Hormone-driven syndromes · Renal & GI

GI Hormones MCQ

Gastrin, secretin, CCK, GIP, motilin, and somatostatin: what each does, which cell makes it, and the clinical syndromes they reveal (Zollinger–Ellison, gallstones, incretin effect, octreotide use). 11 board-style MCQs.

11 practice MCQsQuick-reference tableMnemonics + clinical pearlsFull distractor explanations
High-yield review

Concept summary and clinical relevance.

Quick-reference structure first, then detailed coverage. Mnemonics in amber, clinical pearls in blue.

GI hormones coordinate digestion: when to release acid, when to release bile, when to dump bicarbonate, when to release insulin in response to a meal. Each hormone has a single dominant action: learn the cell that makes it, the trigger, and the function. The clinical syndromes (Zollinger–Ellison, gallstone pain, incretin effect, octreotide indications) follow naturally.

GI hormones: at a glance
HormoneCell / sourceTriggerMain action
GastrinG cells (stomach antrum)Peptides, distension, vagus↑ HCl from parietal cells; ↑ gastric motility
SecretinS cells (duodenum)Acidic chyme (low pH)↑ pancreatic HCO₃⁻; ↓ gastric acid
CCKI cells (duodenum, jejunum)Fatty acids, amino acidsContracts gallbladder; ↑ pancreatic enzymes; slows gastric emptying
GIPK cells (duodenum, jejunum)Glucose, fats, amino acids↑ insulin (incretin effect); ↓ gastric acid
MotilinSmall intestineFasting stateInitiates migrating motor complexes (MMC)
SomatostatinD cells (pancreas, GI mucosa)Acid, broad GI activityUniversal inhibitor of GI hormones and secretions
Hormone-related syndromes
SyndromeHormone abnormalityKey features
Zollinger–Ellison (gastrinoma)↑ GastrinRefractory peptic ulcers + diarrhea
Gallstone pain (biliary colic)↑ CCK in response to fatty mealsRUQ pain after fatty food
VIPoma (WDHA syndrome)↑ VIPWatery Diarrhea, Hypokalemia, Achlorhydria
Carcinoid syndromeSerotonin (and others)Flushing, diarrhea: treated with octreotide
Clinical pearl, The incretin effect
Oral glucose triggers more insulin release than the same dose given IV: because oral glucose stimulates GIP (and GLP-1) release in the gut, which amplifies pancreatic insulin secretion. This is the basis for incretin-based diabetes drugs: GLP-1 agonists (semaglutide, liraglutide) and DPP-4 inhibitors (sitagliptin) leverage the same pathway.
Clinical pearl, Octreotide: somatostatin's clinical clone
Octreotide (synthetic somatostatin analog) is used for: variceal bleeding (portal hypertension), VIPoma, carcinoid syndrome, gastrinoma (Zollinger–Ellison), and acromegaly (off-label suppression of GH). The “universal off switch” of GI and endocrine secretion has wide clinical utility.
Clinical pearl, Why erythromycin causes diarrhea
Erythromycin is a motilin receptor agonist, it stimulates the same receptors that initiate migrating motor complexes during fasting. The result: increased GI motility and the cramping/diarrhea that's a familiar side effect. This property is occasionally exploited therapeutically (gastroparesis).
Mnemonic, Hormone shorthand
“Gastrin = Gas (acid). Secretin = Sink (bicarb). CCK = Chole-Cyst-Kick (gallbladder). GIP = Glucose Increases Pancreatic insulin. Motilin = Motility. Somatostatin = Stop.”
Mnemonic, VIPoma = WDHA
VIPoma syndrome: Watery Diarrhea, Hypokalemia, Achlorhydria. Treated with octreotide to suppress VIP secretion.

Gastrin: turn on the acid

  • Source: G cells in the stomach antrum.
  • Triggers: dietary peptides, gastric distension, vagal stimulation (via gastrin-releasing peptide).
  • Actions: stimulates parietal cells to release HCl; promotes gastric motility.
  • Clinical: gastrinoma (Zollinger–Ellison) → recurrent peptic ulcers + diarrhea.

Secretin: neutralize the acid

  • Source: S cells in the duodenum.
  • Trigger: acidic chyme entering the duodenum.
  • Actions: stimulates pancreatic HCO₃⁻ secretion to neutralize acid; inhibits gastric acid.

CCK: release bile + enzymes

  • Source: I cells in the duodenum and jejunum.
  • Triggers: fatty acids and amino acids in the duodenum.
  • Actions: contracts the gallbladder, stimulates pancreatic enzyme secretion, slows gastric emptying.
  • Clinical: a fatty meal triggers CCK release → gallbladder contraction → biliary colic if gallstones are present.

GIP, motilin, somatostatin

  • GIP: from K cells; primary incretin: oral glucose stimulates more insulin than IV glucose because of GIP.
  • Motilin: initiates the migrating motor complex during fasting; erythromycin is a motilin agonist (causes diarrhea side effect).
  • Somatostatin: from D cells; inhibits virtually every GI and endocrine hormone. Octreotide is the synthetic analog used for variceal bleeding, VIPoma, carcinoid syndrome, and acromegaly.
Core Recall Check

11 board-style MCQs.

Active recall is the highest-yield study method. Pick an answer, check it, and read why every distractor is wrong.

0 of 11 answered · 0 correct
  1. Question 1
    Easy
    Which cell type secretes gastrin?
  2. Question 2
    Easy
    What is the main action of gastrin?
  3. Question 3
    Moderate
    Which condition is caused by a gastrin-secreting tumor?
  4. Question 4
    Easy
    What is the primary effect of secretin?
  5. Question 5
    Easy
    Which hormone contracts the gallbladder after a meal?
  6. Question 6
    Moderate
    Which hormone slows gastric emptying after a fatty meal?
  7. Question 7
    Moderate
    Which hormone is responsible for the “incretin effect”?
  8. Question 8
    Moderate
    Which hormone stimulates migrating motor complexes during fasting?
  9. Question 9
    Moderate
    Which antibiotic acts as a motilin agonist and can cause diarrhea or cramping?
  10. Question 10
    Easy
    Which hormone is secreted by D cells and broadly inhibits GI hormones?
  11. Question 11
    Moderate
    Which drug is a synthetic somatostatin analog used for variceal bleeding, VIPoma, carcinoid syndrome, and acromegaly?

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Author
Dr. Isaac Sun, DDS

Founder, KYT Dental Services. These MCQs are reviewed by a practicing clinician and offered as an educational reference for dental students.

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