Malabsorption & IBS flashcards
22 high-yield MRCP Part 1 cards from the Intellect Medicos Gastroenterology & Hepatology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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Coeliac disease is strongly associated with HLA-______ (about 90–95%), with most of the rest carrying HLA-DQ8.
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DQ2
Why? Gliadin peptides are deamidated by tissue transglutaminase and presented on these HLA molecules to CD4 T cells. A negative HLA result makes coeliac disease very unlikely.
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Coeliac disease is strongly associated with HLA-DQ2 (about 90–95%), with most of the rest carrying HLA-______.
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DQ8
Why? Gliadin peptides are deamidated by tissue transglutaminase and presented on these HLA molecules to CD4 T cells. A negative HLA result makes coeliac disease very unlikely.
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What are the first-line blood tests for suspected coeliac disease?
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IgA tissue transglutaminase (tTG) antibody plus total IgA.
Why? Total IgA is needed because selective IgA deficiency (more common in coeliac disease) gives a false-negative IgA tTG.
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Which serological tests are used for coeliac disease in a patient with IgA deficiency?
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IgG-based tests: IgG tTG, IgG endomysial antibody or IgG deamidated gliadin peptide (DGP).
Why? IgA-based tests are falsely negative when the patient cannot make IgA.
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What is the gold-standard diagnostic test for coeliac disease, and what does it show?
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Duodenal biopsies at gastroscopy (at least 4 from D2 plus 2 from the bulb): villous atrophy, crypt hyperplasia and increased intraepithelial lymphocytes.
Why? Histology confirms the enteropathy before committing the patient to a lifelong gluten-free diet.
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Which drug gives rapid symptom control in dermatitis herpetiformis, and what must be checked first?
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Dapsone; check G6PD status first.
Why? Dapsone is an oxidant drug that causes haemolysis (and methaemoglobinaemia), which is severe in G6PD deficiency. The long-term treatment is a gluten-free diet.
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Which three cereals must be excluded in a gluten-free diet?
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Wheat, barley and rye.
Why? These contain the gluten proteins (gliadin, hordein, secalin) that trigger the immune response.
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Whipple's disease is caused by ______; duodenal biopsy shows PAS-positive foamy macrophages in the lamina propria.
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Tropheryma whipplei
Why? It is a multisystem infection: diarrhoea, weight loss, arthralgia, lymphadenopathy, pigmentation, neurological signs and culture-negative endocarditis.
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Whipple's disease is caused by Tropheryma whipplei; duodenal biopsy shows ______ in the lamina propria.
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PAS-positive foamy macrophages
Why? It is a multisystem infection: diarrhoea, weight loss, arthralgia, lymphadenopathy, pigmentation, neurological signs and culture-negative endocarditis.
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How is Whipple's disease treated?
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IV ceftriaxone (or IV penicillin) for induction, followed by oral co-trimoxazole for about 12 months.
Why? IV antibiotics that cross the blood–brain barrier are used first because CNS relapse is the main danger.
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What is the treatment for tropical sprue?
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Tetracycline for 3–6 months plus high-dose folic acid (and B12 if deficient).
Why? It is thought to be due to bacterial colonisation after infection in the tropics; it looks like coeliac on biopsy but serology is negative and it responds to antibiotics.
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Small bowel bacterial overgrowth: the first-line test is a ______; the gold standard is jejunal aspirate culture (≥10⁵ CFU/mL).
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hydrogen/methane breath test
Why? Bacteria ferment carbohydrate early in the small bowel, so breath hydrogen rises early.
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Small bowel bacterial overgrowth: the first-line test is a hydrogen/methane breath test; the gold standard is ______ (≥10⁵ CFU/mL).
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jejunal aspirate culture
Why? Bacteria ferment carbohydrate early in the small bowel, so breath hydrogen rises early.
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Which antibiotic is preferred for small bowel bacterial overgrowth?
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Rifaximin.
Why? It is poorly absorbed, so it acts in the gut lumen with few systemic effects. Replace B12, fat-soluble vitamins and iron.
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What is the first-line investigation for bile acid malabsorption?
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SeHCAT scan (retention of a radiolabelled bile acid at 7 days).
Why? Low retention shows bile acids are being lost. Serum C4 (raised) or FGF19 (low) are alternatives where SeHCAT is unavailable.
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What is the first-line treatment for bile acid diarrhoea, and how does it work?
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A bile acid sequestrant such as colestyramine; it binds bile acids in the gut so they cannot cause secretory diarrhoea.
Why? Colesevelam is better tolerated. Sequestrants also bind other drugs, so give other medicines at least 1 hour before or 4–6 hours after.
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Which blood tests does NICE recommend in a patient who meets the IBS criteria, to exclude other causes?
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FBC, ESR, CRP and coeliac serology (tTG or EMA).
Why? These screen for anaemia, inflammation and coeliac disease. Faecal calprotectin helps if IBD is a concern; CA125 if ovarian cancer symptoms in women.
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NICE IBS criteria: abdominal pain relieved by defecation or linked to altered stool frequency/form, plus at least ______ of: altered passage (straining/urgency), bloating, worse with eating, passage of mucus.
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2
Why? Symptoms should have been present for at least 6 months before assessment for IBS.
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What is the first-line drug for diarrhoea-predominant IBS, and its mechanism?
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Loperamide; a peripheral μ-opioid receptor agonist that slows gut transit.
Why? It acts on the myenteric plexus and barely crosses the blood–brain barrier, so it has few central opioid effects.
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Which laxative should be avoided in constipation-predominant IBS?
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Lactulose.
Why? It is fermented by colonic bacteria and worsens bloating. Use bulk-forming (ispaghula) or osmotic macrogol laxatives instead.
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What is the second-line drug for persistent abdominal pain in IBS?
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A low-dose tricyclic antidepressant, e.g. amitriptyline.
Why? It acts as a neuromodulator, reducing visceral pain. First-line for pain is an antispasmodic (mebeverine, hyoscine) or peppermint oil; SSRIs are used if TCAs fail.
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Chronic use of which laxative class causes melanosis coli?
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Anthraquinone stimulant laxatives (e.g. senna, cascara).
Why? They cause colonocyte apoptosis; macrophages engulf the debris and lipofuscin pigment builds up, turning the mucosa brown-black. It is benign.
More Gastroenterology & Hepatology topics
- Oesophagus & dysphagia
- Stomach, H. pylori & GI hormones
- IBD & other colitis
- GI bleeding & diverticular disease
- Viral hepatitis
- Alcohol, fatty & autoimmune liver disease
- Inherited & metabolic liver disease
- Cirrhosis & its complications
- Pancreas & biliary tree
- GI cancer, polyposis & NETs
- Infection, nutrition & pregnancy