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"explanation": "This is a fibrous arch that connects the diaphragmatic crura on either side of the aortic hiatus.",
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"explanation": "The round ligament of the uterus is fibro-muscular connective tissue. It appears like a round band of rope. One side of the round ligament is attached to the superior and lateral aspects of the uterus. The round ligament crosses the pelvis through the deep inguinal ring which then traverses the inguinal canal and enters the labia majora, where it terminates with its fibres blending into the mons pubis.",
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"explanation": "The medial umbilical ligament or Urachus is a fibrous remnant cord connecting the bladder to the umbilicus. A patent urachus is often managed surgically. Causes of a patent urachus include urachal cyst, urachal fistula, urachal diverticulum and urachal sinus.",
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"explanation": "## Summary\n\nThe urinary bladder is the most anterior element of the pelvic viscera and a part of the urinary system. It occupies the pelvic cavity when empty but expands into the abdominal cavity as it fills. It is an extraperitoneal organ.\n\n## Anatomy\n\nThe bladder resembles the shape of a 3D pyramid when empty. It consists of a base, apex, a superior surface and 2 inferolateral surfaces.\n\n* **Base (or fundus)** - shaped like an inverted triangle and faces posterolaterally. At the upper corners of the base, the 2 ureters enter the bladder and at the lower corner of the base the urethra exits the bladder.\n* **Apex** - located superiorly and directed towards the pubic symphysis. The median umbilical ligament (an embryological remnant of the urachus) continues from the apex up the anterior abdominal wall to the umbilicus.\n* **Superior surface** - domed when the bladder is empty and balloons upwards as it fills\n* **Inferolateral surfaces** - located between the levator ani muscles and the adjacent obturator internus muscles\n\nIn the inside of the bladder, the smooth triangular area between the openings of the ureter and the urethra is known as the trigone. The smooth walls of the trigone are distinct from the rest of the bladder which is explained by its embryological origin from the mesonephric ducts.\n\nThe ureters course down the posterior abdominal wall and the posterolateral aspect of the pelvis. They run _inferior to the vas deferens_ in males and _inferior to the broad ligament_ in females to reach the base of the bladder. \n\nThis relation can be remembered as *\"water (ureters) under the bridge\"*. The ureters enter the bladder at an angle through the mucosa and the muscle. A flap valve is created to prevent the backflow of urine (vesicoureteric reflux).\n\nThe neck of the bladder is anchored by ligaments to the pelvis floor and the body of the pubis:\n\n* In females this is the pubovesical ligament\n* In males this is the puboprostatic ligament as it blends with the fibrous capsule of the prostate\n\nThe walls of the bladder are made of smooth muscle and detrusor muscle. The mucosa of the bladder is lined by transitional epithelium which is able to withstand the toxic urine that the bladder holds and the stretching of the bladder as it fills.\n\n**Urethral sphiincters:**\n- Internal urethral sphincter: Located at the base of the bladder and blends with the detrusor muscle. It is under involuntary autonomic control. It is the dominant sphincter for maintaining continence.\n- External urethral sphincter: Located in the perineal pouch. In women this is just inferior to the bladder, in male this is just inferior to the prostate (in the membranous urethra).\n\n[lightgallery]\n\n[lightgallery1]\n\n## Blood Supply\n\n**Arterial:**\n* Superior, middle and inferior vesical arteries - derived from the anterior trunk of the hypogastric\n* Obturator artery\n* Inferior gluteal artery\n* In females additional branches are derived from the uterine and vaginal arteries.\n\n**Venous**\nVenous drainage occurs via a vesical venous plexus that drains into the internal iliac veins.\n\n## Innervation\nThe detrusor muscle has both parasympathetic and sympathetic innervation for micturition and closure of the bladder neck (during ejaculation) respectively. The parasympathetic supply is via the pelvic splanchnic nerves, S2-S4. The preganglionic sympathetic fibres arise from the L1-L2 spinal cord and the postganglionic fibres are from the ganglia within the hypogastric plexus.\n\nSomatic innervation is via the pudenal nerve which innervates the external urethral sphincter. This enables the voluntary control of micturition.\n\n## Function\n* Storage of urine\n* Expulsion of urine through the contraction of the muscles of the bladder\n\n\n## Clinical points\n- Prostate surgery can injury the internal urethral sphincter causing incontinence.\n- The bladder is an extraperitoneal organ but there is peritoneal reflection of it's dome. If there is a rupture of the bladder at the dome, the fluid is leak into the peritoneum. However, if any other part ruptures then the leak will be exxtraperitoneal.\n",
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"explanation": "The uterus is a hollow pear-shaped organ. It is a thick-walled muscular organ connected distally to the vagina and laterally to the uterine tubes. It consists of three parts: the fundus – the top of the uterus, the body – usually the site of implantation and the cervix – the lower part of the uterus linking it with the vagina.",
"id": "10014219",
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"explanation": "This represents the caudal extension of the peritoneal cavity. It may also be known as the rectovaginal/rectouterine pouch in females and the rectovesical pouch in males.",
"id": "10014220",
"label": "c",
"name": "The pouch of Douglas",
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"explanation": "This is the opening of the cervix and the upper part of the uterus",
"id": "10014222",
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"name": "The internal OS",
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"explanation": "This is the muscular tube which connects from the vaginal orifice to the cervix.",
"id": "10014221",
"label": "d",
"name": "Vagina",
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"explanation": "The cervix is the lower, narrower end of the uterus connecting the uterus to the vagina.",
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"explanation": "## Summary\n\nThe cervix is a fibromuscular organ that forms the most inferior part of the uterus and acts as the connection between the vagina inferiorly and the rest of the uterus superiorly. \n\nIt is lined by two types of cells, squamous epithelium inferiorly and columnar epithelium superiorly.\n\n## Anatomy\n\nThe cervix is located between the uterus and the vagina and has two openings\n\n1. The **internal ostium** - which communicates directly with the uterus\n2. The **external ostium** - which communicates directly with the vagina\n\nThe **cervical canal** (the ***endocervix***) lies between the internal and external ostium and is lined with **simple columnar epithelium**. The external ostium is clinically relevant, as it marks the end of the cervical canal.\n\nThe outer part of the cervix which communicates directly with the superior vagina is known as the **ectocervix**, and is lined by **stratified squamous non-keratinised epithelium**.\n\nThe junction between the two types of epithelium is known as the **transitional zone** or **squamocolumnar junction** - this is clinically relevant as in some malignancies and pre-malignancies of the cervix this area may be removed.\n\n[lightgallery]\n\n## Clinical points\nHuman papilloma virus infection (HPV) can cause dysplasia of the cells in the transitional zone which can lead to malignant transformation.",
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"explanation": "This refers to inflammation of the urethra and does not constitute a structural abnormality of the urethra.",
"id": "10014226",
"label": "d",
"name": "Urethritis",
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"explanation": "This is a condition describing symptoms similar to those of a UTI without an underlying infection. The main symptom of this condition is chronic pelvic and urinary tract pain. Interestingly, urethral syndrome is linked to certain allergies and food sensitivities and eliminating these may relieve symptoms.",
"id": "10014227",
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"explanation": "Urethral cancer is rare and may not cause any symptoms in the early stages.",
"id": "10014224",
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"explanation": "This is a benign mass usually occurring after menopause and does not usually cause any symptoms. Common symptoms include pain or bleeding on urinating.",
"id": "10014225",
"label": "c",
"name": "Urethral caruncle",
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"explanation": "Males are more likely to develop urethral strictures due to longer urethras however it can affect females too. Urethral narrowing that may lead to blockage is known as a urethral stricture. Injury often causes stricturing but infections are also known to cause structuring.\nOther symptoms of urethral strictures include pain on micturition, blood in the urine and abdominal pain.",
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"explanation": "## Summary\n\nThe female urethra is an epithelium-lined tube that connects the base of the bladder to the external urethral meatus. It is much shorter than the male urethra.\n\n## Anatomy \n\n- The female urethra is **much shorter** than the male urethra at around **4cm long**. \n- It passes through the **deep perineal pouch** and terminates in the external urethra sphincter or orifice. \n- The **proximal urethra** is lined by **transitional epithelium**, with the distal third containing **stratified squamous epithelium**.\n\n[lightgallery]\n\n## Relations\n- Anterior: Pubic symphysis\n- Posterior: Anterior wall of the vagina. \n- Supeiror: Bladder\n\n## Blood supply\n\nThe **internal pudendal arteries** supply the female urethra, along with the vaginal and **inferior vesical arteries**. \n\n## Innervation\n\nThe pudendal nerve supplies the vesical plexus that innervates the urethra. \n\n## Lymphatic drainage\n\n- Distal urethra and labia: the superficial and deep inguinal nodes\n- Proximal urethra: iliac, obturator, presacral, and para-aortic lymphatic chains\n\n## Clinical points\n\nIt is theorised that because the female urethra is much shorter than the male urethra, it is easier for perineal bacteria to track along the urethra into the bladder causing urinary tract infections (UTIs) and cystitis. This may be one reason why UTIs are more common in females.",
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"explanation": "This forms part of the base of the fossa anteriorly. The sacrotuberous ligament and gluteus maximus form the posterior aspect of the base.",
"id": "10014232",
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"explanation": "This forms the floor of the ischioanal fossa.",
"id": "10014229",
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"id": "10014230",
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"explanation": "This forms part of the lateral wall of the fossa .",
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"explanation": "The annotated space is the ischioanal fossa. The ischioanal fossa is a paired triangular-shaped space lateral to the anal canal. The levator ani muscle forms the roof of this.",
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"explanation": "#### Summary\n\nThe ischioanal fossa is a paired fat filled triangular space located lateral to the anal canal.\n\n#### Anatomy\nThis region is bounded by the ischial tuberosities and the anal canal. The apex of this triangular space is directed towards the pubic symphysis in an anteromedial direction. The base is continuous posteriorly allowing the two ischioanal fossae to communicate. The two fossae are continuous with each other anteriorly and posteriorly to the anal canal.\n\n* **Lateral wall** - formed by the ischium, obturator internus muscle and the sacrotuberous ligament.\n* **Medial wall** - levator ani muscle\n\nThe pudenal canal is a fascial tunnel in the lateral wall of each fossa. The internal pudenal vessels and the pudenal nerve run in this canal and give rise to the inferior rectal vessels and nerve.\n\nFat also fills the ischioanal fossa which extends forwards between the lower surface of the pelvic diaphragm and the upper surface of the perineal membrane.\n\n[lightgallery]\n\n\n#### Clinical points\n\n- The ischioanal fossa is susceptible to the formation of abscesses which can cause fistulation between the anus and the skin. This is particularly seen in Crohn's disease.\n",
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"explanation": "#### Summary\n\nThe ischioanal fossa is a paired fat filled triangular space located lateral to the anal canal.\n\n#### Anatomy\nThis region is bounded by the ischial tuberosities and the anal canal. The apex of this triangular space is directed towards the pubic symphysis in an anteromedial direction. The base is continuous posteriorly allowing the two ischioanal fossae to communicate. The two fossae are continuous with each other anteriorly and posteriorly to the anal canal.\n\n* **Lateral wall** - formed by the ischium, obturator internus muscle and the sacrotuberous ligament.\n* **Medial wall** - levator ani muscle\n\nThe pudenal canal is a fascial tunnel in the lateral wall of each fossa. The internal pudenal vessels and the pudenal nerve run in this canal and give rise to the inferior rectal vessels and nerve.\n\nFat also fills the ischioanal fossa which extends forwards between the lower surface of the pelvic diaphragm and the upper surface of the perineal membrane.\n\n[lightgallery]\n\n\n#### Clinical points\n\n- The ischioanal fossa is susceptible to the formation of abscesses which can cause fistulation between the anus and the skin. This is particularly seen in Crohn's disease.\n",
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"explanation": "## Summary\n\nThe male urethra is an epithelium-lined tube that connects the base of the bladder to the external urethral meatus. It is approximately 20cm long and is incorperated within the prostate in parts. It's main funciton is to facilitate the transit of urine out of the body but also has a similar role in ejaculation.\n\n## Anatomy\n\nThe male urethra has three sections.\n\n- **Prostatic urethra** - the widest and most distensible part. \n\t- It has a long ridge on its posterior wall known as the urethral crest. \n\t- The prostatic urethra connects the neck of the bladder through the prostate gland. \n\t- It is approximately 3cm in length and ends in the membranous urethra. \n\t- The two openings of the ejaculatory duct lie on either side of the summit of the urethral crest. \n\t- This portion of the urethra is lined with **transitional epithelium**. \n- **Membranous urethra** \n\t- Connects the prostatic and penile urethra. \n\t- It is the narrowest part of the urethra and is enclosed by the **external urethral sphincter**. \n\t- The membranous urethra is named as such due to its course through the perineal membrane. \n\t- It is approximately 1-2cm and is lined with **pseudostratified columnar** and **pseudostratified epithelium**.\n- **Penile (spongy) urethra** \n\t- It passes through the corpus spongiosum of the penis and terminates in the **external urethral orifice**. \n\t- It is 15-25cm in length and receives secretions from the bulbourethral glands before dilating in the glans of the penis to create the navicular fossa. \n\t- It is lined by **pseudostratified columnar epithelium** proximally and **nonkeratinising stratified squamous epithelium** distally.\n\n[lightgallery]\n\n[lightgallery1]\n\n[lightgallery2]\n\n## Blood supply\n\nArterial supply depends on the portion:\n- Prostatic - **inferior vesical artery**\n- Membranous - **bulbourethral artery**\n- Penile - **internal pudendal artery**\n\n## Functions\nTransit of:\n- Urine from the bladder to the external urethral orifice\n- Semen from the ejaculatory ducts and prostate to the external urethral orifice.\n\n## Clinical points\n- The most likely site of injury in traumatic urethral injury is the membranous urethra.\n- Post-infection (most commonly gonorrheal) urethral stricture is most likely to affect the penile urethra.",
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"explanation": "## Summary\n\nThe male urethra is an epithelium-lined tube that connects the base of the bladder to the external urethral meatus. It is approximately 20cm long and is incorperated within the prostate in parts. It's main funciton is to facilitate the transit of urine out of the body but also has a similar role in ejaculation.\n\n## Anatomy\n\nThe male urethra has three sections.\n\n- **Prostatic urethra** - the widest and most distensible part. \n\t- It has a long ridge on its posterior wall known as the urethral crest. \n\t- The prostatic urethra connects the neck of the bladder through the prostate gland. \n\t- It is approximately 3cm in length and ends in the membranous urethra. \n\t- The two openings of the ejaculatory duct lie on either side of the summit of the urethral crest. \n\t- This portion of the urethra is lined with **transitional epithelium**. \n- **Membranous urethra** \n\t- Connects the prostatic and penile urethra. \n\t- It is the narrowest part of the urethra and is enclosed by the **external urethral sphincter**. \n\t- The membranous urethra is named as such due to its course through the perineal membrane. \n\t- It is approximately 1-2cm and is lined with **pseudostratified columnar** and **pseudostratified epithelium**.\n- **Penile (spongy) urethra** \n\t- It passes through the corpus spongiosum of the penis and terminates in the **external urethral orifice**. \n\t- It is 15-25cm in length and receives secretions from the bulbourethral glands before dilating in the glans of the penis to create the navicular fossa. \n\t- It is lined by **pseudostratified columnar epithelium** proximally and **nonkeratinising stratified squamous epithelium** distally.\n\n[lightgallery]\n\n[lightgallery1]\n\n[lightgallery2]\n\n## Blood supply\n\nArterial supply depends on the portion:\n- Prostatic - **inferior vesical artery**\n- Membranous - **bulbourethral artery**\n- Penile - **internal pudendal artery**\n\n## Functions\nTransit of:\n- Urine from the bladder to the external urethral orifice\n- Semen from the ejaculatory ducts and prostate to the external urethral orifice.\n\n## Clinical points\n- The most likely site of injury in traumatic urethral injury is the membranous urethra.\n- Post-infection (most commonly gonorrheal) urethral stricture is most likely to affect the penile urethra.",
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"explanation": "## Summary\n\nThe ovaries are paired gonadal organs found within the pelvis. They are responsible for maturation and release of ova as well as important hormonal functions.\n\n## Anatomy\n\nThe ovaries lie **against the wall of the pelvis**. They are prune shaped, with their upper pole associated with the fimbrae of the uterine tubes. The **lower pole** of the ovary is connected to the uterus via a **fibromuscular cord** which runs to the body of the uterus, known as the **ligament of the ovary**.\n\nThis ligament of the ovary **continues** onwards from the **body of the uterus**, back through the broad ligament towards the inguinal canal and then through the canal into the labia majora. The continuation fo the ligament of the ovary is known as the **round ligament of the uterus.**\n\nThe **ligaments** are remnants of the **gubernaculum** that drew the gonads into the pelvis in embryonic life. The ovary is covered by a layer of **cuboidal epithelial cells** which are **continuous with the peritoneum**. The **ova** within the ovary **mature and rupture** to cross the peritoneal cavity to enter the uterine tube.\n\nThe **suspensory ligament of the ovary** carries the the ovarian artery and vein. The **ovarian artery** originates from the **abdominal aorta** and branches through the **mesovarium** to reach the ovary and through the mesometrium of the broad ligament to **anastomose with the uterine artery.**\n\n## Blood supply\n\nThe main blood supply is via the ovarian arteries (direct branches from the abdominal aorta). There is additional blood supply from the uterine arteries.\n\nVenous drainage is via the ovarian vein and the pelvic venous plexus.\n\n## Lymphatic drainiage\n\nThe lymph nodes of the pelvis create a complex network.\n\nThe **common iliac lymph nodes** drain the external, internal and sacral lymph nodes. The **lumbar lymph nodes** then superiorly drain the **common iliac nodes**. It is good to know the **drainage of important female reproductive organs.**\n\n* **ovaries** - aortic nodes - draining to lumbar lymph nodes\n* **uterine tubes** - aortic nodes - draining to lumbar lymph nodes\n* **uterus & cervix** - iliac, sacral, aortic and inguinal lymph nodes\n* **vagina** - superiorly to external iliac nodes, middle to internal iliac nodes and inferiorly to superficial inguinal nodes\n\nThey are **clinically** relevant in the metastasis of **cancer**, and may be removed for diagnostic or curative purposes.\n\n## Clinical points\n- The ovaries can be highly mobile within the pelvis. Occasionally they can rotate round their vascular pedicles leading to compromise of their arterial blood supply. This is called ovarian torsion and is a surgical emergency.\n- Ovarian cancer that spreads to the lymph nodes will first spread to the para-aortic nodes mirroring their venous drainage.",
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"explanation": "The distal expansion of the corpus spongiosum forms the glans penis.",
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"explanation": "## Summary\n\nThe penis is a male appendage used for reproduction and urination. It is formed of the two corpora cavernosa and corpus spongiosum. When filled with blood it becomes erect.\n\n## Anatomy\n\nSuperficial to the perineal membrane in the male is the **root of the penis**. The root of the penis is formed by **three masses** of **erectile tissue**, each surrounded by a tough fibrous sheath. The **crura** of the penis are **attached** to the **inner surface** of each **ischiopubic ramus**. The crura become the **two corpora cavernosa** of the shaft. There is **free communication of blood vessels between the two through perforations** in the fibrous septum along the length of the shaft.\n\nThe third component is the **bulb of the penis**. It lies in the midline against the undersurface of the perineal membrane. The bulb continues in the free shaft of the penis as the **corpus spongiosum** and it extends to form the **glans penis** at the top. The bulb of the penis and **two crura are covered by muscles**, which, when they contract, may assist in initiating and maintaining **erection** of the penis.\n\nErectile tissue contains cork-screw like or **helicline arterioles** that open into **fibrous spaces**. As a result of **parasympathetic stimulation** the smooth muscles of the **arterioles dilate** and the fibrous spaces become taut and distended with arterial blood, resulting in erection of the penis.\n\nTwo **ischiocavernosus** muscles **enclose** the crura over the ischiopubic rami and the **bulbospongiosus** muscle cover the bulb of the penis in the midline. The bulbospongiosus muscle has a **midline raphe** or seam that has a sphincteric action that assists in ejaculation and urination.\n\n[lightgallery]\n\n[lightgallery1]\n\n## Blood supply\n\nThe **deep and dorsal arteries** of the penis divide into many branches, and some end in capillary networks. Blood from **cavernous spaces converges** in vessels from the base of the glans penis, to **form the deep dorsal vein.**\n\n## Innervation\n\nThe nerves of the penis come from the **pudendal and pelvic nerve plexuses.**\n\n## Clinical points\nRupture of the corpus cavernosum (called a ruptured or fracture penis) causes immediiate loss of erection, severe pain and deformity. If it is not surgically repaired it can lead to permanent deformity of the penis when erect.",
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"explanation": "## Summary\n\nThe perineum is a diamond shaped anatomical region located inferior to the pelvic floor. It is found between the thighs. The pelvic outlet forms the peripheral boundary and the pelvic diaphragm formed by the levator ani and the coccygeus muscles forms the ceiling. The walls of the pelvic cavity form the lateral walls inferior to the attachment of the levator ani muscle.\n\n\n[lightgallery]\n\n[lightgallery1]\n\n## Anatomy\n\nThe diamond-shaped perineum is divided into an anterior urogenital triangle and the posterior anal triangle by an imaginary line between the ischial tuberosities.\n\n**Borders:**\n\n* Anterior: inferior border of the pubic symphysis\n* Posterior: tip of the coccyx\n* Lateral: ischiopubic rami and the sacrotuberous ligament\n* Roof: levator ani muscles\n* Base: skin and fascia\n\n## Urogenital triangle\n\nThe urogenital triangle is located anteriorly in the perineum. The borders are:\n\n* Pubic symphysis\n* Ischiopubic rami\n* Imaginary line between the 2 ischial tuberosities\n\nThis triangle is associated with the external genitalia and the urethra. The **perineal membrane** is a fibrous sheet that fills this region. It has a free posterior border and it is anchored by the perineal body.\n\nThe **deep perineal pouch** is a structure that is found superior to the perineal membrane. It contains skeletal muscles, neurovascular tissues, external urethral sphincter and structures unique to males and females:\n\n* Females: vagina\n* Males: bulbourethral glands and the deep transverse perineal muscles\n\nThe **superficial perineal pouch** is located between the perineal membrane and the membranous layer of the superficial fascia. This pouch contains:\n\n* Erectile structures that join together to form the clitoris in females and penis in males\n* Associated skeletal muscles that are attached to the perineal membrane and the adjacent bone\n\nThe perineal fascia continues from the abdominal fascia and consists of the deep and superficial fascia.\n\n## Anal triangle\n\nThe anal triangle is located posteriorly. The borders are:\n\n* Coccyx\n* Sacrotuberous ligaments\n* Imaginary line between the ischial tuberosities\n\nThe anal aperture is located central and it communicates with the ischio-anal fossa on either side. The external anal sphincter is also found in this region (surrounding the anal canal) and consists of 3 parts, from superior to inferior these are: deep, superficial and subcutaneous.\n\n* Deep part - circles the upper part of the anal canal, blends with the fibres of the levator ani muscle\n* Superficial part - surrounds the anal canal. Anchored anteriorly to the perineal body and posteriorly to the coccyx and anococcygeal ligament.\n* Subcutaneous part - flattened disc of muscle that surrounds the anal aperture under the skin\n\n## Blood supply\n\nThe branches of the internal pudenal artery are:\n\n* Inferior rectal artery\n* Perineal artery\n* Branches to the erectile tissue of the penis/clitoris\n\nThere are also other arteries that enter the perineum:\n\n* External pudenal\n* Testicular artery\n* Cremasteric artery\n\nThe veins usually accompany the artery and drain into the internal pudenal vein and joins the internal iliac vein. The deep dorsal vein of the penis/clitoris is the only exception as it connects with a plexus that surrounds the prostate in men and bladder in women.\n\n## Innervation\n\nThe major nerve in this region is the pudenal nerve (S2-S4). The major artery is the internal pudenal artery.\n\nThe pudenal nerve travels along the lateral wall of the ischio-anal fossa in the pudenal canal. This canal also contains the internal pudenal artery and the associated veins. The pudenal nerve has 3 branches which are accompanied by branches of the internal pudenal artery:\n\n* Inferior rectal nerve\n* Perineal nerve\n* Dorsal nerve of the penis/clitoris)\n\n## Clinical points\n\nDamage to teh perineal body (e.g. during childbirth) can lead to weakening of the pelvic floor. This can lead to genital prolaspe or stress incontinence.",
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"explanation": "## Summary\n\nThe prostate gland is located inferior to the neck of the bladder, and posterior to the ampulla of the rectum.\n\n## Anatomy\n\nIt is known for being the size of a walnut, but can be subject to increase in later life - either as a part of a benign prostatic hyperplasia (BPH) process, or as a result of malignancy.\n\nThe prostate has four zones, three of main anatomical importance.\n\n- **Central** zone - this encloses the ejaculatory ducts\n- **Transitional** zone - this encloses the prostatic urethra and is the site of BPH\n- **Peripheral** zone - this is the main bulk of the prostate, and is the area felt on digital rectal examination\n\nThe **fibromuscular stroma** is the tissue found at the apex of the prostate. It contains muscle fibres and connective tissue, but no glandular tissue.\n\n[lightgallery]\n\n[lightgallery1]\n\n## Relations\n\n- Anteriorly: Pubic symphysis\n- Posteriorly: Ampulla of the rectum separated by the fascia of Denonvilliers\n- Superiorly: External urethral sphincter and bladder neck\n- Laterally: Levator ani muscles\n\n## Blood supply\n\nIt receives blood supply from several sources (bilaterally):\n- Inferior vesicular artery\n- Pudendal artery\n- Middle rectal artery\n\nThe veins around teh prostate form a plexus which drain to the internal iliac veins. They also connect to the vertebral venous plexus.\n\n## Function\n\n- The prostate produces seminal fluid which is released during ejaculation.\n- During urintation the muscles int eh central zone conotract closing off the seminal ducts preventing retrograde flow.\n- The prostate converts testosterone to its active form, dihydrotestosterone.\n\n## Clinical points\n- Because of it's relation to the rectum, the prostate can be palpated through a digital rectal exam. However, it is important to remember that the more anterior parts (transitional zone and fibromuscular tissue) cannot be palpated.\n- Because of the close relation between the prostate and the bladder neck, possible complications of prostate surgery are incontinence and retrograde ejaculation.\n- The connections between the prostate venous plexus and the vertebral venous plexus explains why prostate cancer commonly metastasises to the vertebral column.",
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"explanation": "## Summary\n\nThe prostate gland is located inferior to the neck of the bladder, and posterior to the ampulla of the rectum.\n\n## Anatomy\n\nIt is known for being the size of a walnut, but can be subject to increase in later life - either as a part of a benign prostatic hyperplasia (BPH) process, or as a result of malignancy.\n\nThe prostate has four zones, three of main anatomical importance.\n\n- **Central** zone - this encloses the ejaculatory ducts\n- **Transitional** zone - this encloses the prostatic urethra and is the site of BPH\n- **Peripheral** zone - this is the main bulk of the prostate, and is the area felt on digital rectal examination\n\nThe **fibromuscular stroma** is the tissue found at the apex of the prostate. It contains muscle fibres and connective tissue, but no glandular tissue.\n\n[lightgallery]\n\n[lightgallery1]\n\n## Relations\n\n- Anteriorly: Pubic symphysis\n- Posteriorly: Ampulla of the rectum separated by the fascia of Denonvilliers\n- Superiorly: External urethral sphincter and bladder neck\n- Laterally: Levator ani muscles\n\n## Blood supply\n\nIt receives blood supply from several sources (bilaterally):\n- Inferior vesicular artery\n- Pudendal artery\n- Middle rectal artery\n\nThe veins around teh prostate form a plexus which drain to the internal iliac veins. They also connect to the vertebral venous plexus.\n\n## Function\n\n- The prostate produces seminal fluid which is released during ejaculation.\n- During urintation the muscles int eh central zone conotract closing off the seminal ducts preventing retrograde flow.\n- The prostate converts testosterone to its active form, dihydrotestosterone.\n\n## Clinical points\n- Because of it's relation to the rectum, the prostate can be palpated through a digital rectal exam. However, it is important to remember that the more anterior parts (transitional zone and fibromuscular tissue) cannot be palpated.\n- Because of the close relation between the prostate and the bladder neck, possible complications of prostate surgery are incontinence and retrograde ejaculation.\n- The connections between the prostate venous plexus and the vertebral venous plexus explains why prostate cancer commonly metastasises to the vertebral column.",
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"explanation": "## Summary\n\nThe uterus is an extraperitoneal female reproductive organ found in the pelvis. It is connected to the vagina inferiorly via the cervix, sits posterior to the urinary bladder and anterior to the rectum.\n\n[lightgallery]\n\n## Anatomy\n\nThe uterus contains a **fundus, body, uterine cavity and cervical canal** as well as the internal and external openings of the cervix, known as the ostium.\n\n## Relations\n\n- Anterior: urinary bladder- the **vesicouterine pouch** separates the two structures\n- Posterior: rectum - the **rectouterine pouch** or pouch of Douglas separates the two structures. \n- Superior: sigmoid colon\n- Inferior: vagina\n\n\n## Blood supply\n\nThe uterus gets its arterial supply from the **uterine artery**. The uterine veins drain the uterus into a **plexus** contained within the broad ligament.\n\nThe lymphatic drainage of the uterus is to the **aortic, inguinal, iliac and sacral nodes**.\n\n## Innervation\n\nThe uterus is innervated by the **uterovaginal** and **inferior hypogastric plexuses.**\n\n## Clinical points\n- The pouches surrounding the uterus have clinical relevance as excess fluid can build up in them - although some fluid can be considered physiological, if there is a lot this can be a sign of intra-abdominal pathology.\n- The relations of the uterus are important because in aggressive uterine cancer the tumour can extend through the uterus and into adjacent structures. This can make surgical resection extremely challenging if not impossibe.",
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"explanation": "This describes an infective exacerbation of COPD. NICE guidelines recommend antibiotics in this scenario due to the his sputum being purulent. The three oral antibiotics recommended for IECOPD in the first instance are amoxicillin, doxycycline, or clarithromycin. In this case, the patient is penicillin allergic and therefore doxycycline is the only appropriate option.",
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"comment": "HUNKA KUNKA",
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"comment": "Anyone know why this is not CAP?",
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"comment": "(I'm pretty sure) it is CAP but he has COPD therefore he also has IECOPD ",
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"explanation": "# Summary\n\nChronic obstructive pulmonary disease (COPD) is a chronic obstructive disease of the airways with the two main components being chronic bronchitis and emphysema. It usually develops due to smoking, with other risk factors including occupation exposures and air pollution. Patients present with breathlessness, a chronic productive cough and wheeze. Key investigations are spirometry (to confirm obstruction), full blood count (to identify anaemia or polycythaemia) and a chest X-ray to exclude lung cancer or other causes of symptoms. Management includes smoking cessation, pulmonary rehabilitation, consideration of long term oxygen therapy, inhaled or nebulised medical treatment and consideration of other medications e.g. mucolytics. Acute exacerbations of COPD may be infective or non-infective, and can be treated by increasing bronchodilator therapy, oral prednisolone and antibiotics (if an infective cause is suspected).\n\n# Definition\n\nChronic obstructive pulmonary disease (COPD) involves airway obstruction that is usually progressive. It encompasses both emphysema (where alveolar wall destruction leads to enlargement of the distal airspaces) and chronic bronchitis (persistent or recurrent productive cough usually due to mucus hypersecretion). \n\n# Epidemiology\n\nIn the UK 1.2 million people have a diagnosis of COPD, with an estimated 2 million people living with it undiagnosed. It is the 5th commonest cause of death in the UK, causing almost 30,000 deaths per year. \n\nAround 90% of COPD cases in the UK are caused by smoking, with household pollution being a bigger contributing factor in low and middle income countries.\n\n# Risk Factors\n\n- Tobacco smoking and passive smoke exposure\n- Marijuana smoking \n- Occupational exposure to dusts and fumes\n- Household air pollution from wood or coal burning\n- Alpha-1 antitrypsin deficiency\n\nPrognosis is variable, with the following factors associated with higher morbidity and mortality:\n\n- Poor exercise tolerance\n- Smoking\n- Low body mass index\n- Multi-morbidity and frailty\n- Exacerbations requiring admission to hospital or frequent exacerbations\n- Severe obstruction on spirometry (as measured by a lower FEV1)\n- Chronic hypoxia\n- Cor pulmonale\n\n# Pathophysiology\n\nChronic Bronchitis:\n\n- As a protective reaction to smoke or other pollutants, goblet cells hypersecrete mucus in the bronchi and bronchioles of the lungs.\nCilia are not able to remove the excess mucus and so it obstructs the small airways.\nOngoing inflammation causes remodelling and thickening of the airway walls that also contributes to obstruction.\n\nEmphysema:\n\n- Inflammation in the lungs is usually countered by antiproteases such as alpha-1 antitrypsin, however the activity of these is reduced by smoke and other pollutants. \n- Without sufficient antiprotease activity, proteolytic enzymes produced by inflammatory cells break down the walls of the alveoli.\n- This causes enlargement of the terminal airspaces and reduces the surface area available for gas exchange.\n\n# Classification\n\nThe Global Initiative for Chronic Obstructive Lung Disease (GOLD) classifies COPD severity using airflow limitation (as measured by FEV1), severity of symptoms and frequency of exacerbations. \n\n| GOLD Grade | Severity | Post-Bronchodilator FEV₁ (% Predicted) |\n|------------|--------------------------|----------------------------------------|\n| 1 | Mild | ≥ 80% |\n| 2 | Moderate | 50-79% |\n| 3 | Severe | 30-49% |\n| 4 | Very Severe | < 30% |\n\n\nThe two measures used to quantify symptom severity are the CAT (COPD Assessment Test) and the mMRC (modified Medical Research Council) dyspnoea scale which is given below:\n\n| Grade | Description |\n|-------|----------------------------------------------------------------------------------------------------|\n| 0 | I only get breathless with strenuous exercise. |\n| 1 | I get short of breath when hurrying on level ground or walking up a slight hill. |\n| 2 | On level ground, I walk slower than people of the same age because of breathlessness, or I have to stop for breath when walking at my own pace. |\n| 3 | I stop for breath after walking about 100 yards or after a few minutes on level ground. |\n| 4 | I am too breathless to leave the house, or I am breathless when dressing or undressing. |\n\n# Signs and symptoms\n\n- Shortness of breath that worsens with exertion\n- Reduced exercise tolerance\n- Chronic productive cough\n- Recurrent lower respiratory tract infections\n- Wheeze\n- In more advanced cases, systemic symptoms such as weight loss and fatigue may be present\n\nExamination may be normal, though signs may include:\n\n- Wheeze or crackles on auscultation\n- Accessory muscle usage\n- Pursed lip breathing (this creates a small amount of positive end expiratory pressure to prevent the alveoli from collapsing)\n- Cyanosis \n- Hyperinflation of the chest\n- Cachexia\n- Raised JVP and peripheral oedema (indicating cor pulmonale has developed)\n\n# Investigations\n\n- **Spirometry** - the diagnostic investigation for COPD and key to classification of severity, may be used to monitor progression of the disease. A FEV1/FVC ratio <0.7 confirms obstruction.\n\n- **Bloods** - Full blood count looking for polycythaemia (resulting from chronic hypoxaemia) or anaemia (usually anaemia of chronic disease), consider BNP to assess for heart failure (with an **echocardiogram** if suspected, alpha-1 antitrypsin in young patients/minimal smoking history/strong family history\n- **ECG** - the following ECG changes are often seen in advanced COPD with features of e.g. cor pulmonale, and include:\n\t- Right axis deviation\n\t- Prominent P waves in inferior leads\n\t- Inverted P waves in high lateral leads (I, aVL)\n\t- Low voltage QRS\n\t- Delayed R/S transition in leads V1-V6\n\t- P pulmonale\n\t- Right ventricular strain pattern\n\t- RBBB\n\t- Multifocal atrial tachycardia\n\n- **Chest X-ray** - used to rule out other causes of symptoms (e.g. lung cancer, bronchiectasis), may show features of COPD including hyperinflation of the chest with flattening of the hemidiaphragms and bullae.\n\n[lightgallery1]\n\n- **Sputum culture** - during exacerbations to target antibiotic therapy\n\n# Differential diagnosis\n\n- **Asthma:** may coexist with COPD, suspect if onset of symptoms <35, history of atopy, non-smoker, variable or nocturnal symptoms.\n- **Bronchiectasis:** copious secretions and coarse crepitations on examination, triggering factors include severe childhood respiratory tract infections.\n- **Heart Failure:** suspect in patients with ischaemic heart disease, may have orthopnoea and paroxysmal nocturnal dyspnoea.\n- **Interstitial Lung Disease:** dry rather than a productive cough, fine crackles on examination.\n- **Lung cancer:** patients with COPD are usually at higher risk due to smoking history, need to investigate for malignancy in cases with a persistent cough/haemoptysis/weight loss.\n- **Tuberculosis:** similar symptoms, systemic manifestations include fevers and weight loss, consider in at-risk groups.\n\n# Management of Chronic COPD\n\n**Conservative:**\n\n- Patient education, ensure all patients have a personalised self-management plan\n- Smoking cessation support\n- Nutritional support and dietician referral if malnourished\n- Annual influenza and one-off pneumococcal vaccination\n- Pulmonary rehabilitation (refer if grade 3 and above on mMRC dyspnoea scale or a recent admission for an acute exacerbation)\n- Consider referral for respiratory physiotherapy to help with sputum clearance and breathing techniques\n\n**Medical:**\n\n\n- For patients whose activities are limited by breathlessness, start a short-acting beta-2 agonist (SABA, e.g. salbutamol) or short-acting muscarinic antagonist (SAMA, e.g. ipratropium) inhaler\n- The next step depends on if they have features of asthma or steroid responsiveness: if these are present then add a long-acting beta-2 agonist (LABA, e.g. formoterol) and an inhaled corticosteroid (ICS, e.g. beclomethasone). If these are not present then add a LABA and a long-acting muscarinic antagonist (LAMA, e.g. tiotropium). \n- If patients do not respond adequately to this, the third inhaler can then be trialled (i.e. all patients would be on a SABA/SAMA + LABA + LAMA + ICS).\n\nPatients who require further therapy should be referred to a specialist for ongoing management which may include oral steroids, oral theophylline or oral phosphodiesterase-4 inhibitors (e.g. roflumilast).\n\nManagement of stable COPD is can be tailored according to the patient’s clinical phenotype. The following groups are defined according to 2024 NICE guidance:\n\n**Group A**\n \n- **Definition**: Patients with minimal symptoms (mMRC grade 0–1 or CAT score <10) and no history of exacerbations requiring hospitalisation or oral corticosteroids in the last year. \n- **Management**:\n - Start with a **short-acting bronchodilator (SABA or SAMA)** as needed for symptom relief.\n - If symptoms are not controlled, consider switching to a long-acting bronchodilator: \n - **LAMA** or **LABA**, depending on individual tolerance and symptom profile. \n\n**Group B**\n \n- **Definition**: Patients with significant symptoms (mMRC grade ≥2 or CAT score ≥10) but no exacerbations requiring hospitalisation or oral corticosteroids in the last year. \n- **Management**: \n - Initiate treatment with a **LAMA** or **LABA** as maintenance therapy. \n - If symptoms persist despite monotherapy, escalate to **dual therapy (LABA + LAMA)**. \n\n**Group E**\n \n- **Definition**: Patients with frequent exacerbations (≥2 per year or ≥1 requiring hospitalisation) regardless of symptom burden. \n- **Management**: \n - First-line therapy is **LAMA** for exacerbation prevention. \n - If exacerbations persist, escalate to: \n\t - **Dual therapy (LABA + LAMA)**. \n\t - If asthmatic features or steroid responsiveness are present (e.g., eosinophilia or a history of asthma), consider **LABA + ICS**. \n - For patients who continue to experience exacerbations despite dual therapy, switch to **triple therapy (LABA + LAMA + ICS)**. \n\n\n\n| **Group** | **Phenotype** | **Initial Therapy** | **Escalation Therapy** | \n|-------------|--------------------------------|------------------------------|------------------------------------| \n| **Group A** | 0 or 1 moderate exacerbation not leading to hospitalisation | SABA or SAMA as needed | LAMA or LABA | \n| **Group B** | 0 or 1 moderate exacerbation not leading to hospitalisation| LAMA or LABA | LABA + LAMA | \n| **Group E** | 2 or more moderate exacerbations or 1 or more exacerbations leading to hospitalisation\t | LAMA | LABA + LAMA or LABA + LAMA + ICS | \n\n\nOther medical treatments that may be considered include:\n\n- Oral mucolytic therapy - for patients with a chronic cough productive of sputum.\n- Prophylactic antibiotics - in cases of frequent infective exacerbations, should be discussed with a specialist, a common choice would be azithromycin 3x per week.\n- Nebuliser therapy - for patients with disabling breathlessness despite optimised use of inhalers.\n- Long-term oxygen therapy (LTOT) - see below for more details\n\n\n**Surgical:**\n\n- In certain cases of severe COPD when patients have not responded to maximal medical therapies, surgical intervention may be considered. \n- Both the NICE recommended options involve lung volume reduction (which involves removing emphysematous areas of the lung so that the healthy lung can expand) - this can be done either by surgical resection or using bronchoscopy to site a one-way valve in one of the larger airways to collapse the diseased lung. \n\n### Long term oxygen therapy (LTOT)\n\n**The following patients should be referred for assessment for LTOT:**\n\n- Oxygen saturations <92% in air or cyanosis\n- FEV1 <30% predicted (consider referring if <49%)\n- Polycythaemia\n- Peripheral oedema or raised jugular venous pressure (suggesting cor pulmonale)\n\nThis assessment involves ensuring that patients are medically optimised and their COPD is stable (i.e. they’re not recovering from a recent exacerbation). Patients who are current smokers cannot be offered LTOT because of the risk of burns and fires. \n\nPatients then have two ABGs in air at least 3 weeks apart and the following patients should be offered LTOT (with the advice to use the oxygen for at least 15 hours per day):\n\n- PaO2 below 7.3kPa\n- PaO2 7.3-8kPa with any of secondary polycythaemia, peripheral oedema or pulmonary hypertension\n\n# Complications\n\n## Acute exacerbations\n\n- These present with worsening breathlessness, productive cough and wheeze, and patients may be febrile, tachycardic and tachypnoeic. \n- Patients who are clinically well may be treated at home with an increase in their usual inhalers, a short course of oral steroids (usually 30mg prednisolone for 5 days) and oral antibiotics if bacterial infection is suspected. \n- Those who have frequent exacerbations may be given a “rescue pack” of steroids and antibiotics to keep at home and start using in case of an exacerbation (alongside seeking medical help).\n\n- Patients requiring hospital admission should also receive steroids and antibiotics if indicated. \n- They may require nebulised bronchodilators, supplementary oxygen and in case of deterioration respiratory support with non-invasive ventilation may be required. \n- Advanced care planning and ensuring that escalation status is discussed with patients is therefore key, so that if they deteriorate to the point of needing intensive care support it is established whether or not this is appropriate and in line with their wishes.\n\n## Polycythaemia\n\n- Chronic tissue hypoxia as seen in COPD leads to a compensatory overproduction of erythropoietin, which leads to increased red blood cell production (i.e. secondary polycythaemia). \n- This causes an increase in blood viscosity that in turns increases risk of both arterial and venous thrombosis. \n\n\n## Cor Pulmonale\n\nCor pulmonale refers to right ventricular dilation or hypertrophy in response to pulmonary hypertension caused by chronic lung disease - COPD is not the only cause of this but it is the most common.\n\nThe pathophysiology is as follows:\n\n- Changes in the lungs and chronic hypoxaemia cause the walls of the pulmonary arteries to thicken.\n- This increases vascular resistance in the lungs.\n- The right ventricle then has to pump against greater resistance, which causes it to either dilate or hypertrophy.\n- Ultimately this leads to right heart failure, with resulting peripheral oedema, hepatomegaly and elevated jugular venous pressure (JVP).\n\nPeripheral oedema may be treated symptomatically with diuretics and long-term oxygen therapy has been shown to reduce morbidity and mortality. All patients with suspected cor pulmonale should be referred to secondary care.\n\n## Pneumothorax\n\n- COPD is a common cause of secondary pneumothoraces (i.e. a pneumothorax secondary to underlying lung disease). These occur when a bulla ruptures, releasing air into the pleural cavity. \n- Investigations and treatment are as per the BTS guidelines (see Pneumothorax chapter for more details).\n\n## Depression and anxiety\n- Over 1 in 3 people with COPD report symptoms of depression and anxiety so screening for this is important during patient reviews. \n- The COPD Assessment Test (CAT) can be used to assess the impact of COPD on everyday life. \n- Referral to psychological services for support may be appropriate, as well as holistic assessment and management.\n\n# NICE Guidelines\n\n[Click here for the NICE Guidelines](https://www.nice.org.uk/guidance/ng115)\n\n[NICE CKS - COPD](https://cks.nice.org.uk/topics/chronic-obstructive-pulmonary-disease/)\n\n# References\n\n[Patient UK - COPD](https://patient.info/doctor/chronic-obstructive-pulmonary-disease-pro)\n\n[GOLD report 2023](https://goldcopd.org/2023-gold-report-2/)\n\n[Radiopaedia - COPD](https://radiopaedia.org/articles/chronic-obstructive-pulmonary-disease-1?lang=gb)\n\n[Patient UK - Cor Pulmonale](https://patient.info/doctor/cor-pulmonale)",
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"explanation": "# Summary\n\nAdrenal insufficiency is a condition where destruction of the adrenal cortex leads to reduced glucocorticoid production. It can be classified as primary (Addison's disease) or secondary, each with different causes. Key signs and symptoms include hypotension, fatigue, weakness, gastrointestinal symptoms, and increased pigmentation. Initial investigations should focus on levels of sodium, potassium, glucose, cortisol, ACTH, renin, and aldosterone, while further tests should be used to establish the underlying cause. Management includes patient education on 'sick day' rules, glucocorticoid and mineralocorticoid replacement, and regular screening for complications like adrenal crisis and osteoporosis.\n\n# Definition\n\nAdrenal insufficiency is a clinical syndrome that arises due to the insufficient production of glucocorticoids and mineralocorticoids from the adrenal cortex. \n\nIt can be categorized as primary, commonly known as Addison's disease, where the cause lies within the adrenal glands themselves, or secondary, where inadequate stimulation of the adrenal glands by the pituitary or hypothalamus is the culprit.\n\n\n# Epidemiology\n\nAdrenal insufficiency is a relatively rare disease. Primary adrenal insufficiency (Addison's disease) affects approximately 100-140 people per million in developed countries. Secondary adrenal insufficiency is considered more common but accurate prevalence rates are difficult to determine.\n\n# Pathophysiology\n\nAdrenal insufficiency can result from damage to the adrenal cortex or disruptions in the hypothalamus-pituitary-adrenal (HPA) axis. The HPA axis regulates adrenal hormone production. In primary adrenal insufficiency (Addison's disease), the adrenal glands are damaged, while secondary adrenal insufficiency is due to dysfunction in the hypothalamus or pituitary. The lack of cortisol then disrupts feedback mechanisms, leading to elevated adrenocorticotropic hormone (ACTH) levels.\n\n\nPrimary adrenal insufficiency (Addison's disease) can be caused by:\n\n- Auto-immune destruction (most common)\n- Surgical removal of the adrenal glands\n- Trauma to the adrenal glands\n- Infectious diseases, such as tuberculosis (more common in developing countries)\n- Haemorrhage (e.g., Waterhouse-Friderichsen syndrome)\n- Infarction\n- Less commonly, neoplasms, sarcoidosis, or amyloidosis\n\nSecondary adrenal insufficiency can occur due to:\n\n- Congenital disorders\n- Fracture of the base of the skull\n- Pituitary or hypothalamic surgery or Neoplasms in the pituitary or hypothalamus\n- Infiltration or infection of the brain\n- Deficiency of corticotropin-releasing hormone (CRH)\n\n# Signs and Symptoms \n\nClinical features of adrenal insufficiency include:\n\n- Hypotension\n- Fatigue and weakness\n- Gastrointestinal symptoms\n- Syncope\n- Skin pigmentation due to increased ACTH which stimulates production of alpha melanocyte stimulating hormone (MSH).\n\n[lightgallery]\n\nIn the case of auto-immune Addison's disease, approximately 60% of patients may also have vitiligo or other autoimmune endocrinopathies.\n\n[lightgallery1]\n\n# Differential Diagnosis\n\nAdrenal insufficiency can be misdiagnosed as several other conditions, including:\n\n- Chronic fatigue syndrome: Presents with persistent fatigue, cognitive difficulties, and other non-specific symptoms\n- Dehydration or septic shock: Hypotension and tachycardia can mimic adrenal insufficiency\n- Primary psychiatric illnesses: Depression or other psychiatric illnesses may present with fatigue, decreased appetite, and weight loss.\n\n# Investigations\n\n* First line investigations are U+E and serum cortisol, where you may find:\n\t* Hyponatraemia (low sodium)\n\t* Hyperkalaemia (high potassium)\n\t* Low serum cortisol\n- Glucose (typically low)\n- Therefore in a patient with Addison's who is acutely unwell, you would expect a blood gas to show a **hyperkalaemic, hyponatraemic, hypoglycaemic metabolic acidosis**\n- ACTH: High in primary insufficiency, low or low-normal in secondary insufficiency\n- Renin (high in Addison's disease)\n- Aldosterone (low in Addison's disease)\n\nAn ACTH (Short Synacthen) test is the gold standard investigation to confirm the diagnosis.\n\nFurther investigations to establish the cause can include:\n\n- Testing for adrenal auto-antibodies\n- Chest X-ray\n- CT scan of the adrenal glands\n- MRI of the brain\n\n# Management\n\n**Management of adrenal insufficiency involves:**\n\n- Patient education on 'sick day' rules, carrying a steroid card, and wearing a medical alert bracelet\n- Doubling the regular steroid medication dose during any intercurrent illness\n- Replacement of both glucocorticoids (typically with hydrocortisone) and mineralocorticoids (typically with fludrocortisone)\n- Regular screening for complications including an adrenal crisis and osteoporosis\n\n**Management of Addisonian Crisis**\n\nAn Addisonian crisis, a life-threatening condition characterized by severe hypotension and electrolyte imbalances, should be managed with:\n\n- Aggressive fluid resuscitation\n- Administration of intravenous/IM (if no access) steroids STAT\n- Glucose administration if hypoglycaemia is present\n\n# Complications\n* Addisonian crisis (life-threatening adrenal crisis)\n* Severe electrolyte imbalances\n* Cardiovascular collapse\n* Hypoglycemia\n* Side effects of long term corticosteroid use e.g. osteoporosis\n\n# NICE Guidelines\n\n[Click here for NICE CKS on Addison's disease](https://cks.nice.org.uk/topics/addisons-disease/)\n",
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"question": "A 75-year-old woman with a history of polymyalgia rheumatica is found collapsed by her partner. Her partner remarks that she is likely exhausted after her holiday. Her initial VBG shows:\n\n\n||||\n|---------------------------|:-------:|--------------------|\n|Sodium|128 mmol/L|135 - 145|\n|Potassium|6.2 mmol/L|3.5 - 5.3|\n|Urea|8.4 mmol/L|2.5 - 7.8|\n|Fasting Glucose|2.7 mmol/L|3.5 - 5.5|\n\n\nWhat is the most likely cause of her collapse?",
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"comment": "Propanolol for Prophylaxis\nTerlipressin to Treat :)",
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"comment": "endoscopic band ligation is an effective primary prophylaxis option for preventing variceal bleeding in those with contraindications to beta blockers\n\n",
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"explanation": "# Summary\n\nOesophageal and gastric varices are dilated veins that arise due to portal hypertension, often secondary to cirrhosis. They are prone to bleeding due to high portal pressures, posing a significant risk of mortality in patients. Diagnosis involves endoscopy at the time of cirrhosis diagnosis, with treatment centred on haemodynamic resuscitation, blood transfusions, and administration of terlipressin and broad-spectrum antibiotics. Primary prophylaxis is recommended for patients with grade 1 varices with red signs, or grade 2 or 3 varices. Prevention strategies include pharmacological interventions like non-selective beta-blockers and endoscopic variceal band ligation.\n\n# Definition\n\nVarices are dilated veins which are formed due to portal hypertension. They are most commonly secondary to liver cirrhosis and are prone to rupture due to the high pressure in the portal system, leading to significant internal bleeding. Oesophageal varices are abnormally enlarged veins located in the lower part of the oesophagus. Gastric varices are dilated submucosal veins located in the stomach.\n\n# Epidemiology\n\nVarices are common in patients with advanced liver disease. They occur in about 50% of patients with cirrhosis, and variceal bleeding is a leading cause of mortality in these patients. Gastric varices are less common than oesophageal varices but can cause significant gastrointestinal bleeding. They are often more difficult to treat due to their location and the complexity of the vascular structures in the stomach.\n\n# Aetiology\n\nOesophageal varices occur as a result of portal hypertension, often due to cirrhosis. Other causes of portal hypertension include portal vein thrombosis, schistosomiasis, and hepatic fibrosis.\n\n# Signs and Symptoms\n\nPatients with oesophageal varices may be asymptomatic until a variceal bleed occurs. A variceal bleed may present with:\n\n- Haematemesis (vomiting of blood)\n- Melena (black, tarry stools)\n- Palpitations\n- Syncope (fainting)\n- Hypotension (low blood pressure)\n\n# Differential Diagnosis\n\nDifferential diagnoses for oesophageal varices include other causes of upper gastrointestinal bleeding such as:\n\n- **Gastric ulcers:** Symptoms may include epigastric pain, nausea, vomiting, and weight loss.\n- **Duodenal ulcers:** Symptoms may include epigastric pain (especially at night), nausea, vomiting, and weight loss.\n- **Mallory-Weiss tear:** Symptoms may include painful retching followed by the onset of bloody vomiting.\n\n# Investigations\n\n- Endoscopy is the primary investigation for oesophageal varices, allowing for direct visualisation and grading of the varices. \n- Patients with cirrhosis should have a one-off OGD at the time of diagnosis. If patients are found not to have varices at the time of their first endoscopy, a repeat endoscopy should be done every 3 years as surveillance\n\n# Management\nThe management of oesophageal varices includes:\n\n- Resuscitation ensuring haemodynamic stability. This may involve blood transfusions and correction of clotting abnormalities with Vitamin K, FFP, and platelet transfusions.\n- Administration of Terlipressin, a vasopressin analogue that reduces portal pressure and bleeding.\n- Administration of broad-spectrum antibiotics to reduce the risk of bacteraemia and spontaneous bacterial peritonitis.\n- Variceal band ligation via endoscopy for oesophageal varices, and sclerotherapy for gastric varices\n- For uncontrollable bleeding, insertion of a Sengstaken-Blakemore tube may be required.\n- In patients with a history of alcoholism, thiamine may be needed to correct any deficiency.\n\n# Prevention\n\nPrevention strategies for variceal bleeding include the use of non-selective beta-blockers and variceal band ligation. If these fail, patients may be recommended for a transjugular intrahepatic portosystemic shunt (TIPSS).\n\n# References\n\n[NICE CKS - Cirrhosis](https://www.nice.org.uk/guidance/ng50/chapter/Recommendations)\n",
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"explanation": "This does not explain the murmur and is unlikely in a young patient.",
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"comment": "For these questions just keep eliminating, and you are eventually able to get rid of all the other options. Literally whats getting me thru cardio atp",
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"explanation": "# Summary\n\nAnaphylaxis is a medical emergency which often occurs due to a type 1 IgE mediated hypersensitivity reaction to an allergen. It is characterised by the rapid onset of life-threatening airway swelling, bronchospasm and/or circulatory dysfunction. In most cases skin or mucosal changes are also present. Triggers include medications (such as penicillins), foods (such as peanuts) and insect stings. Diagnosis is clinical, with repeated mast cell tryptase levels a useful way to confirm the diagnosis in retrospect. Management strategies include removing the trigger, ABCDE assessment, oxygen administration, and adrenaline administration, amongst other interventions. \n \n# Definition\n \nAnaphylaxis is a rapid onset syndrome of life-threatening airway, breathing or circulatory dysfunction. An immunological reaction occurs when patients are exposed to allergens such as medications, foods (such as peanuts or eggs) and bee or other insect stings. Many cases of anaphylaxis however are idiopathic with no known trigger, or may be mediated by other mechanisms other than the classical type 1 IgE-mediated pathway. \n\n# Epidemiology\n \nApproximately 1 in 1333 people in England have had an episode of anaphylaxis. There are approximately 20-30 deaths per year in the UK, with around half of these being iatrogenic (e.g. due to penicillin).\n \n\n# Aetiology\n \nCommon precipitants of IgE-mediated allergic anaphylaxis include:\n\n- Insect stings\n- Nuts\n- Other foods such as eggs or milk\n- Latex\n- Antibiotics (e.g. penicillins)\n- Intravenous contrast agents\n- Other medications (such as NSAIDs)\n \n\n# Signs and Symptoms\n\nSigns and symptoms are sudden in onset and progress rapidly. To be classed as anaphylaxis, patients need to have life-threatening problems affecting the:\n\n- **Airway** (pharyngeal or laryngeal oedema)\n - Symptoms include difficulty swallowing and breathing, feeling that the throat is closing\n - Signs include stridor, hoarse voice and swelling of the tongue and lips\n- **Breathing** (bronchospasm)\n - Symptoms include difficulty breathing, wheeze and cough\n - Signs include increased work of breathing and respiratory distress, hypoxaemia may cause confusion and cyanosis\n - Patients may fatigue leading to respiratory arrest\n- **Circulation** (anaphylactic shock)\n - Symptoms include dizziness\n - Signs include pallor, clamminess, tachycardia and hypotension\n - Patients may develop arrhythmias and anaphylaxis can lead to cardiac arrest\n\nContinuing with an A to E approach, the following signs and symptoms are often also seen:\n\n- **Disability** (altered neurological state)\n - Symptoms include anxiety and a \"sense of impending doom\"\n - Signs include confusion, agitation and loss of consciousness\n- **Exposure** (skin and mucosal changes)\n - These range from mild erythematous patches to florid generalised rashes\n - Often occur prior to the onset of other symptoms\n - Urticaria (hives) are itchy and can occur anywhere on the skin\n - Angioedema involves swelling of the eyelids and lips (as well as the tongue and throat causing airway obstruction)\n\n**Gastrointestinal** manifestations including abdominal pain, incontinence and vomiting are also commonly seen in cases of anaphylaxis.\n \n[lightgallery]\n\n# Differential Diagnosis\n\n- **Life-threatening asthma exacerbation** \n - Several overlapping features e.g. bronchospasm, tachycardia, reduced levels of consciousness\n - May cause raised mast cell tryptase also \n - Triggers can be similar to anaphylaxis triggers\n - Would not have features of upper airway obstruction e.g. stridor or mucosal/skin changes e.g. urticaria\n- **Other causes of angioedema** \n - e.g. hereditary angioedema, induced by medications e.g. ACE inhibitors\n - Both involve histamine and/or bradykinin mediators\n - No circulatory dysfunction and shock unlike in anaphylaxis\n- **Panic attack** \n - May have tachycardia and tachypnoea accompanied by anxiety and feelings of doom, skin flushing may also occur\n - No signs of airway obstruction or circulatory collapse and symptoms often resolve with reassurance\n- **Vasovagal episode** \n - May occur after triggers e.g. vaccination\n - Mimic features of pallor and loss of consciousness\n - No airway or breathing symptoms unlike in anaphylaxis\n \n# Investigations\n \nAnaphylaxis should be diagnosed clinically based on the above features.\n\nThe following investigations should be carried out in the emergency setting:\n\n- **ECG** - to look for myocardial ischaemia and arrhythmias which may be caused by anaphylaxis\n- **Arterial blood gas** should be considered in hypoxic patients, may show metabolic acidosis due to shock\n- **Bloods for mast cell tryptase** - the first sample should be taken as soon as possible after starting emergency treatment, with a second sample taken within 1 to 2 hours (no later than 4 hours from symptom onset) and a third sample taken after complete recovery (as a baseline)\n\nAn elevated serum tryptase from baseline is a useful confirmatory test for anaphylaxis especially where there is diagnostic uncertainty, although a normal level does not exclude anaphylaxis. \n \n\n# Management\n\n**Emergency management:**\n \n- Early recognition is key - call for help (put out a medical emergency call if in hospital)\n- Remove any ongoing trigger e.g. stop causative medication, remove insect stinger\n- Lie patient flat and elevate legs if hypotensive, or help to a seated position to aid breathing\n- Give intramuscular adrenaline - 0.5ml of 1:1000 (500mcg) in adults, usually into the anterolateral thigh\n- Secure the airway\n- Administer high flow oxygen and ensure monitoring in place (oxygen saturations, blood pressure and ECG)\n- Consider inhaled bronchodilators (salbutamol or ipratropium) for wheeze\n- Give an IV fluid bolus in patients with hypotension or shock, or who do not respond to the initial adrenaline dose\n- IM adrenaline can be repeated after 5 minutes if no response\n- In the case of a cardiac arrest, start CPR and give further adrenaline via the IV or IO route (as intramuscular administration is unreliable in this scenario)\n\n**Once stabilised:**\n\n- Give an non-sedating oral antihistamine (e.g. 10-20mg cetirizine) - if not able to swallow can give IV or IM chlorphenamine \n - This helps to treat cutaneous symptoms of anaphylaxis but is not a first-line treatment as they do not treat life-threatening features\n- Steroids are no longer routinely advised but may be considered in patients with an asthma exacerbation/anaphylaxis overlap or in cases of ongoing shock\n- Observe patients for a **biphasic reaction** (when symptoms of anaphylaxis reoccur without further exposure to a trigger)\n - This occurs in around 5% of patients\n - Patients with severe initial presentations, those who require multiple adrenaline doses or who had a delay in treatment are at increased risk\n - Patients should be risk stratified - those at the lowest risk can be discharged after 2 hours of observation, those at intermediate risk should be observed for at least 6 hours and those at the highest risk for at least 12 hours\n- Prior to discharge, patients and families should be educated about anaphylaxis, what actions to take and the risk of a biphasic reaction\n - Give two adrenaline auto-injectors (e.g. an EpiPen) and demonstrate how to use these\n - Advise on trigger avoidance\n- Refer for follow up in a specialist allergy service\n\n# NICE Guidelines\n\n[NICE - Anaphylaxis: assessment and referral after emergency treatment](Anaphylaxis: assessment and referral after emergency treatment)\n\n[NICE CKS - Angio-oedema and Anaphylaxis](https://cks.nice.org.uk/topics/angio-oedema-anaphylaxis/)\n\n# References\n \n[UK Resuscitation Council Anaphylaxis Guidelines](https://www.resus.org.uk/library/additional-guidance/guidance-anaphylaxis/emergency-treatment)",
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"explanation": "This forms a part of the CURB-65 score (Age > 65).",
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"comment": "This feels like a backward way of testing this knowledge",
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"comment": "toooooooo easssssyyyyyy c'mon Quessyy need to up ur game",
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"explanation": "# Summary\n\nPneumonia is a common infection of the lung parenchyma that involves the alveoli becoming consolidated with inflammatory cells and microorganisms. Key symptoms include fever, malaise, a productive cough and pleuritic chest pain. Investigations include a chest X-ray to detect consolidation, blood tests for inflammatory markers and blood and sputum cultures to look for an underlying cause. Management involves oxygen if hypoxic, IV fluids if required and antibiotics targeted to the causative organism. \n\n# Definition\n\nPneumonia is an inflammatory condition of the lung parenchyma caused by infection. Alveoli become filled with inflammatory cells and microorganisms, leading to consolidation of the lung tissue. This impairs gas exchange and can lead to hypoxia.\n\n# Epidemiology\n\nCommunity-acquired pneumonia has an incidence of 5-10 per 1000 adults in the UK per year. Approximately 22-42% of these cases require admission to hospital. Mortality estimates range from 5 to 14%, with half of these being in people aged over 84 years. \n\n# Aetiology\n\nThe commonest cause of pneumonia is Streptococcus pneumonia, which is usually community-acquired, followed by Haemophilus influenzae and Moraxella catarrhalis. These are referred to as typical pneumonias (as they tend to present with the classic symptoms listed below).\n\nAtypical pneumonias have a variety of atypical features, e.g. a more insidious onset, extra-pulmonary symptoms such as headache and varying appearances on chest imaging. These include Mycoplasma pneumoniae, Legionella pneumophila and Chylmydophila psittaci. \n\nHospital-acquired pneumonias are defined as pneumonia that started 48 hours or longer after admission. Gram negative organisms such as Pseudomonas aeruginosa, as well as Staphylococcus aureus are more common in these environments.\n\nAspiration pneumonias are covered in a separate chapter. \n\n**Specific features of some of these microbiological causes are as follows:**\n\n**Staphylococcal pneumonia**\n\n- A bilateral cavitating bronchopneumonia due to staphylococcal aureus, a gram-positive cocci found in clusters.\n- Commoner in intravenous drug users, elderly patients, or as a superadded bacterial infection in those with influenza.\n\n**Klebsiella pneumonia**\n\n- Usually a cavitating pneumonia affecting the upper lobes presenting with red-currant sputum.\n- It is caused by a gram-negative anaerobic rod.\n- Increased risk in the immunocompromised, elderly and in alcohol excess.\n\n**Mycoplasma pneumonia**\n\n- Presents with flu-like symptoms of arthralgia, myalgia, dry cough and headache.\n- Primarily affects younger patients.\n- Associated with an autoimmune haemolytic anaemia caused by cold agglutinins.\n- May lead to erythema multiforme, Stevens-Johnson syndrome, Guillain-Barre syndrome and meningoencephalitis.\n\n**Legionella pneumonia**\n\n- Fever, myalgia and malaise followed by dyspnoea and a dry cough are typical presenting features.\n- Caused by a gram-negative coccobacillus.\n- Occurs in those exposed to contaminated water e.g. in humidifiers or cooling systems.\n- Typically causes hyponatraemia and deranged liver function tests. \n\n**Chlamydophila psittaci pneumonia**\n\n- An intracellular bacteria acquired from contact with infected birds such as parrots.\n- Features include lethargy, arthralgia, headache, anorexia, dry cough and fever.\n\n# Classification\n\nCommunity-acquired pneumonias are classified using the CURB-65 score to determine severity and guide management.\n\nOne point is awarded for each of the following:\n\n- Confusion \n\n- Urea > 7mmol/L\n\n- Respiratory rate > 30 breaths/min\n\n- Blood pressure < 90 systolic and/or < 60mmHg diastolic\n\n- 65 years or older\n\nThis can be used to estimate 30 day mortality from pneumonia:\n\n- CURB-65 0 - **0.7%** \n\n- CURB-65 1 - **3.2%** \n\n- CURB-65 2 - **13%** \n\n- CURB-65 3 - **17%** \n\n- CURB-65 4 - **41.5%** \n\n- CURB-65 5 - **57%** \n\nA CURB-65 score of 0-1 requires home treatment, 2 should consider hospital admission, 3-5 admit to hospital and consider ITU referral.\n\n# Symptoms\n\n- Fever\n- Malaise\n- Rigors\n- Cough\n- Purulent sputum\n- Pleuritic chest pain\n- Haemoptysis\n\n# Signs\n\n- Tachypnoea\n- Tachycardia\n- Hypotension\n- Cyanosis\n- Pyrexia\n- Dullness to percussion over the consolidated area\n- Increased vocal resonance/ tactile vocal fremitus over the consolidated area\n- Bronchial breathing over the consolidated area\n- Pleural rub may be heard due to inflammation of the adjacent pleura\n\n# Differential Diagnosis\n\n- **Bronchiectasis** - chronic productive cough with copious sputum, may be triggered by a severe lower respiratory tract infection or another condition (e.g. cystic fibrosis)\n- **Tuberculosis** - suspect in patients with risk factors (e.g. TB contact, from endemic area, no fixed abode), haemoptysis and weight loss more common\n- **Lung cancer** - may lead to pneumonia e.g. by obstructing a bronchus with downstream infection, important to consider especially in patients with a history of smoking, weight loss, chronic cough and haemoptysis\n- **Bronchitis** - infection of the bronchi rather than the lower respiratory tract, usually viral and self-resolving \n\n# Investigations\n\n**Bedside:**\n\n- Sputum for microscopy, culture and sensitivity\n- Consider arterial blood gas if hypoxaemic \n- Urinary legionella and pneumococcal antigens\n- ECG to look for complications e.g. atrial fibrillation\n\n**Bloods:**\n\n- Blood cultures if febrile\n- FBC and CRP for inflammatory markers\n- U&Es to look for an AKI\n- LFTs may be deranged e.g. in Legionella, baseline important when giving antibiotics\n- Mycoplasma serology if atypical pneumonia suspected\n- HIV testing should be offered to all patients with recurrent pneumonia (and all patients in a high prevalence area such as London)\n\n**Imaging:**\n\n- Chest X-ray: may show lobar consolidation or bilateral consolidation in atypical infections, parapneumonic effusions may also be seen.\n- CT chest may be indicated in some cases (e.g. suspected underlying malignancy, suspicious findings on X-ray)\n\n[lightgallery]\n\n\n# Management\n\n**Conservative:**\n\n- Oxygen if low saturations\n- IV fluids if dehydrated\n- Analgesia for myalgia or chest pain\n- Escalate for respiratory support (e.g. continuous positive airway pressure or intubation and ventilation) if patients are severely unwell - consider escalation status and patient wishes\n\n**Medical:**\n\n- Oral antibiotics for patients managed in the community (e.g. amoxicillin 500mg three times a day for 5 days)\n- IV antibiotics for those admitted with more severe pneumonia (e.g. co-amoxiclav and clarithromycin)\n- Different regimens are indicated for those with penicillin allergies and local guidelines should be consulted\n- Antibiotics should be tailored to antimicrobial sensitivities when these are resulted\n\nPatients with pneumonia should be followed up with a repeat chest X-ray after 6 to 8 weeks to screen for an underlying lung cancer (as this may be masked on initial imaging by infective changes).\n\n# Complications\n\n- Parapneumonic effusion\n- Empyema\n- Lung abscess\n- Sepsis\n\n# NICE Guidelines\n\n[NICE - Pneumonia in adults](https://www.nice.org.uk/guidance/cg191)\n\n[NICE CKS - Chest Infections](https://cks.nice.org.uk/topics/chest-infections-adult/)\n\n# References\n\n[Radiopaedia - Lobar Pneumonia](https://radiopaedia.org/articles/lobar-pneumonia)",
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"explanation": "# Summary \n\nHaematuria, the presence of blood in the urine, can be divided into macroscopic haematuria, visible to the naked eye, and microscopic haematuria, detectable only through urinalysis. Key causes include conditions affecting the kidney, ureters, and urethra, as well as certain medications and dietary items. Clinically significant signs and symptoms vary based on the underlying cause. Key investigations include urinalysis, urine culture, and urine microscopy, as well as blood tests and imaging of the renal tract. Management strategies depend on the identified cause.\n\n# Definitions\n\n- Macroscopic haematuria: Blood in the urine, visible to the naked eye.\n- Microscopic haematuria: Blood in the urine, detectable only on urinalysis.\n\n\n# Epidemiology\n\nThe prevalence of haematuria varies depending on population characteristics such as age and sex, and the criteria used to define haematuria. In general, haematuria is more common in older individuals and in males. In clinical settings, haematuria is a common finding on urinalysis.\n\n# Aetiology\n\n## Kidney-related causes\n\n- Glomerular: IgA nephropathy, Alport's syndrome, Glomerulonephritis.\n- Non-glomerular: Tumours (Renal cell carcinoma, Wilm's tumour), Nephrolithiasis, Infection, Polycystic kidneys, Trauma, Urethral stricture, Vascular conditions (infarction, renal vein thrombosis), Sickle cell disease, Certain drugs.\n\n## Ureter or Bladder-related causes\n\n- Stones\n- Tumours, particularly **Bladder Cancer**\n- Strictures\n- Infection\n\n## Urethral causes\n\n- Benign prostatic hypertrophy\n- Prostate cancer\n- Prostatitis\n- Trauma\n\n## Other causes\n\n- Menstruation\n- Post-coital\n- Certain medications\n- Viral illness\n\nNB: Anticoagulants doesn’t in itself cause haematuria, it makes any bleeding worse. E.g. renal cancer may present with NVH, but if the patient was taking anticoagulation, this would potentiates the bleeding leading to VH. \n\n# Signs and Symptoms\n\nSigns and symptoms of haematuria are largely dependent on the underlying cause and may include flank pain, abdominal pain, dysuria, frequency, urgency, and systemic symptoms such as fever or weight loss. In cases of macroscopic haematuria, patients may report pink, red, or brown urine.\n\n# Differential Diagnosis\n\nThe differential diagnosis of haematuria includes a broad range of conditions, and the main signs and symptoms of each can help to distinguish between them:\n\n- Glomerular diseases (e.g. IgA nephropathy, Alport's syndrome): Proteinuria, hypertension, oedema.\n- Non-glomerular kidney diseases (e.g. tumours like renal cell carcinoma, Wilm's tumour): Flank pain, mass, haematuria, weight loss.\n- Ureteral stones: Flank pain, haematuria, possibly signs of infection (fever, dysuria).\n- Urethral conditions (e.g. benign prostatic hypertrophy, prostate cancer): Lower urinary tract symptoms (e.g. difficulty urinating, frequency), possibly haematuria.\n- Pseudohaematuria: History of specific drug use or dietary intake. If there is any doubt over the legitimacy of haematuria, a lab sample should be sought. Causes of pseudohaematuria include:\n\t- Medications such as Rifampicin, Chlorzoxazone, Phenazopyridine, Phenothiazine, Doxorubicin, Phensuximide, Phenytoin, Daunomycin\n\t- Dietary items such as berries, beets, rhubarb\n\t- Myoglobin\n\t- Menstruation\n- Haemoglobinuria: Occurs due to haemolysis of red blood cells.\n- Myoglobinuria: Occurs due to muscle breakdown.\n\n# Investigations\n\n- Bedside - urinalysis.\n- Urine culture.\n- Urine microscopy - the type of blood cells seen may indicate the cause; dysmorphic red blood cells suggest glomerular origin, if red cell casts visible this suggests renal origin (precipitate with protein made in renal tubules)\n- Blood tests: Full Blood Count (FBC), Urea and Electrolytes (U+E), Prostate-Specific Antigen (PSA) for men, and coagulation studies.\n- Imaging: Renal tract ultrasound, Computed Tomography of kidneys, ureters, bladder (CT KUB).\n- Cystoscopy.\n- Renal biopsy.\n\n## 2 week wait referral criteria\n\n\n| Bladder cancer | Renal cancer | \n| ------------- |-------------| \n| If they are aged 45 years and over and have: 1) Unexplained visible haematuria without urinary tract infection, or 2) Visible haematuria that persists or recurs after successful treatment of urinary tract infection.| If they are aged 45 years and over and have: 1) Unexplained visible haematuria without urinary tract infection, or 2) Visible haematuria that persists or recurs after successful treatment of urinary tract infection.\r\nIf they are aged 60 years and over and have unexplained non-visible haematuria and either dysuria or a raised white cell count on a blood test. | |\nConsider non-urgent referral for bladder cancer in people aged 60 years and over with recurrent or persistent unexplained urinary tract infection.| | right-aligned |\n\n# Management\n\nManagement strategies are tailored based on the identified cause. They may include medical management for infections, surgical intervention for stones or tumours, lifestyle modification for certain causes of pseudohaematuria, or further specialist management for complex cases.\n\n# References\n\n[BMJ Best Practice: Assessment of visible haematuria](https://bestpractice.bmj.com/topics/en-gb/316)\n\n[British Association of Urological Surgeons: Haematuria](https://www.baus.org.uk/patients/conditions/2/blood_in_the_urine_haematuria)\n\n[Oxford Medical Education: Haematuria](https://www.oxfordmedicaleducation.com/wp-content/uploads/2015/04/Haematuria.protected.pdf)",
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"comment": "DAR SH PuNCH needs more salt = hypovolemic: diuretics (loop, thiazide), Addison's, renal failure - euvolemic: SIADH, hypothyroidism - hypervolemic: psychogenic, nephrotic syndrome, cirrhosis of liver, heart failure",
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"explanation": "# Summary\n\nHyponatraemia is defined as a serum sodium concentration of less than 135 mmol/L. It may develop acutely or chronically, and is often asymptomatic especially in mild cases. There are many causes which may be classified by whether the patient is hypovolaemic, euvolaemic or hypervolaemic. Symptoms are more likely in severe hyponatraemia and where serum sodium has fallen acutely, including headache, nausea and vomiting and confusion. Key investigations include U&Es for sodium, potassium and renal function, cortisol and thyroid function to rule out other causes of hyponatraemia and urinary sodium and osmolality. Management differs depending on the cause of hyponatraemia - what may improve hyponatraemia in some cases may worsen it in others. In severe cases where more rapid correction of sodium is required, hypertonic saline may be administered with close monitoring of sodium levels.\n\n# Definition\n\nNormal serum sodium is between 135-145 mmol/L, and so levels below 135 mmol/L are classified as hyponatraemia. This may be mild (130-135 mmol/L), moderate (125-129 mmol/L) or severe (< 125 mmol/L). Acute cases develop within 48 hours, with most cases considered to be chronic (i.e. over 48 hours duration) if the onset is unclear. \n\n# Epidemiology\n\n- Hyponatraemia is the commonest electrolyte disorder seen in clinical practice\n- Approximately 15-20% of hospital inpatients are hyponatraemia\n- Incidence increases with age and is particularly common in older people who are nursing home residents or in hospital\n- Other risk factors include:\n- Medications (e.g. diuretics, antidepressants)\n- Comorbidities (e.g. chronic kidney disease, heart failure)\n\n# Aetiology\n\n## Hypovolaemic hyponatraemia\n\nBoth sodium and water are lost (but more sodium than water)\n\n- Diarrhoea\n- Vomiting\n- Medications (e.g. thiazide diuretics)\n- Adrenal insufficiency\n- Burns\n- Excessive sweating\n- Cerebral salt-wasting (rare cause of hyponatraemia that occurs due to intracranial disease, e.g. subarachnoid haemorrhage or traumatic brain injury)\n- Salt-wasting nephropathy (e.g. Bartter syndrome)\n- Third space losses (e.g. sepsis, pancreatitis, bowel obstruction)\n\n## Euvolaemic hyponatraemia\n\nNo loss of sodium but total body water increases causing a dilutional effect\n\n- Syndrome of Inappropriate ADH release (SIADH)\n- Beer potomania (alcohol excess combined with low solute intake)\n- Primary polydipsia\n- Hypothyroidism\n- Secondary adrenal insufficiency\n- Exercise-induced hyponatraemia \n- Hypotonic intravenous fluids\n\n## Hypervolaemic hyponatraemia\n\nBoth total body water and sodium increase, with a greater increase in water resulting in oedema\n\n- Heart failure\n- Chronic liver disease\n- Renal disease (nephrotic syndrome, chronic kidney disease or acute kidney injury)\n\n# Signs and Symptoms\n\nMany patients, especially those with mild and/or chronic hyponatraemia are asymptomatic and detected incidentally.\n\nSymptoms and signs include:\n\n- Lethargy\n- Anorexia\n- Headache\n- Nausea and vomiting\n- Muscle cramps\n- Drowsiness\n- Confusion\n- Seizures\n\nPatients may also have features of either dehydration (in hypovolaemic hyponatraemia) or fluid overload (in hypervolaemic hypernatraemia - see separate chapters for details.\n\n# Differential Diagnosis\n\n- **Pseudohyponatraemia** refers to a falsely low serum sodium reading due to an increase in serum lipid or protein content\n- Serum osmolality will usually be normal or high (unlike in true hyponatraemia where it is low)\n- Causes include:\n- Hypertriglyceridemia\n- Hypercholesterolemia\n- Hyperglycaemia\n- Paraproteinaemia (e.g. in multiple myeloma)\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 pseudohyponatraemia\n- **Urine osmolality** is used to assess ADH activity - it will be high (i.e. urine is concentrated) if ADH is acting, e.g. in SIADH, and low (i.e. urine is dilute) if ADH is not acting, e.g. in polydipsia\n- **Urine sodium** can be used to help determine the cause of hyponatraemia; in patients who are hypovolaemic:\n- If urine sodium is appropriately low, this indicates extrarenal salt loss - consider vomiting/diarrhoea/third spacing\n- If urine sodium is high (> 30 mmol/L), this indicates renal salt loss - consider diuretics, adrenal insufficiency or cerebral salt-wasting\n- NB urine osmolality and sodium cannot be interpreted in patients taking diuretics and so these may need to be stopped prior to investigations\n- **Urine dip** looking for blood and protein if renal disease is suspected\n\n**Blood tests:**\n\n- **U&Es** to confirm hyponatraemia and to check potassium and renal function\n- **Serum osmolality** should be low in true hyponatraemia - if this is normal or raised suspect pseudohyponatraemia (hypertonic fluids such as mannitol may cause a true hyponatraemia with a raised serum osmolality)\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- **NT-proBNP** if heart failure is suspected\n- **Liver function tests** if cirrhosis is suspected (e.g. in patients with ascites)\n\n# Management\n\n**Conservative:**\n\n- Identify and treat the underlying cause (e.g. stopping causative medications where possible)\n- Patients with hyponatraemia which is severe, acute or symptomatic should usually be admitted to hospital for treatment\n- Consider referral to the appropriate speciality for advice on management of the underlying cause of hyponatraemia (e.g. cardiology for heart failure, endocrinology for adrenal insufficiency)\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 for SIADH and may also be used in some cases of hypervolaemic hyponatraemia\n\n**Medical:**\n\n- Severe hyponatraemia should be treated with hypertonic saline, usually in the intensive care setting\n- Hypovolaemic hyponatraemia is treated with IV normal saline\n- In some cases of SIADH tolvaptan may be considered - this is a vasopressin V2-receptor antagonist\n- Correction of endocrine abnormalities may be required e.g. levothyroxine for hypothyroidism; corticosteroids for adrenal insufficiency\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[Whittington Hospital Hyponatraemia Guideline](https://www.whittington.nhs.uk/document.ashx?id=6089)",
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"explanation": "# Summary\n\nSub-acute combined degeneration of the cord (SCDC) is a neurological disorder stemming from vitamin B12 deficiency, characterised by the degeneration of the dorsal columns and corticospinal tracts. Key signs and symptoms include symmetrical distal sensory symptoms, diminished vibration sense and proprioception in the legs, and mixed upper and lower motor neuron signs. Investigations primarily involve B12, folate levels, and homocysteine levels, in addition to MRI of the spine and nerve conduction studies. The primary management strategy involves B12 replacement therapy.\n\n# Definition\n\nSub-acute combined degeneration of the cord (SCDC) is a neurological complication associated with vitamin B12 deficiency. It is characterised by degeneration of both the dorsal columns and corticospinal tracts, whilst preserving pain and temperature sensations. It typically manifests as symmetrical sensory symptoms starting distally and progressing proximally, along with varying degrees of ataxia.\n\n# Aetiology\n\nThe underlying cause of SCDC is vitamin B12 deficiency, which can result from various factors including pernicious anemia, malabsorption syndromes, dietary deficiencies, and misuse of nitrous oxide (this causes a **functional** rather than a true B12 deficiency) .\n\n# Signs and Symptoms\n\n- Symmetrical distal sensory symptoms, typically beginning in the feet and progressing to the hands\n- Varying degrees of ataxia\n- Diminished vibration sense and proprioception in the legs\n- Mixed upper and lower motor neuron signs, which may present as exaggerated, diminished, or absent limb reflexes\n- Autonomic bladder or bowel symptoms\n- SCDC may manifest in both the presence and absence of haematological manifestations.\n\n# Investigations\n\nDiagnostic workup for SCDC should include:\n\n- Assessment of B12 and folate levels\n- Homocysteine level analysis; a raised level despite normal B12 could indicate a functional B12 deficiency\n- MRI of the spine to exclude cervical myelopathy\n- Nerve conduction studies, which will primarily show axonal neuropathy\n\n# Management\n\nThe mainstay of treatment for SCDC is:\n\n- Urgent Vitamin B12 replacement, typically using hydroxocobalamin 1 mg IM on alternate days until there is no further improvement, followed by maintenance treatment with hydroxocobalamin 1 mg IM every two months, as per [NICE guidelines](https://cks.nice.org.uk/topics/anaemia-b12-folate-deficiency/).",
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"question": "An 18-year-old male attends the GP complaining of weakness and tingling of their legs. They have just started university and state they are drinking 40 units of alcohol a week and taking nitrous oxide recreationally. They have no other past medical history. On examination, they have a positive Babinski sign bilaterally with brisk ankle jerks and absent knee jerks. They also have loss of proprioception.\n\nWhat is the most likely diagnosis?",
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"explanation": "Whilst this is the most common type of non-small cell lung cancer, it tends to be associated with hypertrophic pulmonary osteoarthropathy rather than hyponatraemia. This would present as bony inflammation in the wrists/ankles.",
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"explanation": "This history suggests lung cancer based on the patient being a smoker combined with the weight loss and haemoptysis. A monophonic wheeze indicates one airway being obstructed rather than multiple, further indicating a possible tumour. Hyponatraemia is caused by paraneoplastic SIADH, which is more commonly associated with small cell lung cancer rather than the other options listed. Furthermore, small cell lung cancer tends to be more centrally located rather than peripherally.",
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"explanation": "# Summary\n\nLung cancers are divided into two main subtypes: small cell and non-small cell, with small cell lung cancers being more aggressive and incurable. Types of non-small cell lung cancer include squamous cell and adenocarcinomas, with several rarer subtypes. Most cases of lung cancer are linked to smoking. Lung cancers may present with chest symptoms such as cough, breathlessness or haemoptysis, systemic symptoms of weight loss and anorexia or symptoms of metastatic disease such as bone pain or seizures. Chest X-ray is the initial investigation of choice, followed by CT chest and a biopsy. Staging scans are done after diagnosis to help plan treatment. Management can be curative or palliative depending on the stage of the cancer, the subtype and the patient’s overall health. It may include chemotherapy, radiotherapy, immunotherapy, targeted therapies to specific mutations and surgery. \n\n\n# Definition\n\nLung cancer refers to a primary malignancy arising from the lung parenchyma or the bronchi. Cancers are classified as small cell (SCLC) or non-small cell (NSCLC), with 80% being non-small cell. The main histological subtypes of NSCLC are squamous cell cancers and adenocarcinomas.\n\n# Epidemiology\n\nLung cancer makes up the largest proportion of cancer deaths of any tumour type, with nearly 35,000 deaths per year in the UK (21% of all cancer deaths). It is the second most common cancer in both males and females (after prostate and breast respectively). \n\nIncidence is strongly related to age, with the highest rates in people aged over 75 years old. Although non-smokers can also get lung cancer, 86% of cases are linked to smoking and so the majority of cases are felt to be preventable.\n\n# Aetiology\n\nRisk factors for lung cancer include:\n\n- Tobacco smoking (e.g. cigarettes, pipes, cigars)\n- Passive smoke exposure\n- Occupational exposures (e.g. beryllium, cadmium, arsenic, asbestos, silica)\n- Radon exposure\n- Family history of lung cancer\n- Radiation to the chest (e.g. in lymphoma treatment)\n- Air pollution\n- Immunosuppression (e.g. HIV, medications)\n- Increasing age\n\n# Classification\n\nLung cancers are classified by the cell of origin of the malignancy. Small cell cancers come from neuroendocrine cells of the lung. Non-small cell cancers are split into adenocarcinomas (coming from alveolar type 2 epithelial cells), squamous cell carcinomas (coming from basal epithelial cells) and large cell carcinomas (which come from a variety of epithelial cells). There are also rarer subtypes of lung cancer such as sarcomatoid or salivary gland-type lung cancers which come under the NSCLC umbrella.\n\nStaging is also an important way to classify lung cancers depending on how advanced they are. TNM (tumour, node, metastasis) staging is used to describe how large the tumour is and where it has spread to. This can then be used to classify lung cancers into stage 1 to 4, where stage 1 is localised and small (under 4cm), stages 2 and 3 are locally advanced and stage 4 is metastatic. \n\n# Signs and symptoms\n\n**Symptoms include:**\n\n- Persistent cough\n- Haemoptysis\n- Dyspnoea especially on exertion\n- Chest pain\n- Weight loss\n- Recurrent chest infections, or infections resistant to treatment\n- Anorexia\n\n**Signs include:**\n\n- Cachexia\n- Finger clubbing\n- Lymphadenopathy (supraclavicular or persistent cervical)\n- If there is lung collapse due to an obstructing tumour - absent breath sounds, trachea deviated towards side of collapse\n- If there is a malignant pleural effusion - stony dull on percussion, decreased breath sounds over affected area\n\n**Other signs and symptoms related to paraneoplastic presentations of lung cancer:**\n\n- **Cushing syndrome** - usually SCLC producing ectopic ACTH, presents with dorsal cervical fat pads, truncal obesity, hypertension, striae and proximal muscle weakness\n- **Syndrome of inappropriate ADH secretion (SIADH)** - usually SCLC, present with symptoms of hyponatraemia e.g. fatigue, nausea, weakness, confusion or seizures\n- **Lambert-Eaton myasthenic syndrome (LEMS)** - usually SCLC, due to autoantibodies to presynaptic calcium channels at the neuromuscular junction develop proximal muscle weakness that improves with repeated movement, as well as autonomic effects such as dry mouth, lightheadedness, constipation, urinary symptoms and erectile dysfunction\n- **Humoral hypercalcaemia of malignancy** - usually squamous cell carcinomas (SCC) that release parathyroid hormone-related protein (PTHrP) that mimics PTH and causes hypercalcaemia, leading to symptoms of bone pain, constipation, anorexia, abdominal pain, excessive thirst and confusion\n- **Hypertrophic pulmonary osteoarthropathy** - usually adenocarcinomas which cause a periosteal reaction of bones, resulting in clubbing and arthritis especially affecting wrists and ankles\n\n# Differential diagnosis\n\n- Lung metastases from another primary cancer (e.g. breast or colorectal cancer)\n- Mesothelioma (cancer of the pleura, strongly related to asbestos exposure)\n- Tuberculosis \n- Bronchiectasis\n\n# Investigations\n\nIn primary care, patients should be referred on a 2 week wait pathway in the following situations:\n\n- Aged 40+ with unexplained haemoptysis\n- Chest X-ray findings suspicious for lung cancer\n\nUrgent chest X-rays (to be done within 2 weeks) should be done for patients aged 40+ who have one of these symptoms and have ever smoked (or two symptoms if they are never smokers):\n\n- Cough\n- Fatigue\n- Shortness of breath\n- Chest pain\n- Weight loss\n- Anorexia\n\nAn urgent chest X-ray should be considered in patients aged 40+ with any of:\n\n- Persistent/recurrent chest infection\n- Finger clubbing\n- Supraclavicular or persistent cervical lymphadenopathy\n- Thrombocytosis\n- Chest signs consistent with lung cancer (e.g. reduced breath sounds, dullness to percussion)\n\nChest X-ray findings include:\n\n- Lung mass (may be rounded or spiculated, squamous cell carcinomas may cavitate)\n- Consolidation (where there is infection downstream of the tumour obstructing an airway)\n- Bulky hilum (especially squamous cell carcinomas which often arise centrally)\n- Lobar collapse (due to bronchial obstruction, especially squamous cell carcinomas)\n- Pleural effusion\n\n[lightgallery]\n\nOther initial investigations include:\n\n- **Sputum cytology** - low sensitivity but may be of use in patients who decline or cannot have a biopsy\n- **Diagnostic thoracocentesis** - i.e. a pleural tap; if a pleural effusion is present this should be done and the fluid sent for cytology as well as cell count, microscopy, culture, glucose, LDG and protein (to determine whether it is a transudate or exudate)\n- **Blood tests** - including FBC for anaemia and thrombocytosis, U&Es for hyponatraemia and baseline renal function, LFTs for baseline liver function (may be deranged in liver metastases), bone profile for hypercalcaemia, CRP for superadded infection, clotting if interventions planned\n- **CT chest with contrast** - should be done after chest X-ray to better characterise any lesion seen and investigate for local spread\n- **Biopsy** - to confirm the diagnosis and subtype of cancer, may be done percutaneously for peripheral tumours or via bronchoscopy for central masses\n\nOnce a lung cancer is diagnosed, further investigations may include:\n\n- **Spirometry** - to assess lung function to determine if a patient is suitable for surgical intervention\n- **CT chest abdomen and pelvis** - to stage the cancer (determine if there are any metastases)\n- **PET-CT scan** - a more sensitive way to stage the cancer and look for local or distant spread\n- **CT or MRI head** - may be done as part of staging investigations if curative treatment is planned, or if there are symptoms suspicious of intracranial metastases \n\n# Management \n\n**Conservative:**\n\n- **Holistic support** and an **MDT approach** (e.g. clinical nurse specialist involvement, palliative care input for troubling symptoms or end of life care, signpost to support e.g. Macmillan groups)\n- **Smoking cessation**\n- Discussions around **advance care planning** where appropriate\n\n**Medical**\n\n- **Chemotherapy** is first line in most cases of small cell lung cancer and stage 3 or 4 non-small cell lung cancer - this is with palliative intent (i.e. not aiming to cure the disease but to prolong life and improve symptoms). It is also offered to some patients prior to (neoadjuvant) or after (adjuvant) curative surgery.\n- **Immunotherapy** is also used especially in advanced non-small cell lung cancer; this includes medications such as pembrolizumab or atezolizumab (again with palliative intent).\n- Other **targeted therapies** exist for patients with specific mutations, e.g. erlotinib for patients with advanced non-small cell lung cancers with EGFR-TK mutations.\n- **Radiotherapy** may be curative (for example in early non-small cell lung cancer) or palliative - it is often combined with chemotherapy or other treatment modalities.\n- **Supportive therapies** include analgesia, oxygen if hypoxic and opioid treatment for breathlessness.\n\n**Surgical**\n\n- **Lobectomy** is the standard curative therapy for early stage lung cancers (which can be open or thoracoscopic in approach).\n- Some small tumours can be removed with a **wedge resection.**\n- More extensive surgery such as a **pneumonectomy** (removal of a lung) may be required depending on the size and location of the tumour, however patients need to have adequate FEV1 on pre-operative spirometry to be appropriate for surgery (over 2L for a pneumonectomy).\n- All patients undergoing surgery should also have **mediastinal and hilar lymph nodes sampled** (to look for metastases) or **resected** (removed) to reduce the chances of recurrence.\n\n# Complications\n\n**Common sites of metastatic spread include:**\n\n- Lymph nodes\n- Liver - this can cause significant pain due to stretching of the liver capsule\n- Brain - may cause nausea and vomiting, headaches, seizures, personality changes, sensory or motor symptoms, dysphasia or cerebellar symptoms, depending on where in the brain is affected\n- Bones - mostly osteolytic metastases, can cause bony pain and pathological fractures; there is a risk of metastatic spinal cord compression with vertebral metastases\n- Adrenal glands - may cause flank pain and adrenal insufficiency\n- The contralateral lung or elsewhere in the ipsilateral lung\n\n**Local complications include:**\n\n- Horner’s syndrome - due to an apical (Pancoast) tumour, causes ipsilateral anhidrosis, miosis and partial ptosis\n- Superior vena cava obstruction (SCVO) - lung cancer is the commonest cause of SCVO, causing symptoms of breathlessness, dizziness, headache and swelling of the face, neck and arms. This is a medical emergency due to the risk of airway obstruction.\n- Malignant pleural effusion\n- Hoarse voice - secondary to invasion of left recurrent laryngeal nerve\n- Persistent lower respiratory tract infection due to obstructing tumour\n- Raised hemidiaphragm secondary to invasion of phrenic nerve\n- Brachial plexus injury secondary to tumour invasion from a Pancoast tumour\n\n# Prognosis\n\nOverall prognosis is poor, with an average 5 year survival rate of 17%. This is lower for small cell lung cancer and for metastatic cancers, both of which have around a 5% 5 year survival. Small cell lung cancers are aggressive and are usually metastatic at the time of presentation, hence curative treatment is not possible\n\nIn early stage cancers survival is better, with 70% of patients with stage 1 NSCLC undergoing curative surgery surviving 5 years from diagnosis.\n\n# NICE Guidelines\n\n[Lung cancer: diagnosis and management](https://www.nice.org.uk/guidance/ng122)\n\n[NICE CKS - recognition and referral of lung and pleural cancers](https://cks.nice.org.uk/topics/lung-pleural-cancers-recognition-referral/)\n\n# References\n\n[Radiopaedia - lung cancer](https://radiopaedia.org/articles/lung-cancer-3?lang=gb)\n\n[Patient UK - lung cancer](https://patient.info/doctor/lung-cancer-pro)\n\n[Cancer Research UK - lung cancer statistics](https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/lung-cancer)",
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"question": "A 67 year old male smoker has haemoptysis and 5kg of weight loss over the last 3 months. On examination, a loud monophonic wheeze is heard over the medial aspect of the right middle zone. His renal profile shows hyponatraemia.\n\nWhat is the most likely diagnosis?",
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"explanation": "This patient is not wheezy and the history does not suggest an asthma/COPD exacerbation. This is unlikely to improve the clinical picture.",
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"explanation": "The history does not describe acute abdomen or other concerning features that could be addressed by a return to theatre such as peritonitis or abdominal distension.",
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"explanation": "Although pneumonia could cause shortness of breath, there is no history of a cough or fever, or description of crackles. Whilst a CXR would definitely be sensible, starting antibiotics based on this presentation alone would not be appropriate.",
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"explanation": "Whilst sudden onset SOB in a post operative patient should always lead to consideration of PE, the Well’s score in this case is 1.5, which means an initial d-dimer would be more appropriate than going straight to a CTPA. Additionally, the examination findings would be inconsistent with the diagnosis of PE.",
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"explanation": "This describes atelectasis, small areas of collapse which often occur following abdominal surgery due to pain on deep breathing and coughing, leading to incomplete clearing of secretions. This is usually managed conservatively at first, with chest physiotherapy and pain relief to allow proper clearing of secretions.",
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"comment": "5W’s- got this from Grey’s anatomy 😁",
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"comment": "how do you know she had a fever? doesn't say in Q",
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"comment": "SoB within 72 hours of surgery, with no signs of DVT/PE. Likely atelectasis = Chest physiotherapy, and position upright",
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"explanation": "# Summary\n\nPost-operative pyrexia, or fever following surgery, can be the result of several causes, commonly remembered by the \"5 Ws\" mnemonic: Wind (pneumonia and atelectasis), Water (urinary tract infection), Wound (infection), Wonder drugs (anesthetic reactions), and Walking (deep vein thrombosis). Timelines for the emergence of these causes can vary, but are typically seen within specific post-op periods. It's essential to recognize these symptoms promptly, carry out the relevant investigations such as cultures, imaging, or blood tests, and initiate appropriate management like antibiotics, anticoagulants, or potentially further surgical intervention.\n\n# Definition\n\nPost-operative pyrexia refers to the development of fever following a surgical procedure, usually classified as a core body temperature above 38 degrees Celsius.\n\n# Epidemiology\n\nPost-operative pyrexia is a common occurrence, especially in the first 48 hours post-surgery due to the systemic inflammatory response. The incidence can vary based on the type and invasiveness of the surgery, patient characteristics, and the perioperative care quality.\n\n# Aetiology\n\nCauses of post-operative pyrexia can be remembered using the **5 Ws** mnemonic:\n\n- **W**ind: Pneumonia and atelectasis (1-2 days post-op)\n- **W**ater: Urinary tract infection (UTI) (>3 days)\n- **W**ound: Surgical site infections (> 5 days)\n- **W**onder drugs: Drug-induced fever, commonly due to anaesthesia\n- **W**alking: Deep vein thrombosis (DVT) (>1 week)\n\nIn addition to these, a developing abscess post-operatively can also cause pyrexia.\n\n# Signs and Symptoms\n\n- **Pneumonia and atelectasis**: Cough, dyspnea, sputum production, chest pain, decreased breath sounds on examination\n- **Urinary tract infection (UTI)**: Dysuria, urgency, frequency, suprapubic pain, foul-smelling urine\n- **Surgical site infections**: Pain, erythema, swelling at the wound site, purulent discharge\n- **Drug-induced fever**: Fever associated with recent drug use, but typically no other localized symptoms\n- **Deep vein thrombosis (DVT)**: Leg pain, swelling, erythema, warmth\n\n# Differential Diagnosis\n\n- **Non-infectious causes of fever**: These could include malignancy, collagen vascular disease, thromboembolism, or medication effects. Main symptoms might include widespread symptoms with no localized signs.\n- **Infection not associated with surgery**: Infections elsewhere in the body may cause fever post-operatively. The signs and symptoms would correspond to the organ system affected.\n- **Abscess formation**: This would typically present with localized signs of infection (redness, pain, swelling) at the site of the abscess.\n\n# Investigations\n\nInvestigations will depend on the suspected underlying cause. They may include:\n\n- **Blood tests**: Full blood count, CRP, blood cultures\n- **Cultures**: Urine, wound, or sputum cultures as applicable\n- **Imaging**: Chest X-ray, CT scan, or ultrasound depending on the suspected site\n\n# Management\n\nThe management of post-operative pyrexia depends on the underlying cause but could include:\n\n- **Antibiotics**: For bacterial infections like pneumonia, UTI, or wound infections\n- **Anticoagulants**: For DVT\n- **Modification or cessation of the offending drug**: For drug-induced fever\n- **Further surgical intervention**: In case of abscess formation or severe wound infection",
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"question": "A 47 year old female has shortness of breath 2 days after her subtotal colectomy. She has reduced air entry in both lung bases and a slightly elevated respiratory rate with normal oxygen saturations. Her calves are soft and non tender.\n\nGiven the likely diagnosis, what is the most appropriate management option?",
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"explanation": "# Summary \n \nPneumonia is a radiological diagnosis, often due to a lower respiratory tract infection causing inflammation of the alveoli and terminal bronchioles, leading to consolidation of bronchopulmonary segment or lobe. Key signs and symptoms include rapid onset of high fever and productive cough for typical bacterial causes. Key investigations include blood tests, sputum culture, urinary antigen tests, and chest x-ray. Management strategies involve use of antibiotics, assessment of severity using CURB-65 score and inpatient treatment for severe cases.\n \n \n# Definition\n \n- Lower Respiratory Tract Infection/ Pneumonia is caused by infection and subsequent inflammation of the alveoli and terminal bronchioles.\n- This leads to an entire bronchopulmonary segment or lobe becoming consolidated, which means that tissue is filled with inflammatory cells and oedema.\n \n \n# Community Acquired Pneumonia (CAP)\n \n \n## Bacterial Causes\n \n \n- Typicals - so called because of the classical rapid onset of symptoms, including high fever and productive cough;\n- Streptococcus pneumoniae (gram +ve cocci found in pairs, also known as 'Pneumococcus')\n- Staphylococcus aureus\n- Haemophilus influenzae (gram -ve rod, potent beta-lactamase producer)\n- Moraxella catarrhalis (gram -coccus, potent beta-lactamase producer)\n- Atypicals: so called because of the more gradual onset of symptoms, which may be non-specific initially (fever, myalgia, dry cough). The organisms are also intracellular;\n- Mycoplasma pneumoniae\n- Chlamydia pneumoniae\n- Legionella pneumophila\n- Coxiella burnettii\n- Chlamydia psittaci\n \n \n## Viral Causes \n \n- Most commonly Influenza A, which can predispose to superadded Staph aureus (or strep pneumoniae) pneumonia.\n- Others: CMV, HSV, VZV\n \n## Fungal Causes\n \nCan be seen after silver staining and microscopy:\n \n- Candida - dimorphic yeast\n- Aspergillus - fungus with hyphae\n- Cryptococcus - encapsulated yeast\n \n \n## Specific Causes \n \nCOPD: \n \n- Pneumococcus still most common\n- Haemophilus influenzae\n- Morexella catarrhalis\n \nCystic Fibrosis:\n \n \n- Staph aureus\n- Pseudomonas aeruginosa\n- Burkholderia cepacia\n \nCauses in Homeless people: malnourished, alcohol or drug dependent, immunosuppressed:\n \n \n- Mycobacterium tuberculosis\n- Aspiration pneumonia (infection with normal flora of mouth and anaerobes, also consider in any patient with an unsafe swallow or with depressed consciousness)\n- Klebsiella pneumoniae (causes 'red-current jelly' sputum, and commonly causes lung abscess formation and empyema)\n \n \nOccupational/travel situations:\n \n- Aerosols from humidifiers and airconditioning (e.g. at holiday resorts) - Legionella pneumophila.\n- Patients can present with diarrhoea and vomiting, develop hepatorenal syndrome and have a low sodium. Severe pneumonia develops, with other rare complications such as:\n- Pancreatitis\n- Peritonitis\n- Myocarditis, endocarditis, pericarditis\n- Glomerulonephritis\n \n \nClosed populations e.g. schools, offices\n \n- Mycoplasma pneumoniae\n- Extra respiratory symptoms:\n- Erythema multiforme, erythema nodosum\n- Guillain-Barre Syndrome (and rarely other neurological complications e.g. aseptic meningitis, cerebellar disease, transverse myelitis).\n- Cold agglutinin production with haemolytic anaemia\n- Chlamydia pneumoniae\n \n \nZoonotic Causes: \n \n- In Abattoir worker, farmer, vets\n- Coxiella burnettii\n- Brucella spp.\n \n- Animal hide importers/sorters\n- Bacillus anthracis\n- Coxiella burnettii\n \n \n- Following exposure to birds\n- Chlamydia psittaci (causes psittacosis)\n- Exposure to bats/bat droppings\n- Histoplasma capsulatum (a fungus, classically affects cave-explorers)\n \n \n## Investigations\n \n \n- Bloods: including FBC, U+Es, CRP, WCC and blood cultures\n- Sputum culture\n- Urinary antigen tests for Legionella and pneumococcus\n- Chest X-Ray\n- Could assess pleural fluid aspirate in patients with pleural effusion\n \n \n## CURB-65 \n \n \n- Use the CURB-65 score to aid in deciding the severity of pneumonia and further management based on this\n- Components (1 point for each if present):\n- Confusion +/-\n- Urea >7\n- Respiratory Rate >30\n- Blood pressure: systolic < 90 or diastolic <60\n- More than 65 years old\n \n \nCURB-65 mortality by score:\n \n- 0 or 1 - 1.5%\n- 2 - about 10%\n- 3 or more - 10% or more \n \n \n \n \n## Management\n \nIf a patient is very unwell, adopt an A-E approach, initiate the sepsis six and seek early senior input.\n \n- Management based on CURB-65 score:\n- 0/1: home-based care, give oral amoxicillin for 5 days (macrolide e.g. clarithromycin, doxycycline or tetracycline if penicillin allergic).\n- 2: hospital-based care, 7-10 day course of dual antibiotic therapy with amoxicillin (IV or oral) and a macrolide\n- 3: Hospital/ITU-based care, 7-10 day course of dual antibiotic therapy with IV co-amoxiclav/ceftriaxone/tazocin and a macrolide.\n \n \n- Atypical and typical community-acquired pneumonia are both managed in the same way initially.\n- Liaise with microbiology to guide targeted antibiotics following culture results e.g. flucloxacillin for staph aureus pneumonia.\n- A repeat chest x-ray is required after 6 weeks to assess for underlying pathology.\n \n \n## Complications\n \n \n- Pleural effusion\n- Empyema (suspect if persistent, swinging fever with leucocytosis found after antibiotic therapy)\n- Abscess (can be caused by S. pneumoniae, Klebsiella, staph aureus). Can develop pyopneumothorax.\n- Pneumothorax\n- Septicemia\n- Atrial fibrillation\n- Post-infective bronchiectasis\n \n \n \n \n# Hospital Acquired Pneumonia\n \n \n## Definition\n \n \nLower respiratory tract infection that develops more than 48 hours after admission to hospital\n \n \n## Risk Factors\n \n \n- Poor hand hygiene and hospital infection control\n- Intubation and ventilation\n \n \n## Causative Organisms\n \n \n- Pseudomonas aeruginosa\n- E. coli\n- Klebsiella pneumoniae\n- Acinetobacter species (can acquire high potency beta-lactamases, known as ESBLs)\n- Serratia species (can acquire high potency beta-lactamases, known as ESBLs)\n \n \n## Investigations\n \nMay include:\n \n- Bloods: including FBC, U+Es, CRP, WCC and blood cultures\n- Sputum culture\n- Urinary antigen tests for Legionella and pneumococcus\n- Chest X-Ray\n- Could assess pleural fluid aspirate in patients with pleural effusion\n \n \n## Management \n \nIf a patient is very unwell, adopt an A-E approach, initiate the sepsis six and seek early senior input and discussion with microbiology. 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Local guidance should be sought.\n \n \n# NICE Guidelines\n \n \n[Click here for NICE CKS on chest infections](https://cks.nice.org.uk/topics/chest-infections-adult/)\n \n[Click here for NICE guidance on antimicrobial prescribing in hospital-acqui",
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"explanation": "# Summary \n\nSmall bowel obstruction is a mechanical impediment in the small bowel leading to clinical symptoms such as bilious or faeculent vomiting, abdominal pain, and distension. Key causes include adhesions, intra-abdominal hernias, Crohn's disease, malignancy, and foreign body ingestion, among others. Noteworthy signs and symptoms include abdominal pain with distension, vomiting, failure to pass flatus or stool, and possible fever. Primary investigations include blood tests, abdominal and chest X-ray, CT abdomen and pelvis, and possibly a diagnostic laparotomy/laparoscopy. 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The incidence of SBO tends to increase with age due to increasing rates of surgery, malignancies, and other predisposing conditions.\n\n# Aetiology\n\n## Factors outside the bowel\n\n- Adhesions\n \n - Most common cause in the Western world\n - Prior intra-abdominal surgeries increase the risk of adhesion development. The larger the operation, the higher the likelihood of adhesion formation.\n- Intra-abdominal hernia\n \n - Incarcerated hernias can precipitate acute obstruction\n\n## Factors relating to the bowel wall\n\n- Crohn's disease - stricturing (rather than fistulating) disease is what specifically causes SBO\n- Appendicitis\n\n## Factors relating to inside the bowel\n\n- Malignancy\n- Foreign body ingestion\n- Gallstone ileus\n\n## Diseases causing small bowel obstruction in children\n\n- Intussusception\n- Volvulus\n- Intestinal atresia\n- Appendicitis\n\n# Signs and Symptoms\n\nSBO typically presents with the following:\n\n- Abdominal pain with distension (Initially colicky pain that becomes continuous)\n- Bloating and vomiting (often bilious)\n- Failure to pass flatus or stool\n- History of abdominal/gynaecological surgery or hernia\n- Tympanic, high-pitched bowel sounds on examination\n- An empty rectum on examination in complete bowel obstruction\n\nPatients may also present with fever and significant fluid depletion. Peritonitis indicates severe bowel obstruction with developing complications (e.g. perforation, especially in closed-loop obstructions), necessitating urgent surgical intervention.\n\nSimple or partial SBO may still result in passing some flatus/stool and present with a mild temperature.\n\nIf untreated, SBO can progress to ischaemic or necrotic bowel, leading to perforation.\n\n\n# Differential Diagnosis\n\n- **Adhesions**: Pain, distention, bilious vomiting, constipation, history of previous surgeries.\n- **Intra-abdominal hernia**: Pain, distention, inability to pass flatus or stool, a palpable mass in the abdomen.\n- **Crohn's Disease**: Abdominal pain, diarrhea, weight loss, fatigue, fever.\n- **Malignancy**: Abdominal pain, weight loss, altered bowel habits, possible presence of blood in the stool.\n- **Foreign body ingestion**: Abdominal pain, possible history of foreign body ingestion, altered bowel habits.\n- **Gallstone ileus**: Abdominal pain, distention, bilious vomiting, history of gallstones or cholecystitis.\n- **Paralytic ileus**: Abdominal pain, distension and absent bowel sounds, often a post-operative complication\n\n# Investigations\n\n\nIn a patient presenting with potential intestinal obstruction, peritonitis is a worrisome sign and the consideration to transfer to theatre must be considered.\n\nBasic investigations include:\n\n- Basic blood tests including FBC, U+Es, and lactate\n - FBC (To identify leukocytosis or anaemia)\n - U+Es (To detect organ dysfunction or signs of hypovolaemia)\n - Lactate (To establish if there is bowel ischaemia or necrosis, though it can be falsely low due to liver metabolism)\n - Amylase (To rule out acute abdomen conditions)\n- Abdominal and chest X-ray\n - Performed in an upright position to detect pneumoperitoneum\n - Absence of air in the rectum can indicate complete obstruction\n\n \n| Feature | Small Bowel Obstruction (SBO) | Large Bowel Obstruction (LBO) |\n|--------------------------------|-------------------------------|------------------------------|\n| **Bowel Wall Thickness** | May be mildly thickened | Often markedly thickened |\n| **Valvulae Conniventes** | May be seen (small intestine) | Not typically seen (large intestine) |\n| **Gas Patterns** | Central or diffuse gas pattern | Peripheral or haustral pattern |\n| **Luminal Air Fluid Levels** | Commonly seen | Less frequently seen |\n| **Stool in Colon** | Minimal or absent | Often present |\n| **\"Bird's Beak\" Sign** | Absent | May be seen in LBO (sigmoid volvulus) |\n| **Peritoneal Fluid** | May be seen due to irritation | Less common unless perforation occurs |\n\n\n[lightgallery]\n\n[lightgallery1]\n\nIn the absence of peritonitis and given the patient's stable condition, the following investigations may be performed:\n\n- CT abdomen and pelvis\n - Best diagnostic test for identifying the underlying cause, the site of obstruction, and whether it's a partial vs. complete obstruction\n- Small bowel contrast study using gastrograffin\n - Used as a therapeutic measure in partial SBO\n - Presence of contrast in rectum 24 hours after ingestion signifies a resolving partial SBO, reducing the need for surgery\n- MRI abdomen\n - Comparable to CT scan, it is useful in young patients to avoid exposure to ionising radiation\n- US abdomen\n - Not as reliable as CT, but can be used in children to avoid ionising radiation exposure\n- Diagnostic laparotomy/laparoscopy\n - Used to distinguish between partial and complete obstruction if imaging doesn't provide clear evidence\n\n# Management\n\n- Begin with resuscitation protocols (ABCDE)\n- Correct fluid and electrolyte imbalances to reduce operative risk before surgery for obstruction\n- Fluid resuscitation and NG tube to aspirate content for decompression ('Drip and suck')\n- Gastrografin can be administered as both a diagnostic and therapeutic measure in cases of partial obstruction. 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"comment": "pyrexia alone doesnt make it severe, need further information to distinguish between rectal mesalazine and iv corticosteroids\n",
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"comment": "Agreed, temperature alone makes it only a moderate flare - which can be managed with mesalazine ",
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"comment": "I guess what made me sway towards steroids is the GP referring to ed. If they needed just rectal ASA GP could have prescribed that themselves",
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"explanation": "# Summary\n\nUlcerative colitis (UC) is a chronic inflammatory disease that affects the large bowel. Symptoms include diarrhoea, urgency, tenesmus, weight loss, and fever. The disease can present with extra-intestinal features such as dermatological (erythema nodosum), ocular (anterior uveitis), musculoskeletal (finger clubbing), and hepatobiliary manifestations (jaundice due to primary sclerosing cirrhosis). Investigations include blood tests, microbiological investigations, endoscopic investigations, and imaging. The management of UC is based on severity and involves inducing and maintaining remission using medications like aminosalicylates, steroids, and biologics. Surgery may be required in severe cases or when medical treatment is unsuccessful. Long-term complications include colorectal cancer, cholangiocarcinoma and colonic strictures.\n\n# Definition\n\nUlcerative colitis (UC) is a chronic relapsing-remitting inflammatory disease that primarily affects the large bowel. It usually affects the rectum first, then can extend to the part of the colon (left-hand-side colitis) or the entire colon (pancolitis). It does not spread beyond the ileocaecal valve or to the small bowel, except where backwash ileitis can occur.\n\n# Epidemiology\n\nUC is the most commonly diagnosed inflammatory bowel disease. It has an annual incidence rate of 10 per 100,000 people and a prevalence rate of 243 per 100,000. Although UC can develop at any age, it most frequently occurs in two peak age groups: 15 to 25 years and 55 to 65 years.\n\n# Aetiology\n\nThe exact cause of UC is unknown, but it is believed to result from a combination of genetic predisposition, environmental factors, and dysregulation of the immune system. There is also a higher incidence of UC among non-smokers and ex-smokers.\n\n# Signs and Symptoms\n\nThe main symptoms of UC are gastrointestinal and systemic. \n\nGastrointestinal symptoms include:\n\n- Diarrhoea often containing blood and/or mucus\n- Tenesmus or urgency\n- Generalised crampy abdominal pain in the left iliac fossa\n\nSystemic symptoms include:\n\n- Weight loss\n- Fever\n- Malaise\n- Anorexia\n\nPhysical examination may reveal general signs such as pallor due to anaemia and clubbing. Abdominal examination may reveal distension or tenderness, and a PR examination may show tenderness, and blood/mucus. \n\n\nExtra-intestinal signs occur in 10-20% of patients and include:\n\n- Dermatological manifestations: erythema nodosum, pyoderma gangrenosum\n- Ocular manifestations: anterior uveitis, episcleritis, conjunctivitis\n- Musculoskeletal manifestations: clubbing, non-deforming asymmetrical arthritis, sacroiliitis\n- Hepatobiliary manifestations: jaundice due to primary sclerosing cholangitis (PSC). 80% of those with PSC have ulcerative colitis.\n- Other features include AA amyloidosis\n\n\n\n\n# Differential Diagnosis\n\nThe differential diagnoses for UC include Crohn's disease, infectious colitis, and ischemic colitis. Key signs and symptoms to differentiate these conditions include:\n\n- Crohn's disease: Abdominal pain, weight loss, diarrhea, oral ulcers, anal fissures, and perianal fistulas.\n- Infectious colitis: Acute onset of diarrhea, fever, and abdominal pain. May be associated with recent antibiotic use, travel, or consumption of contaminated food or water.\n- Ischemic colitis: Sudden onset of abdominal pain, blood in stools, and a history of vascular disease or risk factors.\n\n# Investigations\n\n**Bedside:**\n\n- Microbiological investigations: Stool microscopy (for ova/cysts/parasites), culture and sensitivity, and stool C. difficile toxin to exclude infective colitis\n- Faecal calprotectin: Distinguishes between inflammatory bowel syndrome (normal) and inflammatory bowel disease (raised)\n\n**Bloods:**\n\n- Blood tests: FBC (anaemia and a raised white cell count), ESR/CRP is typically raised, LFTs may show a low albumin\n\n**Imaging/Invasive:**\n\n- Radiological investigations: Abdominal X-ray and erect chest x-ray in acute settings to exclude toxic megacolon and perforation.\n\t- Long-standing UC will show 'lead-pipe' colon on AXR \n- Endoscopic investigations: Colonoscopy, barium enema, and biopsy are used to confirm the diagnosis.\n - Colonoscopy will reveal shows continuous inflammation starting at the rectum that does not go beyond the submucosa with an erythematous mucosa, loss of haustral markings, and pseudopolyps.\n - Biopsy: loss of goblet cells, crypt abscess, and inflammatory cells (predominantly lymphocytes)\n - Barium enema will reveal lead-piping inflammation (secondary to loss of haustral markings), thumb-printing (a marker of bowel wall inflammation), and pseudopolyps (due to areas of ulcerating mucosa adjacent to areas of regenerating mucosa). This is less commonly used nowadays due to the increasing availability of endoscopic investigations\n\n# Truelove and Witt's Criteria for Severity\n\nAn acute exacerbation of ulcerative colitis should be assessed using the Truelove and Witt's severity index.\n\n| | **Mild** | **Moderate** | **Severe** |\n| --------------------------------------------- | ----------------------------------- | ----------------------- | ------------------------------------------------------------------------------------ |\n| **Bowel movements (no. per day)** | Fewer than 4 | 4-6 | 6 or more plus at least one of the features of systemic upset (marked with \\* below) |\n| **Blood in stools** | No more than small amounts of blood | Between mild and severe | Visible blood |\n| **Pyrexia (temperature greater than 37.8°C)** | No | No | Yes |\n| **Pulse rate greater than 90 bpm** | No | No | Yes |\n| **Anaemia (< 10g/100mL)** | No | No | Yes |\n| **Erythrocyte sedimentation rate (mm/hour)** | 30 or below | 30 or below | above 30 |\n\n\n# Management\n\n\n## Mild-moderate disease\n\nThe aim of step 1 treatment is to induce remission. If this does not work after 4 weeks, or symptoms worsen, move to step 2.\n\nThe first step in management for a moderate first presentation is to offer a topical aminosalicylate as first-line treatment. If remission is not achieved within 4 weeks, consider adding an oral aminosalicylate. In acute moderate disease if all other measures haven't worked then a trial of Etrasimod (also known as Velsipity). This is a selective sphingosine 1-phosphate (S1P) receptor modulator.\n\n- **Proctitis and proctosigmoiditis:**\n - Step 1: Topical ASA or oral ASA.\n - Step 2: Consider adding oral prednisolone. If this does not help after 2-4 weeks or symptoms worsen, consider adding oral tacrolimus.\n- **Left sided or extensive disease**\n - Step 1: High dose oral ASA.\n - Step 2: Consider adding oral prednisolone. If this does not help after 2-4 weeks or symptoms worsen, consider adding oral tacrolimus.\n\n## Acute severe disease\n\n- Step 1: IV corticosteroids (if contraindicated or not tolerated, use IV ciclosporin).\n- Step 2: If no improvement in 72 hours or worsening symptoms, add IV ciclosporin or consider surgery (if IV ciclosporin contraindicated or not tolerated, consider infliximab).\n- Step 3: A trial of Etrasimod (also known as Velsipity). This is a selective sphingosine 1-phosphate (S1P) receptor modulator.\n- Indications for emergency surgery:\n - Surgery should be considered in patients with:\n - Acute fulminant ulcerative colitis\n - Toxic megacolon who have little improvement after 48-72 hours of intravenous steroids\n - Symptoms worsening despite intravenous steroids\n\n_Note that an alternative is to initiate rescue therapy (with ciclosporin or infliximab) if the patient has a sub-optimal response to intravenous steroids but is stable enough to delay surgery. Surgery should be considered if patients fail to respond to rescue therapy within 3 days._\n\n## Surgical options\n\n- Panproctocolectomy with permanent end ilesotomy\n- Colectomy with temporary end ileostomy (approximately 3 months later the ileostomy can be reversed by forming an ileorectal anastomosis, an alternative option is completion proctectomy with a permanent end ileostomy or ileal pouch anal anastomosis (IPAA)).\n\n## Indications for elective surgery\n\n- This can be considered in patients in which there is failure to induce remission by medical means.\n- Surgical options include: panproctocolectomy with permanent end ileostomy or IPAA. An alternative is a total colectomy with ileorectal anastomosis (i.e. no stoma).\n\n# Complications\n\n## Short-term/acute complications\n\n- Toxic megacolon: this describes a severe form of colitis, and is seen in around 15% of ulcerative colitis patients.\n- Massive lower gastrointestinal haemorrhage: this occurs in up to 3% of patients.\n\n## Long-term complications\n\n- Colorectal cancer: this occurs in 3-5% of patients. There is a higher risk with disease duration, severity and extent of colitis, and concomitant primary sclerosing cholangitis (PSC).\n\n_NICE guidance suggests offering colonoscopy surveillance to high risk patients._\n\n- Cholangiocarcinoma: ulcerative colitis approximately doubles the risk of cholangiocarcinoma.\n- Colonic strictures: these can cause large bowel obstruction.\n\n## Variable-term complications\n\n- Primary Sclerosing Cholangitis: this is characterised by inflammation and fibrosis of the extra- and intra-hepatic biliary tree and affects 3-7% of patients with ulcerative colitis. 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"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/)",
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"explanation": "Bilateral pleural effusions would be an unusual presentation of pleural metastases. Bilateral alveolar oedema is more in keeping with heart failure.",
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"comment": "Just say heart failure. DEAR GOD!",
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"comment": "Correct me if i'm wrong but pleural metastases from malignancy are typically unilateral",
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"explanation": "# Summary\r\n\r\nCardiomyopathy is a group of heart muscle diseases characterised by structural and functional abnormalities of the myocardium in the absence of other heart conditions. The four main types are dilated cardiomyopathy (DCM), restrictive cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (ARVC), and Hypertrophic Cardiomyopathy (HCM). DCM is the most common type and occurs when a patient has dilated ventricles and impaired systolic function, restrictive cardiomyopathy involves impaired diastolic filling and ARVC is characterised by fatty fibrous material replacing the myocardium, primarily in the right ventricle. HCM is discussed in a separate section. Takotsubo cardiomyopathy is a rare, non-ischemic form triggered by stress, resulting in transient apical ballooning of the heart muscle. Each type has different causes, symptoms, and management approaches.\r\n\r\n# Definition \r\n\r\nCardiomyopathies are a group of diseases that have structural and functional abnormalities of the myocardium usually in the absence of coronary artery disease, hypertension, valvular disease or congenital heart disease. \r\n\r\n# Epidemiology \r\n\r\nCardiomyopathy can often go undiagnosed and the prevalence depends on the subtype. Dilated cardiomyopathy is the most common and impacts approximately 1 in 2500 people per year. Takotsubo cardiomyopathy is, however, rare and estimated to impact 1% of those who present with troponin positive chest pain. \r\n\r\n# Pathophysiology\r\n\r\nThe pathophysiology of cardiomyopathies depends on the subtype. \r\n\r\n# Classification \r\n\r\nThere are four main types of cardiomyopathy:\r\n\r\n1. Dilated (DCM): most common \r\n3. Restrictive\r\n4. Arrhythmogenic right ventricular cardiomyopathy (ARVC)\r\n5. Hypertrophic (HCM): discussed in separate section\r\n\r\nCardiomyopathies can also be considered as to whether they are primary, mixed, or secondary (although this is not a perfect system). Primary cardiomyopathies are disease processes confined to the heart (e.g. HOCM or ARVC). Mixed cardiomyopathies refer to those with a genetic disposition to a cardiomyopathy that is triggered by a secondary process (DCM or restrictive). Secondary cardiomyopathies refer to systemic or multi-organ processes that impact the myocardium (e.g. hyperthyroidism or sarcoidosis).\r\n\r\nTakotsubo is a rare, acquired primary cardiomyopathy that will also be briefly discussed in this section. \r\n\r\nEach cardiomyopathy will be discussed separately. \r\n\r\n# Dilated Cardiomyopathy (DCM) \r\n\r\nDilated cardiomyopathy refers to a dilated heart with impaired systolic function (HFrEF). It is the most common cardiomyopathy. Causes include idiopathic, alcohol, Cocksackie B virus (via an acute myocarditis), or wet beri beri. DCM can be found in association with cardiovascular disease, but in order to classify as a cardiomyopathy the the degree of myocardial dysfunction cannot be purely explained by hypertension, valve disease or ischaemic heart disease. \r\n\r\n## Causes \r\n\r\nDilated cardiomyopathy (DCM) has a number of possible causes.\r\n\r\n* Ischaemic changes, hypertension, or valvular disease can, with time, manifest with DCM. These individuals tend to have a genetic predisposition. \r\n* Genetic and congenital - may be related to familial dilated cardiomyopathy, however some sporadic gene mutations may be responsible for idiopathic cases.\r\n* Toxin-related - excessive alcohol consumption leads to myocardial dysfunction and subsequent DCM. Cocaine is also associated with ischaemia and DCM. Other medications which lead to cardiomyopathy include anthracycline chemotherapy (Doxorubicin), Cyclophosphamide, antiretroviral drugs (Zidovudine), Chloroquine and Clozapine.\r\n* Infiltrative - haemochromatosis, amyloidosis and sarcoidosis are known to cause DCM.\r\n* Peripartum - a rare cause of DCM, with unclear aetiology.\r\n* Thyrotoxicosis - the exact mechanism of this is uncertain, but thought to be related to the effects of thyroid hormone on cardiac function.\r\n* Infectious - DCM can occur secondary to myocarditis, or as a direct result of infection from HIV, Lyme disease and Chagas disease.\r\n* Idiopathic - when other potential causes have been ruled out\r\n\r\n## Symptoms and Signs \r\n\r\nCommon symptoms are those related to heart failure: \r\n\r\n* Exertional dyspnoea \r\n* Orthopnoea \r\n* Paroxysmal nocturnal dyspnoea\r\n* Peripheral oedema\r\n\r\nOther symptoms relate to consequences of the cardiomyopathy\r\n\r\n* Palpitations (atrial fibrillation or ventricular tachycardia)\r\n* Syncope/pre-syncope with conduction disturbance\r\n* Sudden cardiac death\r\n\r\nCommon signs: \r\n\r\n* Displaced apex beat\r\n* S3 gallop rhythm (rapid ventricular filling)\r\n* Murmur of mitral regurgitation (due to displacement of the valve leaflets)\r\n* Signs of heart failure (such as oedema, hepatomegaly, ascites, raised JVP).\r\n\r\n## Investigations \r\n\r\n* ECG: poor R wave progression. \r\n* Echocardiogram: diagnostic, showing a globular, dilated heart with reduced ejection fraction. \r\n* Role for cardiac MRI and endomyocardial biopsy. \r\n\r\n## Management \r\n\r\nManagement of DCM involves addressing the trigger (e.g. alcohol abstinence in alcohol-induced DCM). Further medical management surrounds HFrEF optimisation with diuretics (symptom relief) and beta-blockers, ACE-I, and mineralocorticoid antagonists. \r\n\r\n# Restrictive cardiomyopathy\r\n\r\nRestrictive cardiomyopathy involves non-dilated, non-hypertrophied ventricles with impaired diastolic filling but with normal or near-normal systolic function. \r\n\r\n## Causes \r\n\r\n* Familial non-infiltrative cardiomyopathy (inherited genetic disorders)\r\n* Infiltrative:\r\n * Amyloidosis\r\n * Sarcoidosis\r\n * Gaucher disease\r\n * Hurler syndrome\r\n * Fatty infiltration\r\n* Storage:\r\n * Haemochromatosis\r\n * Fabry disease\r\n * Glycogen storage disorders\r\n* Others:\r\n * Diabetic cardiomyopathy\r\n * Scleroderma\r\n * Hypereosinophilic syndrome (Loeffler's)\r\n * Radiation\r\n * Chemotherapy (anthracyclines like Doxorubicin and Daunorubicin)\r\n\r\n## Symptoms and Signs \r\n\r\nPresentation is often similar to heart failure or can be difficult to clinically distinguish from constrictive pericarditis. Patients may present with predominantly right ventricular failure symptoms due to reduced venous return. Up to 75% of patients will have associated atrial fibrillation. \r\n\r\n## Investigation \r\n\r\n* Echocardiogram: shows thickened ventricular walls and valves, with impaired ventricular filling and preserved systolic function. \r\n* Cardiac MRI: useful in distinguishing between restrictive cardiomyopathy and constrictive pericarditis. \r\n\r\n## Management\r\n\r\nManagement of restrictive cardiomyopathy also revolves around addressing the underlying cause (e.g. steroids for sarcoidosis). There is no specific treatment for restrictive cardiomyopathy but involves diuretics for symptom relief and anticoagulation for atrial fibrillation. \r\n\r\n# Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)\r\n\r\nIn ARVC, fatty fibrous material replaces the myocardium. It is caused by genetic defects in desmosomes. It is usually inherited in an autosomal dominant fashion. It primarily involves the right ventricle and can be seen on echocardiogram with hypokinetic segments of the free wall of the right ventricle. As suggested by the name, the main symptoms of ARVC relate to palpitations, syncope or cardiac sudden death due to the development of dangerous arrhythmias. \r\n\r\n\r\n# Takotsubo Cardiomyopathy \r\n\r\nTakotsubo (octopus pot) cardiomyopathy refers to a non-ischaemic cardiomyopathy associated with transient, apical ballooning of the myocardium usually triggered by stress ('Broken Heart' syndrome). It is suspected in those with troponin-positive chest pain, who have a history of a significant stressor, ST elevation on ECG, and normal coronary arteries on angiogram. Echocardiogram reveals classical apical ballooning due to severe hypokinesis of mid and apical segments with preservation of basal segments. The treatment is largely supportive and most patients completely recover within two months. \r\n\r\n# NICE Guidelines\r\n[NICE Guidance on Chronic Heart Failure](<https://www.nice.org.uk/guidance/ng106>)\r\n\r\n# References\r\n[National Institute of Health Information on Cardiomyopathies](<https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4072838/>)",
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"explanation": "# Summary\n \n \nSubfertility is defined as the diminished ability of a couple to conceive a child, which may be due to a variety of definable causes or an unexplained failure to conceive over a two-year period. Key signs and symptoms vary based on the underlying cause but generally revolve around the inability to achieve pregnancy despite regular unprotected sexual intercourse. Investigations typically include hormonal studies, semen analysis, and imaging studies. The management of infertility is dependent on the underlying cause and often involves a combination of lifestyle modifications, medical interventions, and assistive reproductive technology. \n \n \n \n# Definition\n \nInfertility is the diminished ability of a couple to conceive a child. This may result from a definable cause such as ovulatory, tubal, or sperm problems, or may be an unexplained failure to conceive over a two-year period despite regular (3-4 times a week) unprotected sexual intercourse.\n \n \n \n# Epidemiology\n \n \nStatistically, a couple stands an 80% chance of conceiving within one year if the woman is younger than 40 years, they do not use contraception, and they have regular intercourse (3-4 times per week). This overall probability increases to 90% if considered over two years.\n \n \n# Aetiology\n\n \nFactors affecting natural fertility include:\n \n - Increasing age\n - Obesity\n - Smoking\n - Tight-fitting underwear (males)\n - Excessive alcohol consumption\n - Anabolic steroid use\n - Illicit drug use\n \n \n\nCauses of infertility can be classified into:\n \n \n - **Genetic causes:** This includes Turner's syndrome (XO) and Kleinfelter's syndrome (XXY).\n - **Ovulation/endocrine disorders:** Examples are polycystic ovary syndrome, pituitary tumours, Sheehan's syndrome, hyperprolactinaemia, Cushing's syndrome, and premature ovarian failure.\n - **Tubal abnormalities:** These can be due to congenital anatomical abnormalities or adhesions secondary to pelvic inflammatory disease (often caused by chlamydia or gonorrhoea).\n - **Uterine abnormalities:** These include bicornate uterus, fibroids, and Asherman's syndrome (uterine adhesions).\n - Endometriosis\n - **Cervical abnormalities:** These include cervical damage after biopsy or LLETZ procedure.\n - **Testicular disorders:** Disorders such as cryptorchidism, varicocele, testicular cancer, and congenital testicular defects fall in this category.\n - **Ejaculatory disorders:** These include obstruction of the ejaculatory system and disorders of ejaculation such as retrograde ejaculation and premature ejaculation.\n \n \n# Investigations\n \n \nInvestigations for infertility are divided into those for men and women. \n\n*For women:*\n\n**Bedside:**\n \n- Thorough history, including past medical history, sexual history and details of past pregnancies. \n- Speculum and bimanual examination: To investigate physical anomalies (e.g. large fibroids). \n- STI screen\n \n \n**Bloods:**\n \n - Serum progesterone testing (performed 7 days before the end of the menstrual cycle): A rise in progesterone indicates that the corpus luteum has formed and is releasing progesterone due to occurrence of ovulation.\n - Prolactin\n - LH/FSH \n - Anti-mullerian hormone (AMH): Measure of ovarian reserve\n - TFTs \n\n \n**Imaging:**\n \n- Transvaginal ultrasound scan: To identify any physical anomalies of the uterus, and check antral follicle count (measure of ovarian reserve)\n- Hysterosalpingography: Assess tubal patency.\n- Laparsocopy and dye: Assess tubal patency in presence of co-morbidities (e.g. PID, ectopic pregnancy, endometriosis). \n\n\n*For men:*\n\n**Bedside:**\n \n- Thorough history, including past medical history, sexual history and details of past pregnancies. \n- Testicular examination: To investigate visible physical anomalies (e.g. varicocele). \n- Semen analysis: To evaluate sperm count, motility, and morphology. \n \n \n**Bloods:**\n \n - Serum testosterone \n - LH/FSH \n - TFTs \n \n \n# Management\n \n \nThe management of infertility is tailored to the underlying cause but may include:\n \n**Conservative:**\n\n - Weight loss\n - Smoking cessation \n - Reduction of alcohol intake\n - Stress-reduction strategies\n\n**Medical:**\n\nMedications may be used for ovulation induction, such as: \n\n - Clomiphene\n - FSH and LH injections\n - GnRH or DA agonists\n\n \n**Surgical:**\n \n - Assisted reproductive technology, including in vitro fertilisation or intracytoplasmic sperm injection.\n\n\nIn addition to all of the above, if an underlying cause of infertility is found (e.g. fibroids, endometriosis), then those causes should be managed. \n\n\n# NICE Guidelines\n\n[Click here for NICE Guidelines on fertility problems](https://www.nice.org.uk/guidance/cg156)\n\n[Click here for NICE Guidelines on infertility](https://cks.nice.org.uk/topics/infertility/)\n\n# References \n\n[BMJ Best Practice](https://bestpractice.bmj.com/topics/en-gb/498)\n\n[Fields et al., 2023 - BMJ](https://www.bmj.com/bmj/section-pdf/187753?path=/bmj/346/7896/Practice.full.pdf)",
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"explanation": "This would be appropriate for giant cell arteritis, which would present with pain and tenderness over the temporal arteries, along with systemic upset.",
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"explanation": "This would be the correct treatment for giant cell arteritis with no visual involvement. As the patient has no pain or tenderness over the temporal arteries, giant cell arteritis is unlikely.",
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"comment": "Can't believe I misread the question as \"which one of the following mx plans is the cause of her condition\"...",
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"comment": "Good question",
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"comment": "so you asking me for management without giving me investigations, say less",
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"comment": "you haven't said that there is no tenderness over the temporal artery and temporal arteritis can cause painless loss of vision??",
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"explanation": "# Summary\n\nSudden painless visual loss is an emergency presentation with a variety of causes including retinal artery or vein occlusions, optic nerve ischaemia, retinal detachment or vitreous haemorrhage. History and ophthalmological examination may be sufficient for diagnosis, with additional investigations including blood tests, imaging such as a B-scan (eye ultrasound) or a temporal artery biopsy in suspected giant cell arteritis. Management varies significantly based on the underlying cause, for example in retinal artery occlusion attempting to dislodge the embolus, aspirin and referral for both stroke and ophthalmology follow up.\n \n# Definition\n\nSudden painless visual loss has a broad differential of causes - we will cover the main ones here. It should be differentiated from visual loss associated with pain (e.g. acute angle closure glaucoma) and transient visual loss (e.g. amaurosis fugax). Retinal examination is usually key to the diagnosis, although there may be specific features in the history that indicate a particular diagnosis.\n \n# Differential Diagnosis\n\n\n## Central retinal vein occlusion\n\n- Shares risk factors with other forms of venous thromboembolism, including older age, cardiovascular disease, hypercoagulability and the combined oral contraceptive pill\n- History is of sudden unilateral painless visual loss with no other associated symptoms typically\n- Retinal examination shows widespread haemorrhage with dilated tortuous veins - this is described as a \"stormy-sunset\" appearance\n- Investigations include basic bloods including blood glucose, lipids, serum protein electrophoresis (looking for diabetes, hyperlipidaemia and myeloma respectively as these are all risk factors) and young patients may require a thrombophilia and autoimmune screen\n- There is no specific management other than addressing any underlying conditions found\n- Two important complication is neovascularisation causing glaucoma (which is treated with laser therapy) and macular oedema (treated with anti-VEGF injections)\n \n## Central retinal artery occlusion\n \n- Also presents with sudden unilateral painless visual loss with no other specific symptoms\n- On examination patients have a relative afferent pupillary defect and fundoscopy shows a pale retina with a cherry red spot at the macula\n- Risk factors include atrial fibrillation, valvular heart disease, carotid artery stenosis, thrombophilia and atherosclerosis\n- Investigations should include an ECG looking for arrhythmias, bloods including a coagulation screen, glucose, ESR and lipid profile to look for risk factors, and a carotid artery doppler to look for carotid stenosis. An echocardiogram may be needed if valvular heart disease or endocarditis is suspected.\n- Management involves attempting to dislodge the embolus if the patient has presented within 90 minutes of symptom onset - this may involve ocular massage, IV acetazolamide or anterior chamber paracentesis\n- A retinal artery occlusion is a type of ischaemic stroke and so should be treated with 300mg aspirin for 14 days initially with stroke team referral for follow up\n- The main complication is neovascularisation due to ischaemia\n\n [lightgallery1]\n \n## Ischaemic optic neuropathy\n \n- This is a broad term that describes optic nerve damage due to a lack of blood supply\n- It can be classified as anterior or posterior, with visible optic disc swelling characterising anterior ischaemic optic neuropathy (AION)\n- AION can be further divided into arteritic and non-arteritic AION, with the usual cause of arteritic AION being giant cell arteritis (GCA)\n- History may reveal other symptoms of GCA e.g. temporal headache, scalp tenderness and jaw claudication and there may also be systemic symptoms or features of polymyalgia rheumatica such as proximal weakness, fatigue and weight loss\n- Fundoscopy shows a swollen optic disc acutely, which becomes pale due to optic atrophy\n- Investigations include basic bloods including an ESR for GCA, and a HbA1c and lipid profile for non-arteritic anterior ischaemic optic neuropathy (NAION)\n- For GCA, a duplex ultrasound of the temporal artery should be done +/- a temporal artery biopsy\n- Management of GCA is with high-dose steroids and rheumatological referral\n- NAION management is upportive and involves optimisation of risk factors e.g. hypertension\n\n## Retinal detachment\n \n- This may be secondary to traction where the retinal is pulled away (e.g. in proliferative diabetic retinopathy or trauma) or exudative causes where subretinal fluid causes the detachment (e.g. due to inflammation or malignancy)\n- Patients present with floaters and peripheral flashes followed by a \"curtain\" or \"shadow\" falling over their vision\n- Fundoscopy shows a pale grey area of retina ballooning forward and a retinal tear may be seen\n- Diagnosis is usually clinical, however if the diagnosis is unclear is can be confirmed with a B-scan (ultrasound of the eye) to look for detachment of the retina\n- Management is usually surgical in cases of tractional retinal detachment, with either a pars plana vitrectomy or a scleral buckle\n \n## Vitreous haemorrhage\n\n- This occurs due to bleeding of the retinal vessels\n- These are often vessels that are new and fragile due to neovascularisation, most commonly due to proliferative diabetic retinopathy\n- Trauma and retinal detachment can also cause vitreous haemorrhage\n- Symptoms include sudden floaters and blurred vision or visual loss\n - When the bleed is large enough to cause visual loss, the retina is difficult to view on fundoscopy and the red reflex is absent\n- Management may be conservative with follow up to look for retinal detachment\n- Patients should avoid heavy lifting in case they dislodge a clot leading to further bleeding\n- Laser therapy should be considered for patients with neovascularisation to prevent further bleeding\n- Vitrectomy surgery may be required in some cases to remove the blood\n\n[lightgallery]\n\n# NICE Guidelines\n\n[NICE CKS - Retinal Detachment](https://cks.nice.org.uk/topics/retinal-detachment/)\n\n[NICE CKS - Giant Cell Arteritis](https://cks.nice.org.uk/topics/giant-cell-arteritis/)\n\n# References\n\n[Royal College of Ophthalmologists - Retinal Vein Occlusion Guidelines](https://www.rcophth.ac.uk/wp-content/uploads/2015/07/Retinal-Vein-Occlusion-Guidelines-2022.pdf)\n\n[Patient UK - Retinal Artery Occlusion](https://patient.info/doctor/retinal-artery-occlusions)\n\n[Patient UK - Vitreous Haemorrhage](https://patient.info/doctor/vitreous-haemorrhage-pro)",
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"question": "A 43-year old woman experiences sudden-onset painless visual loss. She has a history of rheumatoid arthritis and poorly controlled type 2 diabetes mellitus.\n\nWhich of the following management plans is likely to treat the cause of her condition?",
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"answer": false,
"explanation": "Mycoplasma cannot be detected on conventional light microscopy.",
"id": "10015735",
"label": "e",
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"explanation": "Mycoplasma is not a virus. Without the mention of the cough, herpes simplex could have a likely cause of the erythema multiformae.",
"id": "10015732",
"label": "b",
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"explanation": "Urinary antigen testing is useful for legionella and pneumococcus, rather than mycoplasma.",
"id": "10015734",
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"explanation": "The diagnosis is most likely mycoplasma pneumoniae, for which serology is the best test (from those provided). The rash the patient is experiencing is erythema multiformae, which can be caused by mycoplasma, a common cause of pneumonia in young adults. The patient has evidence of haemolysis as indicated by the low haemoglobin level and elevated reticulocytes which can occur in the context of mycoplasma. Additional testing may show elevated Cold agglutinin titers and a positive Coombs test. It often causes outbreaks amongst those in crowded areas/living conditions, such as university students.",
"id": "10015731",
"label": "a",
"name": "Serology",
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"explanation": "Mycoplasma is not a retrovirus.",
"id": "10015733",
"label": "c",
"name": "RT-PCR",
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"comment": "How am I supposed to diagnose from 2 sentences :(",
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"comment": "Someone who did an undergrad in a lab based subject defo wrote this ",
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"comment": "aka a looooooser",
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"comment": "The pt need to go back and practice hx taking if that is the only hx they are giving the GP......",
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"explanation": "# Summary\n\nPneumonia is a common infection of the lung parenchyma that involves the alveoli becoming consolidated with inflammatory cells and microorganisms. Key symptoms include fever, malaise, a productive cough and pleuritic chest pain. Investigations include a chest X-ray to detect consolidation, blood tests for inflammatory markers and blood and sputum cultures to look for an underlying cause. Management involves oxygen if hypoxic, IV fluids if required and antibiotics targeted to the causative organism. \n\n# Definition\n\nPneumonia is an inflammatory condition of the lung parenchyma caused by infection. Alveoli become filled with inflammatory cells and microorganisms, leading to consolidation of the lung tissue. This impairs gas exchange and can lead to hypoxia.\n\n# Epidemiology\n\nCommunity-acquired pneumonia has an incidence of 5-10 per 1000 adults in the UK per year. Approximately 22-42% of these cases require admission to hospital. Mortality estimates range from 5 to 14%, with half of these being in people aged over 84 years. \n\n# Aetiology\n\nThe commonest cause of pneumonia is Streptococcus pneumonia, which is usually community-acquired, followed by Haemophilus influenzae and Moraxella catarrhalis. These are referred to as typical pneumonias (as they tend to present with the classic symptoms listed below).\n\nAtypical pneumonias have a variety of atypical features, e.g. a more insidious onset, extra-pulmonary symptoms such as headache and varying appearances on chest imaging. These include Mycoplasma pneumoniae, Legionella pneumophila and Chylmydophila psittaci. \n\nHospital-acquired pneumonias are defined as pneumonia that started 48 hours or longer after admission. Gram negative organisms such as Pseudomonas aeruginosa, as well as Staphylococcus aureus are more common in these environments.\n\nAspiration pneumonias are covered in a separate chapter. \n\n**Specific features of some of these microbiological causes are as follows:**\n\n**Staphylococcal pneumonia**\n\n- A bilateral cavitating bronchopneumonia due to staphylococcal aureus, a gram-positive cocci found in clusters.\n- Commoner in intravenous drug users, elderly patients, or as a superadded bacterial infection in those with influenza.\n\n**Klebsiella pneumonia**\n\n- Usually a cavitating pneumonia affecting the upper lobes presenting with red-currant sputum.\n- It is caused by a gram-negative anaerobic rod.\n- Increased risk in the immunocompromised, elderly and in alcohol excess.\n\n**Mycoplasma pneumonia**\n\n- Presents with flu-like symptoms of arthralgia, myalgia, dry cough and headache.\n- Primarily affects younger patients.\n- Associated with an autoimmune haemolytic anaemia caused by cold agglutinins.\n- May lead to erythema multiforme, Stevens-Johnson syndrome, Guillain-Barre syndrome and meningoencephalitis.\n\n**Legionella pneumonia**\n\n- Fever, myalgia and malaise followed by dyspnoea and a dry cough are typical presenting features.\n- Caused by a gram-negative coccobacillus.\n- Occurs in those exposed to contaminated water e.g. in humidifiers or cooling systems.\n- Typically causes hyponatraemia and deranged liver function tests. \n\n**Chlamydophila psittaci pneumonia**\n\n- An intracellular bacteria acquired from contact with infected birds such as parrots.\n- Features include lethargy, arthralgia, headache, anorexia, dry cough and fever.\n\n# Classification\n\nCommunity-acquired pneumonias are classified using the CURB-65 score to determine severity and guide management.\n\nOne point is awarded for each of the following:\n\n- Confusion \n\n- Urea > 7mmol/L\n\n- Respiratory rate > 30 breaths/min\n\n- Blood pressure < 90 systolic and/or < 60mmHg diastolic\n\n- 65 years or older\n\nThis can be used to estimate 30 day mortality from pneumonia:\n\n- CURB-65 0 - **0.7%** \n\n- CURB-65 1 - **3.2%** \n\n- CURB-65 2 - **13%** \n\n- CURB-65 3 - **17%** \n\n- CURB-65 4 - **41.5%** \n\n- CURB-65 5 - **57%** \n\nA CURB-65 score of 0-1 requires home treatment, 2 should consider hospital admission, 3-5 admit to hospital and consider ITU referral.\n\n# Symptoms\n\n- Fever\n- Malaise\n- Rigors\n- Cough\n- Purulent sputum\n- Pleuritic chest pain\n- Haemoptysis\n\n# Signs\n\n- Tachypnoea\n- Tachycardia\n- Hypotension\n- Cyanosis\n- Pyrexia\n- Dullness to percussion over the consolidated area\n- Increased vocal resonance/ tactile vocal fremitus over the consolidated area\n- Bronchial breathing over the consolidated area\n- Pleural rub may be heard due to inflammation of the adjacent pleura\n\n# Differential Diagnosis\n\n- **Bronchiectasis** - chronic productive cough with copious sputum, may be triggered by a severe lower respiratory tract infection or another condition (e.g. cystic fibrosis)\n- **Tuberculosis** - suspect in patients with risk factors (e.g. TB contact, from endemic area, no fixed abode), haemoptysis and weight loss more common\n- **Lung cancer** - may lead to pneumonia e.g. by obstructing a bronchus with downstream infection, important to consider especially in patients with a history of smoking, weight loss, chronic cough and haemoptysis\n- **Bronchitis** - infection of the bronchi rather than the lower respiratory tract, usually viral and self-resolving \n\n# Investigations\n\n**Bedside:**\n\n- Sputum for microscopy, culture and sensitivity\n- Consider arterial blood gas if hypoxaemic \n- Urinary legionella and pneumococcal antigens\n- ECG to look for complications e.g. atrial fibrillation\n\n**Bloods:**\n\n- Blood cultures if febrile\n- FBC and CRP for inflammatory markers\n- U&Es to look for an AKI\n- LFTs may be deranged e.g. in Legionella, baseline important when giving antibiotics\n- Mycoplasma serology if atypical pneumonia suspected\n- HIV testing should be offered to all patients with recurrent pneumonia (and all patients in a high prevalence area such as London)\n\n**Imaging:**\n\n- Chest X-ray: may show lobar consolidation or bilateral consolidation in atypical infections, parapneumonic effusions may also be seen.\n- CT chest may be indicated in some cases (e.g. suspected underlying malignancy, suspicious findings on X-ray)\n\n[lightgallery]\n\n\n# Management\n\n**Conservative:**\n\n- Oxygen if low saturations\n- IV fluids if dehydrated\n- Analgesia for myalgia or chest pain\n- Escalate for respiratory support (e.g. continuous positive airway pressure or intubation and ventilation) if patients are severely unwell - 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"comment": "if the systolic bp was less than 90 would be answer bc DC Cardioversion?",
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"comment": "I think the principle here is that you don't cardiovert AF if there is a clear reversible cause. Most of cases of AF in an unwell patient IS them being unwell (sepsis, electrolyte imbalances, etc). \n\nSo you would treat the cause first (e.g. fluids and abx), then reassess :)",
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"comment": "Also you don't cardiovert after 48 hours for risk of dislodging a possible clot (formed as the result of the AF) which could go on to cause a CVA",
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"comment": "yes and no. If you thought the patient would die faster than rehydrating them would increase the bp, yes. If you were willing to continuously monitor BP and watch it rise while having the crash team nearby ready to cardiovert, then I don't see why not wait for the bolus to go through",
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To be classified as having septic shock, patients need to be persistently hypotensive, requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more **and** have a lactate of over 2 mmol/L despite adequate fluid resuscitation. \n\n# Epidemiology\n\n- Due to variations in coding and definitions, statistics related to admissions to hospital with sepsis tend to be inconsistent\n- Approximately 200,000 people are admitted to hospital with sepsis per year\n- Approximately 20% of these (40,000 per year) require intensive care admission\n- Mortality is also approximately 20%, with deaths estimated at up to 48,000 per year in the UK\n- Men are more commonly affected than women\n- Patients at the extremes of age (infants under a year and people aged over 75) are more at risk\n\n# Aetiology\n\n- The commonest sources of infection are respiratory, genitourinary, renal and gastrointestinal \n- Most causative pathogens are bacteria, although fungal, parasitic and viral infections can also lead to sepsis\n- The commonest organisms identified are Staphylococcus aureus, Escherichia coli and Pseudomonas species\n- In 50% of sepsis cases, no causative pathogen is identified \n\n**Risk factors** for sepsis include:\n\n- Pregnancy\n- Recent miscarriage or abortion\n- Frailty\n- Immunocompromise due to chronic comorbidities e.g. HIV, diabetes, sickle cell disease\n- Immunosuppression secondary to medications e.g. chemotherapy, steroids\n- Recent surgery or trauma\n- Skin breaks or infections\n- Drug or alcohol misuse\n- Indwelling lines or catheters\n\n# Signs and Symptoms\n\nSymptoms include:\n\n- General malaise\n- Fevers, sweats or chills\n- Localising signs of infection e.g. rashes, dysuria\n- Decreased urine output\n- Confusion\n- Breathlessness\n- Nausea and vomiting\n- Myalgia\n \nOn examination, signs include:\n \n- Tachycardia\n- Hypotension\n- Pyrexia or hypothermia\n- Dehydration e.g. dry mucous membranes\n- Altered mental state including delirium\n- Irritability\n- Respiratory distress e.g. tachypnoea, accessory muscle usage\n- Cyanosis and hypoxia\n- Delayed capillary refill time\n- Cool extremities\n- Skin appears mottled or ashen\n\n# Differential Diagnosis\n\n- **Acute alcohol withdrawal** causes altered mental state, tachycardia and sweating; patients are usually tremulous and may have withdrawal seizures if severe\n- **Acute haemorrhage** may cause hypovolaemic shock with signs of shock including tachycardia, hypotension, delayed capillary refill and cool extremities; differentiated by signs of bleeding which may be overt or more subtle (e.g. abdominal pain)\n- **Diabetic ketoacidosis** causes malaise, tachypnoea (with Kussmaul breathing), dehydration and confusion; metabolic acidosis may be seen in both but in diabetic ketoacidosis glucose will be very high\n- **Pulmonary embolism** may cause tachycardia, hypotension, respiratory distress and a low-grade fever; may have haemoptysis and pleuritic chest pain (which could also be seen in sepsis secondary to pneumonia) - CTPA can be used to differentiate if unclear\n- **Thyrotoxicosis** produces similar symptoms of confusion and fevers and signs of tachycardia; thyroid function testing shows high T4 and suppressed TSH\n- **Drug reactions** e.g. neuroleptic malignant syndrome - shares features of fever, confusion, labile blood pressure and sweating; differentiated by a recent history of antipsychotic use, no localising signs of infection\n\n# Investigations \n\nThe **Sepsis Six** involves taking three key measures (as well as giving three key treatments):\n\n- **Blood cultures** ideally prior to antibiotic administration\n- **Lactate** (i.e. a blood gas - venous or arterial)\n- **Urine output** (which may involve inserting a urinary catheter)\n\nOther **bedside tests** should include:\n\n- **Capillary blood glucose** as hypo or hyperglycaemia may contribute to confusion\n- **Urine pregnancy test** in women of childbearing age\n- **Urine dip** and send for **MC&S** looking for evidence of urinary tract infection\n- **ECG** as in any acutely unwell patient, looking for arrhythmias and ischaemic changes\n\n**Blood tests** should include:\n\n- **FBC** and **CRP** for inflammatory markers\n- **U&Es** looking for evidence of acute kidney injury\n- **LFTs** as a baseline prior to giving antibiotics, may be deranged in sepsis\n- **Coagulation screen** as this may be deranged in sepsis\n\n**Imaging** should include:\n\n- **Chest X-ray** as part of a septic screen\n\nOther investigations should be targeted at a suspected underlying cause, e.g. respiratory or wound swabs, other imaging e.g. a CT abdomen or echocardiogram or special tests e.g. lumbar puncture when stable.\n\n# Management \n \nThe three things that should be given as part of the **Sepsis Six** are:\n\n- IV fluid resuscitation (usually a 500ml bolus over 15 minutes initially)\n- Supplementary oxygen to target saturations of 94-98% (88-92% if at risk of type 2 respiratory failure)\n- Broad-spectrum IV antibiotics (as per local guidelines)\n\nOther **conservative** management considerations involve:\n\n- Close monitoring of observations, fluid balance, clinical condition and bloods including serial lactate measurement\n- Early escalation for senior review and inform intensive care as may require interventions such as inotropes or vasopressors\n\nOther **medical** management involves:\n\n- Modify antibiotic therapy if a source of infection is identified or microbiological results become available\n- Further IV fluids may be required however this should be done with careful fluid balance monitoring\n\n**Surgical** management involves:\n\n- Source control, e.g. draining abscesses or debriding infected tissue\n- Infected devices may need to be removed\n \n# Complications\n\n- **Multi-organ failure** including renal failure, heart failure, acute respiratory distress syndrome and cholestasis\n- **Coagulopathy** including disseminated intravascular coagulation\n- **Delirium** which may be associated with long-term cognitive impairment e.g. difficulty concentrating and memory loss\n- **Mental health impacts** including anxiety, depression and post-traumatic stress disorder\n- **Secondary infections** which are often hospital-acquired\n- **Polyneuropathy** i.e. critical illness polyneuropathy, characterised by generalised weakness and sensory loss\n- **Death**\n\n# Prognosis\n\n- Overall mortality has been estimated at around 20-30%\n- This increases to 64% in patients aged over 85 years\n- Patients with septic shock also have higher mortality (40-60%) \n- Risk of death in survivors remains raised after recovery (15% of sepsis survivors die within a year of discharge, with 6-8% more dying each year for the following 5 years) \n\n# NICE Guidelines\n\n[NICE - Sepsis: recognition, diagnosis and early management](https://www.nice.org.uk/guidance/ng51)\n\n[NICE CKS - Sepsis](https://cks.nice.org.uk/topics/sepsis/)\n\n# References \n \n[UK Sepsis Trust](https://sepsistrust.org/)\n\n[Patient UK - Sepsis](https://patient.info/doctor/sepsis-septicaemia-pro)",
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"question": "A 75 year old man is brought to the emergency department after being found unwell at home. His ECG shows evidence of fast atrial fibrillation.\n\nObservations show:\n\n* Pulse rate 130\n\n* Blood pressure 96/64\n\n* Temperature 38.8 degrees celcius\n\n* Respiratory rate 24 breaths/minute\n\nWhat is the most appropriate next step in management?",
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"explanation": "The patient's insidious presentation and normal libido suggests an organic cause for his erectile dysfunction.",
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"explanation": "The patient's insidious presentation and normal libido suggests an organic cause for his ED. Further, SSRIs may cause/exacerbate erectile dysfunction.",
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"explanation": "The patient's insidious presentation and normal libido suggests an organic cause for his ED. As sildenafil is contraindicated due to his nitrate use (concurrent use of both of these may cause profound hypotension), this is the most appropriate management.",
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"explanation": "# Summary\n\nErectile dysfunction (ED) is a common condition that involves the inability to achieve or maintain an erection sufficient for satisfactory sexual performance. It can be a result of a variety of factors, such as vascular disease, autonomic neuropathy, medications, psychogenic factors, endocrine causes, pelvic surgery, and anatomical abnormalities. Key investigations include a detailed sexual and psychological history and blood tests to evaluate hormone levels and overall health. Management strategies include psychosexual therapy, oral phosphodiesterase inhibitors like Sildenafil, vacuum aids, intra-cavernosal injections, and the use of prostheses. Sildenafil has certain contraindications and requires caution in certain patient populations.\n\n# Definition\n\nErectile dysfunction (ED) is defined as the consistent or recurrent inability to attain and/or maintain penile erection sufficient for satisfactory sexual performance.\n\n# Epidemiology\n\nErectile dysfunction is common, particularly among older men. It affects more than 50% of men aged over 60. However, ED is not considered a normal part of aging and can affect men at any age.\n\n# Aetiology\n\nSeveral factors can contribute to erectile dysfunction, including:\n\n- Vascular disease: Atherosclerosis can lead to impaired blood flow to the penis, leading to ED.\n- Autonomic neuropathy: This can cause penile denervation, most commonly seen in conditions like diabetes or with excessive alcohol intake.\n- Medications: Certain drugs, such as antihypertensive agents, can cause ED.\n- Psychogenic: Anxiety, depression, and other psychological factors can contribute to ED.\n- Endocrine causes: Conditions like prolactinoma and hypogonadism can cause hormonal imbalances leading to ED.\n- Pelvic surgery: Procedures involving the bladder, prostate, or other pelvic structures can damage nerves and blood vessels, leading to ED.\n- Anatomical abnormalities: Conditions like Peyronie's disease, characterized by fibrous scar tissue inside the penis, can cause ED.\n\n# Signs and Symptoms\n\nThe primary symptom of erectile dysfunction is the inability to achieve or maintain an erection sufficient for sexual intercourse. This can also lead to:\n\n- Reduced sexual desire\n- Difficulty in ejaculation\n- Anxiety or depression related to sexual performance\n- Signs which suggest an organic cause is more likely - lack tumescence, slow-onset, normal libido.\n- Signs which suggest a psychogenic cause - if situational, high levels of stress, still having early morning erections. \n\n# Differential Diagnosis\n\nConditions with similar symptoms include:\n\n- Premature ejaculation: Characterized by uncontrolled ejaculation either before or shortly after sexual penetration.\n- Hypogonadism: Characterized by low testosterone levels, resulting in low sex drive, fatigue, and mood changes.\n- Peyronie's disease: Presents with a significant bend in the penis during erection, which can interfere with sexual function.\n\n# Investigations\n\nEvaluating erectile dysfunction includes:\n\n- A detailed sexual and psychological history to identify potential contributing factors.\n\t- Generally, if there is acute onset, the cause is most likely psychogenic and if the onset is more gradual there is more likely to be an organic cause (e.g. atherosclerosis).\n- Blood tests: Full blood count, urea and electrolytes, thyroid function tests, lipid profile, testosterone, and prolactin to evaluate overall health and hormonal status.\n\t- ED can sometimes be the first presentation of sequalae of cardiovascular disease and so presentation should prompt investigation of cardiovascular health.\n\n# Management\n\nManagement strategies for erectile dysfunction include:\n\n- Psychosexual therapy to address any underlying psychological factors.\n- Oral phosphodiesterase inhibitors, such as Sildenafil, to enhance the effect of nitric oxide, increasing blood flow to the penis.\n\t- Side effects - headache, flushing, hypotension, blue tinge to vision (memory aid: little blue pill). \n- Vacuum erection devices to draw blood into the penis by applying negative pressure.\n- Intra-cavernosal injections to directly increase blood flow.\n- Penile prostheses for cases resistant to other treatments.\n\n# Contraindications and cautions of Sildenafil\n\nSildenafil, while an effective treatment for ED, has specific contraindications and requires caution in certain patients:\n\n- Contraindicated in: \n\t- Individuals taking nitrates\n\t- Hypertension/hypotension\n\t- Arrhythmias\n\t- Unstable angina\n\t- Stroke\n\t- Recent myocardial infarction.\n- Caution in:\n\t- Patients with angina\n\t- Peptic ulcer\n\t- Liver or kidney impairment\n\t- Peyronie's disease\n\t- Those on complex antihypertensive regimes\n\n\t\n# NICE Guidelines\n\n[NICE Clinical Knowledge Summary (CKS): Erectile dysfunction](https://cks.nice.org.uk/topics/erectile-dysfunction/)\n\n# References\n\n[BMJ Best Practice: Erectile Dysfunction](https://bestpractice.bmj.com/topics/en-gb/213)\n\n[British National Formulary (BNF): Sildenafil](https://bnf.nice.org.uk/drug/sildenafil.html)\n",
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"question": "A 45-year-old man visits his GP complaining of erectile dysfunction. He describes a gradual onset of symptoms, and is frustrated that while he has normal libido, he cannot maintain an erection. He has diabetes and a history of angina, for which he takes metformin and isosorbide mononitrate.\n\nWhat is the most appropriate management for his symptoms?",
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"explanation": "The presence of casts on microscopy suggests a glomerular pathology, for which a renal biopsy would be the gold standard for diagnosis.",
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"explanation": "This would be indicated to visualise the urinary bladder if red blood cells (rather than red cell casts) were seen. A cystoscopy may be paired with a US KUB or CT urogram.",
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"comment": "Painless haematuria - bladder cancer???",
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"comment": "currently, only patients older than 45 with visible haematuria not resolved by usual UTI treatment (or patients above 60 with non visible haematuria) need be referred for bladder cancer (they get a flexi cystoscopy). In this case, the patient is younger and has intermittent episodes rather than persistent haematuria so bladder cancer is further down on differentials and in any case not warranting a 2ww. ",
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"comment": "The red cell casts point to a glomerular pathology, as red cells get squeezed through the glomerulus. Bladder cancer would not present with red cell casts",
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"comment": "cut them all\n",
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"explanation": "## Summary \n\nGlomerular disease is kidney disease affecting the glomerulus. It can be classified according to its presenting clinical syndrome, eg. nephrotic or nephritic syndrome, the histological appearances, the cause or by the underlying systemic disease.\n\n|Nephritic syndrome| Nephrotic syndrome|\n|:---|:---|\n|IgA nephropathy|Minimal change disease (MCD)|\n|RPGN (rapidly progressive GN) (ANCA + vasculitis, anti-GBM)|Membranous GN|\n|Membranoproliferative GN (MPGN)|Focal segmental glomerulosclerosis (FSGS)|\n|Post-infectious GN|MPGN|\n|Henoch–Schönlein purpura (HSP)/IgA vasculitis|IgA nephropathy|\n|SLE | SLE|\n|| Diabetes|\n| |Amyloid|\n\nDiagnosis is usually made using clinical presentation, histology obtained by a kidney biopsy and immunology.\n\n**It is important to distinguish between nephritic and nephrotic syndrome in examination questions however it is often less clear cut in day to day practice.**\n\n## Nephritic syndrome\n\n### Definition\nNephritic syndrome presents with renal impairment, haematuria and non-nephrotic-range proteinuria (+/++ on the urine dipstick). There may be oliguria, with water retention and HTN.\n\n\n### Causes\n\n\nIt is important to consider the conditions that can cause a nephritic picture. These can be remembered as:\n\n\n**SHARP AIM**\n\n\n- **S**LE\n- **H**SP\n- **A**nti-GBM disease (also known as Goodpasture's disease)\n- **R**PGN\n- **P**ost-infectious GN, eg. streptococcal, infective endocarditis\n- **A**lport syndrome\n- **I**gA nephropathy (also known as Berger's disease)\n- **M**PGN\n\n### Investigations\n- Urine dipstick\n- Urine micsrocopy, looking for red-cell casts\n- Urine PCR\n- FBC, U&Es, LFT, bone profile, CRP, ESR\n- Nephritic screen: ANA (inc. dsDNA), ANCA, anti-GBM, C3/C4\n- USS kidneys, ureters and bladder (KUB)\n- Kidney biopsy\n\n## IgA nephropathy (IgAN)\n\n\n### Definition\n\n\nA type of GN characterised by IgA deposition in the mesangium. \n\nThis is the most common type of GN worldwide.\n\n\n### Cause\n\n\n- The pathophysiology is not completely understood\n- It is thought there is an increased propensity to form IgA immune complexes that are lodged in the mesangium of the glomerulus\n- IgA deposition combined with activation of the complement pathway and cytokine release leads to glomerular injury\n\n\n### Clinical features\n\n\n- Typically, patients present with recurrent gross or microscopic haematuria following **12–72 h** of an upper respiratory-tract infection or GI infection\n- It is more common in patients aged 20–30\n- Mild proteinuria may be present\n- HTN may be present\n- Rare cases may present with a nephrotic syndrome, or a rapidly progressive GN where they rapidly progress to acute renal failure\n- It can be associated with HSP/IgA vasculitis, chronic liver disease, inflammatory bowel disease (IBD) and skin and joint disorders, eg. psoriasis\n\n\n### Investigations\n\n\n- First-line investigation includes a urinalysis and MC&S:\n\t- Urinalysis is typically positive for blood ± protein; it is rare for patients to present with nephrotic-range proteinuria\n\t- Urine microscopy will usually show presence of dysmorphic red blood cells which suggests bleeding from the glomerulus\n- The gold-standard method for diagnosis is renal biopsy:\n\t- This shows diffuse mesiangial IgA immune complex deposition\n- Serum IgA is elevated in approximately 50% of patients\n\n\n### IgA nephropathy *vs* post-streptococcal GN (PSGN)\n\n\nIgAN can be differentiated from PSGN by the following features:\n\n- IgAN occurs 1–2 days post-infection *vs* 1–3 weeks post-infection in PSGN.\n- Renal biopsy in IgAN shows IgA immune-complex deposits *vs* IgG immune-complex deposits in PSGN.\n\n\n### Management\n\nThe mainstay of treatment is supportive and aimed at reducing cardiovascular risk:\n\n- Dietary salt restriction\n- Treatment of proteinuria (>0.5 g/day) with an ACE-i/ARB\n- Treatment of HTN\n\nPatients are risk stratified into those who are at low risk of progression to CKD and ESKD and those at high risk:\n\n- Those at high risk of progression are considered for treatment with corticosteroids.\n- Immunosuppresion should be offered for those who present with an RPGN.\n\n### Prognosis\n\nProgression to ESKD occurs in ~30% of patients after 10–25 years from diagnosis.\n\n## Further reading and references\n[Patient UK: Glomerulonephritis](https://patient.info/doctor/glomerulonephritis-pro)\n\n## Post-streptococcal glomerulonephritis (PSGN)\n\n### Definition\n\n\nPSGN is a type of immune-complex-mediated GN that can occur 1–3 weeks after a streptococcal upper respiratory-tract infection. It is more common in children than adults.\n\nGN can occur after other types of bacterial infection; however, PSGN or infective endocarditis are the most commonly encountered causes.\n\n\n### Cause\n\n\n- It is caused by certain strains of group A β-haemolytic streptococci.\n- Pathogenesis is not fully understood but main theories suggest that there is immune-complex deposition, neutrophil infiltration and complement activation in the glomerulus causing inflammation and/or proliferation.\n\n\n### Clinical features\n\n\n- Patients typically present with sudden onset of haematuria, oliguria, HTN and/or oedema 1–3 weeks post-infection\n- Patients may also be asymptomatic with microscopic haematuria\n\n### Investigations\n\n\n- First-line investigation includes a urinalysis and MC&S:\n\t- Urinalysis is typically positive for blood ± protein\n\t- Urine microscopy will usually show presence of dysmorphic red blood cells which suggests bleeding from the glomerulus\n- An FBC may show raised white cells, suggestive of an infective process\n- U&Es often show an AKI\n- Immunoglobulins, complement (low C3 levels commonly found) and autoantibodies (such as raised anti-streptolysin titre, raised DNAse B titre) can help support the diagnosis\n- Blood cultures are indicated in patients with fever\n- The gold-standard method for diagnosis in adults is a renal biopsy:\n\t- The classical finding is subepithelial 'humps' on electron microscopy\n\n### IgA nephropathy *vs* post-streptococcal glomerulonephritis\n\n\nPSGN can be differentiated from IgAN by the following features:\n\n- PSGN occurs 1–3 weeks post-infection *vs* 1–2 days post-infection in **IgAN**<!---Any reason for these double asterisks?-->\n- Renal biopsy in PSGN shows IgG immune-complex deposits in PSGN *vs* IgA immune-complex deposits in IgAN\n\n\n### Management\n\n\nThe infective course is usually self-limiting, and management of AKI is as per any cause of AKI.\n\n\n### Prognosis\n\n\nPrognosis following resolution of AKI is good; however, some patients may go on to develop CKD.\n\n## Infection-associated glomerulonephritis\n\nInfection-associated GN is an acute nephritis associated with infection.\n\n| Bacterial | Viral | Fungal | Parasitic |\n|:---|:---|:---|:---|\n| Streptococcal (PSGN) | Hepatitis B | Candida | Malaria |\n| Staphylococcal | EBV, CMV | | Toxoplasmosis |\n| Pneumococcal | Influenza, mumps, rubella | | Schistosomiasis | \n\n## Membranoproliferative glomerulonephritis (MPGN)\n\n### Definition\n\nMPGN is also known as mesangiocapillary GN (MCGN); it is a term used to describe the histopathological picture on kidney biopsy.\n\n### Cause\n\nThere are many causes; however, the important ones to be aware of for the MRCP exams are:\n\n- Hepatitis C\n- Mixed cryoglobulinaemia\n- Monoclonal gammopathies\n\nIt is thought to be caused by immune-complex deposition and complement activation.\n\n### Clinical features\n\nPatients more commonly present with a nephritic rather than nephrotic picture and AKI. The clue to the diagnosis will be the underlying aetiology, eg. hepatitis C.\n\n### Investigations\n\n- First-line investigations include urinalysis and MC&S:\n\t- Urinalysis is typically positive for blood ± protein\n\t- Urine microscopy will usually show presence of dysmorphic red blood cells which suggests bleeding from the glomerulus\n- An acute renal screen should be sent which may identify the underlying cause\n- The gold-standard method for diagnosis in adults is a renal biopsy:\n\t- The classical finding is a 'double contour' of the basement membrane\n\n### Management\n\nGeneral measures include supportive measures are aimed at reducing cardiovascular risk:\n\n- Dietary salt restriction\n- Treatment of proteinuria (>0.5 g/d) with ACE-i/ARB\n- Treatment of HTN\n\nIf there is an underlying cause, eg. HCV, it should be treated appropriately. In some cases of MPGN, treatment with immunosuppression might be considered.\n\n### Prognosis\n\nAround 50% of patients progress to ESKD by 10 years.\n\n## Anti-glomerular basement membrane (anti-GBM) disease \n\nAnti-GBM disease is a rare cause of RPGN; it used to be known as Goodpasture syndrome.\n\n### Cause\n\n\nAnti-GBM disease is caused by antibodies to the non-collagenous domain (NC1) of the ⍺3 chain of type IV collagen.\n\n\nThese antibodies are directed against antigens found on the GBM in the kidneys and in the lung alveoli, leading to the presentation with pulmonary–renal syndrome.\n\n### Clinical features\n\n- Haemoptysis and pulmonary haemorrhage\n- AKI, often severe and rapidly progressive, leading to renal failure\n- It is more common in males\n- There are two peaks in age of presentation: 20–30 years and 60–70 years\n\n### Investigations\n\n- Urinalysis and MC&S:\n\t- Urinalysis is typically positive for blood ± protein\n\t- Urine microscopy will usually show presence of dysmorphic red blood cells which suggests bleeding from the glomerulus\n- U&Es to assess degree of AKI and whether dialysis is indicated\n- pH to assess degree of acidosis and whether dialysis is indicated\n- CXR/CT to identify and assess the degree of pulmonary haemorrhage\n- An acute renal screen to identify the cause:\n\t- **anti-GBM** should be specifically requested for patients presenting with pulmonary–renal syndrome; this will be positive\n\t- ANCA may be positive; the patient should be managed per anti-GBM\n- Renal biopsy is the gold standard for diagnosis:\n\t- this will show focal and segmental necrotising crescents and linear IgG standing along the basement membrane\n\n\n### Management\n\n\nThe pillars of therapy in anti-GBM disease involve:\n\n\n1. Removoval of the circulating antibody:\n\t- achieved with plasma exchange which removes the pathogenic circulating antibodies. \t\n2. Immunosuppression to stop further production of antibodies:\n\t- normally achieved with high-dose oral prednisolone and cyclophosphamide.\n\t- relapse of the disease is very rare and maintenance immunosuppression is not usually indicated.\n\n### Prognosis\n\n\n- If untreated the disease is fatal\n- Patients who present with severe AKI and require dialysis have a very poor renal prognosis\n\n### References and further reading\n[Vasculitis UK: Anti-GBM](https://www.vasculitis.org.uk/about-vasculitis/anti-gbm-goodpastures-disease)\n\n## ANCA-associated vasculitis (AAV)\n\nAAV includes granulomatosis with polyangitis (GPA), eosinophilic granulomatosis with polyangitis (EGPA) and microscopic polyangitis (GPA). They are pulmonary–renal syndromes associated with positive ANCAs.\n\n#### ANCA\n\nThere are two types of circulating ANCAs: cANCA and pANCA\n\n- cANCA is named as such for producing cytoplasmic staining patterns\n\t- **cANCA** reacts with **anti-proteinase-3 (PR3)** antigens in the cytoplasm of the neutrophils\n- pANCA is so called for producing perinuclear staining patterns\n\t- **pANCA** reacts with **myeloperoxidase (MPO)** in the lysosomes of monocytes\n\n#### Granulomatosis with polyangiitis (GPA)\n\n\n- Also known as Wegners granulomatosis\n- The majority of patients with GPA are **cANCA positive (anti-PR3)**\n- GPA is characterised by upper respiratory-tract symptoms, pulmonary haemorrhage (70%), RPGN and signs of systemic vasculitis\n- Kidney biopsy shows a focal and segmental necrotising GN which is pauci-immune\n\n### Eosinophilic granulomatosis with polyangiitis (EGPA)\n\n\n- Also known as Churg Strauss\n- The majority of patients with EGPA are **pANCA positive (anti-MPO)**\n- EGPA is characterised by allergic asthma, rhinitis and eosinophilia\n- Approximately 30% have renal involvement; 50% of these present with an RPGN\n- Kidney biopsy shows a focal and segmental necrotising GN with eosinophilic infiltration\n\n\n#### Microscopic polyangiitis (MPA)\n\n\n- The majority of patients with MPA are **pANCA positive (anti-MPO)**\n- MPA is characterised by pulmonary haemorrhage (30%), RPGN and signs of systemic vasculitis\n- Kidney biopsy shows a focal and segmental necrotising GN which is pauci-immune\n\n### Management\n\nManagement is with immunosuppression and consists of an induction and maintenance phase.\n\nThe indications for dialysis are as for other causes of AKI.\n\n### References and further reading\n\n[Vasculitis UK: GPA](https://www.vasculitis.org.uk/about-vasculitis/gpa-granulomatosis-with-polyangiitis) \n[Vasculitis UK: MPA](https://www.vasculitis.org.uk/about-vasculitis/microscopic-polyangiitis) \n[Vssculitis UK: EGPA](https://www.vasculitis.org.uk/about-vasculitis/churg-strauss-syndrome)\n\n",
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"question": "A 32-year-old gentleman has three episodes of red urine that have now resolved. A urine microscopy shows red cell casts, with no white cells and no bacteria seen.\n\nWhat is the single most appropriate investigation for definitive diagnosis?",
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"explanation": "Thrombi in the venous circulation (e.g. DVTs) tend to stay within the veins and cause pulmonary emboli. In this case, the thrombus appears to have moved into the arterial circulation, causing a stroke. A reason for this could be a cardiac defect such as a patent foramen ovale, which would be detected on a bubble echocardiogram.",
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"comment": "What's this doing in paediatrics?!",
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"comment": "Congenital cardiac anomalies are a paediatric topic (since usually are detected in childhood). Sometimes they are detected late (ie. in this 29y F). That's the rationale behind their categorisation. :) ",
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"comment": "good damn question! I didn't read it properly",
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"comment": "shout out to the ox medics who have finals in less than a week, pls tell me you also got this wrong :'(",
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"comment": "Hayley Bieber had a TIA and had this bubble echo done if anyone wants a story to go with PFO! It's on her Youtube :)",
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"explanation": "# Summary\n \n\nAtrial septal defect (ASD) is a prevalent cardiac malformation caused by a hole in the septum secundum during development, leading to communication between the left and right atria. Patients may be asymptomatic, but often an ejection systolic murmur can be incidentally discovered on auscultation. ASDs are typically confirmed by echocardiogram, and management can range from conservative to surgical interventions, depending on the severity of the defect. Routine echocardiograms are employed for ongoing surveillance. Major complications can include heart failure and paradoxical embolisms.\n \n\n# Definition\n \n\nAn atrial septal defect (ASD) is a cardiac malformation where a hole exists between the left and right atria. This is commonly due to a defect in the septum secundum during cardiac embryonic development.\n \n\n# Epidemiology\n \n\nASD is a common congenital heart defect, accounting for approximately 10% of all cases of congenital heart disease. Patent foramen ovale is believed to be present in 15-35% of the adult population. The prevalence is higher in females compared to males in a 2:1 ratio. \n \n\n# Aetiology\n \n\nThe development of an ASD arises from the malformation of the septum secundum during embryonic cardiac development. The majority are idiopathic and sporadic, with no known underlying cause. \n\nRisk factors include:\n\n- Maternal alcohol consumption and smoking in the first and second trimester \n- Rubella infection during pregnancy\n- Maternal diabetes\n- Family history of secundum ASD \n- Certain syndromes (i.e. Noonan's syndrome, Down's syndrome)\n \n \n# Classification\n \n- Secundum ASD\n - A defect in the fossa ovalis \n - The **most common** form of ASD.\n- Primum ASD\n - Defect in the lower atrial wall.\n - Often accompanied by mitral valve abnormalities or part of atrioventricular septal defects (AVSD). \n- Sinus Venosus ASD\n - Associated with pulmonary vein abnormalities \n \n\n# Signs and Symptoms\n \n\n- Often asymptomatic.\n- Incidental finding of an ejection systolic murmur on auscultation, loudest on the lower-left sternal edge, due to the flow of blood through the pulmonary valve.\n- Decompensated patients may present in heart failure with signs and symptoms such as shortness of breath, fatigue, oedema, and rapid heart rate.\n- On auscultation, there may be: \n - Fixed (does not vary with respiration) split second heart sound\n - Soft systolic ejection murmur heard best at upper left sternal border \n \n\n# Differential Diagnosis\n \n\n - **Ventricular septal defect**: Characterised by a loud holosystolic murmur at the left lower sternal border, possible cyanosis, and potentially failure to thrive in infants.\n - **Patent ductus arteriosus**: Noted by a continuous \"machinery\" murmur, wide pulse pressure, and bounding pulses.\n - **Pulmonic stenosis**: Presents with a systolic murmur at the left upper sternal border, and there may be cyanosis with severe stenosis.\n \n\n# Investigations\n \n\n- ECG:\n - May be normal or show tall p waves due to right atrial enlargement \n- Chest x-ray:\n - Typically normal, but if the defect is large, cardiomegaly may be seen.\n- Echocardiogram:\n - Diagnostic investigation\n - May reveal abnormal blood flow between the atria\n- Further imaging may be done based on specialist advice (i.e. cardiac MRI) \n \n\n# Management\n \n\n - Management strategies depend on the severity of the lesion.\n - Most ASDs are managed conservatively.\n - Surgical closure of the ASD, or via a transcatheter approach, may be necessary for larger defects or those causing significant symptoms or complications.\n - Routine echocardiograms are used to monitor ASDs for changes over time.\n \n\n# Complications\n \n\n - Heart failure: typically develops in patients' twenties or thirties if the ASD is left untreated.\n - Paradoxical embolisms: this occurs when a blood clot passes from the right side of the heart to the left through an ASD, potentially leading to a stroke.\n - Migraine \n - Pulmonary vascular disease\n - Atrial fibrillation and flutter \n\n# Prognosis\n \nIf surgery is indicated, most patients will have a normal life expectancy following surgical intervention. Isolated ASDs have overall greater prognosis than when associated with additional structural defects. Poor prognosis is seen in patients who develop pulmonary vascular disease. \n\n# NICE Guidelines\n\n[NICE Guidelines on Endovascular closure of atrial septal defect](https://www.nice.org.uk/guidance/ipg96) \n \n \n# References\n \n\n [Information from the British Heart Foundation](https://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwjkhqnzrOPrAhVIe8AKHXXmAboQFjATegQIBhAB&url=https%3A%2F%2Fwww.bhf.org.uk%2F-%2Fmedia%2Ffiles%2Fpublications%2Fchildren-and-young-people%2Fc16understanding-your-childs-heart-atrial-septal-defect0213.pdf&usg=AOvVaw08EipaGMZRboeeJ9xxqbB6)\n \n [Patient Info Atrial Septal Defect](https://patient.info/doctor/atrial-septal-defect-pro)",
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"question": "A 29-year-old female has a dense left-sided hemiparesis. A CT head shows no evidence of haemorrhage, but an MRI brain shows an area of infarcted tissue. She is found to have a right-sided deep vein thrombosis and has a history of being immobilised following a tibial plateau fracture. She has never had any miscarriages and has no family history of clotting pathologies.\n\nWhich investigation is best for confirming why she has had a stroke?",
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"explanation": "Whilst trauma can cause subdural haemorrhages, the hyperdense (white) appearance suggests this is acute. Historical trauma would not account for an acute subdural haemorrhage.",
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"comment": "Chronic alcohol use over head trauma because they aren't elderly?",
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"comment": "If it was a recent head trauma, then yes it would be relevant but it was chronic so unlikely to have caused the subdural bleed",
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"comment": "'Historical' head trauma could mean that it happened a few hours ago though",
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"explanation": "\n### Summary\n\nA subdural haematoma (SDH) is a neurological condition characterized by the accumulation of venous blood between the dura mater and arachnoid mater, often following minor trauma in elderly patients. It can present with a reduced Glasgow Coma Scale (GCS), and is commonly seen in patients with fluctuating GCS. Diagnosis is typically established through a CT scan, with the appearance of the clot varying based on its age. Management strategies largely depend on the stage of the haematoma, with craniotomy indicated for acute haemorrhages, and burr holes recommended for chronic haemorrhages.\n\n### Definition\n\nA subdural haematoma is characterised by the accumulation of venous blood in the potential space between the dura mater and arachnoid mater of the brain.\n\n### Epidemiology\n\nSubdural haematomas typically occur in elderly individuals, particularly those over 65 years of age. It is often a consequence of minor trauma, leading to shearing forces that tear bridging veins between the cortex and dura mater. Risk factors include:\n\n- Advancing age (>65 years old)\n- Bleeding disorders or anticoagulant therapy\n- Chronic alcohol use\n- Trauma.\n\n### Aetiology\n\nThe haematoma results from shearing forces that tear the bridging veins between the cortex and dura mater. These forces commonly arise from minor head traumas but can also occur spontaneously in patients with bleeding disorders, anticoagulant therapy, or chronic alcohol use.\n\n### Signs and Symptoms\n\nClinical presentation of a subdural haematoma varies but may include:\n\n- Headache\n- Nausea or vomiting\n- Confusion\n- Fluctuating GCS\n- Behavioural change.\n\n\n### Differential Diagnosis\n\nDifferential diagnoses for subdural haematoma include:\n\n- Epidural haematoma: Characterized by a brief loss of consciousness, followed by a \"lucid interval\" and then rapid neurological deterioration.\n- Traumatic brain injury: Symptoms may include headache, confusion, lightheadedness, dizziness, blurred vision, or tired eyes.\n- Stroke: Presents with sudden numbness or weakness, especially on one side of the body, confusion, trouble speaking or understanding, trouble seeing in one or both eyes, and trouble walking, dizziness, or loss of balance or coordination.\n- Dementia: Gradual cognitive decline without fluctuating GCS.\n- Migraine: Recurrent headaches that might be accompanied by nausea, vomiting, and sensitivity to light and sound.\n\n### Investigations\n\nDiagnosis of a subdural haematoma is primarily established through a CT scan. \n\nThe appearance of the clot varies based on its age:\n\n- Hyperacute phase (<1 hour): The clot may appear isodense, with underlying cerebral oedema.\n- Acute phase (<3 days): The clot appears as a crescent-shaped hyperdense extra-axial collection over the affected hemisphere.\n- Sub-acute phase (3 days to 3 weeks): The clot appears more isodense compared to the adjacent cortex, making identification more difficult. Contrast-enhanced CT or MRI can aid identification. There may be associated mass effect causing midline shift and sulcal effacement.\n- Chronic phase (>3 weeks): The haematoma appears hypodense relative to the adjacent cortex.\n\n[lightgallery]\n\n[lightgallery1]\n\nFurther investigations may include:\n\n- Routine blood tests including FBC, Renal Profile, Liver Function Tests\n- Clotting profile (to assess for coagulopathy)\n\n### Management\n\nManagement of a subdural haematoma depends on the stage, patient’s premorbid baseline, and functional status. Many cases are managed conservatively, especially if there is no midline shift or cerebral oedema. However, for more severe cases, neurosurgical referral is required.\n\n- **Conservative management**: If no significant midline shift or cerebral oedema.\n\t- For patients taking the DOAC dabigatran, Idarucizumab is a licensed NICE-approval reversal agent which can be given.\n- **Surgical management**: In cases where intervention is necessary, options include:\n - **Craniotomy**: Typically for acute haemorrhages.\n - **Burr holes**: Typically for chronic haemorrhages.\n",
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"explanation": "# Summary\n\nSpinal cord compression (SCC) is a medical emergency that can lead to permanent neurological disability. It causes symptoms of weakness and sensory disturbance below the level of the compression, back pain deep and bladder and bowel involvement (incontinence, constipation or retention). Upper motor neurone signs are seen. Causes include trauma, malignancy (especially metastatic spinal cord compression), disc prolapse or compression by an abscess or epidural haematoma. An MRI of the whole spine is the key investigation. Management depends on the underlying cause; high dose steroids and referral to neurosurgery for consideration of decompression are key. \n\n\n# Definition\n\nSpinal cord compression (SCC) is a form of myelopathy caused by pressure on the cord by a variety of causes. It causes an upper motor neurone lesion, unlike the lower motor neurone signs seen in cauda equina syndrome, where compression is below the level of L1. \n\n\n# Epidemiology\n\n- Spinal cord injury affects approximately 15.4 million people globally\n- Trauma causes the most cases worldwide, with falls, road traffic accidents and violence being the most common precipitants\n- In the UK, there are around 4400 new cases of spinal cord injury per year\n- Metastatic spinal cord compression (MSCC) is the leading cause in the UK \n- In around a quarter of patients, MSCC is their first presentation of malignancy \n\n\n# Aetiology\n\n- **Trauma** - typically due to vertebral fractures or dislocation of facet joints; the cord may be severed in significant trauma\n- **Malignancy i.e. MSCC** - either due to pathological collapse of vertebrae or compression by growing tumours\n- **Infection** including abscess formation and chronic infections such as tuberculosis \n- **Epidural haematoma** where blood accumulates in the epidural space, compressing the cord\n- **Intervertebral disc prolapse** although this is much more rare than lumbar disc prolapses causing cauda equina syndrome\n\n\n\n\n# Signs and Symptoms\n\n**Symptoms include:**\n\n\n- Back pain, which is typically:\n- Severe\n- Progressive\n- Aggravated by straining e.g. coughing\n- Difficulty walking\n- Weakness below the level compressed (typically bilateral and symmetrical)\n- Numbness below the level compressed\n- Urinary or faecal incontinence\n- Urinary retention\n- Constipation\n\n\n**Signs seen (below the level of the lesion):**\n\n\n- Hypertonia\n- Hyperreflexia (although reflexes may be absent at the level compressed)\n- Clonus\n- Upgoing plantars\n- Sensory loss (a \"sensory level\")\n\n\nSymptoms and signs of an underlying cause may also be present, e.g. weight loss and fatigue in a patient with MSCC, fevers in a patient with tuberculosis. \n\n\n# Differential Diagnosis\n\n- **Transverse Myelitis** causes inflammation of the cord that presents similarly to SCC; it may be seen in the context of chronic demyelinating diseases such as Multiple Sclerosis or Neuromyelitis Optica (where other manifestations e.g. optic neuritis may be present)\n- **Cauda Equina Syndrome** is usually caused by herniation of a lumbar disc compressing the cauda equina; bowel and bladder disturbances may be present but signs are lower motor neurone (e.g. flaccid rather than spastic paralysis)\n- **Peripheral Neuropathy** also causes symptoms of weakness and sensory loss, signs are lower motor neurone rather than upper and distribution differs depending on aetiology (e.g. symptoms often unilateral in compression neuropathies)\n- **Spinal metastases** and other causes of back pain (e.g. musculoskeletal), especially if the predominant symptom is pain with minimal neurological symptoms and signs\n- **Sciatica** refers to pain in the lower back, buttocks and posterior legs caused by nerve root compression usually secondary to disc herniation in the lumbar spine; weakness can also occur but MRI will differentiate this from SCC\n\n\n# Investigations\n\nAn **MRI whole spine** is the key investigation\n\n\n- The whole spine should be imaged as there may be compression at multiple levels\n- In cases of suspected MSCC, this should be done within 24 hours as per NICE guidelines\n- Patients with suspected spinal metastases (e.g. back pain) with no neurological signs or symptoms suggestive of MSCC should have their MRI within 1 week\n\n\nIn some cases other imaging modalities may be used, e.g. **whole-body CT** in the context of major trauma. CT may also be used in patients for whom MRI is contraindicated.\n\n\nOther investigations indicated depend on the presentation and suspected aetiology:\n\n\n- Do a **bladder scan** if suspected urinary retention \n- An **ECG** and **baseline blood tests** should be done in anticipation of possible emergency surgical decompression (including a **group and save** and **clotting**)\n- In cases where MSCC is the first presentation of malignancy, further investigations are required to determine where the primary cancer is (guided by history and examination)\n- This may include further imaging e.g. a CT of the chest, abdomen and pelvis\n- Bloods may be done for tumour markers e.g. PSA in men\n- Biopsy is usually required to confirm the diagnosis\n\n# Management\n\n- Management depends on the underlying cause as well as the patient's background \n- Patients with traumatic spinal cord injuries should be transferred to a major trauma centre\n- General principles include:\n- Immobilise the patient and nurse with spinal precautions (e.g. log-rolling)\n- Regular repositioning to prevent pressure ulceration in immobile patients\n- Analgesia for pain\n- VTE prophylaxis \n- Catheterise if in urinary retention\n- Counselling and rehabilitation is key, with multidisciplinary input (e.g. physiotherapy) \n\n**Using MSCC as an example:**\n\n- Start high-dose steroids (usually 16mg dexamethasone initially) in patients with suspected MSCC - this reduces oedema helping to relieve compression\n- A proton pump inhibitor (PPI) should also be given to prevent peptic ulceration caused by steroids\n- Blood glucose should be monitored for hyperglycaemia secondary to steroids\n- Refer to neurosurgery urgently for consideration of surgical decompression (other options include vertebroplasty or kyphoplasty)\n- Patients unsuitable for surgery may have radiotherapy for spinal metastases - this can also be used as an adjuvant after surgery\n- Spinal braces may be used in patients not suitable for surgery to help with pain management and spinal stability\n- Oncology input is key both for diagnosis in patients without a known malignancy and for ongoing management (e.g. chemotherapy)\n\n\n# NICE Guidelines\n\n\n[NICE - Spinal injury: assessment and initial management](https://www.nice.org.uk/guidance/ng41/)\n\n\n[NICE - Spinal metastases and metastatic spinal cord compression](https://www.nice.org.uk/guidance/ng234)\n\n\n# References\n\n[Patient UK - Spinal Cord Compression](https://patient.info/doctor/spinal-cord-compression)\n\n\n[World Health Organisation - Spinal Cord Injury](https://www.who.int/news-room/fact-sheets/detail/spinal-cord-injury)",
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"explanation": "Given that the most likely cause here is a migraine it would be unnecessary to perform a MRI. A CT head would often be performed acutely to exclude an intercranial haemorrhage but this would not be a likely diagnosis given the overall clinical picture.",
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"comment": "When would you use sumatriptan over NSAIDs for migraine?",
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"comment": "If they have a CI including gastric ulcers/ bleeding or if it's not well controlled with NSAID/Paracetamol then GP will consider using sumatriptan along with paracetamol/NSAID to terminate an attack ",
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"comment": "it sounds like a cluster headache fromt he description , did anyone else think that ?",
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"comment": "nausea makes migraine more likely",
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"comment": "where's the cluster at g",
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"comment": "nah definitely go with triptans over NSAIDs",
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"comment": "Imagine someone tells you they're having the worst headache of their life and you whack out some ibuprofen lol",
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"comment": "Anyone that's ever had a migraine is screaming right now",
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"comment": "Would you not want to rule out meningitis and SAH?",
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"comment": "\"worst headache of his life\" and hyperacute presentation, is this not more indicative for SAH?",
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"comment": "no meningism ",
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"comment": "but it says no photophobia on exam? surely sudden 10/10 headache + nausea is more consistent with cluster?",
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"comment": "You would always rule out a SAH in this scenario before assuming its anything less sinister",
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"explanation": "# Summary\r\n\r\nMigraine is a common neurological disorder characterised by recurrent, unilateral, throbbing headaches often preceded by an aura such as visual or sensory symptoms. Migraines can last between 4-72 hours and often result in photophobia and phonophobia. Key signs and symptoms include a unilateral headache, a pulsating character, impairment or worsened by daily activities, and presence of nausea, vomiting or photophobia. Diagnosis is often based on clinical history, focusing on the presence of an aura. Management strategies include avoidance of triggers, prophylaxis with medications such as Propranolol, Topiramate or Amitriptyline, and managing acute attacks with oral triptans alongside Paracetamol or an NSAID.\r\n\r\n# Definition\r\n\r\nMigraine is a primary headache disorder characterised by intense episodes of debilitating headaches, usually unilateral and pulsating in nature. Symptoms may be preceded by an 'aura' which manifests as visual disturbances or sensory changes. The pain usually lasts from 4-72 hours and can be accompanied by nausea, vomiting, photophobia, and phonophobia.\r\n\r\n# Epidemiology\r\n\r\nMigraines are one of the most prevalent neurological disorders worldwide, affecting roughly 12% of the global population. It is more common in women, with a male to female ratio of approximately 1:3, likely related to hormonal influences. The peak incidence occurs between the ages of 30-39.\r\n\r\n# Aetiology\r\n\r\nThe exact cause of migraines is not fully understood, but it is likely a combination of genetic and environmental factors. \n\nThe triggering factors are variable and can include certain foods, changes in weather, stress, hormonal changes, and certain medications such as oral contraceptives.\r\n\r\n# Signs and Symptoms\r\n\r\n- Aura (usually visual or sensory symptoms preceding the headache)\r\n- Unilateral throbbing headache\r\n- Photophobia and phonophobia\r\n- Nausea and/or vomiting\r\n\r\nThe International Headache Society criteria for migraine without aura:\r\n\r\n| Criteria | Description |\r\n| -------- | ------------------------------------------------------------ |\r\n| A | At least five attacks fulfilling criteria B-D |\r\n| B | Headache attacks lasting 4-72 hours (untreated or unsuccessfully treated) |\r\n| C | Headache has at least two of the following four characteristics: <br>1. Unilateral location <br>2. Pulsating quality <br>3. Moderate to severe pain intensity <br>4. Aggravation by or causing avoidance of routine physical activity |\r\n| D | During headache, at least one of the following: <br>1. Nausea and/or vomiting <br>2. Photophobia and phonophobia |\r\n| E | Not better accounted for by another ICHD-3 diagnosis |\r\n\r\n# Differential Diagnosis\r\n\r\nMigraines must be differentiated from other conditions that present with severe headache. Some of these include:\r\n\r\n- Tension-type headache: Bilateral, band-like pressure or tightness, not worsened with physical activity, no associated nausea or vomiting.\r\n- Cluster headache: Severe, unilateral, orbital, supraorbital and/or temporal pain lasting 15-180 minutes, occurring up to 8 times a day, associated with autonomic symptoms like ptosis, miosis, lacrimation.\r\n- Subarachnoid hemorrhage: Sudden-onset severe headache, often described as \"the worst headache of my life\", associated with nausea, vomiting, and possible loss of consciousness.\r\n- Giant cell arteritis: New headache in a person over 50 years, scalp tenderness, jaw claudication, visual disturbances, elevated ESR and CRP.\r\n\r\n# Investigations\r\n\r\nDiagnosis is primarily clinical, based on the history and examination. \n\nA headache diary is important to help identify triggers and response to treatment.\n\nIf secondary causes of headaches are suspected, further investigations may be warranted, such as neuroimaging (MRI or CT) or blood tests (ESR, CRP for giant cell arteritis).\r\n\r\n# Acute Management\r\n\n- **Avoidance of triggers**: \n - Identify and avoid potential triggers like certain foods, stress, and poor sleep.\n- **Medications for acute attacks**: \n - **Triptans** (e.g., Sumatriptan) – avoid in patients with ischaemic heart disease.\n - **Paracetamol** or an **NSAID** (e.g., Ibuprofen) can be used in combination with triptans.\n - **Anti-emetics** (e.g., Metoclopramide)\n- **Special considerations**:\n - Female patients with migraine with aura should avoid the **combined oral contraceptive pill** due to increased risk of ischaemic stroke.\n\n# Prophylaxis\n\n- Medications:\n - **Propranolol** (contraindicated in asthma).\n - **Topiramate**.\n - **Amitriptyline**.\n - **Candesartan**.\n- Injections:\n\t- Greater Occipital Nerve Block\n\t- Botulinum Toxin Injection \n- **Newer treatments**:\n - **Rimegepant** (per NICE guidance, May 2023):\n - Used for preventing episodic migraine.\n - Suitable when at least 3 preventive treatments have failed.\n - Indicated for adults with 4-15 migraine attacks per month.\n\nRegular use of acute migraine medications (e.g., triptans, NSAIDs) more than 10-15 days per month can lead to **medication overuse headache (MOH)**.\n\nPatients should be counseled on limiting the use of acute treatments to prevent MOH.\n\n## References\r\n\r\n[Click here for NICE Clinical Knowledge Summaries on Migraines](https://cks.nice.org.uk/topics/migraine/)",
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"question": "A 19-year-old man is referred to the emergency department by his GP after he experiences 'one of the worst headaches of his life'. He describes a throbbing pain above his right eye, accompanied by severe nausea and light intolerance.\n\nObservations show:\n* Temperature 37.2 degrees celsius\n* Heart rate 76 beats/minute\n* Blood pressure 124/85mmHg\n* Respiratory rate 14 breaths/minute\n\nOn examination, he looks well although is obviously in pain. There are no focal neurological deficits, nuchal rigidity, or photophobia.\n\nGiven the most likely diagnosis, what is the most appropriate management?",
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"explanation": "Ethosuximide is usually used for generalised absence seizures, rather than tonic-clonic seizures.",
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"comment": "Why would a seizure at work be high risk? I'd argue being in a hospital to have a seizure is possible the best place to have one?",
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"comment": "Imagine having a seizure during a procedure ",
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"comment": "Yeah talking more about the risk of a seizure occurring and impacting on what is going on i.e in surgery or when doing procedures",
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"comment": "that must be a joke and it is funny!",
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"comment": "As a group, we have terrible chat ",
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"comment": "Surely you would ask if they wish to start a family \n",
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"comment": "doesn't matter if she's childbearing age = no sodium valproate",
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"comment": "What if it was a woman who did not want to have children but is of child bearing age\n",
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"comment": "its the fact it can cause teratogenicity, just cos they dont want kids they can still get pregnant",
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"comment": "Why did I read it as male 💀",
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"comment": "we're all a bit sexist :/",
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"comment": "Talking bout oui a lot, oh you speak French now ",
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"explanation": "# Summary\n\nEpilepsy is a neurological disorder characterised by an enduring predispotion to generate epileptic seizures. Affecting around 50 million people globally, it is one of the most common neurological conditions. Seizures can be either focal or generalised, with various triggers and symptoms. Differential diagnoses include syncope, transient ischemic attacks (TIA), migraines, panic disorder, and non-epileptic attack disorder (NEAD). Treatment primarily involves antiseizure medications (ASMs), tailored to the type of epilepsy, with surgery and psychological support as additional options in refractory cases. Complications include status epilepticus, psychiatric issues, and Sudden unexpected death in epilepsy (SUDEP).\n\n# Definition\n\nEpilepsy is a neurological disorder characterised by an enduring predisposition to generate epileptic seizures and the neurobiological, cognitive, psychological, and social consequences of this condition. \n\nSeizures are transient occurrences of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain. \n\n# Epidemiology\n\nEpilepsy affects approximately 50 million people worldwide, making it one of the most common neurological disorders.\n\nIt has a lifetime prevalence of 7.6 per 100 people. \n\nIncidence rates vary depending on age, with higher rates in the very young and the elderly. Both males and females are affected equally.\n\n# Aetiology\n\nThere is a strong debate amongst epileptologists regarding the classification of epilepsy syndromes by aetiology. \n\nBroadly, epilepsy syndromes can be classified into:\n\n1. Idiopathic Generalised Epilepsies (IGEs):\n\n- Childhood Absence Epilepsy\n- Juvenile Absence Epilepsy\n- Juvenile Mycolonic Epilspy\n- Generalised Tonic Clonic Seizures Alone\n\n2. Structural aetiology:\n\n- Acquired\n\t- Stroke\n\t- Trauma\n- Genetic\n\t- Malformations of cortical development \n\n3. Genetic aetiology\n4. Infectious aetiology\n4. Metabolic aetiology\n5. Immune aetiology\n6. Unknown aetiology\n\n\n# Signs and symptoms\n\nSigns and symptoms vary between focal and generalized seizures:\n\n- **Focal seizures**: \n - *With impaired consciousness ('complex')*: patients lose consciousness, usually post an aura or at seizure onset. Commonly originate from the temporal lobe, and post-ictal symptoms such as confusion are common.\n - *Without impaired consciousness ('simple')*: patients retain consciousness, experiencing only focal symptoms. Post-ictal symptoms are absent.\n - *Evolving to a bilateral, convulsive seizure ('secondary generalised')*: patients first experience a focal seizure that evolves into a generalized seizure, typically tonic-clonic.\n\n- **Generalized seizures**:\n - *Absence seizures*: brief pauses for less than 10 seconds.\n - *Tonic-clonic seizures*: characterized by loss of consciousness, stiffening (tonic), and jerking (clonic) of limbs. Post-ictal confusion is common.\n - *Myoclonic seizures*: sudden jerks of a limb, trunk, or face.\n - *Atonic seizures*: sudden loss of muscle tone, causing the patient to fall, with consciousness retained.\n\nSpecific epilepsy syndromes to note:\n\n- Temporal lobe epilepsy\n - Associated with complex partial seizures\n - Can present with initial sensory auras e.g. smelling burnt toast, feelings of deja vu or jamai vu (feeling unfamiliar in familiar surroundings), automatisms such as lip smacking\n - Patients often exhibit postictal confusion after each episode\n- Jacksonian March\n\t- A type of focal motor seizure that progressively 'marches' through adjacent areas of the brain\n\t- Typically starts in the hand or face then gradually spreads to other muscle groups following the smatotopic organisation of the motor cortex (starting from hand and spreading to arm, shoulder and face)\n\t- The seizure may progress into a generalised tonic clonic seizure\n\t- Often associated with structural brain lesions\n- Todd's Paresis\n\t- Refers to temporary postictal weakness or paralysis following a seizure\n\t- Usually lasts minutes to hours but can last up to 48 hours \n\t- Usually unilateral but can be bilateral\n\t- It is transient so the patient will reover following resolution of the postictal state\n\n\n\n# Differential diagnosis\n\nThe differential diagnosis for seizures includes:\n\n- **Syncope**: characterized by a sudden, transient loss of consciousness and postural tone followed by spontaneous recovery. Triggered by low blood flow to the brain.\n- **Transient Ischemic Attack (TIA)**: brief episodes of focal neurologic dysfunction caused by ischemia that does not cause lasting brain injury. Symptoms depend on the brain area affected.\n- **Migraines**: characterized by recurrent headaches often accompanied by a variety of symptoms such as visual disturbances (auras), nausea, vomiting, dizziness, extreme sensitivity to sound, light, touch and smell, and tingling or numbness in the extremities or face.\n- **Panic Disorder**: sudden periods of intense fear that may include palpitations, sweating, shaking, shortness of breath, numbness, or a feeling that something terrible is going to happen.\n- **Non-Epileptic Attach Disorder (NEAD)**: characterized by episodes that resemble epileptic seizures but occur without abnormal electrical activity in the brain. NEAD is often associated with psychological or emotional stress, and symptoms may include convulsions, loss of consciousness, or other seizure-like movements. Diagnosis is confirmed by video EEG monitoring, showing no seizure activity during an episode.\n\n# Investigations\n\nDiagnostic workup of epilepsy includes:\n\n- Detailed history and neurological examination\n- Collateral history and, if present, reviewing any videos of previous episodes (with the patient's consent)\n- Imaging such as CT or MRI\n- Electroencephalogram (EEG)\n\t- Video-EEG telemetry can also be considered in select cases\n- Other investigations can be considered to investigate contributory causes which include blood tests, lumbar puncture and more advanced imaging investigations.\n\n\n# Management\n\nThe goal of epilepsy treatment is to minimize seizures and optimise the patient's quality of life via a biopsychosocial model.\n\nAntiseizure medications (ASMs) remain the mainstay of treatment, with the specific drug chosen based on seizure type, patient age, comorbidities, potential side effects, and the patient's personal considerations. \n\nPrinciples of epilepsy ASM management include:\n\n- Aim for optimum quality of life through seizure control, balanced against potential side effects, particularly teratogenesis in women of childbearing age.\n- Initiation of medication may not always be appropriate after a \"provoked\" first seizure; discuss such cases with a specialist.\n- The choice of antiepileptic drugs involves complexity due to the lack of head-to-head trials comparing different medications.\n- Interactions with other medications, particularly with phenytoin and carbamazepine, should be considered.\n- Issues regarding teratogenicity, particularly with valproate, which carries a high risk of neural tube defects, should be considered. Lamotrigine is a better choice for women of childbearing age.\n\nSpecific ASMs:\n\n- According to [NICE Guidelines](https://bnf.nice.org.uk/treatment-summaries/epilepsy/#focal-seizures-with-or-without-secondary-generalisation), Lamotrigine or Levetiracetam should be considered as first-line for focal seizures. \n- Sodium valproate can be offered as first-line for myoclonic seizures in males.\n- Ethosuximide is the drug of choice for absence seizures.\n- Carbamazepine may worsen myoclonic seizures.\n\nSurgical intervention may be an option in cases where AEDs are ineffective. \n\nPsychological support is a vital part of comprehensive epilepsy management.\n\nSpecific guidance on patients presenting with a 'first fit':\n\n- Usual protocols will advise to refer to outpatient neurology following a patient's first seizure\n- Most neurologists would start an ASM after a second seizure, unless there is a specific structural cause or a second fit would be unacceptable to the patient. \n- Following a discussion regarding the risks and benefits of starting an ASM, patients are given information on reducing risks e.g. driving advice or taking showers rather than baths. \n- Patient education via leaflets or online websites are utilised heavily as part of the initial discussions and further follow up or advice is usually relayed via a dedicated epilepsy nurse\n\n# Complications\n\nComplications of epilepsy include:\n\n- **Status epilepticus**: Seizures lasting more than 5 minutes, necessitating immediate medical intervention OR more than 2 seizures within 5 minutes without returning to normal between each seizure.\n- **Psychiatric complications**: Increased risk of depression and suicide.\n- **Sudden unexpected death in epilepsy (SUDEP)**: Thought to occur due to excessive electrical activity inducing a cardiac arrhythmia and subsequent death.\n\n# Side Effects of Anti-Epileptic Drugs\n\nSide effects of common anti-epileptic drugs include:\n\n- **Topiramate**: Abdominal pain, cognitive impairment, confusion, mood changes, muscle spasm, nausea and vomiting, nephrolithiasis, tremor, weight loss.\n- **Lamotrigine**: Blurred vision, arthralgia, ataxia, diarrhoea, dizziness, headache, insomnia, rash, tremor.\n- **Carbamazepine**: Ataxia, blood disorders, blurring of vision, fatigue, hyponatraemia, skin problems.\n- **Sodium Valproate**: Ataxia, Anaemia, confusion, gastric irritation, haemorrhage, hyponatraemia, tremor, weight gain.\n- **Phenytoin**: Acne, anorexia, constipation, dizziness, gingival hypertrophy, hirsutism, insomnia, rash, tremor.\n\n# Driving Guidance\n\nThe DVLA has issued guidelines on driving with medical conditions, including epilepsy:\n\n- For car/motorbike licence: reapply after 6 months for a one-off seizure, or after 1 year for more than one seizure. After a seizure following a change in anti-epileptic medications, reapply to drive if the seizure was more than 6 months ago or you've been back on the previous medication for 6 months.\n- For bus/coach/lorry licence: reapply after 5 years for a one-off seizure if no anti-epileptic medications have been taken during this period. For more than one seizure, reapply after 10 seizure-free years during which no anti-epileptic medication has been taken.\n\nThe DVLA's complete guidelines for epilepsy and driving can be found [here](https://www.gov.uk/epilepsy-and-driving).\n\n# References\n\n[ILAE Guidelines](https://www.ilae.org/guidelines)\n\n[NICE Guidelines](https://www.nice.org.uk/guidance/ng217)\n\n[Driving Guidance on Gov.uk](https://www.gov.uk/epilepsy-and-driving)\n",
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"learningPoint": "Valproate is contraindicated in women of childbearing age due to its high risk of teratogenic effects, making levetiracetam a preferred first-line treatment for generalized tonic-clonic seizures because of its safer profile during pregnancy.",
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"question": "A 32-year-old female junior doctor is seen in a 'first fit' clinic after experiencing a generalised tonic-clonic seizure. They are awaiting further investigations, however the decision is made to start anti-epipleptic medication as the risk that a seizure at work would pose is very high. They have no known drug allergies and a past medical history of hypothyroidism.\n\nWhat would be the most appropriate medication to start?",
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"explanation": "Hepatitis C is more classically associated with chronic illness with most infected patients experiencing no acute symptoms within 6 months of infection. Hepatitis C may cause chronic liver disease, with corresponding signs such as spider naevi, ascites, caput medusae.",
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"explanation": "Hepatocellular carcinoma is unlikely to present acutely and would classically be associated with a background of chronic hepatitis B, C, or alcoholism. Constitutional symptoms such as weight loss and night sweats may be present.",
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"explanation": "Pregnant women are at increased risk of contracting acute HEV infection after eating raw or undercooked meat, especially pork. These patients are at higher risk of developing severe complications including fulminant acute liver failure which can be fatal.",
"id": "10015786",
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"explanation": "This is a sensible differential however the vignette points towards an infective picture with the recent BBQ. Pork in particular is a major reservoir of HEV. In addition, most cases would be unlikely to cause such a severe presentation.",
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"explanation": "Hepatitis A normally runs a self-limiting course. It is unlikely to cause such a severe clinical picture.",
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"comment": "didnt understand why but based on questions in terms of acute viral hepatitis causes\n\nforeign travel= hep A\noverall most common= hep A\n\npregnant=hepE\npork=hepE\nBBQ=hepE",
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"comment": "wow this hit hard...",
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"comment": "This is why pork is haram kids\n",
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"comment": "mashallah brother \n",
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"comment": "Way to remember it: hepatitis E in pregnancEE",
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"comment": "I cooked the chicken",
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"comment": "this is so sad .. ",
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"comment": "\"Pigs sleep and root in sh*t, that's a filthy animal. I don't eat nothin' that ain't got sense enough to disregard its own feces.\"",
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"comment": "Hepatitis E for enormous belly (pregnancy)",
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"comment": "well that took a turn....",
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"explanation": "### Summary\n\nHepatitis means inflammation of the liver and may be caused by a range of infectious and non-infectious aetiologies.\n\nAll infectious hepatitis cases are notifiable diseases in the UK.\n\nThe most common causes of viral hepatitis in the UK are hepatitis A, B and C viruses. These can all cause acute disease, but HBV and HCV can also cause chronic infection. The latter can lead to liver fibrosis and hepatocellular carcinoma.\n\nOther causes of viral hepatitis include:\n\n- Hepatitis D Virus (can cause chronic hepatitis)\n- Hepatitis E Virus\n- CMV\n- EBV\n- Adenovirus\n\nClinical Features:\n\n- Malaise and fatigue\n* Nausea and vomiting\n* Right upper quadrant pain\n* diarrhoea (may have pale stools and dark urine)\n* Jaundice\n* Hepatomegaly\n* Splenomegaly and lymphadenopathy\n* Liver failure: characterised by hepatic encephalopathy, jaundice, ascites and abnormal clotting.\n* Other causes of acute hepatitis include drugs, toxins, alcohol, EBV, CMV, hepatitis E, leptospirosis, and malaria.\n\n### Hepatitis A\n\n- Virus type and transmission route\n\t* RNA picornavirus, transmitted by the faecal-oral route (occasionally through food sources or through anal sex)\n- Epidemiology of Hepatitis A\n\t- Prevalence is high in developing countries.\n\t- Increasing age is the only fundamental determinant of disease severity, with the most significant morbidity and mortality in those over 50 years old.\n\t- Travelers and those at risk can be offered immunisation\n- Presentation of Hepatitis A\n* Flu-like symptoms followed by jaundice, pale stools (in some), dark urine and abdominal pain.\n* Incubation period of 2-6 weeks\n* Complete recovery can take up to 6 months.\n- Investigations of Hepatitis A:\n\t- IgM and IgG antibodies to HAV.\n- Management of Hepatitis A\n\t- Management is largely supportive\n\n### Hepatitis B\n\n- Virus type\n\t- dsDNA virus of the Hepadnaviridae family\n- Hepatitis B Virus Epidemiology\n\t- The most common cause of hepatitis globally\n\t- High prevalence regions include sub-Saharan Africa, Asia and the Pacific Islands.\n\t- The disease is declining in children and adolescents in the UK due to routine vaccination\n- The incubation period is usually 60-90 days.\n- Hepatitis B Virus transmission\n\t* Transmission is via infected blood or body fluids\n\t* Vaginal/anal intercourse\n\t* Transfusion\n\t* Vertical transmission (in 90% of pregnancies where the mother is HBeAg positive, and 10% where this is negative).\n\t* In developing countries, infection is mostly in childhood through vertical or horizontal transmission. In areas of low endemicity (such as the UK), infections are mostly acquired in adulthood.\n* Hepatitis B Infection features\n\t* Only 5% of children have jaundice and severe symptoms, but the majority cannot clear the infection and develop chronic disease.\n\t- 30-50% of adults experience jaundice, fever, malaise, darkening of urine and lightening of stool. Some develop fulminant liver failure with decompensation (ascites, encephalopathy etc.). The risk of developing chronic disease is low (<5%).\n- Serology of Hepatitis B (**See detailed section below**)\n\t- HBsAg is detected 3-5 weeks after infection. If present for >6 months, this defines carrier status (5-10% of infections).\n\t- In carriers, HBeAg-positive patients are the most infectious.\n\t- If HBeAg-negative (and anti-HBe-antibody positive), they have lower infectivity.\n\t- Antibodies to HBsAg (anti-HBs) indicate previous vaccination\n\t- Antibodies to hep B core antigen (anti-HBc) indicate past infection.\n\t- Patients with chronic infection who are HBeAg -ve may have an immune escape phase when the virus mutates despite anti-HBe antibodies being present. These patients are the main pool for the spread in the UK, so all chronically infectious patients need yearly screens to identify this.\n\t- Patients with acute infection have raised IgM to HBcAg, which is negative in chronic infection.\n- Management of Hepatitis B\n\t- Only adults who are HBsAg-positive, have compensated liver disease, are pregnant or are of a young age may be referred for treatment\n\t- Peginterferon alfa-2a is the first line, with tenofovir and entecavir as second-line alternatives.\n\n### Hepatitis B Serology Interpretation\n\t\n\n#### I. Hepatitis B Surface Antigen (HBsAg)\n\nThis is the first detectable viral antigen in the course of infection and is a marker of active infection.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| Positive | Possible acute or chronic Hepatitis B infection |\n| Negative | No active Hepatitis B infection |\n\n#### II. Hepatitis B Surface Antibody (anti-HBs)\n\nThis is an antibody produced by the immune system in response to the Hepatitis B surface antigen. It confers immunity against HBV.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| Positive | Immunity to Hepatitis B (due to past infection or vaccination) |\n| Negative | No immunity to Hepatitis B |\n\n#### III. Hepatitis B Core Antigen (HBcAg)\n\nThis antigen is not detectable in the blood but triggers the production of core antibodies.\n\n#### IV. Hepatitis B Core Antibody (anti-HBc)\n\nIt can be present in both acute and chronic infection. IgM anti-HBc appears early in the infection and indicates a recent infection. IgG anti-HBc remains indefinitely and indicates past exposure.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| IgM Positive | Acute or recent Hepatitis B infection |\n| IgG Positive | Past Hepatitis B infection or chronic infection |\n\n#### V. Hepatitis B e Antigen (HBeAg)\n\nThis is a marker of high replicative activity, indicating a high degree of infectivity.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| Positive | High level of Hepatitis B replication; high infectivity |\n| Negative | Lower levels of Hepatitis B replication; lower infectivity |\n\n#### VI. Hepatitis B e Antibody (anti-HBe)\n\nIt appears after the clearance of HBeAg and indicates lower infectivity.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| Positive | Lower level of Hepatitis B replication; lower infectivity |\n| Negative | Higher levels of Hepatitis B replication; higher infectivity |\n\n#### VII. Hepatitis B DNA (HBV DNA)\n\nThis test measures the amount of Hepatitis B viral load in the blood.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| Positive | Active Hepatitis B replication |\n| Negative | No active Hepatitis B replication |\n\n#### VII. Hepatitis B DNA (HBV DNA)\n\nThis test measures the amount of Hepatitis B viral load in the blood.\n\n| Result | Interpretation |\n| ------- | -------------- |\n| Positive | Active Hepatitis B replication |\n| Negative | No active Hepatitis B replication |\n\n#### Summary\n\nBelow is a table summarizing the serological patterns associated with different stages of Hepatitis B infection:\n\n\n| Status/Marker | HBsAg | anti-HBs | IgM anti-HBc | IgG anti-HBc | HBeAg | anti-HBe | HBV DNA |\n| ------------- | ------- | --------- | ------------ | ------------ | ------- | --------- | ------- |\n| Acute HBV Infection with Immunity | Positive | Negative | Positive | Positive | Positive | Negative | Positive |\n| Chronic HBV Infection | Positive | Negative | Negative | Positive | Positive/Negative | Positive/Negative | Positive/Negative |\n| Immune due to Natural Infection | Negative | Positive | Negative | Positive | Negative | Positive | Negative |\n| Immune due to Hepatitis B Vaccination | Negative | Positive | Negative | Negative | Negative | Negative | Negative |\n\n\n\n\n### Hepatitis C\n\n- Virus type\n\t- RNA virus of the Flaviviridae family, with six major genetic types (genotypes 1 and 3 are most common in the UK, and genotype one is associated with more prolonged treatment and worse prognosis).\n- Hepatitis C Virus transmission\n\t- Transmitted via exchange of blood (the vast majority) and bodily fluids:\n\t* Intravenous drug use\n\t* Blood transfusion\n\t* Haemodialysis (rare in the UK)\n\t* Sexual transmission (less than 1% per year of relationship, but rate higher if co-infected with HIV)\n\t* Needlestick injuries in healthcare facilities - 3% risk of transmission.\n\t* Perinatal infection from infected mother.\n* Incubation period of 6-9 weeks.\n* Natural history of Hepatitis C:\n\t- Most infections are asymptomatic\n\t- Only 15-25% clear the virus; 75% go on to develop chronic infection\n\t- Patients with chronic infection have persistently high LFTs\n\t- Cirrhosis develops in 20-30%.\n\t- 1-4% of patients with cirrhosis develop hepatocellular carcinoma, and 2-5% develop liver failure.\n- Investigations of Hepatitis C\n\t- Anti-HCV serology - 90% are positive three months after infection, but it may take many months to become positive for some.\n\t- HCV RNA - if positive for more than two months, it needs to be treated.\n- Management of Hepatitis C\n\t- Symptomatic treatment in the early stages of the disease\n\t- Drug therapy should be considered for all patients and depends on the genotype of the virus. Nucleoside analogues are generally preferred, e.g. Sofosbuvir, and often lead to undetectable viral loads\n\t- Antivirals have a proven benefit in basically every patient, irrespective of the amount of cirrhosis and fibrosis\n\t- Manage any underlying cirrhosis\n\n### Hepatitis D\n\n- Virus type:\n\t- RNA virus\n- Hepatitis D viral transmission:\n\t- Infected blood products\n\t- Intravenous drug use\n\t- Sexual intercourse\n- Hepatitis D only occurs as a superinfection in patients with concurrent hepatitis B infection; consider this as a differential in a patient with established hepatitis B who has a sudden deterioration in hepatic function/decompensated liver disease.\n- Investigation in Hepatitis D:\n\t- Hepatitis D (IgM, IgG) antibody test\n- Management:\n\t- Pegylated interferon-alpha (low success rates)\n- Prevention:\n\t- No hepatitis D vaccination is available\n\t- Hepatitis B vaccination may be preventative (the patient needs to develop hepatitis B first to then develop hepatitis D).\n\n### Hepatitis E\n\n- Virus type:\n\t- Single-stranded RNA virus\n- Hepatitis E viral transmission:\n\t- faecal-oral transmission\n\t- Contaminated food\n\t\t- Classically transmitted through undercooked pork and seafood\n\t- Vertical transmission\n- Incubation period of 2-9 weeks\n- Endemic regions include Asia, the Middle East, Africa, and Central America\n- Pregnant women are at risk of severe disease; may develop fulminant hepatitis.",
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"explanation": "While this may be useful in the context of symptoms suggestive of diabetes mellitus, it is not the single most important investigation here in view of the likely pancreatic cancer.",
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"comment": "Only differential I had was lymphoma",
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"comment": "Where does it talk about his new onset diabetes?? ",
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"comment": "Pancreatic cancer can cause obstruction of the pancreatic duct, leading to autodigestion of the pancreas and thus *drum roll* diabetes. These questions make sense, but only with hind sight. I was staring at this with my jaw dropped ngl\n",
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"comment": "According to NICE Guidelines, a fasting blood glucose level of 7.0 mmol/L (126 mg/dL) or higher is diagnostic for diabetes.",
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"comment": "got the question right but the described location of lymphadenopathy is rubbish. Should be left supraclavicular",
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"comment": "I think it's not lymphadenopathy since it's painful. The swelling is thrombophlebitis",
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"comment": "I genuinely thought the arm swelling was on the outside aspect of his arm, like a lump on the top of his deltoid or something. Never imagined they were talking about lymphadenopathy lol",
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"question": "A 75 year old man with no previous medical history presents with 7 kg of weight loss over the last three months. He has a tender palpable swelling in his left arm. He says that he has noticed a few similar swellings over the past few months. He appears jaundiced. His recent fasting blood glucose was 7.0 mmol/lL (normal range 3.5-5.5 mmol/L).\n\nWhich of the following investigations is most likely to reveal the underlying diagnosis?",
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"explanation": "This would be useful in treating Addison's disease, which can cause hypotension and dizziness, but not the diarrhoea or murmur. There are no other autoimmune features or skin pigmentation mentioned which would make this diagnosis more likely.",
"id": "10015797",
"label": "b",
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"explanation": "This presentation is consistent with carcinoid syndrome, due to serotonin production from a tumour. The symptoms of carcinoid syndrome include diarrhoea, flushing, hypotension, and predominantly right sided heart murmurs, which are consistent with the symptoms described in the scenario.",
"id": "10015796",
"label": "a",
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"explanation": "This presentation is not consistent with coeliac disease.",
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"explanation": "Infective endocarditis is not an unreasonable differential, however the lack of a fever or risk factors for bacterial endocarditis make this less likely.",
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"comment": "is the murmur bc carcinoid tumours cause pulmonary htn therefore tricuspid regurg?",
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"comment": "from what i believe its that the hepatic metastases may result in direct exposure of the heart to serotonin, which induces plaque-like deformities on the tricuspid valve, and in turn induces valve regurgitation",
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"explanation": "# Summary\n\nCarcinoid tumours are rare, slow-growing neural crest tumours that secrete serotonin. They originate from neuroendocrine tissue commonly in the appendix and small intestine. Key symptoms may include abdominal pain, diarrhoea, flushing, wheezing, and pulmonary stenosis. Diagnosis typically involves assessment of hormone levels, imaging studies, and tissue biopsy. Management strategies primarily include pharmacological therapy, such as Octreotide to inhibit tumour products, and surgical resection when feasible.\n\n# Definition\n\nCarcinoid tumours are a type of neuroendocrine tumour that are typically slow-growing and can potentially become malignant. They often originate in the appendix and small intestine, with approximately 5-10% of these tumours secreting hormones, notably serotonin.\n\nThis is different to **carcinoid syndrome,** which is when the presence of liver metastases impair hepatic excretion of serotonin during first pass metabolism resulting in increased serotonergic symptoms.\n\n# Epidemiology\n\nCarcinoid tumours are relatively rare. They account for less than 1% of all malignancies. The incidence is approximately 1-2 cases per 100,000 people per year.\n\n# Aetiology\n\nCarcinoid tumours are tumours of neuroendocrine cells, which are distributed throughout the body and are concentrated in areas such as the gastrointestinal tract and lungs.\n\n# Signs and Symptoms\n\nPatients with carcinoid tumours may present with:\n\n- Abdominal pain\n- Diarrhoea\n- Flushing\n- Wheezing\n- Pulmonary stenosis\n\nThese symptoms are primarily due to the effects of serotonin and its breakdown products on the systemic circulation. Patients with gastrointestinal carcinoid tumours usually only experience these symptoms if they have liver metastases, which allow tumour products to enter the systemic circulation without first undergoing metabolism in the liver.\n\n# Differential Diagnosis\n\nThe main differential diagnoses include:\n\n- Irritable Bowel Syndrome (IBS): Characterised by abdominal pain, bloating, and altered bowel habits.\n- Inflammatory Bowel Disease (IBD): Manifests with abdominal pain, diarrhoea, and possible systemic symptoms such as weight loss and fatigue.\n- Mastocytosis: This condition can cause flushing, abdominal pain, diarrhoea, and wheezing, similar to carcinoid syndrome.\n\n# Investigations\n\nKey investigations for carcinoid tumours include:\n\n- Hormone level assessment: Measuring the level of 5-HIAA (5-hydroxyindoleacetic acid), a breakdown product of serotonin, in the urine can help identify carcinoid tumours.\n- Imaging: CT, MRI, or Octreotide scans can help identify the location and extent of the tumour.\n- Tissue biopsy: A definitive diagnosis is made through histopathological examination of biopsy material.\n\n# Management\n\nTreatment for carcinoid tumours can involve:\n\n- Pharmacological treatment: Octreotide, a somatostatin analogue, is often used to inhibit the production of hormones by the tumour.\n- Surgery: Resection of the tumour can be considered to alleviate symptoms and prevent further growth or metastasis.\n- Other treatments such as embolisation, radiofrequency ablation, or chemotherapy may be considered based on the individual patient's clinical condition and extent of disease.\n\n# References\n\n[NHS conditions - Carcinoid syndrome](https://www.nhs.uk/conditions/carcinoid-syndrome/)",
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"explanation": "In the first instance, weight loss, avoiding large meals,avoiding acidic/spicy foods, avoiding caffeine/alcohol, and quitting smoking should be implemented along with a proton pump inhibitor or H2 blocker.",
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"explanation": "# Summary\n\nA hiatus hernia is a medical condition where abdominal contents protrude through an enlarged oesophageal hiatus in the diaphragm. There are two main types: sliding, which makes up 80% of cases and rolling, which makes up the remaining 20%. The condition is primarily diagnosed through barium swallows, endoscopy, and oesophageal manometry. Management strategies range from lifestyle changes to medication and surgery in severe cases. \n\n# Definition\n\nA hiatus hernia is a medical condition that occurs when abdominal contents protrude through an enlarged oesophageal hiatus in the diaphragm.\n\n# Epidemiology\n\nThe prevalence of hiatus hernia increases with age and is more common in individuals with certain risk factors.\n\nRisk factors for hiatus hernia include:\n\n- Obesity\n- Prior hiatal surgery\n- Increased intra-abdominal pressure, such as from chronic cough, multiparity, or ascites\n\n# Aetiology\n\nThere are two main types of hiatus hernias:\n\n1. **Sliding hiatal hernia** (80%): Here, the gastro-oesophageal junction slides up into the chest. This results in a less competent sphincter and consequent acid reflux. Treatment is similar to Gastroesophageal reflux disease (GORD).\n2. **Rolling hiatal hernia** (20%): In this type, the gastro-oesophageal junction stays in the abdomen, but part of the stomach protrudes into the chest alongside the oesophagus. This type requires more urgent treatment since volvulus can lead to ischemia and necrosis.\n\n[lightgallery1]\n\n# Signs and Symptoms\n\nSymptoms of a hiatus hernia include:\n\n- Heartburn\n- Dysphagia\n- Regurgitation\n- Odynophagia\n- Shortness of breath\n- Chronic cough\n- Chest pain\n\n# Differential Diagnosis\n\nConditions to consider in the differential diagnosis of hiatus hernia include:\n\n- Gastroesophageal reflux disease (GORD): Heartburn, regurgitation, difficulty swallowing\n- Gastritis: Abdominal pain, nausea, vomiting\n- Peptic ulcer: Abdominal pain, bloating, feeling of fullness\n- Gallstones: Severe abdominal pain, jaundice, fever\n\n# Investigations\n\nHiatus hernias can be diagnosed using:\n\n- **Barium swallows** (upper GI series), which is the most sensitive method\n- **Endoscopy**\n- **Oesophageal manometry**\n\n[lightgallery]\n\n# Management\n\nManagement of hiatus hernia involves a combination of conservative, medical, and surgical strategies.\n\n## Conservative management\n\nConservative management involves lifestyle changes such as:\n\n- Weight loss\n- Elevating the head of the bed\n- Avoidance of large meals and eating 3-4 hours before bedtime\n- Avoidance of alcohol and acidic foods\n- Smoking cessation as nicotine relaxes the lower oesophageal sphincter. Other substances and medications that can relax the lower oesophageal sphincter include chocolate, peppermint, caffeine, fatty foods, and medications such as calcium-channel blockers, nitrates, and beta-blockers\n\n## Medical management\n\nMedical management involves the use of proton pump inhibitors (PPIs) for 4-8 weeks before assessing response.\n\n## Surgical management\n\nSurgical management includes Nissen's fundoplication in cases of medication-resistance or patient preference. This procedure involves closing the defect by tightening the crura and wrapping the gastric fundus around the lower oesophageal sphincter. Urgent surgery is required in the presence of haemorrhage, volvulus, ischaemia, necrosis or obstruction.",
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"comment": "Why does costochondritis, cause ECG changes? ",
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"__typename": "QuestionComment",
"comment": "it.... doesn't",
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"comment": "Why I am seeing ST elevation in V1-2 and T wave inversion?",
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"comment": "There is no st elevation. T wave inversion is normal in right leads so V1 and AVR and will almost always have it. In Afro Caribbean’s it can be normal V1-3 (obvs use clinical context though) ",
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"__typename": "QuestionComment",
"comment": "Actually never mind I see the possible st elevation but the t wave inversion point still stands ",
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"comment": "The ST elevation in V1-2 isnt significant enough to be counted as such - would need to be at least 2 small squares to be considered elevation in precordial leads (V1-6) ",
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"comment": "Is anyone else seeing ST elevation or is it just me?",
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"comment": "ST elevation in leads V1-2 ",
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"comment": "don't think its high enough to be considered true ST elevation :)",
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"comment": "STEMI criteria: 1 mm ST elevation in at least 2 contiguous leads except in V2-V3 where the cutoff is >2.5mm in men under 40, >2mm in men over 40 and 1.5mm in women. Don't think he quite makes the cutoff",
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"comment": "tbh don't think there is ST elevation BUT in young, fit men you might see benign ST elevation. It's pretty normal",
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"comment": "tbh don't think there is ST elevation BUT in young, fit men you might see benign ST elevation. It's pretty normal",
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"comment": "Must be my gran having a faff about in V4 my bad",
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"comment": "would there not be signs of hypertrophy in V2-V3?",
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"comment": "is their rhythm irregularly irregular??",
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"comment": "some people just ain't built for the grind. stay hard",
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"comment": "Maybe it was leg day? How do you know it's chest day ffs",
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"explanation": "# Summary\r\n\r\nAcute coronary syndrome (ACS) refers to a set of symptoms and signs that occur due to reduced blood flow to the heart at rest. It encompasses 3 distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). In the case of infarction, this is a medical emergency requiring urgent treatment. ACS is most commonly caused by the rupture of atherosclerotic plaques in coronary arteries leading to further narrowing, and potentially complete occlusion, of these critical blood vessels. Diagnosis involves clinical evaluation, ECGs, and troponin levels. Treatment strategies differ for STEMI and NSTEMI/unstable angina but include oxygen therapy if hypoxic, antiplatelet medication, glyceryl trinitrates, morphine, and percutaneous coronary intervention (PCI). Post-MI management includes aspirin, dual antiplatelet therapy, beta-blockers, ACE inhibitors, high-dose statins, and cardiac rehabilitation. There are many complications to be aware of post-ACS and these include arrhythmias, heart failure, and cardiac tamponade, and others.\r\n\r\n# Definition \r\n\r\nAcute coronary syndrome is a set of symptoms and signs that occur due to decreased blood flow to the heart at rest. It broadly refers to three distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI). \r\n\r\n# Epidemiology \r\n\r\nIn the UK, there are over 80,000 hospital admissions due to ACS every year. Coronary artery disease remains the largest cause of death in the UK. \r\n\r\n# Pathophysiology\r\n\r\nCoronary artery disease refers to the narrowing of coronary arteries by atherosclerosis and plaque formation. In stable angina, when the demand for myocardial oxygen increases with exertion, narrowed coronary arteries cannot meet this increased demand leading to myocardial ischaemia and pain. Conversely, in ACS, the symptoms occur at rest. This is because there is sudden plaque rupture and clot formation in the narrowed coronary arteries. If there is partial occlusion of the coronary artery this leads to ischaemia and chest pain at rest (unstable angina). If the coronary artery becomes more occluded or fully occluded this leads to significant hypoperfusion of the myocardium and ultimately leads to infarction (death) of the myocardial tissue (NSTEMI or STEMI). \r\n\r\n# Risk Factors\r\n\r\nCoronary artery disease and the development of plaques can be attributed to non-modifiable and modifiable risk factors. Modifiable risk factors must be addressed in the management of IHD. \r\n\r\n* Non-modifiable:\r\n * Age\r\n * Male sex\r\n * Family history\r\n * Ethnicity (particularly South Asians)\r\n* Modifiable:\r\n * Smoking\r\n * Hypertension\r\n * Hyperlipidaemia\r\n * Hypercholesterolaemia\r\n * Obesity\r\n * Diabetes\r\n * Stress\r\n * High fat diets\r\n * Physical inactivity\r\n\r\n# Classification \r\n\r\nAcute coronary syndrome can be split up into three distinct diagnoses: \r\n\r\n1. **Unstable angina**: caused by partial occlusion of a coronary artery. Troponin negative chest pain with normal/abnormal ECG signs. \r\n2. **Non-ST Elevation Myocardial Infarction**: caused by severe but incomplete occlusion of a coronary artery. Troponin positive chest pain without ST elevation. \r\n3. **ST-Elevation Myocardial Infarction**: caused by complete occlusion of a coronary artery. Troponin positive chest pain with ST elevation on ECG. \r\n\r\n*Myocardial Ischaemia vs. Myocardial Infarction and the Release of Troponin*\r\n\r\nIt is important at this stage to distinguish between angina (stable angina is on exertion and unstable angina is at rest) and myocardial infarction. Angina refers to myocardial ischaemia that causes chest pain but does not lead to the death of myocardial tissue and does not lead to a troponin rise. In myocardial infarction, the hypoperfusion of the myocardium is so profound that it leads to the death of myocardial tissue. It is when there is myocardial tissue death that troponin is released into the bloodstream and a troponin rise is found on blood tests.\r\n\r\n*Type 2 Myocardial Infarction* \r\n\r\nIt is also important to mention that some patient may have myocardial infarctions due to cardiac hypoperfusion for other reasons (e.g. severe sepsis, hypotension, hypovolaemia or coronary artery spasm). These are usually termed type 2 myocardial infarctions and may not require the conventional treatment outlined below. \r\n\r\n# Symptoms and Signs\r\n\r\n* Chest pain - the classical presentation can be considered in terms of the SOCRATES mnemonic:\r\n * Site - Central/left sided\r\n * Onset - Sudden\r\n * Character - Crushing ('like someone is sitting on your chest')\r\n * Radiation - Left arm, neck and jaw\r\n * Associated symptoms - Nausea, sweating, clamminess, shortness of breath, sometimes vomiting or syncope\r\n * Timing - Constant\r\n * Exacerbating/relieving factors - Worsened by exercise/exertion and may be improved by GTN\r\n * Severity - Often extremely severe\r\n* Atypical presentations may include:\r\n * Epigastric pain\r\n * No pain (more common in elderly and **patients with diabetes**):\r\n * Acute breathlessness\r\n * Palpitations\r\n * Acute confusion\r\n * Diabetic hyperglycaemic crises\r\n * Syncope\r\n\r\n# Differential Diagnoses\r\n\r\nIt is important to remember that there are non-MI causes of chest pain and these should be considered when making a diagnosis:\r\n\r\n* Cardiac\r\n * Myocarditis\r\n * Pericarditis\r\n * Cardiomyopathy\r\n * Valvular disease\r\n * Cardiac trauma\r\n* Pulmonary\r\n * PE\r\n * Pneumonia\r\n * Pneumothorax\r\n* Vascular\r\n * Aortic dissection\r\n* GI\r\n * Oesophageal spasm\r\n * Oesophagitis\r\n * Peptic ulcer\r\n * Pancreatitis\r\n * Cholecystitis\r\n* MSK\r\n * Rib fracture\r\n * Costochondritis\r\n * Muscle injury\r\n * Herpes zoster\r\n\r\n# Diagnosis of ACS \r\n\r\nDiagnosis depends on a combination of clinical, ECG and biochemical findings which helps distinguish between the various types of ACS.\r\n\r\n* Unstable angina - cardiac chest pain at rest + abnormal/normal ECG + **normal troponin**.\r\n* NSTEMI - cardiac chest pain at rest + abnormal/normal ECG (but not ST-elevation) + **raised troponin**\r\n* STEMI - cardiac chest pain at rest + **persistent ST-elevation/new LBBB** (note that there is no need for a troponin in this case).\r\n\r\n## Diagnosis of STEMI\r\n\r\n* ST segment elevation **>2mm** in adjacent chest leads\r\n* ST segment elevation **>1mm** in adjacent limb leads\r\n* New left bundle branch block (LBBB) with chest pain or suspicion of MI\r\n\r\n## Diagnosis of NSTEMI\r\n\r\nDiagnosis of NSTEMI requires two of the following:\r\n\r\n* Cardiac chest pain\r\n* Newly abnormal ECG which does not demonstrate ST-elevation e.g. ST depression, T wave inversion or non-specific changes. \r\n* Raised troponin (with no other reasonable explanation)\r\n\r\n# Investigations\r\n\r\n## Bedside \r\n\r\n* ECG \r\n\t* Looking for ST-elevation, LBBB or other ST abnormalities\r\n\t* This is the most important investigation and should not be delayed for other investigations (e.g. bloods) because this will define immediate management.\r\n\t* If an ECG shows STEMI then troponin is essentially irrelevant and the patient requires immediate treatment.\r\n\r\n## Bloods \r\n\r\n* Troponin: performed **at least 3 hours** after pain starts. It will also need to be repeated (usually 6 hours after the first level) in order to demonstrate a dynamic troponin rise. \r\n* Renal function: good renal function is required for coronary angiogram +/- PCI due to the use of contrast. \r\n* HbA1c and lipid profile: looking for modifiable risk factors for coronary artery disease. \r\n* FBC and CRP - rule out infectious causes of chest pain\r\n* D-dimer - may be used in _appropriate_ patients to rule out PE. *Be very careful about who you do a D-dimer on!*\r\n\r\n## Imaging \r\n\r\n* CXR: should be completed in all those presenting with a chest symptoms. It will help to rule out other causes of chest pain (e.g. pneumothorax) and look for complications of a large MI (e.g. pulmonary oedema in acute heart failure). \r\n\r\n# ECG Interpretation - Cardiac Territories and Affected Vessels\r\n\r\nThe importance of a 12-lead ECG is that it allows one to view electrical activity of the heart from different \"views\". In MI (particularly STEMI) this allows you to understand which territory (and therefore which vessel) is being affected.\r\n\r\n| Location of ST elevation | Area of myocardium | Coronary artery |\r\n| -------------------------- | ------------------ | -------------------- |\r\n| II, III, aVF | Inferior | RCA |\r\n| V1-2 | Septal | Proximal LAD |\r\n| V3-4 | Anterior | LAD |\r\n| V5-6 | Apex | Distal LAD/ LCx/ RCA |\r\n| I, aVL | Lateral | Lcx |\r\n| V7-V9 (ST depression V1-3) | Posterolateral | RCA/ LCx |\r\n\r\n\r\nRCA: right coronary artery, LAD: left anterior descending, LCx: Left circumflex\r\n\r\n[lightgallery]\r\n\r\n[lightgallery2]\r\n\r\n[lightgallery3]\r\n\r\n[lightgallery4]\r\n\r\n\r\nNSTEMIs may also show T wave abnormalities (such as ST depression and T wave inversions) in vascular territories as above. However, changes can also often not include all the specific leads of that territory in an NSTEMI.\r\n\r\n# Troponin Interpretation\r\n\r\nTroponin is a myocardial protein that is released into the bloodstream when cardiac myocytes are damaged. Serum levels typically rise **3 hours** after myocardial infarction begins.\r\n\r\nDifferent hospitals have differing guidelines (and assays) for interpretations of results. In general there are three groups of troponin levels:\r\n\r\n* Low - definitely no myocardial cell death. The patient is not having an MI although they may be experiencing unstable angina.\r\n* Mildly raised - This is an equivocal result and may be due to other non-MI related factors (see below). These patients usually need a <u>6-12 hour repeat test</u>.\r\n * If repeat troponin is raised on the repeat they are having an MI.\r\n * If repeat troponin is stable or falling then they are unlikely to be having an MI.\r\n* Definitely raised with sequential dynamic troponin rises - MI confirmed (be aware of the possibility of a Type 2 MI)\r\n\r\n## Non-ACS causes of a raised troponin\r\n\r\nAlthough troponin is often used diagnose myocardial infarction, there are in fact many causes of a raised troponin:\r\n\r\n* Myocardial infarction\r\n* Pericarditis\r\n* Myocarditis\r\n* Arrythmias\r\n* Defibrillation\r\n* Acute heart failure\r\n* Pulmonary embolus\r\n* Type A aortic dissection\r\n* Chronic kidney disease\r\n* Prolonged strenuous exercise\r\n* Sepsis\r\n\r\nIt is therefore critical to have good clinical grounds to test a troponin in order to avoid unnecessary treatments and investigations.\r\n\r\n# Management\r\n\r\nAcute management depends on the type of acute coronary syndrome. It is broadly split into the management of STEMI and the management of NSTEMI/unstable angina. \r\n\r\n# Management of STEMI\r\n\r\n[lightgallery5]\r\n\r\nFor emergencies, always follow A-E structure. \r\n\r\n1. Targeted oxygen therapy (aiming for sats >90%)\r\n2. Loading dose of **PO aspirin 300mg**\r\n - Note that some hospital protocols will also call for a loading dose of a second anti-platelet agent such as clopidogrel (300mg) or ticagrelor (180mg)\r\n - For those going on to have PCI, NICE guidance suggests adding prasugrel (if not on anti-coagulation) or clopidogrel (if on anti-coagulation)\r\n3. **Sublingual GTN spray** - for symptom relief\r\n4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart\r\n5. Primary percutaneous coronary intervention (PPCI) for those who:\r\n - Present **within 12 hours of onset of pain** AND\r\n - Are **<2 hours** since <u>first medical contact</u>\r\n\r\nRemember that (particularly in STEMI) _time is heart_ therefore urgent treatment, escalation, and delivery of PPCI is critical to good outcomes.\r\n\r\n# Management of NSTEMI/Unstable Angina\r\n\r\n[lightgallery6]\r\n\r\nFor emergencies, always follow A-E structure. \r\n\r\n1. Targeted oxygen therapy (aiming for sats >90%)\r\n2. Loading dose of **PO aspirin 300mg** and fondaparinux\r\n * Patients should have their 6 month mortality score (often the GRACE score) calculated as early as possible - all those who are anything other than lowest risk should also be given **prasugrel or ticagrelor** unless they have a high risk of bleeding where **PO clopidogrel 300mg** is more appropriate.\r\n3. **Sublingual GTN spray** - for symptom relief\r\n4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart\r\n5. Start antithrombin therapy such as **treatment dose low molecular weight heparin** or **fondaparinux** if they are for an immediate angiogram\r\n6. Patients with <u>high 6 month risk of mortality</u> should be offered an angiogram within 96 hours of symptom onset.\r\n\r\nNote that management of unstable angina is similar to that of NSTEMI with aspirin for all patients and fondaparinux and early angiography for those at high risk.\r\n\r\n# Post-MI management\r\n\r\n[lightgallery7]\r\n\r\n* ALL patients post-MI patients should be started on the following 5 drugs:\r\n 1. **Aspirin 75mg OM** + second anti-platelet (**clopidogrel 75mg OD** or **ticagrelor 90mg OD**)\r\n 2. **Beta blocker (normally bisoprolol)**\r\n 3. **ACE-inhibitor (normally ramipril)**\r\n 4. **High dose statin (e.g. Atorvastatin 80mg ON)**\r\n* All patients should have an **ECHO** performed to assess systolic function and any evidence of heart failure should be treated.\r\n* All patients should be referred to **cardiac rehabilitation**.\r\n* Patients who have been treated without angiography should be considered for ischaemia testing to assess for inducible ischaemia. \r\n\r\n# Complications\r\n\r\n* Ventricular arrhythmia\r\n* Recurrent ischaemia/infarction/angina\r\n* Acute mitral regurgitation\r\n* Congestive heart failure\r\n* 2nd, 3rd degree heart block\r\n* Cardiogenic shock\r\n* Cardiac tamponade\r\n* Ventricular septal defects\r\n* Left ventricular thrombus/aneurysm\r\n* Left/right ventricular free wall rupture\r\n* Dressler's Syndrome\r\n* Acute pericarditis\r\n\r\n## Ventricular Arrhythmias\r\n\r\n* Ventricular arrhythmias can occur as a consequence of MI, during cardiac catheterisation, or after reperfusion.\r\n* Most post-MI ventricular arrhythmias are short lived and self-resolve.\r\n* However if sustained VT or VF occurs they should be treated as per the Advanced Life Support protocols.\r\n\r\n## Recurrent Ischaemia/Infarction/Angina\r\n\r\n* Occasionally inserted stents can thrombose requiring reintervention.\r\n* New infarcts can occur in different vascular territories - this is less likely in the age of PCI where all territory are imaged during the procedure.\r\n* Angina and chest pain can continue for some time after an MI and is more common in NSTEMI patients.\r\n\r\n## Congestive Heart Failure\r\n\r\n* Heart failure can occur as a consequence of impairment heart muscle function secondary to ischaemia.\r\n* It should be treated as any other acute heart failure.\r\n* Ventricular function may improve over months as the heart muscle recovers.\r\n\r\n## Heart Block\r\n\r\n* Various levels of heart block are common - particularly following **inferior** infarcts (because the right coronary artery supplies the SAN).\r\n* These may be treated with:\r\n * Simple observation (as many will revert back to sinus rhythm)\r\n * Transcutaneous/venous pacing (if symptomatic)\r\n * Permanent pacing (if failing to resolve)\r\n\r\n## Left Ventricular Thrombus/Aneurysm\r\n\r\n* Aneurysm can occur following an anterior MI where the myocardium can be susceptible to wall stress leading to an aneurysm.\r\n* It may be silent, cause arrhythmias or embolic events.\r\n* It is definitely diagnosed on ECHO but ECG may show persisting ST elevation.\r\n* Thrombus can form either within an above described aneurysm or around hypokinetic regions of the myocardium.\r\n* Thrombi can embolise causing complications such as stroke, acute limb ischaemia and mesenteric ischaemia.\r\n\r\n## Left/Right Ventricular Free Wall Rupture\r\n\r\n* Necrosis of the free walls of either ventricle can lead to rupture allowing blood into the pericardial space.\r\n* This leads to a rapid tamponade and normally leads to cardiac arrest/death within seconds.\r\n* Treatment includes pericardiocentesis and surgery but prognosis is extremely poor.\r\n\r\n## Acute Mitral Regurgitation\r\n\r\n* This can occur because of papillary muscle rupture and carries a poor prognosis. Occurs commonly due to infero-osterior MI. \r\n* This presents with:\r\n * Pansystolic murmur heard best at the apex\r\n * Severe and sudden heart failure\r\n* It is diagnosed on echocardiogram and may require surgical correction.\r\n\r\n## Ventricular Septal Defect\r\n\r\n* Interventricular septal rupture is a short-term complications of myocardial infarction.\r\n* Rupture caused by an anterior infarct is generally apical and simple.\r\n* Rupture caused by an inferior infarct is generally basal and more complex.\r\n* Without reperfusion, septal rupture typically occurs within the first week after the infarction.\r\n* Features of septal rupture include:\r\n * Shortness of breath\r\n * Chest pain\r\n * Heart failure\r\n * Hypotension\r\n * Harsh, loud pan-systolic murmur along the left sternal border.\r\n * Palpable parasternal thrill.\r\n* Diagnosis is with echocardiogram.\r\n* Patients are managed with emergency cardiac surgery.\r\n\r\n## Dressler's syndrome\r\n\r\n* Dressler's syndrome or post-infarction pericarditis typically presents with persistent fever and pleuritic chest pain **2-3 weeks** or up to a few months after an MI.\r\n* Note that patients can get pericarditis immediately following MI which is NOT considered Dressler's syndrome.\r\n* Symptoms usually resolve after several days.\r\n* Occasionally it can also present with features of pericardial effusion and has become relatively uncommon since the introduction of PCI.\r\n* Management: **high dose aspirin**\r\n\r\n# Prognosis \r\n\r\nDue to the development of PPCI and post-MI care (cardiac rehabilitation) the mortality rates following myocardial infarction continue to decline. Those patients who go on to develop heart failure after myocardial infarction have a significantly worse prognosis than those who do not. \r\n\r\n# NICE Guidelines\r\n\n[NICE Guidelines for Unstable Angina and NSTEMI](https://www.nice.org.uk/guidance/cg94)\r\n\n[NICE Guidelines for STEMI](https://www.nice.org.uk/guidance/cg167)\r\n\r\n# References\r\n\r\n[Patient UK Information on Acute Coronary Syndrome](<https://patient.info/doctor/acute-coronary-syndrome-pro>)",
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"comment": "he would have hypoglycaemia not hyper if he had addison's bc less cortisol- whereas here he's got diabetes due to the iron deposits in the pancreas presumably",
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"explanation": "Discoid lupus and other causes of scarring alopecia may be investigated with an ANA and other blood tests, however the scenario describes the patient being otherwise well with no obvious skin lesions.",
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"comment": "would hair thinning around the scalp not fit with male pattern baldness which would indicate high androgen levels?",
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"comment": "would thyroid disorder present with only hair loss?",
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"comment": "So it says only do androgen testing if there's other symptoms present, but it's ok to do thyroid testing when there's no other symptoms present?? Thyroid disease would have so many other signs IRL!!! Dumb rationale in the answers here.",
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"comment": "why is this not alopecia areata?",
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"comment": "wouldnt she have had to had other features eg thryoid symptoms or tiredness and then you check TFTs and ferritin - said she is otherwise well ?",
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"comment": "why not PCOS? surely more likely",
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"explanation": "# Summary\n\nHypothyroidism, a prevalent endocrine disorder, arises due to the inadequate production of thyroid hormones, critical for metabolism and energy utilisation. Patients often present with a spectrum of signs and symptoms affecting various body systems. These encompass peripheral features like dry skin and brittle hair, head and neck manifestations such as macroglossia and a puffy face, cardiac indicators like bradycardia and cardiomegaly, and neurological deficits, including carpal tunnel syndrome and cerebellar ataxia. An assortment of causes underlies this condition, including autoimmune, iatrogenic, congenital, and iodine-related factors. Diagnosis hinges on comprehensive investigations aimed at identifying the underlying etiology, and management primarily revolves around hormone replacement therapy, with levothyroxine. Ongoing monitoring and management considerations are crucial to optimize treatment outcomes.\n\n\n# Definition\n\n\n\nHypothyroidism is an endocrine disorder characterized by an insufficient production of thyroid hormones, which are crucial for metabolism and energy utilization in the body. \n\n\n# Epidemiology\n\n\n\nHypothyroidism exhibits a higher prevalence among females and escalates with age. Globally, it ranks as one of the most common endocrine disorders, with variations in its etiology across regions. While iodine deficiency remains a prominent cause worldwide, Hashimoto's thyroiditis predominates in the UK.\n\n\n\n# Aetiology\n\n\nThe aetiology of hypothyroidism can be categorized into:\n\n- Autoimmune causes: Hashimoto's thyroiditis, Atrophic thyroiditis and Autoimmune polyendocrine syndromes.\n- Iatrogenic causes: Surgical removal of the thyroid, Radioablation, and Radiation therapy.\n- Congenital causes: Thyroid aplasia and Pendred syndrome (defect in thyroxine synthesis).\n- Iodine deficiency/excess related causes: Infiltrative disorders, Sarcoidosis and Haemochromatosis.\n\n\n# Signs and Symptoms\n\n\n\nThe signs and symptoms of hypothyroidism cover a wide range and can be categorised under:\n\n- Peripheral Features: Dry, thick skin, Brittle hair, Scanty secondary sexual hair.\n\t- Queen Anne's sign - loss of outer 1/3 of eyebrows \n- Cold intolerance, may result in wearing additional layers of clothing\n- Head and Neck Features: Macroglossia, puffy face, goitre (depending on cause).\n- Cardiac Features: bradycardia, cardiomegaly.\n- Neurological Features: Carpal tunnel syndrome, slow relaxing reflexes, cerebellar ataxia, peripheral neuropathy, difficulty concentrating\n- Joint pain\n- Menorrhagia\n\n\n# Differential Diagnosis\n\n\n\nGiven the wide range of symptoms, the differential diagnosis for hypothyroidism is broad and may include:\n\n- Iron deficiency anaemia: fatigue, weakness, pallor, shortness of breath.\n- Chronic fatigue syndrome: persistent fatigue, unrefreshing sleep, cognitive impairment.\n- Depression: persistent low mood, lack of interest, feelings of guilt, sleep and appetite changes.\n\n# Investigations\n\n\nInvestigations are aimed at determining the underlying cause of hypothyroidism:\n\n- First line investigations would include thyroid function tests, which would show a low T3/4 and raised TSH.\n- Antibody testing (Anti-TPO, Anti-thyroglobulin, Anti-TSH receptor) is used to identify autoimmune causes.\n- Imaging and biopsy may be used to identify congenital and infiltrative causes.\n- Iodine levels can be assessed to determine whether deficiency or excess is contributing to hypothyroidism.\n\n# Management\n\n* The primary therapeutic strategy for hypothyroidism revolves around hormone replacement therapy, with levothyroxine as the first-line treatment. \n* Review the patient and recheck TSH levels every 3 months after initiation of LT4 therapy and adjust the dose according to symptoms and TFT results. Once the TSH level is stable (2 similar measurements within the reference range 3 months apart), check TSH annually\n\t* During pregnancy, the dose of levothyroxine is usually increased by 25-50mcg due to increased metabolic demands\n* Compliance with medication and lifestyle recommendations is crucial. \n* This management approach aids in averting complications such as osteoporosis and cardiac arrhythmias associated with untreated or poorly managed hypothyroidism.\n\n\n\n# NICE Guidelines\n\n\n[Click here for NICE CKS on hypothyroidism](https://cks.nice.org.uk/topics/hypothyroidism/).",
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"explanation": "IVIG and plasmapharesis may be used to treat PML which does not typically cause ring enhancing lesions.",
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"explanation": "LP may be contraindicated due to increased intracranial pressure and in the context of HIV neurocomplications is more likely to be a part of the workup for cryptococcal meningitis.",
"id": "10015823",
"label": "c",
"name": "Perform a therapeutic lumbar puncture",
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"explanation": "Toxoplasmosis serology in the blood has no diagnostic bearing on whether cerebral toxoplasmosis exists and is often falsely positive.",
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"explanation": "This case describes a most likely case of toxoplasmosis due to the neuroimaging findings as multiple ring enhancing lesions in HIV are virtually diagnostic of toxoplasmosis. This is the correct answer, as treating toxoplasmosis often involves medical management and monitoring to see whether imaging and symptoms improve. Folate is often co-adminstered with sulfadiazine as it can lead to folate deficiency.",
"id": "10015821",
"label": "a",
"name": "Administer sulfadiazine and pyramethamine",
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"explanation": "Brain biopsies are very invasive and are associated with a host of complications, dexamathesone should be avoided for two reasons, there is very little mass effect and oedema in this case and it could cause an improvement in imaging and confoundthe picture of whether the treatment is working.",
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"comment": "u just made my day ",
"createdAt": 1738692305,
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"comment": "Stop asking for \"appropriate course of action\" and specify whether you want the diagnosis or the treatment!",
"createdAt": 1700140055,
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"comment": "why so butthurt",
"createdAt": 1710544543,
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"comment": "how do you know this is not cryptococcus neoformans? ",
"createdAt": 1717088959,
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"comment": "its just ring enhancing lesions is toxo buzzword, cryptococcus is non-enhancing i think",
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"comment": "does not cause ring enhancing cns lesions",
"createdAt": 1736945112,
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"explanation": "# Summary\n \n\nNeurological differentials in HIV encompass a range of neurological disorders that may occur in individuals with HIV, due to the direct viral effects or secondary to opportunistic infections or malignancies. Key conditions include stroke, meningitis, toxoplasmosis, primary CNS lymphoma, progressive multifocal leukoencephalopathy (PML), cytomegalovirus (CMV) encephalitis, and HIV-associated neurocognitive disorder (HAND). Primary identification hinges on clinical signs and symptoms, supplemented by diagnostic investigations such as lumbar puncture, neuroimaging, and laboratory tests. Management strategies primarily involve antiretroviral therapy, condition-specific medications, and supportive care.\n \n\n# Definition\n \n\nNeurological differentials in HIV are neurological conditions that may present in HIV-positive individuals. These may be directly caused by the virus, arise from the immunocompromised state induced by HIV, or occur as a side-effect of antiretroviral treatment.\n \n\n# Epidemiology\n \n\nNeurological complications in HIV are common and can occur at any stage of the disease. They affect a significant portion of individuals living with HIV, with incidence increasing as the disease progresses and the immune system becomes further compromised.\n \n\n# Aetiology\n \n\nThe aetiology of neurological differentials in HIV varies, with factors including the direct effects of the HIV virus on the nervous system, the secondary effects of a weakened immune system that allow opportunistic infections and malignancies, and side effects from antiretroviral therapy.\n \n\n \n\n# Differential Diagnosis\n \n\n| | **Clinical features** | **Diagnostic tests** | **CD4 count** (cells/microlitre) |\n|---|---|---|---|\n|**Ischaemic stroke** |Acute-onset symptoms including facial weakness, speech abnormalities, leg weakness, focal neurology | CT head: hypoattenuation, loss of grey-white matter differentiation, hyperattenuation in an artery |\n|**Meningitis** |Headache, neck stiffness, photophobia, systemic features (subacute symptoms are more likely to be due to Cryptococcal meningitis which presents in immunocompromised people) | Lumbar puncture* | Cryptococcal meningitis <200 |\n| **Cerebral toxoplasmosis** |Focal neurology, visual changes, altered mental status, headache | Serology positive; CT/MRI: ring-enhancing lesions involving the basal ganglia | <200 |\n| **Primary CNS lymphoma** | Headaches, focal neurology, seizures, visual changes | CT/MRI: classically homogenous appearance, but variable especially in immunocompromise | <100 |\n|**Progressive multifocal leukencephalopathy**| Altered mental status, motor deficits, ataxia, visual changes, seizures | CT/MRI: asymmetric periventricular & subcortical involvement |\n| **CMV encephalitis**| Altered mental status, focal neurology, meningism | MRI: T2/FLAIR non-specific increased signal in white matter; lumbar puncture consistent with viral meningitis* | <100 |\n| **HIV-associated neurocognitive disorder**|Progressive cognitive impairment ranging from mild cognitive impairment to HIV-associated dementia |Neurocognitive testing abnormal; CT/MRI normal| <100 |\n\n\n\n \n\n# Investigations\n \n\nDiagnostic investigations depend on the suspected condition and may include:\n \n\n - Lumbar puncture, which is particularly useful in meningitis\n - Blood tests including serology for toxoplasmosis\n - Glucose measurement, especially in acute presentations\n - Neuroimaging (CT, MRI)\n - Biopsy in selected cases\n - HIV viral load and CD4 count\n \n*Lumbar puncture in meningitis: differentiating features\n\n| | **Appearance** | **Predominant cell type** | **Culture** | **Protein** | **Glucose** |\n|---|---|---|---|---|---|\n| **Bacterial meningitis** | Clear or turbid | **Polymorphonuclear** cells (i.e. neutrophils) | Positive | Raised | **Reduced** |\n| **Aseptic (viral) meningitis** | Clear or slightly turbid | **Lymphocytes** | Negative | Raised | **Normal** |\n| **Tuberculous meningitis** | Clear or slightly turbid, fibrin web | **Lymphocytes** + polymorphonuclear cells | Negative gram stain; acid-fast bacilli positive (auramine staining) | Raised | **Reduced** |\n\nN.b. **Cryptococcal meningitis** may give any of the above results, so should be considered as a differential in any HIV or immunocompromised patient. Classically the opening pressure is very high, and this is a poor prognostic sign. If suspected, request **cryptococcal antigen** or **India Ink** staining.\n\n# Management\n \n\nManagement depends on the specific neurological condition, but in general, the following strategies may be employed:\n \n\n - Initiation or optimization of antiretroviral therapy (ART)\n - Condition-specific medications\n - Ischaemic stroke: antiplatelet therapy & risk factor modification\n - Meningitis: antibiotics, antivirals or antifungals (for cryptococcal meningitis: amphotericin B and a 2nd agent)\n - Cerebral toxoplasmosis: pyrimethamine, sulfadiazine and calcium folinate\n - CMV encephalitis: ganciclovir and foscarnet\n - Supportive care (pain management, physiotherapy, occupational therapy)\n - Neuropsychological support in cases of cognitive impairment\n\n# NICE guidelines\n\n[NICE CKS: Meningitis - bacterial meningitis and meningococcal disease](https://cks.nice.org.uk/topics/meningitis-bacterial-meningitis-meningococcal-disease/)\n\n[NICE: meningitis (bacterial) and meningococcal disease: recognition, diagnosis and management](https://www.nice.org.uk/guidance/ng240/resources/meningitis-bacterial-and-meningococcal-disease-recognition-diagnosis-and-management-pdf-66143949881029)\n\n[NICE CKS: Scenario: Established HIV infection](https://cks.nice.org.uk/topics/hiv-infection-aids/management/established-hiv-infection/)\n\n# References\n\n[Lancet Neurology: HIV infection and stroke: current perspectives and future directions](https://pmc.ncbi.nlm.nih.gov/articles/PMC3460367/#:~:text=Between%201%25%20and%205%25%20of,cerebral%20ischaemic%20lesions%20at%20autopsy.&text=There%20was%20little%20correlation%20between,in%20series%20that%20assessed%20this.)\n\n[Immunity, Inflammation and Disease: Neurological disorders in HIV: hope despite challenges](https://onlinelibrary.wiley.com/doi/full/10.1002/iid3.591)\n\n[BMJ Best Practice: Overview of meningitis](https://bestpractice.bmj.com/topics/en-gb/111?q=Overview%20of%20meningitis&c=suggested)\n\n[BMJ Best Practice: Toxoplasmosis](https://bestpractice.bmj.com/topics/en-gb/557)\n\n[BMJ Best Practice: Assessment of HIV-related mental status changes](https://bestpractice.bmj.com/topics/en-gb/900)\n\n[BMJ Best Practice: Encephalitis](https://bestpractice.bmj.com/topics/en-gb/436)\n\n[BMJ Best Practice: Ischaemic stroke](https://bestpractice.bmj.com/topics/en-gb/3000114)\n\n[BMJ Best Practice: Fungal meningitis](https://bestpractice.bmj.com/topics/en-gb/541)\n\n[Radiopaedia: Lymphomas of the central nervous system](https://radiopaedia.org/articles/lymphomas-of-the-central-nervous-system?lang=gb#nav_clinical-presentation)\n\n[Radiopaedia: Immunodeficiency-associated CNS lymphomas](https://radiopaedia.org/articles/immunodeficiency-associated-cns-lymphomas?lang=gb#nav_radiographic-features)\n\n[Radiopaedia: Progressive multifocal leukencephalopathy](https://radiopaedia.org/articles/progressive-multifocal-leukoencephalopathy?lang=gb#nav_radiographic-features)\n\n[Radiopaedia: Cytomegalovirus encephalitis](https://radiopaedia.org/articles/cytomegalovirus-encephalitis?lang=gb#nav_radiographic-features)",
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"question": "A 38-year-old HIV positive man comes to the emergency department with headache and fever for the last two days. He denies neck stiffness and photophobia. A CT Head shows multiple ring enhancing lesions with no mass effect.\n\nWhat is the most appropriate course of action?",
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"explanation": "Incorrect. Amaurosis fugax is a transient, painless loss of vision, often described as a curtain descending over the eye, usually lasting seconds to minutes. This patient’s visual loss is not transient, making amaurosis fugax unlikely.",
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"explanation": "Incorrect. Optic neuritis is associated with painful vision loss, typically in younger patients, and is often linked to multiple sclerosis. The painless vision loss and systemic symptoms in this case make optic neuritis unlikely.",
"id": "10015835",
"label": "e",
"name": "Optic neuritis",
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"explanation": "Correct. This patient’s sudden, painless visual loss, along with a relative afferent pupillary defect and pale, swollen optic disc, is characteristic of arteritic AION, most often caused by giant cell arteritis (GCA). The patient’s weight loss and jaw discomfort (jaw claudication) further support this diagnosis. GCA is a medical emergency, requiring urgent treatment with corticosteroids to prevent further vision loss.",
"id": "10015831",
"label": "a",
"name": "Arteritic anterior ischemic optic neuropathy (AION)",
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"explanation": "Incorrect. Vitreous haemorrhage typically presents with floaters or a sudden, painless loss of vision but would not cause a swollen optic disc or a relative afferent pupillary defect, which are seen in this case.",
"id": "10015834",
"label": "d",
"name": "Vitreous haemorrhage",
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"votes": 358
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"explanation": "Incorrect. Non-arteritic AION typically presents similarly but lacks systemic symptoms like weight loss or jaw claudication, which are seen in arteritic AION secondary to giant cell arteritis. The visual loss in non-arteritic AION is also usually less severe.",
"id": "10015832",
"label": "b",
"name": "Non-arteritic anterior ischemic optic neuropathy (AION)",
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"__typename": "QuestionComment",
"comment": "Yeh no stress doc its just an eye. ",
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"comment": "Ignorance is bliss",
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"comment": "She will be even more ignorant to her surroundings when she loses here eyesight. Good for her :D",
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"comment": "Her priorities are right, she has two eyes but only one chance to win over 90 minutes. ",
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"comment": "Never heard of arteritic anterior ischaemic ",
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"explanation": "# Summary\n\nSudden painless visual loss is an emergency presentation with a variety of causes including retinal artery or vein occlusions, optic nerve ischaemia, retinal detachment or vitreous haemorrhage. History and ophthalmological examination may be sufficient for diagnosis, with additional investigations including blood tests, imaging such as a B-scan (eye ultrasound) or a temporal artery biopsy in suspected giant cell arteritis. Management varies significantly based on the underlying cause, for example in retinal artery occlusion attempting to dislodge the embolus, aspirin and referral for both stroke and ophthalmology follow up.\n \n# Definition\n\nSudden painless visual loss has a broad differential of causes - we will cover the main ones here. It should be differentiated from visual loss associated with pain (e.g. acute angle closure glaucoma) and transient visual loss (e.g. amaurosis fugax). Retinal examination is usually key to the diagnosis, although there may be specific features in the history that indicate a particular diagnosis.\n \n# Differential Diagnosis\n\n\n## Central retinal vein occlusion\n\n- Shares risk factors with other forms of venous thromboembolism, including older age, cardiovascular disease, hypercoagulability and the combined oral contraceptive pill\n- History is of sudden unilateral painless visual loss with no other associated symptoms typically\n- Retinal examination shows widespread haemorrhage with dilated tortuous veins - this is described as a \"stormy-sunset\" appearance\n- Investigations include basic bloods including blood glucose, lipids, serum protein electrophoresis (looking for diabetes, hyperlipidaemia and myeloma respectively as these are all risk factors) and young patients may require a thrombophilia and autoimmune screen\n- There is no specific management other than addressing any underlying conditions found\n- Two important complication is neovascularisation causing glaucoma (which is treated with laser therapy) and macular oedema (treated with anti-VEGF injections)\n \n## Central retinal artery occlusion\n \n- Also presents with sudden unilateral painless visual loss with no other specific symptoms\n- On examination patients have a relative afferent pupillary defect and fundoscopy shows a pale retina with a cherry red spot at the macula\n- Risk factors include atrial fibrillation, valvular heart disease, carotid artery stenosis, thrombophilia and atherosclerosis\n- Investigations should include an ECG looking for arrhythmias, bloods including a coagulation screen, glucose, ESR and lipid profile to look for risk factors, and a carotid artery doppler to look for carotid stenosis. An echocardiogram may be needed if valvular heart disease or endocarditis is suspected.\n- Management involves attempting to dislodge the embolus if the patient has presented within 90 minutes of symptom onset - this may involve ocular massage, IV acetazolamide or anterior chamber paracentesis\n- A retinal artery occlusion is a type of ischaemic stroke and so should be treated with 300mg aspirin for 14 days initially with stroke team referral for follow up\n- The main complication is neovascularisation due to ischaemia\n\n [lightgallery1]\n \n## Ischaemic optic neuropathy\n \n- This is a broad term that describes optic nerve damage due to a lack of blood supply\n- It can be classified as anterior or posterior, with visible optic disc swelling characterising anterior ischaemic optic neuropathy (AION)\n- AION can be further divided into arteritic and non-arteritic AION, with the usual cause of arteritic AION being giant cell arteritis (GCA)\n- History may reveal other symptoms of GCA e.g. temporal headache, scalp tenderness and jaw claudication and there may also be systemic symptoms or features of polymyalgia rheumatica such as proximal weakness, fatigue and weight loss\n- Fundoscopy shows a swollen optic disc acutely, which becomes pale due to optic atrophy\n- Investigations include basic bloods including an ESR for GCA, and a HbA1c and lipid profile for non-arteritic anterior ischaemic optic neuropathy (NAION)\n- For GCA, a duplex ultrasound of the temporal artery should be done +/- a temporal artery biopsy\n- Management of GCA is with high-dose steroids and rheumatological referral\n- NAION management is upportive and involves optimisation of risk factors e.g. hypertension\n\n## Retinal detachment\n \n- This may be secondary to traction where the retinal is pulled away (e.g. in proliferative diabetic retinopathy or trauma) or exudative causes where subretinal fluid causes the detachment (e.g. due to inflammation or malignancy)\n- Patients present with floaters and peripheral flashes followed by a \"curtain\" or \"shadow\" falling over their vision\n- Fundoscopy shows a pale grey area of retina ballooning forward and a retinal tear may be seen\n- Diagnosis is usually clinical, however if the diagnosis is unclear is can be confirmed with a B-scan (ultrasound of the eye) to look for detachment of the retina\n- Management is usually surgical in cases of tractional retinal detachment, with either a pars plana vitrectomy or a scleral buckle\n \n## Vitreous haemorrhage\n\n- This occurs due to bleeding of the retinal vessels\n- These are often vessels that are new and fragile due to neovascularisation, most commonly due to proliferative diabetic retinopathy\n- Trauma and retinal detachment can also cause vitreous haemorrhage\n- Symptoms include sudden floaters and blurred vision or visual loss\n - When the bleed is large enough to cause visual loss, the retina is difficult to view on fundoscopy and the red reflex is absent\n- Management may be conservative with follow up to look for retinal detachment\n- Patients should avoid heavy lifting in case they dislodge a clot leading to further bleeding\n- Laser therapy should be considered for patients with neovascularisation to prevent further bleeding\n- Vitrectomy surgery may be required in some cases to remove the blood\n\n[lightgallery]\n\n# NICE Guidelines\n\n[NICE CKS - Retinal Detachment](https://cks.nice.org.uk/topics/retinal-detachment/)\n\n[NICE CKS - Giant Cell Arteritis](https://cks.nice.org.uk/topics/giant-cell-arteritis/)\n\n# References\n\n[Royal College of Ophthalmologists - Retinal Vein Occlusion Guidelines](https://www.rcophth.ac.uk/wp-content/uploads/2015/07/Retinal-Vein-Occlusion-Guidelines-2022.pdf)\n\n[Patient UK - Retinal Artery Occlusion](https://patient.info/doctor/retinal-artery-occlusions)\n\n[Patient UK - Vitreous Haemorrhage](https://patient.info/doctor/vitreous-haemorrhage-pro)",
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"question": "A 70 year old female patient presents with sudden onset, painless visual loss. Examination reveals a relative afferent pupillary defect and a pale, swollen optic disc. Over the past month she had noted weight loss and discomfort in her jaw after talking for long periods on the phone, but had not sought medical input. \n\nWhat is the most likely diagnosis? ",
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"__typename": "QuestionChoice",
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"explanation": "An urgent referral may be warranted if LFTs show evidence of hepatitis or the patient has concerning symptoms such as fever/abdominal pain.",
"id": "10015838",
"label": "c",
"name": "Urgent referral to gastroenterology",
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"explanation": "Not investigating jaundice is inappropriate.",
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"explanation": "The most likely diagnosis is Gilbert's syndrome, a benign condition where hyperbilirubinaemia occurs in the absence of liver disease. LFTs are required to check for an acute hepatitis and confirm that there are no other derangements other than an isolated rise in unconjugated bilirubin.",
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"explanation": "Antimalarials are not indicated empirically in this case. The patient has no symptoms of malaria and Egypt is not an endemic area.",
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"name": "Treat with chloroquine",
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"explanation": "An urgent referral may be warranted if LFTs show evidence of hepatitis or the patient has concerning symptoms such as fever/abdominal pain.",
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"__typename": "QuestionComment",
"comment": "Or you could examine the patient who is sitting in front of you?",
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"comment": "love the inclusion",
"createdAt": 1717257739,
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"comment": "ta7ya misr, ta7ya sisi, ta7ya zift el quesmed dah. el as2ila dool zay el zift. ",
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"comment": "yo doc phone up language line for me pls",
"createdAt": 1719197890,
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"comment": "translation: long live egypt, long live sisi, long live this (expletive) quesmed, what are these (expletive) questions.\n\nFor further info: Ta7ya Masr - Song by Ahmed Sheb; absolute bangerrr\nSisi: the current dictator of Egypt",
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"comment": "what does ramadan have to do with this?",
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"comment": "gilbert syndrome can present during illness, fasting or exercise",
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"comment": "in another question about gilberts - answer was reassure ? and the pt had jaundice ",
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"comment": "I think bc he came back from a high-risk country you want to exclude hepatitis just in case",
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"explanation": "# Summary\n\nGilbert's syndrome is a benign autosomal recessive condition characterized by decreased activity of the enzyme that conjugates bilirubin with glucuronic acid due to a mutation in the UGT1A1 gene. Patients may remain asymptomatic or experience mild, intermittent jaundice during periods of stress, fasting, infection, or exercise. Diagnosis is typically confirmed with blood tests revealing mildly elevated bilirubin though otherwise norma liver function tests and a full blood count. No specific treatment is required for this condition. \n\n# Definition\n\nGilbert's syndrome is an inherited, autosomal recessive disorder where the liver does not properly process bilirubin. This is due to a mutation in the UGT1A1 gene, resulting in decreased activity of the enzyme that conjugates bilirubin with glucuronic acid.\n\n\n# Signs and Symptoms\n\nPatients with Gilbert's syndrome may often be asymptomatic. However, they may also experience intermittent mild jaundice triggered by stress, fasting, infection or exercise\n\n# Differential diagnosis\n\nThe main differential diagnoses for Gilbert's syndrome are other causes of jaundice, such as:\n\n- Hepatitis: presenting with symptoms such as fatigue, nausea, abdominal pain, dark urine, and pale stools\n- Hemolytic anemia: characterized by symptoms including fatigue, weakness, shortness of breath, and a rapid heart rate\n- Cholestasis: marked by pruritus, dark urine, pale stools, and steatorrhea\n\n# Investigations\n\nBlood tests show mildly elevated bilirubin but otherwise normal liver function tests and full blood count. A split bilirubin would show a raised unconjugated hyperbilirubinaemia.\n\n# Management\n\nGilbert's syndrome is a benign condition that requires no specific treatment. Management strategies typically involve monitoring the patient's condition and providing reassurance about its benign nature.",
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"question": "A 25-year-old man comes to the GP as his skin has become yellow. He denies any other symptoms. He has returned from visiting family in Egypt a few weeks ago and is currently observing Ramadan.\n\nWhat is the most appropriate management plan?",
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"explanation": "This is incorrect. Screening is often aimed at conditions that can significantly impact health and quality of life, not necessarily those that are terminal.",
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"name": "The condition screened for must be eventually terminal",
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"explanation": "The Wilson and Jungner criteria were established in 1968 by James Wilson and Gunnar Jungner, and they set forth principles for evaluating the suitability of a screening program for a disease. These criteria include several important aspects that a condition must meet for a screening program to be effective. This is one of the key criteria, as it is crucial to understand the progression of a disease to determine the optimal point for screening and intervention.",
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"explanation": "Treatment options do not need to be surgical. They can be medical, lifestyle changes, or other forms of intervention.",
"id": "10015845",
"label": "e",
"name": "There must be an acceptable surgical treatment for the disease",
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"__typename": "QuestionChoice",
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"explanation": "While recognizing symptomatic stages can be useful, the criteria emphasize early detection before symptoms appear, rather than focusing on late stages.",
"id": "10015844",
"label": "d",
"name": "There must be a recognisable late symptomatic stage of the disease",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Screening programs can be periodic rather than one-time events. The frequency depends on the natural history of the disease and the effectiveness of early detection, eg, breast and cervical cancer screening tests are performed every 5-years typically.",
"id": "10015843",
"label": "c",
"name": "Screening must be one off",
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"__typename": "QuestionComment",
"comment": "Got roasted by a consultant in gynae-oncology clinic for this",
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"comment": "a whole year from ur comment my friend, i also got roasted ",
"createdAt": 1735249965,
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"comment": "Knowledge of disease:\nThe condition should be important.\nThere must be a recognisable latent or early symptomatic stage.\nThe natural course of the condition, including development from latent to declared disease, should be adequately understood.\nKnowledge of test:\nSuitable test or examination.\nTest acceptable to population.\nCase finding should be continuous (not just a 'once and for all' project).\nTreatment for disease:\nAccepted treatment for patients with recognised disease.\nFacilities for diagnosis and treatment available.\nAgreed policy concerning whom to treat as patients.\nCost considerations:\nCosts of case finding (including diagnosis and treatment of patients diagnosed) economically balanced in relation to possible expenditures on medical care as a whole.",
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"explanation": "# Summary\n \n \nCervical cancer is the 3rd most common cancer worldwide and the 4th largest cause of cancer death. It is primarily caused by persistent human papillomavirus (HPV) infection and is commonly squamous cell carcinoma. The key clinical features include vaginal discharge, bleeding, discomfort, and changes in urinary or bowel habits. Investigations involve an urgent colposcopy and CT scans for staging. Management strategies depend on the stage of cancer and the patient's fertility desires, ranging from conisation and radical trachelectomy for early-stage cancers to radiotherapy and chemotherapy for more advanced cases.\n \n \n# Definition\n \n \nCervical cancer is a type of cancer that occurs in the cells of the cervix (the lower part of the uterus that connects to the vagina). The majority of cervical cancers are squamous cell carcinomas. \n \n \n# Epidemiology\n \n \nCervical cancer is the 4th most common cancer in women worldwide. In the UK, it is the 14th most common cancer amongst women.\nOver 90% of cervical cancer deaths and similarly higher prevalence is seen in low- and middle-income countries (LMICs), highlighting inequity in access to HPV-prevention (vaccination), cervical cancer screening and treatment options between LMICs and high-income countries. \n \n \n# Aetiology\n \nCervical cancer is strongly associated with persistent human papilloma virus (HPV) infection. The majority of cases are squamous cell carcinoma.\n \nRisk factors for cervical cancer include: \n \n - HPV 16 and 18 infection (accounts for 70% of cases)\n - Multiple sexual partners\n - Smoking\n - Immunosuppression (e.g. HIV or organ transplants)\n \n \n# Signs and symptoms\n \n \nMost cases of cervical cancer are picked up asymptomatically at cervical screening. Other clinical features include:\n \n - Vaginal discharge\n - Bleeding (e.g. postcoital or with micturition or defaecation)\n - Vaginal discomfort\n - Urinary or bowel habit change\n - Suprapubic pain\n - Abnormal white/red patches on the cervix.\n - Pelvic bulkiness on PV examination\n - Mass felt on PR examination\n \n \n# Differential diagnosis\n \n \nThe differential diagnosis for cervical cancer includes other causes of abnormal vaginal bleeding or discharge such as vaginitis, cervicitis, endometrial cancer, and cervical polyps. Key signs and symptoms of these differentials include:\n \n \n1. **Vaginitis:** itching, burning, pain, and abnormal discharge\n2. **Cervicitis:** abnormal discharge, pelvic pain, and postcoital bleeding\n3. **Endometrial cancer:** abnormal vaginal bleeding, pelvic pain, and unintentional weight loss\n4. **Cervical polyps:** abnormal vaginal bleeding, discharge, and pain during intercourse\n \n \n# Investigations\n\n**Bedside:**\n\n* Speculum examination (with sample for cytology and HPV testing) \n\n**Bloods:**\n\n* FBC (anaemia)\n* LFTs (liver involvement)\n* U&Es (renal involvement) \n\n**Imaging:**\n\n* CT chest/abdomen/pelvis (for staging)\n\n**Invasive:** \n\n* Colposcopy (urgent) and cervical biopsy \n \n\n# Management\n \n \nThe treatment for cervical cancer depends on the stage of the cancer, and also whether the woman wants to retain fertility.\n \n \n - For very small cancers in stage IA treatment options include conisation with free margins if aiming to spare fertility. Conisation is done using a scalpel (cold-knife conisation), laser, or electrosurgical loop, and is usually performed as an outpatient.\n - Radical trachelectomy can be done for slightly more advanced, yet still early-stage cancers when the aim is to spare fertility. This involves removal of the cervix, the upper vagina and pelvic lymph nodes.\n - Where maintaining fertility is not an aim a laparoscopic hysterectomy and lymphadenectomy is offered for women for early-stage cancer.\n - For invasive, infiltrating and early metastatic cancer a radical (Wertheim's) hysterectomy can be performed which involves removal of the uterus, primary tumour, pelvic lymph nodes, and sometimes the upper third of the vagina and uterovesical and uterosacral ligaments.\n - If the cancer has spread outside the cervix and uterus, then surgical management is often unlikely to be curative. These cancers are treated with radiotherapy and/or chemotherapy.\n \n# Complications \n\n* Surgical complications: bladder dysfunction, leg oedema (due to lymphadenectomy), preterm birth \n* Radiation complications: vaginal stenosis, vaginal atrophy, bladder dysfunction, urethral strictures\n\n# Prognosis \n\nCervical cancer is preventable through screening. Mortality has decreased significantly as a result of improved treatment and screening programmes. Overall 5-year survival is 67%. However, this varies based on stage of disease at diagnosis:\n\n* Stage I: >90%\n* Stage II-III: 50-70%\n* Stage IV: <20%\n\n# Cervical Screening\n \n \n - For all women and people with a cervix between the age of 25-64 years. \n - Cervical sample is taken and tested for high-risk HPV viruses. \n - From 24 to 49 women are called every three years, and afterwards every five years.\n- The idea behind the screening process is to identify dyskaryotic cells which are pre-cancerous allowing management before invasive cancer can develop.\n \n \n## Outcomes in screening\n \n \nOutcomes from screening can be as follows:\n \n \n - Anybody with a negative HPV test is returned to routine recall.\n - Anybody with a positive HPV test has cytological testing. \n - Patients who are HPV positive but have negative cytology results should have a repeat HPV test in 12 months and again at 24 months if still positive. If they remain positive at 24 months they should be referred to colposcopy.\n - In some cases the sample may be inadequate, in which case the smear should be repeated. If it still not adequate for the next two samples, then the woman should be referred for colposcopy.\n \n \n# HPV Vaccination\n \n \n - Girls and boys aged 12 to 13 years are offered the HPV vaccine as part of the NHS vaccination programme\n - The vaccine helps protect against cancers caused by HPV, including cervical cancer, some mouth and throat cancers and some cancers of the anal and genital areas. It also helps protect against genital warts\n - Gardasil is the vaccination used and protects against HPV types 6, 11, 16, 18, 31, 33, 45, 52 and 58\n \n# NICE Guidelines\n \n [Click here for NICE CKS on Cervical cancer](https://cks.nice.org.uk/topics/cervical-cancer-hpv/)\n \n \n [Click here for NICE CKS on Cervical cancer screening](https://cks.nice.org.uk/topics/cervical-screening/)\n \n \n# References\n \n[Cancer UK](https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/cervical-cancer) \n[NHS Page](https://www.nhs.uk/conditions/cervical-cancer/)",
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"question": "A 27 year old woman attends her routine screening cervical smear appointment at the practice. During the appointment, she asks you to define what the term 'screening test' actually means.\n\nAccording to the Wilson and Jungner criteria of screening tests, which of the following answers makes up part of the criteria?",
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"explanation": "Pregnant women should be advised to quit smoking in its entirety and helped to do so, there is no evidence switching to e-cigarettes is beneficial.",
"id": "10015850",
"label": "e",
"name": "Advise to switch to e-cigarettes",
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"__typename": "QuestionChoice",
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"explanation": "Vareniciline may be useful in smoking cessation but is contraindicated in pregnancy.",
"id": "10015848",
"label": "c",
"name": "Offer Varenicline",
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"votes": 537
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"explanation": "Bupropion may be useful in smoking cessation but is contraindicated in pregnancy.",
"id": "10015847",
"label": "b",
"name": "Offer Bupropion",
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"answer": false,
"explanation": "This is inappropriate as maternal smoking is associated with a host of adverse birth outcomes including infant death, preterm birth, low birth weight and poor intrauterine growth.",
"id": "10015849",
"label": "d",
"name": "Advise to quit after delivery",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "All pregnant woman should be advised to stop smoking immediately and assisted with nicotine replacement therapy to help them quit.",
"id": "10015846",
"label": "a",
"name": "Offer nicotine replacement therapy",
"picture": null,
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"__typename": "QuestionComment",
"comment": "Shoutout to 2% of people telling her to keep smoking",
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"explanation": "# Summary\n\nSmoking is a major public health issue, leading to premature death and multiple health conditions including cancers, COPD and cardiovascular diseases. Encouraging smoking cessation is therefore an important aspect of health promotion. The main strategies include behavioural therapies and pharmacotherapies, which include nicotine replacement therapy (NRT), bupropion, and varenicline. E-cigarettes and vaping are popular aids to smoking cessation and may be offered alongside behavioural support.\n\n# Epidemiology\n\nSmoking is the single biggest cause of premature death in the UK. There are around 10 million active smokers and approximately 50% will eventually die from smoking related conditions (on average 10 years earlier than non-smokers).\n\nConditions associated with smoking include:\n\n- Cancer - smoking is the commonest cause of lung cancer, and contributes to the development of many other tumour types\n- COPD\n- Cardiovascular disease - including stroke, ischaemic heart disease and peripheral vascular disease\n- Peptic ulcers\n- Pregnancy complications (e.g. stillbirth, birth defects, low birth weight)\n- Infertility\n- Osteoporosis\n- Dementia\n- Dental disease\n\nPassive smoking (exposure to second-hand smoke) is also associated with increased risk of lung cancer and heart disease as well as asthma, chest infections and otitis media in children.\n\n# Nicotine Withdrawal Symptoms\n\nWhen attempting to stop smoking, people may experience a variety of unpleasant symptoms due to both physical and psychological dependence on smoking and nicotine. \n\nMost people find they improve within 2-3 weeks of stopping smoking although some may last longer.\n\nSymptoms include:\n\n- Mood changes (irritability, frustration, anger, anxiety, depression)\n- Insomnia\n- Poor concentration\n- Increased appetite and weight gain\n- Restlessness\n- Cravings for cigarettes\n\n# Management\n\n- Patients should be asked if they smoke at every opportunity\n- Those who do smoke should be offered Very Brief Advice (VBA), also known as the 3 As:\n- **Ask** patients if they smoke\n- **Advise** those who smoke that the best way to quit is with specialist support\n- **Act** refer to smoking cessation services if they wish to quit\n- Those who do not want to quit smoking should be offered advice about harm reduction and encouraged to seek support if they are considering quitting\n- Harm reduction strategies include:\n- Cutting down with or without NRT \n- Temporarily stopping smoking with or without NRT\n- Using an e-cigarette\n\n## Behavioural Advice\n\n- Abrupt quitting is the most effective way to stop smoking\n- Encourage patients to set a quit date\n- After this date they should commit to not smoking at all (\"not a puff\" rule)\n- Think about ways to avoid other people smoking and situations in which they would usually smoke\n- Discuss individual barriers to stopping smoking\n- Signpost to resources e.g. free helplines, phone apps\n- Individual and group support services are also available \n- Offer follow up and ongoing support\n\n## Medical Management\n\nOnly one of the following should be prescribed at any time.\n\n- **Nicotine replacement therapy (NRT)**\n\t- Reduces cravings and nicotine withdrawal symptoms\n\t- Multiple formulations are available including patches, gums, sprays and lozenges\n\t- Should be started on the day of quitting\n\t- Common side-effects include nausea, dizziness, vivid dreams and palpitations\n\t- Combination NRT is the most effective - this involves using a patch for 'background' cravings and a short-acting preparation (e.g. a mouth spray) for 'breakthrough' cravings\n- **Bupropion**\n\t- Acts by inhibiting reuptake of dopamine and noradrenaline\n\t- Tablet taken once a day for 6 days then twice a day for 7-9 weeks\n\t- Should be started 7-14 days before the quit date\n\t- Contraindicated in:\n\t- Epilepsy (decreases seizure threshold)\n\t- Eating disorders\n\t- Bipolar disorder\n\t- Brain tumours\n\t- Current benzodiazepine or alcohol withdrawal\n\t- Pregnancy and breast-feeding\n\t- Important side-effects include insomnia, hypersensitivity reactions and rarely seizures\n- **Varenicline**\n\t- Works as a partial nicotinic receptor agonist\n\t- Taken as an oral medication which is uptitrated in dose over the first week\n\t- Start 7-14 days before the quit date, usually continued for 12 weeks\n\t- Contraindicated in pregnancy and end-stage renal disease\n\t- Important side-effects include psychiatric effects (e.g. suicidal thoughts, depression and hallucinations), nausea and headaches\n- **E-cigarettes**\n\t- These are not licensed medications and are not available on the NHS currently but patients may wish to buy them \n\t- Patients should be advised that there is not enough evidence to know whether there are long-term harms of vaping\n\t- However, available evidence suggests that vaping is significantly less harmful than smoking and can help people stop smoking\n\t- Advise patients using e-cigarettes to stop smoking tobacco completely\n\n# Prognosis\n\nAround half of people using NHS Stop Smoking services are successful in quitting at four weeks, with evidence suggesting that people who stop smoking for a month are five times more likely to quit long term. \n\nStopping smoking before the age of 50 halves the risk of dying of smoking-related disease.\n\n\n# NICE Guidelines\n\n[NICE - Tobacco dependence](https://www.nice.org.uk/guidance/ng92)\n\n[NICE CKS - Smoking Cessation](https://cks.nice.org.uk/topics/smoking-cessation/)\n\n# References\n\n[Action on Smoking and Health](https://ash.org.uk/)\n\n[NHS advice on e-cigarettes](https://www.nhs.uk/live-well/quit-smoking/using-e-cigarettes-to-stop-smoking/)\n\n[National Centre for Smoking Cessation and Training](https://www.ncsct.co.uk/)",
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"question": "A 25 year old woman comes to the GP asking for help quitting smoking as she has recently discovered she is pregnant.\n\nWhat is the most appropriate management?",
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"answer": false,
"explanation": "Aciclovir is not used to treat molluscum contagiosum, steroid creams are used, whilst antibiotics may be indicated if secondary infection occurs.",
"id": "10015854",
"label": "d",
"name": "Trial a course of aciclovir",
"picture": null,
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"__typename": "QuestionChoice",
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"explanation": "Whilst cryotherapy may be used for molluscum contagiosum, this option does not address the possible immunocompromise.",
"id": "10015853",
"label": "c",
"name": "Refer for excision and cryotherapy",
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"explanation": "The history and examination describe molluscum contagiosum, caused by the poxvirus. Whilst harmless in children, in adults when they persist and are widespread in the manner described they are suggestive of underlying immunocompromise, therefore HIV testing is indicated.",
"id": "10015851",
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"explanation": "This is inappropriate due to widespread nature of the rash and lengthy duration.",
"id": "10015852",
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"__typename": "QuestionChoice",
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"explanation": "This is not appropriate as we are not concerned about a dermatological malignancy.",
"id": "10015855",
"label": "e",
"name": "2 week referral to dermatology",
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"comment": "He waited 2 years…",
"createdAt": 1704401460,
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"comment": "My God, These Derm Questions Are Absolute AIDS",
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"comment": "Nobody's got aids, and I don't want to hear that word in here again!",
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"comment": "literally he has aids",
"createdAt": 1719677357,
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"comment": "People downvoting me clearly aren't cultured Sopranos fans...",
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"comment": "my thought process was \"might as well test for HIV before telling him to go home\"",
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"comment": "i htought becuase hes worried about them - to use cryotherapy \n",
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"explanation": "# Summary\n\n\nMolluscum contagiosum, a viral skin infection caused by the molluscum contagiosum virus (MCV), primarily presents as small, pearly papules with central umbilication, often occurring on the genitals. Diagnosis is usually made through visual inspection, and a full STI screen is advised for patients with genital manifestations. While the infection typically resolves spontaneously within 18 months, distressing cosmetic implications may warrant treatment such as cryotherapy.\n\n\n# Definition\n\n\nMolluscum contagiosum is a common, contagious skin infection caused by the molluscum contagiosum virus, a member of the poxvirus family.\n\n\n# Epidemiology\n\n\nMolluscum contagiosum exhibits a worldwide distribution with an estimated prevalence of about 8000 cases per 100,000 population annually. The infection is particularly prevalent among children and adolescents. In the UK, the incidence of new cases was reported to be 261 per 100,000 in 2015.\n\n\n# Aetiology\n\n\nThe aetiologic agent of molluscum contagiosum is the molluscum contagiosum virus (MCV), a virus from the poxvirus family. Transmission occurs primarily through direct skin-to-skin contact.\n\n\n# Signs and Symptoms\n\n\nClinical manifestations of molluscum contagiosum include:\n\n\n- Small, smooth, pearly-colored papules with a central area of umbilication\n- These lesions can occur anywhere on the body, but they are most commonly found on the genitals\n- In immunocompromised patients, lesions can be extra-genital and particularly prevalent on the face\n- When the lesions are present on the eyelid margin, they can cause irritation, redness and follicular conjunctivitis, characterised by small lymphoid tissue elevations on the tarsal conjunctiva.\n\n\n# Differential Diagnosis\n\n\nThe main differential diagnoses for molluscum contagiosum include:\n\n\n- **Basal cell carcinoma**: Presents as pearly nodules with telangiectasia, often on sun-exposed skin\n- **Genital warts**: These typically appear as flesh-coloured, cauliflower-like growths in the genital area\n- **Herpes simplex virus infection**: Characterised by painful clusters of vesicles, usually on an erythematous base\n- **Keratoacanthoma**: Rapidly growing, keratin-filled nodule that may resemble a volcano\n\n\n# Investigations\n\n\nDiagnosis of molluscum contagiosum is primarily clinical, made using visual inspection. However, in case of genital molluscum, a full sexually transmitted infection (STI) screen is advised for all presenting patients to rule out co-existing STIs.\n\n\n# Management\n\n\nMolluscum contagiosum is usually self-limiting and clears up spontaneously within 12-18 months. However, management strategies can be employed to speed up recovery and limit the spread of the virus. These include:\n\n\n- Cryotherapy: This involves freezing the lesions with liquid nitrogen, which can speed up lesion clearing. \n- Topical treatments: These aim to stimulate an immune response or directly disrupt the virus, and include ingredients such as salicylic acid, potassium hydroxide, and imiquimod. \n- Curettage: This involves scraping off the lesions under local anaesthesia, but is usually reserved for smaller outbreaks due to the risk of scarring.\n\n\nPatient education on avoiding direct skin-to-skin contact and sharing personal items can help prevent the spread of the virus. Patients at higher risk of complications (for example, ocular molluscum contagiosum or immunocompromise) should be referred to secondary care.\n\n\n# NICE Guidelines\n\n\n[NICE Information on Molluscum Contagiosum](https://cks.nice.org.uk/topics/molluscum-contagiosum/)",
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"explanation": "# Summary\n\nAn squamous cell carcinoma (SCC) is a malignant tumour of epidermal keratinocytes that is often locally invasive and can sometimes metastasise (unlike BCC, where this is rare). Key signs and symptoms include keratinised, scaly, irregular nodules that may ulcerate and display an everted edge. The key investigation method is an excision biopsy, and primary management involves surgical excision with possible adjunctive treatments like Mohs micrographic surgery or radiotherapy.\n\n# Definition\n\nAn squamous cell carcinoma (SCC) is a locally invasive malignant tumour of epidermal keratinocytes. SCCs can cause pain, tenderness or bleeding and grow over weeks or months. SCCs sometimes metastasise, which can be fatal. By definition, since this is a cancer, there is invasion of the basement membrane.\n\n\n# Risk factors\n\n- Family history or previous history\n- Genetic syndromes, for example Xeroderma Pigmentosum, an autosomal recessive condition that reduces the ability of the body to repair UV damage to DNA through nucleotide excision repair, essential for repairing the pyrimidine dimers formed from sun damage.\n- Pale skin/light hair (always burns, never tans phenotype - Fitzpatrick type I or II skin)\n- High levels of sun or UV exposure - for example through occupation, sunburn, or use of sun-beds\n- Immunosuppression: where HPV viruses are thought to play a key role \n- Chronic inflammation - for example, a Marjolin ulcer, which is when a cutaneous SCC develops in the site of a chronically inflamed ulcer or scars \n- Predisposing lesions - these are pre-malignant lesions that occur due to sun-damage and may transition into SCC if not treated: \n\t- Actinic (solar) keratosis: usually asymptomatic but can be mildly pruritic. They appear as scaly, keratotic, rough lesions, either plaques or papules. \n\t- Bowen's Disease: also known as intraepidermal SCC or SCC in situ. Tumour cells are confined to the epidermis. Bowen's disease appears as an irregular, red, keratinised, scaly plaques.\n- Smoking \n- Old age and male sex\n\n\t[lightgallery]\n\t\n# Clinial Features\n\n- SCCs of the skin can appear as keratinised, scaly, irregular nodules. On occasion, the keratin may be so developed that it forms a horn or a plug.\n- They may be ulcerating, and have an everted edge\n- Often in sun exposed areas. There may be background sun-damage, for example wrinkled skin and actinic keratoses. \n- The lesions may be polypoid\n- The lesion is usually slow growing, over months\n- Any complications are usually from local invasion; distant metastasis is rare, but can occur\n- Pain, tenderness, and bleeding may be present\n\n[lightgallery1]\n\n# Investigations\n\n\n- Diagnosis is usually made by excision biopsy with a 4mm margin (treatment and diagnosis at the same time, based on clinical suspicion) \n- Sometimes, a punch biopsy is the first investigation that is performed (for example if the lesion is especially large), later requiring an excision biopsy with a 4mm margin.\n- A 6mm margin is required for high risk lesions, which are defined as:\n\t- 2cm+ diameter\n\t- Location on the ear, lip, face, hands, feet, or genitals\n\t- Elderly or immunosuppressed\n\t- Histological features: thicker than 2mm, poor differentiation, blood or nerve involvement, invasion of subcutaneous tissue\n\t\n\n# Management\n\n- Almost always treated surgically with excision using a 4mm margin (6mm for high risk lesions)\n- Mohs micrographic surgery is sometimes used:\n\t- Tisue is removed and examined under a microscope in real time, to ensure that all the cancerous cells are removed but the maximum amount of healthy tissue is preserved. \n\t- This is done especially if the area is ill-defined macroscopically, or if the area where the cancer is affecting is in need of preservation (for example, ear lobe or nose)\n- Radiotherapy may sometimes be required\n- Other options include curettage and cautery, topical 5-flourouracil, topical imiquimod, and cryotherapy if the lesion appears low risk (small, flat, and superficial), or in the case of suspected actinic keratoses or Bowen's disease\n- Lifestyle advice to prevent further lesions (sun block)\n- Plastic surgery input may be required if the lesion is particularly tricky to remove\n- Prognosis is very favourable (a 5 year survival of 99%) if the SCC is detected early\n\n# References\n\n[Squamous cell carcinoma - DermNet NZ](https://dermnetnz.org/topics/cutaneous-squamous-cell-carcinoma)\n",
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"explanation": "# Summary\n\nDelirium, also known as acute confusional state, is a frequent condition, primarily observed among elderly individuals. It manifests through symptoms such as disorientation, hallucinations, inattention, memory problems, mood or personality changes, and disturbed sleep. Comprehensive investigation includes physical examination and infection screen. Management focuses on treating the underlying cause, optimising the patient's environment, and, in severe cases, considering sedative measures.\n\n# Definition\n\nDelirium is an acute and fluctuating disturbance in attention and cognition, often accompanied by a change in consciousness. It is typically reversible and frequently seen in the elderly, particularly in inpatient settings. It manifests in three subtypes:\n\n* **Hyperactive** Delirium: Marked by increased psychomotor activity, restlessness, agitation, and hallucinations.\n* **Hypoactive** Delirium: Characterised by lethargy, reduced responsiveness, and withdrawal.\n* **Mixed** Delirium: Combines features of both hyperactive and hypoactive delirium.\n\n# Epidemiology\n\nDelirium is a common condition, predominantly affecting elderly people, and is seen in up to 30% of elderly inpatients. The incidence increases with age, severity of illness, and the presence of pre-existing cognitive impairment.\n\n# Aetiology\n\nThe causes of delirium can be multifactorial and are remembered using the mnemonic DELIRIUMS:\n\n- D: Drugs and Alcohol (Anti-cholinergics, opiates, anti-convulsants, recreational)\n- E: Eyes, ears and emotional disturbances\n- L: Low Output state (Myocardial Infarction, Acute Respiratory Distress Syndrome, Pulmonary Embolism, Congestive Heart Failure, Chronic Obstructive Pulmonary Disease)\n- I: Infection\n- R: Retention (of urine or stool)\n- I: Ictal (related to seizure activity)\n- U: Under-hydration/Under-nutrition\n- M: Metabolic disorders (Electrolyte imbalance, thyroid disorders, Wernicke's encephalopathy)\n- (S): Subdural hematoma, Sleep deprivation\n\n# Signs and Symptoms\n\nDelirium can present in a number of different ways, including:\n\n- Disorientation\n- Hallucinations - visual or auditory\n- Inattention\n- Memory problems\n- Change in mood or personality. **Sundowning** is agitation and confusion worsening in the late afternoon or evening.\n- Disturbed sleep\n\nPatients may be hypoactive (sedated) or hyperactive (very agitated), and these presentations can fluctuate over time. Hyperactive delirium is easily seen due to the presentation, while hypoactive delirium can be easily missed as patients may appear more withdrawn.\n\n# Differential Diagnosis\n\nDelirium can mimic several other conditions and it's crucial to consider the following in differential diagnosis, each with its key signs and symptoms:\n\n- Dementia: Characterized by gradual onset, stable consciousness level, and progressive decline in cognitive function.\n- Psychosis: May present with hallucinations and delusions, but usually with preserved orientation and memory.\n- Depression: May exhibit poor concentration and slow cognition, but typically with a stable consciousness level and often accompanied by pervasive feelings of sadness or guilt.\n- Stroke: Abrupt onset with focal neurologic signs and specific deficits in speech, motor, or sensory function.\n \n# Investigations\n\n- 4AT and CAM are commonly used tools for delirium assessment.\n\nInitial investigations should include a comprehensive physical examination and infection screen. Additional investigations should be guided by clinical suspicion based on the patient's history and physical examination. These may include:\n\n- Bedside - bladder scan, review medications, ECG (arrhythmias, ischaemic changes that could cause hypoperfusion) urine MC&S - you should not perform urine dipstick if >65 as they are less sensitive in this age group.\n- Bloods: FBC, urea and electrolyes, liver function tests, thyroid function tests, and blood cultures.\n- Imaging: chest X-ray, or ultrasound of the abdomen. Neuroimaging with CT or MRI head is reserved for those without a clear identifiable cause.\n\n\n# Management\n\nManagement of delirium primarily focuses on treating the underlying cause. Non-pharmacological strategies should be the first line, which include:\n\n- Providing an environment with good lighting\n- Maintaining a regular sleep-wake cycle\n- Regular orientation and reassurance\n- Ensuring the patient's glasses and hearing aids are used if needed\n\nFor patients who are extremely agitated and potentially a danger to themselves or others, pharmacological interventions such as small doses of haloperidol or lorazepam. Olanzapine may also be considered however, these should be used with caution, especially in the elderly, due to the risk of side effects. \n\n# NICE Guidelines\n\nFor more information, see [NICE CKS on delirium](https://cks.nice.org.uk/topics/delirium/).",
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"comment": "yes all images on quested since the new update ",
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"comment": "Am I not seeing ghon lesions?",
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"comment": "CURB-65 of 2 which means that the treatment is amoxicillin ( not co-amoxiclav) + clarithromycin ",
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"comment": "You could test but his history isn't really suggestive of TB. He's not reported to have night sweats, haemoptysis, etc. TB often also doesn't come on acutely like the above case, it generally presents as a cough for > 3 weeks. \n",
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Mortality estimates range from 5 to 14%, with half of these being in people aged over 84 years. \n\n# Aetiology\n\nThe commonest cause of pneumonia is Streptococcus pneumonia, which is usually community-acquired, followed by Haemophilus influenzae and Moraxella catarrhalis. These are referred to as typical pneumonias (as they tend to present with the classic symptoms listed below).\n\nAtypical pneumonias have a variety of atypical features, e.g. a more insidious onset, extra-pulmonary symptoms such as headache and varying appearances on chest imaging. These include Mycoplasma pneumoniae, Legionella pneumophila and Chylmydophila psittaci. \n\nHospital-acquired pneumonias are defined as pneumonia that started 48 hours or longer after admission. 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**0.7%** \n\n- CURB-65 1 - **3.2%** \n\n- CURB-65 2 - **13%** \n\n- CURB-65 3 - **17%** \n\n- CURB-65 4 - **41.5%** \n\n- CURB-65 5 - **57%** \n\nA CURB-65 score of 0-1 requires home treatment, 2 should consider hospital admission, 3-5 admit to hospital and consider ITU referral.\n\n# Symptoms\n\n- Fever\n- Malaise\n- Rigors\n- Cough\n- Purulent sputum\n- Pleuritic chest pain\n- Haemoptysis\n\n# Signs\n\n- Tachypnoea\n- Tachycardia\n- Hypotension\n- Cyanosis\n- Pyrexia\n- Dullness to percussion over the consolidated area\n- Increased vocal resonance/ tactile vocal fremitus over the consolidated area\n- Bronchial breathing over the consolidated area\n- Pleural rub may be heard due to inflammation of the adjacent pleura\n\n# Differential Diagnosis\n\n- **Bronchiectasis** - chronic productive cough with copious sputum, may be triggered by a severe lower respiratory tract infection or another condition (e.g. cystic fibrosis)\n- **Tuberculosis** - suspect in patients with risk factors (e.g. TB contact, from endemic area, no fixed abode), haemoptysis and weight loss more common\n- **Lung cancer** - may lead to pneumonia e.g. by obstructing a bronchus with downstream infection, important to consider especially in patients with a history of smoking, weight loss, chronic cough and haemoptysis\n- **Bronchitis** - infection of the bronchi rather than the lower respiratory tract, usually viral and self-resolving \n\n# Investigations\n\n**Bedside:**\n\n- Sputum for microscopy, culture and sensitivity\n- Consider arterial blood gas if hypoxaemic \n- Urinary legionella and pneumococcal antigens\n- ECG to look for complications e.g. atrial fibrillation\n\n**Bloods:**\n\n- Blood cultures if febrile\n- FBC and CRP for inflammatory markers\n- U&Es to look for an AKI\n- LFTs may be deranged e.g. in Legionella, baseline important when giving antibiotics\n- Mycoplasma serology if atypical pneumonia suspected\n- HIV testing should be offered to all patients with recurrent pneumonia (and all patients in a high prevalence area such as London)\n\n**Imaging:**\n\n- Chest X-ray: may show lobar consolidation or bilateral consolidation in atypical infections, parapneumonic effusions may also be seen.\n- CT chest may be indicated in some cases (e.g. suspected underlying malignancy, suspicious findings on X-ray)\n\n[lightgallery]\n\n\n# Management\n\n**Conservative:**\n\n- Oxygen if low saturations\n- IV fluids if dehydrated\n- Analgesia for myalgia or chest pain\n- Escalate for respiratory support (e.g. continuous positive airway pressure or intubation and ventilation) if patients are severely unwell - consider escalation status and patient wishes\n\n**Medical:**\n\n- Oral antibiotics for patients managed in the community (e.g. amoxicillin 500mg three times a day for 5 days)\n- IV antibiotics for those admitted with more severe pneumonia (e.g. co-amoxiclav and clarithromycin)\n- Different regimens are indicated for those with penicillin allergies and local guidelines should be consulted\n- Antibiotics should be tailored to antimicrobial sensitivities when these are resulted\n\nPatients with pneumonia should be followed up with a repeat chest X-ray after 6 to 8 weeks to screen for an underlying lung cancer (as this may be masked on initial imaging by infective changes).\n\n# Complications\n\n- Parapneumonic effusion\n- Empyema\n- Lung abscess\n- Sepsis\n\n# NICE Guidelines\n\n[NICE - Pneumonia in adults](https://www.nice.org.uk/guidance/cg191)\n\n[NICE CKS - Chest Infections](https://cks.nice.org.uk/topics/chest-infections-adult/)\n\n# References\n\n[Radiopaedia - Lobar Pneumonia](https://radiopaedia.org/articles/lobar-pneumonia)",
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"explanation": "# Summary\n\nSarcoidosis is an inflammatory disease characterised by granuloma formation in various organs, with the most commonly affected being the lungs. Symptoms include fever, polyarthralgia, erythema nodosum, dry cough, dyspnoea, fatigue and weight loss. Investigations include blood tests (with calcium and serum ACE being important), chest X-ray and biopsy of a granuloma. Management depends on the severity of disease and may include NSAIDs, corticosteroids and other immunosuppressants.\n\n# Definition\n\nSarcoidosis is a multi-system disease that is characterised by the formation of non-caseating granulomas around the body. This leads to inflammation and scarring in the organs affected, most commonly the lungs and skin. Other organs affected include the nerves, the brain, the heart, the liver and the eyes.\n\n# Epidemiology\n\nIn the UK, there are approximately 4,500 new diagnoses of sarcoidosis each year, with a prevalence around 1 in 10,000 people. Prevalence varies significantly depending on region, with the highest rates seen in Northern Europe (e.g. Sweden, Finland and Denmark). Some ethnicities are more at risk than others, with people of African descent being affected more often and with more severe disease.\n\nPeak onset is in adults aged between 30 and 55 years old, and it is slightly more common in women than men.\n\n# Aetiology\n\nThe cause of sarcoidosis is not known, with the main theories being that it is an inflammatory response to a yet unidentified environmental exposure or infection, or that is is caused by autoimmunity.\n\nA small percentage of cases are familial and the wide variation in prevalence across different populations suggests that genetic factors are likely to contribute to its development.\n\n# Signs and Symptoms\n\n**Pulmonary manifestations**\n\n- Dry cough\n- Dyspnoea\n- Reduced exercise tolerance\n- Chest pain\n- Clubbing\n- Fine crackles on auscultation\n\n**Dermatological manifestations**\n\n- Erythema nodosum (inflammation of subcutaneous fat leading to tender nodules especially on the shins)\n- Lupus pernio (red/purple plaques and nodules on the face)\n- Hyper or hypopigmentation of the skin\n\n**Neurological manifestations**\n\n- Meningitis\n- Peripheral neuropathy\n- Facial nerve palsy (may be bilateral)\n- Headache\n- Seizures/encephalopathy\n\n**Ocular manifestations**\n\n- Uveitis\n- Keratoconjunctivitis sicca\n- Glaucoma\n\n**Cardiac manifestations**\n\n- Arrhythmias\n- Restrictive cardiomyopathy\n- Syncope\n\n**Abdominal manifestations**\n\n- Hepatomegaly\n- Splenomegaly\n- Renal stones\n\n**Systemic manifestations**\n\n- Fatigue\n- Weight loss\n- Arthralgia\n- Low-grade fevers\n- Lymphadenopathy\n- Enlarged parotid glands\n\n**Lofgren's syndrome** refers to the acute onset of:\n\n- Fever\n- Polyarthralgia\n- Erythema nodosum\n- Bilateral hilar lymphadenopathy (seen on chest X-ray)\n\n**Heerfordt's syndrome** refers to the combination of:\n\n- Fever\n- Uveitis\n- Parotid swelling\n- Facial nerve palsy\n\n# Differential Diagnosis\n\n- **Tuberculosis:** may present very similarly with chronic cough, night sweats, weight loss, bilateral hilar lymphadenopathy so important to rule out (see investigations).\n- **Lymphoma:** also may present with unexplained weight loss, fever, night sweats and lymphadenopathy, pulmonary symptoms less predominant, can be distinguished on biopsy.\n- **Other causes of interstitial lung disease:** similar pulmonary features of dyspnoea, cough and chest pain, and may have weight loss and malaise. Extrapulmonary features (e.g. rashes and hypercalcaemia) seen in sarcoidosis help to differentiate.\n\n# Investigations\n\n**Bedside investigations include:**\n\n- **ECG** looking for arrhythmias or changes related to hypercalcaemia (e.g. QT shortening)\n- **Mantoux test** looking for evidence of exposure to tuberculosis (an important differential)\n- **Lung function testing** - if pulmonary sarcoidosis suspected\n- **Ophthalmological examination** if ocular sarcoidosis suspected\n\n**Blood tests include:**\n\n- **FBC** may show lymphopenia, anaemia or raised white cells\n- **LFTs** for liver disease\n- **Renal function** for renal impairment (not common in sarcoidosis)\n- **Bone profile** for hypercalcaemia\n- **ESR** may be raised due to chronic inflammation\n- **Serum ACE** is elevated in around 60% and normalises if the disease resolves (with or without treatment)\n\n**Imaging studies include:**\n\n- **Chest X-ray** can be used to stage sarcoidosis as below:\n\t- Stage 1 - Bilateral hilar lymphadenopathy (BHL)\n\t- Stage 2 - BHL with peripheral infiltrates\n\t- Stage 3 - Peripheral infiltrates alone\n\t- Stage 4 - Pulmonary fibrosis\n- **High-resolution CT chest** should be done if sarcoidosis suspected on chest X-ray to further assess for pulmonary fibrosis \n- **PET scanning** may be used if there is ongoing diagnostic uncertainty\n- **Echocardiogram** if cardiac disease is suspected\n\n**Other investigations include:**\n\n- **Biopsy** is required to confirm the diagnosis in most cases (with a classic presentation of chronic pulmonary disease or a clear case of Lofgren's syndrome being exceptions) - this is looking for the classic finding of noncaseating granulomas\n- **Bronchoalveolar lavage** may also be done in suspected pulmonary sarcoidosis, with classic findings of raised lymphocytes and an elevated CD4/CD8 ratio\n\n[lightgallery]\n\n# Management\n\n**Conservative treatment includes:**\n\n- Patient education and support\n- Smoking cessation\n- **No active treatment is needed in many cases of sarcoidosis** \n\n**Medical treatment includes:**\n\n- Steroids e.g. oral prednisolone with a higher dose at induction which is then reduced to a lower maintenance dose\n- Second line immunosuppressants (e.g. if steroids contraindicated or not effective) include methotrexate, mycophenolate or azathioprine\n- Third line treatment is usually with biologics (e.g. infliximab)\n\n**Note - Medical treatment should be started only if sarcoidosis symptoms are affecting quality of life or there is significant risk of morbidity or mortality from sarcoidosis**\n\n**Surgical treatment includes:**\n\n- Rarely in severe cases of pulmonary sarcoidosis a lung transplant may be considered\n- In cases of pulmonary sarcoidosis complicated by aspergilloma, surgical management of haemoptysis is sometimes required\n\n# Complications\n\n- Pulmonary fibrosis (stage IV pulmonary sarcoidosis\n- Cor pulmonale\n- Pulmonary hypertension\n- Aspergillomas can form in cavities left by granulomatous pulmonary disease\n- Arrhythmias and sudden death in cardiac sarcoidosis\n- Low mood and anxiety\n- Complications of long-term steroid use (e.g. osteoporosis, hyperglycaemia)\n\n# Prognosis\n\n- In general prognosis is good, with two-thirds of people experiencing disease remission within 2-5 years (usually with no treatment required).\n- Around 20% of people develop chronic disease requiring treatment\n- Remission is more common in earlier stages of sarcoidosis\n- Only 6-8% of people with sarcoidosis have a reduced life expectancy, with the commonest cause of death being pulmonary disease (interstitial lung disease and pulmonary hypertension)\n\n# NICE Guidelines\n\n[NICE CKS - Sarcoidosis](https://cks.nice.org.uk/topics/sarcoidosis/)\n\n# References\n\n[Patient UK - Sarcoidosis](https://patient.info/doctor/sarcoidosis-pro)\n\n[Radiopaedia - Sarcoidosis](https://radiopaedia.org/articles/sarcoidosis-1?lang=gb)",
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"comment": "where does it say she is having vertigo??",
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"comment": "Dizzy when tying shoelaces i.e. vertigo triggered by change in head position, which is characteristic of BPPV",
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"comment": "to be pedantic, the answer says \"She describes vertigo and dizziness...\", implying these are seperate symptoms not interchangeable terms, though she also feels \"the room spinning\".\n\nOverall, I still agree with @BO that this was [clumsily?] intended to highlight vertigo ",
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"comment": "is this not a correct investigation for vertebrobasilar insufficiency which would make sense with the history and the specific head movement? ",
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"comment": "Dix-hallpike - for Diagnosis (D) \nEpley for treatment (if anyone else can't remeber which is which for BPPV)",
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"comment": "BUT SHE HAD A FALL WHY>>>>>",
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"explanation": "# Summary\n\nBenign Paroxysmal Positional Vertigo (BPPV) is a condition characterised by sudden episodes of vertigo, typically following head movement. It is the most common cause of vertigo, particularly in the elderly due to calcium deposition within the semicircular canals. The key signs and symptoms include sudden attacks of rotational vertigo lasting for 30 seconds to 1 minute, triggered by changing head positions. There are no associated auditory symptoms. Diagnosis is made using the Dix-Hallpike manoeuvre, and management primarily involves the Epley manoeuvre. \n\n# Definition\n\nBenign Paroxysmal Positional Vertigo (BPPV) is a medical condition characterised by sudden, episodic attacks of vertigo induced by changes in head position. This condition is due to detachment of otoliths in the inner ear, which results in hair cell stimulation and subsequent vertigo symptoms.\n\n# Epidemiology\n\nBPPV is the leading cause of vertigo and is especially prevalent within the elderly population. This increased prevalence is largely attributed to the accumulation of calcium deposits, known as cholelithiasis, within the semicircular canals of the inner ear.\n\n# Aetiology\n\nBPPV arises due to a detachment of otoliths from the utricle of the inner ear. These detached particles can migrate into the semicircular canals, where they stimulate hair cells and lead to symptoms of vertigo.\n\n# Signs and Symptoms\n\nKey clinical features of BPPV include:\n\n- Vertigo attacks provoked by specific head movements, such as turning the head to one side while in bed or looking upwards\n- Episodes of rotational vertigo lasting between 30 seconds to 1 minute\n- Absence of auditory symptoms\n- Recurrent episodes, often resolving naturally over weeks to months\n\n# Differential Diagnosis\n\nDifferential diagnoses for BPPV include other conditions that can cause vertigo such as Meniere's disease, vestibular neuritis, and labyrinthitis. Key signs and symptoms for these conditions include:\n\n- Meniere's disease: episodic vertigo, tinnitus, hearing loss, and a sensation of fullness in the ear\n- Vestibular neuritis: sudden onset of severe vertigo, nausea, and imbalance lasting for several days\n- Labyrinthitis: vertigo, hearing loss, and tinnitus\n\n# Investigations\n\nThe primary diagnostic test for BPPV is the Dix-Hallpike manoeuvre. This test involves a series of specific head movements that provoke the characteristic vertigo and nystagmus associated with BPPV.\n\n[Click here for more information](https://www.thebsa.org.uk/wp-content/uploads/2014/04/HM.pdf)\n\n# Management\n\nThe mainstay of BPPV management is the Epley manoeuvre. This therapeutic manoeuvre aims to move the detached otoliths out of the semicircular canal and back to the utricle where they originate.\n\n[Click here for more information](https://www.racgp.org.au/download/Documents/AFP/2013/January/February/201301handi.pdf)\n\n# References\n\n[Click here for NICE CKS on benign paroxysmal positional vertigo](https://cks.nice.org.uk/topics/benign-paroxysmal-positional-vertigo/)",
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"question": "A 78-year-old woman was brought in by ambulance following a fall at home. She describes recently feeling unsteady on her feet and dizzy with the room spinning, when tying her shoelaces. She has hypertension, type 2 diabetes, knee osteoarthritis and COPD. On examination, her gait and balance were normal, with no focal neurology.\n\nWhich of the following is likely to diagnose the underlying cause of her fall?",
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"explanation": "Bronchoconstriction can cause respiratory distress in infants, however a wheeze rather than stridor would be found on examintation. The history and examination is more consistent with an inhaled foreign body.",
"id": "10035733",
"label": "b",
"name": "Nebulised salbutamol",
"picture": null,
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"explanation": "Anaphylaxis is an important differential for respiratory distress and stridor, however is is accompanied by hypotension, and allergic symptoms such as angioedema. The history and examination is more consistent with an inhaled foreign body.",
"id": "10035735",
"label": "d",
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"explanation": "The history and examination is consistent with an inhaled foreign body. The immediate management is a rigid bronchoscopy to remove it. Foreign body inhalations are often unwitnessed in children and it is an important differential for anyone presenting with stridor and respiratory distress. Although not common practice, this question has appeared in previous writers' MLA AKT exams so we have included it in our bank.",
"id": "10035732",
"label": "a",
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"picture": null,
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"explanation": "Croup is a common cause of stridor in children and can also cause respiratory distress, this would be treated with steroids. However, the onset would not be so sudden and there is usually a history of low grade fever and coryzal illness. The history and examination is more consistent with an inhaled foreign body.",
"id": "10035734",
"label": "c",
"name": "Dexamethasone, STAT dose",
"picture": null,
"votes": 2338
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"explanation": "The sudden onset and lack of temperature in this patient is not consistent with an infectious cause of respiratory distress. The history and examination is more consistent with an inhaled foreign body.",
"id": "10035736",
"label": "e",
"name": "Amoxicillin",
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"comment": "Would CXR be indicated at all?",
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"comment": "If it's already suspected that the kiddy has eaten the forbidden plastic chocolate brick then you are already there with the grabber to remove it with a bronchoscopy. A CXR would only confirm the diagnosis but exposure them to extra radiation and you would still need to go in with the scope. Hope this helps / makes sense :D ",
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"comment": "thanks uncs",
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"explanation": "# Summary\n\nForeign Body Ingestion (FBI) refers to the swallowing of objects that are not intended to be ingested. Clinical manifestations vary from being asymptomatic to significant morbidity, including esophageal obstruction or perforation, depending on the type and location of the foreign body. Most instances can be managed conservatively, but high-risk objects may necessitate invasive interventions such as endoscopy or open surgery. High-risk objects include batteries, large objects, absorbent materials, magnets swallowed with metal objects, lead-based objects, and objects containing toxins.\n\n# Definition\n\nForeign Body Ingestion is a common pediatric complaint and involves the swallowing of objects not intended for ingestion. While most foreign bodies pass harmlessly through the gastrointestinal tract, some can cause significant complications.\n\n# Epidemiology\n\nForeign Body Ingestion is a prevalent issue among children, particularly those between the ages of six months to three years. This high incidence is attributed to their oral exploratory behavior. Most ingested objects pass spontaneously without causing complications, but a subset may pose a significant health risk.\n\n# Aetiology\n\nObjects often ingested include coins, toys, jewelry, batteries, and food items. The list of potentially ingestible items is virtually limitless but varies based on cultural, environmental, and individual factors. High-risk objects include batteries, large objects that may become trapped at the pylorus, absorbent materials that may cause obstruction, magnets swallowed with metal objects, lead-based objects, and objects containing toxins.\n\n# Signs and Symptoms\n\nThe clinical presentation can range from asymptomatic to significant morbidity. Symptoms include, but are not limited to:\n\n- Drooling\n- Difficulty swallowing or painful swallowing\n- Refusal to eat\n- Chest, throat, or abdominal pain\n- Vomiting\n- Blood in the stool\n\nThe onset and type of symptoms can be influenced by the size, shape, location, and nature of the foreign body.\n\n# Differential Diagnosis\n\nConsider the following conditions in a patient presenting with symptoms suggestive of foreign body ingestion:\n\n- Gastroenteritis: Characterized by nausea, vomiting, diarrhea, abdominal pain.\n- Esophagitis or Gastritis: These could present with similar symptoms of painful swallowing, refusal to eat, and abdominal pain.\n- Appendicitis: Presents with abdominal pain, loss of appetite, nausea, and vomiting.\n- Esophageal stricture or tumor: Can present with difficulty swallowing, chest pain, weight loss, and regurgitation of food or fluids.\n\n# Investigations\n\nInvestigations are unnecessary in an asymptomatic child with a low-risk ingestion. In symptomatic patients or those who have ingested high-risk objects, investigations may include:\n\n- Plain radiography: Most commonly used and can detect radio-opaque objects.\n- Computed Tomography (CT): Offers better sensitivity and specificity for detecting radiolucent foreign bodies.\n- Direct visualization with endoscopy: Useful when there is a high index of suspicion, even if radiological studies are negative.\n\n# Management\n\nThe majority of foreign bodies that are swallowed can be managed conservatively, including observation and symptomatic treatment. High-risk objects such as batteries, sharp objects, or large objects may require endoscopic or surgical removal. Clinicians should provide clear discharge instructions regarding potential complications and when to seek immediate medical attention.\n\n# References\n\n[BMJ Best Practice: Foreign Body Ingestion](https://bestpractice.bmj.com/topics/en-gb/1050)",
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"question": "A 10-month old girl is rushed into the Emergency Department with sudden onset cough, respiratory distress, and noisy breathing. This started 20 minutes ago whilst at a playdate, and she had previously been well. On examination she is making a high-pitched inspiratory sound whilst breathing and is coughing ineffectively. There is no wheeze, rash, or angioedema. Her respiratory rate is elevated at 48 (30-40) and she is tachycardic at 152 bpm (80-140), her other vital signs are normal.\n\nWhat is the most appropriate management?",
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"explanation": "This is only indicated in tonsillitis that is very severe and impairs the patient's ability to swallow which is not the case here.",
"id": "10035811",
"label": "e",
"name": "IV maintenance fluids",
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"votes": 35
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"explanation": "This patient has a Centor score of 2 and therefore, does not warrant antibiotics. Oral penicillin V would be used if they had a Centor score of 3 or more.",
"id": "10035809",
"label": "c",
"name": "Oral penicillin V",
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"votes": 4641
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"explanation": "This patient has a Centor score of 2. Therefore, antibiotics are not warranted. IV antibiotics would be used if the patient were septic or had severe consequences from the tonsillitis that impaired their ability to swallow safely.",
"id": "10035808",
"label": "b",
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"explanation": "This patient is presenting with features of tonsillitis. As his Centor score is only 2 (tonsillar exudate and absence of a cough) antibiotics are not warranted currently. Antibiotics are only given if the Centor score is 3 or above. Therefore, this patient requires analgesia and appropriate safety netting to return in case the symptoms do not resolve. \n\n[NICE guidelines](https://www.nice.org.uk/guidance/ng84/chapter/Recommendations) currently advise using the **original** Centor scoring criteria, which **does not include age.** The modified/McIsaac Centor score, which is available via MDCalc however, does include age, which is why some users may have calculated this patient's score as 3.\n",
"id": "10035807",
"label": "a",
"name": "Encourage regular paracetamol and fluid intake",
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{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This patient has a Centor score of 2 and therefore, they do not warrant antibiotics. Oral clarithromycin would be an option if they had a Centor score of 3 or more and a penicillin allergy.",
"id": "10035810",
"label": "d",
"name": "Oral clarithromycin",
"picture": null,
"votes": 234
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{
"__typename": "QuestionComment",
"comment": "the one thing medicine gave me was teaching me how to finesse the system with a telephone call to get abx for my recurrent tonsillitis",
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"comment": "Isnt the centor score 3 because of the age as well??? \n+1 age between 3-14, +1 exudate, +1 no cough",
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"comment": "Only modified Centor includes age which NICE doesn't use :(",
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"comment": "If you use FEVERPAIN score then is score = 4...consider abx",
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"comment": "Exactly :’)",
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"__typename": "QuestionComment",
"comment": "Need to spend more time in GP",
"createdAt": 1718976723,
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"comment": "its just 3 (purulent tonsils, inflamed tonsils, no cough) 2-3 is apparently a delayed abx prescription so giving PenV now is wrong i guess?",
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"comment": "I work in OOH...",
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"comment": "fever, tonsilar exudate, no cough - I count 3..",
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"comment": "Temp is 37.4 so not considered a fever",
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"explanation": "# Summary\n \nTonsillitis is an acute inflammation of the tonsils, often with a purulent exudate in bacterial cases. The most common cause of tonsillitis are viruses, however, the most common bacterium causing tonsillitis is Streptococcus pyogenes (group A streptococcus). The CENTOR criteria can be used to determine the likelihood of a bacterial infection, and management of bacterial tonsillitis often involves antibiotic treatment. Key signs and symptoms can include tonsillar exudate, tender anterior cervical lymphadenopathy, fever over 38 degrees Celsius, and absence of a cough. \n \n# Definition\n \n\nTonsillitis is a form of pharyngitis characterised by acute inflammation of the tonsils, often with a purulent exudate present in bacterial tonsillitis.\n \n\n# Epidemiology\n \n\nIn the UK, tonsillitis is a common condition that predominantly affects children and adolescents, with an estimated 7.4% of GP consultations for children under 15 years involving a sore throat or tonsillitis as the primary reason for the visit.\n \n\n# Aetiology\n \n\nThe most common causative organism of tonsillitis is Streptococcus pyogenes (group A streptococcus). Epstein-Barr virus (EBV) is another common cause.\n \nRisk factors for tonsillitis include:\n \n - Age 5-15 years\n - Immunodeficiency \n - Family history of tonsillitis \n - Close contact with an infected individual \n \n\n# Signs and Symptoms \n \n - Sore throat \n - The child may also complain of referred pain in the ears or a headache \n - Changes to the sound of the child's voice or cry \n - Purulent and inflamed tonsils\n - Lymphadenopathy \n \n\n# Differential Diagnosis\n \n\nDifferential diagnoses for tonsillitis include the following:\n \n\n - **Bacterial Tonsillitis**: Main signs and symptoms include cervical lymphadenopathy, tonsillar exudate, and fever.\n - **Viral Tonsillitis**: Symptoms are often milder, and accompanied by coryzal symptoms (i.e. cough, rhinorrhoea). \n - **Infectious Mononucleosis**: Also known as glandular fever, this is more common in teenagers. This presents with enlarged tonsils, fatigue and occasionally with splenomegaly. \n - **Hand, foot and mouth disease**: This is caused by the Coxsackie virus, and will feature blisters on the tonsils and roof of the child's mouth. Blisters may also be found on the feet and hands.\n \n\n# Investigations\n \n\nThe CENTOR criteria can be used to indicate the likelihood of a sore throat being due to a bacterial infection. The criteria are as follows:\n \n\n 1. Tonsillar exudate\n 2. Tender anterior cervical lymphadenopathy\n 3. Fever over 38 degrees Celsius\n 4. Absence of a cough\n \n\n [lightgallery]\n \n\nEach of the CENTOR criteria scores 1 point, with a maximum score of 4. A score of 0, 1 or 2 is thought to be associated with a 3 to 17% likelihood of isolating Streptococcus. A score of 3 or 4 is thought to be associated with a 32 to 56% likelihood of isolating Streptococcus.\n\nAlternatively, the FeverPAIN score can be used. The criteria for this include:\n\n- **Fever**\n- **P**us on tonsils\n- **A**ttended within 3 days of symptom onset\n- **I**nflamed tonsils\n- **N**o cough or coryza \n\nDiagnosis is usually clinical, however, in some cases, further investigations may include:\n\n- Throat swab for microscopy and culture\n- Monospot (heterophile antibody) test for glandular fever \n \n\n# Management\n \n\nBacterial tonsillitis with a CENTOR criteria score of 3/4, FeverPAIN score of 4 or 5, or evidence of systemic upset/immunosuppression warrants prescribing antibiotics:\n \n\n- 1st line: Penicillin V PO QDS for 5-10 days\n - Dose is dependent on age, see BNFc for dosing \n- Alternative in penicillin allergy: Clarithromycin/Erythromycin PO BD for 5 days\n - Dose is dependent on age, see BNFc for dosing \n\nFor patients with a CENTOR score of 0-2 or FeverPAIN score of 0 or 1:\n\n- Advise that antibiotics are not needed as they do not tend to alter how long symptoms last and may cause side effects such as diarrhoea and nausea.\n- Conservative management including paracetamol for analgesia and ensuring adequate fluid intake. \n\nIf the child is systemically very unwell or has severe complications, consider referring the child to the hospital. \n\n# Complications\n\n- Quinsy (peritonsillar abscess)\n- Acute otitis media \n- If tonsillitis is due to Group A beta haemolytic step:\n - Rheumatic fever\n - Syndenham's chorea \n - Glomerulonephritis \n - Scarlet fever \n\n# Prognosis \n\nTonsillitis is usually self-resolving within 3-4 days. Some children will have recurrent tonsillitis, and this recurrence may be reduced by smoking cessation for the parents or through tonsillectomy. \n\nTonsillectomy may be indicated for severe recurrent tonsillitis (more than 7 episodes/year for one year, more than 5 episodes/year for two years and more than 3 episodes per year for 3 years). This may be done via diathermy or coblation. \n\n\n# NICE Guidelines\n\n[NICE Guidelines Sore Throat (acute)](https://www.nice.org.uk/guidance/ng84) \n\n[NICE Flowsheet on Antimicrobial Prescribing](https://www.nice.org.uk/guidance/ng84/resources/sore-throat-acute-in-adults-antimicrobial-prescribing-visual-summary-pdf-11315864557) \n \n\n# References\n \n[NHS Information on Tonsillitis](https://www.nhs.uk/conditions/tonsillitis/)\n\n[Patient Info Tonsillitis](https://patient.info/doctor/tonsillitis-pro) \n\n[Great Ormond Street Hospital Tonsillectomy](https://www.gosh.nhs.uk/conditions-and-treatments/procedures-and-treatments/your-child-having-his-or-her-tonsils-andor-adenoids-removed/)",
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"question": "A 13-year-old boy presents to General Practice complaining of a sore throat for the last four days with no cough. He is able to eat and drink. He has no past medical history, is not taking any medications and has no allergies. Examination reveals no lymphadenopathy but there is swelling of the tonsils bilaterally with exudate. His observations are:\n\n- Temperature 37.4 degrees Celsius\n- Pulse 78 bpm\n- Respiratory rate 15\n- Oxygen saturation 98% on room air.\n\nWhat is most appropriate management plan?",
"sbaAnswer": [
"a"
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"explanation": "This is a common presentation and examination finding in ankylosing spondylitis.",
"id": "10035764",
"label": "c",
"name": "Tenderness at the sacroiliac joints",
"picture": null,
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},
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"__typename": "QuestionChoice",
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"explanation": "Heberden's nodes are common findings in patients presenting with osteoarthritis. They present as prominent bony outgrowths that can be palpated on the outer aspect of the distal interphalangeal joints. This patient likely has osteoarthritis due to her age and the fact that her symptoms appear to be activity-related, and are therefore worse in the evening. As the stiffness in her joints lasts less than 30 minutes in the morning it is unlikely to be an inflammatory arthropathy.",
"id": "10035762",
"label": "a",
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"explanation": "Episcleritis is a finding in many rheumatological conditions, including rheumatoid arthritis and enteropathic arthritis.",
"id": "10035766",
"label": "e",
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"explanation": "This is a feature of rheumatoid arthritis (RA). The other features of RA are swan neck and boutonniere deformities, as well as ulnar deviation of the wrist. RA is the most common inflammatory arthropathy but usually affects younger patients.",
"id": "10035763",
"label": "b",
"name": "Z-shaped deformity of the thumb",
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"explanation": "This is a feature of rheumatoid arthritis (RA). Other features include z-shaped deformities of the thumbs, boutonniere's deformities, and ulnar deviation of the wrist. RA is the most common inflammatory arthropathy but usually affects younger patients.",
"id": "10035765",
"label": "d",
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"comment": "Signs of osteoarthritis on the hand can be remembered by \"TBH\" \nT:Thumb CMC squaring.\nB:Bouchard's nodes (affecting the proximal IPJ)\nH:Heberden's nodes (affecting distal IPJ)\nand if ur Arab u know HAB3D means i'll go far away rather than closer so Heberden's nodes (distal rather than proximal affected) !!",
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"comment": "hello fellow Arab <3",
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"comment": "I remember that Herberdens are outer because it's like the Outer Hebrides ",
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"comment": "حبعد!!!! كلش فرحت لان شفت عربي ههههههه نايس تو ميت يو 🥰",
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"comment": "How would you differentiate this from rheumatoid nodules",
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"explanation": "# Summary\n\nOsteoarthritis (OA) is a chronic, degenerative joint disease characterised by loss of articular cartilage, remodelling of bone with osteophyte formation and mild synovitis. The main risk factor is older age, although obesity, joint injury and genetics also contribute. Presentation is with gradual onset pain that is worse with activity, with associated functional limitations. The most commonly affected joints are the knees, hips and small joints of the hands. Diagnosis is clinical, and severity of disease on X-ray does not correlate well with severity of symptoms. Management should be individualised, with important components being exercise, simple analgesia and optimisation of risk factors (such as maintaining a healthy weight). Where there is ongoing pain and disability, options include intra-articular steroid injections and surgical intervention (such as joint replacement).\n\n# Definition\n\nOsteoarthritis (OA) is the commonest form of arthritis, which is characterised by degenerative changes affecting the entirety of joints affected. Cartilage is lost, the subchondral bone becomes sclerosed with formation of osteophytes and subchondral cysts and there is inflammation of the synovial membrane lining the joint capsule (synovitis). \n\n# Epidemiology\n\n- Approximately 10 million people in the UK have osteoarthritis\n- More women than men are affected\n- Average age of onset is 55 \n- The commonest joint affected is the knee, followed by the hip then the hand\n\n# Aetiology\n\nOsteoarthritis develops due to a combination of factors, with important contributors including:\n\n- Older age\n- Female sex\n- Overweight or obesity\n- Family history of OA\n- Previous joint injury\n- Joint damage due to inflammation (e.g. in patients with inflammatory arthritis)\n- Physical inactivity and reduced muscle strength\n- Low bone density \n- Deformities such as development dysplasia of the hip or leg length discrepancy\n- Stresses on joints due to occupational factors (e.g. repetitive squatting or kneeling) or exercise\n\n# Signs and Symptoms\n\nKey symptoms include:\n\n- Pain in the affected joint exacerbated by use\n- Pain may radiate e.g to the thigh, knee and ankle in hip OA, or to the wrist in hand OA\n- Joints may feel stiff (although prolonged morning stiffness is suggestive of inflammatory arthritis)\n- Functional limitations such as difficulty opening jars (hand OA) or mobilising (knee or hip OA)\n- Locking or giving way of the knee\n\nExamination findings include:\n\n- Restricted and painful range of motion (e.g. in hip OA internal rotation with the hip flexed is particularly painful)\n- Crepitus (friction between bone and cartilage) \n- Affected joints may appear swollen or enlarged\n- A small effusion may form, especially when the knee is affected\n- Synovitis may present with mild soft tissue swelling, tenderness and warmth\n- Muscle wasting and weakness can result from disuse atrophy\n- Joint instability\n- An antalgic gait (\"limping\") in knee OA\n- Trendelenburg gait in hip OA (due to weak abductors patients lurch towards the affected hip)\n- Deformities, including:\n- Heberden's nodes (bony nodules over the distal interphalangeal joints) \n- Bouchard's nodes (bony nodules over the proximal interphalangeal joints) \n- Fixed flexion of the first carpometacarpal joint with hyperextension of the distal joints\n- This may lead to squaring of the joint with subluxation and remodelling\n- Ulnar or radial deviation of joints in the hand may occur\n- In severe hip OA the leg may be shortened due to fixed flexion and external rotation\n- Varus (most commonly) or valgus deformities of the knees \n\n# Differential Diagnosis\n\n- **Inflammatory arthritis** such as rheumatoid arthritis, ankylosing spondylitis; pain that improves with activity and morning stiffness lasting over 30 minutes are differentiating factors, systemic symptoms such as malaise and weight loss may be present\n- **Septic arthritis** is an important differential for all patients presenting with an acutely painful swollen joint (which may occur in an acute flare of osteoarthritis); patients may be systemically unwell with fevers\n- **Fracture** e.g. of the tibial plateau may mimic OA symptoms of pain and limited mobility; usually the patient is unable to weight bear with swelling of the affected area; a history of trauma should be elicited\n- **Malignancy** including bone metastases, multiple myeloma or sarcoma may cause mechanical pain leading to functional limitations; red flags include weight loss, night sweats, persistent pain not relieved by rest and night pain\n- **Greater trochanteric pain syndrome** most commonly occurs in middle-aged women and causes lateral hip pain and tenderness worsened by activity; it may also radiate to the lateral knee\n- **Iliotibial band syndrome** presents with lateral knee pain worse with activity, which is often accompanied by clicking or clunking sounds when the knee is moved; occurs most commonly due to repetitive knee flexion e.g. cyclists or runners \n- **Meniscal tear** may occur after an injury involving a twisting or pivoting movement; similar symptoms of pain, swelling, locking and giving way of the knee and range of motion may be limited on examination\n- **Trigger thumb** may mimic OA of the hand with pain, clicking and catching when the thumb is flexed; a nodule may be palpable in the tendon\n- **Ganglion cysts** occur more commonly in people with OA and present as soft tissue swellings e.g. at the base of the thumb; often asymptomatic but may cause pain and limit movement of the joint\n\n# Investigations\n\nDiagnosis of OA is clinical and can be made without any investigations in a patient of 45 or older if there are no features suggesting another underlying cause of symptoms.\n\nIf there is diagnostic uncertainty or a rapid deterioration in symptoms, **X-rays** of affected joints may be of use. Typical findings can be remembered with the mnemonic \"LOSS\":\n\n- **L**oss or narrowing of joint space due to thinning of cartilage\n- **O**steophytes i.e. formation of new bony spurs at the joint margins\n- **S**ubchondral sclerosis i.e. increased bone density beneath the cartilage\n- **S**ubchondral cysts which are fluid-filled sacs in the subchondral bone\n\n[lightgallery]\n\nHowever, severity of OA features on X-ray may not correlate well with severity of clinical disease.\n\nOther investigations if the diagnosis is in doubt should be targeted to the differential suspected, and may include:\n\n- Further imaging such as MRI to look for ligament or cartilage damage (e.g. a meniscal tear)\n- Joint aspiration with synovial fluid analysis to exclude septic arthritis or crystal arthritis\n- Blood tests for inflammatory markers, rheumatoid factor and anti-CCP (for example) if rheumatoid arthritis is suspected\n\nBaseline bloods for renal function and full blood count should be considered in all patients starting NSAID treatment, especially older patients who are at higher risk of adverse effects.\n\n# Management\n\n**Conservative management:**\n\n- Patient education and advice on self-care e.g. appropriate footwear\n- Weight loss advice and signposting to services in patients with excess body weight\n- Exercise has many benefits including strengthening muscles, improving fitness, reducing pain and improving function\n- Options include online fitness programmes designed for people with arthritis, physiotherapy and supervised exercise sessions\n- Physiotherapy services may also be able to offer manual therapies and joint supports such as braces or splints to reduce load and improve instability\n- Occupational health input may be needed in patients with functional impairment to assess their working environment and suggest adaptations\n- Patients should be asked about psychosocial stressors and support offered e.g. for associated depression and anxiety\n- Occupational therapy input may be helpful to advise on aids and devices to assist with activities of daily living (e.g. walking sticks, sock aids, grab rails, tap turners)\n- Podiatry input may be useful to assess the biomechanics of joint pain and advise on orthotic devices such as insoles\n- Referral to a pain management service may be appropriate for patients who have not responded to maximal medical (and if appropriate, surgical) management of OA\n- Assess falls risk and consider referral to specialist services for patients at risk (e.g. those with abnormal gait or balance, or who have had a fall in the last year)\n\n**Medical management:**\n\n- First-line analgesia is with topical NSAIDs (such as ibuprofen gel) - patients should be made aware that some systemic absorption may occur\n- If this is ineffective or unsuitable, oral NSAIDs should be considered (with a PPI for gastroprotection if there are risk factors for gastrointestinal side effects)\n- Paracetamol or weak opioids (e.g. codeine) may also be used in the short-term\n- Topical capsaicin is another option, especially for knee OA\n- Intra-articular steroid injections may be considered if other treatments are not effective, and/or to enable therapeutic exercise\n\n**Surgical management:**\n\n- Patients with OA of the hip, knee or shoulder who have symptoms significantly impacting quality of life despite optimal medical management should be considered for orthopaedic referral\n- The usual operation offered is an arthroplasty (joint replacement)\n- Rehabilitation before and after surgery is key to optimising outcomes\n\n# Complications\n\n- Joint deformities (as above)\n- Increased risk of falls\n- Functional limitations, e.g. hand OA may making writing, turning keys or fasting buttons challenging\n- Reduced mobility \n- Sleep difficulties\n- Low mood and anxiety\n- Chronic pain\n\n# Prognosis\n\n- Not all cases of OA are progressive and the disease course is variable\n- OA of the hands generally has a good prognosis, especially interphalangeal joint involvement\n- Hip OA has a poorer prognosis with many patients requiring arthroplasty\n- Knee arthroplasties for OA are also common however many patients' symptoms improve or remain stable with time \n- Intermittent flares of OA may occur, where symptoms increase in intensity suddenly\n- Flares tend to last for a few days before improving\n\n# NICE Guidelines\n\n[NICE CKS - Osteoarthritis](https://cks.nice.org.uk/topics/osteoarthritis)\n\n[NICE - Osteoarthritis in over 16s: diagnosis and management](https://www.nice.org.uk/guidance/ng226/)\n\n# References\n\n[WHO fact sheet - Osteoarthritis](https://www.who.int/news-room/fact-sheets/detail/osteoarthritis)\n\n[BNF Treatment Summaries - Osteoarthritis](https://bnf.nice.org.uk/treatment-summaries/osteoarthritis/)\n\n[Patient UK - Osteoarthritis](https://patient.info/doctor/osteoarthritis-pro)",
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"question": "A 65-year-old lady presents to the GP with joint pain affecting both of her hands for the last three months. She also reports stiffness in her hands that lasts for 10 minutes when she wakes up. Her hands feel worse towards the end of the day. She has no relevant past medical history.\n\nWhich of the following is the most likely examination finding in this patient?",
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"a"
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173,464,637 | false | 50 | null | 6,495,160 | null | false | [] | null | 20,023 | {
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"answer": false,
"explanation": "This would be appropriate for patients with suspected urosepsis. This patient does not present with any features of sepsis e.g. hypotension and therefore does not require a stat dose of gentamicin.",
"id": "10038324",
"label": "e",
"name": "STAT dose IV gentamicin 5mg/kg",
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"explanation": "According to [NICE CKS guidelines](https://cks.nice.org.uk/topics/urinary-tract-infection-lower-women/management/acute-uti-no-visible-haematuria-not-pregnant-or-catheterized/), this is the second-line antibiotic regimen where nitrofurantoin and trimethoprim are contraindicated (see other explanations), or where there is no improvement in symptoms.",
"id": "10038320",
"label": "a",
"name": "PO Pivmecillinam 400mg initial dose, then 200 mg TDS for three days",
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"explanation": "Methotrexate is listed as a severe interaction with trimethoprim in the BNF, due to the increased risk of haematological side effects that can be fatal. This is a very important drug interaction to remember.",
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"name": "PO Trimethoprim 200mg BD for three days",
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"explanation": "G6PD deficiency is listed as a contra-indication to nitrofurantoin in the BNF.",
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"name": "PO Nitrofurantoin 100mg BD for three days",
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"explanation": "The BNF advises that ciprofloxacin be used with caution in patients with G6PD deficiency. Furthermore, this medication would be more appropriate for patients with acute pyelonephritis managed in the community. The lack of additional symptoms in this patient i.e. flank pain or features of sepsis makes acute pyelonephritis unlikely. ",
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"comment": "So focussed on the G6PD stuff I didn't even see the methotrexate god",
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"comment": "Shush",
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"comment": "PSA is the only reason i got this",
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"comment": "Still didn't get it :/",
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"comment": "Got my finals tomorrow and still only getting 40% on mocks :/",
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"explanation": "# Summary \n\nLower urinary tract infections (LUTIs), often manifesting as cystitis, typically involve the infection of the bladder. Primarily caused by transurethral ascent of colonic commensals like E. coli, symptoms include urinary frequency, dysuria, urgency, foul-smelling urine, and suprapubic pain. Investigations are generally limited to a urine dipstick test for leucocytes and nitrites, while management involves oral nitrofurantoin or trimethoprim, and conservative measures. A key differential diagnosis is pyelonephritis, a urinary tract infection affecting the kidneys. Pyelonephritis exhibits more severe symptoms like fever, malaise, loin pain, and vomiting, and requires hospital admission and intravenous antibiotics.\n\n# Definition \n\nA lower urinary tract infection (LUTI) is generally defined as an infection of the bladder, often manifesting as cystitis.\n\n# Aetiology \n\nLUTIs are caused by the transurethral ascent of colonic commensals, most commonly **E. coli**.\n\n# Signs and symptoms\n\nPatients with LUTIs generally present with:\n\n- Urinary frequency\n- Dysuria\n- Urgency\n- Foul-smelling urine\n- Suprapubic pain\n- Clinical examination may be normal or reveal suprapubic tenderness.\n\nRed flag symptoms such as haematuria, loin pain, rigors, nausea, vomiting, and altered mental state may indicate more serious infection, and these patients may have/are at risk of developing pyelonephritis (see below) and likely need referral to A&E.\n\n\n# Investigations\n\nFor LUTIs:\n\n- Urine dipstick is positive for leucocytes and nitrites in most cases.\n- In uncomplicated cases, no further investigations are required.\n- In children, men, and pregnant women a mid-stream urine sample should be sent.\n\nNB: Urine dipstick is unreliable in women aged older than 65 years and those who are catheterised.\n\nIf being managed in secondary care due to red flag symptoms consider:\n\n- If there are signs of systemic upset consider routine blood tests such as FBC, U+E, and CRP.\n- For uncomplicated UTIs, imaging is rarely required, but if there are concerns over antecedents/complications such as urinary retention/obstruction, an USS bladder/kidney scan would be the first port of call.\n\n# Management \n\n[lightgallery]\n\n[lightgallery1]\n\nFor LUTIs:\n\n- First line management is with oral nitrofurantoin or trimethoprim. Antibiotic duration can vary (see below) however in women the standard course length is 3 days.\n- The patient should be advised on conservative measures to reduce the risk of further infection e.g. regular fluid intake, post-coital voiding.\n\n## Specific situations\n\n**UTI in Men:**\n\n- Empirical antibiotic drug treatment (if no cultures with sensitivities) with trimethoprim or nitrofurantoin for **7 days.**\n- Refer to urology if there are ongoing symptoms despite treatment, if there is an underlying risk factor for UTIs (e.g. urinary calculi, suspected obstruction, previous GU surgery), or if there are recurrent episodes of UTI.\n\n**UTI during Pregnancy (with no haematuria):**\n\n- First-line antibiotics are nitrofurantoin (but *avoid at term),* for **7 days.**\n- If nitrofurantoin is not suitable due to e.g. renal function, or there is no improvement in symptoms, consider second-choice antibiotics such as amoxicillin/cefalexin for 7 days.\n\n\n# NICE Guidelines\n\n[Click here for NICE CKS on urinary tract infection (lower) - women](https://cks.nice.org.uk/topics/urinary-tract-infection-lower-women/)\n\n[Click here for NICE CKS on pyelonephritis - acute](https://cks.nice.org.uk/topics/pyelonephritis-acute/)\n",
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"question": "A 55-year-old woman presents to the GP clinic with pain on passing urine for the past three days. She is otherwise well in herself. She has a past medical history of G6PD deficiency and rheumatoid arthritis, for which she takes methotrexate. She does not take any other medication and has no known drug allergies.\n\nShe has a temperature of 36.5 degrees Celsius, pulse 65 bpm, BP 125/86 mmHg.\n\nUrine dipstick shows 2+ leukocytes and 3+ nitrites.\n\nThe GP decides to prescribe a course of antibiotics for this patient. Which is the most appropriate regimen to prescribe?",
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"explanation": "This is not a first-line investigation for possible ankle fractures and would be more suited for assessing ligament damage.",
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"explanation": "The Ottawa rules recommend an ankle X-ray if following an ankle injury, a patient has pain in the malleolar zone and one of the following; 1) Inability to weight bear immediately after the injury and on examination, 2) Bony tenderness along the distal 6 cm of the posterior edge of the fibula or tip of the lateral malleolus, or 3) Bony tenderness along the distal 6cm of the posterior edge of the tibia or tip of the medial malleolus. As this patient meets these criteria, an ankle X-ray should be carried out in order to rule out ankle fracture.",
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"name": "Immediate surgical reduction and fixation",
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"explanation": "This would not be appropriate as the patient meets the criteria for an ankle X-ray.",
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"explanation": "# Indication\n\nThe Ottawa ankle rules are a decision aid for use in the assessment of acute ankle injuries and the need for radiological imaging. It was developed to reduce the number of unnecessary x-rays being performed, as many ankle injuries do not display a fracture and can be managed conservatively.\n\n# Requirement for x-ray if there is malleolar pain\n\nAnkle x-ray is required only if there is pain in the malleolar zone and any of:\n\n- Bone tenderness at the posterior edge or tip of the lateral malleolus\n- Bone tenderness at the posterior edge or tip of the medial malleolus\n- Inability to bear weight both immediately and in emergency department for four steps.\n\n# Requirement for x-ray if there is midfoot pain\n\nFoot x-ray is only required if there is midfoot zone pain and any of the below:\n\n- Bone tenderness at base of the fifth metatarsal.\n- Bone tenderness at navicular bone.\n- Inability to bear weight both immediately and in emergency department for four steps.\n\n# Reasons why the Ottawa Ankle Rules may not be accurate\n\nIt is important also to use clinical judgement and appreciate this decision aid might not be accurate if:\n\n- The patient is intoxicated or has reduced consciousness\n- The patient has other distracting painful injuries\n- The patient has evidence of reduced sensation in the lower limb\n\n# References\n\n[- The Ottawa Ankle Rules](http://www.theottawarules.ca/ankle_rules)\n[- BMJ Best Practice: Ankle Fractures](https://bestpractice.bmj.com/topics/en-gb/385/)",
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"question": "A 19-year-old female inverts her right ankle whilst playing football. Immediately after the injury she is only able to take two steps using her right foot. On examination, her foot is swollen and bruised and she is extremely tender over her right lateral malleolus. Her foot is warm and well perfused and her dorsalis pedis pulse is palpable. She is unable to weight bear at the time of examination.\n\nWhat is the most appropriate way to manage this injury?",
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"explanation": "This is incorrect. Patients >40 years old are at a greater risk of developing Dupuytren’s contracture.",
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"explanation": "This is incorrect. Patients who smoke are at greater risk of developing Dupuytren’s contracture.",
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"explanation": "This is incorrect. Patients of Northern European descent are at greater risk of developing Dupuytren’s contracture.",
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"explanation": "The condition described here is Dupuytren’s contracture, which is a progressive flexion contracture of the fingers due to connective tissue proliferation and nodule formation in the palm. Positive family history is a significant risk factor for the development of Dupuytren’s contracture.",
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"explanation": "This is incorrect. Male patients are at a greater risk of developing Dupuytren’s contracture.",
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"explanation": "# Summary\n\nDupuytren's contracture is a hand deformity that gradually develops due to fibrotic thickening of the palmar fascia, most notably affecting the 4th and 5th digits. Risk factors include idiopathic origins, diabetes, chronic alcohol use with associated liver disease, familial history, AIDS, and Peyronie's disease. The condition is primarily diagnosed through clinical evaluation, and management ranges from conservative measures like physiotherapy and exercises to surgical fasciectomy.\n\n# Definition\n\nDupuytren's contracture is a pathophysiological condition characterised by the progressive, fibrotic thickening of the palmar fascia that results in permanent flexion deformity of the affected fingers, predominantly the 4th and 5th digits.\n\n# Epidemiology\n\nDupuytren's contracture most commonly affects individuals of Northern European descent and males more frequently than females, with the prevalence increasing with age. The condition often presents in individuals over the age of 50. It's estimated that about 4-6% of the population in the United States suffers from this condition, with a significantly higher prevalence noted in individuals of Scandinavian descent, where it may affect up to 30% of the population.\n\n# Aetiology\n\nDupuytren's contracture may arise due to a variety of factors:\n\n- Idiopathic: This is the most prevalent cause.\n- Diabetes: Chronic diabetes heightens the risk.\n- Excess alcohol use with chronic liver disease: Higher incidence is correlated with chronic liver disease and heavy alcohol consumption.\n- Family history: There is often a genetic predisposition.\n- AIDS: A higher incidence has been noted in HIV patients.\n- Peyronie's disease: An association has been noted with this connective tissue disorder.\n\n# Signs and Symptoms\n\nThe key clinical features of Dupuytren's contracture include:\n\n- Fixed flexion deformity of the 4th and 5th digit\n- Contraction at the metacarpophalangeal and interphalangeal joints\n- In many instances, a symmetrical and bilateral presentation\n\n[lightgallery]\n\n# Differential Diagnosis\n\nThe differential diagnosis for Dupuytren's contracture primarily includes:\n\n- **Trigger finger**: This is characterised by finger stiffness, clicking, and a sensation of locking or catching when the finger is bent and straightened.\n- **Carpal tunnel syndrome**: Symptoms include numbness, tingling, and weakness in the hand, particularly affecting the thumb and the first three fingers.\n- **Diabetic cheiroarthropathy**: This presents with limited joint mobility and a thick, tight, waxy skin on the back of the hands.\n\n# Investigations\n\nDiagnosis of Dupuytren's contracture is primarily clinical, based on presentation of typical symptoms and findings on physical examination.\n\n# Management\n\nThe management strategies for Dupuytren's contracture are:\n\n- Conservative measures: These include physiotherapy and exercises to help maintain finger mobility and strength.\n- Surgical intervention: Surgical fasciectomy may be considered when conservative management is ineffective. This procedure involves the removal of the thickened tissue and creation of a z-shaped scar to mitigate recurrence.\n\n# External link\n\n[Click here for more information on Dupuytren's contractures](https://teachmesurgery.com/orthopaedic/wrist-and-hand/dupuytrens-contracture/)",
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"question": "A 46-year-old male has thickening of tissue and palpable nodules over the fourth and fifth digits on the palm of his right hand. The fingers are slightly flexed, and the patient is unable to flatten his right hand on the table.\n\nGiven the likely diagnosis, which of the following is a risk factor for the development of this condition?",
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"explanation": "This history is more concerning for malignancy given the development of a growing, painful bony lesion in an adolescent. Patients would be less likely to develop pseudogout at this age and X-ray would be more likely to show chondrocalcinosis (calcification of cartilage).",
"id": "10017158",
"label": "c",
"name": "Pseudogout",
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"explanation": "This more commonly affects patients over the age of 40. Lytic lesions with ‘fluffy popcorn calcification’ are the characteristic X-ray findings.",
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"label": "b",
"name": "Chondrosarcoma",
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"explanation": "This is the most common primary bone malignancy which typically affects adolescent males. A history of retinoblastoma is a risk factor for the development of osteosarcoma and the ‘sunburst appearance’ (formation of new bone in a specific pattern) is a classic finding on X-ray.",
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"explanation": "Whilst trauma can present with pain and swelling, the developing size of the swelling means malignancy is more likely and needs to be excluded.",
"id": "10017160",
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"name": "Trauma to the distal femur",
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"__typename": "QuestionChoice",
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"explanation": "This is a disease which causes inflammation of the growth plate and presents with pain and swelling of the tibial tuberosity rather than distal femur. This history and the X-ray findings are much more suggestive of malignancy.",
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"explanation": "# Summary\n\nOsteosarcoma, Ewing's Sarcoma, and Chondrosarcoma are all examples of primary bone malignancies, which, while rare, are significant health concerns that are typically treated in specialist orthopaedic/oncology units. These cancers can present with common symptoms such as painful, warm swellings and systemic symptoms like fever and anaemia. Key investigations include X-rays, which may reveal specific patterns characteristic of these diseases, such as Codman's triangle in osteosarcoma or 'onion skin' periosteal reaction in Ewing's sarcoma. Management strategies vary, but often include surgical resection, radiation therapy, and systemic chemotherapy.\n\n# Definition\n\nPrimary bone malignancies are rare cancers that originate in the bone, rather than spreading from other areas of the body (metastatic disease). They include various types, most notably osteosarcoma, Ewing's sarcoma, and chondrosarcoma.\n\n# Epidemiology\n\nSecondary tumours arising from metastatic disease are the most common type of malignancy encountered in bone. Primary bone tumours, including osteosarcoma, Ewing's sarcoma, and chondrosarcoma, are relatively rare and usually treated in specialist orthopaedic/oncology units.\n\n# Aetiology\n\nThe exact causes of primary bone cancers are not entirely understood, although genetic factors, previous radiation exposure, and certain bone conditions such as Paget's disease may increase the risk.\n\n# Signs and symptoms\n\n- **Osteosarcoma:** Typically presents with a warm, painful swelling, often around the knee.\n- **Ewing's Sarcoma:** Presents as a painful, warm, enlarging mass along long bone diaphysis. Systemic symptoms, such as fever and anaemia, may also be present, and blood tests may reveal a raised ESR and WCC.\n- **Chondrosarcoma:** Occurs in older patients (>40) and often presents with pain and a lump.\n\n# Differential diagnosis\n\nWhen presented with a patient experiencing bone pain and swelling, several conditions should be considered:\n\n- **Osteomyelitis:** Presents with bone pain, fever, and possibly swelling and erythema. Blood tests may show raised inflammatory markers.\n- **Benign bone tumours (e.g., osteoid osteoma, osteoblastoma):** Often present with localized pain that may be worse at night.\n- **Metastatic bone disease:** Can present with bone pain and fractures. May be associated with weight loss and a history of cancer elsewhere in the body.\n\n# Investigations\n\nThe main diagnostic tool for primary bone cancers is an X-ray, which can reveal unique patterns:\n\n- **Osteosarcoma:** Periosteal reaction with Codman's triangle and a sunburst appearance. \n\n[lightgallery1]\n\n- **Ewing's Sarcoma:** 'Onion skin' periosteal reaction. \n\n[lightgallery]\n\n- **Chondrosarcoma:** Lytic lesion with 'fluffy popcorn' calcification.\n\nFurther investigations can include blood tests, biopsy, MRI, CT scan, and bone scan.\n\n# Management\n\nTreatment for primary bone cancers often involves multidisciplinary teams and may include surgical resection, radiation therapy, and systemic chemotherapy. The specifics of treatment depend on the type, location, and stage of the cancer, as well as the patient's overall health.",
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"question": "A 14-year-old boy has a painful swelling just above his right knee, which is growing in size. A knee X-ray shows a ‘sunburst appearance’ of the distal right femur. He has a past medical history of retinoblastoma.\n\nWhat is the most likely diagnosis?",
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"explanation": "This is a classic presentation of reactive arthritis (triad arthritis, urethritis and conjunctivitis). It is usually caused by gastrointestinal/genituo-urinary infections. Given the urinary symptoms, arranging urinary NAAT testing is likely to be diagnostic of the causative organism.",
"id": "10017161",
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"name": "Arrange urinary NAAT testing",
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"explanation": "Whilst gastrointestinal infections can trigger reactive arthritis, there is no mention of diarrhoea or other GI symptoms, whilst there is suspicion for urethral infection.",
"id": "10017165",
"label": "e",
"name": "Obtain stool cultures for PCR and culture",
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"explanation": "This would be appropriate management for a confirmed crystal arthropathy (e.g. gout/pseudogout). However, the symptoms are far more suggestive of a reactive arthritis with active underlying infection, which would need to be treated on top of symptomatic analgesia.",
"id": "10017163",
"label": "c",
"name": "Commence colchicine and discharge with safety netting advice",
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"__typename": "QuestionChoice",
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"explanation": "Whilst a red, hot and swollen joint should always raise suspicion for septic arthritis, this would likely lead to limited range of motion and be exquisitely tender on palpation. Although joint aspiration may be useful, this history (and lack of fever) is far more suggestive of a reactive arthritis.",
"id": "10017162",
"label": "b",
"name": "Arrange urgent joint aspiration",
"picture": null,
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This would be more useful in a scenario with suspected meniscal or ligament injury following trauma. It additionally would be unlikely to be used as a first line investigation.",
"id": "10017164",
"label": "d",
"name": "Arrange urgent knee MRI",
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"comment": "Would you not want to rule out septic arthritis? ",
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"comment": "true, but the q asks for management given most likely dx, and whilst you need to rule out septic arthritis, it isn't the most likely dx. ",
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"comment": "If I'm not wrong you need to rule out septic arthritis first before starting treatment ",
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"explanation": "# Summary\n\nReactive arthritis is a sterile inflammatory arthritis that typically occurs within four weeks of an infection. Infections are often sexually transmitted (e.g. Chlamydia trachomatis) or gastrointestinal (e.g. Salmonella, Shigella or Campylobacter). Patients present with joint pain, stiffness and swelling which is usually asymmetrical and affects few joints, predominantly lower extremity. The classic triad of symptoms is of arthritis, conjunctivitis and urethritis; other associated features include rashes, nail changes and mouth ulcers. Investigations involve testing for the causative infection, synovial fluid analysis to exclude differentials, and X-ray imaging of affected joints. Reactive arthritis is a self-limiting condition in the majority of patients and so management is symptomatic. NSAIDs are usually first line and either local or systemic steroids may be used if NSAIDs are contraindicated or ineffective. If ongoing infection is identified (e.g. Chlamydia) this should be treated and referral to genitourinary medicine made to investigate for other sexually transmitted infections and arrange contact tracing.\n\n# Definition\n\nReactive arthritis (ReA) is a type of inflammatory arthritis that occurs secondary to a recent infection, usually genitourinary or gastrointestinal in nature. It is described as \"sterile\", meaning that the affected joints are not themselves infected. \n\nReactive arthritis was originally referred to as Reiter's syndrome, which refers to the classic triad of conjunctivitis, urethritis and arthritis (remembered with the mnemonic \"can't see, can't pee, can't climb a tree).\n\n# Aetiology\n\n- The triggering infection occurs up to a month before the onset of arthritis\n- Most infections are sexually transmitted (postvenereal ReA) or gastrointestinal (postenteric ReA)\n- Common causative organisms include:\n- Chlamydia trachomatis \n- Campylobacter jejuni\n- Salmonella\n- Shigella\n- Yersinia\n- Less common causes include E coli, HIV, Neisseria gonorrhoea and Mycoplasma pneumoniae\n- Postvenereal ReA is mainly seen in men aged 20-30\n- Postenteric ReA affects both sexes equally\n- There may not be an identifiable triggering infection in all cases\n- Patients who are HLA-B27 positive have a 50x increased risk of ReA and are more likely to have severe and persistent symptoms\n\n# Signs and Symptoms\n\n- **Arthritis**\n- Typically this is asymmetrical and primarily affects the large joints of the lower limbs\n- Usually oligoarticular (affecting few joints)\n- A small joint polyarthritis in the upper limbs may also occur\n- Axial involvement and sacroiliitis are more common with urogenital rather than enteric ReA\n- **Dactylitis** refers to swelling of an entire digit (finger or toe)\n- **Enthesitis** causes pain and swelling at sites of tendon or ligament insertions into bone\n- Achilles tendonitis and plantar fasciitis are common and cause pain on walking\n- **Keratoderma blennorhagicum** is the classic rash of ReA\n- Pustular lesions form on the palms and soles of the feet \n- These become hyperkeratotic and scaly and form plaques\n- **Circinate balanitis** refers to red or grey plaques with an irregular white margin that form on the penis (the shaft or the glans)\n- **Oral ulceration**\n- **Nail dystrophy**\n- **Eye involvement** may be the first presenting feature, with manifestations including:\n- Conjunctivitis\n- Anterior uveitis\n- Keratitis\n- Episcleritis\n- **Genitourinary features** may occur in both postvenereal and postenteric ReA, including:\n- Urethritis or cervicitis\n- Cystitis\n- Prostatitis\n- Salpingo-oophoritis\n- **Constitutional symptoms** are often present and include:\n- Fevers\n- Malaise\n- Fatigue\n\n[lightgallery] [lightgallery1] [lightgallery2] \n\n# Differential Diagnosis\n\n- **Gonococcal arthritis** occurs in the context of disseminated infection and may present with joint pain and swelling, tenosynovitis and dermatitis - swabs should be taken from relevant sites including the rectum, pharynx, urethra and cervix and synovial fluid cultures may be positive\n- **Other spondyloarthritides** including ankylosing spondylitis, enteric arthritis and psoriatic arthritis can present with similar features of peripheral arthritis, enthesitis and dactylitis however these are not temporally related to a triggering infection and tend not to self-resolve\n- **Viral infections** may cause arthritis as well as extra articular features of fevers, rashes and conjunctivitis e.g. enteroviruses, Coxsackievirus, Chikungunya\n- **Septic arthritis** usually presents with a single inflamed joint accompanied by systemic features of fevers and malaise; aspiration and analysis of synovial fluid is the key investigation\n- **Rheumatic fever** occurs in a similar timeframe to reactive arthritis after initial streptococcal infection (usually a sore throat), and shares features of polyarthritis and rashes (classically erythema marginatum); other features include carditis and chorea\n\n# Investigations\n\n**Bedside tests:**\n\n- **Chlamydia trachomatis and gonorrhoea testing** should be done with nucleic acid amplification tests (NAAT) on urine or a urethral/vulvovaginal swab\n- In patients with a history of oral or anal sexual intercourse, pharyngeal and/or rectal swabs should also be tested\n- Antibiotic sensitivity testing is required for positive samples\n- **Stool MC&S**, **viral PCR** and **Clostridium difficile testing** should be done in patients with ongoing diarrhoea (although usually this has resolved by the time ReA develops)\n- **Aspiration of synovial fluid** should usually be carried out to rule out septic arthritis or crystal arthropathies - in ReA cultures will be negative but white cell count is high\n\n**Blood tests:**\n\n- **FBC** is usually indicative of inflammation with a normocytic anaemia, mildly raised white cell count and thrombocytosis\n- **CRP** and **ESR** are raised acutely and normalise with time\n- **HIV testing** should be offered as people with HIV have an increased risk of ReA\n- Testing for other sexually transmitted infections including **syphilis, hepatitis B and C** should be considered \n- **HLA-B27** is often positive in patients with ReA and is a poor prognostic marker\n- **Serology** for other infections may be indicated e.g. salmonella or shigella\n\n**Imaging:**\n\n- **X-rays** of affected joints which may be normal early on in the disease course\n- Imaging features include erosions, enthesopathy with bony spur formation, loss of joint space and soft tissue swelling\n- Sacroiliitis may be seen on X-ray however **MRI** is more sensitive for joint erosions in the acute phase\n\n# Management\n\n- Patients diagnosed with a sexually transmitted disease (usually Chlamydia trachomatis) should be referred to a sexual health specialist to be assessed for other infections and for contact tracing\n- Patients with chlamydia and their partners should be treated with antibiotics (usually 7 days of oral doxycycline)\n- Otherwise, management of joint symptoms is usually symptomatic with NSAIDs being first-line\n- If NSAIDs are contraindicated or ineffective, local steroid injections for affected joints (or systemic steroids if many joints are affected) may be used\n- Bone and stomach protection should be considered for all patients who require oral steroid treatment\n- In patients with persistent disease, conventional DMARDs should be initiated with sulfasalazine being the preferred medication\n- Biologics can be initiated if conventional DMARDs are ineffective, with anti-TNF agents such as etanercept being first-line options\n- Additional treatment may be required for significant skin involvement, with topical treatments including steroids, salicylic acid and vitamin D analogues\n\n# Prognosis\n\n- In most patients, disease is self-limiting with a duration of around 3 to 5 months\n- However in 25% of patients symptoms persist for longer than 6 months (referred to as chronic ReA) \n- Recurrence of disease may also occur, which may be in response to another infective trigger\n- Secondary osteoarthritis may complicate reactive arthritis due to inflammatory joint damage\n\n# References\n\n[Reactive arthritis: a clinical review](https://www.rcpe.ac.uk/sites/default/files/jrcpe_51_3_jubber.pdf)\n\n[Patient UK - Reactive Arthritis](https://patient.info/doctor/reactive-arthritis-pro)\n\n[Radiopaedia - Reactive Arthritis](https://radiopaedia.org/articles/reactive-arthritis?lang=gb)",
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"question": "A 21-year-old male has a painful left knee. He has also noticed he has a left red eye and pain on urination in the last week. On examination, his knee is swollen and mildly tender, but he has a full range of motion and can weight bear. The patient is afebrile.\n\nGiven the likely diagnosis, what is the most appropriate management?",
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"explanation": "This patient demonstrates conductive hearing loss on the right-hand side on Rinne’s and Weber’s testing. Combined with her history of foul-smelling discharge, this makes cholesteatoma (an abnormal collection of skin cells within the ear) the most likely of these options. All of the other options are causes of sensorineural hearing loss rather than conductive hearing loss.",
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"explanation": "# Summary\nCholesteatoma, despite its name, is neither a tumor nor related to cholesterol. It is a severe but rare complication of chronic otitis media, common in patients aged 5-15 years old. Key signs and symptoms include persistent foul-smelling discharge, headache, and otalgia. Critical investigations include examination of the tympanic membrane, which often reveals a white area in the attic behind the membrane. Management strategies focus on preventing complications, such as facial nerve palsy and central nervous system (CNS) complications, through surgical intervention.\n\n# Definition\nCholesteatoma is a misnomer, as it is neither a tumor nor has relations to cholesterol. It is an abnormal accumulation of skin and squamous epithelium within the middle ear cleft and mastoid air cells.\n\n# Epidemiology\nCholesteatoma is a rare condition, commonly occurring in younger patients, particularly those aged 5-15 years old. It is a severe complication of chronic otitis media.\n\n# Aetiology\nThe primary cause of cholesteatoma is the abnormal accumulation of squamous epithelium and skin cells in the middle ear cleft and mastoid air cells. This unusual build-up often results from chronic otitis media.\n\n# Signs and Symptoms\nKey signs and symptoms of cholesteatoma include:\n- Persistent foul-smelling discharge\n- Headaches\n- Otalgia\n\nUpon examination of the tympanic membrane, a white area is often visible in the attic behind the membrane.\n\n[lightgallery]\n\n# Differential Diagnosis\nDifferential diagnoses for cholesteatoma include:\n- Chronic otitis media: Presents with recurrent ear infections, ear discharge, hearing loss, and ear pain.\n- Otosclerosis: Symptoms include progressive hearing loss, tinnitus, and vertigo.\n- Squamous cell carcinoma: Presents with persistent ear pain, hearing loss, and sometimes facial nerve paralysis.\n\n# Investigations\nCritical investigation for cholesteatoma includes an examination of the tympanic membrane. This examination often reveals a white area in the attic behind the tympanic membrane. More advanced investigations may include CT scans and MRIs to assess the extent of the disease.\n\n# Management\nThe primary management strategy for cholesteatoma is surgical intervention to remove the abnormal skin and squamous epithelium accumulation. This approach helps prevent severe complications such as facial nerve palsy and CNS complications (including meningitis, epidural abscess, and sigmoid sinus thrombosis).\n\n# References\n[Click here for NICE CKS on cholesteatoma](https://cks.nice.org.uk/topics/cholesteatoma/)",
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"question": "A 47-year-old female has foul smelling discharge from her right ear with associated hearing loss. When assessing her hearing with a tuning fork, she hears the sound louder on the right, with the tuning fork placed in the middle of the forehead. On the right, the sound from the tuning fork is heard best when placed on the mastoid process, whilst it is heard best next to the external auditory meatus on the left. She denies any tinnitus or vertigo.\n\nWhat is the most likely diagnosis?",
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"explanation": "Whilst this may be appropriate management after the bleeding had resolved, it is not appropriate initial treatment.",
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"explanation": "This increases the risk of aspiration and the pressure being applied to the bridge of the nose does not compress the likely source of the bleed.",
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"explanation": "# Summary\n \nEpistaxis refers to nosebleeds, which are a common condition ranging significantly in severity. Many are mild and self-limiting with simple first-aid, however larger bleeds may be life-threatening and require rapid intervention and resuscitation. Contributing factors include trauma (e.g. nose-picking), inflammation, drug use (e.g. cocaine), recent surgery, tumours and bleeding diatheses. Management of epistaxis involves a stepwise approach starting with direct pressure on the cartilaginous part of the nose, cautery, nasal packing, followed by interventions such as arterial embolisation or ligation if bleeding is refractory to other treatments. \n \n# Definition\n \nEpistaxis refers to bleeding from the nose - this usually originates from the anterior nasal septum (Little's area and Kiesselbach's plexus specifically) but around 10% of cases are posterior, originating from branches of the sphenopalatine artery. \n \n# Aetiology\n \nMost cases of epistaxis are mild and self-limiting, with no specific underlying cause identified. Factors that may contribute to epistaxis include:\n\n- Trauma (e.g. nose-picking, blunt trauma, septal perforations and foreign bodies in the nose)\n- Oxygen via nasal cannulae (causes drying and irritation of the nasal mucosa)\n- Recent ENT or maxillofacial surgery\n- Tumours, either malignant (e.g. squamous cell carcinomas) or benign (e.g. angiofibromas)\n- Inflammation (e.g. rhinosinusitis, nasal polyps)\n- Alcohol excess\n- Illicit drug use e.g. snorting cocaine \n- Medications such as nasal steroids\n- Vasculitides (e.g. granulomatosis with polyangiitis)\n- Bleeding diatheses (e.g. thrombocytopenia, Von Willebrand disease, haemophilia, antiplatelet or anticoagulant medications)\n- Environmental factors e.g. inhaled irritants, temperature and humidity\n\n# Signs and symptoms\n\nThe major symptom is nasal bleeding - other signs and symptoms may include:\n\n- Bleeding down the throat (which may present as haemoptysis or haematemesis) - may signify posterior epistaxis\n- Bleeding from both nostrils is another sign of possible posterior epistaxis\n- Signs and symptoms of haemodynamic instability if blood loss is significant (e.g. tachycardia, pallor, syncope)\n- Signs and symptoms of an underlying cause (e.g. nasal obstruction and rhinorrhoea may indicate a tumour or nasal polyps)\n\n# Investigations\n\nIn most cases of nosebleeds, no investigations are required.\n\nIf bleeding is significant, a **venous blood gas** and **FBC** should be done to look for anaemia and thrombocytopenia, a **clotting screen** looking for coagulopathy and a **group and save** or **crossmatch** if blood transfusion is required.\n\nInvestigations may also be required if an underlying serious cause is suspected, e.g. imaging or flexible nasendoscopy for a suspected tumour, or specific blood tests for bleeding disorders such as Von Willebrand disease.\n\n# Management\n\n- The first step in management is **direct compression**.\n- The patient should sit forward (minimising bleeding into the nasopharynx), breathing through their mouth, and pinch the cartilaginous part of the nose for 10-15 minutes. \n- Sucking ice cubes, cold drinks or placing an ice pack on the back of the neck can help to reduce bleeding.\n- This is sufficient to resolve the majority of anterior epistaxis.\n- A **topic antiseptic** (e.g. Naseptin or mupirocin) may be prescribed to reduce crusting and rebleeding.\n- If direct compression does not resolve the epistaxis and a bleeding point can be visualised, **cautery** may be performed. \n- This involves applying a local anaesthetic spray with a vasoconstrictor (e.g. lidocaine with phenylephrine) to temporarily halt bleeding, then apply silver nitrate (chemical cautery) or electrocautery to the area. \n- Only one side of the septum should be cauterised to avoid perforation.\n- If a bleeding point cannot be visualised or bleeding continues despite cautery, **nasal packing** may be used. \n- The most common devices used are nasal tampons (e.g. Merocel) or inflatable packs (e.g. Rapid-Rhino). \n- Both nostrils can be packed to increase pressure on the area of bleeding.\n- In cases of posterior epistaxis, **posterior packing** may be required which may involve insertion of a Foley catheter with the balloon inflated to compress the bleeding area.\n- Packing should be left in place for 24-48 hours to ensure bleeding has stopped.\n- If bleeding continues despite packing, a **surgical approach** may be required (e.g examination under anaesthesia with ligation of bleeding vessels) or interventional radiology may perform an **embolisation**.\n- **Tranexamic acid** should be given to all patients with severe bleeding.\n- Antiplatelets and anticoagulants should usually be held - may need speciality input (e.g. cardiology) in difficult cases such as patients with metallic heart valves.\n- Anticoagulation may need to be reversed with haematology input if needed.\n- Patients who are haemodynamically unstable may need resuscitation and blood transfusion.\n\n# Complications\n\n- Anaemia\n- Recurrent epistaxis\n- Hypovolaemia\n- Aspiration of blood and airway compromise\n- Nasal cautery may cause septal perforation\n- Nasal packing may lead to sinusitis, septal haematoma or pressure necrosis\n\n# NICE Guidelines\n\n[NICE CKS - Epistaxis](https://cks.nice.org.uk/topics/epistaxis-nosebleeds/)\n\n# References\n\n[ENT UK - Epistaxis Guideline](https://www.entuk.org/_userfiles/pages/files/guidelines/global%20ent%20guidelines/nosebleeds.pdf)\n \n[Life in the Fast Lane - Epistaxis](https://litfl.com/a-case-of-epistaxis/)\n\n[Patient UK - Epistaxis](https://patient.info/doctor/nosebleed-epistaxis-pro)",
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"comment": "surely they wouldn't even tolerate a PR w a fissure??",
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"explanation": "# Summary\n\nAnal fissures are commonly experienced by patients as severe anal pain or a tearing sensation while passing stools, persisting for hours afterward. Typical signs and symptoms include anal spasms and per rectum (PR) bleeding. Key risk factors are constipation and pregnancy. The initial management is typically conservative, including treatment of constipation and use of topical analgesics and vasodilators. For resistant cases, topical calcium channel blockers or oral medications can be used. Referral to a gastroenterologist is recommended for atypical cases or those suspected of Crohn's disease.\n\n# Definition\n\nAnal fissures are linear tears or cracks in the distal anal canal, often causing severe pain and bleeding during or after bowel movements.\n\n# Epidemiology\n\nAnal fissures are a common condition in the general population. However, they are more frequently encountered in certain groups such as those suffering from chronic constipation and pregnant women, particularly during the third trimester or post-delivery.\n\n# Aetiology\n\nAnal fissures occur due to various causes, most notably:\n\n- Constipation: Hard stools can cause tearing in the distal anal canal.\n- Pregnancy: Increased risk during the third trimester and post-delivery.\n\n# Signs and Symptoms\n\nPatients with anal fissures typically present with the following symptoms:\n\n- Severe anal pain or a tearing sensation during bowel movements, lasting for hours afterward.\n- Anal spasms reported by about 70% of patients.\n- Bright red PR bleeding typically noticed on the stool or the toilet paper.\n- Over 90% of fissures are in the posterior midline, visible on parting the buttocks.\n- In chronic cases, a sentinel pile (skin tag) may be visible.\n- In severe cases, digital rectal examination may not be possible due to pain.\n\n[lightgallery]\n\n# Differential Diagnosis\n\nThe differential diagnosis for anal fissures includes other conditions causing anal pain or bleeding, such as:\n\n- Hemorrhoids: Painful, swollen veins in the lower portion of the rectum or anus. Signs include painless bleeding during bowel movements, itching or irritation in the anal region, discomfort, swelling around the anus, and a lump near the anus.\n- Anal abscess or fistula: Symptoms include anal pain, rectal discharge, bleeding, irritation, and fever.\n- Anal cancer: Symptoms can include anal bleeding, anal itching, a lump or mass at the anal opening, pain or feeling of fullness in the anal area.\n- Inflammatory bowel disease (Crohn's disease or ulcerative colitis): Symptoms include diarrhea, rectal bleeding, abdominal cramps and pain, an urgent need to move the bowels, and weight loss.\n\n# Investigations\n\nInvestigation of anal fissures primarily involves a physical examination, including inspection of the anal area and potentially a digital rectal examination (if tolerable by the patient). Further investigations may be warranted in atypical cases or in those with potential signs of systemic disease like Crohn's disease.\n\n# Management\n\nThe management of anal fissures involves both conservative and pharmacologic strategies:\n\n- Treatment of constipation with the use of laxatives and dietary fiber.\n- Use of topical analgesics, such as lidocaine cream or jelly.\n- Application of topical vasodilators like nifedipine or nitroglycerine.\n- Second-line treatments include topical calcium channel blockers (diltiazem), or oral nifedipine / diltiazem.\n- Patients with atypical anal fissures or symptoms/signs suggestive of Crohn's disease should be referred to a gastroenterologist.\n\n# NICE Guidelines\n\n[NICE CKS - anal fissures](https://cks.nice.org.uk/topics/anal-fissure/)\n\n# References\n\n[NHS - anal fissures](https://www.nhs.uk/conditions/anal-fissure/)",
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"question": "A 28-year-old-male notices bright red blood in the toilet bowel after opening his bowels for the last 3 days. He experiences pain when passing stool. He denies any weight loss or abdominal pain. He usually opens his bowels once a day. There are no palpable masses on rectal examination.\n\nWhat is the most likely diagnosis?",
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"explanation": "Whilst this will present with fever and right upper quadrant pain, the absence of jaundice and presence of Murphy’s sign make this less likely.",
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"explanation": "# Summary\n\nCholecystitis is the inflammation of the gallbladder, typically caused by cholelithiasis, and can present as acute or chronic. The characteristic symptoms are right upper quadrant or epigastric pain, fever, nausea, vomiting, and right upper quadrant tenderness. Murphy's sign is commonly positive. Diagnosis is primarily made with an abdominal ultrasound. Management strategies depend on the severity of the condition, with supportive care and early laparoscopic surgery being the definitive treatment. More severe cases may require intensive treatment unit (ITU) admission and urgent cholecystostomy.\n\n# Definition\n\nCholecystitis refers to the acute or chronic inflammation of the gallbladder, which is commonly precipitated by cholelithiasis, or gallstones. \nCholecystitis can be categorised into acute or chronic forms based on the duration and progression of inflammation, and into calculous or acalculous types based on the presence or absence of gallstones. \n\n# Epidemiology\n\nCholecystitis is a common gastrointestinal disease and one of the major causes of hospital admissions related to gastrointestinal disorders worldwide. It affects women more than men, with an estimated ratio of 2:1. Age is a significant risk factor, with incidence rising in individuals over 40 years of age. Other risk factors include obesity, ethnicity (higher prevalence in Hispanic and Native American populations), rapid weight loss, diabetes, pregnancy, and a family history of gallstones.\n\n# Pathophysiology\n\nCholecystitis predominantly results from the obstruction of the cystic duct by gallstones. This obstruction can lead to an infection in the gallbladder caused by organisms including:\n\n- E.coli (most common)\n- Klebsiella\n- Enterococcus\n\n# Classification\n\nCholecystitis can be classified into two main categories: acute and chronic. Additionally, cholecystitis can be further categorised based on the presence or absence of gallstones.\n\n1. **Acute Cholecystitis:** This is characterised by the sudden onset of inflammation in the gallbladder. It is often associated with the presence of gallstones, particularly when one of these stones obstructs the cystic duct, leading to a buildup of bile and subsequent inflammation. \n\n2. **Chronic Cholecystitis:** This is a long-term, smoldering inflammation of the gallbladder, usually caused by the repeated irritation of gallstones. Over time, chronic cholecystitis can lead to thickening of the gallbladder wall and a decrease in its overall function. Unlike acute cholecystitis, chronic cholecystitis may have milder and more intermittent symptoms, including recurrent abdominal discomfort after meals.\n\n3. **Calculous Cholecystitis:** This type of cholecystitis occurs when gallstones are present in the gallbladder. These stones can obstruct the cystic duct, impair bile flow, and trigger an inflammatory response. Calculous cholecystitis is the most common form of cholecystitis.\n\n4. **Acalculous Cholecystitis:** In contrast, acalculous cholecystitis develops without the presence of gallstones. It is often associated with other underlying medical conditions, such as critical illness, severe trauma, or prolonged fasting, which can lead to gallbladder stasis or ischaemia. Acalculous cholecystitis is less common but can be more severe and challenging to diagnose, as it may not present with the typical gallstone-related symptoms.\n\n\n# Signs and Symptoms\n\nPatients with acute cholecystitis present with:\n\n- Right upper quadrant/epigastric pain, which can radiate to the right shoulder tip if the diaphragm is irritated\n- Fever\n- Nausea and vomiting\n- Right upper quadrant tenderness\n- Positive Murphy's sign\n\nIn cases with associated biliary obstruction, patients may exhibit jaundice, dark urine, and pale stools. However, these are not key features of cholecystitis.\n\n# Differential Diagnosis\n\nThe differential diagnoses for cholecystitis primarily include other conditions that cause right upper quadrant pain. The key signs and symptoms for these conditions are:\n\n- **Acute pancreatitis**: Epigastric pain radiating to the back, nausea and vomiting, tenderness of the abdomen.\n- **Peptic ulcer disease**: Epigastric pain that may be relieved by eating, dark stool (melena), nausea and vomiting.\n- **Hepatitis**: Jaundice, fatigue, pale stools, dark urine, and flu-like symptoms.\n- **Right lower lobe pneumonia**: Cough, fever, shortness of breath, and right-sided abdominal pain.\n\n# Investigations\n\n* The first line investigation for suspected cholecystitis is an ultrasound examination of the abdomen, which can identify gallstones, gallbladder wall thickening, and pericholecystic fluid. \n* Alongside this, blood tests including FBC, U+Es, CRP and LFTs will help reveal if there is an underlying infection/evidence of sepsis, as well as any cholestasis\n* CT abdomen-pelvis (rarely MRI) is helpful to look for complications e.g. perforation, collections\n\n# Management\n\nThe management of cholecystitis varies depending on its subtype and the clinical circumstances. Here's a summary of management for each subtype of cholecystitis:\n\n**Acute Calculous Cholecystitis:**\n\n- **Conservative Management:** In mild cases, patients may be managed conservatively with bowel rest, fasting, and intravenous fluids to relieve symptoms.\n- **Antibiotics:** Antibiotics, often covering common pathogens like Escherichia coli and Klebsiella pneumoniae, are typically prescribed.\n- **Cholecystectomy:** The definitive treatment for acute calculous cholecystitis is laparoscopic cholecystectomy, which is recommended during the same hospital admission or within a week.\n\n**Acalculous Cholecystitis:**\n\n- **Prompt Surgery:** Acalculous cholecystitis is considered a surgical emergency, and prompt cholecystectomy is typically recommended.\n\n**Chronic Cholecystitis:**\n\n- **Elective Cholecystectomy:** For patients with chronic cholecystitis, an elective laparoscopic cholecystectomy may be performed to prevent recurrent episodes and complications.\n- **Symptomatic Management:** In some cases, patients may initially receive symptomatic management and dietary modifications, but surgery is eventually recommended.\n\nFurther research now focuses on timing of intervention, resulting in what is now known as 'hot' vs 'cold' laparoscopic cholecstectomies:\n\n**Hot Elective Cholecystectomy:**\n\n- In cases of acute cholecystitis where the patient's condition has improved with conservative management, but the inflammation is still present, an elective (\"hot\") laparoscopic cholecystectomy should be performed within 6 weeks of the acute episode.\n- This approach balances the need to address the underlying cause with allowing the patient's condition to stabilise.\n\n**Cold Elective Cholecystectomy:**\n\n- In cases of chronic cholecystitis or asymptomatic gallstones, where there is no acute inflammation or infection, an elective (\"cold\") laparoscopic cholecystectomy can be scheduled based on the patient's convenience and availability.\n- This approach avoids the urgency associated with acute inflammation.\n\nIn summary, the management of cholecystitis includes conservative measures, antibiotics, and surgical intervention, depending on the subtype and clinical circumstances. Elective laparoscopic cholecystectomy is recommended for both acute calculous cholecystitis (after symptom resolution) and chronic cholecystitis. The timing of surgery may vary, with \"hot\" cholecystectomy addressing acute inflammation and \"cold\" cholecystectomy focusing on non-urgent cases.\n\n### Complications of Laparoscopic Cholecystectomies\n\nWhile the exact prevalence can vary, complications occur in a small but significant proportion of patients undergoing cholecystectomy. Post-cholecystectomy syndrome is seen in approximately 10-15% of patients.\n\n- **Haemorrhage:** Rapid hypotension or development of a retroperitoneal haematoma. May require surgical intervention if severe.\n- **Post-cholecystectomy syndrome:** Symptoms include colicky abdominal pain, diarrhea, vague abdominal pain, and jaundice. Management is symptomatic with e.g. anti-spasmodics for pain and nausea.\n- **Bile duct injury:** Presents with dark-colored urine and stools, potentially progressing to chemical peritonitis, causing abdominal pain and distension. Sometimes this requires surgical intervention.\n- **Pneumoperitoneum:** Trapped air in the subcutaneous space can lead to subcutaneous emphysema, pneumothorax, or air embolism.\n\n# Complications\n\n\n1. **Empyema:** This occurs when the gallbladder becomes filled with pus due to a severe infection. It can lead to systemic infection and sepsis if not treated promptly.\n\n2. **Gangrenous Cholecystitis:** In severe cases of cholecystitis, the gallbladder tissue may become necrotic (dead) due to impaired blood flow. This condition is known as gangrenous cholecystitis and can lead to tissue perforation, abscess formation, or peritonitis.\n\n3. **Perforation:** Prolonged inflammation can cause the gallbladder to rupture or perforate, leading to bile leakage into the abdominal cavity. This is a life-threatening emergency requiring immediate surgery.\n\n4. **Abscess Formation:** A collection of pus can develop within or around the gallbladder, leading to an abscess. Abscesses may require drainage and antibiotic therapy.\n\n5. **Bile Duct Obstruction:** Inflammation or gallstones can cause blockage of the common bile duct, leading to jaundice, pancreatitis, or cholangitis (bile duct infection).\n\n6. **Chronic Cholecystitis Complications:** Long-term inflammation of the gallbladder may lead to scarring, thickening of the gallbladder walls, and impaired gallbladder function. This can result in chronic abdominal pain and discomfort.\n\n\n# NICE Guidelines\n\n[Click here to see the NICE guidelines on cholecystitis](https://cks.nice.org.uk/topics/cholecystitis-acute/)",
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"question": "A 45-year-old female has a fever and constant upper abdominal pain. She denies any diarrhoea or recent travel history. On general inspection, she has no scleral icterus. On palpation, she is extremely tender in the right upper quadrant pain on palpation, particularly when taking a deep breath in.\n\nWhat is the most likely diagnosis?",
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"explanation": "# Overview\n\nThe Mental Capacity Act (MCA) includes provisions that allow people to plan for their care in advance, for a situation in the future where they do not have the capacity to make decisions. Two of these are Advanced Statements and Advanced Decisions. An individual can make both an Advanced Statement and an Advance Decision.\n\n# Definition of Advanced Decisions\n\nAn Advanced Decision, short for Advanced Decision to Refuse Treatment, is a legally binding document. Its purpose is to ensure that an individual can refuse a specific treatment(s) that they do not want to have in the future.\n\n# Advanced Decision Criteria\n\nIn order for an Advanced Decision to be legally binding, it must meet certain criteria:\n\n _It must be valid (this means it must have been made at a time when the individual had capacity to make that decision)._\n\n _It must be applicable (this means the wording must be specific to the medical circumstances, and not vague or unclear)._\n\n _It must have been made when the individual was over 18, and fully informed about their decision._\n\n _It must not have been made under the influence or duress of other people_\n\n _It must be written down, be signed and witnessed (if it concerns a refusal of life-saving treatment)_\n\n# What Can Advanced Decisions Cover?\n\nTreatments that can be refused include life-sustaining treatments. It cannot refuse basic care (such as washing), food or drink by mouth, measures designed purely for comfort (e.g. painkillers), or treatment for a mental health condition if the individual is sectioned under the Mental Health Act. It can also not demand specific treatment or something that is illegal (e.g. assisted dying).\n\n# Definition of Advanced Statement\n\nAn Advance Statement is sometimes called a \"Statement of Wishes and Care Preferences\". It allows an individual to make general statements about their wishes, beliefs, feelings and values and how these influence their preferences for their future care and treatment.\n\nAn Advance Statement is not by itself legally binding, but legally must be taken into consideration when making a \"best interests\" decision on someone's behalf under the Mental Capacity Act (MCA), 2005. This is because one of the criteria of the MCA is that a patient's \"wishes, feelings, beliefs and values\" must be taken into consideration; an Advanced Statement provides evidence of this.\n\n# Advanced Statement information included\n\nInformation that can be included in an Advanced Statement can be anything that is important to the individual. This might include:\n\n _Religious or spiritual views, and those that might relate to care_\n\n _Food preferences_\n\n _Information about your daily routine_\n _Where you would like to be cared for (in hospital, at home, in a care home etc.)_\n\n _Any people who you would like to be consulted when best interests decisions are being made on your behalf (however this does not give the same legal power as creating a Lasting Power of Attorney)_\n\n# What Can Advanced Statement Cover?\n\nAn Advanced Statement can be made verbally, but it is better to write it down so there is clear documented evidence of an individual's wishes and views. Copies of the Advanced Statement can be given to anyone the individual wishes to have a copy (e.g. their GP, carers and relatives).",
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"question": "A 45-year-old male with motor neuron disease would like to find out if it is possible to establish which medical treatments they do not want to have in future, if they were no longer able to make these decisions for themselves.\n\nHow can they do this in a way which is legally binding?",
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"comment": "Just wondering if the pt's classmate had impetigo, and if so is that a red herring for eczema herpeticum, which is a HSV infection?",
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"explanation": "# Summary\n \n\nFever and rash is a frequent emergency presentation in paediatrics, often due to a non-specific viral infection. Key considerations include septicaemia; slapped cheek syndrome; Hand, foot and mouth disease; Scarlet fever; Measles; Urticaria; Chickenpox; Roseola, and Rubella. Depending on the specific presentation and diagnosis, management strategies range from supportive care to initiation of antibiotics or antiviral medication.\n \n\n# Definition\n \n\nA fever is a temporary elevation in the body's thermoregulatory set-point, typically by more than 1–1.5 °C. In children, a fever is usually defined as a rectal temperature over 38.0 °C (100.4 °F). A rash refers to any change in skin colour, texture, or overall appearance.\n \n\n# Epidemiology\n \n\nFever and rash commonly present in paediatric populations, predominantly due to non-specific viral infections, often unidentified. The specific epidemiology varies according to the underlying cause.\n \n\n# Aetiology\n \n\nFever and rash in children can be caused by a multitude of conditions including:\n \n\n - Septicaemia\n - Slapped cheek syndrome (Fifth Disease or Parvovirus B19)\n - Hand, Foot and Mouth disease\n - Scarlet fever\n - Measles\n - Urticaria (hives)\n - Chickenpox\n - Roseola\n - Rubella\n \n\n# Signs and symptoms\n \n\n - **Erythema toxicum (erythema toxicum neonatorum):** This is a benign rash in newborns which consists of erythematous macules (flat red patches) papules (small bumps) and pustules. The eruption waxes and wanes over several days and rarely for more than a day.\n - **Threadworm**: also known as pinworm, presents with an itchy bum, especially at night, and may also be visible in faeces.\n - **Septicaemia**: Rapid development of a non-blanching purpuric skin rash, lethargy, headache, fever, rigors, vomiting.\n - **Slapped cheek syndrome**: Rash on both cheeks, fever, upper respiratory tract infection symptoms.\n \n\n [lightgallery]\n \n\n - **Hand, foot, and mouth disease**: Blisters on hands and feet, grey ulcerations in the buccal cavity, fever, lethargy.\n \n\n [lightgallery1]\n \n\n [lightgallery2]\n \n\n - **Scarlet fever**: Coarse red rash on the cheeks, sore throat, headache, fever, 'sandpaper' texture rash, bright red tongue.\n \n\n [lightgallery3]\n \n\n [lightgallery4]\n \n\n - **Measles**: Erythematous, blanching maculopapular rash, fever, cough, runny nose, conjunctivitis, Koplik spots.\n \n\n [lightgallery5]\n \n\n [lightgallery6]\n \n\n - **Urticaria**: Raised, itchy red rashes, usually not accompanied by fever.\n \n\n [lightgallery7]\n \n\n - **Chickenpox**: Maculopapular vesicular rash that crusts over and forms blisters.\n \n\n [lightgallery8]\n \n\n - **Roseola**: Lace-like red rash across the whole body, high fever.\n \n\n [lightgallery9]\n \n\n - **Rubella**: Rash that starts on the head and spreads to the trunk, postauricular lymphadenopathy.\n \n\n [lightgallery10]\n \n\n# Differential Diagnosis\n \n\nThe differential diagnosis of a child with fever and rash is extensive and includes:\n \n\n - **Septicaemia**: The key signs include rapid development of a non-blanching purpuric skin rash, lethargy, headache, fever, rigors, and vomiting.\n - **Trauma**: Presents with localised rash or bruising, often with a clear history of injury.\n - **Liver disease**: Accompanied by jaundice, pruritus, and other systemic symptoms.\n - **Drug Reaction (e.g., antiepileptics)**: Rash may be accompanied by other signs of drug reaction, like itchiness or wheezing.\n - **Vasculitis**: Can present with fever, weight loss, and multi-system symptoms.\n - **Thrombocytopaenia**: Accompanied by mucosal bleeding and petechiae.\n - **Coagulopathy**: Similar to thrombocytopenia, patients may have petechiae and mucosal bleeding.\n - **Malignancy**: Presents with fatigue, unexplained weight loss, and systemic symptoms.\n - **Disseminated intravascular coagulation (DIC)**: Accompanied by systemic symptoms of sepsis or malignancy.\n \n\n# Investigations\n \nOften is a clinical diagnosis based on appearance of the rash and the associated symptoms. \n \nInvestigations may include:\n \n\n - Blood tests (FBC, Coagulation profile)\n - Blood cultures\n - Viral serology\n - Skin biopsy\n \n \n\n# Management\n \n\nManagement varies depending on the condition causing fever and rash:\n \n\n - **Septicaemia**: Immediate broad-spectrum IV antibiotics, notify a senior paediatrician.\n - **Slapped cheek syndrome**: Generally self-limiting, symptomatic treatment.\n - **Hand, foot, and mouth disease**: Generally self-limiting, symptomatic treatment.\n - **Scarlet fever**: Treated with antibiotics, usually phenoxymethylpenicillin.\n - **Measles**: Supportive management and immunisation is crucial.\n - **Urticaria**: Antihistamines and/or steroids, identify and avoid triggers.\n - **Chickenpox**: Supportive treatment, antiviral treatment for high-risk groups.\n - **Roseola**: Self-limiting, supportive management.\n - **Rubella**: Self-limiting, supportive management, immunisation for prevention.\n - **Threadworm**: Education on good hand hygiene, and oral mebendazole for the child **and** family.\n \n\n# References\n \n\n[NHS page on Rashes in babies and children](https://www.nhs.uk/conditions/rashes-babies-and-children/)",
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"question": "A 6-year-old boy with a history of eczema and asthma has a fever and multiple monomorphic lesions on his face, arms and trunk. His dad mentions his classmate at school last week had a golden crusted rash on their face.\n\nWhat is the next most appropriate management step?",
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"explanation": "# Summary\n\n\nTumour lysis syndrome is a potentially lethal condition caused by the rapid death of tumour cells often following chemotherapy or rapid progression of haematological malignancies, resulting in the massive release of intracellular contents. It is an oncological emergency. Patients commonly present with acute-onset dysuria/oliguria, abdominal pain, or weakness. Key investigations include measurements of U&E (showing raised potassium and phosphate), calcium (typically low), uric acid (raised), and ECG to detect metabolic abnormalities and life-threatening arrhythmias. Initial management involves the correction of electrolyte abnormalities and intravenous fluid administration.\n\n\n# Definition\n\n\nTumour lysis syndrome is a serious metabolic disorder caused by the rapid death of tumour cells in response to chemotherapy. This results in a massive release of intracellular contents into the bloodstream, leading to significant electrolyte imbalances.\n\n\nTumour lysis syndrome is most commonly associated with aggressive, rapidly proliferating tumours such as acute leukaemia and high-grade lymphomas, particularly after the initiation of cytotoxic therapy. \n\n\n# Aetiology\n\n\nThe syndrome occurs due to the rapid release of intracellular contents from dying tumour cells, often following chemotherapy. It can however also be caused by high-grade lymphomas and acute leukaemias. This leads to hyperuricaemia, hyperphosphatemia, hyperkalaemia, and hypocalcaemia. These metabolic abnormalities lead to the clinical manifestations including acute kidney injury and arrhythmias.\n\n\n# Signs and symptoms\n\n\nPatients may present with symptoms related to electrolyte abnormalities and hyperuricaemia, which include:\n\n\n* Dysuria or oliguria\n* Abdominal pain\n* Weakness\n* Nausea or vomiting\n* Muscle cramps\n* Seizures\n* Cardiac arrhythmias\n* Gout/joint swelling\n\n\n# Differential diagnosis\n\n\nDifferential diagnosis should consider other causes of similar symptoms and laboratory abnormalities, such as:\n\n\n* **Acute kidney injury**: while tumour lysis syndrome can cause AKI, other causes should be considered. For example, patients may have significant dehydration or have received nephrotoxic drugs contributing to AKI. Careful history-taking and the absence of other features of tumour lysis syndrome should raise suspicion of AKI due to other causes. It is important to note though, that AKI can cause significant electrolyte abnormalities, so careful monitoring is required.\n* **Isolated hyperkalaemia**: presents with muscle weakness, fatigue, palpitations, and potentially life-threatening cardiac arrhythmias. Patients may have a history of renal failure or taking potassium-sparing medications. Uric acid, phosphate and calcium levels would be normal.\n* **Isolated hyperphosphateamia**: presents with muscle cramps, itching, and perioral tingling or numbness. Uric acid and potassium would be normal.\n* **Isolated hypocalcaemia**: presents with numbness and tingling in the hands, feet, and around the mouth, muscle cramps, and seizures. Uric acid, potassium and phosphate would be normal\n\n\n# Investigations\n\n\nKey investigations for tumour lysis syndrome include:\n\n* Basic observations\n* U&E: Potassium and phosphate are usually raised, raised Cr suggestive of AKI/renal failure.\n* Calcium: Typically low in tumour lysis syndrome.\n* Uric acid: Usually elevated.\n* ECG: To assess risk of arrhythmias caused by electrolyte abnormalities.\n* Hyperkalaemia may cause tented T waves, broad QRS, flattened P-wave and a prolonged PR interval. \n* Hypocalcaemia may cause a prolonged QT interval.\n\n\n# Management\n\n\nManagement of tumour lysis syndrome primarily focuses on:\n\n\n* Correction of electrolyte imbalances & mitigation of arrhythmia risk.\n* For example in severe hyperkalaemia, calcium gluconate is given followed by an insulin-dextrose infusion or nebulised salbutamol. Further management may include calcium resonium to prevent further potassium absorption from the gut.\n* Severe hypocalcaemia may require parenteral replacement.\n* Dialysis may be required in severe cases.\n* Administration of intravenous fluids to help flush out the intracellular contents released by the dying tumour cells.\n* Medications: rasburicase (a recombinant form of the urate oxidase enzyme) transforms uric acid into allantoin. Allantoin is more soluble in urine than uric acid, and more easily eliminated by the kidney.\n\n\n### Prevention \n\n\n* Low/intermediate risk patients can be managed with a combination of adequate hydration and allopurinol. \n* Rasburicase (a recombinant form of the urate oxidase enzyme) can be used as a prophylactic agent in adults with hyperuricaemia that is inadequately managed by allopurinol or febuxostat.\n\n\n# References\n\n[British Society for Haemotology: Management of Tumour Lysis Syndrome in Adults and Children with Haematological Malignancies](https://b-s-h.org.uk/guidelines/guidelines/management-of-tumour-lysis-syndrome-in-adults-and-children-with-haematological-malignancies)\n\n[Patient.info: Oncological emergencies](https://patient.info/doctor/oncological-emergencies#tumour-lysis-syndrome)",
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"explanation": "Mycoplasma genitalium is a bacterium without a cell wall that can cause urethritis. While it is intracellular, it is less common than Chlamydia trachomatis and typically associated with persistent or recurrent urethritis rather than acute symptoms as seen in this case.",
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"explanation": "Chlamydia trachomatis is the most common cause of sexually transmitted urethritis in young men. It is an obligate intracellular bacterium, which fits the NAAT findings. It typically presents with dysuria and a clear or white urethral discharge.",
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"explanation": "Treponema pallidum is the causative organism of syphilis, a sexually transmitted infection that can cause painless genital ulcers (primary syphilis) or systemic symptoms (secondary syphilis). It is a spirochete, not an obligate intracellular bacterium, and is not associated with urethritis.",
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"explanation": "Trichomonas vaginalis is a motile protozoan, not a bacterium. It is a rare cause of urethritis in men and is typically associated with frothy discharge and irritation, not the white discharge and dysuria seen here.",
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"explanation": "# Summary\n \n\nUrethral discharge is a common symptom often associated with sexually transmitted infections (STIs) such as gonorrhoea and chlamydia, or non-specific/non-gonococcal urethritis. Less common causes include infections by Ureaplasma urealyticum, Trichomoniasis, herpes simplex, and E.coli, as well as conditions like cystitis and pyelonephritis. Trauma or a foreign body in the urethra can also be responsible. Key signs and symptoms, in addition to urethral discharge, can include dysuria, pruritis, or haematuria. Investigations typically involve laboratory tests such as urinalysis and cultures, alongside polymerase chain reaction (PCR) for detecting specific pathogens. Management primarily revolves around antimicrobial therapy, symptom relief, and partner notification and treatment.\n \n\n# Definition\n \n\nUrethral discharge refers to any abnormal fluid that is expelled from the urethra, aside from urine and semen. This discharge can be the result of an infection, inflammation, or other conditions affecting the urinary tract.\n\n# Epidemiology\n\nUrethral discharge is a common presenting symptom of urethritis, of which the most common causes are sexually transmitted infections including chlamydia and gonorrhoea.\n \n\n# Aetiology\n \n\nCauses of urethral discharge include:\n \n\n- *Neisseria gonorrhoeae*, or gonococcal urethritis, which typically presents 2-5 days after exposure\n- Non-gonococcal urethritis (NGU) - common causes include*Chlamydia trachomatis* and *Mycoplasma genitalium*. Other causes of NGU include:\n - Infections: *Ureaplasma urealyticum, Trichomonas vaginalis*, herpes simplex virus, adenovirus, lower & upper urinary tract infections\n - Non-infectious: trauma to the urethra, irritants, foreign body\n\n\n# Signs and Symptoms\n \n\nCommon symptoms associated with urethral discharge and urethritis include:\n \n\n- Mucoid and/or purulent urethral discharge\n- Dysuria, haematuria\n- Pruritis, erythema and irritation\n- Associated lymphadenopathy in groin/inguinal region\n \n\n# Differential Diagnosis\n \n\n- **Gonorrhoea**: Characterised by a purulent, often copious urethral discharge, dysuria, and less commonly, testicular discomfort.\n- **Chlamydia**: Presents with a mucoid or watery discharge, dysuria, testicular discomfort, and possibly conjunctivitis.\n- **Non-specific urethritis** (NSU) or non-gonococcal urethritis (NGU): Discharge, dysuria, and occasionally urethral pruritus.\n- **Ureaplasma urealyticum**: Causes dysuria and urethral discharge, less commonly associated with testicular discomfort.\n- **Trichomoniasis**: Causes pruritus, dysuria, and a frothy, yellow-green discharge with a foul smell.\n- **Herpes simplex virus**: Painful vesicles or ulcers, possible urethral discharge, and systemic symptoms like fever.\n- **E.coli**: Typically presents as a urinary tract infection (UTI) with dysuria, frequency, urgency, and occasionally haematuria.\n- **Cystitis**: Lower urinary tract infection causing dysuria, frequency, urgency, and suprapubic pain.\n- **Pyelonephritis**: An upper urinary tract infection causing flank pain, fever, nausea/vomiting, dysuria, frequency, and urgency.\n- **Trauma**: Painful urination, possible blood in the urine or at the urethral meatus, and history of trauma.\n- **Foreign body**: Pain, possible blood at the urethral meatus, history of foreign body insertion.\n \n\n# Investigations\n \nClinical assessment of urethral discharge should include:\n\n- **History** including symptoms, sexual history and past medical history\n- **Examination** including genitalia, lymph node palpation and digital rectal examination to assess for prostatitis\n- Bedside tests including **urinalysis** and **observations**\n\nLaboratory tests to consider include:\n\n- Nucleic acid amplification testing (**NAAT**) for *N. gonorrhoea*, *C. trachomatis* and *M. genitalium*.\n- Swabs/first-void urine sample for **microscopy and culture** for *Trichomonas*\n- **HIV** testing\n- **Urine microscopy and culture** for urinary tract infection\n- **Blood tests** including FBC, U&Es & CRP, especially if systemic symptoms are present\n \n\n# Management\n\nIf a sexually transmitted infection is suspected or diagnosed, patients should be referred to a genito-urinary medicine (GUM) clinic. Management involves:\n \n\n- Antibiotic therapy targeting the suspected pathogen based on clinical presentation, or following cultures and sensitivities\n - Empirical treatment usually involves doxycycline 100mg twice daily for seven days. Alternatives include azithromycin or ofloxacin.\n - If gonococcal urethritis is suspected, ceftriaxone is usually first-line\n - If Trichomoniasis is suspected, this should be treated with oral metronidazole\n- Symptom management (for example, pain relief)\n- Partner notification and treatment to prevent reinfection\n \n\n# NICE guidelines\n \n\n[NICE CKS: Urethritis](https://cks.nice.org.uk/topics/urethritis-male/)\n\n[NICE CKS: Gonorrhoea](https://cks.nice.org.uk/topics/gonorrhoea/)\n\n[NICE CKS: Trichomoniasis](https://cks.nice.org.uk/topics/trichomoniasis/)\n\n \n# References\n\n\n[BASHH guideline: Non-gonococcal urethritis](https://www.bashhguidelines.org/media/1051/ngu-2015.pdf)\n\n[BMJ Best Practice: Urethritis](https://bestpractice.bmj.com/topics/en-gb/54)",
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"question": "A 21-year-old man presents to his GP with a 3-day history of white urethral discharge and dysuria. He is sexually active and recently began a casual relationship. Nucleic acid amplification testing (NAAT) confirms that his condition is caused by an obligate intracellular bacterium.\n\nWhat is the most likely causative organism?",
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"explanation": "Sodium would usually be low due to increased ADH levels leading to hypervolaemic hyponatraemia.",
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"explanation": "Serum triglycerides would likely be raised in nephrotic syndrome.",
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"explanation": "This would likely be raised in nephrotic syndrome. This is due to a combination of increased production and impaired catabolism/clearance of LDLs.",
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"explanation": "This describes a case of minimal change disease, a form of nephrotic syndrome. It commonly follows viral upper respiratory tract infections. This classically causes a low serum albumin and elevated serum triglycerides/cholesterol.",
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"explanation": "# Summary\n \n\nMinimal Change Disease (MCD) is the leading cause of nephrotic syndrome in children, responsible for roughly 70% of cases. It shows minimal changes to nephrological structures on light microscopy. Typically characterised by the presence of oedema and frothy urine, MCD often follows a viral upper respiratory tract infection. Key investigations include urine tests and possibly a kidney biopsy. Management strategies primarily involve corticosteroid therapy, fluid restriction, and reduced salt intake. It can lead to complications like spontaneous peritonitis, thrombosis, renal damage, and an increased risk of infections.\n \n\n# Definition\n \n\nMinimal Change Disease is a condition that primarily affects the kidneys. Despite causing significant clinical symptoms, the disease is marked by minimal or no changes visible under light microscopy in nephrological structures. However, more subtle changes can be detected using electron microscopy. This condition is the most common cause of nephrotic syndrome in children, and while it may also affect adults, it is much less common in this population.\n \n\n# Epidemiology\n \n\n - The incidence of minimal change disease is 2 per 100,000 children in the UK per year. \n - Minimal Change Disease most commonly affects children aged 1-8 years old.\n - It is the primary cause of nephrotic syndrome in children, accounting for around 70% of all cases.\n \n\n# Aetiology\n \n\nWhile the exact cause of Minimal Change Disease is unknown, it has been associated with certain factors:\n \n\n - Recent viral upper respiratory tract infection\n - There may be an immune response causing damage to the kidneys.\n - Being male (2x more prevalent in boys than girls)\n - Being South Asian (4-6x more prevalent compared to white British children)\n \n\n# Signs and Symptoms\n \n\nPatients with Minimal Change Disease typically present with:\n \n\n - Oedema, including facial swelling and puffiness around the eyes most prominent in the morning, followed by pedal oedema \n - Frothy urine, caused by excessive protein in the urine (proteinuria)\n - Fatigue\n - Weight gain due to fluid retention\n\n# Differential Diagnosis\n \n\nIn a patient presenting with symptoms suggestive of nephrotic syndrome, several other conditions should be considered:\n \n\n - **Focal segmental glomerulosclerosis (FSGS)**: Presents with proteinuria, hypertension, and oedema. However, FSGS often progresses to kidney failure and responds less well to corticosteroids compared to MCD.\n - **Membranous nephropathy**: Characterized by heavy proteinuria, hypertension, and oedema. It typically affects adults and is less common in children.\n - **Secondary causes of nephrotic syndrome**: Conditions such as diabetes, lupus, or certain infections and medications can lead to nephrotic syndrome.\n \n\n# Investigations\n \n\nPatients suspected to have Minimal Change Disease should undergo:\n \n\n - Urine tests: to identify proteinuria and to look for blood or white blood cells\n - Urine protein : creatinine >200 mg/mmol \n - Blood tests: to check for low albumin and elevated cholesterol\n - Hypoalbuminaemia defined by serum albumin < 25 g/L\n - Kidney biopsy: often reserved for patients who do not respond to initial treatment, to confirm diagnosis. Light microscopy of renal biopsy specimens from patients with MCD shows minimal to no change, hence the name.\n \n\n# Management\n \n\nThe treatment of Minimal Change Disease involves:\n \n\n- Corticosteroid therapy: Prednisolone is the first-line treatment, used for 4 weeks. \n- Second-line therapy: Includes other oral immunosuppressive agents such as ciclosporin if initial treatment fails.\n- Fluid restriction and reduced salt intake: To manage oedema and prevent further complications.\n - Fluid can be restricted to 750 mL/day for children < 5 years, or 1,000 mL/day for children over the age of 5. \n- Diuretics (i.e. furosemide) may be used to reduce fluid overload.\n - If severe, IV albumin infusions may also be used to manage hypoalbuminaemia. \n\nChildren are also advised to have the pneumococcal vaccine due to relative immunodeficiency and the use of immunosuppressive medications. \n \n# Complications\n \nComplications of minimal change disease include:\n \n- Infection\n - Through the loss of immunoglobulins in urine, the children are at increased risk of infections\n - Antibiotic prophylaxis is not routinely recommended \n- Thrombosis due to loss of anti-thrombin III in the urine and hypovolaemic state \n - Consider DVT, PE and cerebral venous sinus thrombosis in a child presenting with leg, chest or head pain\n- Steroid-related side effects (i.e. hyperglycaemia/diabetes, hypertension, psychosis and sleep disturbance) \n- Vitamin D deficiency \n- Hypertension \n- Hypercholesterolaemia \n \n\n# Prognosis\n\nInitially, over 80% of children respond to high-dose prednisolone. Factors associated with poor response to steroid treatment include age <1 year or >10 years, hypertension at presentation, macroscopic haematuria, and a family history of nephrotic syndrome. \n\nThe long-term prognosis, however, for Minimal Change Disease varies:\n \n\n - 1/3 of patients resolve completely and never have another episode.\n - 1/3 have further relapses requiring additional steroid treatment.\n - 1/3 are dependent on continued steroid/immunosuppression therapy.\n\n \nPatients require monitoring via urinary dipsticks. \n \n\n# References\n\n[NHS Nephrotic syndrome in children](https://www.nhs.uk/conditions/nephrotic-syndrome/) \n \n [BMJ Best Practice Summary](https://bestpractice.bmj.com/topics/en-gb/940)\n \n [National Kidney Federation Minimal Change Nephropathy](https://www.kidney.org.uk/minimal-change-nephropathy#:~:text=Minimal%20change%20causes%20fluid%20retention,This%20is%20not%20usually%20affected.)",
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"question": "A 5-year-old boy has facial swelling. His mother states he had a cough and runny nose the week prior to the swelling. His urine dipstick shows 3+ protein.\n\nGiven the likely diagnosis, which of the following investigation results would you expect to see?",
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"explanation": "This history does not mention any of the main features of EUPD, including impulsive behaviour or difficulty maintaining relationships.",
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"comment": "The stem doesn't describe the fact the 'compulsion' is required to dispel the negative feelings associated with the 'obsession' though? It describes it as two separate symptoms? idk",
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"explanation": "# Summary\n\nObsessive-Compulsive Disorder (OCD) is a debilitating psychiatric condition characterized by intrusive thoughts and repetitive behaviors. According to both ICD-11 and DSM-V criteria, individuals with OCD experience distressing obsessions, leading to compulsive rituals that consume significant time and impair daily functioning. Affecting 1-3% of the population, OCD often emerges in adolescence, with a chronic course. Biological factors, including genetic and neurobiological elements, contribute to its etiology. While cognitive-behavioral therapy and pharmacotherapy prove effective in management, complications such as impaired quality of life underscore the need for comprehensive, early intervention. \n\n# Definition\n\nObsessive-compulsive disorder (OCD) is characterized by recurrent obsessional thoughts or compulsive acts or, commonly, both, which cause significant functional impairment and/or distress.\n\n**ICD-11 Criteria:**\n\n- Presence of obsessions, compulsions, or both.\n- Time-consuming (more than one hour a day) or causes significant impairment.\n- Not attributed to another medical or mental disorder.\n\n**DSM-V Criteria:**\n\n- Presence of obsessions, compulsions, or both.\n- Time-consuming or cause significant distress/impairment.\n- Not attributable to another medical or mental disorder.\n\n# Epidemiology\n\n- Affects approximately 1-3% of the population.\n- Onset often in adolescence or early adulthood.\n- Variable course, with chronicity common.\n\n# Aetiology\n\n- **Biological Factors:** Genetic predisposition, neurobiological abnormalities.\n- **Psychological Factors:** Early life experiences, cognitive processes. Often co-exists with other mental health conditions.\n- **Environmental Factors:** Trauma, stressors.\n\n# Clinical Features\n\n- **Obsessions:** Intrusive, unwanted thoughts or images causing distress.\n- **Compulsions:** Repetitive behaviors or mental acts aimed at reducing anxiety.\n- Significant time investment and interference with daily life.\n\nSymptom severity can be assessed using the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS). With scores: 8 - 15 = Mild OCD, 16 - 23 = Moderate OCD, 24 - 31 = Severe OCD, 32 - 40 = extremely severe OCD.\n\n\n# Differential Diagnosis\n\n\n- **Generalized Anxiety Disorder (GAD)**\n - *Similarity:* Intrusive thoughts.\n - *Difference:* GAD involves excessive worry across various domains, while OCD focuses on specific obsessive themes and compulsive rituals.\n\n- **Major Depressive Disorder (MDD)**\n - *Similarity:* Intrusive thoughts and impaired daily functioning.\n - *Difference:* MDD primarily involves persistent low mood, whereas OCD centers on anxiety-provoking obsessions and compulsions.\n\n- **Body Dysmorphic Disorder (BDD)**\n - *Similarity:* Preoccupation with appearance.\n - *Difference:* BDD centers on perceived flaws, while OCD involves intrusive thoughts unrelated to personal appearance.\n\n- **Social Anxiety Disorder (SAD)**\n - *Similarity:* Avoidance behaviors.\n - *Difference:* SAD's avoidance stems from fear of social scrutiny, while OCD avoidance is driven by anxiety related to obsessions.\n\n- **Trichotillomania (Hair-Pulling Disorder)**\n - *Similarity:* Repetitive behaviors.\n - *Difference:* Trichotillomania involves compulsive hair pulling, distinct from OCD's varied ritualistic behaviors.\n\n- **Hoarding Disorder**\n - *Similarity:* Compulsive behaviors.\n - *Difference:* Hoarding focuses on difficulty discarding possessions, while OCD involves rituals unrelated to possessions.\n\n- **Post-Traumatic Stress Disorder (PTSD)**\n - *Similarity:* Intrusive thoughts.\n - *Difference:* PTSD results from trauma exposure, whereas OCD involves persistent, non-trauma-related obsessions.\n\n- **Autism Spectrum Disorder (ASD)**\n - *Similarity:* Repetitive behaviors.\n - *Difference:* ASD features repetitive behaviors related to restricted interests, distinct from OCD's varied rituals.\n\n# Management\n\nManagement of OCD is stratified according to the severity of the condition:\n\n* Mild functional impairment:\n\t* Low-intensity cognitive-behavioural therapy (CBT), including exposure and response prevention (ERP)\n- Moderate functional impairment:\n\t- Offer a choice of intensive CBT including ERP **or** an SSRI\n\t- Escitalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline are all licensed for the treatment of OCD in adults\n\t- Clomipramine is an alternative to SSRI if the person prefers clomipramine or has had a previous good response to it, or if an SSRI is contraindicated\n- Severe functional impairment: \n\t- Combined treatment with intensive CBT (including ERP) **and** an SSRI \n- If a medication is effective, it should be continued for a minimum of 12 months. Once they have taken an SSRI or clomipramine for 12 months after remission (symptoms are not clinically significant and the person is fully functioning for at least 12 weeks), review the need for continued treatment.\n\n\n# NICE Guidelines\n\n[NICE CKS - OCD](https://cks.nice.org.uk/topics/obsessive-compulsive-disorder/)",
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"question": "A 30-year-old PhD student is particularly stressed about her upcoming viva and would like to learn about therapy options.\n\nOn further history taking, she describes distressing images flashing into her mind and she often feels she is unable to leave the house without turning the lights on and off multiple times.\n\nWhat is the most likely diagnosis?",
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"explanation": "This is UKMEC Category 1 (no restriction on use) unless the patient is a known carrier of gene mutations associated with breast cancer.",
"id": "10017228",
"label": "c",
"name": "Family history of breast cancer",
"picture": null,
"votes": 365
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is UKMEC Category 2 (but would be UKMEC Category 4 if the patient was over 35).",
"id": "10017230",
"label": "e",
"name": "Smoking 20 cigarettes a day",
"picture": null,
"votes": 385
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is the only UKMEC Category 4 (absolute contraindication) option on the list for the combined oral contraceptive pill, due to the risk of thrombotic complications.",
"id": "10017226",
"label": "a",
"name": "Antiphospholipid syndrome",
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"votes": 3311
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"explanation": "This is UKMEC Category 1 (no restriction on use), although enzyme-inducing anti-epileptic drugs may reduce the effectiveness of oral contraceptives, so an alternative form of contraception (such as a patch) may be recommended.",
"id": "10017227",
"label": "b",
"name": "Taking anti-epileptic medications",
"picture": null,
"votes": 172
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is UKMEC Category 2 (advantages generally outweigh risks) and is therefore not an absolute contraindication.",
"id": "10017229",
"label": "d",
"name": "Rheumatoid arthritis",
"picture": null,
"votes": 13
}
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"explanation": "# Overview\n\n\nThere are numerous contraindications and cautions related to the use of the combined hormonal contraception (CHC) including the combined oral contraceptive pill (COCP), combined contraceptive transdermal patch and the vaginal ring.\n\n\nThe UK Medical Eligibility Criteria (UKMEC) provides guidance on the suitability of contraception options:\n\n\n- UKMEC 4: a situation where the use of the method of contraception represents an unacceptable health risk\n- UKMEC 3: a situation where the theoretical or proven risks usually outweigh the advantages of using the method\n- UKMEC 2: a situation where the advantages of using the method generally outweigh the risks\n- UKMEC 1: a situation for which there is no restriction for the use of the method\n\n\n# UKMEC 4 conditions for use of combined hormonal contraception\n\n\nThese are conditions or situations where the use of combined hormonal contraception represents an unacceptable health risk:\n\n\n- <6 weeks postpartum and breastfeeding\n- <3 weeks postpartum, not breastfeeding, with other risk factors for VTE\n- Age ≥35 and smoking ≥15 cigarettes/day\n- Consistently elevated blood pressure (systolic ≥160 mmHg or diastolic ≥100 mmHg)\n- Vascular disease (e.g. coronary heart disease, peripheral vascular disease intermittent claudication, hypertensive retinopathy)\n- Current or past ischaemic heart disease (including angina)\n- Current or past stroke (including TIA)\n- History of VTE (including PE and DVT)\n- Current VTE (even if on anticoagulation)\n- Planned major surgery with prolonged immobilisation\n- Known thrombogenic mutations (e.g. factor V Leiden)\n- Complicated valvular and congenital heart disease (e.g. with pulmonary hypertension)\n- Cardiomyopathy with impaired cardiac function\n- Atrial fibrillation\n- Migraine with aura, at any age\n- Current breast cancer\n- Severe or decompensated liver disease e.g. cirrhosis\n- Certain liver tumours e.g. hepatocellular adenoma, malignant hepatocellular carcinoma)\n- Systemic lupus erythematosus (SLE) with positive antiphospholipid antibodies\n- Any other condition with positive antiphospholipid antibodies\n\n\n# UKMEC 3 conditions for use of combined hormonal contraception\n\n\nThese are situations where the theoretical or proven risks usually outweigh the advantages of using combined hormonal contraception.\n\n\n- <3 weeks postpartum, not breastfeeding, without other risk factors for VTE\n- 3-6 weeks postpartum, not breastfeeding, with other risk factors for VTE\n- Age >35 years and smoking <15 cigarettes/day\n- Age >35 and stopped smoking <1 year ago\n- BMI ≥35 kg/m2\n- History of bariatric surgery, With BMI ≥35 kg/m2\n- Adequately controlled hypertension\n- Consistently elevated blood pressure (systolic >140–159 mmHg or diastolic >90–99 mmHg)\n- Complicated organ transplant (e.g. if graft failure or rejection)\n- Multiple risk factors for cardiovascular disease (e.g smoking, diabetes, hypertension, obesity, dyslipidaemia)\n- Undiagnosed breast mass or symptoms (for initiating CHC)\n- Carriers of known breast cancer gene mutations (e.g. BRCA1/BRCA2)\n- Past breast cancer\n- Diabetes with nephropathy, retinopathy, neuropathy or other vascular disease\n- Viral hepatitis with acute flare (for initiating CHC)\n- Family history of VTE in a first-degree relative age <45 years\n- Immobility (unrelated to surgery) (e.g. wheelchair use, debilitating illness)\n- Migraine without aura, at any age (continuing CHC)\n- History (≥5 years ago) of migraine with aura, any age\n- Gallbladder disease (if symptomatic or receiving medical therapy)\n- History of cholestasis thought to be due to CHC\n\n\n# UKMEC 2 conditions for use of combined hormonal contraception\n\n\nThese are situations where the advantages of using CHC generally outweigh the risks\n\n\n- Age ≥40 years\n- ≥6 weeks to <6 months postpartum and primarily breastfeeding\n- 3 to <6 weeks postpartum and not breastfeeding\n- Age <35 years and smoking\n- Age ≥35 years and stopped smoking ≥1 year ago\n- BMI ≥30–34 kg/m2\n- History of bariatric surgery with BMI ≥30‒34 kg/m2\n- Uncomplicated organ transplant\n- History of high blood pressure during pregnancy\n- Dyslipidaemia\n- Family history of VTE in a first-degree relative age ≥45 years\n- Planned major surgery without prolonged immobilisation\n- Superficial venous thrombosis\n- Uncomplicated valvular or congenital heart disease (i.e. not on medication, asymptomatic, not requiring regular cardiology review)\n- Cardiomyopathy with normal cardiac function\n- Long QT syndrome\n- Non-migrainous (mild or severe) headache (continuation of CHC)\n- Migraine without aura, at any age (initiation of CHC)\n- Idiopathic intracranial hypertension (IIH)\n- Unexplained vaginal bleeding\n- Cervical intraepithelial neoplasia (CIN)\n- Cervical cancer, awaiting treatment/surgery\n- Undiagnosed breast mass/breast symptoms (continuation of CHC)\n- Diabetes with no vascular disease\n- Previous gallbladder disease treated by cholecystectomy\n- Asymptomatic gallbladder disease\n- History of pregnancy related cholestasis\n- Acute flare of viral hepatitis (continuation of CHC)\n- Focal nodular hyperplasia of the liver\n- Inflammatory bowel disease (IBD) (including Crohn’s disease and ulcerative colitis)\n- Sickle cell disease\n- Rheumatoid arthritis\n- Systemic lupus erythematosus (SLE) without positive antiphospholipid antibodies\n\n\nMultiple conditions that are UKMEC 2 may overall make the risks outweigh the benefits.\n\n\n# References\n\n\n[Click here to see the UKMEC summary sheet on contraception](https://www.fsrh.org/standards-and-guidance/documents/ukmec-2016-summary-sheets/)",
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"question": "A 21-year-old female would like to discuss contraceptive options. Her preference is for the combined oral contraceptive pill as she is aware it can be beneficial in the treatment of acne, and she wants a form of contraception which is readily reversible.\n\nWhich of the following represents an absolute contraindication for the combined oral contraceptive pill?",
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"explanation": "Diabetic patients who are fasting should be placed at the beginning of the surgical list to minimise the duration of the fast and the complications of suboptimal glucose control, which include dizziness, sweating, palpitations and, if severe, loss of consciousness.",
"id": "10017231",
"label": "a",
"name": "A 43 year old insulin-dependant diabetic lady undergoing a hernia repair",
"picture": null,
"votes": 3975
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "Although this case may prove difficult from an anaesthetics point of view due to the difficulties with controlling blood pressure and risk of catecholamine surge during surgery, limiting fasting duration in a patient with diabetes takes priority.",
"id": "10017233",
"label": "c",
"name": "A 21 year old man undergoing an elective surgery to remove a pheochromocytoma",
"picture": null,
"votes": 165
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "Infectious patients should be placed at the end of the surgical list to reduce the risk of infecting other patients.",
"id": "10017234",
"label": "d",
"name": "A 45 year old patient with miliary tuberculosis undergoing an elective lobectomy",
"picture": null,
"votes": 146
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is no particular reason why this patient should be placed at the start of the list.",
"id": "10017232",
"label": "b",
"name": "An 88 year old man undergoing an elective hip replacement surgery",
"picture": null,
"votes": 68
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is no particular reason why this patient should be placed at the start of the list.",
"id": "10017235",
"label": "e",
"name": "A 44 year old lady undergoing an elective laparoscopic cholecystectomy",
"picture": null,
"votes": 38
}
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"explanation": "# COPD\n\nPatients with COPD are at higher risk of post-op complications than other patients because of their impaired respiratory function. It is therefore advisable to arrange the following tests before surgery:\n\n- Lung function tests\n- Chest x-ray\n- Arterial blood gas (if the patient is known to retain carbon dioxide)\n\nFurthermore, it is prudent to encourage patients to give up smoking before the operation and to start chest physio early after the operation.\n\n# Drugs to stop\n\n- **Cardiovascular drugs:** Clopidogrel should be stopped 7 days before surgery, warfarin should be (generally) stopped 5 days before surgery and instead patients should be on low molecular weight heparin until the night before, ACE inhibitors should be stopped the day before surgery.\n- **Combined oral contraceptive pill** should be stopped 4-6 weeks before surgery, and re-started at least 2 weeks after surgery (when the patient is mobile). This reduces the risk of DVT.\n\n# Patients taking steroids\nWhen the body experiences acute stress (e.g. illness, trauma, surgery), the steroid demand increases. \n\nPatients on long term steroids cannot respond to this demand because their adrenal function is suppressed.\n\nTherefore, patients who are on long term steroids usually need more steroids than usual during periods of physiological stress e.g. surgery or acute illness.\n\n\n## Management\n\nPeri-operative management is as follows:\n\n1. Switch oral steroids to 50-100mg IV hydrocortisone.\n2. If there is associated hypotension then fludrocortisone can be added.\n3. For minor operations oral prednisolone can be restarted immediately post-operatively. If the surgery is major then they may require IV hydrocortisone for up to 72 hours post-op.\n\n# Diabetes\nPeri-operative management of diabetes, both non-insulin-dependent (type 2 diabetes) and insulin-dependent (type 1 diabetes), involves careful monitoring and adjustment of medication regimens to mitigate the risk of peri-operative complications. The need for specific peri-operative management in diabetics arises due to physiological changes in response to stress (such as surgery), combined with the patient's underlying metabolic disorder. Surgical stress can induce hyperglycemia, and alterations in medication timing or dosage may be necessary due to fasting or changes in renal function.\n\n## Potential complications\n\n- **Hyperglycemia**: Characterised by blood glucose levels >180 mg/dL, symptoms include polyuria, polydipsia, and unexplained weight loss.\n- **Hypoglycemia**: Characterised by blood glucose levels <70 mg/dL, symptoms include palpitations, tremor, sweating, anxiety, and confusion.\n- **Diabetic Ketoacidosis (DKA)**: Common in type 1 diabetics, symptoms include polyuria, polydipsia, nausea, vomiting, abdominal pain, and fruity-smelling breath.\n- **Lactic Acidosis**: A potential complication of metformin use, especially in renal impairment. Symptoms include abdominal discomfort, nausea, vomiting, muscle pain, and rapid breathing.\n\n\n## Management\n\n\n| Drug | Plan |\n| ---------------------------- | ---------------------------------------------- |\n| Metformin (taken once daily) | Take during the morning of surgery |\n| DDP-IV inhibitors | Take during the morning of surgery |\n| GLP-1 analogues | Take during the morning of surgery |\n| SGLT-2 inhibitors | Omit the day of surgery due to the risk of DKA |\n\nFor insulin-dependent diabetics, key principles are:\n\n1. Schedule the patient as early on the theatre list as possible, minimising the amount of time the patient is nil by mouth.\n2. If on long-acting insulin, this should be continued but reduced by 20%.\n3. Stop any other insulin and begin sliding scale insulin infusion from when the patient is placed nil by mouth.\n4. Continue infusion until the patient is able to eat post-operatively.\n5. Switch to the normal insulin regimen around their first meal.\n\n*For some operations (particularly those that do not require contrast media) metformin does not need to be stopped, but one should always consider the risk of lactic acidosis.\n\nAfter surgery, all oral medications should generally be restarted the morning following surgery.\n\n\n\n# NICE Guidelines\n\n[NICE Guidelines on Diabetes management during the Peri-operative period](https://bnf.nice.org.uk/treatment-summaries/diabetes-surgery-and-medical-illness/)",
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"question": "You are a foundation year one doctor on a general surgery rotation and are reviewing the cases for the list for the next few days.\n\nWhich of the following cases should be placed at the start of the surgical list for the day?",
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"__typename": "QuestionSBA",
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect, she may drink water up to 2 hours before surgery.",
"id": "10017239",
"label": "d",
"name": "She should not drink for 6 hours before surgery",
"picture": null,
"votes": 264
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect, orange juice with pulp does not constitute a clear fluid and therefore should not be consumed 2 hours before surgery. It can be consumed 6 hours before her operation, however.",
"id": "10017237",
"label": "b",
"name": "She may have a glass of orange juice with pulp 2 hours before surgery",
"picture": null,
"votes": 19
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "This is incorrect, tomato soup does not constitute a clear fluid and therefore should be consumed at least 6 hours before surgery.",
"id": "10017238",
"label": "c",
"name": "She may have tomato soup 2 hours before surgery",
"picture": null,
"votes": 8
},
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is correct, clear fluids (black coffee, black tea, water) can be drank up to 2 hours before surgery.",
"id": "10017236",
"label": "a",
"name": "She may drink water 2 hours before surgery",
"picture": null,
"votes": 3700
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "The current recommendation is to abstain from eating for 6 hours before surgery and clear fluids 2 hours before.",
"id": "10017240",
"label": "e",
"name": "She should fast overnight",
"picture": null,
"votes": 266
}
],
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"explanation": "# Pre-operative Fasting\n\n**Oral Fluids**:\n\n- **Clear Fluids**: Patients should be informed that they are allowed to consume clear fluids until 2 hours before their scheduled operation. Clear fluids encompass water, fruit juice without pulp, coffee or tea without milk, and ice lollies.\n\n\n\n**Intravenous Fluids**:\n\n- **Intraoperative Maintenance**: During surgery, practitioners are advised to consider using intravenous crystalloid solutions to maintain fluid balance.\n\n**Food:**\n\nPatients are generally advised to have their last meal/solid food/non-clear fluids for at least 6 hours before their surgery.\n",
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"id": "56",
"name": "Anaesthetics and Intensive Care Medicine",
"typeId": 2
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"question": "A 49 year old patient is scheduled to undergo an elective cholecystectomy next week for long standing biliary colic. She asks whether she can eat and drink prior to her surgery.\n\nWhich of the following is true regarding her pre-operative eating and drinking?",
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"__typename": "QuestionChoice",
"answer": true,
"explanation": "This is the correct answer. The imaging findings heavily suggest an occupational exposure to asbestos with pleural plaques and mesothelioma. All deaths related to industrial disease must be reported to the coroner.",
"id": "10017241",
"label": "a",
"name": "Refer death to the coroner",
"picture": null,
"votes": 2978
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is nothing to suggest that the circumstances of the death warrant an incident form. This may be required in cases where an incident (e.g. medication error) is thought to have contributed to an adverse outcome.",
"id": "10017244",
"label": "d",
"name": "Submit a critical incident form",
"picture": null,
"votes": 198
},
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"__typename": "QuestionChoice",
"answer": false,
"explanation": "There is nothing to suggest this patient is infectious at present.",
"id": "10017242",
"label": "b",
"name": "Notify local microbiology lead",
"picture": null,
"votes": 63
},
{
"__typename": "QuestionChoice",
"answer": false,
"explanation": "To certify a death you must have seen the patient in the last 14 days before death or after death and must have provided care in the last illness before death. As this case needs a coroner referral, this is not appropriate and should not be handed over to a colleague who has likely not seen the patient.",
"id": "10017243",
"label": "c",
"name": "Handover to night team doctor to verify and certify death",
"picture": null,
"votes": 35
},
{
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"comment": "Correct me if I am wrong, but aren't all deaths within 24 hours of presentation to hospital with no precipitating event referred to the coroner",
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"comment": "Yes: \nThe following deaths should be reported to the coroner\nunexpected or sudden deaths\nwhen the doctor attending the deceased did not see them within 28 days before death\nthis was increased from 14 days during the COVID pandemic\nif a death occurs within 24 hours of hospital admission\naccidents and injuries\nsuicide\nindustrial injury or disease (e.g. asbestosis)\ndeaths occurring as a result of ill treatment, starvation or neglect\nthe death occurred during an operation or before recovery from the effect of an anaesthetic\npoisoning, including taking illicit drugs\nstillbirths - if there is doubt as to whether the child was born alive\nprisoner or people in police custody\nservice disability pensioners",
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"explanation": "# Summary\n\nLung cancers are divided into two main subtypes: small cell and non-small cell, with small cell lung cancers being more aggressive and incurable. Types of non-small cell lung cancer include squamous cell and adenocarcinomas, with several rarer subtypes. Most cases of lung cancer are linked to smoking. Lung cancers may present with chest symptoms such as cough, breathlessness or haemoptysis, systemic symptoms of weight loss and anorexia or symptoms of metastatic disease such as bone pain or seizures. Chest X-ray is the initial investigation of choice, followed by CT chest and a biopsy. Staging scans are done after diagnosis to help plan treatment. Management can be curative or palliative depending on the stage of the cancer, the subtype and the patient’s overall health. It may include chemotherapy, radiotherapy, immunotherapy, targeted therapies to specific mutations and surgery. \n\n\n# Definition\n\nLung cancer refers to a primary malignancy arising from the lung parenchyma or the bronchi. Cancers are classified as small cell (SCLC) or non-small cell (NSCLC), with 80% being non-small cell. The main histological subtypes of NSCLC are squamous cell cancers and adenocarcinomas.\n\n# Epidemiology\n\nLung cancer makes up the largest proportion of cancer deaths of any tumour type, with nearly 35,000 deaths per year in the UK (21% of all cancer deaths). It is the second most common cancer in both males and females (after prostate and breast respectively). \n\nIncidence is strongly related to age, with the highest rates in people aged over 75 years old. Although non-smokers can also get lung cancer, 86% of cases are linked to smoking and so the majority of cases are felt to be preventable.\n\n# Aetiology\n\nRisk factors for lung cancer include:\n\n- Tobacco smoking (e.g. cigarettes, pipes, cigars)\n- Passive smoke exposure\n- Occupational exposures (e.g. beryllium, cadmium, arsenic, asbestos, silica)\n- Radon exposure\n- Family history of lung cancer\n- Radiation to the chest (e.g. in lymphoma treatment)\n- Air pollution\n- Immunosuppression (e.g. HIV, medications)\n- Increasing age\n\n# Classification\n\nLung cancers are classified by the cell of origin of the malignancy. Small cell cancers come from neuroendocrine cells of the lung. Non-small cell cancers are split into adenocarcinomas (coming from alveolar type 2 epithelial cells), squamous cell carcinomas (coming from basal epithelial cells) and large cell carcinomas (which come from a variety of epithelial cells). There are also rarer subtypes of lung cancer such as sarcomatoid or salivary gland-type lung cancers which come under the NSCLC umbrella.\n\nStaging is also an important way to classify lung cancers depending on how advanced they are. TNM (tumour, node, metastasis) staging is used to describe how large the tumour is and where it has spread to. This can then be used to classify lung cancers into stage 1 to 4, where stage 1 is localised and small (under 4cm), stages 2 and 3 are locally advanced and stage 4 is metastatic. \n\n# Signs and symptoms\n\n**Symptoms include:**\n\n- Persistent cough\n- Haemoptysis\n- Dyspnoea especially on exertion\n- Chest pain\n- Weight loss\n- Recurrent chest infections, or infections resistant to treatment\n- Anorexia\n\n**Signs include:**\n\n- Cachexia\n- Finger clubbing\n- Lymphadenopathy (supraclavicular or persistent cervical)\n- If there is lung collapse due to an obstructing tumour - absent breath sounds, trachea deviated towards side of collapse\n- If there is a malignant pleural effusion - stony dull on percussion, decreased breath sounds over affected area\n\n**Other signs and symptoms related to paraneoplastic presentations of lung cancer:**\n\n- **Cushing syndrome** - usually SCLC producing ectopic ACTH, presents with dorsal cervical fat pads, truncal obesity, hypertension, striae and proximal muscle weakness\n- **Syndrome of inappropriate ADH secretion (SIADH)** - usually SCLC, present with symptoms of hyponatraemia e.g. fatigue, nausea, weakness, confusion or seizures\n- **Lambert-Eaton myasthenic syndrome (LEMS)** - usually SCLC, due to autoantibodies to presynaptic calcium channels at the neuromuscular junction develop proximal muscle weakness that improves with repeated movement, as well as autonomic effects such as dry mouth, lightheadedness, constipation, urinary symptoms and erectile dysfunction\n- **Humoral hypercalcaemia of malignancy** - usually squamous cell carcinomas (SCC) that release parathyroid hormone-related protein (PTHrP) that mimics PTH and causes hypercalcaemia, leading to symptoms of bone pain, constipation, anorexia, abdominal pain, excessive thirst and confusion\n- **Hypertrophic pulmonary osteoarthropathy** - usually adenocarcinomas which cause a periosteal reaction of bones, resulting in clubbing and arthritis especially affecting wrists and ankles\n\n# Differential diagnosis\n\n- Lung metastases from another primary cancer (e.g. breast or colorectal cancer)\n- Mesothelioma (cancer of the pleura, strongly related to asbestos exposure)\n- Tuberculosis \n- Bronchiectasis\n\n# Investigations\n\nIn primary care, patients should be referred on a 2 week wait pathway in the following situations:\n\n- Aged 40+ with unexplained haemoptysis\n- Chest X-ray findings suspicious for lung cancer\n\nUrgent chest X-rays (to be done within 2 weeks) should be done for patients aged 40+ who have one of these symptoms and have ever smoked (or two symptoms if they are never smokers):\n\n- Cough\n- Fatigue\n- Shortness of breath\n- Chest pain\n- Weight loss\n- Anorexia\n\nAn urgent chest X-ray should be considered in patients aged 40+ with any of:\n\n- Persistent/recurrent chest infection\n- Finger clubbing\n- Supraclavicular or persistent cervical lymphadenopathy\n- Thrombocytosis\n- Chest signs consistent with lung cancer (e.g. reduced breath sounds, dullness to percussion)\n\nChest X-ray findings include:\n\n- Lung mass (may be rounded or spiculated, squamous cell carcinomas may cavitate)\n- Consolidation (where there is infection downstream of the tumour obstructing an airway)\n- Bulky hilum (especially squamous cell carcinomas which often arise centrally)\n- Lobar collapse (due to bronchial obstruction, especially squamous cell carcinomas)\n- Pleural effusion\n\n[lightgallery]\n\nOther initial investigations include:\n\n- **Sputum cytology** - low sensitivity but may be of use in patients who decline or cannot have a biopsy\n- **Diagnostic thoracocentesis** - i.e. a pleural tap; if a pleural effusion is present this should be done and the fluid sent for cytology as well as cell count, microscopy, culture, glucose, LDG and protein (to determine whether it is a transudate or exudate)\n- **Blood tests** - including FBC for anaemia and thrombocytosis, U&Es for hyponatraemia and baseline renal function, LFTs for baseline liver function (may be deranged in liver metastases), bone profile for hypercalcaemia, CRP for superadded infection, clotting if interventions planned\n- **CT chest with contrast** - should be done after chest X-ray to better characterise any lesion seen and investigate for local spread\n- **Biopsy** - to confirm the diagnosis and subtype of cancer, may be done percutaneously for peripheral tumours or via bronchoscopy for central masses\n\nOnce a lung cancer is diagnosed, further investigations may include:\n\n- **Spirometry** - to assess lung function to determine if a patient is suitable for surgical intervention\n- **CT chest abdomen and pelvis** - to stage the cancer (determine if there are any metastases)\n- **PET-CT scan** - a more sensitive way to stage the cancer and look for local or distant spread\n- **CT or MRI head** - may be done as part of staging investigations if curative treatment is planned, or if there are symptoms suspicious of intracranial metastases \n\n# Management \n\n**Conservative:**\n\n- **Holistic support** and an **MDT approach** (e.g. clinical nurse specialist involvement, palliative care input for troubling symptoms or end of life care, signpost to support e.g. Macmillan groups)\n- **Smoking cessation**\n- Discussions around **advance care planning** where appropriate\n\n**Medical**\n\n- **Chemotherapy** is first line in most cases of small cell lung cancer and stage 3 or 4 non-small cell lung cancer - this is with palliative intent (i.e. not aiming to cure the disease but to prolong life and improve symptoms). It is also offered to some patients prior to (neoadjuvant) or after (adjuvant) curative surgery.\n- **Immunotherapy** is also used especially in advanced non-small cell lung cancer; this includes medications such as pembrolizumab or atezolizumab (again with palliative intent).\n- Other **targeted therapies** exist for patients with specific mutations, e.g. erlotinib for patients with advanced non-small cell lung cancers with EGFR-TK mutations.\n- **Radiotherapy** may be curative (for example in early non-small cell lung cancer) or palliative - it is often combined with chemotherapy or other treatment modalities.\n- **Supportive therapies** include analgesia, oxygen if hypoxic and opioid treatment for breathlessness.\n\n**Surgical**\n\n- **Lobectomy** is the standard curative therapy for early stage lung cancers (which can be open or thoracoscopic in approach).\n- Some small tumours can be removed with a **wedge resection.**\n- More extensive surgery such as a **pneumonectomy** (removal of a lung) may be required depending on the size and location of the tumour, however patients need to have adequate FEV1 on pre-operative spirometry to be appropriate for surgery (over 2L for a pneumonectomy).\n- All patients undergoing surgery should also have **mediastinal and hilar lymph nodes sampled** (to look for metastases) or **resected** (removed) to reduce the chances of recurrence.\n\n# Complications\n\n**Common sites of metastatic spread include:**\n\n- Lymph nodes\n- Liver - this can cause significant pain due to stretching of the liver capsule\n- Brain - may cause nausea and vomiting, headaches, seizures, personality changes, sensory or motor symptoms, dysphasia or cerebellar symptoms, depending on where in the brain is affected\n- Bones - mostly osteolytic metastases, can cause bony pain and pathological fractures; there is a risk of metastatic spinal cord compression with vertebral metastases\n- Adrenal glands - may cause flank pain and adrenal insufficiency\n- The contralateral lung or elsewhere in the ipsilateral lung\n\n**Local complications include:**\n\n- Horner’s syndrome - due to an apical (Pancoast) tumour, causes ipsilateral anhidrosis, miosis and partial ptosis\n- Superior vena cava obstruction (SCVO) - lung cancer is the commonest cause of SCVO, causing symptoms of breathlessness, dizziness, headache and swelling of the face, neck and arms. This is a medical emergency due to the risk of airway obstruction.\n- Malignant pleural effusion\n- Hoarse voice - secondary to invasion of left recurrent laryngeal nerve\n- Persistent lower respiratory tract infection due to obstructing tumour\n- Raised hemidiaphragm secondary to invasion of phrenic nerve\n- Brachial plexus injury secondary to tumour invasion from a Pancoast tumour\n\n# Prognosis\n\nOverall prognosis is poor, with an average 5 year survival rate of 17%. This is lower for small cell lung cancer and for metastatic cancers, both of which have around a 5% 5 year survival. Small cell lung cancers are aggressive and are usually metastatic at the time of presentation, hence curative treatment is not possible\n\nIn early stage cancers survival is better, with 70% of patients with stage 1 NSCLC undergoing curative surgery surviving 5 years from diagnosis.\n\n# NICE Guidelines\n\n[Lung cancer: diagnosis and management](https://www.nice.org.uk/guidance/ng122)\n\n[NICE CKS - recognition and referral of lung and pleural cancers](https://cks.nice.org.uk/topics/lung-pleural-cancers-recognition-referral/)\n\n# References\n\n[Radiopaedia - lung cancer](https://radiopaedia.org/articles/lung-cancer-3?lang=gb)\n\n[Patient UK - lung cancer](https://patient.info/doctor/lung-cancer-pro)\n\n[Cancer Research UK - lung cancer statistics](https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/lung-cancer)",
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