Master Medical Physiology II: Detailed notes on Gastrin, pancreatic auto-digestion, fat digestion, satiety mechanisms, and thyroid cardiovascular effects.
--- --- 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: - Hypothalamic integration of satiety signals - Activation of POMC/CART neurons in arcuate nucleus - Inhibition of NPY/AgRP neurons (hunger centers) - Brainstem processing of vagal afferent signals Metabolic Factors: - Increased blood glucose and amino acid levels - Enhanced insulin sensitivity - Metabolic switching from hunger to fed state Integration: - Hypothalamic nuclei integrate peripheral signals - Modulation of feeding behavior through higher brain centers - Coordination with autonomic nervous system responses --- 5. Effects of Thyroid Hormone on Cardiovascular System Question: List the effects of thyroid hormone on the cardiovascular system Answer: Thyroid hormones (T3 and T4) have profound effects on cardiovascular function: Cardiac Effects: - Increased heart rate: Direct chronotropic effect on SA node - Increased contractility: Enhanced myocardial contractile force (positive inotropic effect) - Increased cardiac output: Result of increased HR and stroke volume - Shortened cardiac cycle: Reduced diastolic filling time Vascular Effects: - Decreased peripheral vascular resistance: Vasodilation in peripheral tissues - Increased blood volume: Enhanced erythropoiesis and plasma volume - Improved endothelial function: Enhanced nitric oxide production - Increased coronary blood flow: Meets increased metabolic demands Blood Pressure Changes: - Widened pulse pressure: Increased systolic, decreased diastolic pressure - Systolic hypertension: Common in hyperthyroidism - Enhanced sensitivity to catecholamines: Increased β-adrenergic receptor expression Electrophysiological Effects: - Shortened action potential duration: Altered ion channel expression - Increased conduction velocity: Enhanced AV node conduction - Arrhythmia predisposition: Particularly atrial fibrillation Metabolic Cardiovascular Effects: - Increased oxygen consumption: Enhanced cellular metabolism - Increased heat production: Cardiovascular adaptation to thermoregulation - Enhanced calcium cycling: Improved sarcoplasmic reticulum function --- 6. Physiological Functions of Pancreatic Hormone Glucagon Question: Briefly discuss the physiological functions of the Pancreatic Hormone Glucagon Answer: Glucagon, secreted by alpha cells of pancreatic islets, serves as the primary counter-regulatory hormone to insulin: Hepatic Effects: - Glycogenolysis: Stimulates glycogen breakdown to glucose - Gluconeogenesis: Promotes glucose synthesis from amino acids, lactate, and glycerol - Ketogenesis: Enhances fatty acid oxidation and ketone body production - Inhibits glycogen synthesis: Blocks glycogen synthase activity Metabolic Functions: - Lipolysis: Activates hormone-sensitive lipase in adipose tissue - Protein catabolism: Promotes amino acid mobilization for gluconeogenesis - Maintains blood glucose: Prevents hypoglycemia during fasting states - Metabolic switching: Shifts from glucose utilizat