Gastro Flashcards

Question

Question: What are the key features of an ectopic pregnancy?

Answer 1

Location: Right or left iliac fossa Notes: Pain, history of amenorrhoea for 6-9 weeks, vaginal bleeding may be present.

Answer 2

Location: Central abdominal pain radiating to the back Notes: Sudden collapse or sub-acute presentation, developing shock, history of cardiovascular disease.

Answer 3

Location: Central abdominal pain Notes: History of atrial fibrillation or cardiovascular disease, diarrhoea, rectal bleeding, metabolic acidosis.

Answer 4

The rapid onset of hepatocellular dysfunction leading to a variety of systemic complications.

Answer 5

Paracetamol overdose Alcohol Viral hepatitis (usually A or B) Acute fatty liver of pregnancy

Answer 6

Jaundice Coagulopathy: raised prothrombin time Hypoalbuminaemia Hepatic encephalopathy Renal failure is common ('hepatorenal syndrome')

Answer 7

Prothrombin time Albumin level

Answer 8

They do not always accurately reflect the synthetic function of the liver. The synthetic function is better assessed by looking at the prothrombin time and albumin level.

Answer 9

Oesophageal varices and peptic ulcer disease.

Answer 10

Haematemesis is the vomiting of blood, often bright red but may sometimes be described as 'coffee ground'.

Answer 11

Melena is the passage of altered blood per rectum, typically black and 'tarry'.

Answer 12

A raised urea level may be seen due to the 'protein meal' of the blood.

Answer 13

Usually a large volume of fresh blood. Swallowed blood may cause melena. Often associated with haemodynamic compromise. May stop spontaneously but re-bleeds are common until appropriately managed.

Answer 14

Small volume of fresh blood, often streaking vomit. Melena is rare. Often ceases spontaneously. Usually history of antecedent GORD-type symptoms.

Answer 15

Small low-volume bleeds are more common, tending to present as iron deficiency anaemia. Erosion into a significant vessel may produce considerable haemorrhage and haematemesis.

Answer 16

May present with haematemesis, melena, and epigastric discomfort. The pain often occurs several hours after eating.

Answer 17

Glasgow-Blatchford score: Used at first assessment to decide whether patients can be managed as outpatients or not. Rockall score: Used after endoscopy to provide a percentage risk of rebleeding and mortality.

Answer 18

To assess the risk of needing treatment for an upper GI bleed and to help decide whether patients can be managed as outpatients.

Answer 19

ABC (Airway, Breathing, Circulation) Wide-bore intravenous access × 2 Platelet transfusion if actively bleeding and platelet count < 50 x 10*9/litre Fresh frozen plasma if fibrinogen level < 1 g/litre, or prothrombin time or activated partial thromboplastin time > 1.5 times normal Prothrombin complex concentrate for patients on warfarin who are actively bleeding

Answer 20

Endoscopy should be offered immediately.

Answer 21

Proton pump inhibitors (PPIs) should not be given before endoscopy to patients with suspected variceal upper GI bleeding. PPIs should be given to patients with non-variceal upper GI bleeding and stigmata of recent haemorrhage shown at endoscopy. If further bleeding occurs, options include repeat endoscopy, interventional radiology, and surgery.

Answer 22

Terlipressin and prophylactic antibiotics should be given at presentation. Band ligation for oesophageal varices. Injections of N-butyl-2-cyanoacrylate for gastric varices. Transjugular intrahepatic portosystemic shunts (TIPS) if bleeding is not controlled.

Answer 23

A: Alcoholic ketoacidosis is a non-diabetic euglycaemic form of ketoacidosis that occurs in people who regularly drink large amounts of alcohol.

Answer 24

A: Alcoholic ketoacidosis occurs because alcoholics often do not eat regularly and may vomit the food they do eat, leading to episodes of starvation and malnutrition.

Answer 25

A: Once malnourished, after an alcohol binge, the body starts to break down body fat, producing ketones, leading to ketoacidosis.

Answer 26

A: The typical metabolic findings in alcoholic ketoacidosis include metabolic acidosis, elevated anion gap, elevated serum ketone levels, and normal or low glucose concentration.

Answer 27

A: The most appropriate treatment for alcoholic ketoacidosis is an infusion of saline and thiamine.

Answer 28

A: Thiamine is administered to avoid Wernicke encephalopathy or Korsakoff psychosis.

Answer 29

A: Alcoholic liver disease covers alcoholic fatty liver disease, alcoholic hepatitis, and cirrhosis.

Answer 30

A: Gamma-GT is characteristically elevated in alcoholic liver disease.

Answer 31

A: An AST:ALT ratio of > 2 is typical, and a ratio of > 3 is strongly suggestive of acute alcoholic hepatitis.

Answer 32

A: Glucocorticoids (e.g., prednisolone) are often used during acute episodes of alcoholic hepatitis.

Answer 33

A: Maddrey's discriminant function (DF) is used to determine who would benefit from glucocorticoid therapy during acute episodes of alcoholic hepatitis.

Answer 34

A: Maddrey's discriminant function (DF) is calculated using prothrombin time and bilirubin concentration.

Answer 35

A: Pentoxyphylline is sometimes used for alcoholic hepatitis.

Answer 36

A: The STOPAH study showed that prednisolone improved survival at 28 days, while pentoxyphylline did not improve outcomes.

Answer 37

A: 5-ASA acts locally as an anti-inflammatory in the colon.

Answer 38

A: 5-ASA may inhibit prostaglandin synthesis.

Answer 39

A: Sulphasalazine is a combination of sulphapyridine (a sulphonamide) and 5-ASA.

Answer 40

A: Side effects include rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, and lung fibrosis.

Answer 41

A: Mesalazine is a delayed release form of 5-ASA that avoids the sulphapyridine side effects seen in patients taking sulphasalazine.

Answer 42

A: Side effects include GI upset, headache, agranulocytosis, pancreatitis, and interstitial nephritis.

Answer 43

A: Olsalazine consists of two molecules of 5-ASA linked by a diazo bond, which is broken by colonic bacteria.

Answer 44

A: Aminosalicylates are associated with agranulocytosis and other haematological adverse effects.

Answer 45

A: FBC is key due to the risk of haematological adverse effects like agranulocytosis.

Answer 46

A: Pancreatitis is 7 times more common in patients taking mesalazine than in those taking sulphasalazine.

Answer 47

A: Angiodysplasia is a vascular deformity of the gastrointestinal tract that predisposes to bleeding and iron deficiency anaemia.

Answer 48

A: There is a debated association between angiodysplasia and aortic stenosis.

Answer 49

A: Angiodysplasia is generally seen in elderly patients.

Answer 50

A: Common features include anaemia and gastrointestinal (GI) bleeding.

Answer 51

A: Upper GI bleeding may present as melena.

Answer 52

A: Lower GI bleeding may present as brisk, fresh red per rectum (PR) bleeding.

Answer 53

A: Diagnostic methods include colonoscopy and mesenteric angiography if there is acute bleeding.

Answer 54

A: Management options include endoscopic cautery or argon plasma coagulation, antifibrinolytics (e.g., tranexamic acid), and oestrogens.

Answer 55

A: Phospholipase A2.

Answer 56

A: COX-1 and COX-2.

Answer 57

A: Prostacyclin (PGI2), Prostaglandin (PGE2), and Thromboxane (TXA2).

Answer 58

A: Vasodilation, decreased platelet aggregation, and decreased uterine tone.

Answer 59

A: Increased pain, temperature, uterine tone, gastric mucus, and decreased gastric acid; varying effects on vascular smooth muscle and airways.

Answer 60

A: Vasoconstriction and increased platelet aggregation.

Answer 61

A: Lipoxygenase.

Answer 62

A: Leukotrienes (LTB4, LTA4, LTC4, LTD4, LTE4).

Answer 63

A: Increased neutrophil chemotaxis.

Answer 64

A: Increased bronchoconstriction.

Answer 65

A: THROMBOxane (THROMBOSIS): promotes platelet aggregation and vasoconstriction.

Answer 66

A: Prostacyclin (PGI2) has the opposite effects: it causes vasodilation and decreases platelet aggregation.

Answer 67

A: Ascites is the abnormal accumulation of fluid in the abdomen.

Answer 68

A: An SAAG > 11 g/L indicates portal hypertension.

Answer 69

A: Cirrhosis, alcoholic liver disease, acute liver failure, and liver metastases.

Answer 70

A: Right heart failure and constrictive pericarditis.

Answer 71

A: Budd-Chiari syndrome, portal vein thrombosis, veno-occlusive disease, myxoedema, hypoalbuminaemia, nephrotic syndrome, and severe malnutrition (e.g., Kwashiorkor).

Answer 72

A: Malignancy (peritoneal carcinomatosis), infections (e.g., tuberculous peritonitis), pancreatitis, bowel obstruction, biliary ascites, postoperative lymphatic leak, and serositis in connective tissue diseases.

Answer 73

A: Reducing dietary sodium.

Answer 74

A: Fluid restriction is sometimes recommended if the sodium is < 125 mmol/L.

Answer 75

A: Aldosterone antagonists (e.g., spironolactone) and loop diuretics.

Answer 76

A: Some authorities add loop diuretics only if the patient does not respond to aldosterone antagonists, while others suggest starting both types of diuretics at first presentation.

Answer 77

A: Therapeutic abdominal paracentesis.

Answer 78

A: Albumin is given to reduce paracentesis-induced circulatory dysfunction and mortality.

Answer 79

A: Paracentesis-induced circulatory dysfunction, high ascites recurrence, hepatorenal syndrome, dilutional hyponatraemia, and high mortality rate.

Answer 80

A: To reduce the risk of spontaneous bacterial peritonitis, especially in cirrhosis with ascites and an ascitic protein of 15 g/L or less.

Answer 81

A: Oral ciprofloxacin or norfloxacin.

Answer 82

A: TIPS may be considered in some patients with ascites related to portal hypertension.

Answer 83

A: Autoimmune hepatitis is a condition of unknown etiology, most commonly seen in young females, characterized by immune system attack on the liver.

Answer 84

A: Other autoimmune disorders, hypergammaglobulinaemia, and HLA B8, DR3.

Answer 85

A: Type I, Type II, and Type III.

Answer 86

A: Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA).

Answer 87

A: Type I autoimmune hepatitis.

Answer 88

A: Anti-liver/kidney microsomal type 1 antibodies (LKM1).

Answer 89

A: Type II autoimmune hepatitis.

Answer 90

A: Soluble liver-kidney antigen.

Answer 91

A: Type III autoimmune hepatitis.

Answer 92

A: Chronic liver disease signs, acute hepatitis (fever, jaundice), amenorrhoea, ANA/SMA/LKM1 antibodies, and raised IgG levels.

Answer 93

A: Inflammation extending beyond the limiting plate, with features like piecemeal necrosis and bridging necrosis.

Answer 94

A: Steroids and other immunosuppressants, such as azathioprine.

Answer 95

A: Liver transplantation.

Answer 96

A: Barrett's oesophagus refers to the metaplasia of the lower oesophageal mucosa, where the usual squamous epithelium is replaced by columnar epithelium.

Answer 97

A: The risk of oesophageal adenocarcinoma is estimated to be 50-100 times higher in patients with Barrett's oesophagus.

Answer 98

A: Barrett's oesophagus is typically identified during an endoscopy for evaluation of upper gastrointestinal symptoms, such as dyspepsia.

Answer 99

A: Short (<3cm) and long (>3cm) segments of metaplasia.

Answer 100

A: The length of the affected segment strongly correlates with the likelihood of identifying metaplasia.

Answer 101

A: The columnar epithelium may resemble that of the cardiac region of the stomach or the small intestine, with features like goblet cells and a brush border.

Answer 102

A: Gastro-oesophageal reflux disease (GORD) is the strongest risk factor for Barrett's oesophagus.

Answer 103

A: Male gender (7:1 ratio), smoking, and central obesity.

Answer 104

A: No, alcohol does not seem to be an independent risk factor for Barrett's oesophagus, though it is associated with both GORD and oesophageal cancer.

Answer 105

A: Barrett's oesophagus itself is asymptomatic, but patients often have coexistent GORD symptoms.

Answer 106

A: High-dose proton pump inhibitors (PPIs) are commonly used, although the evidence for their ability to reduce progression to dysplasia or induce regression is limited.

Answer 107

A: Endoscopy is recommended every 3-5 years for patients with metaplasia (but not dysplasia).

Answer 108

A: Endoscopic intervention is offered if any grade of dysplasia is identified.

Answer 109

A: Options include radiofrequency ablation (preferred first-line treatment, particularly for low-grade dysplasia) and endoscopic mucosal resection.

Answer 110

A: Bile-acid malabsorption is a cause of chronic diarrhoea, which may be primary (excessive bile acid production) or secondary (due to reduced bile acid absorption from an underlying gastrointestinal disorder).

Answer 111

A: It can lead to steatorrhoea and malabsorption of vitamins A, D, E, and K.

Answer 112

A: Secondary causes include ileal disease (e.g., Crohn's disease), cholecystectomy, coeliac disease, and small intestinal bacterial overgrowth.

Answer 113

A: The test of choice is SeHCAT, a nuclear medicine test using a gamma-emitting selenium molecule (75SeHCAT).

Answer 114

A: Scans are done 7 days apart to assess the retention/loss of the radiolabelled 75SeHCAT, which helps evaluate bile acid retention.

Answer 115

A: The main treatment is bile acid sequestrants, such as cholestyramine.

Answer 116

A: Bilirubin is a chemical by-product of the breakdown of heme from red blood cells and other heme-containing proteins (e.g., myoglobin). Heme is processed in macrophages into biliverdin, which is reduced to unconjugated bilirubin.

Answer 117

A: Unconjugated bilirubin binds to albumin in the blood, is taken up by hepatocytes, and is conjugated to become water-soluble. It is then excreted into bile, enters the intestines, and is further processed by intestinal bacteria.

Answer 118

A: Urobilinogen is further processed by intestinal bacteria into urobilin and stercobilin, which are excreted in the faeces. About 10% of urobilinogen re-enters the portal circulation and is excreted in the urine.

Answer 119

A: Raised levels of unconjugated bilirubin may occur due to haemolysis (e.g., autoimmune-mediated haemolytic anaemia) or hepatocyte defects, such as impaired uptake or defective conjugation of bilirubin in liver disease.

Answer 120

A: A mild deficiency of glucuronyl transferase causes Gilbert's Syndrome, while a moderate to severe deficiency can cause Crigler-Najjar Syndrome types I and II. A transient deficiency can contribute to physiological neonatal jaundice.

Answer 121

A: Raised levels of conjugated bilirubin can occur due to defective excretion, such as in Dubin-Johnson Syndrome or cholestasis.

Answer 122

A: Jaundice appears when bilirubin levels exceed 35 µmol/L.

Answer 123

A: Cholestasis can be caused by physical factors (e.g., gallstones, pancreatic or cholangiocarcinoma) or functional factors (e.g., drug-induced, pregnancy-related, post-operative cholestasis).

Answer 124

A: Budd-Chiari syndrome, also known as hepatic vein thrombosis, is a condition where there is thrombosis of the hepatic veins, often associated with underlying haematological or procoagulant conditions.

Answer 125

A: Common causes include polycythaemia rubra vera, thrombophilia (e.g., activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies), pregnancy, and the combined oral contraceptive pill (which accounts for about 20% of cases).

Answer 126

The classic triad includes: Sudden, severe abdominal pain Ascites (abdominal distension) Tender hepatomegaly

Answer 127

A: Ultrasound with Doppler flow studies is very sensitive and should be the initial radiological investigation.

Answer 128

A: Carcinoid syndrome occurs when metastases, typically in the liver, release serotonin into the systemic circulation. It can also occur with lung carcinoids if the mediators are not cleared by the liver.

Answer 129

Flushing (often the earliest symptom) Diarrhoea Bronchospasm Hypotension Right heart valvular stenosis (can also affect the left heart in bronchial carcinoid) Cushing's syndrome (due to ACTH secretion) Pellagra (due to diversion of dietary tryptophan to serotonin)

Answer 130

Urinary 5-HIAA (a breakdown product of serotonin) Plasma chromogranin A

Answer 131

Somatostatin analogues (e.g., octreotide) Cyproheptadine for diarrhoea

Answer 132

A: Cholestyramine is a bile acid sequestrant used to manage hyperlipidaemia, particularly by reducing LDL cholesterol. It is also used in Crohn's disease to treat diarrhoea following bowel resection.

Answer 133

A: Cholestyramine decreases bile acid reabsorption in the small intestine, which leads to an increased conversion of cholesterol to bile acids, reducing LDL cholesterol levels.

Answer 134

Abdominal cramps and constipation Decreased absorption of fat-soluble vitamins (A, D, E, K) Cholesterol gallstones May raise triglyceride levels

Answer 135

A: C. difficile is a Gram-positive, anaerobic, spore-forming bacterium that produces exotoxins leading to pseudomembranous colitis. Overgrowth typically occurs when normal gut flora is suppressed by broad-spectrum antibiotics, particularly second and third-generation cephalosporins.

Answer 136

Use of broad-spectrum antibiotics (especially cephalosporins) Proton pump inhibitors (PPIs) Hospitalization

Answer 137

A: C. difficile produces toxin A and toxin B, which damage intestinal epithelial cells and inflammatory cells, leading to colitis.

Answer 138

Diarrhoea Abdominal pain Raised white blood cell count (WCC) In severe cases, toxic megacolon may develop

Answer 139

A: Diagnosis is made by detecting C. difficile toxin (CDT) in stool samples. C. difficile antigen positivity only indicates exposure, not active infection.

Answer 140

First-line: Oral vancomycin for 10 days Second-line: Oral fidaxomicin Third-line: Oral vancomycin +/− IV metronidazole

Answer 141

Within 12 weeks of symptom resolution: Oral fidaxomicin After 12 weeks: Oral vancomycin or fidaxomicin

Answer 142

A: Oral vancomycin and IV metronidazole, along with specialist advice. Surgery may be considered.

Answer 143

Bezlotoxumab (monoclonal antibody targeting toxin B) – not currently recommended by NICE for recurrence prevention due to cost-effectiveness concerns. Faecal microbiota transplant may be considered for patients with multiple recurrent episodes.

Answer 144

Isolation in a side room until no diarrhoea (types 5-7 on the Bristol Stool Chart) for 48 hours Disposable gloves and aprons for staff Handwashing (alcohol gel does not kill C. difficile spores)

Answer 145

A: Coeliac disease is an autoimmune condition caused by sensitivity to gluten. Repeated exposure leads to villous atrophy, causing malabsorption.

Answer 146

A: Coeliac disease affects around 1% of the UK population.

Answer 147

A: Coeliac disease is strongly associated with HLA-DQ2 (95% of patients) and HLA-DQ8 (80%).

Answer 148

Dermatitis herpetiformis (vesicular, pruritic skin eruption) Autoimmune disorders like type 1 diabetes mellitus and autoimmune hepatitis

Answer 149

Chronic or intermittent diarrhoea Failure to thrive or faltering growth (in children) Persistent gastrointestinal symptoms (nausea, vomiting) Prolonged fatigue Recurrent abdominal pain, cramping, or distension Sudden weight loss Unexplained iron-deficiency anaemia Autoimmune thyroid disease Dermatitis herpetiformis Type 1 diabetes First-degree relatives with coeliac disease

Answer 150

Anaemia (iron, folate, and vitamin B12 deficiency) Hyposplenism Osteoporosis, osteomalacia Lactose intolerance Enteropathy-associated T-cell lymphoma of the small intestine Subfertility and unfavourable pregnancy outcomes Rare cancers (oesophageal cancer, other malignancies)

Answer 151

Complete atrophy of villi with flat mucosa Marked crypt hyperplasia Intraepithelial lymphocytosis Dense mixed inflammatory infiltrate in the lamina propria

Answer 152

Flat mucosa with hyperplastic crypts Dense cellular infiltrate in the lamina propria Increased intraepithelial lymphocytes Vacuolated superficial epithelial cells

Answer 153

A: The gold standard for diagnosing coeliac disease is an endoscopic intestinal biopsy.

Answer 154

Tissue transglutaminase (TTG) antibodies (IgA): First-choice test according to NICE. Endomysial antibodies (IgA): Used to check for selective IgA deficiency, which can cause false-negative results. Anti-gliadin antibodies (IgA or IgG): Not recommended by NICE. Anti-casein antibodies: Found in some patients.

Answer 155

If a patient is already on a gluten-free diet, they should, if possible, reintroduce gluten for at least 6 weeks prior to testing for coeliac disease.

Answer 156

Villous atrophy Crypt hyperplasia Increase in intraepithelial lymphocytes Lamina propria infiltration with lymphocytes

Answer 157

A: While duodenal biopsies are traditionally performed, jejunal biopsies are occasionally performed as well.

Answer 158

A: The primary treatment for coeliac disease is a gluten-free diet.

Answer 159

Wheat: Bread, pasta, pastry Barley: Beer, whisky (although the distillation process removes gluten from whisky) Rye Oats: Some patients may tolerate oats, but it is generally advised to avoid them.

Answer 160

Rice Potatoes Corn (maize)

Answer 161

A: Tissue transglutaminase antibodies may be checked to monitor compliance with the gluten-free diet.

Answer 162

Patients with coeliac disease often experience functional hyposplenism, increasing their risk for infections. All patients are offered the pneumococcal vaccine and should receive a booster every 5 years. The influenza vaccine is recommended on an individual basis.

Answer 163

The three types of colon cancer are: Sporadic (95%) Hereditary non-polyposis colorectal carcinoma (HNPCC), also known as Lynch syndrome (5%) Familial adenomatous polyposis (FAP) (<1%)

Answer 164

Allelic loss of the APC gene (found in >50% of cases) Activation of the K-ras oncogene Deletion of the p53 and DCC tumour suppressor genes

Answer 165

A: HNPCC is an autosomal dominant condition associated with a high risk of colorectal cancer (70-80% of patients develop it). It is caused by mutations affecting genes involved in DNA mismatch repair, leading to microsatellite instability.

Answer 166

MSH2 (60% of cases) MLH1 (30% of cases)

Answer 167

At least 3 family members with colon cancer The cases span at least two generations At least one case diagnosed before the age of 50 years

Answer 168

FAP is a rare autosomal dominant condition where patients develop hundreds of polyps by the age of 30-40 years. It is caused by a mutation in the APC gene, located on chromosome 5, and inevitably leads to colorectal carcinoma.

Answer 169

A: The standard treatment is a total proctocolectomy with ileal pouch-anal anastomosis (IPAA), typically performed in their twenties.

Answer 170

Patients with FAP are also at risk for duodenal tumours. A variant called Gardner’s syndrome can cause: Osteomas of the skull and mandible Retinal pigmentation Thyroid carcinoma Epidermoid cysts on the skin

Answer 171

Constipation is a common primary functional bowel disorder characterized by unsatisfactory defecation. It is defined by: Infrequent stools (<3 times weekly) Difficulty passing stools (straining or discomfort) Seemingly incomplete defecation

Answer 172

Features include: Passage of infrequent, hard stools Difficulty or discomfort with defecation

Answer 173

Investigating and excluding any secondary causes Considering red flag symptoms Excluding faecal impaction Lifestyle measures: Increasing dietary fibre, ensuring adequate fluid intake, and maintaining adequate activity levels First-line laxative: Bulk-forming laxative, such as ispaghula Second-line laxative: Osmotic laxative, such as macrogol

Answer 174

Overflow diarrhoea Acute urinary retention Haemorrhoids

Answer 175

A: Crohn's disease is a form of inflammatory bowel disease (IBD) that can affect any part of the gastrointestinal tract, from the mouth to the anus. It commonly involves the terminal ileum and colon.

Answer 176

Genetic susceptibility Inflammation in all layers of the bowel (including the serosa), leading to strictures, fistulas, and adhesions Disease burden distribution: 80% have small bowel involvement, mostly ileum 50% have ileocolitis 20% have colitis exclusively 30% have perianal disease

Answer 177

A: It typically presents in late adolescence or early adulthood. Main symptoms include: Weight loss and lethargy Diarrhoea (most prominent symptom in adults) Abdominal pain (most prominent symptom in children) Bloody diarrhoea (especially in Crohn's colitis) Perianal disease (e.g., skin tags, ulcers) Extra-intestinal features, more common in colitis or perianal disease

Answer 178

Common features related to disease activity: Pauciarticular, asymmetric arthritis Erythema nodosum Episcleritis Osteoporosis Unrelated to disease activity: Polyarticular, symmetric arthritis Uveitis Pyoderma gangrenosum Clubbing Primary sclerosing cholangitis (more common in ulcerative colitis)

Answer 179

Raised inflammatory markers Increased faecal calprotectin Anaemia Low vitamin B12 and vitamin D

Answer 180

A: C-reactive protein (CRP) correlates well with disease activity in Crohn's disease.

Answer 181

A: Colonoscopy is the investigation of choice for diagnosing Crohn's disease.

Answer 182

Deep ulcers Skip lesions (areas of healthy mucosa interspersed with affected tissue)

Answer 183

Inflammation in all layers (from mucosa to serosa) Goblet cells Granulomas

Answer 184

Small bowel enema is highly sensitive for examining the terminal ileum, with findings such as: Strictures: "Kantor's string sign" Proximal bowel dilation 'Rose thorn' ulcers Fistulae

Answer 185

A: The first step is to advise patients to stop smoking, as smoking worsens Crohn's disease.

Answer 186

Glucocorticoids (oral, topical, or intravenous) Budesonide (alternative for some patients) Enteral feeding with an elemental diet (especially for young children or those concerned about steroid side effects)

Answer 187

5-ASA drugs (e.g., mesalazine) Azathioprine or mercaptopurine (not used as monotherapy) Methotrexate (alternative to azathioprine)

Answer 188

A: Infliximab is used for refractory disease and fistulating Crohn's disease. Patients may continue on azathioprine or methotrexate alongside infliximab.

Answer 189

A: Azathioprine or mercaptopurine is used first-line to maintain remission, with methotrexate as second-line. TPMT activity should be assessed before starting thiopurines.

Answer 190

Ileocaecal resection for stricturing terminal ileal disease Segmental small bowel resections Stricturoplasty Surgery for perianal fistulae (with MRI used to assess fistula complexity)

Answer 191

A: Metronidazole is often used for isolated perianal disease and can also be used for perianal abscesses, in combination with incision and drainage.

Answer 192

Small bowel cancer (standard incidence ratio = 40) Colorectal cancer (lower risk than in ulcerative colitis) Osteoporosis

Answer 193

A: Diarrhoea is defined as > 3 loose or watery stools per day.

Answer 194

Acute diarrhoea: lasts < 14 days Chronic diarrhoea: lasts > 14 days

Answer 195

Gastroenteritis (may be accompanied by abdominal pain or nausea/vomiting) Diverticulitis (left lower quadrant pain, diarrhoea, and fever) Antibiotic therapy, including Clostridioides difficile infections Constipation causing overflow, with alternating diarrhoea and constipation

Answer 196

Irritable Bowel Syndrome (IBS) (abdominal pain, bloating, and change in bowel habit) Ulcerative colitis (bloody diarrhoea, crampy abdominal pain, and weight loss) Crohn's disease (crampy abdominal pain, diarrhoea, malabsorption, mouth ulcers) Colorectal cancer (diarrhoea, rectal bleeding, anaemia, weight loss) Coeliac disease (failure to thrive, diarrhoea, abdominal distension in children; lethargy, anaemia, diarrhoea in adults)

Answer 197

Thyrotoxicosis Laxative abuse Appendicitis Radiation enteritis

Answer 198

The patient is systemically unwell and may need hospital admission There is blood or pus in the stool The patient is immunocompromised Recent use of antibiotics, PPIs, or recent hospitalisation Recent foreign travel Public health indication (e.g., high-risk individuals or suspected food poisoning)

Answer 199

Acute kidney injury Hypokalaemia Hyponatraemia

Answer 200

Diverticulosis refers to the presence of multiple outpouchings (diverticula) in the bowel wall, most commonly in the sigmoid colon. Diverticular disease is reserved for symptomatic cases of diverticulosis.

Answer 201

Increasing age Low-fibre diet

Answer 202

Painful diverticular disease: Symptoms include altered bowel habits and colicky left-sided abdominal pain. A high-fibre diet is recommended to reduce symptoms. Diverticulitis: Infection of a diverticulum, presenting with more severe symptoms (see below).

Answer 203

Left iliac fossa pain and tenderness Anorexia, nausea, and vomiting Diarrhoea Features of infection: pyrexia, raised WBC, and raised CRP

Answer 204

Oral antibiotics

Answer 205

Nil by mouth Intravenous fluids Intravenous antibiotics (typically a cephalosporin and metronidazole)

Answer 206

Abscess formation Peritonitis Obstruction Perforation

Answer 207

Hepatocellular Cholestatic Mixed (overlap between both)

Answer 208

Paracetamol Sodium valproate, phenytoin MAOIs Halothane Anti-tuberculosis drugs: isoniazid, rifampicin, pyrazinamide Statins Alcohol Amiodarone Methyldopa Nitrofurantoin

Answer 209

Combined oral contraceptive pill Antibiotics: flucloxacillin, co-amoxiclav, erythromycin* Anabolic steroids, testosterones Phenothiazines: chlorpromazine, prochlorperazine Sulphonylureas Fibrates Rare causes: nifedipine

Answer 210

Methotrexate Methyldopa Amiodarone

Answer 211

All patients with dysphagia All patients with an upper abdominal mass consistent with stomach cancer Patients aged ≥ 55 years with weight loss and any of the following: Upper abdominal pain Reflux Dyspepsia

Answer 212

Haematemesis Patients aged ≥ 55 years with: Treatment-resistant dyspepsia, or Upper abdominal pain with low haemoglobin levels or raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain Nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain

Answer 213

Review medications for possible causes of dyspepsia Lifestyle advice Trial of full-dose proton pump inhibitor for one month OR a 'test and treat' approach for H. pylori If symptoms persist after either approach, try the alternative approach

Answer 214

Initial diagnosis: Carbon-13 urea breath test Stool antigen test Laboratory-based serology (where locally validated) Test of cure: No need for re-testing if symptoms resolve after treatment If re-testing is required, use carbon-13 urea breath test

Answer 215

A: New-onset dysphagia is a red flag symptom that requires urgent endoscopy, regardless of age or other symptoms.

Answer 216

Dysphagia associated with weight loss, anorexia, or vomiting during eating Past history of Barrett's oesophagus, GORD, excessive smoking or alcohol use

Answer 217

A: Oesophagitis. It may also include odynophagia (painful swallowing) and no systemic symptoms.

Answer 218

HIV Use of steroid inhalers or other immunosuppressive treatments

Answer 219

Dysphagia for both liquids and solids from the start Heartburn, regurgitation of food, and possible complications like cough and aspiration pneumonia

Answer 220

CREST syndrome may present with oesophageal dysmotility, causing dysphagia The lower oesophageal sphincter (LES) pressure is decreased, unlike in achalasia, where LES pressure is increased

Answer 221

A herniation between the thyropharyngeus and cricopharyngeus muscles Symptoms include dysphagia, regurgitation, aspiration, chronic cough, and halitosis. A large pouch may present with a midline lump that gurgles on palpation.

Answer 222

Extraocular muscle weakness or ptosis Dysphagia for both liquids and solids

Answer 223

A sensation of a lump in the throat often associated with anxiety Symptoms are intermittent and often relieved by swallowing, typically painless (if painful, further investigation is needed) Often difficult to swallow saliva

Answer 224

Upper GI endoscopy is required for all patients unless contraindicated Fluoroscopic swallowing studies for motility disorders Full blood count Ambulatory oesophageal pH and manometry studies for conditions like achalasia or GORD being considered for surgery

Answer 225

A: Ferritin is an intracellular protein that binds iron and stores it, releasing it in a controlled manner at sites where iron is required.

Answer 226

300 µg/L in men and postmenopausal women 200 µg/L in premenopausal women

Answer 227

A: Ferritin is an acute phase reactant, meaning it can be elevated during inflammatory conditions even without actual iron overload.

Answer 228

Inflammation (due to ferritin being an acute phase protein) Alcohol excess Liver disease Chronic kidney disease Malignancy

Answer 229

Primary iron overload (e.g., hereditary haemochromatosis) Secondary iron overload (e.g., following repeated blood transfusions)

Answer 230

The best test is transferrin saturation. Normal values: < 45% in females < 50% in males Values above these thresholds suggest iron overload.

Answer 231

A: Ferritin levels may be decreased in cases of iron deficiency anaemia, as the body has less iron available for storage.

Answer 232

A: Measuring serum ferritin levels helps determine whether low hemoglobin and microcytosis are due to iron deficiency.

Answer 233

A: Up to 24% of women and 12% of men have gallstones. Of those, up to 30% may develop cholecystitis.

Answer 234

A: Mixed composition stones (50%), followed by pure cholesterol stones (20%).

Answer 235

A: Colicky right upper quadrant pain, usually postprandially, and worsened after fatty meals.

Answer 236

Abdominal ultrasound Liver function tests For bile duct stones, MRCP or intraoperative imaging may be used.

Answer 237

Symptoms: Colicky abdominal pain, worse postprandially, after fatty foods. Management: Laparoscopic cholecystectomy if gallstones are seen on imaging.

Answer 238

Symptoms: Right upper quadrant pain, fever, Murphy's sign, mild deranged LFTs. Management: Imaging (USS), and cholecystectomy ideally within 48 hours.

Answer 239

Symptoms: Prodromal illness, right upper quadrant pain, swinging pyrexia, systemic illness. Management: Imaging (USS or CT), surgery (subtotal cholecystectomy or percutaneous drainage for unfit patients).

Answer 240

Symptoms: Severe sepsis, jaundice, right upper quadrant pain. Management: Fluid resuscitation, broad-spectrum antibiotics, ERCP.

Answer 241

Symptoms: Small bowel obstruction (may be intermittent). Management: Laparotomy to remove the gallstone from the small bowel.

Answer 242

Symptoms: Patients with intercurrent illness, high fever, gallbladder inflammation without stones. Management: Cholecystectomy if fit; otherwise, percutaneous cholecystostomy.

Answer 243

A: Asymptomatic gallstones in the gallbladder are managed expectantly. However, if stones are in the common bile duct, surgical management should be considered due to complications like cholangitis or pancreatitis.

Answer 244

Bleeding: 0.9% (1.5% with sphincterotomy) Duodenal perforation: 0.4% Cholangitis: 1.1% Pancreatitis: 1.5%

Answer 245

A: Stones can be managed with ERCP or surgical exploration. Small stones <5mm may pass spontaneously and do not require intervention.

Answer 246

A: Around 2% of all cancer diagnoses.

Answer 247

A: Gastric adenocarcinoma, which arises from the glandular epithelium of the stomach lining.

Answer 248

Helicobacter pylori infection Pernicious anaemia and atrophic gastritis Diet (salt, salt-preserved foods, nitrates) Ethnicity (Japan, China) Smoking Blood group A

Answer 249

Abdominal pain (vague, epigastric) Dyspepsia Weight loss and anorexia Nausea and vomiting Dysphagia (particularly if cancer is in the proximal stomach) Overt upper GI bleeding (in minority) Lymphatic spread: Virchow's node (left supraclavicular lymph node) Sister Mary Joseph's node (periumbilical nodule)

Answer 250

Oesophago-gastro-duodenoscopy (OGD) with biopsy. Signet ring cells may be seen, associated with a worse prognosis.

Answer 251

CT scan of the chest, abdomen, and pelvis to check for metastasis. Other options include endoscopic ultrasound, FDG-PET scanning, and pre-operative staging laparoscopy.

Answer 252

Endoscopic mucosal resection Partial gastrectomy Total gastrectomy

Answer 253

A: Chemotherapy may be used as part of the treatment depending on the stage and resectability of the cancer.

Answer 254

A: There is poor correlation between symptoms and endoscopy appearance.

Answer 255

Age > 55 years Symptoms lasting > 4 weeks or persistent despite treatment Dysphagia Relapsing symptoms Weight loss

Answer 256

A: 24-hour oesophageal pH monitoring, which is considered the gold standard test for diagnosis of GORD.

Answer 257

A: GORD is defined as symptoms of oesophagitis secondary to refluxed gastric contents.

Answer 258

A: It should be treated as per the dyspepsia guidelines.

Answer 259

Full dose proton pump inhibitor (PPI) for 1-2 months. If response, switch to low dose treatment as required. If no response, increase to double-dose PPI for 1 month.

Answer 260

Full dose PPI for 1 month. If response, offer low dose treatment, possibly on an as-required basis, with a limited number of repeat prescriptions. If no response, consider H2RA or prokinetic for 1 month.

Answer 261

Oesophagitis Ulcers Anaemia Benign strictures Barrett's oesophagus Oesophageal carcinoma

Answer 262

A: Gilbert's syndrome is an autosomal recessive condition caused by a deficiency of UDP glucuronosyltransferase, leading to defective bilirubin conjugation.

Answer 263

A: The prevalence is approximately 1-2%.

Answer 264

Unconjugated hyperbilirubinaemia (i.e., increased bilirubin in the blood but not in the urine). Jaundice may be seen during intercurrent illness, exercise, or fasting.

Answer 265

A: A rise in bilirubin following prolonged fasting or IV nicotinic acid is suggestive.

Answer 266

A: No treatment is required.

Answer 267

A: Haemochromatosis is an autosomal recessive disorder of iron absorption and metabolism, leading to iron accumulation. It is caused by mutations in the HFE gene on both copies of chromosome 6.

Answer 268

A: The prevalence is approximately 1 in 200 people of European descent, making it more common than cystic fibrosis.

Answer 269

Fatigue Erectile dysfunction Arthralgia (especially of the hands) 'Bronze' skin pigmentation Diabetes mellitus Stigmata of chronic liver disease (hepatomegaly, cirrhosis) Cardiac failure (due to dilated cardiomyopathy) Hypogonadism (due to cirrhosis and pituitary dysfunction) Arthritis (especially of the hands)

Answer 270

Cardiomyopathy Skin pigmentation Liver cirrhosis (if not advanced) Diabetes mellitus Hypogonadotrophic hypogonadism Arthropathy

Answer 271

Liver cirrhosis (once developed) Cardiac failure (due to dilated cardiomyopathy) Arthropathy (joint damage)

Answer 272

A: There are rare cases where families exhibit classic features of genetic haemochromatosis but have no mutation in the HFE gene.

Answer 273

A: Transferrin saturation is considered the most useful marker for screening for haemochromatosis.

Answer 274

A: Ferritin should also be measured, though it is not usually abnormal in the early stages of iron accumulation.

Answer 275

Transferrin saturation > 55% in men or > 50% in women Raised ferritin (e.g. > 500 µg/L) and iron Low TIBC (total iron-binding capacity)

Answer 276

Liver function tests Molecular genetic testing for the C282Y and H63D mutations MRI to quantify liver and/or cardiac iron Liver biopsy (if suspected hepatic cirrhosis)

Answer 277

A: Venesection (phlebotomy) is the first-line treatment.

Answer 278

Transferrin saturation should be kept below 50% Serum ferritin concentration should be kept below 50 µg/L

Answer 279

A: Desferrioxamine may be used as a second-line treatment.

Answer 280

A: Helicobacter pylori is a Gram-negative bacterium.

Answer 281

Chemotaxis away from low pH areas, using its flagella to burrow into the mucous lining to reach the epithelial cells. Secretion of urease, which converts urea to NH3, resulting in alkalinization of the acidic environment and increased bacterial survival.

Answer 282

A: Helicobacter pylori releases bacterial cytotoxins (e.g., CagA toxin) that disrupt the gastric mucosa.

Answer 283

Peptic ulcer disease (95% of duodenal ulcers, 75% of gastric ulcers) Gastric cancer B cell lymphoma of MALT tissue (regression in 80% after eradication) Atrophic gastritis

Answer 284

A: The role of H. pylori in GORD is unclear, and there is currently no role for eradication of H. pylori in GORD management.

Answer 285

A 7-day course of: Proton pump inhibitor (PPI) + amoxicillin + (clarithromycin OR metronidazole)

Answer 286

A 7-day course of: Proton pump inhibitor (PPI) + metronidazole + clarithromycin

Answer 287

The patient consumes a drink containing carbon isotope 13 (13C) enriched urea. H. pylori urease breaks down the urea. After 30 minutes, the patient exhales into a tube, and mass spectrometry calculates the amount of 13C CO2.

Answer 288

Sensitivity: 95-98% Specificity: 97-98%

Answer 289

It should not be performed: Within 4 weeks of antibacterial treatment. Within 2 weeks of antisecretory drugs (e.g., proton pump inhibitors).

Answer 290

The exact cause is not fully understood but involves excess absorption of ammonia and glutamine from the bacterial breakdown of proteins in the gut.

Answer 291

A: Yes, hepatic encephalopathy is associated with both acute liver failure and chronic liver disease (such as cirrhosis). Chronic cirrhosis patients may develop subtle symptoms (e.g., mild cognitive impairment) before more recognizable features.

Answer 292

Confusion, altered GCS (Glasgow Coma Scale) Asterixis ("liver flap"): Arrhythmic negative myoclonus (3-5 Hz) Constructional apraxia: Inability to draw a 5-pointed star Triphasic slow waves on EEG Raised ammonia levels (though rarely measured)

Answer 293

Grade I: Irritability Grade II: Confusion, inappropriate behavior Grade III: Incoherent, restless Grade IV: Coma

Answer 294

Infection (e.g., spontaneous bacterial peritonitis) GI bleed Post-TIPSS (transjugular intrahepatic portosystemic shunt) Constipation Drugs (e.g., sedatives, diuretics) Hypokalaemia Renal failure Increased dietary protein (uncommon)

Answer 295

Lactulose (to promote ammonia excretion and increase ammonia metabolism by gut bacteria). Rifaximin may be added for secondary prophylaxis.

Answer 296

A: Lactulose promotes the excretion of ammonia and enhances ammonia metabolism by gut bacteria.

Answer 297

A: Rifaximin is thought to modulate gut flora, leading to decreased ammonia production.

Answer 298

Embolisation of portosystemic shunts Liver transplantation in selected patients

Answer 299

HBsAg is the first marker to appear in hepatitis B infection. If present for 1-6 months, it indicates acute disease. If present for > 6 months, it indicates chronic disease (i.e., infective).

Answer 300

Anti-HBs implies immunity (either from exposure or immunisation). It is negative in chronic disease.

Answer 301

Anti-HBc implies previous or current infection. IgM anti-HBc appears during acute or recent hepatitis B infection and is present for about 6 months. IgG anti-HBc persists for a longer time.

Answer 302

HBeAg is a marker of HBV replication and infectivity. It results from the breakdown of the core antigen from infected liver cells and indicates high infectivity.

Answer 303

Anti-HBs positive All other markers (HBsAg, anti-HBc, HBeAg) negative.

Answer 304

Anti-HBc positive HBsAg negative

Answer 305

Anti-HBc positive HBsAg positive Anti-HBs negative.

Answer 306

HBsAg indicates ongoing infection. Acute infection if present for 1-6 months. Chronic infection (carrier) if present for > 6 months.

Answer 307

Anti-HBc negative suggests the patient has been immunized (i.e., no previous infection).

Answer 308

Nausea and vomiting Anorexia Myalgia Lethargy Right upper quadrant (RUQ) pain Risk factors: foreign travel, intravenous drug use.

Answer 309

Caused by congestive heart failure. Liver pain occurs due to liver stretching. In severe cases, cirrhosis may develop.

Answer 310

RUQ pain, intermittent Usually begins abruptly and subsides gradually Often occurs after eating Nausea is common The patient may be female, in their forties, fat, and fair (a generalization).

Answer 311

Similar to biliary colic but more severe and persistent pain. Pain may radiate to the back or right shoulder. The patient may be pyrexial. Murphy’s sign is positive (arrest of inspiration on palpation of RUQ).

Answer 312

Infection of the bile ducts, often secondary to gallstones. Triad of symptoms: Fever (rigors are common) RUQ pain Jaundice

Answer 313

Small bowel obstruction caused by an impacted gallstone. May occur if a fistula forms between a gangrenous gallbladder and the duodenum. Symptoms: abdominal pain, distension, vomiting.

Answer 314

Persistent biliary colic, anorexia, jaundice, and weight loss. Courvoisier sign (palpable RUQ mass) Sister Mary Joseph nodes (periumbilical lymphadenopathy) Virchow node (left supraclavicular adenopathy).

Answer 315

Severe epigastric pain (usually due to alcohol or gallstones). Vomiting is common. Examination may reveal tenderness, ileus, and low-grade fever. Cullen’s sign (periumbilical discoloration) and Grey-Turner’s sign (flank discoloration) are rare but described.

Answer 316

Painless jaundice is the classical presentation. Pain is a relatively common symptom. Anorexia and weight loss are common.

Answer 317

Malaise, anorexia, weight loss. RUQ pain tends to be mild. Jaundice is uncommon.

Answer 318

Chronic hepatitis B is the most common cause globally. Chronic hepatitis C is the most common cause in Europe

Answer 319

Liver cirrhosis (secondary to various conditions including hepatitis B & C, alcohol use, haemochromatosis, and primary biliary cirrhosis). Other risk factors include: Alpha-1 antitrypsin deficiency Hereditary tyrosinosis Glycogen storage disease Aflatoxin exposure Drugs (oral contraceptive pill, anabolic steroids) Porphyria cutanea tarda Male sex Diabetes mellitus and metabolic syndrome

Answer 320

Tends to present late. Features of liver cirrhosis or liver failure may be seen, such as: Jaundice Ascites RUQ pain Hepatomegaly Pruritus Splenomegaly Decompensation in a patient with chronic liver disease. Raised AFP (Alpha-fetoprotein).

Answer 321

Patients with liver cirrhosis secondary to hepatitis B & C or haemochromatosis. Men with liver cirrhosis secondary to alcohol use. Screening may involve ultrasound and alpha-fetoprotein (AFP) levels.

Answer 322

Surgical resection Liver transplantation Radiofrequency ablation Transarterial chemoembolisation Sorafenib (a multikinase inhibitor).

Answer 323

Wilson's disease (a genetic disorder that causes copper accumulation in the liver).

Answer 324

In early disease, the liver may be enlarged. In later stages, the liver may decrease in size. The liver is typically non-tender and firm.

Answer 325

Can be caused by metastatic spread or a primary hepatoma. The liver is hard and has an irregular edge.

Answer 326

The liver is firm, smooth, and tender. The liver edge may be pulsatile.

Answer 327

Viral hepatitis Glandular fever Malaria Abscesses (pyogenic, amoebic) Hydatid disease Haematological malignancies Haemochromatosis Primary biliary cirrhosis Sarcoidosis Amyloidosis

Answer 328

Splanchnic vasodilation leads to reduced systemic vascular resistance. The kidneys sense an "underfill" and activate the renin-angiotensin-aldosterone system (RAAS). This causes renal vasoconstriction, but it is insufficient to counteract the splanchnic vasodilation.

Answer 329

Type 1 HRS: Rapid progression: Doubling of serum creatinine to >221 µmol/L or halving creatinine clearance to <20 ml/min within 2 weeks. Very poor prognosis. Type 2 HRS: Slow progression: The prognosis is poor, but patients may survive longer.

Answer 330

Vasopressin analogues (e.g., terlipressin): Improve splanchnic vasoconstriction. Volume expansion with 20% albumin: To increase circulatory volume. Transjugular intrahepatic portosystemic shunt (TIPSS): To reduce portal pressure.

Answer 331

Liver transplantation is the ideal treatment, but it is often difficult due to the patient's condition and a shortage of donors.

Answer 332

Crohn's disease (CD): Diarrhoea is usually non-bloody, with more prominent weight loss and upper gastrointestinal symptoms. Ulcerative colitis (UC): Bloody diarrhoea is more common, with abdominal pain in the left lower quadrant and tenesmus.

Answer 333

Crohn's disease (CD): Gallstones are more common due to reduced bile acid reabsorption. Ulcerative colitis (UC): Primary sclerosing cholangitis is more common.

Answer 334

Crohn's disease (CD): Inflammation can affect any part of the gastrointestinal tract from the mouth to anus, with skip lesions, and inflammation affects all layers of the bowel wall. Ulcerative colitis (UC): Inflammation starts in the rectum and is continuous, never extending beyond the ileocaecal valve. It affects only the mucosa and submucosa.

Answer 335

Crohn's disease (CD): Features granulomas, increased goblet cells, and inflammation of all layers from mucosa to serosa. Ulcerative colitis (UC): No granulomas, depletion of goblet cells, and inflammation is limited to the mucosa and submucosa, with crypt abscesses and neutrophil migration

Answer 336

Crohn's disease (CD): Deep ulcers, skip lesions, and a cobble-stone appearance. Ulcerative colitis (UC): Widespread ulceration with adjacent mucosa showing pseudopolyps.

Answer 337

Crohn's disease (CD): Small bowel enema shows Kantor's string sign, proximal bowel dilation, rose thorn ulcers, and fistulae. Ulcerative colitis (UC): Barium enema shows loss of haustrations, pseudopolyps, and in long-standing disease, the colon appears narrow and short (drainpipe colon).

Answer 338

Unconjugated hyperbilirubinaemia. Gilbert's syndrome: Autosomal recessive, mild deficiency of UDP-glucuronyl transferase, benign condition.

Answer 339

Unconjugated hyperbilirubinaemia. Crigler-Najjar syndrome, type 1: Autosomal recessive, absolute deficiency of UDP-glucuronosyl transferase, does not survive to adulthood. Crigler-Najjar syndrome, type 2: Less severe, may improve with phenobarbital.

Answer 340

Conjugated hyperbilirubinaemia. Dubin-Johnson syndrome: Autosomal recessive, mutation in MRP2 (canalicular multidrug resistance protein 2), defective hepatic excretion of bilirubin. Grossly black liver, benign.

Answer 341

Conjugated hyperbilirubinaemia. Rotor syndrome: Autosomal recessive, defect in hepatic uptake and storage of bilirubin, benign.

Answer 342

A: Serum iron indicates the amount of circulating iron in the blood.

Answer 343

A: Raised TIBC can indicate iron deficiency anaemia (IDA), pregnancy, or be due to oestrogen use.

Answer 344

A: Transferrin saturation is calculated by the formula: serum iron / TIBC.

Answer 345

A: Raised ferritin can indicate inflammatory disorders.

Answer 346

A: Low ferritin suggests iron deficiency anaemia (IDA).

Answer 347

A: Transferrin receptors are increased in iron deficiency anaemia (IDA).

Answer 348

Serum iron: Reduced TIBC: Reduced Ferritin: Normal or raised Anemia type: Normochromic/hypochromic, normocytic

Answer 349

Abdominal pain Bloating Change in bowel habit

Answer 350

Abdominal pain relieved by defecation or associated with altered bowel frequency or stool form, plus 2 of the following: Altered stool passage (straining, urgency, incomplete evacuation) Abdominal bloating, distension, tension, or hardness Symptoms made worse by eating Passage of mucus

Answer 351

Lethargy Nausea Backache Bladder symptoms

Answer 352

Rectal bleeding Unexplained/unintentional weight loss Family history of bowel or ovarian cancer Onset after 60 years of age

Answer 353

Full blood count (FBC) ESR/CRP (Erythrocyte Sedimentation Rate/C-Reactive Protein) Coeliac disease screen (tissue transglutaminase antibodies)

Answer 354

A: Antispasmodic agents

Answer 355

A: Laxatives (avoid lactulose)

Answer 356

A: Loperamide

Answer 357

A: If optimal or maximum tolerated doses of previous laxatives from different classes have not helped and they have had constipation for at least 12 months.

Answer 358

A: Low-dose tricyclic antidepressants (e.g., amitriptyline 5-10 mg)

Answer 359

A: Cognitive behavioural therapy, hypnotherapy, or psychological therapy

Answer 360

Have regular meals and take time to eat Avoid missing meals or leaving long gaps between eating Drink at least 8 cups of fluid per day, especially water or other non-caffeinated drinks Restrict tea and coffee to 3 cups per day Reduce intake of alcohol and fizzy drinks Consider limiting intake of high-fibre foods Reduce intake of 'resistant starch' found in processed foods Limit fresh fruit to 3 portions per day Avoid sorbitol for diarrhoea For wind and bloating, consider increasing intake of oats and linseeds

Answer 361

A: Acute mesenteric ischaemia, chronic mesenteric ischaemia, and ischaemic colitis

Answer 362

A: Increasing age, atrial fibrillation, other causes of emboli (endocarditis, malignancy), cardiovascular disease risk factors (smoking, hypertension, diabetes), and cocaine use

Answer 363

A: Abdominal pain, rectal bleeding, diarrhoea, fever, elevated white blood cell count, and lactic acidosis

Answer 364

A: CT scan

Answer 365

A: An embolism resulting in occlusion of an artery supplying the small bowel, often the superior mesenteric artery

Answer 366

A: Severe, sudden onset abdominal pain out-of-keeping with physical exam findings

Answer 367

A: Urgent surgery

Answer 368

A: Intestinal angina

Answer 369

A: Colicky, intermittent abdominal pain

Answer 370

A: Acute but transient compromise in blood flow to the large bowel, more likely in 'watershed' areas like the splenic flexure pain gets worse after eating, when the bowel requires more blood flow for its increased energy demands for digestion

Answer 371

A: 'Thumbprinting' due to mucosal oedema/haemorrhage

Answer 372

A: Supportive care, with surgery required in a minority of cases if conservative measures fail

Answer 373

A: Generalised peritonitis, perforation, or ongoing haemorrhage

Answer 374

A: Shock liver

Answer 375

A: Diffuse hepatic injury resulting from acute hypoperfusion

Answer 376

A: No, it is not an inflammatory process

Answer 377

A: In the presence of an inciting event (e.g., cardiac arrest) and marked increases in aminotransferase levels (exceeding 1000 international units/L or 50 times the upper limit of normal)

Answer 378

A: Exceeding 1000 international units/L or 50 times the upper limit of normal

Answer 379

A: Acute kidney injury (tubular necrosis) or other end-organ dysfunction

Answer 380

A: Alcohol, non-alcoholic fatty liver disease (NAFLD), and viral hepatitis (B and C)

Answer 381

A: Liver biopsy

Answer 382

A: Transient elastography and acoustic radiation force impulse imaging

Answer 383

A: Fibroscan

Answer 384

A: It uses a 50-MHz wave passed into the liver from a small transducer on the end of an ultrasound probe to measure the 'stiffness' of the liver, which is a proxy for fibrosis

Answer 385

People with hepatitis C virus infection Men who drink over 50 units of alcohol per week and women who drink over 35 units of alcohol per week for several months People diagnosed with alcohol-related liver disease

Answer 386

A: An upper endoscopy to check for varices

Answer 387

A: Liver ultrasound every 6 months (+/- alpha-fetoprotein)

Answer 388

A Body Mass Index (BMI) of less than 18.5

Answer 389

Greater than 10%

Answer 390

Unintentional weight loss greater than 5% within the last 3-6 months

Answer 391

MUST (Malnutrition Universal Screen Tool)

Answer 392

BMI, recent weight change, and the presence of acute disease

Answer 393

Dietician support

Answer 394

A 'food-first' approach with clear instructions (e.g., 'add full-fat cream to mashed potato')

Answer 395

They should be taken between meals, rather than instead of meals

Answer 396

A disorder of pigmentation of the bowel wall.

Answer 397

Pigment-laden macrophages.

Answer 398

Laxative abuse.

Answer 399

Anthraquinone compounds such as senna.

Answer 400

Loss of hydrogen ions or gain of bicarbonate, typically due to kidney or gastrointestinal issues.

Answer 401

Vomiting / aspiration (e.g. peptic ulcer, pyloric stenosis, nasogastric suction) Diuretics Liquorice, carbenoxolone Hypokalaemia Primary hyperaldosteronism Cushing's syndrome Bartter's syndrome

Answer 402

Activation of the renin-angiotensin II-aldosterone (RAA) system, causing Na+ reabsorption in exchange for H+ in the distal convoluted tubule, leading to alkalosis.

Answer 403

Vomiting or diuretics cause Na+ and Cl- loss, leading to activation of the RAA system and increased aldosterone, resulting in H+ loss and alkalosis.

Answer 404

In hypokalaemia, K+ shifts from cells into extracellular fluid (ECF), and to maintain neutrality, H+ shifts into cells, causing alkalosis.

Answer 405

Mainly used in the management of nausea.

Answer 406

Gastro-oesophageal reflux disease (GERD) Gastroparesis (particularly secondary to diabetic neuropathy) Combined with analgesics for migraine treatment

Answer 407

Extrapyramidal effects (e.g., acute dystonia, oculogyric crisis, especially in children and young adults) Diarrhoea Hyperprolactinaemia Tardive dyskinesia Parkinsonism

Answer 408

In bowel obstruction, but it may be helpful in paralytic ileus.

Answer 409

Non-alcoholic fatty liver disease (NAFLD).

Answer 410

Steatosis (fat in the liver) Steatohepatitis (fat with inflammation, non-alcoholic steatohepatitis, NASH) Fibrosis and cirrhosis in progressive disease.

Answer 411

Insulin resistance, as NAFLD is considered the hepatic manifestation of the metabolic syndrome.

Answer 412

NASH is similar to alcoholic hepatitis but occurs in the absence of alcohol abuse.

Answer 413

Obesity Type 2 diabetes mellitus Hyperlipidaemia Jejunoileal bypass Sudden weight loss/starvation

Answer 414

Usually asymptomatic Hepatomegaly ALT > AST Increased echogenicity on ultrasound

Answer 415

No routine screening for NAFLD. For incidental findings (e.g., fatty liver on ultrasound), use the enhanced liver fibrosis (ELF) blood test to check for advanced fibrosis.

Answer 416

FIB4 score NAFLD fibrosis score FibroScan (liver stiffness measurement using transient elastography)

Answer 417

Lifestyle changes, particularly weight loss, along with monitoring.

Answer 418

Adenocarcinoma.

Answer 419

Adenocarcinoma: Lower third, near the gastroesophageal junction. Squamous cell cancer: Upper two-thirds of the oesophagus.

Answer 420

Gastro-oesophageal reflux disease (GORD) Barrett's oesophagus Smoking Obesity

Answer 421

Smoking Alcohol Achalasia Plummer-Vinson syndrome Diets rich in nitrosamines

Answer 422

Dysphagia.

Answer 423

Anorexia and weight loss Vomiting Odynophagia Hoarseness Melaena Cough

Answer 424

Upper GI endoscopy with biopsy.

Answer 425

Endoscopic ultrasound (preferred for locoregional staging) CT scanning of the chest, abdomen, and pelvis (initial staging) FDG-PET CT for detecting occult metastases Laparoscopy to detect occult peritoneal disease

Answer 426

Surgical resection, typically an Ivor-Lewis type oesophagectomy.

Answer 427

Anastomotic leak, which can lead to mediastinitis, especially with an intrathoracic anastomosis.

Answer 428

Adjuvant chemotherapy.

Answer 429

Dysphagia (due to oesophageal webs) Glossitis Iron-deficiency anaemia

Answer 430

Iron supplementation Dilation of oesophageal webs

Answer 431

Severe vomiting leads to painful mucosal lacerations at the gastroesophageal junction, causing haematemesis. Common in alcoholics.

Answer 432

Severe vomiting causes oesophageal rupture.

Answer 433

Adenocarcinoma (over 80% of pancreatic tumours) Typically occurs at the head of the pancreas.

Answer 434

Increasing age Smoking Diabetes Chronic pancreatitis Hereditary non-polyposis colorectal carcinoma Multiple endocrine neoplasia BRCA2 gene mutation KRAS gene mutation

Answer 435

Painless jaundice Pale stools, dark urine, and pruritus Cholestatic liver function tests Abdominal masses: Hepatomegaly (due to metastases) Gallbladder (Courvoisier's law: palpable gallbladder in painless obstructive jaundice is unlikely to be due to gallstones) Epigastric mass (from the primary tumour) Anorexia, weight loss, epigastric pain Loss of exocrine function (steatorrhoea) Loss of endocrine function (diabetes mellitus) Atypical back pain Migratory thrombophlebitis (Trousseau's sign)

Answer 436

High-resolution CT scan Ultrasound has a sensitivity of around 60-90%. Imaging may show the "double duct" sign (simultaneous dilatation of the common bile and pancreatic ducts).

Answer 437

Whipple's resection (pancreaticoduodenectomy) for lesions in the head of the pancreas. Side effects: dumping syndrome and peptic ulcer disease. Adjuvant chemotherapy following surgery. ERCP with stenting for palliation in advanced cases.

Answer 438

Bleeding, accounting for around three-quarters of complications.

Answer 439

Haematemesis.

Answer 440

Melaena Hypotension Tachycardia

Answer 441

The gastroduodenal artery.

Answer 442

ABC approach (Airway, Breathing, Circulation) as with any upper gastrointestinal haemorrhage. IV proton pump inhibitor. Endoscopic intervention as first-line treatment

Answer 443

Urgent interventional angiography with transarterial embolization. Surgery (approximately 10% of patients).

Answer 444

Sudden onset epigastric pain, which later becomes more generalized. Patients may describe syncope

Answer 445

Plain x-rays, particularly an upright (erect) chest x-ray.

Answer 446

It is useful for detecting free air under the diaphragm, which is seen in approximately 75% of patients with a perforated peptic ulcer.

Answer 447

Helicobacter pylori infection: 95% of duodenal ulcers 75% of gastric ulcers Drugs: NSAIDs, SSRIs, corticosteroids, bisphosphonates Zollinger-Ellison syndrome: Rare cause due to excessive gastrin secretion from a gastrin-secreting tumor. The role of alcohol and smoking is unclear.

Answer 448

Duodenal ulcers: More common than gastric ulcers. Epigastric pain when hungry, relieved by eating. Gastric ulcers: Epigastric pain worsened by eating.

Answer 449

First-line tests: Urea breath test or stool antigen test.

Answer 450

If Helicobacter pylori is negative: Proton pump inhibitors (PPIs) are prescribed until the ulcer heals. If Helicobacter pylori is positive: Eradication therapy should be given.

Answer 451

Pernicious anaemia is an autoimmune disorder that affects the gastric mucosa, leading to vitamin B12 deficiency. It is the most common cause of vitamin B12 deficiency.

Answer 452

Intrinsic factor antibodies: Bind to intrinsic factor and block the vitamin B12 binding site. Gastric parietal cell antibodies: Lead to reduced acid production and atrophic gastritis, decreasing intrinsic factor production and vitamin B12 absorption.

Answer 453

Anaemia features: lethargy, pallor, dyspnoea. Neurological features: Peripheral neuropathy (symmetrical, affecting legs more than arms). Subacute combined degeneration of the spinal cord (weakness, ataxia, paresthesias). Neuropsychiatric symptoms (memory loss, confusion, depression). Other features: mild jaundice (lemon tinge), atrophic glossitis (sore tongue).

Answer 454

Full blood count: Macrocytic anaemia (may be absent in 30% of cases). Hypersegmented polymorphs. Low WCC and platelets may also be seen. Vitamin B12 levels: = 200 ng/L is generally considered normal. Antibodies: Anti-intrinsic factor antibodies (high specificity but low sensitivity). Anti-gastric parietal cell antibodies (high sensitivity but low specificity).

Answer 455

Vitamin B12 replacement: No neurological features: 3 injections per week for 2 weeks, then every 3 months. With neurological features: More frequent doses of B12 injections (hydroxycobalamin). Folic acid supplementation may be required. Oral B12 may be effective for maintenance, but is not commonly used yet.

Answer 456

Increased risk of gastric cancer. Haematological and neurological features as discussed above.

Answer 457

Peutz-Jeghers syndrome is an autosomal dominant condition characterized by numerous hamartomatous polyps in the gastrointestinal tract and pigmented freckles on the lips, face, palms, and soles. Although the polyps themselves have no malignant potential, about 50% of patients will die from another gastrointestinal tract cancer by age 60.

Answer 458

Hamartomatous polyps in the gastrointestinal tract, primarily in the small bowel. Small bowel obstruction, often due to intussusception. Gastrointestinal bleeding. Pigmented lesions on the lips, oral mucosa, face, palms, and soles.

Answer 459

Management is generally conservative unless complications, such as small bowel obstruction or gastrointestinal bleeding, develop.

Answer 460

A pharyngeal pouch, also known as Zenker's diverticulum, is a posteromedial diverticulum through Killian's dehiscence. This is a triangular area in the pharyngeal wall between the thyropharyngeus and cricopharyngeus muscles.

Answer 461

Dysphagia (difficulty swallowing) Regurgitation Aspiration Neck swelling that gurgles on palpation Halitosis (bad breath)

Answer 462

Investigation typically involves a barium swallow combined with dynamic video fluoroscopy to visualize the diverticulum during swallowing.

Answer 463

Management is surgical, with procedures such as diverticulectomy or myotomy, depending on the size and symptoms.

Answer 464

Primary biliary cholangitis (formerly known as primary biliary cirrhosis) is a chronic autoimmune liver disorder that causes progressive damage to interlobular bile ducts, leading to cholestasis and potentially cirrhosis.

Answer 465

PBC is more common in females, with a female to male ratio of 9:1.

Answer 466

Sjogren's syndrome (in up to 80% of patients) Rheumatoid arthritis Systemic sclerosis Thyroid disease

Answer 467

Fatigue Pruritus (itching) Cholestatic jaundice Raised ALP on routine liver function tests (LFTs)

Answer 468

Liver failure Hepatomegaly and splenomegaly Xanthelasmas and xanthomata Hyperpigmentation, especially over pressure points Right upper quadrant pain in 10% of patients

Answer 469

Itching (pruritus) in a middle-aged woman.

Answer 470

Immunology: Anti-mitochondrial antibodies (AMA) M2 subtype are highly specific and present in 98% of cases. Imaging: Ultrasound or MRCP to exclude extrahepatic biliary obstruction.

Answer 471

Ursodeoxycholic acid: Slows disease progression and improves symptoms. Cholestyramine: Used for pruritus.

Answer 472

Cirrhosis and portal hypertension (leading to ascites and variceal hemorrhage) Osteomalacia and osteoporosis Increased risk of hepatocellular carcinoma (20-fold)

Answer 473

If bilirubin > 100 (PBC is a major indication for liver transplantation). Recurrence in grafts is possible but not typically problematic.

Answer 474

Primary sclerosing cholangitis is a biliary disease characterized by inflammation and fibrosis of intra and extra-hepatic bile ducts, leading to cholestasis.

Answer 475

Ulcerative colitis (4% of UC patients have PSC; 80% of PSC patients have UC) Crohn's disease (less common than with UC) HIV

Answer 476

Cholestasis Jaundice Pruritus Raised bilirubin and ALP Right upper quadrant pain Fatigue

Answer 477

Endoscopic retrograde cholangiopancreatography (ERCP) or Magnetic resonance cholangiopancreatography (MRCP): Show multiple biliary strictures with a 'beaded' appearance. p-ANCA may be positive. Limited role for liver biopsy: It may show fibrous, obliterative cholangitis often described as 'onion skin'.

Answer 478

Cholangiocarcinoma (in 10% of patients) Increased risk of colorectal cancer

Answer 479

PPIs cause irreversible blockade of the H+/K+ ATPase enzyme on gastric parietal cells, reducing gastric acid production.

Answer 480

Hyponatraemia Hypomagnesaemia Osteoporosis (increased risk of fractures) Microscopic colitis Increased risk of Clostridium difficile infections

Answer 481

Staphylococcus aureus (in children) Escherichia coli (in adults)

Answer 482

Drainage (typically percutaneous) Antibiotics: Amoxicillin + Ciprofloxacin + Metronidazole If penicillin allergic: Ciprofloxacin + Clindamycin

Answer 483

Hypophosphataemia (hallmark symptom) Hypokalaemia Hypomagnesaemia Abnormal fluid balance

Answer 484

Shift from fat to carbohydrate metabolism: Refeeding causes a switch to carbohydrate metabolism, stimulating insulin secretion. Intracellular movement of phosphate: Phosphate is moved intracellularly for ATP and 2,3-diphosphoglycerate production. Decreased phosphate stores: Chronic malnutrition depletes phosphate stores, and refeeding increases demand, leading to hypophosphataemia.

Answer 485

Cardiac dysfunction: Impaired myocardial contractility, heart failure, arrhythmias Respiratory failure: Muscle weakness affecting the diaphragm and intercostal muscles Neurological complications: Confusion, seizures, coma Haematological effects: Reduced oxygen release from haemoglobin, hemolysis Rhabdomyolysis: Muscle breakdown due to impaired ATP production

Answer 486

If no food intake for >5 days: Refeed at no more than 50% of requirements for the first 2 days.

Answer 487

SBBOS is a disorder characterized by excessive amounts of bacteria in the small bowel, leading to gastrointestinal symptoms such as chronic diarrhoea, bloating, flatulence, and abdominal pain.

Answer 488

Neonates with congenital gastrointestinal abnormalities Scleroderma Diabetes mellitus

Answer 489

Chronic diarrhoea Bloating and flatulence Abdominal pain (Note: Many of these features overlap with irritable bowel syndrome.)

Answer 490

Hydrogen breath test (most commonly used) Small bowel aspiration and culture (less often used due to invasiveness and difficult-to-reproduce results) Antibiotic trial (sometimes used as a diagnostic approach)

Answer 491

Correction of the underlying disorder Antibiotic therapy: Rifaximin (treatment of choice due to relatively low resistance) Co-amoxiclav or metronidazole (also effective in most patients)

Answer 492

SBP is a form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis. It involves spontaneous infection of the ascitic fluid.

Answer 493

Ascites Abdominal pain Fever

Answer 494

Paracentesis: Neutrophil count > 250 cells/µL The most common organism found on ascitic fluid culture is Escherichia coli (E. coli).

Answer 495

Intravenous cefotaxime is typically administered to treat SBP.

Answer 496

Patients with a history of SBP Patients with ascitic fluid protein < 15 g/L and a Child-Pugh score of at least 9 or hepatorenal syndrome NICE recommends oral ciprofloxacin or norfloxacin for patients with cirrhosis and ascites and an ascitic protein level of 15 g/L or less until the ascites resolves.

Answer 497

Alcoholic liver disease is a marker of poor prognosis in SBP.

Answer 498

UC is a form of inflammatory bowel disease (IBD) that causes continuous inflammation starting at the rectum, which never spreads beyond the ileocaecal valve.

Answer 499

UC peaks in people aged 15-25 years and in those aged 55-65 years.

Answer 500

Bloody diarrhoea Urgency Tenesmus Abdominal pain, particularly in the left lower quadrant Extra-intestinal features

Answer 501

Colonoscopy + biopsy is the typical diagnostic tool. Flexible sigmoidoscopy is preferred in severe cases to reduce the risk of perforation. Findings: Red, raw mucosa that bleeds easily No inflammation beyond the submucosa (unless fulminant) Widespread ulceration with adjacent mucosa appearing as pseudopolyps Crypt abscesses formed by neutrophils

Answer 502

Loss of haustrations Superficial ulceration and pseudopolyps Long-standing disease: Colon appears narrow and short, known as drainpipe colon

Answer 503

Arthritis: pauciarticular, asymmetric (related to disease activity) Erythema nodosum Episcleritis Osteoporosis

Answer 504

Primary sclerosing cholangitis is much more common in UC.

Answer 505

Polyarticular, symmetric arthritis Uveitis Pyoderma gangrenosum Clubbing

Answer 506

UC: Primary sclerosing cholangitis is more common, uveitis is more common, and extra-intestinal features often relate to disease activity (e.g., arthritis, erythema nodosum). Crohn's disease: Episcleritis is more common, and the disease can present with additional complications like perianal disease.

Answer 507

Stress Medications NSAIDs Antibiotics Cessation of smoking

Answer 508

Flares are classified as mild, moderate, or severe based on the number of stools and the presence of systemic disturbance.

Answer 509

Fewer than four stools daily, with or without blood No systemic disturbance Normal ESR and C-reactive protein values

Answer 510

Four to six stools a day Minimal systemic disturbance

Answer 511

More than six stools a day, containing blood Evidence of systemic disturbance, e.g.: Fever Tachycardia Abdominal tenderness, distension, or reduced bowel sounds Anaemia Hypoalbuminaemia

Answer 512

Patients with severe disease should be admitted to hospital for further management.

Answer 513

Inducing remission Maintaining remission

Answer 514

Mild: < 4 stools/day, small amount of blood Moderate: 4-6 stools/day, varying blood, no systemic upset Severe: > 6 bloody stools/day + systemic upset (fever, tachycardia, anaemia, raised inflammatory markers)

Answer 515

Topical (rectal) aminosalicylate (mesalazine) If no remission after 4 weeks, add oral aminosalicylate If still no remission, add topical or oral corticosteroid

Answer 516

Topical (rectal) aminosalicylate If no remission after 4 weeks, add high-dose oral aminosalicylate or switch to high-dose oral aminosalicylate + topical corticosteroid If still no remission, add oral corticosteroid

Answer 517

Topical (rectal) aminosalicylate and high-dose oral aminosalicylate If no remission after 4 weeks, stop topical treatments and offer oral aminosalicylate + oral corticosteroid

Answer 518

IV steroids (first-line treatment in hospital) If no improvement after 72 hours, consider adding IV ciclosporin or surgery

Answer 519

Proctitis/proctosigmoiditis: Topical (rectal) aminosalicylate daily or intermittently OR oral aminosalicylate + topical aminosalicylate Left-sided and extensive UC: Low-dose oral aminosalicylate for maintenance

Answer 520

Oral azathioprine or oral mercaptopurine

Answer 521

Oesophageal varices, which can rupture, leading to a potentially life-threatening upper gastrointestinal bleed.

Answer 522

ABC (Airway, Breathing, Circulation) resuscitation Blood transfusion if needed Correct clotting: FFP, vitamin K, platelet transfusions Vasoactive agents: Terlipressin (first-line) Octreotide (alternative) Prophylactic IV antibiotics (quinolones) Endoscopy (endoscopic variceal band ligation)

Answer 523

Terlipressin (first-line) Shown to reduce mortality and prevent rebleeding Octreotide (alternative, but terlipressin is preferred)

Answer 524

Terlipressin (or octreotide) Prophylactic IV antibiotics (quinolones)

Answer 525

Endoscopic variceal band ligation (EVBL) Superior to endoscopic sclerotherapy

Answer 526

Sengstaken-Blakemore tube (temporary measure to control bleeding)

Answer 527

Transjugular Intrahepatic Portosystemic Shunt (TIPSS) Connects the hepatic vein to the portal vein Common complication: exacerbation of hepatic encephalopathy

Answer 528

Propranolol Reduces rebleeding and mortality compared to placebo

Answer 529

Endoscopic variceal band ligation (EVL) for medium to large oesophageal varices

Answer 530

PPI cover is given to prevent EVL-induced ulceration after variceal band ligation.

Answer 531

Every two weeks until all varices are eradicated.

Answer 532

A type of colonic polyp with the potential for malignant transformation. It secretes large amounts of mucous, which can lead to electrolyte disturbances.

Answer 533

Asymptomatic in the vast majority of cases. Possible non-specific lower gastrointestinal symptoms. Secretory diarrhoea may occur in some cases.

Answer 534

Hypokalaemia (due to excessive mucous secretion).

Answer 535

Microcytic anaemia (commonly due to chronic blood loss).

Answer 536

Villous adenomas have the potential to undergo malignant transformation, making them a significant risk factor for colon cancer.

Answer 537

Night blindness, due to impaired visual function related to insufficient retinal production.

Answer 538

Alcohol excess (thiamine supplements are routinely recommended for alcoholics). Malnutrition.

Answer 539

Wernicke's encephalopathy: nystagmus, ophthalmoplegia, and ataxia. Korsakoff's syndrome: amnesia and confabulation. Dry beriberi: peripheral neuropathy. Wet beriberi: dilated cardiomyopathy.

Answer 540

Angular cheilitis, which is inflammation and cracking at the corners of the mouth.

Answer 541

Hartnup's disease: A hereditary disorder that reduces absorption of tryptophan. Carcinoid syndrome: Increased metabolism of tryptophan to serotonin, leading to lower niacin production.

Answer 542

Pellagra, which presents with the 3 Ds: Dermatitis: Typically a sun-exposed, scaly rash. Diarrhoea: Gastrointestinal upset. Dementia: Cognitive changes, confusion, and neurological symptoms.

Answer 543

Isoniazid therapy: A medication used to treat tuberculosis that can interfere with vitamin B6 metabolism.

Answer 544

Peripheral neuropathy: Numbness, tingling, and weakness in the limbs. Sideroblastic anemia: Anemia caused by impaired hemoglobin production due to ineffective erythropoiesis.

Answer 545

Gingivitis and loose teeth Poor wound healing Bleeding from gums, hematuria, and epistaxis (nosebleeds) General malaise: Fatigue, weakness, and irritability.

Answer 546

Defective collagen synthesis due to impaired hydroxylation of proline and lysine, leading to capillary fragility and increased bleeding tendency.

Answer 547

Severe malnutrition Drug and alcohol abuse Limited access to fruits and vegetables, often seen in poverty.

Answer 548

Whipple's disease is caused by infection with Tropheryma whippelii.

Answer 549

Malabsorption (diarrhoea, weight loss) Large-joint arthralgia Lymphadenopathy Skin (hyperpigmentation, photosensitivity) Pleurisy and pericarditis Neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus

Answer 550

Diagnosis is confirmed by jejunal biopsy, which shows macrophages containing Periodic Acid-Schiff (PAS) granules.

Answer 551

Oral co-trimoxazole for one year is often used, as it has the lowest relapse rate. Sometimes, the treatment may begin with a course of IV penicillin before oral co-trimoxazole.

Answer 552

Zollinger-Ellison syndrome is a condition characterized by excessive levels of gastrin due to a gastrin-secreting tumour, commonly located in the first part of the duodenum or pancreas.

Answer 553

The majority of gastrin-secreting tumours are found in the first part of the duodenum, with the second most common location being the pancreas.

Answer 554

Multiple gastroduodenal ulcers Diarrhoea Malabsorption

Answer 555

The best initial diagnostic test is the fasting gastrin levels.

Answer 556

The secretin stimulation test is used to further confirm the diagnosis of Zollinger-Ellison syndrome after elevated fasting gastrin levels.

Answer 557

Wilson's disease is an autosomal recessive disorder characterized by excessive copper deposition in tissues due to increased copper absorption from the small intestine and decreased hepatic copper excretion. It is caused by a defect in the ATP7B gene on chromosome 13.

Answer 558

The onset of symptoms is usually between 10-25 years. Children often present with liver disease, whereas young adults typically show neurological symptoms.

Answer 559

Hepatitis Cirrhosis

Answer 560

Basal ganglia degeneration (particularly in the putamen and globus pallidus) Speech, behavioural, and psychiatric problems Other symptoms: asterixis, chorea, dementia, parkinsonism

Answer 561

Kayser-Fleischer rings are green-brown rings in the periphery of the iris caused by copper accumulation in Descemet's membrane. They are present in about 50% of patients with isolated hepatic Wilson's disease and 90% of those with neurological involvement.

Answer 562

Renal tubular acidosis (especially Fanconi syndrome) Haemolysis Blue nails

Answer 563

Slit lamp examination for Kayser-Fleischer rings Reduced serum caeruloplasmin Reduced total serum copper (95% of plasma copper is carried by ceruloplasmin) Increased free (non-ceruloplasmin-bound) serum copper Increased 24-hour urinary copper excretion Genetic analysis of the ATP7B gene for confirmation

Answer 564

Penicillamine (chelates copper) as traditional first-line treatment Trientine hydrochloride as an alternative chelating agent Tetrathiomolybdate is a newer agent currently under investigation

Answer 565

colorectal then endometrial

Answer 566

right iliac fossa

Answer 567

vomiting, thoracic pain, subcutaneous emphysema

Answer 568

examination of scrotum for infection/torsion

Answer 569

first solids then liquids

Answer 570

cholestyramine

Answer 571

After endoscopy

Answer 572

gastric carcinoma

Answer 573

gallstone ileus

Answer 574

hyperbilirubinaemia

Answer 575

colonoscopy, sigmoidoscopy in severe flare

Answer 576

chronic hep b anti HBc IgG shows long term antibodies produced anti HBc IgM negative means it is not acute

Answer 577

IV phopshate

Answer 578

propanalol

Answer 579

give stimulant laxative -> senna

Answer 580

of 8-24 hours after presentation and consumed more than 150mg/kg