mcg atropine:*\r\n\r\n* Risk of asystole: recent asystole, mobitz type II block, complete heart block + broad QRS, ventricular pauses >3s. \r\n* **1st line** = administer **500 micrograms atropine IV**. Alternatively, **transcutaenous pacing** or **isoprenaline** or **adrenaline** or **alternative drugs** including aminophylline, adrenaline, glucagon (in beta-blocker or calcium channel blocker overdose). \r\n\r\n*If there are no adverse signs and there is no risk of asystole*\r\n\r\n* Observe\r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines on Pacing](<https://www.nice.org.uk/guidance/ta88/chapter/2-clinical-need-and-practice>) \r\n\r\n# References\r\n\r\n[Life in the Fast Lane Heart Block ECG Summary](https://litfl.com/heart-block-and-conduction-abnormalities/)\r\n\r\n[Resuscitation Council Adult Bradycardia Algorithm](<https://www.resus.org.uk/sites/default/files/2020-05/G2015_Adult_bradycardia.pdf>)", "files": null, "highlights": [], "id": "619", "pictures": [ { "__typename": "Picture", "caption": "First degree heart block.", "createdAt": 1665036193, "id": "769", "index": 0, "name": "First Degree Heart Block.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/o84o7ha81665036171703.jpg", "path256": "images/o84o7ha81665036171703_256.jpg", "path512": "images/o84o7ha81665036171703_512.jpg", "thumbhash": "tkgCA4D41rmEiOhnqX+d+sc=", "topic": null, "topicId": null, "updatedAt": 1708373886 }, { "__typename": "Picture", "caption": "Mobitz type I.", "createdAt": 1665036183, "id": "694", "index": 1, "name": "Mobitz Type I.png", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/6waeua8n1665036171702.jpg", "path256": "images/6waeua8n1665036171702_256.jpg", "path512": "images/6waeua8n1665036171702_512.jpg", "thumbhash": "OCgCBYJ2hmZwd4d+dwhmf4ePcvcX", "topic": null, "topicId": null, "updatedAt": 1708373886 }, { "__typename": "Picture", "caption": "Complete heart block.", "createdAt": 1665036193, "id": "764", "index": 3, "name": "Complete heart block.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/sfujefok1665036171701.jpg", "path256": "images/sfujefok1665036171701_256.jpg", "path512": "images/sfujefok1665036171701_512.jpg", "thumbhash": "sUgCC4AFanekjIh5f4jHT4Y=", "topic": null, "topicId": null, "updatedAt": 1708373886 }, { "__typename": "Picture", "caption": "Mobitz type II.", "createdAt": 1665036192, "id": "738", "index": 2, "name": "Mobitz Type II.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/pzhhne1c1665036171703.jpg", "path256": "images/pzhhne1c1665036171703_256.jpg", "path512": "images/pzhhne1c1665036171703_512.jpg", "thumbhash": "oDgGBICveHeLd3d3h3h/nKf5Nw==", "topic": null, "topicId": null, "updatedAt": 1708373886 } ], "typeId": 2 }, "chapterId": 619, "demo": null, "entitlement": null, "id": "3433", "name": "Heart Block", "status": null, "topic": { "__typename": "Topic", "id": "59", "name": "ECG Interpretation", "typeId": 4 }, "topicId": 59, "totalCards": null, "typeId": null, "userChapter": null, "userNote": null, "videos": [] }, "conceptId": 3433, "conditions": [], "difficulty": 1, "dislikes": 0, "explanation": null, "highlights": [], "id": "6355", "isLikedByMe": 0, "learningPoint": null, "likes": 2, "multiAnswer": null, "pictures": [ { "__typename": "Picture", "caption": null, "createdAt": 1639016494, "id": "357", "index": 0, "name": "2-1 heart block.png", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/xcxyxbyl1639016494016.jpg", "path256": "images/xcxyxbyl1639016494016_256.jpg", "path512": "images/xcxyxbyl1639016494016_512.jpg", "thumbhash": "tigGAoKHZ8aLh/iHR3xwtAg=", "topic": { "__typename": "Topic", "id": "35", "name": "Cardiology", "typeId": 2 }, "topicId": 35, "updatedAt": 1708373886 } ], "prescribeAnswer": null, "presentations": [], "psaSectionId": null, "qaAnswer": null, "question": "A 75-year-old man is brought to the emergency department by ambulance with a collapse. He reportedly lost consciousness with no pre-syncopal symptoms, was unconscious for approximately 20 seconds, and regained consciousness quickly. He reports this has happened twice in the last few weeks. Part of the rhythm strip from his ECG performed by the ambulance service may be seen below.\n\n[lightgallery]\n\nWhich of the following is the most suitable treatment for this patient?", "sbaAnswer": [ "a" ], "totalVotes": 7115, "typeId": 1, "userPoint": null }

[]

{ "__typename": "QuestionSBA", "choices": [ { "__typename": "QuestionChoice", "answer": false, "explanation": "There is no indication that this patient has an arrhythmia, angina or hypertension which are the indications for verapamil. In fact, you should avoid calcium channel blockers in heart failure as they are negatively inotropic so can further exacerbate heart failure by reducing cardiac function", "id": "31781", "label": "d", "name": "Verapamil", "picture": null, "votes": 1266 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "There are no indications for ibuprofen in this patient and, in fact, non-steroidal anti-inflammatory drugs (NSAIDs) should be avoided in heart failure", "id": "31782", "label": "e", "name": "Ibuprofen", "picture": null, "votes": 40 }, { "__typename": "QuestionChoice", "answer": true, "explanation": "Implantation of a cardiac resynchronisation therapy (CRT) device is indicated in patients with heart failure and a wide QRS complex on their ECG", "id": "31778", "label": "a", "name": "Implantation of a cardiac resynchronisation therapy (CRT) pacemaker device", "picture": null, "votes": 2789 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "There is no indication that this patient is she haemodynamically unstable and requires cardioversion", "id": "31779", "label": "b", "name": "Synchronised Direct current (DC) cardioversion", "picture": null, "votes": 1357 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "There is no indication that this patient has an arrhythmia which is what amiodarone is used to treat", "id": "31780", "label": "c", "name": "Amiodarone", "picture": null, "votes": 3592 } ], "comments": [ { "__typename": "QuestionComment", "comment": "its not an arrthymia cox there is no tachycardia", "createdAt": 1736727332, "dislikes": 1, "id": "60391", "isLikedByMe": 0, "likes": 6, "parentId": null, "questionId": 6356, "replies": [], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Malignant Syndrome", "id": 15952 } }, { "__typename": "QuestionComment", "comment": "this is incorrect. peri arrest guidelines say if they have acute heart failure then its DC cardioversion", "createdAt": 1738587441, "dislikes": 0, "id": "62217", "isLikedByMe": 0, "likes": 1, "parentId": null, "questionId": 6356, "replies": [], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Sydney Sweeney", "id": 30184 } } ], "concept": { "__typename": "Concept", "chapter": { "__typename": "Chapter", "explanation": "# Summary\r\n\r\nHeart failure (HF) is a clinical syndrome characterised by the heart's inability to pump enough blood to meet the body's needs. It is a common condition primarily affecting the elderly population. HF can be classified based on various factors, such as the type of dysfunction (systolic or diastolic), the onset (acute or chronic), and the severity of symptoms (NYHA classification). The clinical features of HF differ depending on whether it primarily affects the left or right ventricle, but broadly include fatigue, shortness of breath, and peripheral oedema. Diagnosis involves evaluating symptoms, NT-pro-BNP levels, and echocardiography. Management includes lifestyle modifications, medical therapy, and, in some severe cases, cardiac resynchronisation therapy. The prognosis for HF varies, but approximately 50% of those diagnosed are alive at 5 years.\r\n\r\n# Definition \r\n\r\nHeart failure (HF), also known as congestive heart failure (CHF) and congestive cardiac failure (CCF), is defined as the failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body.\r\n\r\n# Epidemiology \r\n\r\n* HF is common: the prevalence in the UK is estimated at 1-2%.\r\n\r\n* HF primarily affects the elderly population: the average age of diagnosis is 75 years old. The incidence of HF has been increasing with the ageing population.\r\n\r\n* In Europe and North America the most common causes are coronary artery disease, hypertension, and valvular disease.\r\n\r\n* Although Chagas disease is a rare cause in Europe and North America, it is a significant cause of heart failure in Central/South America.\r\n\r\n# Pathophysiology\r\n\r\nThe pathophysiology for HF is diverse and depends on the aetiology of the HF. \r\n\r\n# Classification \r\n\r\nHF can be classified in different ways. It can be classified as being low output vs. high output HF, predominantly systolic or diastolic dysfunction, whether the process has been acute or chronic, or by the severity of symptoms (and consideration for predominantly left or right ventricle features). \r\n\r\n## Low-output HF vs. High-output HF \r\n\r\nLow-output HF is much more common than high-output HF. Low-output HF occurs when cardiac output is reduced due to a primary problem with the heart and the heart is unable to meet the body's needs. Conversely, high-output HF refers to a heart that has a normal cardiac output, but there is an increase in peripheral metabolic demands that the heart is unable to meet. \r\n\r\nThe common causes of low-output HF will be further discussed below. Common causes of high-output HF include: \r\n\r\n* Anaemia\r\n* Arteriovenous malformation\r\n* Paget's disease\r\n* Pregnancy\r\n* Thyrotoxicosis\r\n* Thiamine deficiency (wet Beri-Beri)\r\n\r\nThese can be remembered with the AAPPTT mnemonic. \r\n\r\n## Systolic vs. Diastolic HF\r\n\r\nSystolic dysfunction refers to an impairment of ventricular contraction. The ventricles are able to fill well, but the heart is unable to pump the blood sufficiently out of the ventricle due to impaired myocardial contraction during systole (reduced ejection fraction). Common causes include: ischaemic heart disease, dilated cardiomyopathy, myocarditis or infiltration (haemochromatosis or sarcoidosis). \r\n\r\nIn comparison, diastolic dysfunction refers to the inability of the ventricles to relax and fill normally, hence the heart is still able to pump well but pumps out less blood per contraction due to reduced diastolic filling (preserved ejection fraction). Common causes include: uncontrolled chronic hypertension (significant left ventricular hypertrophy reduces filling of the left ventricle), hypertrophic cardiomyopathy, cardiac tamponade, and constrictive pericarditis. \r\n\r\n## Acute vs. Chronic HF \r\n\r\nHF can also be classified according to the time of onset. Acute HF occurs with new-onset HF symptoms (acute mitral regurgitation following an MI) or an acute deterioration in a patient with known, chronic HF. In comparison, chronic HF progresses more slowly and may take many years to develop. \r\n\r\n## Severity of Symptoms\r\n\r\n**New York Heart Association (NYHA) Classification of HF**\r\n\r\nThe NYHA Classification system is used to classify HF through the severity of symptoms. It runs from Class I (no limitation) to Class IV (discomfort at rest). \r\n\r\n* Class I - no limitation in physical activity, and activity does not cause undue fatigue, palpitations or dyspnoea.\r\n* Class II - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitations and/or dyspnoea.\r\n* Class III - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary).\r\n* Class IV - inability to carry on any physical activity without discomfort, with symptoms occurring at rest. If any activity takes place, discomfort increases.\r\n\r\n# Symptoms and Signs\r\n\r\nThe clinical features of HF can be considered according to the ventricle most impacted. However, a common presenting complaint for all types of heart failure is **fatigue**. \r\n\r\n\r\n## Clinical features of left heart failure (LHF)\r\n\r\nLHF, or left ventricular failure (LVF), causes pulmonary congestion (pressure builds up in the LHS of the heart and there is backpressure to the lungs) and systemic hypoperfusion.\r\n\r\n### Symptoms \r\n\r\n* Shortness of breath on exertion\r\n* Orthopnoea\r\n* Paroxysmal nocturnal dyspnoea\r\n* Nocturnal cough (± pink frothy sputum)\r\n* **Fatigue**\r\n\r\n### Signs \r\n\r\n* Tachypnoea\r\n* Bibasal fine crackles on auscultation of the lungs\r\n* Cyanosis\r\n* Prolonged capillary refill time \r\n* Hypotension\r\n* Less common signs: pulsus alternans (alternating strong and weak pulse), S3 gallop rhythm (produced by large amounts of blood striking compliant left ventricle), features of functional mitral regurgitation. \r\n\r\n## Clinical features of right heart failure \r\n\r\nRight heart failure causes venous congestion (pressure builds up behind the right heart) and pulmonary hypoperfusion (reduced right heart output).\r\n\r\n### Symptoms \r\n\r\n* Ankle swelling \r\n* Weight gain \r\n* Abdominal swelling and discomfort \r\n* Anorexia and nausea \r\n\r\n### Signs\r\n\r\n* Raised JVP\r\n* Pitting peripheral oedema (ankle to thighs to sacrum)\r\n* Tender smooth hepatomegaly\r\n* Ascites\r\n* Transudative pleural effusions (typically bilaterally)\r\n\r\n*NB. Sometimes left-sided heart failure can lead to pulmonary congestion which in turn also pushes the right ventricle into failure. In these cases, signs and symptoms of both left and right-sided heart failure may be present. This is congestive cardiac failure.* \r\n\r\n# Differential Diagnoses\r\n\r\n* **Chronic Obstructive Pulmonary Disease (COPD)** \r\n\t* **Similarities**: both may present with dyspnoea (and significant respiratory distress) and fatigue. \r\n\t* **Differences**: in heart failure, the shortness of breath is typically worse on lying flat (orthopnoea) and may be accompanied by paroxysmal nocturnal dyspnoea and peripheral oedema. Shortness of breath in COPD tends to be worse with exertion and is likely accompanied by other symptoms including chronic productive cough, wheeze and a significant smoking history. \r\n\r\n* **Acute Respiratory Distress Syndrome** \r\n\t* **Similarities**: both may present with shortness of breath, tachypnoea and respiratory distress. Both lead to the accumulation of fluid in the lungs and impaired gaseous exchange leading to hypoxaemia. \r\n\t* **Differences**: the underlying pathology between the two is different. Heart failure is a result of raised pressures in pulmonary capillaries, whereas ARDS is usually due to increased pressures in pulmonary capillaries secondary to a large insult (e.g. pneumonia, aspiration, or trauma). They can be distinguished by taking pulmonary capillary wedge pressures. \r\n\r\n* **Renal Failure** \r\n\t* **Similarities**: fluid retention and peripheral overload. \r\n\t* **Differences**: other signs and symptoms will allow distinction between HF and renal failure. In the latter, you may find uraemic symptoms(nausea, anorexia, uraemic flap) and potentially signs of renal replacement therapy. \r\n\r\n* **Liver Failure** \r\n\t* **Similarities**: fluid retention and peripheral overload especially ascites. \r\n\t* **Differences**: liver failure patients will present with other signs and symptoms including jaundice, hepatic encephalopathy and chronic liver disease signs (gynaecomastia, spider naevi, and excoriations). \r\n\r\n\r\n# Investigations\r\n\r\nIf a stable patient is presenting to the GP with suspected chronic heart failure, investigations should be carried out as per NICE guidelines. \r\n\r\n**1st line = NT-pro-BNP level**\r\n\r\nNT-pro-BNP is released by the ventricles in response to myocardial stretch. It has a high negative predictive value.\r\n\r\nInterpret NT-pro-BNP results as follows: \r\n\r\n* >2000ng/L (236pmol/L): refer urgently for specialist assessment and TTE <2 weeks. \r\n* 400-2000ng/L (47-236pmol/L): refer for specialist assessment and TTE <6 weeks. \r\n* If <400ng/L: diagnosis of heart failure is less likely. \r\n\r\n**Arrange a 12-lead ECG in all patients** \r\n\r\nECG may be normal or hint at underlying aetiology (ischaemic changes or arrhythmias). \r\n\r\n**Transthoracic echocardiogram (TTE)**\r\n\r\nAn echocardiogram will confirm the presence and degree of ventricular dysfunction.\r\n\r\n* Ventricular dysfunction is normally measured by the ejection fraction (EF). \r\n * EF <40% = HF with reduced ejection fraction (HFrEF, systolic dysfunction). \r\n * EF >40% but with raised BNP = HF with preserved ejection fraction (HFpEF, diastolic dysfunction).\r\n * EF 50-70% with normal BNP = normal. \r\n\r\n**Other Investigations:** \r\n\r\n* **Bloods**: U&E (renal function for medication and hyponatraemia), LFTS (deranged LFTs suggest hepatic congestion), TFTs (hyperthyroidism and high-output HF), glucose and lipid profile (modifiable CV risk factors)\r\n\r\n* **CXR**: CXR findings in heart HF can be remembered by the ABCDEF mnemonic:\r\n * A: **Alveolar** oedema (with 'batwing' perihilar shadowing)\r\n * B: **Kerley B** lines (caused by interstitial oedema)\r\n * C: **Cardiomegaly** (cardiothoracic ratio >0.5)\r\n * D: upper lobe blood **diversion**\r\n * E: **Pleural effusions** (typically bilateral transudates)\r\n * F: **Fluid in the horizontal fissure**\r\n\r\n[lightgallery]\r\n\r\n[lightgallery1] \r\n\r\n# Management\r\n\r\n## Conservative management\r\n\r\n* Weight loss if BMI >30. \r\n* Smoking cessation \r\n* Salt and fluid restriction - improves mortality\r\n* Supervised exercise-based group rehabilitation programme for people with heart failure. \r\n\r\nOffer annual influenza and one-off pneumococcal vaccinations for patients diagnosed with heart failure. \r\n\r\n## Medical management\r\n\r\n**Symptom management**: \r\n\r\n* For fluid overload, prescribe loop diuretics (e.g. furosemide or bumetanide). These do not affect overall mortality from heart failure. \r\n\r\n\r\n**Management which improves mortality**:\r\n \r\n1st line = ACE-I and beta-blocker \r\n\r\n* Consider ARB if intolerant to ACE-I. \r\n* Consider hydralazine if intolerant to ACE-I/ARB. \r\n\r\nIf symptoms persist and NYHA Class 3 or 4 consider adding:\r\n\r\n* Aldosterone antagonists = spironolactone or eplerenone. \r\n* Hydralazine and a nitrate for Afro-Caribbean patients. \r\n* Ivabradine if in sinus rhythm and impaired EF. \r\n* Digoxin = useful in those with AF. This <u>worsens</u> mortality but improves morbidity.\r\n\r\nNICE also advices seeking specialist guidance for prescribing **SGLT2 inhibitors** (dapagliflozin or empagliflozin). These should be given in symptomatic chronic heart failure with preserved or reduced ejection fraction, or as an add-on for patients already optimised with ACE-i/ARB/sacubitril-valsartan (i.e. combination), beta-blockers and aldosterone antagonists.\r\n\r\n**BASH Mnemonic**\r\n\r\n* BASH medications demonstrate a mortality benefit in patients with HFrEF = Beta-blockers, ACE-inhibitors/ARB, Spironolactone and Hydralazine. \r\n* There are no medications that improve mortality in diastolic heart failure. \r\n\r\n[lightgallery2]\r\n\r\n# Surgical/Interventional management \r\n\r\n* Cardiac resynchronisation therapy\r\n* Implantable cardiac defibrillators (ICDs) are indicated if the following criteria are fulfilled: \r\n * QRS interval <120ms, high risk sudden cardiac death, NYHA class I-III\r\n * QRS interval 120-149ms without LBBB, NYHA class I-III\r\n * QRS interval 120-149ms with LBBB, NYHA class I\r\n\r\n## Adverse effects of heart failure medications\r\n\r\nThe common side-effects for different heart failure medications are listed below\r\n\r\n* **Beta blockers**: Bradycardia, hypotension, fatigue, dizziness\r\n* **ACE inhibitors**: Hyperkalaemia, renal impairment, dry cough, lightheadedness, fatigue, GI disturbances, angioedema\r\n* **Spironolactone**: Hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/hair growth in women, changes in libido\r\n* **Furosemide**: Hypotension, hyponatraemia/kalaemia,\r\n* **Hydralazine/nitrates**: Headache, palpitations, flushing\r\n* **Digoxin**: Dizziness, blurred vision, GI disturbances\n* **SGLT-2 inhibitors:** Thrush, UTIs, DKA in patients with pre-existing diabetes\r\n\r\n# Prognosis \r\n\r\nIt is estimated that >50% of people diagnosed with HF will survive after 5 years. Approximately 35% will be alive in 10 years. \r\n\r\n# NICE Guidelines\r\n\r\n[NICE Guidelines on Acute Heart Failure](https://www.nice.org.uk/guidance/cg187/chapter/1-Recommendations)\n\n[NICE Guidelines on Chronic Heart Failure](https://cks.nice.org.uk/topics/heart-failure-chronic)\r\n\r\n# References \r\n\r\n[2022 Stat Pearls Summary of Congestive Heart Failure](https://www.ncbi.nlm.nih.gov/books/NBK430873)", "files": null, "highlights": [], "id": "610", "pictures": [ { "__typename": "Picture", "caption": "A chest x-ray of a patient with multiple signs of heart failure.", "createdAt": 1665036253, "id": "1086", "index": 0, "name": "Heart failure x-ray.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/0vo39uij1665036171716.jpg", "path256": "images/0vo39uij1665036171716_256.jpg", "path512": "images/0vo39uij1665036171716_512.jpg", "thumbhash": "KQgGBoBJ+IeAinqLeXVniHh2AAAAAAA=", "topic": null, "topicId": null, "updatedAt": 1708373886 }, { 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"explanation": null, "highlights": [], "id": "6356", "isLikedByMe": 0, "learningPoint": "Cardiac resynchronisation therapy (CRT) is beneficial for heart failure patients with wide QRS complexes to improve cardiac function and symptoms.", "likes": 7, "multiAnswer": null, "pictures": [], "prescribeAnswer": null, "presentations": [], "psaSectionId": null, "qaAnswer": null, "question": "An 80 year old female is admitted to hospital with heart failure. Her ECG demonstrates sinus rhythm with wide QRS complexes of approximately 190ms. Her blood pressure is 130/85 mmHg, her heart rate is 78 bpm.\n\nWhich of the following is indicated in this patient?", "sbaAnswer": [ "a" ], "totalVotes": 9044, "typeId": 1, "userPoint": null }

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{ "__typename": "QuestionSBA", "choices": [ { "__typename": "QuestionChoice", "answer": false, "explanation": "She is haemodynamically stable and apyrexial and therefore intravenous antibiotics are not indicated at this point", "id": "31786", "label": "d", "name": "IV erythromycin", "picture": null, "votes": 589 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "This patient has a known penicillin allergy and therefore flucloxacillin is contraindicated", "id": "31784", "label": "b", "name": "Oral flucloxacillin", "picture": null, "votes": 1306 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "This patient has a known penicillin allergy and therefore co-amoxiclav is contraindicated", "id": "31787", "label": "e", "name": "IV co-amoxiclav", "picture": null, "votes": 95 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "This patient has a known penicillin allergy and therefore flucloxacillin is contraindicated", "id": "31785", "label": "c", "name": "IV flucloxacillin", "picture": null, "votes": 120 }, { "__typename": "QuestionChoice", "answer": true, "explanation": "As a penicillin allergic patient, this is the most appropriate antibiotic. As she is haemodynamically stable and apyrexial, oral antibiotics are appropriate", "id": "31783", "label": "a", "name": "Oral erythromycin", "picture": null, "votes": 6501 } ], "comments": [], "concept": { "__typename": "Concept", "chapter": { "__typename": "Chapter", "explanation": "# Summary\n \n\nMastitis is an inflammation of the breast, often associated with lactation in postpartum women, referred to as puerperal mastitis. Key signs and symptoms include localised pain, tenderness, redness and heat in the breast, along with systemic symptoms such as fever, rigours, myalgia, fatigue, nausea and headache. Diagnosis is primarily clinical. Ultrasound may be used if a breast abscess is suspected. Management strategies focus on reassurance about continued breastfeeding, advice on milk removal, analgesia, antibiotics, and in severe cases, surgical intervention.\n \n\n# Definition\n \n\nMastitis is the inflammation of the breast tissue, which can be with or without an infection. When associated with lactation in postpartum women, the condition is specified as puerperal mastitis. Alternatively, mastitis can be seen in women who are not breastfeeding.\n \n\n# Epidemiology\n \n\nNon-lactational mastitis is significantly less common than lactational mastitis, and its most common in women with immunodeficiency and diabetes. \n \n\n# Aetiology\n \nMastitis unrelated to pregnancy and breastfeeding is typically due to obstruction of the ducts from cellular debris. This can result in a local inflammatory response in non-infectious mastitis. \n\nIn infectious mastitis, bacteria from the skin can then enter the ducts, causing inflammation and may progress to peri-areolar abscesses. The most common causative pathogen is Staphylococcus aureus. \n\nRisk factors for non-lactational mastitis include:\n\n- Cigarette smoking\n- Nipple rings \n- Diabetes mellitus\n- Immunocompromise \n \n\n# Signs and Symptoms\n \n\nMastitis diagnosis is primarily clinical, based on characteristic local and systemic symptoms.\n \n\n - Localised symptoms: Painful, tender, red, and hot breast.\n - Systemic symptoms: Fever, rigours, myalgia, fatigue, nausea, and headache.\n - Additional information: The condition is usually unilateral and tends to present within the first week postpartum.\n \n\nIn some cases, mastitis may develop into a breast abscess, manifesting as a fluctuant, tender mass with overlying erythema.\n \n\n# Differential Diagnosis\n \n\nThe differential diagnosis for mastitis should include other conditions that also cause breast pain and inflammation:\n \n\n - **Breast abscess**: Fluctuant mass, tenderness, overlying erythema, systemic signs of infection.\n - **Inflammatory breast cancer**: Swelling, skin changes resembling orange peel, nipple inversion, axillary lymphadenopathy.\n - **Breast engorgement**: Typically bilateral and associated with milk stasis, painful, and tense breasts.\n \n\n# Investigations\n \n\nWhile the diagnosis of mastitis is primarily clinical, further investigations may be necessary in certain circumstances.\n \n\n - Ultrasound: Utilised to identify a potential abscess, appearing as a collection of pus.\n - Additional information: Early referral to secondary care is vital if an abscess is suspected.\n \n\n# Management\n \n\nManaging mastitis involves multiple strategies:\n \n\n - Provide analgesia to manage symptoms (i.e. paracetamol, ibuprofen)\n\t - Warm and cold compresses may also help.\n - Antibiotics may be considered if acute pain, severe symptoms or symptoms lasting more than 12-24 hours, fever or positive cultures \n\t - Flucloxacillin or clindamycin for those with penicillin allergy\n\t - Treatment is indicated for 10-14 days.\n - In cases where the condition does not improve, consider intravenous antibiotics (i.e. vancomycin) or ultrasound to evaluate for the presence of a breast abscess.\n - Patients may also benefit from antifungal therapy (i.e. nystatin) for concomitant nipple candidiasis \n\n \n# Complications\n \nComplications of mastitis include:\n \n - Breast abscess\n - Recurrence:\n\t - More common if treatment is delayed or too short in duration \n \n\n# NICE Guidelines\n \n[NICE CKS on mastitis and breast abscess](https://cks.nice.org.uk/topics/mastitis-breast-abscess/)\n\n# References\n\n[BMJ Best Practice Mastitis and Breast Abscess](https://bestpractice.bmj.com/topics/en-gb/1084)\n\n[Patient Info Benign Breast Diseas](https://bestpractice.bmj.com/topics/en-gb/1084) \n\n[NHS Mastitis](https://www.nhs.uk/conditions/mastitis/)", "files": null, "highlights": [], "id": "340", "pictures": [], "typeId": 2 }, "chapterId": 340, "demo": null, "entitlement": null, "id": "345", "name": "Lactational Breast abscess", "status": null, "topic": { "__typename": "Topic", "id": "55", "name": "Breast Disease", "typeId": 2 }, "topicId": 55, "totalCards": 5, "typeId": null, "userChapter": null, "userNote": null, "videos": [] }, "conceptId": 345, "conditions": [], "difficulty": 1, "dislikes": 1, "explanation": null, "highlights": [], "id": "6357", "isLikedByMe": 0, "learningPoint": "In breastfeeding women with a breast abscess, oral erythromycin is a suitable antibiotic choice for those allergic to penicillin.", "likes": 3, "multiAnswer": null, "pictures": [], "prescribeAnswer": null, "presentations": [], "psaSectionId": null, "qaAnswer": null, "question": "A 33-year-old woman presents to the out of hours general practitioner with a tender, fluctuant mass in her left breast, with associated erythema of the overlying skin. She is currently breast feeding. A breast abscess is confirmed on ultrasound and percutaneous drainage is performed uneventfully.\n\nHer observations are as follows:\n\nPulse 80 beats per minute\n\nRespiratory rate 17 breaths per minute\n\nBlood pressure 115/75mmHg\n\nTemperature 37.2°\n\nShe looks otherwise well, and is alert and orientated. Her renal function and liver function is within normal limits and she has an allergy to penicillin\n\nWhich of the following is the most appropriate antibiotic therapy?", "sbaAnswer": [ "a" ], "totalVotes": 8611, "typeId": 1, "userPoint": null }

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{ "__typename": "QuestionSBA", "choices": [ { "__typename": "QuestionChoice", "answer": false, "explanation": "Trastuzumab (Herceptin) is only useful in HER2 positive breast cancers", "id": "31791", "label": "d", "name": "Trastuzumab", "picture": null, "votes": 384 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "This is a hormone therapy (LHRH agonist) used in the treatment of prostate cancer", "id": "31792", "label": "e", "name": "Goserelin", "picture": null, "votes": 94 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "This is not a treatment for breast cancer. In fact, HRT can increase a patient's risk of breast cancer", "id": "31790", "label": "c", "name": "Hormone replacement therapy (HRT)", "picture": null, "votes": 97 }, { "__typename": "QuestionChoice", "answer": true, "explanation": "This is correct. Anastrozole is an aromatase inhibitor which is used for ER positive breast cancer in post-menopausal women", "id": "31788", "label": "a", "name": "Anastrozole", "picture": null, "votes": 6223 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Tamoxifen is indicated in pre- and peri-menopausal women with ER-positive breast cancer not previously treated with tamoxifen", "id": "31789", "label": "b", "name": "Tamoxifen", "picture": null, "votes": 2012 } ], "comments": [ { "__typename": "QuestionComment", "comment": "Unlikely but are we outright assuming she's post-menopause?", "createdAt": 1672189406, "dislikes": 3, "id": "15592", "isLikedByMe": 0, "likes": 0, "parentId": null, "questionId": 6358, "replies": [ { "__typename": "QuestionComment", "comment": "At 70? That's not much of an assumption mate", "createdAt": 1682781512, "dislikes": 0, "id": "22945", "isLikedByMe": 0, "likes": 2, "parentId": 15592, "questionId": 6358, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Anterior Gallbladder", "id": 5111 } }, { "__typename": "QuestionComment", "comment": "Bruh... she's 70!!", "createdAt": 1683647465, "dislikes": 0, "id": "23863", "isLikedByMe": 0, "likes": 1, "parentId": 15592, "questionId": 6358, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "FastFiringNeuron", "id": 33525 } }, { "__typename": "QuestionComment", "comment": "70 is the new 30", "createdAt": 1684247832, "dislikes": 0, "id": "24801", "isLikedByMe": 0, "likes": 2, "parentId": 15592, "questionId": 6358, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Al", "id": 19078 } } ], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Chronic Haemophilus", "id": 13970 } }, { "__typename": "QuestionComment", "comment": "Good question", "createdAt": 1682409127, "dislikes": 0, "id": "22612", "isLikedByMe": 0, "likes": 2, "parentId": null, "questionId": 6358, "replies": [], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Gland Hereditary", "id": 6697 } } ], "concept": { "__typename": "Concept", "chapter": { "__typename": "Chapter", "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)", "files": null, "highlights": [], "id": "343", "pictures": [], "typeId": 2 }, "chapterId": 343, "demo": null, "entitlement": null, "id": "343", "name": "Breast Cancer", "status": null, "topic": { "__typename": "Topic", "id": "55", "name": "Breast Disease", "typeId": 2 }, "topicId": 55, "totalCards": 56, "typeId": null, "userChapter": null, "userNote": null, "videos": [ { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "343", "name": "Breast Cancer" } ], "demo": false, "description": null, "duration": 522.07, "endTime": null, "files": null, "id": "149", "live": false, "museId": "NwAyTxS", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/oncology.png", "title": "Genetic syndromes and Cancer", "userViewed": false, "views": 271, "viewsToday": 42 } ] }, "conceptId": 343, "conditions": [], "difficulty": 2, "dislikes": 1, "explanation": null, "highlights": [], "id": "6358", "isLikedByMe": 0, "learningPoint": "Anastrozole is an aromatase inhibitor indicated for the treatment of oestrogen receptor-positive breast cancer in post-menopausal women.", "likes": 9, "multiAnswer": null, "pictures": [], "prescribeAnswer": null, "presentations": [], "psaSectionId": null, "qaAnswer": null, "question": "A 70-year-old female is referred to the breast clinic with a left breast lump. A biopsy is obtained which shows a ductal carcinoma which is oestrogen receptor (ER) positive, HER2 negative, and progestogen receptor (PR) negative.\n\nWhich of the following medical therapies is indicated for the management of this patient's breast cancer?", "sbaAnswer": [ "a" ], "totalVotes": 8810, "typeId": 1, "userPoint": null }

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{ "__typename": "QuestionSBA", "choices": [ { "__typename": "QuestionChoice", "answer": true, "explanation": "Hyperkalaemia is defined as serum potassium concentration >5.5mmol/L, and can be further categorised as mild (5.5-5.9 mmol/l), moderate (6.0-6.4 mmol/l) or severe (≥ 6.5 mmol/l).\n\nModerate or severe hyperkalaemia, or any hyperkalaemia with ECG changes should be treated with insulin/dextrose or insulin/glucose infusion, particularly if the patient is systemically unwell (e.g. with an AKI). Insulin promotes potassium to shift into cells and the dextrose is to counteract the hypoglycaemic effects of insulin.\n\nAccording to the UK Kidney Association Guidelines, Calcium Gluconate should only be given if (1) there is severe hyperkalaemia >6.5 mmol/l irregardless of ECG changes or (2) there is mild to moderate (5.5-6.5 mmol/l) hyperkalaemia in the presences of ECG changes.\n\n", "id": "31793", "label": "a", "name": "Insulin and dextrose infusion", "picture": null, "votes": 2356 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Dialysis is considered for some patients with refractory hyperkalaemia where other less invasive treatments have failed", "id": "31797", "label": "e", "name": "Dialysis", "picture": null, "votes": 225 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "According to the UK Kidney Association Guidelines, Calcium Gluconate should only be given if (1) there is severe hyperkalaemia >6.5 mmol/l irregardless of ECG changes or (2) there is mild to moderate (5.5-6.5 mmol/l) hyperkalaemia in the presences of ECG changes.", "id": "31794", "label": "b", "name": "Calcium gluconate", "picture": null, "votes": 2556 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "This would not directly treat the hyperkalaemia and if sustained over a long period may risk overloading the patient", "id": "31796", "label": "d", "name": "Increase rate of 0.9% NaCl to 500ml/hr", "picture": null, "votes": 334 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "According to the latest Renal guidelines, a moderate hyperkalaemia should be treated with insulin/dextrose or insulin/glucose infusion, particularly if the patient is systemically unwell (e.g. with an AKI), to prevent further deterioration", "id": "31795", "label": "c", "name": "Continue current treatment", "picture": null, "votes": 1078 } ], "comments": [], "concept": { "__typename": "Concept", "chapter": { "__typename": "Chapter", "explanation": "# Summary\n\nHyperkalaemia is a potentially life-threatening electrolyte abnormality, defined as a serum potassium concentration greater than 5.5mmol/L. A potassium of 6.0-6.5 mmol/L is classed as moderate hyperkalaemia, and > 6.5 mmol/L is classed as severe. Causes include acute or chronic renal impairment, medications such as ACE inhibitors, adrenal insufficiency and rhabdomyolysis. Pseudohyperkalaemia is also common and occurs when there is haemolysis of the blood collected that causes potassium to leak from cells. Key investigations include an ECG, a blood gas to confirm hyperkalaemia is true, and U&Es for renal function. Management depends on the severity of hyperkalaemia and may include calcium gluconate or calcium carbonate to stabilise the myocardium and insulin-dextrose infusion to drive potassium into the cells, as well as treating the cause of hyperkalaemia. Potassium binders such as sodium zirconium cyclosilicate (Lokelma) may also be used. The main complication is cardiac conduction abnormalities, with possible findings including tall tented T waves, flattened P waves, bradyarrhythmias and QRS widening with bizarre morphology. \n\n# Definition\n\nHyperkalaemia is a common electrolyte abnormality that is defined as an abnormally high serum potassium. The normal range is 3.5-5.0 mmol/L, with a level of > 5.5 mmol/L generally described as hyperkalaemia. It is seen in around 1-10% of hospital inpatients and is often asymptomatic.\n\n# Aetiology\n\n- Impaired excretion of potassium\n - Acute kidney injury\n - Chronic kidney disease\n - Medications (ACE inhibitors, potassium sparing diuretics, NSAIDs, heparin, trimethoprim, ciclosporin)\n - Type 4 renal tubular acidosis\n - Hypoadrenalism (e.g. Addison's disease)\n- Increased potassium intake\n - Oral intake (especially if combined with impaired excretion)\n - Excessive IV potassium\n- Increased cellular release \n - Metabolic acidosis\n - Hyperglycaemia\n - Rhabdomyolysis\n - Tumour lysis syndrome\n - Packed red blood cell transfusion\n - Digoxin toxicity\n - Beta blockers\n - Severe burns\n - Hyperkalaemic periodic paralysis\n\n# Classification\n\nThe European Resuscitation Guidelines stratify severity of hyperkalaemia as follows:\n\n||Serum potassium (mmol/L)|\n|--------------------------|------------------------------------|\n|**Mild**|5.5–5.9|\n|**Moderate**|6.0–6.4|\n|**Severe**|≥6.5|\n\n# Signs and Symptoms\n\nHyperkalaemia is often asymptomatic and only detected on blood tests - there may be symptoms or signs of the underlying cause however (e.g. dark urine in rhabdomyolysis)\n\n**Symptoms include:**\n\n- Palpitations\n- Fatigue\n- Chest pain\n- Shortness of breath\n- Paralysis\n\n**Signs include:**\n\n- Arrhythmias (e.g. bradycardia)\n- Reduced muscle power +/- flaccid paralysis\n- Hyporeflexia\n\n# Differential Diagnosis\n\n**Pseudohyperkalaemia** is common and refers to an artifactual increase in potassium in the sample tested - causes of this include:\n\n- Prolonged tourniquet time\n- Difficult venepuncture\n- Excessive fist clenching\n- Delayed specimen processing\n- Contamination with potassium EDTA anticoagulant in FBC bottles\n- Thrombocytosis\n- Leukocytosis\n\n# Investigations\n\n- **Blood gas** to confirm hyperkalaemia rapidly and check acid-base status and lactate\n- **ECG** to look for cardiac conduction abnormalities associated with hyperkalaemia. ECG changes include tall-tented T waves, PR prolongation, p wave flattening and QRS broadening.\n- **U&Es** to confirm hyperkalaemia, check sodium (may be an associated hyponatraemia e.g. in adrenal insufficiency) and renal function\n\n# Management \n\n**Conservative management:**\n\n- Stop any potassium-containing fluids\n- Address any underlying causes e.g. stop any contributing medications where possible, manage constipation\n- Consider advising the patient on a low potassium diet (e.g. in patients with chronic kidney disease) - dietician referral may be helpful\n- Patients with ECG changes may require cardiac monitoring\n- Mild-moderate cases of hyperkalaemia without ECG changes may be managed by addressing the underlying cause alone\n\n**Medical management:**\n\n- Patients with ECG changes or severe hyperkalaemia require treatment\n- Give 10 ml of IV 10% calcium carbonate or 30ml of IV 10% calcium gluconate immediately\n- This does not reduce serum potassium but acts to stabilise the myocardium and reduce the risk of arrhythmias\n- Further doses may be given if required\n- Give an insulin and glucose infusion (e.g. 10 units of Actrapid in 50 ml of 50% glucose over 15-30 minutes\n- This reduces serum potassium by shifting potassium into cells, however does not eliminate potassium from the body\n- Nebulised salbutamol may be given in addition which has the same effect\n- Potassium binders may be considered to eliminate potassium via the gut, especially in patients with chronic or refractory hyperkalaemia\n- Newer agents such as sodium zirconium cyclosilicate (Lokelma) are better tolerated than older resins (e.g. sodium polystyrene sulfonate)\n- Furosemide may also be useful to increase urinary potassium excretion especially in patients with fluid overload\n- Consider sodium bicarbonate for patients with acidosis and hyperkalaemia\n- Medical treatment may be required to correct the cause of hyperkalaemia (e.g. IV fluids for a pre-renal AKI or rhabdomyolysis)\n\n**Interventional management:**\n\n- Refractory hyperkalaemia despite medical therapy is an indication for emergency dialysis\n\n# Complications\n\nThe main complication of hyperkalaemia is cardiac conduction abnormalities and arrhythmias which in the most severe cases may cause cardiac arrest - changes in order of increasing severity are:\n\n1. Tall tented T-waves\n2. Flattened P-waves\n3. Prolonged PR interval\n4. Widened QRS complexes\n5. Idioventricular rhythms (bradycardia of ventricular origin)\n6. Sine wave pattern (pre-terminal rhythm)\n7. Ventricular fibrillation/asystole\n\n# References\n\n[BNF Treatment Summary - Hyperkalaemia](https://bnf.nice.org.uk/treatment-summaries/hyperkalaemia/)\n\n[The Renal Association - Treatment of Acute Hyperkalaemia in Adults](https://www.ukkidney.org/sites/default/files/RENAL%20ASSOCIATION%20HYPERKALAEMIA%20GUIDELINE%20-%20JULY%202022%20V2_0.pdf)\n\n[Patient UK - Hyperkalaemia in adults](https://patient.info/doctor/hyperkalaemia-in-adults)\n\n[Whittington Hospital Hyperkalaemia Guideline](https://www.whittington.nhs.uk/document.ashx?id=6250)\n\n[Life in the Fast Lane - Hyperkalaemia](https://litfl.com/hyperkalaemia-ecg-library/)", "files": null, "highlights": [], "id": "153", "pictures": [ { "__typename": "Picture", "caption": "ECG changes seen in someone with hyperkalaemia.", "createdAt": 1665036193, "id": "791", "index": 0, "name": "Hyperkalaemia ecg.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/6f36tetq1665036171704.jpg", "path256": "images/6f36tetq1665036171704_256.jpg", "path512": "images/6f36tetq1665036171704_512.jpg", "thumbhash": "dSgCA4Dp5seGh/lnSImAlAg=", "topic": null, "topicId": null, "updatedAt": 1713538168 } ], "typeId": 2 }, "chapterId": 153, "demo": null, "entitlement": null, "id": "154", "name": "Hyperkalaemia", "status": null, "topic": { "__typename": "Topic", "id": "36", "name": "Clinical Chemistry", "typeId": 2 }, "topicId": 36, "totalCards": 50, "typeId": null, "userChapter": null, "userNote": null, "videos": [ { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "154", "name": "Hyperkalaemia" } ], "demo": false, "description": null, "duration": 401.54, "endTime": null, "files": null, "id": "184", "live": false, "museId": "6i8cnZd", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/chemistry.png", "title": "Hyperkalaemia ", "userViewed": false, "views": 112, "viewsToday": 4 }, { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "154", "name": "Hyperkalaemia" } ], "demo": false, "description": null, "duration": 3507.09, "endTime": null, "files": null, "id": "333", "live": false, "museId": "PWmnGPT", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/nephrology.png", "title": "Quesmed Tutorial: Renal and Electrolytes", "userViewed": false, "views": 1031, "viewsToday": 44 } ] }, "conceptId": 154, "conditions": [], "difficulty": 3, "dislikes": 20, "explanation": null, "highlights": [], "id": "6359", "isLikedByMe": 0, "learningPoint": null, "likes": 3, "multiAnswer": null, "pictures": [], "prescribeAnswer": null, "presentations": [], "psaSectionId": null, "qaAnswer": null, "question": "An inpatient being treated for an acute kidney injury (AKI) has their potassium level returned at 6.2 mmol/L (normal range 3.5-5.3 mmol/L). The day before it had been 5.9 mmol/L. There are no hyperkalaemic changes on the ECG.\n\n\nThey are being managed with intravenous (IV) 0.9% NaCl at 100ml/hr. They feel well and have no symptoms to report.\n\n\nWhat is the best next step for this patient?", "sbaAnswer": [ "a" ], "totalVotes": 6549, "typeId": 1, "userPoint": null }

[]

{ "__typename": "QuestionSBA", "choices": [ { "__typename": "QuestionChoice", "answer": true, "explanation": "Trimethoprim inhibits tubular creatinine secretion, leading to an increase in serum creatinine independent of the true glomerular filtration rate (GFR). This leads to a falsely low eGFR as creatinine concentration is used in the calculation of GFR", "id": "31798", "label": "a", "name": "Trimethoprim", "picture": null, "votes": 2750 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Nitrofurantoin is not a nephrotoxic itself and will not cause an increase in serum creatinine, however, it is contraindicated in those with renal impairment due to reduced renal elimination of the antibiotic in these patients", "id": "31799", "label": "b", "name": "Nitrofurantoin", "picture": null, "votes": 1435 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Statins may cause rhabdomyolysis which leads to an increased creatinine level but this would be due to a **true** decrease in glomerular filtration rate", "id": "31802", "label": "e", "name": "Atorvastatin", "picture": null, "votes": 815 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Ramipril is an ACE inhibitor which is a nephrotoxic. It may cause an increase in serum creatinine but this is because of a **true** decrease in glomerular filtration rate", "id": "31801", "label": "d", "name": "Ramipril", "picture": null, "votes": 2850 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Bisoprolol is not a nephrotoxic and has no effect on serum creatinine", "id": "31800", "label": "c", "name": "Bisoprolol", "picture": null, "votes": 432 } ], "comments": [ { "__typename": "QuestionComment", "comment": "Fun fact trimethoprim has a chemical structure very close to the potassium sparing diuretic amiloride and is also well known to cause a rise in potassium in addition to falsely elevated creatinine (esp when used with ACEi etc)", "createdAt": 1682518819, "dislikes": 0, "id": "22721", "isLikedByMe": 0, "likes": 9, "parentId": null, "questionId": 6360, "replies": [], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": ";-;", "id": 21686 } }, { "__typename": "QuestionComment", "comment": "So just to confirm she has new onset AKI that is causing her confusion/delirium (explained by the high creatine) and the low eGFR (that is usually indicative of CKD which she has no history of) is caused by the trimethoprim?", "createdAt": 1683285807, "dislikes": 0, "id": "23442", "isLikedByMe": 0, "likes": 1, "parentId": null, "questionId": 6360, "replies": [], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Lateral Kinase", "id": 3545 } }, { "__typename": "QuestionComment", "comment": "could someone please explain the \"true rise\" bit for ramipril? I dont get it ", "createdAt": 1707678458, "dislikes": 0, "id": "41339", "isLikedByMe": 0, "likes": 1, "parentId": null, "questionId": 6360, "replies": [ { "__typename": "QuestionComment", "comment": "By reducing angiotensin II levels, ramipril dilates the efferent arteriole. This lowers the pressure within the glomerulus, which can reduce the glomerular filtration rate (GFR). As a result, waste products like creatinine may not be filtered out as efficiently, leading to an increase in blood creatinine levels.", "createdAt": 1723826815, "dislikes": 0, "id": "54697", "isLikedByMe": 0, "likes": 1, "parentId": 41339, "questionId": 6360, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Wilsons CT", "id": 66995 } } ], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Neoplasia Nightshift", "id": 46473 } } ], "concept": { "__typename": "Concept", "chapter": { "__typename": "Chapter", "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.", "files": null, "highlights": [], "id": "1784", "pictures": [], "typeId": 2 }, "chapterId": 1784, "demo": null, "entitlement": null, "id": "1968", "name": "Trimethoprim and renal function", "status": null, "topic": { "__typename": "Topic", "id": "33", "name": "Nephrology", "typeId": 2 }, "topicId": 33, "totalCards": null, "typeId": null, "userChapter": null, "userNote": null, "videos": [] }, "conceptId": 1968, "conditions": [], "difficulty": 3, "dislikes": 21, "explanation": null, "highlights": [], "id": "6360", "isLikedByMe": 0, "learningPoint": "Trimethoprim can falsely lower estimated glomerular filtration rate (eGFR) by inhibiting tubular creatinine secretion, affecting serum creatinine levels.", "likes": 9, "multiAnswer": null, "pictures": [], "prescribeAnswer": null, "presentations": [], "psaSectionId": null, "qaAnswer": null, "question": "A 60-year-old lady presents to the emergency department with confusion. She has the following blood tests:\n\n\n||||\n|---------------------------|:-------:|--------------------|\n|Sodium|136 mmol/L|135 - 145|\n|Potassium|4 mmol/L|3.5 - 5.3|\n|Urea|6 mmol/L|2.5 - 7.8|\n|Creatinine|300 µmol/L|60 - 120|\n|eGFR|15 mL/min/1.73m²|> 60|\n\n\nHer previous blood tests from 2 months ago suggest that her baseline creatinine is approximately 70umol/L.\n\n\nThere is no information on the computer system about her medications but you find the following medications in her bag: trimethoprim, nitrofurantoin, bisoprolol, ramipril, and atorvastatin.\n\n\nWhich of the following medications would lead to a falsely low estimated glomerular filtration rate (eGFR)?", "sbaAnswer": [ "a" ], "totalVotes": 8282, "typeId": 1, "userPoint": null }

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{ "__typename": "QuestionSBA", "choices": [ { "__typename": "QuestionChoice", "answer": false, "explanation": "Patients with SIADH are usually euvolaemic or hypervolaemic. Clinical dehydration suggests other causes for hyponatraemia such as secondary to diuretics or acute kidney injury", "id": "31807", "label": "e", "name": "Clinical dehydration", "picture": null, "votes": 67 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "A low serum cortisol and hyponatraemia suggests Addison's disease", "id": "31805", "label": "c", "name": "Low serum cortisol", "picture": null, "votes": 57 }, { "__typename": "QuestionChoice", "answer": true, "explanation": "In SIADH there are high levels of antidiuretic hormone (ADH) in the blood. This leads to increased retention of water, but not sodium. There is therefore low levels of salt in the blood and therefore low plasma osmolality. Urine produced is more concentrated (as less water is excreted) and has more sodium, leading to a high urine osmolality and high urine sodium level. Urine osmolality greater than plasma osmolality can only be induced by inappropriately high levels of ADH in the bloodstream", "id": "31803", "label": "a", "name": "Urine osmolality greater than plasma osmolality", "picture": null, "votes": 4929 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Hypothyroidism is one of the potential causes for SIADH and so TFTs should be checked when investigating for SIADH. However, whether TFTs are normal or abnormal has no bearing on the diagnosis of SIADH", "id": "31806", "label": "d", "name": "Normal thyroid function tests (TFTs)", "picture": null, "votes": 55 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "In SIADH, due to increased water retention secondary to the high levels of ADH, concentrated urine with high sodium levels is produced (high urine osmolality). As excessive sodium is being excreted and water is excessively retained, plasma sodium is low and plasma osmolality is high. Therefore, by definition, urine osmolality will be greater than plasma osmolality", "id": "31804", "label": "b", "name": "Plasma osmolality greater than urine osmolality", "picture": null, "votes": 1539 } ], "comments": [ { "__typename": "QuestionComment", "comment": "how is this diagnostic if urine osmolarity is higher than plasma in healthy patients? ", "createdAt": 1666536864, "dislikes": 0, "id": "13990", "isLikedByMe": 0, "likes": 0, "parentId": null, "questionId": 6361, "replies": [ { "__typename": "QuestionComment", "comment": "SIADH is inappropriate activation of V2 (aquaporin) receptor so more water is reabsorbed back into the capillaries lowering urine water volume. Lower urine water volume means that theres more solutes in the urine so the osmolality would be higher. Osmolality is the measure of how many substances are dissolved in 1kg of water.", "createdAt": 1683141267, "dislikes": 0, "id": "23328", "isLikedByMe": 0, "likes": 1, "parentId": 13990, "questionId": 6361, "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Zzzzzeba", "id": 33138 } } ], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Jaundice Myopathy", "id": 18355 } } ], "concept": { "__typename": "Concept", "chapter": { "__typename": "Chapter", "explanation": "# Summary\n\nSyndrome of Inappropriate ADH secretion (SIADH) refers to excessive antidiuretic hormone (ADH) release, causing water to be retained resulting in a euvolemic hyponatraemia. There are a wide range of causes including medications, malignancy, central nervous system (CNS) disorders and infections. Patients may be asymptomatic and detected through an incidental finding of a low serum sodium, or may present with features of severe hyponatraemia (e.g. confusion, seizures) and/or the underlying cause of SIADH. Key investigations include U&Es for sodium, cortisol and thyroid function to rule out other causes of hyponatraemia and urinary sodium and osmolality (which will be greater than 30 mmol/L and 100 mOsm/kg respectively). First-line management is with fluid restriction to 500-1000 ml/day, as well as treating the underlying cause (e.g. stopping causative medications). Severe cases may require hypertonic saline, and resistant cases may be treated with tolvaptan (an vasopressin V2-receptor antagonist).\n\n# Definition\n\nSyndrome of Inappropriate ADH secretion (SIADH) is an important cause of hyponatraemia that occurs when there is inappropriate release of antidiuretic hormone (ADH) outside of normal homeostatic mechanisms, which leads to reduced urine output. The increase in total body water effectively dilutes serum sodium, leading to hyponatraemia. \n\nNormally, ADH (also referred to as vasopressin) is produced in the hypothalamus and released from the posterior pituitary when serum osmolality is high. It acts to normalise osmolality by acting on the distal convoluted tubules and collecting ducts of the kidney to stimulate increased water reabsorption. \n\nSIADH may involve excessive release of ADH from the pituitary gland or production of ADH by an abnormal non-pituitary source (e.g. a tumour).\n\n# Aetiology\n\nSIADH has a wide range of causes - these are some examples:\n\n- Pulmonary causes:\n\t- Pneumonia\n\t- Chronic Obstructive Pulmonary Disease (COPD)\n\t- Tuberculosis (TB)\n- Central Nervous System (CNS) disorders:\n\t- Meningitis\n\t- Stroke\n\t- Subarachnoid haemorrhage\n\t- Traumatic brain injury\n\t- Psychosis\n- Malignancies:\n\t- Small cell lung cancer\n\t- Pancreatic cancer\n\t- Lymphoma\n\t- Mesothelioma\n\t- Thymoma\n\t- Nasopharyngeal cancer\n- Medications:\n\t- Carbamazepine\n\t- Selective Serotonin Reuptake Inhibitors (SSRIs)\n\t- Opiates\n\t- Anti-psychotics\n\t- Cyclophosphamide\n- Other: \n\t- HIV\n\t- Surgery\n\t- Acute intermittent porphyria\n\t- Idiopathic\n\n# Signs and Symptoms\n\nSIADH presents with a euvolaemic hyponatraemia, and so patients may be asymptomatic or present with features of the underlying cause (e.g. pneumonia).\n\nSigns and symptoms of hyponatraemia are more likely to develop in severe cases and where sodium has fallen rapidly:\n\n- Lethargy\n- Anorexia\n- Headache\n- Nausea and vomiting\n- Muscle cramps\n- Drowsiness\n- Confusion\n- Seizures\n\n# Differential Diagnosis\n\nSee the Hyponatraemia chapter for a full list of differentials - other causes of a euvolaemic hyponatraemia include:\n\n- **Beer potomania** is a cause of hyponatraemia in the context of alcohol excess combined with low solute intake due to a poor diet\n- **Primary polydipsia** occurs when people drink excessive amounts of water, leading to polyuria with dilute urine (as opposed to the smaller volume of concentrated urine seen in SIADH)\n- **Hypothyroidism** may cause hyponatraemia in severe cases; patients will usually have other symptoms such as fatigue, cold intolerance and constipation\n- **Adrenal insufficiency** causes hyponatraemia with hyperkalaemia; other features include hypotension, abdominal pain and weakness\n- **Exercise-induced hyponatraemia** occurs during or in the 24 hours following prolonged exercise (e.g. running a marathon), usually due to excess intake of hypotonic fluids\n- **Hypotonic intravenous fluids** such as 5% dextrose or 0.45% saline may lead to iatrogenic hyponatraemia\n\n# Investigations\n\n**Bedside:**\n\n- **Venous blood gas** to confirm hyponatraemia - if there is a significant discrepancy between the sodium on the gas and the U&Es, suspect pseudohyponatremia (see Hyponatraemia chapter for details) \n- **Urine osmolality** will be high (> 100 mOsm/kg)\n- **Urine sodium** will be high (> 30 mmol/L)\n- NB urine osmolality and sodium cannot be interpreted in patients taking diuretics and so these need to be stopped prior to investigations\n\n**Blood tests:**\n\n- **U&Es** to confirm hyponatraemia; urea will also likely be low due to dilution\n- **Serum osmolality** will be low (< 280 mOsm/kg)\n- **Thyroid function tests** to exclude hypothyroidism as a cause of hyponatraemia\n- **9am serum cortisol** to exclude adrenal insufficiency as a cause of hyponatraemia\n\n**Imaging:**\n\n- **Chest X-ray** if there is no obvious cause of SIADH as an initial screen for malignancy and pulmonary disease (e.g. tuberculosis, pneumonia)\n- **CT chest, abdomen and pelvis** and **MRI head** may be considered to exclude occult malignancy if there is no identified cause\n\n# Management\n\n**Conservative:**\n\n- Identify and treat the underlying cause (e.g. stopping causative medications where possible)\n- Patients with suspected SIADH in primary care should be referred to endocrinology to confirm the diagnosis and advise on treatment\n- Closely monitor sodium levels and ensure these are corrected no faster than 8-10 mmol/L per 24 hours \n- Fluid restriction is the first-line management in most cases, usually to 500-1000 ml/day \n\n**Medical:**\n\n- Severe hyponatraemia should be treated with hypertonic saline, usually in the intensive care setting\n- In some cases (e.g. SIADH resistant to fluid restriction), tolvaptan may be considered - this is a vasopressin V2-receptor antagonist\n\n# Complications\n\n- **Cerebral oedema** may complicate severe and/or acute hyponatraemia and may be life-threatening - patients develop raised intracranial pressure with symptoms of vomiting, headache, seizures and coma\n- **Central pontine myelinolysis** is a complication of rapid correction of hyponatraemia - patients may present with confusion, ataxia, spastic quadriparesis and pseudobulbar palsy with dysphagia and dysarthria\n- Chronic hyponatraemia, especially in the elderly, increases the risk of **falls** as well as **cognitive impairment**\n\n# NICE Guidelines\n\n[NICE CKS - Hyponatraemia](https://cks.nice.org.uk/topics/hyponatraemia/)\n\n# References\n\n[Life in the Fast Lane - Hyponatraemia](https://litfl.com/hyponatraemia/)\n\n[Life in the Fast Lane - SIADH](https://litfl.com/siadh-syndrome-of-inappropriate-adh-secretion/)\n\n[Whittington Hospital Hyponatraemia Guideline](https://www.whittington.nhs.uk/document.ashx?id=6089)", "files": null, "highlights": [], "id": "152", "pictures": [], "typeId": 2 }, "chapterId": 152, "demo": null, "entitlement": null, "id": "153", "name": "Syndrome of Inappropriate ADH release (SIADH)", "status": null, "topic": { "__typename": "Topic", "id": "36", "name": "Clinical Chemistry", "typeId": 2 }, "topicId": 36, "totalCards": 10, "typeId": null, "userChapter": null, "userNote": null, "videos": [ { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "153", "name": "Syndrome of Inappropriate ADH release (SIADH)" } ], "demo": false, "description": null, "duration": 251.73, "endTime": null, "files": null, "id": "374", "live": false, "museId": "PXMSwJ1", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/oncology.png", "title": "Superior Vena Cava Obstruction", "userViewed": false, "views": 79, "viewsToday": 2 }, { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "153", "name": "Syndrome of Inappropriate ADH release (SIADH)" } ], "demo": false, "description": null, "duration": 1027.09, "endTime": null, "files": null, "id": "376", "live": false, "museId": "akpx4rY", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/chemistry.png", "title": "Syndrome of Inappropriate ADH release (SIADH)", "userViewed": false, "views": 108, "viewsToday": 7 }, { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "153", "name": "Syndrome of Inappropriate ADH release (SIADH)" } ], "demo": false, "description": null, "duration": 6426.6, "endTime": null, "files": null, "id": "324", "live": false, "museId": "7AeyDdA", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/chemistry.png", "title": "Quesmed Tutorial: Medical Emergencies", "userViewed": false, "views": 949, "viewsToday": 49 }, { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "153", "name": "Syndrome of Inappropriate ADH release (SIADH)" } ], "demo": false, "description": null, "duration": 373.7, "endTime": null, "files": null, "id": "582", "live": false, "museId": "XWiHgAL", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/chemistry.png", "title": "Lung Cancer 5", "userViewed": false, "views": 5, "viewsToday": 0 }, { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "153", "name": "Syndrome of Inappropriate ADH release (SIADH)" } ], "demo": false, "description": null, "duration": 3495.64, "endTime": null, "files": null, "id": "579", "live": false, "museId": "FkiyEVw", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/respiratory.png", "title": "Quesmed Tutorial: Lung Cancer", "userViewed": false, "views": 132, "viewsToday": 17 } ] }, "conceptId": 153, "conditions": [], "difficulty": 1, "dislikes": 2, "explanation": null, "highlights": [], "id": "6361", "isLikedByMe": 0, "learningPoint": null, "likes": 2, "multiAnswer": null, "pictures": [], "prescribeAnswer": null, "presentations": [], "psaSectionId": null, "qaAnswer": null, "question": "A 73-year-old man is being investigated for hyponatraemia (serum Na 129 mmol/L; normal range 135-145 mmol/L) which was found on routine blood tests.\n\n\nWhich of the following results would be diagnostic of syndrome of inappropriate antidiuretic hormone secretion (SIADH)?", "sbaAnswer": [ "a" ], "totalVotes": 6647, "typeId": 1, "userPoint": null }

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{ "__typename": "QuestionSBA", "choices": [ { "__typename": "QuestionChoice", "answer": false, "explanation": "This is an autoimmune condition causing blistering urticarial lesions. This can sometimes have mucosal involvement. It is not drug induced, as this question is implying is the cause of this man's rash. It does not normally produce systemic symptoms", "id": "31809", "label": "b", "name": "Bullous Pemphigoid", "picture": null, "votes": 174 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Pyoderma gangrenosum usually manifests as a painful pustule or nodule with rapid progression. There is normally just one nodule, and is usually on the lower limbs. There is no mucosal involvement. It can sometimes be accompanied by fever and systemic symptoms", "id": "31810", "label": "c", "name": "Pyoderma gangrenosum", "picture": null, "votes": 285 }, { "__typename": "QuestionChoice", "answer": true, "explanation": "Stevens-Johnson syndrome typically produces a maculopapular rash with target lesions. There is normally mucosal involvement, as can be seen in the image above. Stevens-Johnson syndrome is usually drug-induced. This will require a hospital admission for treatment", "id": "31808", "label": "a", "name": "Stevens-Johnson syndrome", "picture": null, "votes": 8069 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "SCC would not establish over such a short time frame", "id": "31811", "label": "d", "name": "Squamous cell carcinoma (SCC) of the skin", "picture": null, "votes": 29 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Eczema herpeticum is a disseminated infection of a herpes virus that produces itchy blisters or punched-out erosions. It is normally seen in children with eczema. It can be accompanied by systemic symptoms such as fever", "id": "31812", "label": "e", "name": "Eczema herpeticum", "picture": null, "votes": 145 } ], "comments": [], "concept": { "__typename": "Concept", "chapter": { "__typename": "Chapter", "explanation": "# Summary\n\nStevens-Johnson syndrome (SJS) is a serious, immune-complex-mediated hypersensitivity disorder often triggered by medication or, less commonly, viral, bacterial, or fungal infections. Clinically, it's characterized by symptoms resembling an upper respiratory tract infection, followed by erythematous macules and mucosal ulceration, affecting less than 10% of the body surface. Diagnosis is usually clinical, supplemented by skin biopsy. Management is largely supportive, with a focus on skin and eye care.\n\n# Definition\n\nStevens-Johnson syndrome (SJS) is an immune-complex-mediated hypersensitivity disorder. It ranges from mild to severe forms, part of a spectrum that includes toxic epidermal necrolysis (TEN) at its most severe end.\n\n# Epidemiology\n\nSJS is a rare disorder, with an incidence estimated between 2.6 to 6.1 cases per million people annually. It affects both genders and all age groups, although some studies suggest a slightly higher incidence in females and middle-aged adults.\n\n# Pathophysiology\n\nThe predominant cause of SJS is adverse drug reactions, most commonly from sulfonamides, beta-lactams (penicillins and cephalosporins), antiepileptics, allopurinol, and NSAIDs. Infectious agents, particularly viral pathogens like herpes simplex virus, Epstein-Barr virus, HIV, influenza, and hepatitis, can also trigger SJS. Bacterial and fungal infections are much less common causes.\n\n# Signs and Symptoms\n\n- SJS often presents within a week of medication intake, initially resembling an upper respiratory tract infection with symptoms such as cough, cold, fever, and sore throat.\n- Erythematous macules, later becoming target-shaped, appear after a few days.\n- Flaccid blisters develop and the Nikolsky sign is positive.\n- SJS affects less than 10% of the body surface, in contrast to TEN, which involves more than 30% of the skin.\n- Mucosal ulceration is seen in at least two of the following: conjunctiva, mouth, urethra, pharynx, or gastrointestinal tract. \n\nSJS has a 10% mortality rate, primarily due to dehydration, infection, or disseminated intravascular coagulation. In comparison, TEN has a 30% mortality rate.\n\n[lightgallery]\n\n# Differential Diagnosis\n\nThe differential diagnosis of SJS includes:\n\n- Erythema Multiforme: Characterized by target lesions, typically on the hands and feet, and less severe mucosal involvement.\n- Drug Rash with Eosinophilia and Systemic Symptoms (DRESS): Presents with fever, rash, and internal organ involvement, often with a delay of 2-6 weeks after drug exposure.\n- Acute Generalized Exanthematous Pustulosis (AGEP): Noted for the rapid development of numerous small non-follicular sterile pustules on a background of edematous erythema.\n\n# Investigations\n\nThe diagnosis of SJS is primarily clinical but can be supported by a skin biopsy, which can reveal necrotic keratinocytes and a sparse lymphocytic infiltrate.\n\n# Management\n\nManagement of SJS is largely supportive, focusing on skin care and prevention of ocular complications through timely ophthalmology referrals. Patients may require hospitalization for fluid and electrolyte management, pain control, and potential treatment of secondary infections.\n\n# References\n\n[Click here for more information on Stevens-Johnson syndrome](https://patient.info/doctor/stevens-johnson-syndrome)", "files": null, "highlights": [], "id": "881", "pictures": [ { "__typename": "Picture", "caption": null, "createdAt": 1639016501, "id": "358", "index": 0, "name": "Stevens-johnson-syndrome.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/ivp2xhmg1639016499928.jpg", "path256": "images/ivp2xhmg1639016499928_256.jpg", "path512": "images/ivp2xhmg1639016499928_512.jpg", "thumbhash": "lecFHAgnNocIyIxsWKgIdINAOA==", "topic": { "__typename": "Topic", "id": "4", "name": "Dermatology", "typeId": 2 }, "topicId": 4, "updatedAt": 1708373886 } ], "typeId": 2 }, "chapterId": 881, "demo": null, "entitlement": null, "id": "924", "name": "Stevens-Johnson syndrome ", "status": null, "topic": { "__typename": "Topic", "id": "4", "name": "Dermatology", "typeId": 2 }, "topicId": 4, "totalCards": 11, "typeId": null, "userChapter": null, "userNote": null, "videos": [] }, "conceptId": 924, "conditions": [], "difficulty": 1, "dislikes": 2, "explanation": null, "highlights": [], "id": "6362", "isLikedByMe": 0, "learningPoint": "Stevens-Johnson syndrome is a severe drug-induced condition characterised by a maculopapular rash, often with mucosal involvement, requiring urgent medical attention.", "likes": 5, "multiAnswer": null, "pictures": [ { "__typename": "Picture", "caption": null, "createdAt": 1639016501, "id": "358", "index": 0, "name": "Stevens-johnson-syndrome.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/ivp2xhmg1639016499928.jpg", "path256": "images/ivp2xhmg1639016499928_256.jpg", "path512": "images/ivp2xhmg1639016499928_512.jpg", "thumbhash": "lecFHAgnNocIyIxsWKgIdINAOA==", "topic": { "__typename": "Topic", "id": "4", "name": "Dermatology", "typeId": 2 }, "topicId": 4, "updatedAt": 1708373886 } ], "prescribeAnswer": null, "presentations": [], "psaSectionId": null, "qaAnswer": null, "question": "A 40-year-old man presents to the accident and emergency department with a painful rash which has established quickly over the last few hours. He is pyrexial and reports general arthralgia. He was started on a course of amoxicillin for sinusitis the preceding day. He has no significant past medical or dermatological history.\n\nHis rash can be seen below.\n\n[lightgallery]\n\nWhich of the following is the most likely diagnosis in this patient?", "sbaAnswer": [ "a" ], "totalVotes": 8702, "typeId": 1, "userPoint": null }

[]

{ "__typename": "QuestionSBA", "choices": [ { "__typename": "QuestionChoice", "answer": false, "explanation": "The glomerular basement membrane is the kidneys - there will be IgG/C3 deposition in glomerulonephritis (eg. post-infectious)", "id": "31816", "label": "d", "name": "The glomerular basement membrane", "picture": null, "votes": 756 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Immunofluorescence will detect IgG and/or C3 on the epithelial cell surface in pemphigus vulgaris", "id": "31814", "label": "b", "name": "Epithelial cell surface", "picture": null, "votes": 500 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "IgG staining in intercellular space is seen in all types of pemphigus (except IgA pemphigus)", "id": "31815", "label": "c", "name": "Intercellular space", "picture": null, "votes": 199 }, { "__typename": "QuestionChoice", "answer": false, "explanation": "Bullous disorders affect the epidermal layer and basement membrane rather than the dermis", "id": "31817", "label": "e", "name": "The dermis", "picture": null, "votes": 1725 }, { "__typename": "QuestionChoice", "answer": true, "explanation": "This is correct. Bullous pemphigoid is an autoimmune condition caused by antibodies against hemidesmosome proteins in the epithelial basement membrane", "id": "31813", "label": "a", "name": "The epidermal basement membrane", "picture": null, "votes": 5304 } ], "comments": [ { "__typename": "QuestionComment", "comment": "this is the lowest yield question i have ever seen", "createdAt": 1653243528, "dislikes": 5, "id": "11090", "isLikedByMe": 0, "likes": 26, "parentId": null, "questionId": 6363, "replies": [], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Hypertension Hematoma", "id": 1943 } }, { "__typename": "QuestionComment", "comment": "Should spend more time on the wards....", "createdAt": 1685092523, "dislikes": 18, "id": "26307", "isLikedByMe": 0, "likes": 4, "parentId": null, "questionId": 6363, "replies": [], "user": { "__typename": "User", "accessLevel": "subscriber", "displayName": "Al", "id": 19078 } } ], "concept": { "__typename": "Concept", "chapter": { "__typename": "Chapter", "explanation": "### Summary\n\nBullous Pemphigoid and Pemphigus Vulgaris are both autoimmune blistering disorders with different blister locations and antigens involved. The clinical features, investigations, and treatments are similar, with steroids forming the mainstay of treatment. \n\n### Bullous Pemphigoid\n\n#### Definition\n\nOne of the autoimmune blistering disorders characterised by tense subepidermal blisters\n\n#### Pathophysiology\n\n- Autoantibodies targeting the hemidesmosomes that bind the basal keratinocytes of the epidermis to the basement membrane. The antigens are the BP180 and BP230 components of hemidesmosomes\n- This causes the development of tense, sub-epidermal blisters that are not readily deroofed\n- On immunoflouresence, this produces a linear pattern of immunoflouresence along the basement membrane\n- Autoantibodies may also be identified in the circulation\n- May sometimes represent a paraneoplastic process, so a careful history and examination is important\n- Other associations include drugs (PD-1 inhibitors in melanoma, ACEi and penicillamine), psoriasis treatment (phototherapy), injury to skin, neurological disease, and genetics\n\n#### Clinical Features\n\n- Usually affects older people\n- Prodrome of itch, irritation, erythematous, eczematous, urticarial skin changes, followed by tense subepidermal blisters\n- Nikolsky's sign is negative\n- The mucous membrane's are spared, except for the cicatrial variant (characterised by marked scarring and predilection for the mucous membranes) \n\n[lightgallery]\n\n#### Investigations\n\n- Biopsy for immunoflouresence from lesion edge\n- Anti BP180/BP230 antibodies circulating\n\n#### Treatment\n\n- Topical potent steroids at onset of symptoms e.g. itch\n- Doxycycline for anti-inflammatory effect\n- Systemic steroids (0.5-1mg/kg of prednisolone), continued until no further lesions for one year. Then tapered very gradually over many, many months\n- Steroid sparing agents include azathioprine and mycophenolate if relapse during steroid withdrawal\n- The cicatrial variant is particularly difficult to treat \n\n### Pemphigus Vulgaris\n\n#### Definition\n\nOne of the autoimmune blistering skin conditions characterised by flaccid intra-epidermal blisters.\n\n#### Pathophysiology\n\n- IgG autoantibodies are targeted against desmosomes, structures that link keratinocytes to other keratinocytes within the epidermis\n- The specific antigens are desmoglein 1 and desmoglein 3\n- This leads to the development of blisters within the epidermis, which are flaccid and often deroofed\n- Immunoflouresence shows a fish-net/chicken-wire pattern of staining within the epidermis\n- Drug triggers have been noted (such as ACEi and penicillamine), and it may be associated with an underlying malignancy as a paraneoplastic phenomenon\n\n#### Clinical Features\n\n- Flaccid, thin walled blisters leading to erosions across the body \n- Mucous membranes may be involved\n- Nikolsky's sign is positive\n- Patients can be quite unwell with pemphigus vulgaris and mortality is high without treatment\n\n[lightgallery1]\n\n#### Investigations\n\n- Biopsy for immunoflouresence from the edge of the lesion\n- Detection of autoantibodies against desmoglein 1 and desmoglein 3 using indirect immunofluorescence (IIF) or enzyme-linked immunosorbent assay (ELISA)\n\n#### Treatment\n\n- Treatment is very similar to Bullous Pemphigoid, with oral predniosolone\n- Risk of secondary bacterial infections is high and these often need treating with antibiotics \n\n### Memory Aid\n\nPemphigu**s** = **s**uperficial blisters, pemphigoi**d** = **d**eep blisters\n\nHere's a table comparing the two conditions:\n\n| | Bullous pemphigoid | Pemphigus vulgaris |\n| ------------- |:-------------:| :-----:|\n| Pathophysiology | IgG antibodies against hemidesmosomal proteins, primarily BP180 and BP230 | IgG antibodies against desmoglein 1 and desmoglein 3|\n| Clinical features | Tense, subepidermal blisters, rarely mucous membrane involvement | Painful, fragile blisters and erosions, mucous membrane involvement (oral membranes almost always)|\n| Investigation findings | Direct immunofluorescence (DIF) demonstrates linear IgG and complement along the basement membrane zone; Indirect immunofluorescence (IIF) or ELISA detects circulating antibodies against BP180 and BP230 | DIF demonstrates intercellular IgG deposits in the epidermis; IIF or ELISA identifies antibodies against desmoglein 1 and desmoglein 3 |\nTreatment | High-potency topical corticosteroids for local disease, oral corticosteroids for extensive involvement; immunosuppressive medications (AZT, MMF) for severe or refractory cases | High-dose systemic corticosteroids to induce remission, topical steroids for mucous membranes; adjunctive immunosuppressive agents (AZT, MMF, rituximab) to reduce corticosteroid dependence|\n\n\n\n### References\n[Bullous pemphigoid - DermNet NZ](https://dermnetnz.org/topics/bullous-pemphigoid)\n\n[Pemphigus vulgaris - DermNet NZ](https://dermnetnz.org/topics/pemphigus-vulgaris)\n", "files": null, "highlights": [], "id": "862", "pictures": [ { "__typename": "Picture", "caption": "An example of pemphigus vulgaris", "createdAt": 1665036196, "id": "936", "index": 1, "name": "Pemphigoid 2.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/hu6ye3eq1665036171729.jpg", "path256": "images/hu6ye3eq1665036171729_256.jpg", "path512": "images/hu6ye3eq1665036171729_512.jpg", "thumbhash": "mjgKDQIG0sY5a4SomHqIiQekZlBZ", "topic": null, "topicId": null, "updatedAt": 1708373886 }, { "__typename": "Picture", "caption": "An example of bullous pemphigoid.", "createdAt": 1665036195, "id": "906", "index": 0, "name": "Pemphigoid.jpeg", "overlayPath": null, "overlayPath256": null, "overlayPath512": null, "path": "images/b9j2eq141665036171717.jpg", "path256": "images/b9j2eq141665036171717_256.jpg", "path512": "images/b9j2eq141665036171717_512.jpg", "thumbhash": "pRgGDQT0OiSip1WUd2iFeAKJKLCY", "topic": null, "topicId": null, "updatedAt": 1708373886 } ], "typeId": 2 }, "chapterId": 862, "demo": null, "entitlement": null, "id": "908", "name": "Pemphigus and Pemphigoid", "status": null, "topic": { "__typename": "Topic", "id": "4", "name": "Dermatology", "typeId": 2 }, "topicId": 4, "totalCards": 5, "typeId": null, "userChapter": null, "userNote": null, "videos": [ { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "908", "name": "Pemphigus and Pemphigoid" } ], "demo": false, "description": null, "duration": 3472.41, "endTime": null, "files": null, "id": "311", "live": false, "museId": "m1dDZby", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/dermatology.png", "title": "Quesmed Tutorial: Dermatology", "userViewed": false, "views": 799, "viewsToday": 49 }, { "__typename": "Video", "concepts": [ { "__typename": "Concept", "id": "908", "name": "Pemphigus and Pemphigoid" } ], "demo": false, "description": null, "duration": 299.97, "endTime": null, "files": null, "id": "268", "live": false, "museId": "YqTp3Y1", "osceStation": null, "startTime": null, "status": null, "thumbnail": "images/videos/dermatology.png", "title": "Pemphigus and Pemphigoid", "userViewed": false, "views": 69, "viewsToday": 3 } ] }, "conceptId": 908, "conditions": [], "difficulty": 2, "dislikes": 4, "explanation": null, "highlights": [], "id": "6363", "isLikedByMe": 0, "learningPoint": "In bullous pemphigoid, IgG and C3 are located at the epidermal basement membrane, indicating an autoimmune response against hemidesmosome proteins.", "likes": 7, "multiAnswer": null, "pictures": [], "prescribeAnswer": null, "presentations": [], "psaSectionId": null, "qaAnswer": null, "question": "A patient presents with blistering of the skin. Bullous pemphigoid is suspected. Direct immunofluorescence is carried out and detects IgG and C3 in a linear pattern.\n\nIn what location would the IgG and C3 be located to confirm a diagnosis of bullous pemphigoid?", "sbaAnswer": [ "a" ], "totalVotes": 8484, "typeId": 1, "userPoint": null }