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.
