MBMP2300: Medical Physiology II - Complete OmpathStudy

--- SECTION A: SHORT ANSWER QUESTIONS (SAQs) Question 1: Pathophysiology of Protein-Energy Malnutrition Answer: Protein-energy malnutrition (PEM) is a systemic condition resulting from inadequate protein and/or energy intake, leading to multiple physiological disruptions. Key Pathophysiological Mechanisms: Metabolic Adaptation : Body shifts from anabolic to catabolic state, breaking down muscle proteins for energy Hormonal Changes : Decreased insulin, growth hormone, and IGF-1; increased cortisol and glucagon Immune Dysfunction : Reduced lymphocyte production, impaired cell-mediated immunity, increased infection susceptibility Gastrointestinal Changes : Villous atrophy, decreased digestive enzyme production, malabsorption Cardiovascular Effects : Decreased cardiac output, bradycardia, hypotension Clinical Manifestations: Kwashiorkor: Edema, fatty liver, skin changes (protein deficiency with adequate calories) Marasmus: Severe wasting, no edema (overall caloric deficiency) Growth retardation, delayed wound healing, increased mortality risk --- Question 2: Gastrointestinal Absorption of Amino Acids Answer: [DIAGRAM: Small Intestine Cross-Section] Lumen → Brush Border → Enterocyte → Portal Circulation Proteins → Peptides → Amino Acids → Absorption Absorption Process: Protein Digestion : Stomach pepsin and pancreatic enzymes break proteins into peptides Final Digestion : Brush border peptidases convert peptides to amino acids Transport Mechanisms : Sodium-dependent transporters : For neutral, acidic, and basic amino acids Sodium-independent transporters : For some amino acids Peptide transporters : PEPT1 for di- and tripeptides Location : Primarily in duodenum and jejunum Regulation : Enhanced by insulin, growth hormone, and dietary protein intake Clinical Significance : Defects lead to aminoaciduria and malnutrition --- Question 3: Migrating Motor Complex (MMC) Answer: The MMC is a cyclical pattern of intestinal motility occurring during fasting states, consisting of four distinct phases. Phase Characteristics: Phase I (45-60 minutes) : Quiescent period with minimal contractions Phase II (30-45 minutes) : Irregular, intermittent contractions Phase III (5-15 minutes) : Intense, regular contractions ("housekeeper waves") Phase IV (5-15 minutes) : Transitional period between cycles Functions: Sweeps undigested food residues toward colon Prevents bacterial overgrowth in small intestine Maintains intestinal hygiene Propels secretions and debris Regulation : Controlled by motilin hormone, vagal stimulation, and enteric nervous system Clinical Importance : Disrupted in diabetes, irritable bowel syndrome, and bacterial overgrowth --- Question 4: Functions and Regulation of Cholecystokinin (CCK) Answer: CCK is a peptide hormone released by I-cells in the duodenum and jejunum in response to fats and proteins. Primary Functions: Gallbladder Contraction : Stimulates bile release for fat digestion Pancreatic Enzyme Secretion : Triggers release of digestive enzymes Gastric Emptying : Slows gastric emptying to allow proper digestion Satiety Signal : Acts on brain to reduce food intake Sphincter of Oddi Relaxation : Allows bile and pancreatic juice flow Regulation: Stimuli : Fatty acids, amino acids, peptides in duodenum Inhibition : Somatostatin, completed digestion Feedback : Negative feedback from pancreatic enzymes Clinical Significance : Deficiency leads to poor fat digestion and gallbladder dysfunction --- Question 5: Production of Cortisol Answer: Cortisol is a glucocorticoid hormone produced by the zona fasciculata of the adrenal cortex. Production Pathway: Hypothalamus : Releases CRH (Corticotropin-Releasing Hormone) Anterior Pituitary : Secretes ACTH (Adrenocorticotropic Hormone) Adrenal Cortex : Produces cortisol from cholesterol via steroidogenesis Biosynthesis Steps: Cholesterol → Pregnenolone → Progesterone → 17α-hydroxyprogesterone → 11-deoxycortisol → Cortisol Key enzymes: 21-hydroxylase, 11β-hydroxylase Regulation: Stimulation : ACTH, stress, hypoglycemia, inflammation Inhibition : Negative feedback on hypothalamus and pituitary Circadian Rhythm : Peak in early morning, lowest at night Transport : 90% bound to cortisol-binding globulin (CBG) --- Question 6: Pathophysiology of Graves' Disease Answer: Graves' disease is an autoimmune hyperthyroid condition caused by thyroid-stimulating immunoglobulins (TSI). Pathophysiological Mechanism: Autoimmune Process : TSI antibodies bind to TSH receptors Thyroid Stimulation : Continuous stimulation leads to excess hormone production Thyroid Enlargement : Diffuse goiter formation Metabolic Acceleration : Increased T3 and T4 cause hypermetabolism Clinical Manifestations: Metabolic : Weight loss, heat intolerance, increased appetite Cardiovascular : Tachycardia, palpitations, atrial fibrillation Neurological : Anxiety, tremor, insomnia, irritability Ocular : Exophthalmos, diplopia (Graves' ophthalmopathy) Dermatological : Warm, moist skin; pretibial myxedema Laboratory