Medical Physiology Paper II — Questions and OmpathStudy

Good Luck Daktari SECTION A: SHORT ANSWER QUESTIONS (Total – 60 Marks) Each question carries 5 marks. All questions are compulsory. Gastrin is a peptide hormone secreted by G cells in the antrum of the stomach. Stimulated by peptides/amino acids, stomach distension, and vagal stimulation (via GRP) . Increases gastric motility by enhancing contractions of the gastric smooth muscle . Promotes gastric emptying by increasing the tone of the lower esophageal sphincter , relaxing the pyloric sphincter , and stimulating antral contractions . Indirectly stimulates motility of the small intestine via increased gastrin-mediated secretions. Enhances peristaltic movements , thus aiding in mixing and propulsion of gastric contents. Excess gastrin (e.g., in Zollinger-Ellison syndrome ) can lead to hyper-motility and diarrhea . Inhibition of Pancreatic Autodigestion Pancreatic enzymes are synthesized and secreted as inactive zymogens (e.g., trypsinogen). Trypsinogen is activated only in the duodenum by enterokinase (enteropeptidase) . The pancreas also secretes trypsin inhibitor (e.g., SPINK1 ) to prevent premature trypsin activation. Compartmentalization of enzymes in zymogen granules within acinar cells prevents cytoplasmic exposure. The ductal cells secrete bicarbonate , flushing enzymes into the duodenum and diluting them. Any prematurely activated trypsin is rapidly inactivated by autolysis or inhibitors . Disruption of these safety mechanisms (e.g., in pancreatitis) leads to autodigestion . Process of Digestion of Fats Begins in the mouth (lingual lipase) and stomach (gastric lipase) – minor role. Major digestion occurs in the small intestine , especially duodenum and jejunum . Emulsification by bile salts increases surface area for enzyme action. Pancreatic lipase (with colipase ) hydrolyzes triglycerides into monoglycerides and free fatty acids . These products form micelles with bile salts for transport to the intestinal brush border . Absorbed into enterocytes , where triglycerides are re-esterified . Packaged into chylomicrons and transported via lacteals into lymphatics . Physiology Behind Satiety After a Heavy Meal Stomach distension activates mechanoreceptors that signal the hypothalamus (satiety center) via vagal afferents . Cholecystokinin (CCK) is released from the duodenum in response to fats and proteins, slowing gastric emptying and promoting satiety. Insulin and GLP-1 rise postprandially and act on the arcuate nucleus of the hypothalamus to inhibit hunger. Leptin (from adipose tissue) exerts longer-term satiety effects but contributes postprandially. PYY from the ileum/colon also contributes to delayed gastric emptying and reduced appetite . Serotonin (from enterochromaffin cells) contributes to early satiety by modulating enteric and central pathways. Integration of neural and hormonal signals leads to inhibition of the lateral hypothalamic (hunger) center and activation of the ventromedial nucleus (satiety center) . Effects of Thyroid Hormones on the Cardiovascular System Increased heart rate (positive chronotropic effect) : Thyroid hormones enhance the sensitivity of the heart to catecholamines, increasing heart rate. Increased cardiac output : Both heart rate and stroke volume are elevated, leading to an increase in cardiac output. Increased myocardial contractility (positive inotropic effect) : Thyroid hormones increase the force of myocardial contraction. Peripheral vasodilation : Thyroid hormones cause vasodilation in peripheral vessels, lowering systemic vascular resistance. Increased blood volume : Thyroid hormones increase sodium and water retention by the kidneys, contributing to increased blood volume. Arrhythmias : Hyperthyroidism can lead to arrhythmias, including atrial fibrillation, due to increased myocardial excitability. Enhanced oxygen consumption : Increased metabolic rate from thyroid hormones raises myocardial oxygen demand. Physiological Functions of the Pancreatic Hormone Glucagon Increases blood glucose levels : Glucagon stimulates glycogenolysis in the liver, converting stored glycogen to glucose. Promotes gluconeogenesis : Stimulates the liver to produce glucose from non-carbohydrate precursors (e.g., amino acids). Stimulates lipolysis : Glucagon activates the breakdown of stored triglycerides into free fatty acids and glycerol. Increases ketogenesis : In periods of fasting, glucagon stimulates the liver to convert fatty acids to ketone bodies. Inhibits insulin secretion : Glucagon reduces insulin secretion to prevent hypoglycemia during fasting. Enhances protein catabolism : Glucagon increases the breakdown of proteins to provide amino acids for gluconeogenesis. Supports muscle energy needs : Although it has limited direct action on muscle, glucagon increases available glucose and fatty acids for energy. Countercurrent Multiplier System in the Kidneys (Short notes with diagram) DIAGRAM Descending limb : Permeable to water, but not solutes; water is reabsorbed into the surr