Medical Physiology II (Paper 2)

--- ** --- **PROGRAMME:** Bachelor of Medicine and Bachelor of Surgery (MBChB)**YEAR OF STUDY:** Year 2**UNIT CODE:** MBMP 2300B**UNIT TITLE:** Medical Physiology II**PAPER:** Two**DATE:** 3rd July, 2019**TIME:** 2:00 PM**DURATION:** 1 Hour 45 Minutes --- ### **INSTRUCTIONS TO CANDIDATES:** - This paper consists of **two sections**: **Section A** and **Section B**. - **Section A**: Answer **all questions** (Multiple Choice and Short Answer Questions). - **Section B**: Answer **any two (2) essay questions**. - Write your **registration number** clearly on every answer booklet used. - Begin each question on a **new page**. - Marks for each question are indicated in the exam booklet. - Adhere strictly to the time allocated. --- Physiology SAQ Answers - 5 Marks Each ## 1. Role of Gastrin in Gastro-intestinal Motility **Question:** Write short notes on the role of Gastrin in Gastro-intestinal motility **Answer:** Gastrin is a peptide hormone secreted by G cells in the gastric antrum and duodenum that plays crucial roles in gastrointestinal motility: **Gastric Motility Effects:** - Stimulates gastric smooth muscle contractions, enhancing gastric mixing and churning - Increases antral contractions, promoting gastric emptying - Enhances lower esophageal sphincter (LES) tone, preventing gastroesophageal reflux **Small Intestinal Effects:** - Stimulates duodenal and jejunal peristalsis - Coordinates migrating motor complexes (MMCs) during fasting periods - Promotes segmentation contractions for mixing **Colonic Effects:** - Stimulates colonic motility and mass movements - Enhances ileocecal valve function **Mechanism:** Gastrin acts through CCK-B receptors on smooth muscle cells and enteric neurons, activating calcium-dependent pathways that increase contractility and coordinate peristaltic waves throughout the digestive tract. --- ## 2. Inhibition of Auto-digestion of the Pancreas **Question:** Briefly explain how Auto-digestion of the Pancreas is inhibited **Answer:** The pancreas protects itself from auto-digestion through multiple protective mechanisms: **Enzyme Synthesis as Inactive Precursors:** - Proteolytic enzymes are synthesized as inactive zymogens (trypsinogen, chymotrypsinogen, proelastase) - Stored in zymogen granules within acinar cells - Activated only after secretion into the duodenum **Protease Inhibitors:** - Pancreatic secretory trypsin inhibitor (PSTI) blocks premature trypsin activation - Serine protease inhibitor Kazal type 1 (SPINK1) provides additional protection - α1-antitrypsin in plasma neutralizes any leaked enzymes **Cellular Compartmentalization:** - Strict separation between synthesis, storage, and secretion compartments - Zymogen granules maintain acidic pH preventing activation - Regulated exocytosis prevents intracellular enzyme release **Ductal Bicarbonate Secretion:** - High bicarbonate concentration in pancreatic juice neutralizes any acidic conditions - Maintains optimal pH for enzyme stability during transport **Rapid Enzyme Clearance:** - Efficient drainage through pancreatic duct system - Quick transit to duodenum prevents accumulation --- ## 3. Process of Fat Digestion **Question:** Briefly highlight the process of digestion of fats **Answer:** Fat digestion occurs through a coordinated process involving mechanical, chemical, and enzymatic breakdown: **Oral Phase:** - Minimal digestion occurs - Lingual lipase begins triglyceride hydrolysis (10-30% of total) - Mechanical breakdown through chewing **Gastric Phase:** - Gastric lipase continues fat hydrolysis - Gastric acid and pepsin help break down fat-protein complexes - Gastric churning creates crude emulsification **Intestinal Phase - Emulsification:** - Bile salts from gallbladder create stable emulsions - Reduces fat droplet size from 1mm to 1μm - Phospholipids and proteins aid emulsification **Pancreatic Enzyme Action:** - Pancreatic lipase hydrolyzes triglycerides to monoglycerides and fatty acids - Colipase facilitates lipase binding to lipid interface - Phospholipase A2 breaks down phospholipids - Cholesterol esterase hydrolyzes cholesterol esters **Micelle Formation:** - Bile salts form mixed micelles with digestion products - Facilitates absorption at brush border membrane - Fat-soluble vitamins (A, D, E, K) incorporated into micelles **Absorption:** - Occurs primarily in jejunum - Passive diffusion into enterocytes - Reformation into chylomicrons for lymphatic transport --- ## 4. Physiology of Satiety Following Heavy Meal **Question:** Following a heavy meal, discuss the physiology behind Satiety **Answer:** Satiety after a heavy meal involves complex hormonal, neural, and mechanical mechanisms: **Mechanical Factors:** - Gastric distension activates stretch receptors in stomach wall - Vagal afferents signal fullness to brainstem - Increased intragastric pressure triggers satiety reflexes **Hormonal Signals:** - **Cholecystokinin (CCK):