Medical Physiology II (Paper 2) — Notes OmpathStudy

--- --- 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): Released from duodenal I-cells, promotes satiety through vagal pathways Glucagon-like peptide-1 (GLP-1): Secreted by L-cells, slows gastric emptying and reduces appetite Peptide YY (PYY): Released from ileum and colon, inhibits gastric motility and food intake Leptin: Increases from adipose tissue, provides long-term satiety signaling Neural Mechanisms: Hypoth