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Q1: Definition and the three mechanisms (2 min)
Examiner: "What do you understand by the term 'malabsorption', and how do you classify its mechanisms?"
Model answer: Malabsorption is impaired absorption of macro- and micronutrients across the gut. I classify it into three mechanistic-anatomical sites of failure: luminal (defective intraluminal digestion — pancreatic exocrine insufficiency, bile-salt deficiency, SIBO, lactase deficiency); mucosal (defective uptake — coeliac disease, tropical sprue, Crohn's, radiation enteritis, Whipple disease); and transport/post-mucosal (defective delivery — short bowel, post-gastrectomy, intestinal lymphangiectasia). The classification matters because each mechanism maps onto a specific investigation and treatment.
Q2: Clinical features and site clues (2 min)
Examiner: "A patient has steatorrhoea. How does the pattern of deficiency help you localise the cause?"
Model answer: Steatorrhoea is the hallmark — pale, bulky, greasy, foul-smelling, difficult-to-flush stool; faecal fat over 7 g/day. The deficiency pattern localises the lesion: iron and folate deficiency point to proximal small-bowel mucosal disease (coeliac, sprue); vitamin B12 deficiency implicates the terminal ileum (resection, Crohn's, tropical sprue, pernicious anaemia); calcium, vitamin D and the fat-soluble vitamins A, D, E, K are lost in any fat-malabsorption state. Pancreatic insufficiency notably causes steatorrhoea without anaemia because the proximal mucosa is intact.
Q3: Investigations — the targeted ladder (3 min)
Examiner: "Walk me through your investigation of a patient with suspected malabsorption."
Model answer: First I confirm malabsorption and map deficiencies — FBC, iron studies, B12, folate, calcium, albumin, 25-OH vitamin D, clotting/INR, magnesium. Then I localise the cause: coeliac serology — anti-tTG IgA plus total serum IgA (essential to exclude IgA deficiency, which affects ~2-5% of coeliacs); faecal elastase-1 for pancreatic exocrine insufficiency (low under 200, very low under 100); breath tests — glucose/lactulose for SIBO, lactose hydrogen for lactose malabsorption; stool for microscopy/culture and faecal calprotectin. For mucosal disease I proceed to endoscopy with duodenal biopsies (4-6 distal duodenum plus 1-2 bulb), graded by the Marsh classification — Marsh I intraepithelial lymphocytosis, Marsh II crypt hyperplasia, Marsh III villous atrophy. Imaging — CT/MR enterography, MRCP — for structural disease. Crucially, I take coeliac serology and biopsy BEFORE any gluten-free diet.
Q4: Management principles and cause-specific therapy (3 min)
Examiner: "What is the principle of treatment, and how would you manage SIBO and short bowel syndrome?"
Model answer: The governing principle is treat the underlying cause first, then replace deficiencies — never just replace nutrients blindly. For SIBO I give rifaximin 550 mg PO TDS for 14 days, with rotating antibiotics for relapse, address any structural/motility cause, and correct anaemia. For short bowel syndrome the ladder is anti-diarrhoeals (loperamide, codeine), a PPI to reduce gastric hypersecretion, PERT, oral rehydration, octreotide to reduce secretions, and teduglutide — a GLP-2 analogue, 0.05 mg/kg SC daily — which is the only drug proven to enhance intestinal adaptation and reduce parenteral nutrition dependence. If the gut is too short (under ~100 cm without colon) or oral/enteral nutrition fails, I start parenteral nutrition with long-term monitoring for line sepsis, PN-liver disease and metabolic bone disease.
Q5: Complications, pitfalls and a nasty peripheral question (2 min)
Examiner: "What are the complications of untreated coeliac disease, and what is the one error you must not make at diagnosis?"
Model answer: Untreated coeliac causes iron/B12/folate anaemia, osteoporosis and osteomalacia, infertility and recurrent miscarriage, hyposplenism, and malignancy — especially enteropathy-associated T-cell lymphoma (EATL) and small-bowel adenocarcinoma; refractory coeliac disease is a precursor of EATL. The error not to make is starting a gluten-free diet before serology and biopsy — this normalises both and makes the diagnosis impossible for months. I also always remember to check total IgA with anti-tTG IgA, because IgA-deficient coeliacs have falsely normal serology.