MRCP Physiology: GI Secretions & Hormones (MRCP Part 1)

TL;DR: 

For MRCP Part 1, gastrointestinal secretions and hormones are tested as applied physiology rather than rote biochemistry. You must understand who secretes what, what stimulates or inhibits secretion, and how drugs or disease modify these pathways. This guide covers the examinable scope, high-yield mechanisms, common traps, and a short worked MCQ to help you score reliably.

Why GI secretions & hormones matter in MRCP Part 1

GI physiology is a recurring theme in MRCP Part 1 because it integrates basic science with clinical reasoning. Questions often look simple—acid secretion, diarrhoea, pancreatic enzymes—but are designed to test whether you understand regulation, feedback, and final common pathways.

Importantly, this topic overlaps with pharmacology (PPIs, H₂ blockers), pathology (Zollinger–Ellison syndrome, ileal disease), and surgery (vagotomy). A solid grasp here reduces cognitive load across multiple systems.

For context, this topic sits within the broader MRCP Part 1 syllabus published by MRCP(UK):👉 https://www.mrcpuk.org/mrcpuk-examinations/part-1/syllabus

Examinable scope (what the exam expects)

You are not expected to memorise molecular pathways in detail. The exam consistently focuses on:

• Regulation of gastric acid secretion

• Major GI hormones and their actions

• Neural vs hormonal control

• Pancreatic exocrine secretion

• Bile, bile salts, and enterohepatic circulation

• Mechanisms of diarrhoea (especially secretory)

Questions are usually framed as:

• “Which hormone is released in response to…?”

• “Which pathway is blocked by this drug?”

• “What happens after vagotomy or ileal resection?”

Five most tested subtopics (high yield)

1. Gastric acid secretion (very high yield)

Cell: Parietal cell Final pathway: H⁺/K⁺-ATPase (proton pump)

Key stimulants:

• Acetylcholine → M3 receptor → ↑ intracellular Ca²⁺

• Gastrin → CCK-B receptor → ↑ Ca²⁺

• Histamine → H₂ receptor → ↑ cAMP

All three converge on the proton pump. This is why:

• PPIs are more potent than H₂ blockers

• Acid secretion persists after vagotomy (histamine still works)

2. Gastrin

Actions commonly tested:

• ↑ Gastric acid secretion (mainly via ECL cell histamine release)

• ↑ Gastric mucosal growth

• ↑ Gastric motility

Regulation:

• Stimulated by peptides, amino acids, vagal input

• Inhibited by low gastric pH (negative feedback)

Classic association: Zollinger–Ellison syndrome (gastrinoma).

3. Pancreatic exocrine secretion

A favourite area for clean physiology questions.

• Secretin

  • Released from duodenal S cells

  • Stimulus: acidic chyme

  • Effect: ↑ bicarbonate-rich pancreatic secretion

• Cholecystokinin (CCK)

  • Released from I cells

  • Stimulus: fats and amino acids

  • Effect: ↑ enzyme-rich pancreatic secretion, gallbladder contraction

Exam pearl:

Secretin = bicarbonate, CCK = enzymes.

4. Bile and bile salts

Commonly tested in malabsorption scenarios.

Key points:

• Bile salts are synthesised from cholesterol

• Reabsorbed in the terminal ileum

• Enterohepatic circulation conserves bile salts

Clinical link:

• Ileal disease or resection → bile salt loss → fat malabsorption + diarrhoea

5. Intestinal fluid secretion & diarrhoea

Secretory diarrhoea is a classic applied question.

• Chloride secretion via CFTR drives water movement

• cAMP and cGMP increase secretion

• Cholera toxin → ↑ cAMP → profuse watery diarrhoea

Clue in the stem: diarrhoea persists despite fasting.

Summary table: major GI hormones

Hormone	Source	Main action
Gastrin	G cells (antrum)	↑ gastric acid, mucosal growth
Secretin	S cells (duodenum)	↑ pancreatic bicarbonate
CCK	I cells (duodenum/jejunum)	↑ pancreatic enzymes, gallbladder contraction
GIP	K cells	↑ insulin, ↓ gastric acid
Motilin	Small intestine	Migrating motor complex

This level of detail is sufficient for MRCP Part 1.

Mini-case (SBA style)

Question: A 48-year-old man undergoes truncal vagotomy for refractory peptic ulcer disease. Which mechanism of gastric acid secretion is most reduced post-operatively?

A. Histamine-mediated cAMP increaseB. Gastrin release from G cellsC. Acetylcholine stimulation of parietal cellsD. Proton pump activityE. Carbonic anhydrase activity

Correct answer: C. Acetylcholine stimulation of parietal cells

Explanation: Vagotomy removes cholinergic input to parietal cells. Gastrin and histamine pathways remain intact, so acid secretion is reduced but not abolished—an important physiological distinction tested in MRCP Part 1.

Five common traps examiners use

• Confusing secretin with CCK

• Assuming vagotomy abolishes all acid secretion

• Mixing up cAMP and Ca²⁺ pathways

• Forgetting enterohepatic circulation of bile salts

• Memorising hormone lists without understanding stimuli

Practical study-tip checklist

• Learn GI hormones as stimulus → hormone → effect

• Always link secretions to cell type and receptor

• Draw simple flow diagrams instead of long notes

• Pair physiology with pharmacology (PPIs, H₂ blockers)

• Test weekly using timed MCQs rather than passive reading

For structured practice, use a high-quality MRCP question bank such as the Crack Medicine QBank:👉 https://crackmedicine.com/qbank/

FAQs

How detailed is GI physiology in MRCP Part 1?

Conceptual understanding is prioritised. Focus on regulation and applied physiology rather than molecular detail.

Are GI hormones tested on their own?

Rarely. They are usually embedded in clinical or pharmacological scenarios.

Do I need to memorise hormone structures?

No. Structures are not required for MRCP Part 1—functions and control are.

Is gastric acid secretion more important than other GI topics?

Yes. Acid secretion is one of the most frequently tested physiology themes.

What’s the fastest way to revise this topic?

Active recall with MCQs and summary tables, followed by focused review of weak areas.

Ready to start?

GI secretions and hormones are easy marks if you understand the mechanisms. Consolidate this topic with regular question practice, benchmark yourself using full mock exams, and integrate physiology with pharmacology early in your MRCP Part 1 preparation.

Sources

• MRCP(UK) Part 1 Syllabus: https://www.mrcpuk.org/mrcpuk-examinations/part-1/syllabus

• Guyton & Hall. Textbook of Medical Physiology.

• Boron WF, Boulpaep EL. Medical Physiology.