Gastro Flashcards
Question: What is achalasia?
Achalasia is a disorder characterized by failure of oesophageal peristalsis and inability to relax the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus. This results in a contracted LOS and a dilated oesophagus above it.
Question: What are the clinical features of achalasia?
Dysphagia of both liquids and solids
Variation in severity of symptoms
Heartburn
Regurgitation of food
Cough and aspiration pneumonia (in severe cases)
Malignant change in a small number of patients
Question: What is the most important investigation for achalasia?
Oesophageal manometry is considered the most important diagnostic test, showing excessive LOS tone that does not relax upon swallowing.
Question: What are the characteristic findings on barium swallow in achalasia?
Grossly expanded oesophagus
Fluid level
‘Bird’s beak’ appearance, indicating narrowing at the LOS
Question: What is seen on a chest x-ray in achalasia?
Wide mediastinum
Fluid level in the oesophagus
Question: What are the treatment options for achalasia?
Pneumatic (balloon) dilation is the preferred first-line treatment due to quicker recovery and less invasiveness.
Surgical intervention with a Heller cardiomyotomy is considered if symptoms are recurrent or persistent.
Botulinum toxin injection can be used in high surgical risk patients.
Drug therapy (e.g., nitrates, calcium channel blockers) has limited use due to side effects.
Question: What is a common way to think about the potential causes of acute abdominal pain?
The location of the pain. Conditions often cause pain in specific regions of the abdomen, although some conditions, like appendicitis, may start with generalized pain before localizing to a particular area.
Question: Which condition typically presents with central abdominal pain before localizing to the right iliac fossa?
Appendicitis.
Question: What are some infective causes of acute abdominal pain?
Gastroenteritis
Appendicitis
Diverticulitis
Pyelonephritis
Cholecystitis
Cholangitis
Pelvic inflammatory disease
Hepatitis
Pneumonia
Question: What are some inflammatory causes of acute abdominal pain?
Pancreatitis
Peptic ulcer disease
Question: What are some vascular causes of acute abdominal pain?
Ruptured abdominal aortic aneurysm
Mesenteric ischaemia
Myocardial infarction
Question: What are some traumatic causes of acute abdominal pain?
Ruptured spleen
Perforated viscus (e.g., oesophagus, stomach, bowel)
Question: What are some metabolic causes of acute abdominal pain?
Renal/ureteric stone
Diabetic ketoacidosis
Question: What are the key features of biliary colic?
Location: Right upper quadrant
Notes: Caused by a gallstone lodged in the bile duct, typically provoked by eating a fatty meal, no fever, and normal inflammatory markers.
Question: What are the key features of acute cholecystitis?
Location: Right upper quadrant
Notes: Inflammation/infection of the gallbladder secondary to impacted gallstones, positive Murphy’s sign, fever, and raised inflammatory markers.
Question: What are the key features of ascending cholangitis?
Location: Right upper quadrant
Notes: Bacterial infection of the biliary tree, commonly due to gallstones, Charcot’s triad (RUQ pain, fever, jaundice) in 20-50% of patients.
Question: What are the key features of acute pancreatitis?
Location: Epigastrium, radiating to the back
Notes: Usually due to alcohol or gallstones, very severe pain, tenderness, ileus, and low-grade fever.
Question: What are the key features of peptic ulcer disease?
Location: Epigastrium
Notes: History of NSAID use or alcohol excess, duodenal ulcers relieved by eating, gastric ulcers worsened by eating, features of upper GI haemorrhage.
Question: What are the key features of appendicitis?
Location: Right iliac fossa
Notes: Pain starts centrally, localizes to RIF, anorexia, tachycardia, low-grade pyrexia, tenderness in RIF, Rovsing’s sign.
Question: What are the key features of acute diverticulitis?
Location: Left lower quadrant
Notes: Colicky pain, diarrhea (sometimes bloody), fever, raised inflammatory markers, and white cells.
Question: What are the key features of intestinal obstruction?
Location: Central
Notes: History of malignancy or previous operations, vomiting, not opened bowels recently, ‘tinkling’ bowel sounds.
Question: What are the key features of renal colic?
Location: Loin pain radiating to the groin
Notes: Severe but intermittent pain, patients are restless, visible or non-visible haematuria may be present.
Question: What are the key features of acute pyelonephritis?
Location: Loin pain
Notes: Fever, rigors, and vomiting.
Question: What are the key features of urinary retention?
Location: Suprapubic
Notes: Caused by obstruction to bladder outflow, more common in men with a history of benign prostatic hyperplasia.
Question: What are the key features of an ectopic pregnancy?
Location: Right or left iliac fossa
Notes: Pain, history of amenorrhoea for 6-9 weeks, vaginal bleeding may be present.
Question: What are the key features of a ruptured abdominal aortic aneurysm?
Location: Central abdominal pain radiating to the back
Notes: Sudden collapse or sub-acute presentation, developing shock, history of cardiovascular disease.
Question: What are the key features of mesenteric ischaemia?
Location: Central abdominal pain
Notes: History of atrial fibrillation or cardiovascular disease, diarrhoea, rectal bleeding, metabolic acidosis.
Question: What does acute liver failure describe?
The rapid onset of hepatocellular dysfunction leading to a variety of systemic complications.
Question: What are common causes of acute liver failure?
Paracetamol overdose
Alcohol
Viral hepatitis (usually A or B)
Acute fatty liver of pregnancy
Question: What are the key features of acute liver failure?
Jaundice
Coagulopathy: raised prothrombin time
Hypoalbuminaemia
Hepatic encephalopathy
Renal failure is common (‘hepatorenal syndrome’)
Question: Which tests best assess the synthetic function of the liver in acute liver failure?
Prothrombin time
Albumin level
Question: Why are traditional ‘liver function tests’ not always reliable in acute liver failure?
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.
Question: What are the most common causes of acute upper gastrointestinal (GI) bleeding?
Oesophageal varices and peptic ulcer disease.
Question: What is haematemesis and how is it typically presented?
Haematemesis is the vomiting of blood, often bright red but may sometimes be described as ‘coffee ground’.
Question: What is melena and how is it typically presented?
Melena is the passage of altered blood per rectum, typically black and ‘tarry’.
Question: What might a raised urea level indicate in the context of upper GI bleeding?
A raised urea level may be seen due to the ‘protein meal’ of the blood.
Question: What are the typical presenting features of oesophageal varices?
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.
Question: What are the presenting features of oesophagitis?
Small volume of fresh blood, often streaking vomit.
Melena is rare.
Often ceases spontaneously.
Usually history of antecedent GORD-type symptoms.
Question: What are the presenting features of a gastric ulcer?
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.
Question: What are the presenting features of a duodenal ulcer?
May present with haematemesis, melena, and epigastric discomfort.
The pain often occurs several hours after eating.
Question: What are the two scores used for risk assessment in upper GI bleeding?
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.
Question: What is the Blatchford score used for?
To assess the risk of needing treatment for an upper GI bleed and to help decide whether patients can be managed as outpatients.
Question: What is the initial resuscitation approach for patients with acute upper GI bleeding?
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
Question: What should be done for patients with severe upper GI bleeding after initial resuscitation?
Endoscopy should be offered immediately.
Question: What are the management recommendations for non-variceal upper GI bleeding?
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.
Question: What are the management recommendations for variceal upper GI bleeding?
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.
Q: What is alcoholic ketoacidosis?
A: Alcoholic ketoacidosis is a non-diabetic euglycaemic form of ketoacidosis that occurs in people who regularly drink large amounts of alcohol.
Q: What lifestyle factors contribute to alcoholic ketoacidosis?
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.
Q: How does the body react to malnutrition in alcoholic ketoacidosis?
A: Once malnourished, after an alcohol binge, the body starts to break down body fat, producing ketones, leading to ketoacidosis.
Q: What are the typical metabolic findings in alcoholic ketoacidosis?
A: The typical metabolic findings in alcoholic ketoacidosis include metabolic acidosis, elevated anion gap, elevated serum ketone levels, and normal or low glucose concentration.
Q: What is the most appropriate treatment for alcoholic ketoacidosis?
A: The most appropriate treatment for alcoholic ketoacidosis is an infusion of saline and thiamine.
Q: Why is thiamine administered in the treatment of alcoholic ketoacidosis?
A: Thiamine is administered to avoid Wernicke encephalopathy or Korsakoff psychosis.
Q: What conditions are covered under alcoholic liver disease?
A: Alcoholic liver disease covers alcoholic fatty liver disease, alcoholic hepatitis, and cirrhosis.
Q: What investigation finding is characteristically elevated in alcoholic liver disease?
A: Gamma-GT is characteristically elevated in alcoholic liver disease.
Q: What AST:ALT ratio is strongly suggestive of acute alcoholic hepatitis?
A: An AST:ALT ratio of > 2 is typical, and a ratio of > 3 is strongly suggestive of acute alcoholic hepatitis.
Q: What medication is often used during acute episodes of alcoholic hepatitis?
A: Glucocorticoids (e.g., prednisolone) are often used during acute episodes of alcoholic hepatitis.
Q: What is Maddrey’s discriminant function (DF) used for in alcoholic hepatitis?
A: Maddrey’s discriminant function (DF) is used to determine who would benefit from glucocorticoid therapy during acute episodes of alcoholic hepatitis.
Q: What factors are used to calculate Maddrey’s discriminant function (DF)?
A: Maddrey’s discriminant function (DF) is calculated using prothrombin time and bilirubin concentration.
Q: What alternative medication is sometimes used for alcoholic hepatitis?
A: Pentoxyphylline is sometimes used for alcoholic hepatitis.
Q: What did the STOPAH study show about the treatments for alcoholic hepatitis?
A: The STOPAH study showed that prednisolone improved survival at 28 days, while pentoxyphylline did not improve outcomes.
Q: What is the primary action of 5-aminosalicyclic acid (5-ASA) in the colon?
A: 5-ASA acts locally as an anti-inflammatory in the colon.
Q: What might 5-ASA inhibit as part of its mechanism of action?
A: 5-ASA may inhibit prostaglandin synthesis.
Q: What is sulphasalazine composed of?
A: Sulphasalazine is a combination of sulphapyridine (a sulphonamide) and 5-ASA.
Q: What are some side effects of the sulphapyridine component in sulphasalazine?
A: Side effects include rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, and lung fibrosis.
Q: What is mesalazine?
A: Mesalazine is a delayed release form of 5-ASA that avoids the sulphapyridine side effects seen in patients taking sulphasalazine.
Q: What are some side effects common to mesalazine?
A: Side effects include GI upset, headache, agranulocytosis, pancreatitis, and interstitial nephritis.
Q: What is olsalazine?
A: Olsalazine consists of two molecules of 5-ASA linked by a diazo bond, which is broken by colonic bacteria.
Q: What haematological adverse effects are associated with aminosalicylates?
A: Aminosalicylates are associated with agranulocytosis and other haematological adverse effects.
Q: Why is FBC a key investigation in an unwell patient taking aminosalicylates?
A: FBC is key due to the risk of haematological adverse effects like agranulocytosis.
Q: How much more common is pancreatitis in patients taking mesalazine compared to those taking sulphasalazine?
A: Pancreatitis is 7 times more common in patients taking mesalazine than in those taking sulphasalazine.
Q: What is angiodysplasia?
A: Angiodysplasia is a vascular deformity of the gastrointestinal tract that predisposes to bleeding and iron deficiency anaemia.
Q: What is a debated association related to angiodysplasia?
A: There is a debated association between angiodysplasia and aortic stenosis.
Q: In which patient population is angiodysplasia generally seen?
A: Angiodysplasia is generally seen in elderly patients.
Q: What are common features of angiodysplasia?
A: Common features include anaemia and gastrointestinal (GI) bleeding.
Q: How does upper GI bleeding from angiodysplasia typically present?
A: Upper GI bleeding may present as melena.
Q: How does lower GI bleeding from angiodysplasia typically present?
A: Lower GI bleeding may present as brisk, fresh red per rectum (PR) bleeding.
Q: What diagnostic methods are used for angiodysplasia?
A: Diagnostic methods include colonoscopy and mesenteric angiography if there is acute bleeding.
Q: What are the management options for angiodysplasia?
A: Management options include endoscopic cautery or argon plasma coagulation, antifibrinolytics (e.g., tranexamic acid), and oestrogens.
Q: What enzyme converts phospholipids to arachidonic acid?
A: Phospholipase A2.
Q: Which enzymes convert arachidonic acid to endoperoxides?
A: COX-1 and COX-2.
Q: What are the products of endoperoxides in arachidonic acid metabolism?
A: Prostacyclin (PGI2), Prostaglandin (PGE2), and Thromboxane (TXA2).
Q: What are the effects of prostacyclin (PGI2)?
A: Vasodilation, decreased platelet aggregation, and decreased uterine tone.
Q: What are the effects of prostaglandin (PGE2)?
A: Increased pain, temperature, uterine tone, gastric mucus, and decreased gastric acid; varying effects on vascular smooth muscle and airways.
Q: What are the effects of thromboxane (TXA2)?
A: Vasoconstriction and increased platelet aggregation.
Q: What enzyme converts arachidonic acid to HPETEs?
A: Lipoxygenase.
Q: What are the products of HPETEs in arachidonic acid metabolism?
A: Leukotrienes (LTB4, LTA4, LTC4, LTD4, LTE4).
Q: What is the function of LTB4?
A: Increased neutrophil chemotaxis.
Q: What is the function of leukotrienes LTA4, LTC4, LTD4, and LTE4?
A: Increased bronchoconstriction.
Q: What mnemonic helps remember the function of thromboxane (TXA2)?
A: THROMBOxane (THROMBOSIS): promotes platelet aggregation and vasoconstriction.
Q: How does prostacyclin (PGI2) function in relation to thromboxane (TXA2)?
A: Prostacyclin (PGI2) has the opposite effects: it causes vasodilation and decreases platelet aggregation.
Q: What is ascites?
A: Ascites is the abnormal accumulation of fluid in the abdomen.
Q: What does an SAAG (Serum-Ascites Albumin Gradient) > 11 g/L indicate?
A: An SAAG > 11 g/L indicates portal hypertension.
Q: What liver disorders can cause ascites with an SAAG > 11 g/L?
A: Cirrhosis, alcoholic liver disease, acute liver failure, and liver metastases.
Q: What cardiac conditions can cause ascites with an SAAG > 11 g/L?
A: Right heart failure and constrictive pericarditis.
Q: What are some other causes of ascites with an SAAG > 11 g/L?
A: Budd-Chiari syndrome, portal vein thrombosis, veno-occlusive disease, myxoedema, hypoalbuminaemia, nephrotic syndrome, and severe malnutrition (e.g., Kwashiorkor).
Q: What causes ascites with an SAAG < 11 g/L?
A: Malignancy (peritoneal carcinomatosis), infections (e.g., tuberculous peritonitis), pancreatitis, bowel obstruction, biliary ascites, postoperative lymphatic leak, and serositis in connective tissue diseases.
Q: What is a key part of managing ascites?
A: Reducing dietary sodium.
Q: When is fluid restriction recommended in ascites management?
A: Fluid restriction is sometimes recommended if the sodium is < 125 mmol/L.
Q: What are common diuretics used in the management of ascites?
A: Aldosterone antagonists (e.g., spironolactone) and loop diuretics.
Q: When are loop diuretics added in the treatment of ascites?
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.
Q: What is the treatment for tense ascites?
A: Therapeutic abdominal paracentesis.
Q: Why is albumin ‘cover’ needed during large-volume paracentesis?
A: Albumin is given to reduce paracentesis-induced circulatory dysfunction and mortality.
Q: What complications can arise from large-volume paracentesis (> 5 litres)?
A: Paracentesis-induced circulatory dysfunction, high ascites recurrence, hepatorenal syndrome, dilutional hyponatraemia, and high mortality rate.
Q: What is the role of prophylactic antibiotics in ascites management?
A: To reduce the risk of spontaneous bacterial peritonitis, especially in cirrhosis with ascites and an ascitic protein of 15 g/L or less.
Q: What antibiotics are recommended for prophylaxis in ascites with cirrhosis?
A: Oral ciprofloxacin or norfloxacin.
Q: When might a transjugular intrahepatic portosystemic shunt (TIPS) be considered in ascites management?
A: TIPS may be considered in some patients with ascites related to portal hypertension.
Q: What is autoimmune hepatitis?
A: Autoimmune hepatitis is a condition of unknown etiology, most commonly seen in young females, characterized by immune system attack on the liver.
Q: What are some recognized associations with autoimmune hepatitis?
A: Other autoimmune disorders, hypergammaglobulinaemia, and HLA B8, DR3.
Q: What are the three types of autoimmune hepatitis based on circulating antibodies?
A: Type I, Type II, and Type III.
Q: What antibodies are associated with Type I autoimmune hepatitis?
A: Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA).
Q: Which type of autoimmune hepatitis affects both adults and children?
A: Type I autoimmune hepatitis.
Q: What antibodies are associated with Type II autoimmune hepatitis?
A: Anti-liver/kidney microsomal type 1 antibodies (LKM1).
Q: Which type of autoimmune hepatitis affects children only?
A: Type II autoimmune hepatitis.
Q: What antibodies are associated with Type III autoimmune hepatitis?
A: Soluble liver-kidney antigen.
Q: Which type of autoimmune hepatitis affects middle-aged adults?
A: Type III autoimmune hepatitis.
Q: What are common features of autoimmune hepatitis?
A: Chronic liver disease signs, acute hepatitis (fever, jaundice), amenorrhoea, ANA/SMA/LKM1 antibodies, and raised IgG levels.
Q: What is a key finding in liver biopsy for autoimmune hepatitis?
A: Inflammation extending beyond the limiting plate, with features like piecemeal necrosis and bridging necrosis.
Q: What is the main treatment for autoimmune hepatitis?
A: Steroids and other immunosuppressants, such as azathioprine.
Q: What is the treatment option for patients with severe autoimmune hepatitis or liver failure?
A: Liver transplantation.
Q: What is Barrett’s oesophagus?
A: Barrett’s oesophagus refers to the metaplasia of the lower oesophageal mucosa, where the usual squamous epithelium is replaced by columnar epithelium.
Q: What is the risk of oesophageal adenocarcinoma in Barrett’s oesophagus?
A: The risk of oesophageal adenocarcinoma is estimated to be 50-100 times higher in patients with Barrett’s oesophagus.
Q: How is Barrett’s oesophagus typically identified?
A: Barrett’s oesophagus is typically identified during an endoscopy for evaluation of upper gastrointestinal symptoms, such as dyspepsia.
Q: What are the two subtypes of Barrett’s oesophagus?
A: Short (<3cm) and long (>3cm) segments of metaplasia.
Q: What does the length of the affected segment in Barrett’s oesophagus correlate with?
A: The length of the affected segment strongly correlates with the likelihood of identifying metaplasia.
Q: What are the histological features of Barrett’s oesophagus?
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.
Q: What is the single strongest risk factor for Barrett’s oesophagus?
A: Gastro-oesophageal reflux disease (GORD) is the strongest risk factor for Barrett’s oesophagus.
Q: What are other risk factors for Barrett’s oesophagus?
A: Male gender (7:1 ratio), smoking, and central obesity.
Q: Does alcohol independently increase the risk of Barrett’s oesophagus?
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.
Q: What are the typical symptoms of Barrett’s oesophagus?
A: Barrett’s oesophagus itself is asymptomatic, but patients often have coexistent GORD symptoms.
Q: What is the first-line management for Barrett’s oesophagus?
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.
Q: How often should endoscopic surveillance be done for patients with Barrett’s oesophagus with metaplasia?
A: Endoscopy is recommended every 3-5 years for patients with metaplasia (but not dysplasia).
Q: What is the management for Barrett’s oesophagus if dysplasia is identified?
A: Endoscopic intervention is offered if any grade of dysplasia is identified.
Q: What are the treatment options for dysplasia in Barrett’s oesophagus?
A: Options include radiofrequency ablation (preferred first-line treatment, particularly for low-grade dysplasia) and endoscopic mucosal resection.
Q: What is bile-acid malabsorption?
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).
Q: What can bile-acid malabsorption lead to?
A: It can lead to steatorrhoea and malabsorption of vitamins A, D, E, and K.
Q: What are some secondary causes of bile-acid malabsorption?
A: Secondary causes include ileal disease (e.g., Crohn’s disease), cholecystectomy, coeliac disease, and small intestinal bacterial overgrowth.
Q: What is the test of choice for investigating bile-acid malabsorption?
A: The test of choice is SeHCAT, a nuclear medicine test using a gamma-emitting selenium molecule (75SeHCAT).
Q: How does the SeHCAT test work?
A: Scans are done 7 days apart to assess the retention/loss of the radiolabelled 75SeHCAT, which helps evaluate bile acid retention.
Q: What is the main treatment for bile-acid malabsorption?
A: The main treatment is bile acid sequestrants, such as cholestyramine.
Q: What is bilirubin and how is it formed?
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.
Q: What happens to unconjugated bilirubin after it is released into the bloodstream?
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.
Q: What is the fate of urobilinogen produced in the intestines?
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.
Q: What causes raised levels of unconjugated bilirubin?
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.
Q: What conditions are associated with a glucuronyl transferase deficiency?
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.
Q: What causes raised levels of conjugated bilirubin?
A: Raised levels of conjugated bilirubin can occur due to defective excretion, such as in Dubin-Johnson Syndrome or cholestasis.
Q: At what bilirubin level does jaundice typically appear?
A: Jaundice appears when bilirubin levels exceed 35 µmol/L.
Q: What are the two main categories of causes of cholestasis?
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).
Q: What is Budd-Chiari syndrome?
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.
Q: What are the common causes of Budd-Chiari syndrome?
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).
Q: What is the classic triad of symptoms in Budd-Chiari syndrome?
The classic triad includes:
Sudden, severe abdominal pain
Ascites (abdominal distension)
Tender hepatomegaly
Q: What is the most sensitive initial investigation for Budd-Chiari syndrome?
A: Ultrasound with Doppler flow studies is very sensitive and should be the initial radiological investigation.
Q: What is Carcinoid Syndrome and when does it usually occur?
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.
Q: What are the key features of Carcinoid Syndrome?
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)
Q: What are the key investigations for Carcinoid Syndrome?
Urinary 5-HIAA (a breakdown product of serotonin)
Plasma chromogranin A
Q: What is the management for Carcinoid Syndrome?
Somatostatin analogues (e.g., octreotide)
Cyproheptadine for diarrhoea
Q: What is Cholestyramine used for?
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.
Q: How does Cholestyramine work?
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.
Q: What are the main adverse effects of Cholestyramine?
Abdominal cramps and constipation
Decreased absorption of fat-soluble vitamins (A, D, E, K)
Cholesterol gallstones
May raise triglyceride levels
Q: What is Clostridioides difficile (C. difficile) and what causes its overgrowth?
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.
Q: What are the key risk factors for developing C. difficile infection?
Use of broad-spectrum antibiotics (especially cephalosporins)
Proton pump inhibitors (PPIs)
Hospitalization
Q: What are the two exotoxins produced by C. difficile and their effects?
A: C. difficile produces toxin A and toxin B, which damage intestinal epithelial cells and inflammatory cells, leading to colitis.
Q: What are the typical symptoms of C. difficile infection?
Diarrhoea
Abdominal pain
Raised white blood cell count (WCC)
In severe cases, toxic megacolon may develop
Q: How is C. difficile infection diagnosed?
A: Diagnosis is made by detecting C. difficile toxin (CDT) in stool samples. C. difficile antigen positivity only indicates exposure, not active infection.
Q: What are the treatment options for first-time C. difficile infection?
First-line: Oral vancomycin for 10 days
Second-line: Oral fidaxomicin
Third-line: Oral vancomycin +/− IV metronidazole
Q: How is recurrent C. difficile infection treated?
Within 12 weeks of symptom resolution: Oral fidaxomicin
After 12 weeks: Oral vancomycin or fidaxomicin
Q: What is the management for life-threatening C. difficile infection?
A: Oral vancomycin and IV metronidazole, along with specialist advice. Surgery may be considered.
Q: What are some other therapies for C. difficile infection?
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.
Q: How should C. difficile infection be managed to prevent spread in a hospital setting?
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)
Q: What is coeliac disease and what causes it?
A: Coeliac disease is an autoimmune condition caused by sensitivity to gluten. Repeated exposure leads to villous atrophy, causing malabsorption.
Q: What is the prevalence of coeliac disease in the UK?
A: Coeliac disease affects around 1% of the UK population.
Q: Which genetic markers are strongly associated with coeliac disease?
A: Coeliac disease is strongly associated with HLA-DQ2 (95% of patients) and HLA-DQ8 (80%).
Q: What are some conditions associated with coeliac disease?
Dermatitis herpetiformis (vesicular, pruritic skin eruption)
Autoimmune disorders like type 1 diabetes mellitus and autoimmune hepatitis
Q: What are some key symptoms that should prompt screening for coeliac disease?
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
Q: What are some complications of coeliac disease?
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)
Q: What do duodenal biopsies show in coeliac disease?
Complete atrophy of villi with flat mucosa
Marked crypt hyperplasia
Intraepithelial lymphocytosis
Dense mixed inflammatory infiltrate in the lamina propria
Q: What are the histological features of coeliac disease at higher magnification?
Flat mucosa with hyperplastic crypts
Dense cellular infiltrate in the lamina propria
Increased intraepithelial lymphocytes
Vacuolated superficial epithelial cells
Q: What is the gold standard for diagnosing coeliac disease?
A: The gold standard for diagnosing coeliac disease is an endoscopic intestinal biopsy.
Q: What are the serological tests used in the diagnosis of coeliac disease?
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.
Q: What is the role of the gluten-free diet in the diagnosis of coeliac disease?
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.
Q: What are the histological findings on a duodenal biopsy in coeliac disease?
Villous atrophy
Crypt hyperplasia
Increase in intraepithelial lymphocytes
Lamina propria infiltration with lymphocytes
Q: Are jejunal biopsies performed in coeliac disease diagnosis?
A: While duodenal biopsies are traditionally performed, jejunal biopsies are occasionally performed as well.
Q: What is the primary treatment for coeliac disease?
A: The primary treatment for coeliac disease is a gluten-free diet.
Q: Which foods contain gluten and should be avoided by patients with coeliac disease?
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.
Q: Which foods are typically safe (gluten-free) for patients with coeliac disease?
Rice
Potatoes
Corn (maize)
Q: How is compliance with a gluten-free diet monitored in coeliac disease?
A: Tissue transglutaminase antibodies may be checked to monitor compliance with the gluten-free diet.
Q: Why are vaccinations important in the management of coeliac disease?
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.
Q: What are the three types of colon cancer?
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%)
Q: What genetic mutations are commonly associated with sporadic colorectal cancer?
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
Q: What is HNPCC (Lynch syndrome)?
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.
Q: Which genes are most commonly mutated in HNPCC?
MSH2 (60% of cases)
MLH1 (30% of cases)
Q: What are the diagnostic criteria for HNPCC based on the Amsterdam criteria?
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
Q: What is Familial Adenomatous Polyposis (FAP)?
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.
Q: What is the standard treatment for patients with FAP?
A: The standard treatment is a total proctocolectomy with ileal pouch-anal anastomosis (IPAA), typically performed in their twenties.
Q: What additional risks do patients with FAP face?
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
Q: What is constipation?
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
Q: What are the features of constipation?
Features include:
Passage of infrequent, hard stools
Difficulty or discomfort with defecation
Q: What are the steps in the management of constipation?
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
Q: What are some complications of constipation?
Overflow diarrhoea
Acute urinary retention
Haemorrhoids
Q: What is Crohn’s disease?
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.
Q: What are the main pathophysiological features of Crohn’s disease?
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
Q: When does Crohn’s disease typically present and what are the main symptoms?
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
Q: What are some common extra-intestinal features of Crohn’s disease?
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)
Q: What are the common investigations for Crohn’s disease?
Raised inflammatory markers
Increased faecal calprotectin
Anaemia
Low vitamin B12 and vitamin D
Q: What blood test is useful in assessing Crohn’s disease activity?
A: C-reactive protein (CRP) correlates well with disease activity in Crohn’s disease.
Q: What is the investigation of choice for Crohn’s disease?
A: Colonoscopy is the investigation of choice for diagnosing Crohn’s disease.
Q: What endoscopic findings are suggestive of Crohn’s disease?
Deep ulcers
Skip lesions (areas of healthy mucosa interspersed with affected tissue)
Q: What histological findings are characteristic of Crohn’s disease?
Inflammation in all layers (from mucosa to serosa)
Goblet cells
Granulomas
Q: What imaging technique is highly sensitive for examining the terminal ileum in Crohn’s disease?
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
Q: What is the first step in managing Crohn’s disease?
A: The first step is to advise patients to stop smoking, as smoking worsens Crohn’s disease.
Q: What are the first-line medications for inducing remission in Crohn’s disease?
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)
Q: What medications can be used second-line for inducing remission in Crohn’s disease?
5-ASA drugs (e.g., mesalazine)
Azathioprine or mercaptopurine (not used as monotherapy)
Methotrexate (alternative to azathioprine)
Q: What is the role of infliximab in Crohn’s disease management?
A: Infliximab is used for refractory disease and fistulating Crohn’s disease. Patients may continue on azathioprine or methotrexate alongside infliximab.
Q: How is Crohn’s disease remission maintained?
A: Azathioprine or mercaptopurine is used first-line to maintain remission, with methotrexate as second-line. TPMT activity should be assessed before starting thiopurines.
Q: What surgical interventions are commonly required for Crohn’s disease?
Ileocaecal resection for stricturing terminal ileal disease
Segmental small bowel resections
Stricturoplasty
Surgery for perianal fistulae (with MRI used to assess fistula complexity)
Q: What is the role of metronidazole in Crohn’s disease?
A: Metronidazole is often used for isolated perianal disease and can also be used for perianal abscesses, in combination with incision and drainage.
Q: What are the complications of Crohn’s disease?
Small bowel cancer (standard incidence ratio = 40)
Colorectal cancer (lower risk than in ulcerative colitis)
Osteoporosis
Q: What is the definition of diarrhoea according to the World Health Organisation?
A: Diarrhoea is defined as > 3 loose or watery stools per day.
Q: What is the difference between acute and chronic diarrhoea?
Acute diarrhoea: lasts < 14 days
Chronic diarrhoea: lasts > 14 days
Q: What are some common causes of acute diarrhoea?
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
Q: What conditions are associated with chronic diarrhoea?
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)
Q: What are some other conditions associated with diarrhoea?
Thyrotoxicosis
Laxative abuse
Appendicitis
Radiation enteritis
Q: When should a stool sample be taken in a primary care setting for diarrhoea?
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)
Q: What blood tests might be indicated for severe diarrhoea?
Acute kidney injury
Hypokalaemia
Hyponatraemia
Q: What is the difference between diverticulosis and diverticular disease?
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.
Q: What are the main risk factors for diverticulosis?
Increasing age
Low-fibre diet
Q: How can diverticulosis present?
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).
Q: What is the classical presentation of diverticulitis?
Left iliac fossa pain and tenderness
Anorexia, nausea, and vomiting
Diarrhoea
Features of infection: pyrexia, raised WBC, and raised CRP
Q: How is mild diverticulitis treated?
Oral antibiotics
Q: How is severe diverticulitis treated?
Nil by mouth
Intravenous fluids
Intravenous antibiotics (typically a cephalosporin and metronidazole)
Q: What are the complications of diverticulitis?
Abscess formation
Peritonitis
Obstruction
Perforation
Q: What are the three types of drug-induced liver disease?
Hepatocellular
Cholestatic
Mixed (overlap between both)
Q: Which drugs typically cause a hepatocellular pattern of liver injury?
Paracetamol
Sodium valproate, phenytoin
MAOIs
Halothane
Anti-tuberculosis drugs: isoniazid, rifampicin, pyrazinamide
Statins
Alcohol
Amiodarone
Methyldopa
Nitrofurantoin
Q: Which drugs are most likely to cause cholestasis (and sometimes hepatitis)?
Combined oral contraceptive pill
Antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
Anabolic steroids, testosterones
Phenothiazines: chlorpromazine, prochlorperazine
Sulphonylureas
Fibrates
Rare causes: nifedipine
Q: Which drugs are associated with liver cirrhosis?
Methotrexate
Methyldopa
Amiodarone
Q: What are the urgent referral criteria for dyspepsia based on the 2015 NICE guidelines?
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
Q: What are the non-urgent referral criteria for dyspepsia based on the 2015 NICE guidelines?
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
Q: What is the step-wise approach to manage undiagnosed dyspepsia?
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
Q: What are the tests recommended by NICE for diagnosing H. pylori infection?
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
Q: What is the general red flag for dysphagia?
A: New-onset dysphagia is a red flag symptom that requires urgent endoscopy, regardless of age or other symptoms.
Q: What is the classic presentation of oesophageal cancer causing dysphagia?
Dysphagia associated with weight loss, anorexia, or vomiting during eating
Past history of Barrett’s oesophagus, GORD, excessive smoking or alcohol use
Q: What condition may present with dysphagia and heartburn but no weight loss?
A: Oesophagitis. It may also include odynophagia (painful swallowing) and no systemic symptoms.
Q: What are common risk factors for oesophageal candidiasis causing dysphagia?
HIV
Use of steroid inhalers or other immunosuppressive treatments
Q: What is the typical presentation of achalasia causing dysphagia?
Dysphagia for both liquids and solids from the start
Heartburn, regurgitation of food, and possible complications like cough and aspiration pneumonia
Q: What is the relationship between systemic sclerosis and dysphagia?
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
Q: What is a pharyngeal pouch and its associated symptoms?
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.
Q: What additional symptoms may be present in myasthenia gravis causing dysphagia?
Extraocular muscle weakness or ptosis
Dysphagia for both liquids and solids
Q: What is globus hystericus and how does it relate to dysphagia?
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
Q: What are the investigations for dysphagia?
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
Q: What is ferritin and its role in the body?
A: Ferritin is an intracellular protein that binds iron and stores it, releasing it in a controlled manner at sites where iron is required.
Q: When are ferritin levels considered elevated?
300 µg/L in men and postmenopausal women
200 µg/L in premenopausal women
Q: Why can ferritin levels be falsely elevated?
A: Ferritin is an acute phase reactant, meaning it can be elevated during inflammatory conditions even without actual iron overload.
Q: What are the causes of increased ferritin levels without iron overload?
Inflammation (due to ferritin being an acute phase protein)
Alcohol excess
Liver disease
Chronic kidney disease
Malignancy
Q: What are the causes of increased ferritin levels with iron overload?
Primary iron overload (e.g., hereditary haemochromatosis)
Secondary iron overload (e.g., following repeated blood transfusions)
Q: How is iron overload assessed?
The best test is transferrin saturation.
Normal values:
< 45% in females
< 50% in males
Values above these thresholds suggest iron overload.
Q: When are ferritin levels reduced?
A: Ferritin levels may be decreased in cases of iron deficiency anaemia, as the body has less iron available for storage.
Q: How is serum ferritin used in diagnosing iron deficiency anaemia?
A: Measuring serum ferritin levels helps determine whether low hemoglobin and microcytosis are due to iron deficiency.
Q: How common are gallstones?
A: Up to 24% of women and 12% of men have gallstones. Of those, up to 30% may develop cholecystitis.
Q: What is the most common composition of gallstones?
A: Mixed composition stones (50%), followed by pure cholesterol stones (20%).
Q: What are the classic symptoms of gallstones?
A: Colicky right upper quadrant pain, usually postprandially, and worsened after fatty meals.
Q: What is the standard diagnostic workup for suspected gallstones?
Abdominal ultrasound
Liver function tests
For bile duct stones, MRCP or intraoperative imaging may be used.
Q: What are the features and management of biliary colic?
Symptoms: Colicky abdominal pain, worse postprandially, after fatty foods.
Management: Laparoscopic cholecystectomy if gallstones are seen on imaging.
Q: What are the features and management of acute cholecystitis?
Symptoms: Right upper quadrant pain, fever, Murphy’s sign, mild deranged LFTs.
Management: Imaging (USS), and cholecystectomy ideally within 48 hours.
Q: What is gallbladder abscess and how is it managed?
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).
Q: What is cholangitis and its management?
Symptoms: Severe sepsis, jaundice, right upper quadrant pain.
Management: Fluid resuscitation, broad-spectrum antibiotics, ERCP.
Q: What is gallstone ileus and its management?
Symptoms: Small bowel obstruction (may be intermittent).
Management: Laparotomy to remove the gallstone from the small bowel.
Q: What is acalculous cholecystitis and how is it managed?
Symptoms: Patients with intercurrent illness, high fever, gallbladder inflammation without stones.
Management: Cholecystectomy if fit; otherwise, percutaneous cholecystostomy.
Q: How are asymptomatic gallstones managed?
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.
Q: What are the risks of ERCP?
Bleeding: 0.9% (1.5% with sphincterotomy)
Duodenal perforation: 0.4%
Cholangitis: 1.1%
Pancreatitis: 1.5%
Q: What should be done if bile duct stones are found during laparoscopic cholecystectomy?
A: Stones can be managed with ERCP or surgical exploration. Small stones <5mm may pass spontaneously and do not require intervention.
Q: What percentage of all cancer diagnoses is gastric cancer in the developed world?
A: Around 2% of all cancer diagnoses.
Q: What is the most common type of gastric cancer?
A: Gastric adenocarcinoma, which arises from the glandular epithelium of the stomach lining.
Q: What are the risk factors for gastric cancer?
Helicobacter pylori infection
Pernicious anaemia and atrophic gastritis
Diet (salt, salt-preserved foods, nitrates)
Ethnicity (Japan, China)
Smoking
Blood group A
Q: What are the common features of gastric cancer?
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)
Q: What is the diagnostic test for gastric cancer?
Oesophago-gastro-duodenoscopy (OGD) with biopsy.
Signet ring cells may be seen, associated with a worse prognosis.
Q: What is the staging method for gastric cancer?
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.
Q: What are the surgical treatment options for gastric cancer?
Endoscopic mucosal resection
Partial gastrectomy
Total gastrectomy
Q: What is the role of chemotherapy in gastric cancer?
A: Chemotherapy may be used as part of the treatment depending on the stage and resectability of the cancer.
Q: What is the relationship between symptoms and endoscopy appearance in gastro-oesophageal reflux disease (GORD)?
A: There is poor correlation between symptoms and endoscopy appearance.
Q: What are the indications for upper GI endoscopy in suspected GORD?
Age > 55 years
Symptoms lasting > 4 weeks or persistent despite treatment
Dysphagia
Relapsing symptoms
Weight loss
Q: If endoscopy for GORD is negative, what should be considered next?
A: 24-hour oesophageal pH monitoring, which is considered the gold standard test for diagnosis of GORD.
Q: What is gastro-oesophageal reflux disease (GORD) defined as?
A: GORD is defined as symptoms of oesophagitis secondary to refluxed gastric contents.
Q: According to NICE, how should GORD that has not been investigated with endoscopy be treated?
A: It should be treated as per the dyspepsia guidelines.
Q: What is the recommended management for endoscopically proven oesophagitis in GORD?
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.
Q: What is the management for endoscopically negative reflux disease in GORD?
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.
Q: What are the complications of GORD?
Oesophagitis
Ulcers
Anaemia
Benign strictures
Barrett’s oesophagus
Oesophageal carcinoma
Q: What is Gilbert’s syndrome?
A: Gilbert’s syndrome is an autosomal recessive condition caused by a deficiency of UDP glucuronosyltransferase, leading to defective bilirubin conjugation.
Q: What is the prevalence of Gilbert’s syndrome in the general population?
A: The prevalence is approximately 1-2%.
Q: What is the typical presentation of Gilbert’s syndrome?
Unconjugated hyperbilirubinaemia (i.e., increased bilirubin in the blood but not in the urine).
Jaundice may be seen during intercurrent illness, exercise, or fasting.
Q: How is Gilbert’s syndrome investigated?
A: A rise in bilirubin following prolonged fasting or IV nicotinic acid is suggestive.
Q: What is the treatment for Gilbert’s syndrome?
A: No treatment is required.
Q: What is haemochromatosis?
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.
Q: What is the prevalence of haemochromatosis in people of European descent?
A: The prevalence is approximately 1 in 200 people of European descent, making it more common than cystic fibrosis.
Q: What are some early presenting features of haemochromatosis?
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)
Q: What are the reversible complications of haemochromatosis with treatment?
Cardiomyopathy
Skin pigmentation
Liver cirrhosis (if not advanced)
Diabetes mellitus
Hypogonadotrophic hypogonadism
Arthropathy
Q: What are the irreversible complications of haemochromatosis?
Liver cirrhosis (once developed)
Cardiac failure (due to dilated cardiomyopathy)
Arthropathy (joint damage)
Q: How common is it for families to have haemochromatosis without the HFE gene mutation?
A: There are rare cases where families exhibit classic features of genetic haemochromatosis but have no mutation in the HFE gene.
Q: What is the most useful marker for screening for haemochromatosis in the general population?
A: Transferrin saturation is considered the most useful marker for screening for haemochromatosis.
Q: What other test should be measured along with transferrin saturation in screening for haemochromatosis?
A: Ferritin should also be measured, though it is not usually abnormal in the early stages of iron accumulation.
Q: What is the typical iron study profile for a patient with haemochromatosis?
Transferrin saturation > 55% in men or > 50% in women
Raised ferritin (e.g. > 500 µg/L) and iron
Low TIBC (total iron-binding capacity)
Q: What additional tests are done for haemochromatosis after initial screening?
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)
Q: What is the first-line treatment for haemochromatosis?
A: Venesection (phlebotomy) is the first-line treatment.
Q: How is the adequacy of venesection monitored in the management of haemochromatosis?
Transferrin saturation should be kept below 50%
Serum ferritin concentration should be kept below 50 µg/L
Q: What is used as second-line treatment for haemochromatosis if venesection is insufficient?
A: Desferrioxamine may be used as a second-line treatment.
Q: What type of bacteria is Helicobacter pylori?
A: Helicobacter pylori is a Gram-negative bacterium.
Q: What are the main mechanisms by which Helicobacter pylori survives in the acidic gastric environment?
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.
Q: What is the pathogenesis mechanism of Helicobacter pylori?
A: Helicobacter pylori releases bacterial cytotoxins (e.g., CagA toxin) that disrupt the gastric mucosa.
Q: What are some gastrointestinal associations of Helicobacter pylori?
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
Q: What is the role of Helicobacter pylori in Gastro-oesophageal reflux disease (GORD)?
A: The role of H. pylori in GORD is unclear, and there is currently no role for eradication of H. pylori in GORD management.
Q: What is the standard treatment regimen for Helicobacter pylori eradication?
A 7-day course of:
Proton pump inhibitor (PPI) + amoxicillin + (clarithromycin OR metronidazole)
Q: What is the alternative treatment for Helicobacter pylori in penicillin-allergic patients?
A 7-day course of:
Proton pump inhibitor (PPI) + metronidazole + clarithromycin
Q: How does the urea breath test for Helicobacter pylori work?
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.
Q: What are the sensitivity and specificity of the urea breath test for Helicobacter pylori?
Sensitivity: 95-98%
Specificity: 97-98%
Q: What are the limitations of the urea breath test for Helicobacter pylori?
It should not be performed:
Within 4 weeks of antibacterial treatment.
Within 2 weeks of antisecretory drugs (e.g., proton pump inhibitors).
Q: What is the aetiology of hepatic encephalopathy?
The exact cause is not fully understood but involves excess absorption of ammonia and glutamine from the bacterial breakdown of proteins in the gut.
Q: Can hepatic encephalopathy occur in both acute and chronic liver disease?
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.
Q: What are the features of hepatic encephalopathy?
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)
Q: How is hepatic encephalopathy graded?
Grade I: Irritability
Grade II: Confusion, inappropriate behavior
Grade III: Incoherent, restless
Grade IV: Coma
Q: What are common precipitating factors of hepatic encephalopathy?
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)
Q: What is the first-line treatment for hepatic encephalopathy?
Lactulose (to promote ammonia excretion and increase ammonia metabolism by gut bacteria).
Rifaximin may be added for secondary prophylaxis.
Q: How does lactulose work in treating hepatic encephalopathy?
A: Lactulose promotes the excretion of ammonia and enhances ammonia metabolism by gut bacteria.
Q: How does rifaximin work in treating hepatic encephalopathy?
A: Rifaximin is thought to modulate gut flora, leading to decreased ammonia production.
Q: What are the other management options for hepatic encephalopathy?
Embolisation of portosystemic shunts
Liver transplantation in selected patients
Q: What does the presence of HBsAg (Hepatitis B surface antigen) indicate?
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).
Q: What does the presence of anti-HBs (antibodies to hepatitis B surface antigen) indicate?
Anti-HBs implies immunity (either from exposure or immunisation).
It is negative in chronic disease.
Q: What does the presence of anti-HBc (antibodies to hepatitis B core antigen) indicate?
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.
Q: What does the presence of HBeAg (Hepatitis B e antigen) indicate?
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.
Q: What are the key features of a patient with previous immunisation for hepatitis B?
Anti-HBs positive
All other markers (HBsAg, anti-HBc, HBeAg) negative.
Q: What are the key features of a patient with previous hepatitis B infection, not a carrier?
Anti-HBc positive
HBsAg negative
Q: What are the key features of a patient who is a carrier of hepatitis B (chronic infection)?
Anti-HBc positive
HBsAg positive
Anti-HBs negative.
Q: What is the significance of HBsAg in interpreting hepatitis B serology?
HBsAg indicates ongoing infection.
Acute infection if present for 1-6 months.
Chronic infection (carrier) if present for > 6 months.
Q: What does a negative anti-HBc imply?
Anti-HBc negative suggests the patient has been immunized (i.e., no previous infection).
Q: What are the common symptoms of viral hepatitis?
Nausea and vomiting
Anorexia
Myalgia
Lethargy
Right upper quadrant (RUQ) pain
Risk factors: foreign travel, intravenous drug use.
Q: What is congestive hepatomegaly and how does it cause pain?
Caused by congestive heart failure.
Liver pain occurs due to liver stretching.
In severe cases, cirrhosis may develop.
Q: What are the typical features of biliary colic?
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).
Q: What are the key features of acute cholecystitis?
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).
Q: What is ascending cholangitis and how does it present?
Infection of the bile ducts, often secondary to gallstones.
Triad of symptoms:
Fever (rigors are common)
RUQ pain
Jaundice
Q: What is gallstone ileus and its features?
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.
Q: What are the key features of cholangiocarcinoma?
Persistent biliary colic, anorexia, jaundice, and weight loss.
Courvoisier sign (palpable RUQ mass)
Sister Mary Joseph nodes (periumbilical lymphadenopathy)
Virchow node (left supraclavicular adenopathy).
Q: What are the symptoms of acute pancreatitis?
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.
Q: How does pancreatic cancer typically present?
Painless jaundice is the classical presentation.
Pain is a relatively common symptom.
Anorexia and weight loss are common.
Q: What are the typical symptoms of an amoebic liver abscess?
Malaise, anorexia, weight loss.
RUQ pain tends to be mild.
Jaundice is uncommon.
Q: What is the most common cause of hepatocellular carcinoma (HCC) worldwide?
Chronic hepatitis B is the most common cause globally.
Chronic hepatitis C is the most common cause in Europe
Q: What is the main risk factor for developing HCC?
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
Q: How does hepatocellular carcinoma (HCC) typically present?
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).
Q: What high-risk groups should be screened for HCC?
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.
Q: What are the management options for early-stage hepatocellular carcinoma (HCC)?
Surgical resection
Liver transplantation
Radiofrequency ablation
Transarterial chemoembolisation
Sorafenib (a multikinase inhibitor).
Q: Which condition is an exception to the general rule that liver cirrhosis is the main risk factor for HCC?
Wilson’s disease (a genetic disorder that causes copper accumulation in the liver).
Q: What are the key features of hepatomegaly due to cirrhosis?
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.
Q: What are the key features of hepatomegaly due to malignancy?
Can be caused by metastatic spread or a primary hepatoma.
The liver is hard and has an irregular edge.
Q: What are the key features of hepatomegaly in right heart failure?
The liver is firm, smooth, and tender.
The liver edge may be pulsatile.
Q: What are some other causes of hepatomegaly?
Viral hepatitis
Glandular fever
Malaria
Abscesses (pyogenic, amoebic)
Hydatid disease
Haematological malignancies
Haemochromatosis
Primary biliary cirrhosis
Sarcoidosis
Amyloidosis
Q: What is the pathophysiology of hepatorenal syndrome (HRS)?
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.
Q: What are the two types of hepatorenal syndrome (HRS)?
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.
Q: What are the main management options for hepatorenal syndrome (HRS)?
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.
Q: What is the ideal treatment for hepatorenal syndrome (HRS)?
Liver transplantation is the ideal treatment, but it is often difficult due to the patient’s condition and a shortage of donors.
Q: What is a key symptom difference between Crohn’s disease and ulcerative colitis?
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.
Q: What are the differences in extra-intestinal features between Crohn’s disease and ulcerative colitis?
Crohn’s disease (CD): Gallstones are more common due to reduced bile acid reabsorption.
Ulcerative colitis (UC): Primary sclerosing cholangitis is more common.
Q: How does the pathology differ between Crohn’s disease and ulcerative colitis?
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.
Q: What is the difference in histology between Crohn’s disease and ulcerative colitis?
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
Q: How does the endoscopic appearance differ between Crohn’s disease and ulcerative colitis?
Crohn’s disease (CD): Deep ulcers, skip lesions, and a cobble-stone appearance.
Ulcerative colitis (UC): Widespread ulceration with adjacent mucosa showing pseudopolyps.
Q: How does radiology help differentiate Crohn’s disease and ulcerative colitis?
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).
Q: What type of hyperbilirubinaemia is associated with Gilbert’s syndrome?
Unconjugated hyperbilirubinaemia.
Gilbert’s syndrome: Autosomal recessive, mild deficiency of UDP-glucuronyl transferase, benign condition.
Q: What type of hyperbilirubinaemia is associated with Crigler-Najjar syndrome?
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.
Q: What type of hyperbilirubinaemia is associated with Dubin-Johnson syndrome?
Conjugated hyperbilirubinaemia.
Dubin-Johnson syndrome: Autosomal recessive, mutation in MRP2 (canalicular multidrug resistance protein 2), defective hepatic excretion of bilirubin. Grossly black liver, benign.
Q: What type of hyperbilirubinaemia is associated with Rotor syndrome?
Conjugated hyperbilirubinaemia.
Rotor syndrome: Autosomal recessive, defect in hepatic uptake and storage of bilirubin, benign.
Q: What is the significance of serum iron in iron studies?
A: Serum iron indicates the amount of circulating iron in the blood.
Q: What does a raised Total Iron Binding Capacity (TIBC) indicate?
A: Raised TIBC can indicate iron deficiency anaemia (IDA), pregnancy, or be due to oestrogen use.
Q: How is transferrin saturation calculated?
A: Transferrin saturation is calculated by the formula: serum iron / TIBC.
Q: What does raised ferritin indicate?
A: Raised ferritin can indicate inflammatory disorders.
Q: What does low ferritin suggest?
A: Low ferritin suggests iron deficiency anaemia (IDA).
Q: When are transferrin receptors increased?
A: Transferrin receptors are increased in iron deficiency anaemia (IDA).
Q: What are the characteristics of anaemia of chronic disease in terms of serum iron, TIBC, and ferritin?
Serum iron: Reduced
TIBC: Reduced
Ferritin: Normal or raised
Anemia type: Normochromic/hypochromic, normocytic
Q: What symptoms should be present for at least 6 months to consider a diagnosis of IBS?
Abdominal pain
Bloating
Change in bowel habit
Q: What are the criteria for a positive diagnosis of IBS?
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
Q: Which additional symptoms may support the diagnosis of IBS?
Lethargy
Nausea
Backache
Bladder symptoms
Q: What are the red flag features to enquire about when diagnosing IBS?
Rectal bleeding
Unexplained/unintentional weight loss
Family history of bowel or ovarian cancer
Onset after 60 years of age
Q: What primary care investigations are suggested for IBS?
Full blood count (FBC)
ESR/CRP (Erythrocyte Sedimentation Rate/C-Reactive Protein)
Coeliac disease screen (tissue transglutaminase antibodies)
Q: What is the first-line pharmacological treatment for pain in IBS patients?
A: Antispasmodic agents
Q: What is the first-line pharmacological treatment for constipation in IBS patients?
A: Laxatives (avoid lactulose)
Q: What is the first-line pharmacological treatment for diarrhoea in IBS patients?
A: Loperamide
Q: When may linaclotide be considered for constipation in IBS patients?
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.
Q: What is the second-line pharmacological treatment for IBS?
A: Low-dose tricyclic antidepressants (e.g., amitriptyline 5-10 mg)
Q: What psychological interventions may be considered for refractory IBS?
A: Cognitive behavioural therapy, hypnotherapy, or psychological therapy
Q: What general dietary advice is recommended for IBS patients?
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
Q: What are the three main conditions resulting from ischaemia to the lower gastrointestinal tract?
A: Acute mesenteric ischaemia, chronic mesenteric ischaemia, and ischaemic colitis
Q: What are common predisposing factors for bowel ischaemia?
A: Increasing age, atrial fibrillation, other causes of emboli (endocarditis, malignancy), cardiovascular disease risk factors (smoking, hypertension, diabetes), and cocaine use
Q: What are common features of bowel ischaemia?
A: Abdominal pain, rectal bleeding, diarrhoea, fever, elevated white blood cell count, and lactic acidosis
Q: What is the investigation of choice for diagnosing bowel ischaemia?
A: CT scan
Q: What typically causes acute mesenteric ischaemia?
A: An embolism resulting in occlusion of an artery supplying the small bowel, often the superior mesenteric artery
Q: How does acute mesenteric ischaemia usually present?
A: Severe, sudden onset abdominal pain out-of-keeping with physical exam findings
Q: What is the management for acute mesenteric ischaemia?
A: Urgent surgery
Q: What is chronic mesenteric ischaemia also known as?
A: Intestinal angina
Q: How does chronic mesenteric ischaemia present?
A: Colicky, intermittent abdominal pain
Q: What is ischaemic colitis and where is it more likely to occur?
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
Q: What investigation finding is characteristic of ischaemic colitis on an abdominal x-ray?
A: ‘Thumbprinting’ due to mucosal oedema/haemorrhage
Q: What is the usual management for ischaemic colitis?
A: Supportive care, with surgery required in a minority of cases if conservative measures fail
Q: What are the indications for surgery in ischaemic colitis?
A: Generalised peritonitis, perforation, or ongoing haemorrhage
Q: What is another term for ischaemic hepatitis?
A: Shock liver
Q: What causes ischaemic hepatitis?
A: Diffuse hepatic injury resulting from acute hypoperfusion
Q: Is ischaemic hepatitis an inflammatory process?
A: No, it is not an inflammatory process
Q: How is ischaemic hepatitis diagnosed?
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)
Q: What level of aminotransferase increase is associated with ischaemic hepatitis?
A: Exceeding 1000 international units/L or 50 times the upper limit of normal
Q: What other conditions often occur in conjunction with ischaemic hepatitis?
A: Acute kidney injury (tubular necrosis) or other end-organ dysfunction
Q: What are the primary causes of liver cirrhosis?
A: Alcohol, non-alcoholic fatty liver disease (NAFLD), and viral hepatitis (B and C)
Q: What traditional method was used for diagnosing liver cirrhosis?
A: Liver biopsy
Q: What are some newer techniques recommended by NICE for diagnosing liver cirrhosis?
A: Transient elastography and acoustic radiation force impulse imaging
Q: What is transient elastography commonly known as?
A: Fibroscan
Q: How does transient elastography work?
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
Q: Who should be offered transient elastography according to NICE recommendations?
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
Q: What additional investigation does NICE recommend for patients with a new diagnosis of cirrhosis?
A: An upper endoscopy to check for varices
Q: What regular screening does NICE recommend for patients with cirrhosis to check for hepatocellular cancer?
A: Liver ultrasound every 6 months (+/- alpha-fetoprotein)
How does NICE define malnutrition based on BMI?
A Body Mass Index (BMI) of less than 18.5
What percentage of unintentional weight loss within the last 3-6 months defines malnutrition according to NICE?
Greater than 10%
How does NICE define malnutrition with a BMI of less than 20?
Unintentional weight loss greater than 5% within the last 3-6 months
What tool is mostly used for screening malnutrition?
MUST (Malnutrition Universal Screen Tool)
What factors does the MUST score take into account?
BMI, recent weight change, and the presence of acute disease
What is the first step in the management of malnutrition recommended by NICE for high-risk patients
Dietician support
What approach does NICE recommend for managing malnutrition before considering oral nutritional supplements (ONS)?
A ‘food-first’ approach with clear instructions (e.g., ‘add full-fat cream to mashed potato’)
How should oral nutritional supplements (ONS) be taken if they are used?
They should be taken between meals, rather than instead of meals
Q: What is Melanosis coli?
A disorder of pigmentation of the bowel wall.
Q: What does histology of Melanosis coli show?
Pigment-laden macrophages.
Q: With what is Melanosis coli associated?
Laxative abuse.
Q: Which type of laxatives are especially associated with Melanosis coli?
Anthraquinone compounds such as senna.
Q: What causes metabolic alkalosis?
Loss of hydrogen ions or gain of bicarbonate, typically due to kidney or gastrointestinal issues.
Q: What are common causes of metabolic alkalosis?
Vomiting / aspiration (e.g. peptic ulcer, pyloric stenosis, nasogastric suction)
Diuretics
Liquorice, carbenoxolone
Hypokalaemia
Primary hyperaldosteronism
Cushing’s syndrome
Bartter’s syndrome
Q: What mechanism leads to metabolic alkalosis?
Activation of the renin-angiotensin II-aldosterone (RAA) system, causing Na+ reabsorption in exchange for H+ in the distal convoluted tubule, leading to alkalosis.
Q: How does vomiting or diuretics contribute to metabolic alkalosis?
Vomiting or diuretics cause Na+ and Cl- loss, leading to activation of the RAA system and increased aldosterone, resulting in H+ loss and alkalosis.
Q: How does hypokalaemia cause metabolic alkalosis?
In hypokalaemia, K+ shifts from cells into extracellular fluid (ECF), and to maintain neutrality, H+ shifts into cells, causing alkalosis.
Q: What is the primary use of metoclopramide?
Mainly used in the management of nausea.
Q: What are other uses of metoclopramide?
Gastro-oesophageal reflux disease (GERD)
Gastroparesis (particularly secondary to diabetic neuropathy)
Combined with analgesics for migraine treatment
Q: What are common adverse effects of metoclopramide?
Extrapyramidal effects (e.g., acute dystonia, oculogyric crisis, especially in children and young adults)
Diarrhoea
Hyperprolactinaemia
Tardive dyskinesia
Parkinsonism
Q: When should metoclopramide be avoided?
In bowel obstruction, but it may be helpful in paralytic ileus.
Q: What is the most common cause of liver disease in the developed world?
Non-alcoholic fatty liver disease (NAFLD).
Q: What spectrum of disease does NAFLD encompass?
Steatosis (fat in the liver)
Steatohepatitis (fat with inflammation, non-alcoholic steatohepatitis, NASH)
Fibrosis and cirrhosis in progressive disease.
Q: What is thought to be the key mechanism leading to steatosis in NAFLD?
Insulin resistance, as NAFLD is considered the hepatic manifestation of the metabolic syndrome.
Q: What is the main difference between non-alcoholic steatohepatitis (NASH) and alcoholic hepatitis?
NASH is similar to alcoholic hepatitis but occurs in the absence of alcohol abuse.
Q: What are common associated factors with NAFLD?
Obesity
Type 2 diabetes mellitus
Hyperlipidaemia
Jejunoileal bypass
Sudden weight loss/starvation
Q: What are the typical features of NAFLD?
Usually asymptomatic
Hepatomegaly
ALT > AST
Increased echogenicity on ultrasound
Q: What does NICE recommend for the investigation of NAFLD?
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.
Q: What are the non-invasive tests recommended if the ELF blood test is unavailable?
FIB4 score
NAFLD fibrosis score
FibroScan (liver stiffness measurement using transient elastography)
Q: What is the mainstay of management for NAFLD?
Lifestyle changes, particularly weight loss, along with monitoring.
Q: What is the most common type of oesophageal cancer in the UK and the US?
Adenocarcinoma.
Q: What is the location of adenocarcinoma and squamous cell cancer in the oesophagus?
Adenocarcinoma: Lower third, near the gastroesophageal junction.
Squamous cell cancer: Upper two-thirds of the oesophagus.
Q: What are the common risk factors for adenocarcinoma of the oesophagus?
Gastro-oesophageal reflux disease (GORD)
Barrett’s oesophagus
Smoking
Obesity
Q: What are the common risk factors for squamous cell carcinoma of the oesophagus?
Smoking
Alcohol
Achalasia
Plummer-Vinson syndrome
Diets rich in nitrosamines
Q: What is the most common presenting symptom of oesophageal cancer?
Dysphagia.
Q: What are some other possible symptoms of oesophageal cancer?
Anorexia and weight loss
Vomiting
Odynophagia
Hoarseness
Melaena
Cough
Q: What is the preferred diagnostic method for oesophageal cancer?
Upper GI endoscopy with biopsy.
Q: What are the methods used for staging oesophageal cancer?
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
Q: What is the treatment for operable oesophageal cancer (T1N0M0)?
Surgical resection, typically an Ivor-Lewis type oesophagectomy.
Q: What is a major surgical challenge after oesophagectomy for oesophageal cancer?
Anastomotic leak, which can lead to mediastinitis, especially with an intrathoracic anastomosis.
Q: Besides surgery, what other treatment is commonly given to oesophageal cancer patients?
Adjuvant chemotherapy.
Q: What are the features of Plummer-Vinson syndrome?
Dysphagia (due to oesophageal webs)
Glossitis
Iron-deficiency anaemia
Q: What is the treatment for Plummer-Vinson syndrome?
Iron supplementation
Dilation of oesophageal webs
Q: What is Mallory-Weiss syndrome and what causes it?
Severe vomiting leads to painful mucosal lacerations at the gastroesophageal junction, causing haematemesis.
Common in alcoholics.
Q: What is Boerhaave syndrome?
Severe vomiting causes oesophageal rupture.
Q: What is the most common type of pancreatic cancer?
Adenocarcinoma (over 80% of pancreatic tumours)
Typically occurs at the head of the pancreas.
Q: What are some associations with pancreatic cancer?
Increasing age
Smoking
Diabetes
Chronic pancreatitis
Hereditary non-polyposis colorectal carcinoma
Multiple endocrine neoplasia
BRCA2 gene mutation
KRAS gene mutation
Q: What are the classic features of pancreatic cancer?
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)
Q: What is the investigation of choice for pancreatic cancer diagnosis?
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).
Q: What is the treatment for resectable pancreatic cancer?
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.
Q: What is the most common complication of peptic ulcer disease?
Bleeding, accounting for around three-quarters of complications.
Q: What is the most common presenting symptom of acute bleeding in peptic ulcer disease?
Haematemesis.
Q: What are other features of acute bleeding in peptic ulcer disease?
Melaena
Hypotension
Tachycardia
Q: What is the most common source of a significant gastrointestinal bleed in peptic ulcer disease?
The gastroduodenal artery.
Q: What is the initial approach to managing acute bleeding in peptic ulcer disease?
ABC approach (Airway, Breathing, Circulation) as with any upper gastrointestinal haemorrhage.
IV proton pump inhibitor.
Endoscopic intervention as first-line treatment
Q: What should be done if endoscopic intervention fails in acute bleeding from peptic ulcer disease?
Urgent interventional angiography with transarterial embolization.
Surgery (approximately 10% of patients).
Q: What are the typical symptoms of perforation secondary to peptic ulcer disease?
Sudden onset epigastric pain, which later becomes more generalized.
Patients may describe syncope
Q: What is the first form of imaging recommended for suspected perforation of peptic ulcer disease?
Plain x-rays, particularly an upright (erect) chest x-ray.
Q: What is the diagnostic significance of an upright chest x-ray in suspected perforation of peptic ulcer disease?
It is useful for detecting free air under the diaphragm, which is seen in approximately 75% of patients with a perforated peptic ulcer.
Q: What are the main risk factors for peptic ulcer disease?
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.
Q: What are the key features of duodenal and gastric ulcers?
Duodenal ulcers:
More common than gastric ulcers.
Epigastric pain when hungry, relieved by eating.
Gastric ulcers:
Epigastric pain worsened by eating.
Q: How is Helicobacter pylori tested in suspected peptic ulcer disease?
First-line tests: Urea breath test or stool antigen test.
Q: What is the management for peptic ulcer disease based on Helicobacter pylori status?
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.
Q: What is the cause of pernicious anaemia?
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.
Q: What antibodies are involved in the pathophysiology of pernicious anaemia?
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.
Q: What are the key features of pernicious anaemia?
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).
Q: What investigations are done for pernicious anaemia?
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).
Q: How is pernicious anaemia treated?
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.
Q: What are the complications of pernicious anaemia?
Increased risk of gastric cancer.
Haematological and neurological features as discussed above.
Q: What is Peutz-Jeghers syndrome?
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.
Q: What are the key features of Peutz-Jeghers syndrome?
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.
Q: How is Peutz-Jeghers syndrome managed?
Management is generally conservative unless complications, such as small bowel obstruction or gastrointestinal bleeding, develop.
Q: What is a pharyngeal pouch (Zenker’s diverticulum)?
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.
Q: What are the common features of a pharyngeal pouch (Zenker’s diverticulum)?
Dysphagia (difficulty swallowing)
Regurgitation
Aspiration
Neck swelling that gurgles on palpation
Halitosis (bad breath)
Q: How is a pharyngeal pouch (Zenker’s diverticulum) investigated?
Investigation typically involves a barium swallow combined with dynamic video fluoroscopy to visualize the diverticulum during swallowing.
Q: How is a pharyngeal pouch (Zenker’s diverticulum) managed?
Management is surgical, with procedures such as diverticulectomy or myotomy, depending on the size and symptoms.
Q: What is primary biliary cholangitis (PBC)?
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.
Q: What is the gender distribution for primary biliary cholangitis (PBC)?
PBC is more common in females, with a female to male ratio of 9:1.
Q: What are common associations with primary biliary cholangitis (PBC)?
Sjogren’s syndrome (in up to 80% of patients)
Rheumatoid arthritis
Systemic sclerosis
Thyroid disease
Q: What are the early clinical features of primary biliary cholangitis (PBC)?
Fatigue
Pruritus (itching)
Cholestatic jaundice
Raised ALP on routine liver function tests (LFTs)
Q: What are late-stage clinical features of primary biliary cholangitis (PBC)?
Liver failure
Hepatomegaly and splenomegaly
Xanthelasmas and xanthomata
Hyperpigmentation, especially over pressure points
Right upper quadrant pain in 10% of patients
Q: What is the classic presentation of primary biliary cholangitis (PBC)?
Itching (pruritus) in a middle-aged woman.
Q: How is primary biliary cholangitis (PBC) diagnosed?
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.
Q: What is the first-line treatment for primary biliary cholangitis (PBC)?
Ursodeoxycholic acid: Slows disease progression and improves symptoms.
Cholestyramine: Used for pruritus.
Q: What are the complications of primary biliary cholangitis (PBC)?
Cirrhosis and portal hypertension (leading to ascites and variceal hemorrhage)
Osteomalacia and osteoporosis
Increased risk of hepatocellular carcinoma (20-fold)
Q: When is liver transplantation considered in primary biliary cholangitis (PBC)?
If bilirubin > 100 (PBC is a major indication for liver transplantation).
Recurrence in grafts is possible but not typically problematic.
Q: What is primary sclerosing cholangitis (PSC)?
Primary sclerosing cholangitis is a biliary disease characterized by inflammation and fibrosis of intra and extra-hepatic bile ducts, leading to cholestasis.
Q: What are the associations with primary sclerosing cholangitis (PSC)?
Ulcerative colitis (4% of UC patients have PSC; 80% of PSC patients have UC)
Crohn’s disease (less common than with UC)
HIV
Q: What are the common features of primary sclerosing cholangitis (PSC)?
Cholestasis
Jaundice
Pruritus
Raised bilirubin and ALP
Right upper quadrant pain
Fatigue
Q: How is primary sclerosing cholangitis (PSC) diagnosed?
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’.
Q: What are the complications of primary sclerosing cholangitis (PSC)?
Cholangiocarcinoma (in 10% of patients)
Increased risk of colorectal cancer
Q: What is the mechanism of action of proton pump inhibitors (PPI)?
PPIs cause irreversible blockade of the H+/K+ ATPase enzyme on gastric parietal cells, reducing gastric acid production.
Q: What are the common adverse effects of proton pump inhibitors (PPI)?
Hyponatraemia
Hypomagnesaemia
Osteoporosis (increased risk of fractures)
Microscopic colitis
Increased risk of Clostridium difficile infections
Q: What are the most common organisms found in pyogenic liver abscesses?
Staphylococcus aureus (in children)
Escherichia coli (in adults)
Q: What is the typical management of a pyogenic liver abscess?
Drainage (typically percutaneous)
Antibiotics:
Amoxicillin + Ciprofloxacin + Metronidazole
If penicillin allergic: Ciprofloxacin + Clindamycin
Q: What metabolic abnormalities occur in refeeding syndrome?
Hypophosphataemia (hallmark symptom)
Hypokalaemia
Hypomagnesaemia
Abnormal fluid balance
Q: What is the pathophysiology of hypophosphataemia in refeeding syndrome?
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.
Q: What are the clinical consequences of hypophosphataemia in refeeding syndrome?
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
Q: What is the recommended approach to prevent refeeding syndrome?
If no food intake for >5 days: Refeed at no more than 50% of requirements for the first 2 days.
Q: What is small bowel bacterial overgrowth syndrome (SBBOS)?
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.
Q: What are the risk factors for SBBOS?
Neonates with congenital gastrointestinal abnormalities
Scleroderma
Diabetes mellitus
Q: What are common features of SBBOS?
Chronic diarrhoea
Bloating and flatulence
Abdominal pain
(Note: Many of these features overlap with irritable bowel syndrome.)
Q: How is SBBOS diagnosed?
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)
Q: What is the treatment for SBBOS?
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)
Q: What is spontaneous bacterial peritonitis (SBP)?
SBP is a form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis. It involves spontaneous infection of the ascitic fluid.
Q: What are the common features of SBP?
Ascites
Abdominal pain
Fever
Q: How is SBP diagnosed?
Paracentesis: Neutrophil count > 250 cells/µL
The most common organism found on ascitic fluid culture is Escherichia coli (E. coli).
Q: What is the treatment for SBP?
Intravenous cefotaxime is typically administered to treat SBP.
Q: Who should receive antibiotic prophylaxis for SBP?
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.
Q: What is a marker of poor prognosis in SBP?
Alcoholic liver disease is a marker of poor prognosis in SBP.
Q: What is ulcerative colitis (UC)?
UC is a form of inflammatory bowel disease (IBD) that causes continuous inflammation starting at the rectum, which never spreads beyond the ileocaecal valve.
Q: What is the peak incidence age for ulcerative colitis?
UC peaks in people aged 15-25 years and in those aged 55-65 years.
Q: What are common symptoms in the initial presentation of UC?
Bloody diarrhoea
Urgency
Tenesmus
Abdominal pain, particularly in the left lower quadrant
Extra-intestinal features
Q: How is UC diagnosed?
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
Q: What are the barium enema findings in UC?
Loss of haustrations
Superficial ulceration and pseudopolyps
Long-standing disease: Colon appears narrow and short, known as drainpipe colon
Q: What are common extra-intestinal features of UC?
Arthritis: pauciarticular, asymmetric (related to disease activity)
Erythema nodosum
Episcleritis
Osteoporosis
Q: Which extra-intestinal feature is much more common in UC than Crohn’s disease?
Primary sclerosing cholangitis is much more common in UC.
Q: What are extra-intestinal features unrelated to disease activity in UC?
Polyarticular, symmetric arthritis
Uveitis
Pyoderma gangrenosum
Clubbing
Q: What are the differences in extra-intestinal features between UC and Crohn’s disease?
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.
Q: What factors are often linked to flares of ulcerative colitis?
Stress
Medications
NSAIDs
Antibiotics
Cessation of smoking
Q: How are flares of ulcerative colitis classified?
Flares are classified as mild, moderate, or severe based on the number of stools and the presence of systemic disturbance.
Q: What characterizes a mild flare of ulcerative colitis?
Fewer than four stools daily, with or without blood
No systemic disturbance
Normal ESR and C-reactive protein values
Q: What characterizes a moderate flare of ulcerative colitis?
Four to six stools a day
Minimal systemic disturbance
Q: What characterizes a severe flare of ulcerative colitis?
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
Q: What should be done for patients with evidence of severe ulcerative colitis?
Patients with severe disease should be admitted to hospital for further management.
Q: What are the two main phases in the management of ulcerative colitis?
Inducing remission
Maintaining remission
Q: How is ulcerative colitis classified by severity?
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)
Q: How is mild-to-moderate proctitis treated?
Topical (rectal) aminosalicylate (mesalazine)
If no remission after 4 weeks, add oral aminosalicylate
If still no remission, add topical or oral corticosteroid
Q: How is mild-to-moderate proctosigmoiditis and left-sided ulcerative colitis treated?
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
Q: How is extensive ulcerative colitis treated?
Topical (rectal) aminosalicylate and high-dose oral aminosalicylate
If no remission after 4 weeks, stop topical treatments and offer oral aminosalicylate + oral corticosteroid
Q: What is the first-line treatment for severe ulcerative colitis?
IV steroids (first-line treatment in hospital)
If no improvement after 72 hours, consider adding IV ciclosporin or surgery
Q: How is remission maintained after mild-to-moderate ulcerative colitis flare?
Proctitis/proctosigmoiditis:
Topical (rectal) aminosalicylate daily or intermittently
OR oral aminosalicylate + topical aminosalicylate
Left-sided and extensive UC:
Low-dose oral aminosalicylate for maintenance
Q: How is remission maintained after severe relapse or 2+ exacerbations in the past year?
Oral azathioprine or oral mercaptopurine
Q: What is the main complication of portal hypertension in liver cirrhosis?
Oesophageal varices, which can rupture, leading to a potentially life-threatening upper gastrointestinal bleed.
Q: What are the initial steps in the acute treatment of variceal haemorrhage?
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)
Q: What vasoactive agents are used in the acute treatment of variceal haemorrhage?
Terlipressin (first-line)
Shown to reduce mortality and prevent rebleeding
Octreotide (alternative, but terlipressin is preferred)
Q: What should be given before endoscopy in patients with suspected variceal haemorrhage?
Terlipressin (or octreotide)
Prophylactic IV antibiotics (quinolones)
Q: What is the preferred endoscopic treatment for variceal haemorrhage?
Endoscopic variceal band ligation (EVBL)
Superior to endoscopic sclerotherapy
Q: What is used in cases of uncontrolled variceal haemorrhage?
Sengstaken-Blakemore tube (temporary measure to control bleeding)
Q: What is used if standard measures fail in variceal haemorrhage management?
Transjugular Intrahepatic Portosystemic Shunt (TIPSS)
Connects the hepatic vein to the portal vein
Common complication: exacerbation of hepatic encephalopathy
Q: What is the first-line prophylaxis for variceal haemorrhage?
Propranolol
Reduces rebleeding and mortality compared to placebo
Q: What is the recommended endoscopic treatment for the primary prevention of variceal bleeding?
Endoscopic variceal band ligation (EVL) for medium to large oesophageal varices
Q: What is the role of proton pump inhibitors (PPI) in variceal haemorrhage management?
PPI cover is given to prevent EVL-induced ulceration after variceal band ligation.
Q: What is the interval for endoscopic variceal band ligation (EVL) in the primary prevention of variceal haemorrhage?
Every two weeks until all varices are eradicated.
Q: What is a villous adenoma?
A type of colonic polyp with the potential for malignant transformation. It secretes large amounts of mucous, which can lead to electrolyte disturbances.
Q: What are the typical symptoms of a villous adenoma?
Asymptomatic in the vast majority of cases.
Possible non-specific lower gastrointestinal symptoms.
Secretory diarrhoea may occur in some cases.
Q: What electrolyte disturbances can be associated with villous adenomas?
Hypokalaemia (due to excessive mucous secretion).
Q: What type of anaemia may be seen in patients with villous adenomas?
Microcytic anaemia (commonly due to chronic blood loss).
Q: What is the potential malignant risk associated with villous adenomas?
Villous adenomas have the potential to undergo malignant transformation, making them a significant risk factor for colon cancer.
Q: What is a common consequence of vitamin A deficiency?
Night blindness, due to impaired visual function related to insufficient retinal production.
Q: What are the common causes of thiamine (B1) deficiency?
Alcohol excess (thiamine supplements are routinely recommended for alcoholics).
Malnutrition.
Q: What conditions are associated with thiamine deficiency?
Wernicke’s encephalopathy: nystagmus, ophthalmoplegia, and ataxia.
Korsakoff’s syndrome: amnesia and confabulation.
Dry beriberi: peripheral neuropathy.
Wet beriberi: dilated cardiomyopathy.
Q: What is the main clinical consequence of riboflavin (B2) deficiency?
Angular cheilitis, which is inflammation and cracking at the corners of the mouth.
Q: What are the causes of niacin (B3) deficiency?
Hartnup’s disease: A hereditary disorder that reduces absorption of tryptophan.
Carcinoid syndrome: Increased metabolism of tryptophan to serotonin, leading to lower niacin production.
Q: What is the clinical condition caused by niacin deficiency?
Pellagra, which presents with the 3 Ds:
Dermatitis: Typically a sun-exposed, scaly rash.
Diarrhoea: Gastrointestinal upset.
Dementia: Cognitive changes, confusion, and neurological symptoms.
Q: What is a common cause of vitamin B6 deficiency?
Isoniazid therapy: A medication used to treat tuberculosis that can interfere with vitamin B6 metabolism.
Q: What are the clinical consequences of vitamin B6 deficiency?
Peripheral neuropathy: Numbness, tingling, and weakness in the limbs.
Sideroblastic anemia: Anemia caused by impaired hemoglobin production due to ineffective erythropoiesis.
Q: What are the features of vitamin C deficiency (scurvy)?
Gingivitis and loose teeth
Poor wound healing
Bleeding from gums, hematuria, and epistaxis (nosebleeds)
General malaise: Fatigue, weakness, and irritability.
Q: How does vitamin C deficiency affect collagen?
Defective collagen synthesis due to impaired hydroxylation of proline and lysine, leading to capillary fragility and increased bleeding tendency.
Q: What are common causes of vitamin C deficiency (scurvy)?
Severe malnutrition
Drug and alcohol abuse
Limited access to fruits and vegetables, often seen in poverty.
Q: What is the cause of Whipple’s disease?
Whipple’s disease is caused by infection with Tropheryma whippelii.
Q: What are the key features of Whipple’s disease?
Malabsorption (diarrhoea, weight loss)
Large-joint arthralgia
Lymphadenopathy
Skin (hyperpigmentation, photosensitivity)
Pleurisy and pericarditis
Neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus
Q: How is Whipple’s disease diagnosed?
Diagnosis is confirmed by jejunal biopsy, which shows macrophages containing Periodic Acid-Schiff (PAS) granules.
Q: What is the management for Whipple’s disease?
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.
Q: What is Zollinger-Ellison syndrome?
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.
Q: What is the most common location for gastrin-secreting tumours in Zollinger-Ellison syndrome?
The majority of gastrin-secreting tumours are found in the first part of the duodenum, with the second most common location being the pancreas.
Q: What are the main features of Zollinger-Ellison syndrome?
Multiple gastroduodenal ulcers
Diarrhoea
Malabsorption
Q: What is the best initial diagnostic test for Zollinger-Ellison syndrome?
The best initial diagnostic test is the fasting gastrin levels.
Q: What is the secretin stimulation test used for in Zollinger-Ellison syndrome?
The secretin stimulation test is used to further confirm the diagnosis of Zollinger-Ellison syndrome after elevated fasting gastrin levels.
Q: What is Wilson’s disease?
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.
Q: What is the typical onset age for Wilson’s disease?
The onset of symptoms is usually between 10-25 years. Children often present with liver disease, whereas young adults typically show neurological symptoms.
Q: What are the liver-related features of Wilson’s disease?
Hepatitis
Cirrhosis
Q: Describe the neurological features of Wilson’s disease.
Basal ganglia degeneration (particularly in the putamen and globus pallidus)
Speech, behavioural, and psychiatric problems
Other symptoms: asterixis, chorea, dementia, parkinsonism
Q: What are Kayser-Fleischer rings?
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.
Q: What are other non-neurological and non-hepatic features of Wilson’s disease?
Renal tubular acidosis (especially Fanconi syndrome)
Haemolysis
Blue nails
Q: What are the key investigations for diagnosing Wilson’s disease?
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
Q: What is the management for Wilson’s disease?
Penicillamine (chelates copper) as traditional first-line treatment
Trientine hydrochloride as an alternative chelating agent
Tetrathiomolybdate is a newer agent currently under investigation
What cancers are most associated with HNPCC
colorectal then endometrial
Where is the abdominal mass felt in crohns
right iliac fossa
What is the triad for Boerhaaves syndrome
vomiting, thoracic pain, subcutaneous emphysema
What other examination is important to do in a male presenting with RIF pain
examination of scrotum for infection/torsion
oesophageal cancer pattern of dysphagia with food
first solids then liquids
What is the most common area affected in UC
rectum
Beaded appearance on ERCP
PSC
First exam done for acute mesenteric ischaemia
lactate
Treatment for ongoing diarrhoea after Crohns resection
cholestyramine
When should you give PPIs for endoscopy of variceal bleeding
After endoscopy
What cancer is pernicious anaemia linked to
gastric carcinoma
small bowel obstruction and air in the biliary tree
gallstone ileus
What causes itch in cholestasis
hyperbilirubinaemia
How do you investigate mallory weiss tear
endoscopy
In UC, how do you diagnose and what do you do in a severe flare
colonoscopy, sigmoidoscopy in severe flare
What is the most common side effect of metoclopramide
diarrhoea
HBsAg +, anti HBc IgG +, anti HBc IgM -
chronic hep b
anti HBc IgG shows long term antibodies produced
anti HBc IgM negative means it is not acute
How do you treat hypophosphataemia in refeeding syndrome
IV phopshate
what medication would you give to reduce portal hypertension
propanalol
if a patient has constipation due to opioids, what should you do
give stimulant laxative -> senna
most likely cause of spontaneous bacterial peritonitis
e coli
what level of paracetamol overdose necessitates NAC
of 8-24 hours after presentation and consumed more than 150mg/kg
