OIA2004 INTRODUCTION TO THE PHYSIOLOGY OF GIT

Gastrointestinal Tract (GIT)

A continuous tube extending from the mouth to the anus, responsible for digestion and absorption.

Mucosa

The innermost layer of the GIT, involved in secretion, absorption, and protection.

Submucosa

A layer under the mucosa providing elasticity and containing the submucosal nerve plexus.

Muscularis Externa

A smooth muscle layer responsible for peristalsis and mixing movements.

Serosa

The outermost layer secreting fluid to prevent friction.

Intrinsic Nerve Plexuses

The enteric nervous system (ENS), consisting of the myenteric and submucosal plexuses.

Extrinsic Nerves

Autonomic nerves (sympathetic and parasympathetic) that regulate GIT activity.

Gastrointestinal Hormones

Chemical messengers released by endocrine cells to regulate digestion.

Pacemaker Cells (Interstitial Cells of Cajal)

Generate slow-wave potentials that drive smooth muscle contractions.

Gastrointestinal Motility

Controlled by smooth muscle contraction and neural/hormonal inputs.

Peristalsis

Rhythmic contractions that propel food through the GIT.

Segmentation

Alternating contractions that mix food with digestive secretions.

Gastric Mucosal Barrier

Protective mechanisms preventing acid damage to the stomach lining.

Gastric Emptying Rate

The speed at which stomach contents move into the duodenum.

Acid-Base Regulation in GIT

Achieved through bicarbonate secretion and pH balance.

HCl Secretion Mechanism

CO2 + H2O → CAH2CO3 → H+ + HCO3−

Henderson-Hasselbalch Equation (for pH regulation)

pH=pKa+log⁡[A−][HA]

Chloride Shift in Parietal Cells

HCO3− is exchanged for Cl−, leading to HCl secretion.

Proton Pump Function

H+/K+-ATPase actively transports H+ into the stomach lumen.

Helicobacter pylori (H. pylori)

A bacterium responsible for peptic ulcers by breaking the mucosal barrier.

NSAIDs (e.g., aspirin, ibuprofen)

Can inhibit mucus production, leading to gastric ulcers.

Secretin Hormone

Released in response to acidic chyme; stimulates bicarbonate secretion to neutralize stomach acid.

Cholecystokinin (CCK)

Stimulated by fatty acids; causes gallbladder contraction and enzyme secretion.

Gastric Inhibitory Peptide (GIP)

Inhibits gastric acid secretion and stimulates insulin release.

Gastrin

Stimulates acid secretion and gastric motility.

Histamine

Stimulates acid secretion by acting on H2 receptors.

Acetylcholine (ACh)

Stimulates parietal cells to secrete acid via M3 receptors.

Somatostatin

Inhibits acid secretion by blocking histamine and gastrin release.

Cephalic Phase

Triggered by sight, smell, and taste of food; stimulates gastric secretions.

Gastric Phase

Initiated when food reaches the stomach; major contributor to acid secretion.

Intestinal Phase

Occurs when chyme enters the duodenum; inhibits gastric secretions.

Protein Digestion

Begins in the stomach with pepsin breaking down proteins.

Fat Digestion

Initiated by gastric lipase, but mainly occurs in the small intestine.

Carbohydrate Digestion

Begins in the mouth with amylase, continues in the small intestine.

Mucus Secretion

Protects the stomach lining from acid.

Epithelial Cell Renewal

The stomach lining is replaced every 3 days to prevent damage.

Sympathetic Nervous System (SNS)

Inhibits digestion during stress.

Parasympathetic Nervous System (PNS)

Enhances digestion and secretion.

Peptic Ulcer Disease (PUD)

Caused by H. pylori or NSAIDs leading to mucosal erosion.

Gastroesophageal Reflux Disease (GERD)

Acid reflux due to weakened lower esophageal sphincter.