GI System - Anatomy and Physiology

Note: BD Chaurasia's Human Anatomy is not in the library database. The anatomy content below is drawn from Guyton & Hall (which includes GI anatomy detail) and supplemented with Ganong's structural coverage. The physiology sections are extensively covered from both Guyton and Ganong.

OVERVIEW OF THE GI SYSTEM

1. Mouth → Esophagus → Stomach → Duodenum → Jejunum → Ileum → Cecum → Colon → Rectum → Anus

• Ganong's Review of Medical Physiology, 26e, p. 457

PART I: ANATOMY

1. Layers of the GI Wall (Physiologic Anatomy)

• Guyton & Hall, p. 776

2. GI Smooth Muscle - Syncytial Organisation

• Individual smooth muscle fibers: 200-500 µm long, 2-10 µm diameter
• Arranged in bundles of up to 1000 parallel fibers
• Longitudinal layer: bundles run lengthwise; circular layer: bundles encircle the gut
• Fibers connected by gap junctions - low-resistance pathways for ionic current spread
• Each muscle layer acts as a functional syncytium: an action potential spreads throughout the mass
• Guyton & Hall, p. 776

3. Villi and Crypts (Small Intestine)

• Stem cells at the crypt base give rise to all epithelial cells
• Epithelium turns over every 3-5 days
• Villus cells have extensive microvilli (brush border) with a glycocalyx
• Brush border hydrolases perform final digestion
• Crypt base contains Paneth cells (antimicrobial peptides) and stem cells
• Epithelial layer contains scattered endocrine cells and intraepithelial lymphocytes
• Ganong's Review, p. 458

4. Blood Supply (Splanchnic Circulation)

• Celiac artery - stomach
• Superior mesenteric artery (SMA) - small intestine + proximal large intestine
• Inferior mesenteric artery (IMA) - distal colon and rectum

1. Muscle bundles
2. Intestinal villi
3. Submucosal vessels (for secretion and absorption)

• Guyton & Hall, p. 783

PART II: PHYSIOLOGY

1. Electrical Activity of GI Smooth Muscle

a) Slow Waves (Basic Electrical Rhythm)

• Not action potentials; undulating changes in resting membrane potential
• Amplitude: 5-15 mV
• Frequency varies by region:
  • Stomach body: ~3/min
  • Duodenum: ~13/min
  • Terminal ileum: ~8-9/min
• Generated by Interstitial Cells of Cajal (ICC) - the pacemakers of the gut
• ICCs form a network interposed between muscle layers with synaptic-like contacts to smooth muscle
• Slow waves alone do not cause contraction (except in the stomach)

b) Spike Potentials (True Action Potentials)

• Occur when resting membrane potential rises above -40 mV
• Normal resting membrane potential: -50 to -60 mV
• Frequency: 1-10 spikes/sec
• Duration: 10-20 milliseconds (much longer than nerve action potentials)
• Carried mainly by calcium-sodium channels (slow channels) - NOT fast sodium channels
• Calcium entry during action potential triggers muscle contraction
• Guyton & Hall, p. 776-777

2. Neural Control - Enteric Nervous System (ENS)

3. Motility

Mastication (Chewing)

• Anterior teeth (incisors): cutting; posterior teeth (molars): grinding
• Force: 55 lbs on incisors, 200 lbs on molars
• Controlled by nuclei in the brain stem (motor branch of CN V - trigeminal)
• Chewing reflex: food in mouth → inhibition of jaw muscles → jaw drops → stretch reflex → jaw closure

Swallowing (Deglutition)

• Soft palate rises → closes posterior nares
• Palatopharyngeal folds pull medially → passage only for small food
• Vocal cords appose; larynx rises, epiglottis covers opening
• Upper esophageal sphincter (UES/pharyngoesophageal sphincter) relaxes
• Pharyngeal peristalsis propels bolus into esophagus
• Entire stage: <2 seconds
• Swallowing center: medulla and lower pons
• Afferent: CN V, IX; Efferent: CN V, IX, X, XII

• Primary peristalsis: continuation of pharyngeal peristaltic wave; moves bolus in ~8-10 seconds
• Secondary peristalsis: initiated by distension of esophagus if primary fails to clear bolus
• Lower esophageal sphincter (LES) relaxes as the peristaltic wave approaches
• Guyton & Hall, p. 789-791

Gastric Motility

• Receptive relaxation: fundus relaxes as food enters (mediated by vagus - VIP/NO)
• Mixing movements: antral contractions mix food with gastric juice → chyme
• Gastric emptying: regulated by duodenal receptors; fats and acid slow emptying via enterogastric reflex and hormones (secretin, CCK, GIP)

Small Intestine Motility

• Segmentation contractions: primary mixing movement; divide and re-divide the chyme
• Peristalsis: propulsive; moves chyme aborally at 0.5-2 cm/sec
• Migrating Motor Complex (MMC): housekeeping wave during fasting, every ~90 min; sweeps residue distally (controlled by motilin)

Large Intestine Motility

• Haustral contractions: mixing, slow movement
• Mass movements (mass peristalsis): 1-3 times/day, propel contents rapidly; triggered by gastrocolic reflex
• Defecation reflex: distension of rectum → internal anal sphincter relaxes; external sphincter under voluntary control

4. Secretion

Salivary Secretion

• Produced by parotid, submandibular, and sublingual glands
• Contains: salivary α-amylase (begins starch digestion), mucins (lubrication), IgA, lysozyme
• Saliva is hypotonic
• ~1-1.5 L/day

Gastric Secretion

• Parietal cells: secrete HCl (H⁺/K⁺-ATPase proton pump) and intrinsic factor
  • Stimulated by: acetylcholine (via M3), histamine (via H2, cAMP), gastrin (via CCK-B receptor, Ca²⁺)
  • Inhibited by: somatostatin, prostaglandins, GIP
• Chief cells: secrete pepsinogen (activated to pepsin by HCl)
• G cells (antrum): secrete gastrin
• Mucous cells: secrete mucus + HCO₃⁻ (protect mucosa)
• Output: ~2.5 L/day

1. Cephalic phase (~30%): sight/smell/taste/thought of food → vagus → HCl + pepsin
2. Gastric phase (~60%): food in stomach → distension + amino acids → gastrin → HCl
3. Intestinal phase (~10%): chyme in duodenum; initially stimulatory, then inhibitory

Pancreatic Secretion

• Exocrine pancreas: compound alveolar gland
• Secretin (from S cells, triggered by acid in duodenum): acts on duct cells → large volume, high HCO₃⁻, low enzyme juice (via cAMP)
• CCK (from I cells, triggered by fats and proteins): acts on acinar cells → enzyme-rich juice (via phospholipase C/Ca²⁺)
• Acetylcholine (vagus): also stimulates acinar cells → enzyme release

• Ganong's Review, p. 462-464

Bile

• Secreted by hepatocytes, stored in gallbladder
• CCK causes gallbladder contraction + sphincter of Oddi relaxation
• Bile salts emulsify fats, forming micelles for lipase access
• Bile salts are reabsorbed in terminal ileum (enterohepatic circulation)

5. Absorption

Carbohydrates

• Digested to monosaccharides (glucose, galactose, fructose)
• Glucose and galactose: absorbed via SGLT1 (Na⁺-coupled, active) on apical membrane → GLUT2 on basolateral
• Fructose: absorbed via GLUT5 (facilitated) on apical membrane

Proteins

• Digested to amino acids and di/tripeptides
• Amino acids: Na⁺-coupled transporters (apical)
• Di/tripeptides: PepT1 (H⁺-coupled)

Fats

• Triglycerides → fatty acids + monoglycerides (pancreatic lipase)
• Packaged into micelles with bile salts
• Fatty acids enter enterocytes → reassembled into triglycerides → packaged into chylomicrons
• Chylomicrons exit via lacteals into lymphatics → thoracic duct

Vitamins and Minerals

• Vitamin B12 (cobalamin): requires intrinsic factor; absorbed in terminal ileum
• Iron: absorbed in duodenum as Fe²⁺ via DMT1
• Calcium: absorbed in duodenum, stimulated by 1,25-(OH)₂-vitamin D
• Fat-soluble vitamins (A, D, E, K): absorbed with fat in micelles

Water and Electrolytes

• GI tract handles ~9 liters/day of fluid (2L intake + 7L secretions)
• ~8.9 L is absorbed (small intestine: ~7-8L, colon: ~1.3-1.9L)
• Only ~100-200 mL excreted in feces

6. GI Hormones

7. Blood Flow Regulation in the GI Tract

• Blood flow in each GI region is directly proportional to local metabolic activity
• During active absorption: blood flow in villi can increase up to 8-fold
• Vasodilatory mechanisms: release of cholecystokinin, secretin, GIP, VIP from mucosa; liberation of kinins (kallikrein-kinin system); reduced O₂ tension (reactive hyperemia)
• Portal hypertension: obstruction of portal venous flow → collaterals (esophageal varices, caput medusae, hemorrhoids)
• Guyton & Hall, p. 783-785

8. Defecation

• Mass movements drive feces into rectum
• Rectal distension → intrinsic defecation reflex (via ENS) → internal anal sphincter relaxation (smooth muscle)
• Voluntary contraction of external anal sphincter (skeletal muscle, pudendal nerve) can delay defecation
• Valsalva maneuver, squatting position facilitate defecation

Summary: Key Numbers to Remember