Gastrointestinal Physiology

🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your exam.

Gastrointestinal Physiology — Key Facts for FMGE Core concept: The GI tract digests food and absorbs nutrients through coordinated mechanical and chemical processes regulated by hormones and neural inputs High-yield point: Secretin and CCK are the main enteric hormones; understand how each GI segment handles different nutrients ⚡ Exam tip: Gastric acid secretion has three phases (cephalic, gastric, intestinal) controlled by different stimuli; H. pylori and PPI are clinically important

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🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

Gastrointestinal Physiology — FMGE Study Guide

GI Tract Overview

Layers (wall structure)

• Mucosa: Epithelium, lamina propria, muscularis mucosae
• Submucosa: Connective tissue, blood vessels, Meissner’s plexus
• Muscularis externa: Circular muscle, longitudinal muscle, Auerbach’s plexus
• Serosa (adventitia): Outer connective tissue

Enteric Nervous System (ENS)

• Meissner’s plexus (submucosal): Controls secretion, blood flow
• Auerbach’s plexus (myenteric): Controls motility
• Can function independently of CNS but modulated by it

GI Motility Types

• Segmentation: Rhythmic constrictions in small intestine (mixing)
• Peristalsis: Propulsive waves (sequential circular contraction behind bolus)
• Migrating Motor Complex (MMC): Cyclic fasting pattern (housekeeper of gut)
• Sphincters: Prevent backflow (LES, pylorus, ileocecal valve, internal/external anal sphincters)

Mouth and Esophagus

Salivation

• Parotid (serous), Submandibular (mixed), Sublingual (mucous)
• Salivary amylase: Digests starch (α-amylase)
• Lysozyme, IgA: Antimicrobial
• Functions: Lubrication, digestion, oral health
• Neural control: Parasympathetic (↑salivation - CN VII, IX); Sympathetic (↓salivation, viscous saliva)

Swallowing

• Oral phase (voluntary): Bolus formed, pushed by tongue
• Pharyngeal phase (involuntary): Soft palate elevates, epiglottis covers larynx, pharyngeal constrictors contract
• Esophageal phase: Peristaltic wave; LES relaxes

Lower Esophageal Sphincter (LES)

• Normally closed; relaxes during swallowing
• GERD: LES dysfunction → acid reflux
• Barrett esophagus: Metaplasia of esophageal epithelium due to chronic acid reflux

Stomach

Gastric Secretion

Mucous cells: Secrete mucus and bicarbonate (protective barrier) Parietal cells: Secrete HCl and intrinsic factor Chief cells: Secrete pepsinogen (pepsin precursor) G cells: Secrete gastrin (hormone)

Gastric Acid Secretion

HCl:

• Parietal cell secretes H⁺ (from water) and Cl⁻ (from plasma)
• H⁺-K⁺-ATPase (proton pump): Pumps H⁺ into lumen in exchange for K⁺
• H⁺ from carbonic acid (CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻)
• Intrinsic factor: Required for B12 absorption in terminal ileum

Phases of Gastric Secretion

Cephalic phase (brain):

• Sight, smell, taste, thought of food
• Vagus nerve stimulation
• Acetylcholine → direct stimulation of parietal cells + G cells
• 30% of acid response

Gastric phase (stomach):

• Food distends stomach → local reflexes + gastrin release
• Protein → ↑gastrin → ↑acid
• 60% of acid response

Intestinal phase (intestine):

• Chyme in duodenum → enterogastrones (secretin, CCK, GIP)
• Inhibits gastric secretion and motility
• 10% of acid response

Gastrin

• Secreted by G cells (antrum)
• Stimulus: Protein, distension, vagal stimulation
• Action: ↑HCl secretion, ↑growth of gastric mucosa
• Gastrinoma (Zollinger-Ellison syndrome): Gastrin-secreting tumor → excessive acid → peptic ulcers in unusual locations

GI Hormones

Gastrin: From G cells; ↑acid, ↑growth of gastric mucosa Cholecystokinin (CCK): From I cells in duodenum; ↑gallbladder contraction, ↑pancreatic enzyme secretion, ↓gastric emptying, ↑growth of exocrine pancreas Secretin: From S cells in duodenum; ↑pancreatic bicarbonate secretion, ↓gastric acid secretion GIP (Glucose-dependent Insulinotropic Peptide): From K cells; ↓gastric acid, ↑insulin release Motilin: From M cells; initiates MMC, ↑GI motility Somatostatin: From D cells; inhibits gastrin, secretin, pancreatic secretion; slows GI motility

Peptic Ulcers

• Duodenal ulcers: Associated with H. pylori, normal/below normal acid secretion; pain relieved by eating
• Gastric ulcers: Associated with NSAIDs, may have high acid; pain worsened by eating
• H. pylori: Colonizes antrum → ↑gastrin → ↑acid → ulcer; treat with triple therapy (PPI + clarithromycin + amoxicillin)

Pancreatic Secretion

Exocrine Pancreas

• Bicarbonate-rich fluid (duct cells) + enzyme-rich fluid (acinar cells)
• Trypsinogen, chymotrypsinogen, procarboxypeptidase: Proteases
• Amylase: Digests carbohydrates
• Lipase: Digests fats (with colipase)
• Ribonuclease, deoxyribonuclease: Nucleic acid digestion

Regulation

• CCK: ↑pancreatic enzyme secretion (via vagal afferents)
• Secretin: ↑pancreatic bicarbonate secretion (acid in duodenum)
• Vagal stimulation: ↑enzyme secretion
• Somatostatin: ↓pancreatic secretion

Enzyme Activation

• Trypsinogen → enterokinase (from duodenal mucosa) → trypsin
• Trypsin then activates other proteases (cascade)

Bile and Gallbladder

Bile

• Bile acids (bile salts): Amphipathic; emulsify fats (increase surface area)
• Bilirubin: Waste product from RBC breakdown
• Cholesterol: Excreted in bile
• Lecithin: Phospholipid; helps emulsify fat

Enterohepatic Circulation

• Bile acids released into duodenum → most reabsorbed in terminal ileum → portal vein → liver → rebile secretion
• 95% recycled; 5% lost in stool (requires synthesis of new bile acids)

Gallbladder

• Stores and concentrates bile
• CCK: Stimulates contraction and ejection of bile
• Fat in duodenum → CCK release → gallbladder contracts

Gallstones

• Cholesterol stones: Most common; associated with obesity, female, fertile
• Pigment stones: Black (hemolysis) or brown (infection)

Small Intestine

Absorption Sites

Duodenum: Iron, calcium, folate, glucose, amino acids Jejunum: Most nutrients (carbs, proteins, fats, vitamins) Ileum: B12, bile salts, fat-soluble vitamins, anything remaining

Carbohydrate Digestion

• Pancreatic amylase: Breaks starch to disaccharides
• Disaccharidases (maltase, sucrase, lactase): Break to monosaccharides
• Lactase deficiency: Lactose intolerance → bloating, flatulence, diarrhea with dairy

Protein Digestion

• Pepsin (stomach): Initial proteolysis
• Trypsin, chymotrypsin, carboxypeptidase (pancreas): Peptide bonds
• Aminopeptidases (intestinal brush border): Individual amino acids

Fat Digestion

• Emulsification: Bile salts break large fat globules into small droplets
• Pancreatic lipase: Hydrolyzes triglycerides → monoglycerides + free fatty acids
• Colipase: Anchors lipase to fat-water interface
• Products: Micelles → absorbed by enterocytes → reassembled into triglycerides → chylomicrons → lymphatic system

Vitamins

• Fat-soluble (A, D, E, K): Absorbed with fat; require bile and lipase
• Water-soluble: B vitamins, vitamin C; absorbed directly into portal blood

Large Intestine

Functions

• Water and electrolyte absorption: ~1.5 L/day enters; only ~150 mL lost in stool
• Bacterial metabolism: Ferment undigested carbohydrates → short-chain fatty acids, gases (H₂, CO₂, CH₄)
• Vitamin K synthesis: By bacteria; important for clotting factors
• Fecal storage: Rectum and sigmoid

Defecation

• Mass movement: Propulsive peristalsis (3-4 times/day)
• Rectum distended → internal anal sphincter relaxes (involuntary)
• External anal sphincter: Voluntary control; relax when appropriate

Diarrhea and Constipation

• Secretory diarrhea: Increased Cl⁻ secretion (cholera, ETEC); watery, large volume
• Osmotic diarrhea: Non-absorbed solutes draw water (lactose intolerance, laxatives)
• Motility diarrhea: Decreased transit time (hyperthyroidism, IBS)
• Constipation: Slow transit; hard, dry stools

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