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GI secretions, motility and absorption

14 NEET-PG practice questions on GI secretions, motility and absorption, part of Physiology. The first 14 are below; the first 5 with answers and explanations (tap Show answer after you have chosen), the rest in Learn with a free account.

  1. Question 1 · Medium

    A 24-year-old student from Meghalaya has bloating, flatulence and loose stools within a few hours of drinking milk, but not with other foods. Stool pH is 5.0 and the stool osmotic gap is 140 mOsm/kg. Which investigation best confirms the likely diagnosis?

    1. ASerum anti-tTG IgA antibody
    2. BDuodenal biopsy at endoscopy
    3. CLactose hydrogen breath test
    4. DStool culture for enteric pathogens
    Show answer

    Answer: C · Lactose hydrogen breath test

    Symptoms only after milk, an acidic stool and a high osmotic gap point to lactase deficiency, very common in adults in Asia. Lactose not split by brush-border lactase reaches the colon, where bacteria ferment it to short-chain acids (lowering stool pH) and hydrogen; the unabsorbed sugar draws water in as an osmotic diarrhoea. The lactose hydrogen breath test shows a rise in breath hydrogen after an oral lactose load and is the usual confirmatory test. Avoiding or reducing milk, or taking curd, relieves symptoms.

    • A: Coeliac disease is triggered by gluten, not milk, and would not spare other foods.
    • B: Biopsy is invasive and is not needed for a selective milk intolerance.
    • D: Infection would not be tied to milk alone and would usually give a secretory picture.
  2. Question 2 · Medium

    A 35-year-old woman has had progressive difficulty swallowing both solids and liquids for a year, with regurgitation of undigested food at night. A barium swallow shows a dilated oesophagus with a smooth 'bird's beak' narrowing. Manometry shows absent peristalsis and incomplete relaxation of the lower oesophageal sphincter. Loss of which neurons causes this?

    1. ASympathetic neurons from the coeliac ganglion
    2. BExcitatory myenteric neurons releasing acetylcholine
    3. CInhibitory myenteric neurons releasing NO and VIP
    4. DSubmucosal plexus neurons controlling secretion
    Show answer

    Answer: C · Inhibitory myenteric neurons releasing NO and VIP

    This is achalasia cardia. Relaxation of the lower oesophageal sphincter on swallowing depends on inhibitory neurons of the myenteric (Auerbach) plexus that release nitric oxide and VIP. Their loss leaves the sphincter tonically contracted and abolishes coordinated peristalsis. Treatment aims to disrupt the sphincter: pneumatic dilatation, Heller myotomy or peroral endoscopic myotomy (POEM).

    • A: Sympathetic input is not what relaxes the sphincter on swallowing.
    • B: Loss of cholinergic excitatory neurons would weaken the sphincter, not keep it closed.
    • D: The submucosal (Meissner) plexus controls secretion and local blood flow, not sphincter relaxation.
  3. Question 3 · Hard

    A 4-month-old boy has had chronic diarrhoea, poor weight gain and generalised oedema since birth; serum albumin is 1.9 g/dL. Sweat chloride is normal. In duodenal fluid collected after a test meal, trypsin activity is absent, but adding a small amount of enteropeptidase in the laboratory restores normal trypsin activity. Lipase activity is normal. Which enzyme is deficient?

    1. ATrypsinogen secreted by pancreatic acini
    2. BColipase secreted by pancreatic acini
    3. CAlpha-1 antitrypsin made in the liver
    4. DEnteropeptidase of the duodenal brush border
    Show answer

    Answer: D · Enteropeptidase of the duodenal brush border

    Pancreatic proteases are secreted as inactive zymogens. Enteropeptidase (enterokinase), a brush-border enzyme of the duodenum, cleaves trypsinogen to trypsin, which then activates the other zymogens, so its absence stops protein digestion and causes protein malabsorption and hypoproteinaemic oedema. That adding enteropeptidase restores activity proves trypsinogen is present; normal lipase and sweat chloride exclude generalised pancreatic insufficiency such as cystic fibrosis. Pancreatic enzyme supplements, which contain active proteases, are effective.

    • A: If trypsinogen were missing, adding enteropeptidase could not restore trypsin activity.
    • B: Colipase deficiency impairs fat digestion; it does not abolish trypsin activity.
    • C: Alpha-1 antitrypsin inhibits proteases; its deficiency would not abolish trypsin activity.
  4. Question 4 · Easy

    A 58-year-old man who had a total gastrectomy for carcinoma stomach 3 years ago did not attend follow-up. He now has a macrocytic anaemia, glossitis and numbness of both feet. Loss of which gastric secretion explains this?

    1. AMucus from surface cells
    2. BIntrinsic factor from parietal cells
    3. CGastrin from antral G cells
    4. DPepsinogen from chief cells
    Show answer

    Answer: B · Intrinsic factor from parietal cells

    Parietal cells secrete intrinsic factor along with HCl. Vitamin B12 freed from food binds haptocorrin, then intrinsic factor in the duodenum, and the B12-intrinsic factor complex is absorbed in the terminal ileum through cubilin receptors. After total gastrectomy no intrinsic factor is made, so B12 deficiency develops once liver stores are used up, after a few years. Lifelong parenteral B12 is therefore needed.

    • A: Loss of gastric mucus has no role in B12 absorption.
    • C: Gastrin loss reduces acid drive but is not the cause of B12 deficiency.
    • D: Pepsinogen loss impairs protein digestion only slightly and does not cause B12 deficiency.
  5. Question 5 · Medium

    A 52-year-old woman with long-standing type 1 diabetes has early satiety and vomits undigested food several hours after meals. A gastric emptying scan shows delayed emptying with no obstruction. She is given low-dose erythromycin. What is its mechanism in this setting?

    1. AAgonist at 5-HT4 receptors
    2. BAntagonist at D2 receptors
    3. CAgonist at motilin receptors
    4. DAntagonist at muscarinic receptors
    Show answer

    Answer: C · Agonist at motilin receptors

    Erythromycin is a motilin receptor agonist at doses below its antibiotic dose. Motilin, released cyclically from the upper small intestine during fasting, starts phase III of the migrating motor complex, the strong 'housekeeper' contractions that sweep the stomach and small bowel. Erythromycin mimics this and speeds gastric emptying in diabetic gastroparesis caused by autonomic neuropathy, although tachyphylaxis limits long-term use.

    • A: 5-HT4 agonism is the action of prucalopride (and metoclopramide in part).
    • B: D2 antagonism is how metoclopramide and domperidone act.
    • D: Antimuscarinics slow gastric emptying and would worsen gastroparesis.
  6. Question 6 · Medium

    A 42-year-old man has recurrent ulcers in the distal duodenum and jejunum and chronic diarrhoea despite proton pump inhibitors. Off treatment, his fasting serum gastrin is markedly raised while gastric pH is 1.5. Which test best confirms the likely diagnosis?

    1. AUrea breath test
    2. BSecretin stimulation test
    3. CSerum chromogranin A
    4. DPentagastrin stimulation test

    Answer and explanation in LearnFree account

  7. Question 7 · Medium

    A 50-year-old man on long-term omeprazole has a fasting serum gastrin above the normal range. While explaining this, the resident reviews the control of gastric acid. Consider four statements: 1. Histamine raises parietal cell cAMP through H2 receptors. 2. Gastrin stimulates acid mainly by releasing histamine from ECL cells. 3. Somatostatin from D cells inhibits gastrin release when the antrum is acidic. 4. Parietal cells secrete bicarbonate into the gastric lumen with each H+ ion. Which statements are correct?

    1. A1, 2 and 3 only
    2. B2 and 4 only
    3. C1 and 3 only
    4. D1, 2 and 4 only

    Answer and explanation in LearnFree account

  8. Question 8 · Hard

    A 48-year-old woman has passed about 4 litres of watery stool a day for 6 weeks, and the diarrhoea continues during a 48-hour fast. Serum K+ is 2.6 mmol/L, and gastric acid output is low. Stool Na+ is 105 mmol/L, stool K+ 40 mmol/L and measured stool osmolality 290 mOsm/kg. What is the most likely cause?

    1. ACovert magnesium laxative use
    2. BAdult-onset lactase deficiency
    3. CGastrin-secreting duodenal tumour
    4. DVIP-secreting pancreatic tumour

    Answer and explanation in LearnFree account

  9. Question 9 · Easy

    Acid chyme entering the duodenum releases secretin, which stimulates bicarbonate-rich pancreatic juice. The cells that release secretin are:

    1. AI cells
    2. BG cells
    3. CS cells
    4. DK cells

    Answer and explanation in LearnFree account

  10. Question 10 · Medium

    A 50-year-old woman with active rheumatoid arthritis has Hb 9.8 g/dL, MCV 80 fL, low serum iron, low TIBC and serum ferritin 350 ng/mL. A 3-month course of oral iron did not raise her haemoglobin. What best explains her poor absorption of oral iron?

    1. ALack of gastric acid to reduce dietary iron
    2. BAbsence of DMT1 on the duodenal brush border
    3. CHepcidin causing loss of enterocyte ferroportin
    4. DDeficiency of duodenal cytochrome b ferric reductase

    Answer and explanation in LearnFree account

  11. Question 11 · Medium

    A 30-year-old man with Crohn's disease has had a long segment of terminal ileum resected; his colon is intact. Consider four consequences: 1. Vitamin B12 deficiency. 2. Steatorrhoea from depletion of the bile acid pool. 3. Calcium oxalate kidney stones. 4. Iron deficiency from loss of the main iron-absorbing site. Which are expected?

    1. A1 and 2 only
    2. B1, 2 and 3 only
    3. C2, 3 and 4 only
    4. D1 and 4 only

    Answer and explanation in LearnFree account

  12. Question 12 · Medium

    A 40-year-old woman with known gallstones gets colicky right upper abdominal pain about 30 minutes after a meal of fried puris. Which hormone, released by fat in the duodenum, triggers the gallbladder contraction behind her pain?

    1. AGastric inhibitory peptide
    2. BCholecystokinin
    3. CMotilin
    4. DSecretin

    Answer and explanation in LearnFree account

  13. Question 13 · Medium

    A 45-year-old woman with reflux disease is started on pantoprazole and asks why she must take it 30 minutes before breakfast rather than at bedtime. What is the physiological reason?

    1. AIt has to act before gastrin is released by the meal
    2. BFood prevents the drug from being absorbed
    3. CIt blocks histamine at the H2 receptor
    4. DIt binds only to pumps that are actively secreting

    Answer and explanation in LearnFree account

  14. Question 14 · Medium

    During floods in Assam, a 6-year-old boy in a relief camp has profuse rice-water stools, and Vibrio cholerae is isolated. He improves well on oral rehydration solution. Why does ORS work although the toxin is still active?

    1. ANa+-glucose cotransport by SGLT1 stays intact
    2. BGlucose in ORS blocks the toxin's receptor
    3. CCitrate in ORS neutralises the cholera toxin
    4. DSodium in ORS closes the CFTR chloride channel

    Answer and explanation in LearnFree account

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