Human Phys Final Study Guide PDF

Kidneys Kidney Functions and Nephron Structure 1. General Functions of the Kidneys 1. Filtration: ○ Remove metabolic waste products, toxins, and drugs from the blood. 2. Regulation: ○ Maintain fluid balance, electrolytes, and blood pressure. 3. Acid-Base Balance:...

Kidneys Kidney Functions and Nephron Structure 1. General Functions of the Kidneys 1. Filtration: ○ Remove metabolic waste products, toxins, and drugs from the blood. 2. Regulation: ○ Maintain fluid balance, electrolytes, and blood pressure. 3. Acid-Base Balance: ○ Regulate blood pH by excreting H+ and reabsorbing bicarbonate (HCO3^-). 4. Erythropoiesis Regulation: ○ Release erythropoietin (EPO) to stimulate red blood cell production. 5. Metabolic and Hormonal Roles: ○ Activate vitamin D, and regulate calcium-phosphate metabolism. 2. Filtration Barrier Layers The filtration barrier between the glomerulus and Bowman's capsule consists of: 1. Fenestrated Endothelium: ○ Allows passage of water and small solutes but blocks cells (e.g., red blood cells). 2. Basement Membrane: ○ Prevents passage of large proteins via charge and size selectivity. 3. Podocyte Filtration Slits: ○ Podocytes with slit diaphragms provide another size-selective barrier. 3. Nephron Segments in Order 1. Glomerular Capsule (Bowman’s Capsule): ○ Collects filtrate from the glomerulus. 2. Proximal Convoluted Tubule (PCT): ○ Reabsorbs the majority of water, glucose, and electrolytes. 3. Nephron Loop (Loop of Henle): ○ Descending Limb: Permeable to water; concentrates filtrate. ○ Ascending Limb: Impermeable to water; reabsorbs Na+ and Cl^-. 4. Distal Convoluted Tubule (DCT): ○ Regulates Na+, K+, and pH under hormonal control (e.g., aldosterone).  5. Collecting Duct: ○ Adjusts water reabsorption based on ADH levels; forms concentrated or dilute urine. 4. Nephron and Collecting Duct Relationship Each nephron connects to a collecting duct, which collects processed filtrate (urine) from multiple nephrons. Collecting ducts merge and drain into the renal pelvis. 5. Cortical vs. Juxtamedullary Nephrons Feature Cortical Nephrons Juxtamedullary Nephrons Location Mostly in the renal cortex. Extend deep into the renal medulla. Loop of Short loop. Long loop, essential for urine concentration. Henle Function General filtration and Concentration of urine (via countercurrent reabsorption. mechanisms). Blood Peritubular capillaries. Vasa recta for medullary exchange. Supply 6. Vascular Elements of the Nephron 1. Afferent Arterioles: ○ Deliver blood to the glomerulus. 2. Glomerulus: ○ Network of capillaries that filters plasma into Bowman’s capsule. 3. Efferent Arterioles: ○ Carry blood away from the glomerulus. 4. Peritubular Capillaries: ○ Surround cortical nephron tubules; site of exchange for reabsorption and secretion. 5. Vasa Recta: ○ Surround juxtamedullary nephron loops; maintain the medullary osmotic gradient. 7. Key Renal Processes  Filtration: ○ Plasma filtered into Bowman’s capsule. Reabsorption: ○ Valuable substances (e.g., water, glucose, Na+) reclaimed into the blood. Secretion: ○ Additional waste products actively transported into tubules. 8. Determining Urine Volume and Composition Integration of: 1. Filtration: Determines the starting composition of filtrate. 2. Reabsorption: Adjusts water, ions, and nutrients returned to blood. 3. Secretion: Removes excess ions and waste from blood into the filtrate. 9. Glomerular Filtration Rate (GFR) Definition: ○ Volume of filtrate produced by the kidneys per minute (~125 mL/min). Starling Forces: ○ Glomerular Hydrostatic Pressure (GHP): Pushes fluid out of capillaries into Bowman’s capsule (favors filtration). ○ Capsular Hydrostatic Pressure (CHP): Pressure in the capsule opposing filtration. ○ Glomerular Oncotic Pressure (GOP): Osmotic pull from plasma proteins (opposes filtration). Net Filtration Pressure (NFP): ○ NFP=GHP−(CHP+GOP)NFP = GHP - (CHP + GOP). 10. Water Molecule Pathway Pathway to Urine: 1. Afferent arteriole → Glomerulus → Bowman’s capsule → PCT → Loop of Henle → DCT → Collecting duct → Renal pelvis → Ureter → Bladder → Urethra → Excreted. Pathway to Renal Vein:  1. Afferent arteriole → Glomerulus → Bowman’s capsule → Reabsorbed in PCT → Peritubular capillaries → Renal vein → Systemic circulation. Study Tools 1. Diagram: Nephron Structure Include: ○ Glomerulus, PCT, Loop of Henle, DCT, and collecting duct. ○ Label associated blood vessels: afferent arteriole, glomerulus, efferent arteriole, peritubular capillaries, and vasa recta. 2. Table: Cortical vs. Juxtamedullary Nephrons Aspect Cortical Juxtamedullary Loop Length Short Long Primary Role General filtration Urine concentration Body Fluid Volume and Osmolarity Predictions 1. Net Water Loss or Gain Net Water Loss: ○ Body Fluid Volume: Decreases. ○ Body Fluid Osmolarity: Increases (hyperosmotic state). ○ Urine Volume: Decreases due to increased reabsorption of water under ADH influence. ○ Urine Osmolarity: Increases, concentrating the urine to conserve water. Net Water Gain: ○ Body Fluid Volume: Increases. ○ Body Fluid Osmolarity: Decreases (hyposmotic state). ○ Urine Volume: Increases to excrete excess water. ○ Urine Osmolarity: Decreases, producing dilute urine. 2. Net NaCl Loss or Gain  Net NaCl Loss: ○ Body Fluid Volume: Decreases (water follows Na+). ○ Body Fluid Osmolarity: Decreases (more Na+ loss than water). ○ Urine Production: Increases initially but decreases later as aldosterone promotes Na+ reabsorption. ○ Urine Osmolarity: Decreases initially, as less solute is available for water reabsorption. Net NaCl Gain: ○ Body Fluid Volume: Increases (water follows Na+). ○ Body Fluid Osmolarity: Increases (hyperosmotic state). ○ Urine Production: Increases as the kidneys excrete excess Na+. ○ Urine Osmolarity: Increases, reflecting the higher Na+ concentration. Sodium Reabsorption Mechanisms 3. Primary Active Transport of Na+ Location: Basolateral membrane of tubular cells. Mechanism: ○ Na+/K+ ATPase actively transports Na+ out of tubular cells into the interstitial fluid. ○ This creates a concentration gradient favoring Na+ entry from the tubular lumen into the cells. 4. "Downhill" Entry of Na+ Varies across tubule segments: 1. Proximal Tubule: Na+ entry is coupled with the reabsorption of glucose, amino acids, and other solutes via symporters. 2. Thick Ascending Loop of Henle: Na+ entry is coupled with Cl^- and K+ via the Na+-K+-2Cl^- symporter. 3. Distal Tubule: Na+ entry occurs through Na+-Cl^- symporters. 4. Collecting Duct: Na+ entry is through epithelial sodium channels (ENaCs) regulated by aldosterone. Water Reabsorption and Permeability 5. Coupling of Water Reabsorption with Na+ Water reabsorption occurs via osmosis, following solute reabsorption (Na+). Permeability Varies: ○ Proximal tubule: High permeability due to abundant aquaporins. ○ Loop of Henle: Descending limb: Permeable to water. Ascending limb: Impermeable to water. ○ Collecting duct: Water permeability depends on ADH presence. Vasopressin (ADH) Mechanism 6. Vasopressin (ADH) Mechanism: ○ ADH binds to V2 receptors on collecting duct cells. ○ Increases insertion of aquaporins (AQP2) into the apical membrane. ○ Enhances water reabsorption, concentrating urine. Site of Action: Late distal tubule and collecting duct. 7. Water vs. Osmotic Diuresis Water Diuresis: ○ Increased water excretion due to low ADH levels. ○ Produces dilute urine. Osmotic Diuresis: ○ Increased urine production due to the presence of non-reabsorbed solutes (e.g., glucose in diabetes mellitus). ○ Water follows the solutes, leading to a loss of both water and solutes in urine. Key Concepts Solute Loss and Water Loss: ○ Any solute lost in urine must be accompanied by water.  ○ Water loss can occur independently of solutes, particularly in water diuresis. Active Study Tips 1. Draw It Out: ○ Create a nephron diagram showing Na+ and water reabsorption pathways. ○ Highlight ADH’s role and how aquaporins regulate water reabsorption. 2. Flowchart: ○ Map fluid and osmolarity changes in response to water/Na+ loss or gain. 3. Table: ○ Compare water diuresis vs. osmotic diuresis. Include causes, effects, and urine characteristics. 4. Concept Map: ○ Link Na+ transport, water reabsorption, ADH, and urine concentration changes. Vasopressin (ADH) Influence on Urine Volume and Osmolarity Vasopressin (ADH) is released in response to increased plasma osmolarity or decreased blood volume. It increases water reabsorption in the kidneys by inserting aquaporin-2 channels into the collecting duct's epithelial cells. This reduces urine volume and increases its osmolarity. Role of Na+ in Maintaining Extracellular Fluid Volume Sodium (Na⁺) is the primary extracellular cation, and its concentration governs extracellular fluid volume. Water follows Na⁺ due to osmosis, so Na⁺ retention increases extracellular fluid volume, whereas Na⁺ loss decreases it. This balance is crucial for maintaining blood pressure and overall homeostasis. Sodium Balance, Blood Volume, and Arterial Blood Pressure Sodium Balance: Increased sodium retention raises extracellular fluid volume and blood pressure. Blood Volume: Directly proportional to sodium levels due to osmotic effects. Arterial Blood Pressure: Increased extracellular fluid and blood volume raise arterial pressure, while losses in sodium and water lower it. Renin-Angiotensin System (RAS)  1. Factors Initiating Renin Release: ○ Decreased renal perfusion (low blood pressure). ○ Sympathetic stimulation (β1-adrenergic receptors). ○ Decreased Na⁺ delivery to the macula densa. 2. Pathway from Angiotensinogen to Angiotensin II: ○ Renin converts angiotensinogen (from the liver) into angiotensin I. ○ Angiotensin-converting enzyme (ACE) converts angiotensin I into angiotensin II (ANGII). 3. Effects of ANGII on Target Tissues: ○ Kidneys: Stimulates Na⁺ reabsorption. ○ Adrenal Glands: Promotes aldosterone secretion. ○ Vasculature: Causes vasoconstriction, increasing blood pressure. ○ Brain: Triggers thirst and ADH release. Major Stimuli for Aldosterone Release 1. Increased plasma K⁺ levels (hyperkalemia). 2. Angiotensin II via RAS activation. 3. ACTH (minor influence). 4. Decreased Na⁺ levels or blood volume/pressure. Aldosterone Effect on the Nephron Target Tubule Segments: Distal convoluted tubule and collecting ducts. Transport Mechanisms Altered: ○ Increases Na⁺ reabsorption via epithelial sodium channels (ENaC). ○ Enhances K⁺ excretion by upregulating ROMK channels. ○ Stimulates Na⁺/K⁺-ATPase pumps. Osmoreceptors and Vasopressin Secretion Definition: Specialized neurons in the hypothalamus sensitive to changes in plasma osmolarity. Function: When osmolarity increases, osmoreceptors signal the posterior pituitary to release vasopressin, enhancing water reabsorption and correcting osmolarity. Baroreceptors and Vasopressin Release Definition: Pressure-sensitive receptors in the aortic arch and carotid sinuses. Firing Rates: ○ Decreased blood pressure → Reduced baroreceptor firing → Increased vasopressin release. ○ Increased blood pressure → Enhanced baroreceptor firing → Decreased vasopressin release. Effect: Adjusts blood volume and pressure by influencing water retention. Decreased Extracellular Volume and Na⁺/Water Reabsorption 1. Decreased extracellular volume triggers: ○ Sympathetic activation → Increased renin release. ○ Angiotensin II → Enhances Na⁺ reabsorption in the proximal tubule. ○ Aldosterone → Promotes Na⁺ and water reabsorption in the distal tubule and collecting duct. 2. These mechanisms restore fluid balance and blood pressure. Digestion & Absorption Structures of the GI Tract Proper vs. Accessory Organs GI Tract Proper: Continuous tube including the mouth, esophagus, stomach, small intestine (duodenum, jejunum, ileum), large intestine, rectum, and anus. Accessory Organs: Organs that aid digestion but are not part of the continuous tube, including the salivary glands, liver, pancreas, and gallbladder. Primary Functions of the Digestive System 1. Digestion: Breakdown of macromolecules into absorbable units; occurs in the stomach, small intestine, and mouth. 2. Absorption: Uptake of nutrients into blood/lymph; occurs primarily in the small intestine. 3. Secretion: Release of enzymes, mucus, bile, and acids; occurs in the salivary glands, stomach, pancreas, liver, and small intestine. 4. Motility: Movement of food through the GI tract; occurs via peristalsis and segmentation. Segmental vs. Peristaltic Contractions Segmental Contractions: Mix contents; occur in the small intestine. Peristaltic Contractions: Propel contents forward; occur throughout the GI tract (e.g., esophagus, stomach, intestines). Fluid Balance in the Digestive System Sources: ~9 L enter the GI tract daily (2 L ingestion, 7 L secretions). Exits: ~8.9 L absorbed (7.5 L in the small intestine, 1.4 L in the colon), ~0.1 L excreted. Regulation of GI Function Neural: ENS (local reflexes) and CNS (vagal control). Hormonal: GI hormones like gastrin, CCK, and secretin. Local: Mechanical and chemical stimuli in the GI tract. Integration of ENS and CNS in Regulation ENS: Controls motility and secretion locally. CNS: Influences the ENS through autonomic input (parasympathetic promotes digestion; sympathetic inhibits). Major GI Hormones 1. Gastrin: Stimuli—protein, stomach distension; Target—parietal cells; Effect—stimulates HCl secretion. 2. CCK: Stimuli—fatty acids, amino acids; Target—pancreas, gallbladder; Effect—stimulates enzyme secretion, bile release. 3. Secretin: Stimuli—acidic chyme; Target—pancreas; Effect—stimulates bicarbonate secretion. Three Digestive Phases  1. Cephalic Phase: Stimulated by sight/smell of food. 2. Gastric Phase: Stimulated by food in the stomach. 3. Intestinal Phase: Stimulated by chyme in the small intestine. Composition of Saliva and Functions Mucus: Lubrication. Water: Dissolves food. Salivary Amylase: Begins carbohydrate digestion. Lysozyme: Antimicrobial action. HCl Production by Parietal Cells 1. Carbonic anhydrase catalyzes the formation of H⁺ and HCO₃⁻. 2. H⁺ secreted via H⁺/K⁺ ATPase. 3. Cl⁻ enters the lumen via Cl⁻ channels. Gastric Paracrine Secretions Histamine: Stimulates HCl secretion. Intrinsic Factor: Aids in vitamin B12 absorption. Somatostatin: Inhibits HCl secretion. Integrated Gastric Functions HCl: Protein denaturation, pepsin activation. Pepsin: Protein digestion. Gastric Lipase: Fat digestion. Importance of Stomach's Acidic Environment Low pH activates pepsinogen, denatures proteins, and kills pathogens. Divisions of the Small Intestine Duodenum: Digestion, neutralization of chyme. Jejunum: Primary site of absorption. Ileum: Absorption of bile salts, vitamin B12. Fat Emulsification Emulsifiers: Bile salts from the liver. Importance: Increases fat surface area for enzyme action. Intestinal Structures and Functions Villi/Microvilli: Increase surface area. Brush Border Enzymes: Aid digestion. Crypts: Secrete intestinal fluids. Lacteals: Absorb fats. Absorption of Salts and Water Active Na⁺ transport drives water absorption via osmosis. Secretions of Liver, Pancreas, and Gallbladder Liver: Bile production. Pancreas: Enzymes (amylase, lipase, proteases) and bicarbonate. Gallbladder: Bile storage and release. Neutralization of Acidic Chyme Pancreatic bicarbonate neutralizes acidic chyme in the duodenum. Brush Border Enzymes  Definition: Enzymes anchored to enterocyte membranes. Function: Increase digestion efficiency. Bile Pathway and Gallbladder Function Pathway: Liver → Bile ducts → Gallbladder → Duodenum. Hormone: CCK stimulates bile release. Emulsification by Bile Salts Amphipathic structure surrounds fats, breaking them into micelles for enzymatic digestion. Large Intestine Functions Absorbs water, electrolytes, and forms feces. Protection from Autodigestion Mucus Layer: Protects epithelial cells. Bicarbonate: Neutralizes acid near cells. Effects of Drugs on Gastric Function H2 Antagonists: Block histamine, reducing HCl. Proton Pump Inhibitors: Inhibit H⁺/K⁺ ATPase, reducing acidity. Antacids: Neutralize gastric acid. Importance of Inactive Enzymes Zymogens (e.g., pepsinogen) prevent autodigestion. Found in the stomach and pancreas. Metabolism Fed (Absorptive) vs. Fasted (Post-Absorptive) States Aspect Fed (Absorptive) Fasted (Post-Absorptive) Timing After eating (postprandial) Hours after eating (preprandial) Primary Goal Storage and utilization of ingested Mobilization of energy stores to nutrients maintain homeostasis Hormonal Dominated by insulin Dominated by glucagon, cortisol, Control and epinephrine Energy Dietary glucose, lipids, amino acids Glycogenolysis, lipolysis, Sources gluconeogenesis, proteolysis Processes Anabolism (storage): glycogenesis, Catabolism: glycogenolysis, lipogenesis, protein synthesis gluconeogenesis, lipolysis, ketogenesis Fates of Ingested Biomolecules 1. Energy Production: Immediate ATP synthesis via glycolysis and oxidative phosphorylation. 2. Synthesis: Building blocks for proteins, nucleotides, and membranes. 3. Storage: Excess stored as glycogen (carbohydrates) or triglycerides (lipids). Major Storage Sites for Nutrients 1. Carbohydrates: Stored as glycogen in the liver and skeletal muscle. 2. Lipids: Stored as triglycerides in adipose tissue.  3. Proteins: Stored as functional proteins in skeletal muscle (not a primary energy store). Nutrient Storage Site Composition Carbs Liver, muscle Glycogen (polymer of glucose) Lipids Adipose tissue Triglycerides (fatty acids + glycerol) Proteins Skeletal Amino acids (functional proteins) muscle Definitions Metabolism: Sum of all chemical reactions in the body. Anabolism: Building molecules (e.g., glycogenesis, lipogenesis, protein synthesis). Catabolism: Breaking molecules (e.g., glycolysis, glycogenolysis, proteolysis). Anabolism vs. Catabolism Aspect Anabolism Catabolism Purpose Build molecules, store energy Break molecules, release energy Example Glycogenesis, lipogenesis, protein Glycogenolysis, lipolysis, s synthesis proteolysis Energy Requires ATP Produces ATP Carbohydrate, Lipid, and Protein Metabolism State Carbohydrates Lipids Proteins Fed Glycogenesis, glycolysis Lipogenesis Protein synthesis Faste Glycogenolysis, Lipolysis, Proteolysis, d gluconeogenesis ketogenesis gluconeogenesis Roles of Major Organs in Metabolism Organ Carbohydrates Lipids Proteins Liver Glycogenesis, Lipogenesis, ketogenesis Protein synthesis, gluconeogenesis deamination Adipose Minimal glycogen Lipogenesis, lipolysis None Tissue storage Skeletal Glycogenesis, Fatty acid oxidation Proteolysis during Muscle glycogenolysis during exercise fasting Hormonal Effects on Metabolism Hormone Effect Source Target Tissues Insulin Promotes storage and anabolism β-cells of Liver, muscle, adipose pancreas tissue Glucago Promotes catabolism and glucose α-cells of Liver n release pancreas Cortisol Promotes gluconeogenesis, Adrenal cortex Liver, muscle, adipose proteolysis tissue Blood Glucose Regulation Insulin: Decreases blood glucose by promoting glucose uptake and storage. Glucagon: Increases blood glucose by promoting glycogenolysis and gluconeogenesis. Insulin Reflex Pathway 1. Increased blood glucose → β-cells secrete insulin. 2. Insulin promotes glucose uptake (via GLUT4), glycogenesis, and lipogenesis. 3. Decreased blood glucose provides feedback. Glucagon Reflex Pathway 1. Decreased blood glucose → α-cells secrete glucagon. 2. Glucagon stimulates glycogenolysis and gluconeogenesis in the liver. 3. Blood glucose rises, inhibiting further glucagon release. Exercise and Stress Effects Exercise: Decreases plasma glucose due to muscle uptake; glucagon and epinephrine maintain levels. Stress: Cortisol increases gluconeogenesis and proteolysis. Fuel Use in Skeletal Muscle Exercise: Glucose and fatty acids are primary fuels; anaerobic metabolism produces lactate. Fasting: Fatty acids and ketones are primary fuels. Summary of Metabolic Changes in Diabetes 1. Type 1 Diabetes: Insulin deficiency → hyperglycemia, increased lipolysis, and ketogenesis. 2. Type 2 Diabetes: Insulin resistance → impaired glucose uptake and chronic hyperglycemia. 3. Insulin Excess: Hypoglycemia → confusion, weakness, or coma. Exercise Metabolism Glycolysis Overview Process: Glycolysis is a metabolic pathway that breaks down glucose (a six-carbon molecule) into two molecules of pyruvate (three-carbon molecules). It occurs in 10 enzymatic steps. Location: Cytoplasm of the cell. Reactants: Glucose, 2 NAD+, 2 ATP, 4 ADP, 4 Pi (inorganic phosphate). Products: 2 Pyruvate, 2 NADH, 4 ATP (net gain of 2 ATP). Fates of Pyruvate 1. Presence of Oxygen (Aerobic): Pyruvate enters the mitochondria, where it is converted to acetyl-CoA and further oxidized in the Krebs cycle (citric acid cycle), leading to the production of CO2, NADH, FADH2, and ATP. 2. Absence of Oxygen (Anaerobic): Pyruvate is converted to lactate (via lactate dehydrogenase) in the cytoplasm, regenerating NAD+ for continued glycolysis. ATP Production in Muscle Fibers 1. Phosphagen System: ATP is formed quickly from phosphocreatine; used for short bursts of intense activity. ○ Fuel: Phosphocreatine. 2. Glycolysis: Generates ATP anaerobically from glucose or glycogen; used for moderate-intensity, short-duration activity. ○ Fuel: Glucose, glycogen. 3. Oxidative Phosphorylation: ATP is produced aerobically in mitochondria using the electron transport chain; used for prolonged, low-intensity activity. ○ Fuel: Glucose, glycogen, fatty acids, amino acids. Contribution of Glycolysis During High-Intensity Exercise During high-intensity exercise, glycolysis provides a rapid source of ATP anaerobically. However, it is limited by the accumulation of lactate and hydrogen ions, contributing to muscle fatigue. Muscle Fatigue Mechanisms 1. High-Intensity, Short-Duration Exercise: ○ Accumulation of hydrogen ions (decreasing pH). ○ Depletion of phosphocreatine and ATP. ○ Disruption of calcium handling in muscle cells. 2. Low-Intensity, Long-Duration Exercise: ○ Depletion of glycogen stores. ○ Accumulation of metabolic byproducts (e.g., ammonia). ○ Central fatigue due to reduced neural drive. Muscle Fiber Types 1. Fast-Oxidative-Glycolytic (FOG): ○ Intermediate speed of contraction. ○ Moderate resistance to fatigue. ○ Uses both aerobic and anaerobic metabolism. 2. Slow-Oxidative (SO): ○ Slow contraction speed. ○ High resistance to fatigue. ○ Primarily relies on aerobic metabolism.  3. Fast-Glycolytic (FG): ○ Fast contraction speed. ○ Low resistance to fatigue. ○ Relies on anaerobic glycolysis. Cardiac Output (CO) Definition: The volume of blood pumped by the heart per minute. Units: Liters per minute (L/min). Calculation: CO=Stroke Volume (SV)×Heart Rate (HR)\text{CO} = \text{Stroke Volume (SV)} \times \text{Heart Rate (HR)} Effect of HR and SV on CO Increased HR: Typically increases CO unless it compromises ventricular filling. Increased SV: Directly increases CO. VO2max Definition: The maximum rate of oxygen consumption during intense exercise; indicates aerobic fitness. Blood Gas Changes During Exercise Rest to ~25% Max Effort: Minimal changes; oxygen delivery meets demand. Rest to ~95% Max Effort: ○ Arterial O2: Relatively stable (unless respiratory limitation). ○ Venous O2: Decreases significantly due to increased extraction by muscles. Physiological Responses to Intense Exercise 1. Cardiovascular: Increased HR, SV, and CO; redistribution of blood to active muscles. 2. Ventilatory: Increased ventilation rate and tidal volume.  3. Metabolic: Increased reliance on glycolysis and oxidative phosphorylation. Variables Distinguishing Cardiovascular Fitness VO2max. Lactate threshold. Recovery rate of HR and VO2 after exercise. Hemodynamics and Oxygen Delivery During exercise, increased CO, enhanced vasodilation in active muscles, and higher oxygen extraction improve oxygen delivery. Absolute vs. Relative Oxygen Consumption Absolute VO2: Measured in L/min; does not account for body size. Relative VO2: Measured in mL/kg/min; normalizes for body weight, allowing comparison between individuals. Reproductive Spermatogenesis vs. Spermiogenesis Spermatogenesis: The process of forming mature sperm cells (spermatozoa) from spermatogonia through mitotic and meiotic divisions in the seminiferous tubules. Spermiogenesis: The final stage of spermatogenesis where round spermatids differentiate into elongated, motile spermatozoa without further division. Comparison: Spermatogenesis includes mitosis, meiosis, and differentiation, whereas spermiogenesis only involves morphological changes. Spermatogenesis forms haploid cells, while spermiogenesis prepares them for functionality. Steps of Spermatogenesis 1. Spermatogonia (stem cells) undergo mitosis to produce primary spermatocytes. 2. Primary spermatocytes (diploid) enter meiosis I to form secondary spermatocytes. 3. Secondary spermatocytes (haploid) undergo meiosis II to form spermatids. 4. Spermatids undergo spermiogenesis to develop into spermatozoa. Roles of Sertoli and Leydig Cells: Sertoli Cells: Support and nourish developing sperm, form the blood-testis barrier, and secrete inhibin and androgen-binding protein (ABP). Leydig Cells: Located in interstitial spaces, they secrete testosterone in response to LH. Endocrine Control of Spermatogenesis 1. GnRH from the hypothalamus stimulates the anterior pituitary to release FSH and LH. 2. FSH acts on Sertoli cells to support spermatogenesis and secrete ABP. 3. LH stimulates Leydig cells to produce testosterone, essential for spermatogenesis. 4. Testosterone and inhibin provide negative feedback to the hypothalamus and anterior pituitary. Phases of the Ovarian Cycle 1. Follicular Phase: Follicle growth; granulosa and theca cells produce estrogen. 2. Ovulation: Triggered by an LH surge; release of a mature oocyte. 3. Luteal Phase: Formation and function of the corpus luteum, which secretes progesterone and estrogen. Oogenesis vs. Folliculogenesis Oogenesis: Formation of a mature egg from oogonia through mitosis, meiosis, and maturation. Folliculogenesis: Development of ovarian follicles (structures housing the oocyte). Comparison: Oogenesis involves the oocyte; folliculogenesis involves supporting cells (granulosa, theca). Oogenesis begins before birth; folliculogenesis begins at puberty with each cycle. Corpus Luteum Formation After ovulation, granulosa and theca cells transform into luteal cells, forming the corpus luteum. These cells secrete large amounts of progesterone and some estrogen to support potential pregnancy. Corpus Luteum Degradation If fertilization does not occur, the corpus luteum degenerates into the corpus albicans, a fibrotic remnant. Progesterone and estrogen levels drop, triggering menstruation. Folliculogenesis Stages 1. Primordial Follicle: Inactive oocyte surrounded by squamous granulosa cells. 2. Primary Follicle: Oocyte growth, cuboidal granulosa cells. 3. Secondary Follicle: Formation of theca layer and follicular fluid. 4. Tertiary (Graafian) Follicle: Mature follicle ready for ovulation. Roles of Cells: Granulosa Cells: Support oocytes, produce estrogen, respond to FSH. Theca Cells: Produce androgens, precursors to estrogen. Hypothalamic-Pituitary-Gonad Axis (Female) 1. GnRH stimulates FSH and LH release. 2. FSH promotes follicle growth and estrogen production. 3. LH induces ovulation and corpus luteum formation. 4. Estrogen, progesterone, and inhibin provide feedback regulation. Hormonal Patterns During the Ovarian Cycle Follicular Phase: Rising FSH, LH, and estrogen; low progesterone. Ovulation: Estrogen peaks, triggering an LH surge. Luteal Phase: High progesterone and moderate estrogen; FSH and LH suppressed. Ovulation The release of a secondary oocyte from the mature follicle occurs during the LH surge, following a peak in estrogen. Uterine Cycle Phases 1. Menstrual Phase: Shedding of the endometrial lining. 2. Proliferative Phase: Endometrium thickens under estrogen's influence. 3. Secretory Phase: Progesterone prepares the endometrium for implantation. Oocyte Pathway Ovary → Fimbriae → Fallopian Tube → Uterus. Hormonal Roles in Reproduction GnRH: Stimulates FSH, LH release. FSH: Stimulates follicle growth and Sertoli cell function. LH: Triggers ovulation, Leydig cell function. Estrogen: Supports follicular development, uterine growth. Progesterone: Maintains uterine lining, inhibits GnRH during luteal phase. Inhibin: Suppresses FSH. Fertilization vs. Non-Fertilization Fertilization: Corpus luteum maintained by hCG; high progesterone and estrogen. No Fertilization: Corpus luteum degenerates; hormone levels drop, cycle restarts. Oocyte vs. Sperm Production Oocyte: One gamete per meiosis; meiosis begins in the fetus, completes after fertilization.  Sperm: Four gametes per meiosis; continuous production after puberty. Pregnancy and Ovulation Detection Kits Pregnancy Tests: Detect hCG, accurate post-implantation. Ovulation Tests: Detect LH surge, indicating imminent ovulation. Exam 4 Question Categories Renal Physiology 1. Filtration Membrane ○ Consists of the glomerular endothelium, basement membrane, and podocytes. ○ Filters blood to form the glomerular filtrate. 2. Nephron & Collecting Duct Anatomy ○ Nephron: Functional unit of the kidney with components like Bowman's capsule, proximal tubule, loop of Henle, distal tubule, and collecting duct. 3. Filtration, Reabsorption, Secretion ○ Filtration: Movement of substances from blood to filtrate in Bowman's capsule. ○ Reabsorption: Reclaiming water, ions, and nutrients back into blood. ○ Secretion: Active transport of substances from blood to nephron tubules. 4. GFR & Starling Forces ○ GFR: Rate of filtrate formation in glomeruli, influenced by hydrostatic and osmotic pressures. 5. Renal Clearance ○ Volume of plasma cleared of a substance per unit time, reflecting kidney function. 6. Sodium & Molecular Transport ○ Sodium plays a critical role in ion gradients and reabsorption processes via active and passive transport. 7. Countercurrent Multiplication & Vasa Recta ○ Mechanism in the loop of Henle for concentrating urine, supported by vasa recta to maintain medullary gradient.  8. Hormonal Control ○ ADH, aldosterone, ANP, and renin regulate fluid balance, ion concentrations, and blood pressure. Digestive System 1. Functions ○ Includes ingestion, digestion, absorption, and elimination. 2. Digestive Fluid Balance ○ Coordination of secretions (saliva, bile, pancreatic juice) and absorption of water. 3. GI Hormones ○ Key hormones: Gastrin, CCK, secretin, GIP, and motilin. 4. Digestive Phases ○ Cephalic, gastric, and intestinal phases coordinate digestion. 5. HCl Production & Regulation ○ Parietal cells secrete HCl; regulated by gastrin, histamine, and vagal stimulation. 6. Pepsinogen & Zymogen Activation ○ Pepsinogen (inactive) converts to pepsin (active) in acidic environments. 7. Carbohydrate & Protein Digestion ○ Carbohydrates: Broken down to monosaccharides. ○ Proteins: Hydrolyzed to amino acids by proteases. 8. Fat Digestion & Bile ○ Lipases and bile emulsify fats for absorption. 9. Macronutrient Absorption ○ Nutrients absorbed primarily in the small intestine. 10. Fed/Absorptive State ○ Anabolic processes predominate; glucose used for energy or stored. 11. Fasted/Post-Absorptive State ○ Catabolic processes release stored energy substrates (e.g., glycogenolysis).  12. Blood Glucose & Hormones ○ Insulin and glucagon regulate glucose homeostasis. 13. Amino Acids, Fat & Hormones ○ Metabolism influenced by insulin, glucagon, and other regulatory hormones. 14. Diabetes, Exercise & Hormonal Responses ○ Diabetes disrupts glucose regulation; exercise improves sensitivity and energy metabolism. Reproductive Physiology 1. Spermatogenesis & Spermiogenesis ○ Process of sperm production in seminiferous tubules and maturation. 2. Oogenesis & Folliculogenesis ○ Development of ova in ovaries and maturation of follicles. 3. Gametogenesis Comparison ○ Differences in male (continuous) vs. female (cyclic and finite) gamete production. 4. Granulosa & Theca Cells + Estrogen ○ Granulosa: Estrogen production via aromatase. ○ Theca: Androgen synthesis, precursor for estrogen. 5. Hypothalamic-Pituitary-Gonadal Axis ○ Hormonal regulation of reproduction involving GnRH, LH, and FSH. 6. Ovarian Cycle & Hormones ○ Follicular, ovulatory, and luteal phases orchestrated by FSH, LH, and ovarian hormones. 7. Ovulation & Hormones ○ Triggered by LH surge; essential for releasing a mature oocyte. 8. Uterine Cycle & Hormones ○Menstrual, proliferative, and secretory phases guided by estrogen and progesterone. 9. Hormones & Birth Control/Pregnancy/Menopause  ○ Birth control manipulates hormonal cycles. ○ Pregnancy maintains progesterone and estrogen. ○ Menopause involves estrogen and progesterone decline. With specific reference to feedback loops explain how hormonal birth control such as the combination pill (estrogen + progesterone) works as a contraceptive method Hormonal birth control methods like the combination pill work primarily by disrupting the natural hormonal feedback loops that regulate the menstrual cycle. Here's how this happens with specific reference to feedback loops: 1. Normal Feedback Loops in the Menstrual Cycle: ○ The menstrual cycle is controlled by a feedback loop involving the hypothalamus, pituitary gland, and ovaries. ○ The hypothalamus releases gonadotropin-releasing hormone (GnRH), which stimulates the pituitary to produce luteinizing hormone (LH) and follicle-stimulating hormone (FSH). ○ LH and FSH regulate ovarian functions, such as follicle development and ovulation. ○ The ovaries produce estrogen and progesterone, which provide negative feedback to the hypothalamus and pituitary to modulate hormone levels. 2. Effect of the Combination Pill: ○The combination pill contains synthetic forms of estrogen and progesterone, which mimic the effects of these natural hormones. ○ High levels of these synthetic hormones in the bloodstream create a negative feedback loop that suppresses the release of GnRH from the hypothalamus and LH and FSH from the pituitary gland. 3. Disruption of Ovulation: ○ Without adequate FSH, follicles in the ovaries do not mature. ○ Without the LH surge, ovulation (release of an egg) does not occur. This is the primary contraceptive effect of the combination pill. 4. Additional Contraceptive Mechanisms: ○ Progesterone effects: The synthetic progesterone thickens the cervical mucus, making it more difficult for sperm to travel through the cervix and reach an egg.  ○ Endometrial changes: The endometrium (uterine lining) is kept in a state less conducive to implantation of a fertilized egg. By altering the hormonal feedback loops and physiological conditions necessary for conception, the combination pill effectively prevents pregnancy. Fabian Study Guide Renal Physiology Definitions: 1. Filtration: ○The movement of water and solutes from the blood in the glomerulus into Bowman’s space. ○ Driven by glomerular filtration pressure, it allows small molecules (e.g., water, glucose, sodium) to pass while excluding larger molecules like proteins. 2. Reabsorption: ○ The transfer of substances from the tubular lumen back into the capillaries. ○ Helps reclaim essential molecules such as glucose, amino acids, and sodium. 3. Secretion: ○ The movement of substances from the capillaries into the tubular lumen for excretion. ○ Includes waste products like hydrogen ions (H+) and potassium (K+). Key Nephron Regions: 1. Proximal Tubule: ○ Major site for reabsorption (glucose, amino acids, sodium, water) and secretion (H+, organic acids/bases). 2. Loop of Henle: ○ Concentrates urine via a countercurrent mechanism. ○ Descending limb: Water reabsorption. ○ Ascending limb: Active reabsorption of Na+, Cl– (impermeable to water). 3. Distal Tubule: ○ Fine-tunes sodium and potassium balance under aldosterone control. 4. Collecting Duct:  ○ Regulates water reabsorption via ADH and sodium reabsorption through aldosterone. Filtration, Reabsorption, and Secretion: Filtered substances: Water, glucose, amino acids, ions (Na+, K+, Cl−, HCO3−), urea, and creatinine. Reabsorbed substances: ○ Almost complete: Glucose, amino acids, bicarbonate. ○ Regulated: Sodium, water. Secreted substances: H+, K+, drugs, and organic acids/bases. Hormonal Regulation of Kidney Function: 1. ADH (Antidiuretic Hormone): ○ Increases water reabsorption in the collecting duct by inserting aquaporins into the membrane. ○ Triggered by high plasma osmolality or low blood volume. 2. Aldosterone: ○ Acts on the distal tubule and collecting duct. ○ Enhances sodium reabsorption and potassium secretion by upregulating sodium-potassium pumps and sodium channels. ○ Responds to low blood volume or pressure. 3. Renin in RAAS: ○ Secreted by the juxtaglomerular cells of the kidney in response to low blood pressure. ○ Converts angiotensinogen (from the liver) to angiotensin I, which is further converted to angiotensin II by ACE. ○ Angiotensin II stimulates aldosterone release, vasoconstriction, and thirst. Glomerular Filtration Pressure: 1. Determinants: ○ Hydrostatic pressure: Pressure exerted by blood in the glomerulus (favors filtration).  ○ Osmotic pressure: Opposing force due to plasma proteins in the capillaries. ○ Bowman’s capsule pressure: Opposing force due to fluid in Bowman’s space. 2. Net Filtration Pressure (NFP): ○ NFP=Glomerular hydrostatic pressure−(Plasma osmotic pressure+Bowman’s capsule pressure)\text{NFP} = \text{Glomerular hydrostatic pressure} - (\text{Plasma osmotic pressure} + \text{Bowman’s capsule pressure}). Active Learning Strategies: Flowchart: Filtration: Blood → Glomerulus → Bowman’s space → Filtrate (excludes proteins like albumin). Reabsorption: Proximal tubule → Glucose, Na+, water reclaimed to blood. Secretion: Distal tubule → H+, K+ secreted into tubule for excretion. Venn Diagram: ADH: ○ Directly affects water reabsorption. ○ Dysregulation: Diabetes insipidus (polyuria due to impaired water retention). Aldosterone: ○ Sodium reabsorption, potassium secretion. ○ Dysregulation: Addison’s disease (low sodium retention, hyperkalemia). Practice Calculation: Given: ○ Glomerular hydrostatic pressure = 69 mmHg ○ Plasma osmotic pressure = 30 mmHg ○ Bowman’s capsule pressure = 15 mmHg ○ NFP=69−(30+15)=24 mmHg\text{NFP} = 69 - (30 + 15) = 24 \, \text{mmHg}. If hydrostatic pressure drops to 50 mmHg: ○ NFP=50−(30+15)=5 mmHg\text{NFP} = 50 - (30 + 15) = 5 \, \text{mmHg}. ○ Result: Reduced filtration rate due to lower driving force for filtration. Gastrointestinal Physiology Phases of Digestion: 1. Cephalic Phase:  ○ Trigger: Sight, smell, taste, or thought of food. ○ Nerves and Hormones: Parasympathetic (vagus nerve) stimulates salivary glands, gastric glands, and pancreatic secretions. Gastrin release begins as vagal stimulation primes gastric secretion. 2. Gastric Phase: ○ Trigger: Stomach distension and presence of proteins/peptides. ○ Nerves and Hormones: Parasympathetic (vagus nerve) continues stimulation. Gastrin is released from G cells, promoting acid secretion by parietal cells and stimulating gastric motility. 3. Intestinal Phase: ○ Trigger: Presence of chyme in the small intestine (especially fatty or acidic chyme). ○ Nerves and Hormones: Hormones: Cholecystokinin (CCK), secretin, and gastric inhibitory peptide (GIP). CCK and secretin inhibit gastric emptying while stimulating digestion in the duodenum. Enteric nerves mediate motility and secretory responses. Enzymes and Hormonal Regulation: 1. Gastrin: ○ Role: Stimulates acid production by parietal cells in the stomach. ○ Mechanism: Enhances secretion of hydrochloric acid (HCl) and promotes gastric motility. 2. CCK (Cholecystokinin): ○ Role: Influences bile release and pancreatic enzyme secretion. ○ Mechanism: Stimulates gallbladder contraction, releasing bile into the duodenum. Enhances secretion of digestive enzymes (lipases, amylases, proteases) from the pancreas. 3. Secretin: ○ Role: Stimulates bicarbonate release from the pancreas and bile ducts. ○ Mechanism: Neutralizes acidic chyme in the duodenum, providing an optimal pH for digestive enzymes. Fat Digestion, Absorption, and Transport: 1. Role of Bile: ○ Emulsifies fats into micelles, increasing the surface area for pancreatic lipase action. 2. Absorption of Fatty Acids: ○ Fatty acids and monoglycerides diffuse into intestinal epithelial cells. ○ Inside cells, they are reassembled into triglycerides and packaged into chylomicrons. ○ Chylomicrons are transported via the lymphatic system to the bloodstream. 3. Disruption of Bile Production/Release: ○ Impairs fat emulsification. ○ Leads to incomplete fat digestion and absorption, resulting in steatorrhea (fatty stools). Active Learning Strategies: Flowchart: Step-by-step Fat Digestion: 1. Mouth: Minimal digestion of fats. 2. Stomach: Gastric lipase partially breaks down fats. 3. Small Intestine: CCK triggers bile release and pancreatic enzyme secretion. Bile emulsifies fats; lipase converts triglycerides into free fatty acids and monoglycerides. 4. Absorption: Fatty acids form micelles for transport into epithelial cells, where they are packaged into chylomicrons. 5. Transport: Chylomicrons enter lymphatic vessels (lacteals) and eventually the bloodstream. Case Study: Absence of Gallbladder: Physiological Impact: ○ The gallbladder stores and concentrates bile. Without it, bile flows continuously into the intestine, but in less concentrated amounts.  ○ Fatty meals require higher bile concentrations for effective emulsification. GI Discomfort: ○ Incomplete fat digestion leads to undigested fats in the colon, causing bloating, diarrhea, and cramping. Comparison Table: Hormone Stimulus Target Effects Gastrin Protein in stomach, Parietal cells Increases HCl secretion, enhances stomach distension (stomach) gastric motility CCK Fatty acids, amino Gallbladder, Stimulates bile release, pancreatic acids in duodenum pancreas enzyme secretion, inhibits gastric emptying Secretin Acidic chyme in Pancreas, bile Stimulates bicarbonate secretion, duodenum ducts neutralizes acid Endocrine Physiology Hormonal Regulation of Reproduction: 1. FSH and LH in Follicle Maturation and Ovulation: ○FSH (Follicle-Stimulating Hormone): Promotes the growth and maturation of ovarian follicles. Stimulates granulosa cells to produce estrogen. ○ LH (Luteinizing Hormone): Surge triggers ovulation (release of the oocyte). Stimulates the formation of the corpus luteum and production of progesterone. 2. Negative Feedback of Estrogen and Progesterone on GnRH: ○ Moderate levels of estrogen inhibit GnRH, FSH, and LH to prevent premature follicular growth. ○ High progesterone levels during the luteal phase suppress GnRH, maintaining a stable environment for implantation.  3. Role of Inhibin: ○ Secreted by granulosa cells (follicular phase) and the corpus luteum (luteal phase). ○ Specifically inhibits FSH to prevent the recruitment of additional follicles during the current cycle. Menstrual Cycle Phases and Hormonal Patterns: 1. Follicular Phase: ○ Hormonal Changes: FSH rises, stimulating follicle growth. Rising estrogen (produced by growing follicles) triggers the proliferation of the endometrium. ○ Endometrial Phase: Proliferative phase (thickening of the endometrial lining). ○ Ends with an LH surge, triggering ovulation. 2. Luteal Phase: ○ Hormonal Changes: After ovulation, the corpus luteum produces high progesterone and moderate estrogen. Progesterone prepares the endometrium for implantation and inhibits further follicular development. ○ Endometrial Phase: Secretory phase (glandular secretion and vascularization). ○ If no pregnancy occurs, corpus luteum degenerates, hormone levels drop, and menstruation begins. Hormones Regulating Blood Glucose: 1. Insulin vs. Glucagon: ○ Insulin (fed state): Promotes glucose uptake by cells, glycogenesis, and fat storage. ○ Glucagon (fasting state): Stimulates glycogenolysis and gluconeogenesis to increase blood glucose. 2. Epinephrine and Cortisol (Stress/Exercise): ○ Epinephrine: Increases glycogenolysis and lipolysis for quick energy. ○ Cortisol: Supports long-term energy needs by promoting gluconeogenesis and inhibiting glucose uptake in tissues. Active Learning Strategies: Flowchart: Menstrual Cycle: Days 1-14: Follicular phase. ○ Rising FSH → follicle growth → increased estrogen → endometrial proliferation. ○ Estrogen peak → LH surge → ovulation (~day 14). Days 15-28: Luteal phase. ○ Corpus luteum → progesterone dominance → endometrial secretion phase. ○ Hormone decline → menstruation if no pregnancy. Focus Question: Hormonal Changes After Ovulation: Progesterone rises significantly (produced by the corpus luteum). Estrogen remains moderate. High progesterone marks the luteal phase and supports implantation. Case Study: High Progesterone, Low Estrogen, Last Period 10 Days Ago: ○ She is likely in the early luteal phase. ○ Ovulation likely occurred 2-3 days ago (day ~12-13 of a 28-day cycle). Diagram: Glucose Regulation: High-Carbohydrate Meal: ○ Blood glucose rises → pancreas secretes insulin → glucose uptake by cells, glycogen formation. Prolonged Fasting: ○ Blood glucose drops → pancreas secretes glucagon → glycogen breakdown, gluconeogenesis. Summary Feedback Loops:  1. Insulin Feedback: High glucose → insulin secretion → glucose uptake/storage → glucose level decreases → insulin decreases. 2. Glucagon Feedback: Low glucose → glucagon secretion → glycogen breakdown → glucose level increases → glucagon decreases. Reproductive Physiology Follicular vs. Luteal Phases: 1. Hormone Levels: ○ Follicular Phase (Days 1-14): FSH: Elevated initially to recruit follicles, then declines as inhibin and estrogen increase. LH: Low but steady, with a surge near ovulation (~Day 14). Estrogen: Rises significantly due to growing follicles, peaking just before ovulation. Progesterone: Low throughout the phase. ○ Luteal Phase (Days 15-28): FSH and LH: Decline due to negative feedback from progesterone. Estrogen: Moderate levels maintained by the corpus luteum. Progesterone: Rises significantly, dominating the luteal phase. 2. Transition Between Phases: ○ Marked by the LH surge, which triggers ovulation and the transformation of the dominant follicle into the corpus luteum. Role of Hormones in Ovulation and Follicle Dominance: 1. Dominant Follicle Selection: ○ The follicle with the most FSH receptors and highest estrogen production becomes dominant. ○ Rising estrogen and inhibin suppress FSH, starving other follicles of stimulation. 2. Inhibin’s Role: ○ Secreted by granulosa cells of the dominant follicle. ○ Inhibits FSH to prevent the recruitment of additional follicles during the current cycle. LH and FSH Levels Across Life Stages: 1. Normal Menstrual Cycle: ○ FSH peaks in the early follicular phase and declines. ○ LH surges mid-cycle to trigger ovulation. ○ Progesterone dominates the luteal phase. 2. Pregnancy: ○FSH and LH are suppressed by high levels of hCG (human chorionic gonadotropin), estrogen, and progesterone from the placenta. 3. Menopause: ○FSH and LH levels rise due to the lack of ovarian response and reduced negative feedback from estrogen and inhibin. 4. Hormonal Birth Control: ○ Suppresses FSH and LH by maintaining steady levels of synthetic estrogen and/or progestins, preventing ovulation. Timeline of Hormonal Changes: 1. Days 1-14 (Follicular Phase): ○ FSH rises, then falls. ○ Estrogen rises steadily, peaking before ovulation. ○ LH remains low until a surge on Day 14. 2. Days 15-28 (Luteal Phase): ○ LH and FSH fall after ovulation. ○ Progesterone rises sharply, dominating this phase. ○ Estrogen maintains moderate levels. Disruptions: 1. Menopause: ○ No follicles respond to FSH/LH, leading to high FSH and LH due to lack of negative feedback from estrogen and inhibin. 2. Birth Control:  ○ Suppresses LH and FSH to near baseline, preventing ovulation and follicle development. Case Study: Postmenopausal Female with High LH and FSH: 1. Why are LH and FSH elevated?: ○ Ovaries no longer produce sufficient estrogen or inhibin. ○ Lack of negative feedback leads to elevated LH and FSH secretion by the pituitary. 2. Disrupted Feedback: ○ Loss of ovarian hormones removes suppression of GnRH, leading to unchecked FSH and LH production. Venn Diagram: LH and FSH in Males vs. Females: Hormone Females Males Common Roles LH Triggers ovulation and Stimulates Leydig cells to Promotes steroid hormone supports corpus produce testosterone. synthesis (estrogen, luteum. testosterone). FSH Stimulates follicle Stimulates Sertoli cells for Supports gametogenesis growth and estrogen spermatogenesis. and gonadal function. production. Metabolism and Nutrition Hormonal Control of Metabolism: 1. Insulin: ○ Promotes Glucose Uptake:  Stimulates glucose transport into cells by activating GLUT-4 transporters in muscle and adipose tissue. ○ Glycogen Storage: Enhances glycogen synthesis in the liver and muscle by activating glycogen synthase and inhibiting glycogen breakdown. 2. Glucagon and Epinephrine: ○ Glucagon: Secreted during fasting, stimulates glycogenolysis (glycogen breakdown) and gluconeogenesis in the liver. ○ Epinephrine: Mobilizes energy during stress by promoting glycogenolysis in liver and muscle and enhancing lipolysis in adipose tissue. 3. Cortisol: ○ Released during long-term stress, it supports sustained energy by: Promoting gluconeogenesis. Increasing lipolysis and proteolysis to provide substrates for glucose production. Reducing glucose uptake by peripheral tissues to preserve glucose for vital organs. Digestion and Absorption of Macronutrients: 1. Carbohydrates: ○ Digestion: Begins with salivary amylase in the mouth and continues with pancreatic amylase in the small intestine. ○ Absorption: Glucose is absorbed via the SGLT-1 transporter (sodium-glucose cotransporter) in the small intestine and enters the bloodstream via GLUT-2. 2. Proteins: ○ Digestion: Starts in the stomach with pepsin (active at low pH). Continued by pancreatic proteases like trypsin and chymotrypsin in the small intestine. ○ Absorption: Amino acids are absorbed via sodium-dependent transporters into intestinal epithelial cells and then into the bloodstream. 3. Fats: ○ Digestion:  Bile emulsifies fats, and pancreatic lipase breaks them into fatty acids and monoglycerides. ○ Absorption: Fatty acids and monoglycerides are absorbed into enterocytes, reassembled into triglycerides, and packaged into chylomicrons for transport via the lymphatic system. Effects of pH Changes on Enzyme Activity: 1. Pepsin: ○ Requires an acidic pH (~1.5–3) to be activated from its precursor, pepsinogen. ○ Antacids raise stomach pH, reducing pepsin activity and impairing protein digestion. 2. Impact of Increased Stomach pH: ○ Protein digestion slows due to decreased pepsin activity. ○ Other enzymes like trypsin (active in the alkaline pH of the small intestine) are less affected. Diagrams and Active Learning: 1. Carbohydrate Digestion: ○ Mouth: Salivary amylase begins breaking starch into maltose. ○ Stomach: No carbohydrate digestion (acidic pH denatures amylase). ○ Small Intestine: Pancreatic amylase converts starch to maltose, maltotriose, and dextrins. Brush-border enzymes (e.g., maltase, sucrase, lactase) break these into glucose. ○ Absorption: Glucose enters enterocytes via SGLT-1 (coupled with Na+). Transported to blood via GLUT-2. 2. Case Study: Daily Antacid Use: ○ Effect on Enzyme Activity: Pepsin: Most impacted due to its reliance on acidic pH. Trypsin: Unaffected as it operates in the small intestine at neutral to alkaline pH. ○ Result:  Reduced protein digestion in the stomach, leading to discomfort and nutrient malabsorption. 3. Feedback Loop: Insulin and Glucagon: ○ High-Carbohydrate Meal: Blood glucose rises → pancreas secretes insulin → glucose uptake and glycogen synthesis increase → blood glucose decreases → insulin secretion declines. ○ Fasting: Blood glucose drops → pancreas secretes glucagon → glycogen breakdown and gluconeogenesis increase → blood glucose rises → glucagon secretion declines. Extension: Type I Diabetes/Insulin Resistance: Type I Diabetes: Insulin is absent, leading to unregulated blood glucose levels and reliance on glucagon-driven gluconeogenesis and lipolysis. Insulin Resistance: Cells fail to respond to insulin, causing elevated blood glucose and compensatory hyperinsulinemia. Fluid and Electrolyte Balance Effects of Hydration Status on Renal Water Reabsorption: 1. Role of Vasopressin (ADH): ○ ADH promotes water reabsorption by binding to V2 receptors in the kidney's collecting duct. ○ This stimulates the insertion of aquaporin-2 channels into the apical membrane of the collecting duct cells, allowing water to move from the tubular lumen into the interstitial space. 2. Overhydration (Low ADH): ○ With low ADH levels, aquaporins are absent, reducing water reabsorption. ○ Urine volume: High (dilute urine). ○ Urine concentration: Low. 3. Dehydration (High ADH): ○ With high ADH levels, more aquaporins are inserted, enhancing water reabsorption. ○ Urine volume: Low (concentrated urine). ○ Urine concentration: High. Role of ADH and RAAS in Hydration and Blood Pressure: 1. ACE Inhibitors and RAAS: ○ ACE inhibitors block the conversion of angiotensin I to angiotensin II. ○ Effects: Decreased vasoconstriction. Reduced aldosterone secretion, leading to lower sodium reabsorption and water retention. Lower blood pressure. 2. Stimuli for Renin Secretion: ○ Low blood pressure or volume sensed by juxtaglomerular cells. ○ Low sodium concentration in the distal tubule sensed by the macula densa. ○ Sympathetic nervous system activation. 3. Angiotensin II Effects: ○ Blood Pressure: Vasoconstriction increases systemic resistance, raising blood pressure. ○ Sodium Balance: Stimulates aldosterone secretion, promoting sodium reabsorption in the distal tubule and collecting duct. Enhances sodium and water reabsorption, increasing blood volume and pressure. Electrolyte Movement and Osmotic Gradients: 1. Chloride Movement and Water Transport: ○ Chloride is often co-transported with sodium, and its movement establishes osmotic gradients. ○ Water follows chloride and sodium through osmosis. 2. Impact of Cholera Toxin: ○ Cholera toxin causes excessive chloride secretion into the intestinal lumen via CFTR channels. ○ Disruption: Water follows chloride, leading to massive water loss in the form of diarrhea. Severe dehydration occurs due to osmotic imbalances.  3. Osmotic Balance: ○ Essential for maintaining cell integrity, fluid distribution, and proper organ function. ○ Imbalances in the intestine or kidney can lead to dehydration, edema, or other complications. Active Learning Strategies: 1. Diagram: RAAS: ○ Steps: Renin converts angiotensinogen (from the liver) into angiotensin I. ACE converts angiotensin I into angiotensin II. Angiotensin II acts to increase blood pressure and stimulate aldosterone release. ○ ACE Inhibitors: Block step 2, reducing angiotensin II levels, lowering blood pressure. 2. Case Study: Cholera: ○ Chloride Transport Disruption: Excess chloride in the intestinal lumen creates a high osmotic gradient. Water follows chloride into the lumen, causing diarrhea. ○ Risk of Dehydration: Rapid fluid loss decreases blood volume and blood pressure, leading to potential shock if untreated. 3. Scenario Practice: Alcohol and ADH: ○ Alcohol's Effect: Alcohol inhibits ADH secretion from the posterior pituitary. ○ Result: Reduced aquaporin insertion in the collecting ducts. Increased urine volume and decreased water reabsorption, leading to dilute urine and potential dehydration. Hormonal and Nervous Regulation Sympathetic and Parasympathetic Control in Digestion:  1. Parasympathetic Activation: ○During the cephalic phase (sight, smell, or thought of food), the vagus nerve stimulates: Salivary glands to produce saliva. Gastric glands to secrete gastric juice (acid and enzymes). Pancreatic enzyme release in preparation for digestion. 2. Sympathetic Activation: ○ During stress, sympathetic input: Reduces blood flow to the gastrointestinal tract. Decreases motility and secretions to conserve energy for the “fight-or-flight” response. Hormonal Responses During Stress and Exercise: 1. Epinephrine: ○ Secreted by the adrenal medulla during acute stress. ○ Effect: Stimulates glycogenolysis in the liver and skeletal muscles, releasing glucose into the bloodstream. Promotes lipolysis in adipose tissue to provide fatty acids for energy. 2. Cortisol: ○ Released by the adrenal cortex during prolonged stress or exercise. ○ Effect: Enhances gluconeogenesis (glucose production from non-carbohydrate sources). Mobilizes amino acids and fatty acids as substrates for energy. Baroreceptor Role in Hydration Status: 1. Response to Blood Pressure Changes: ○ Dehydration (Low Blood Pressure): Baroreceptors in the aorta and carotid arteries detect reduced stretch. Signal the hypothalamus to increase sympathetic activity and stimulate vasopressin (ADH) release.  ○ Overhydration (High Blood Pressure): Increased stretch inhibits ADH release, reducing water reabsorption in the kidneys. 2. Role of Vasopressin (ADH): ○ Restores fluid balance by: Increasing water reabsorption in the collecting ducts. Raising blood pressure through vasoconstriction. Active Learning Strategies: 1. Flowchart: Nervous System Regulation in the Cephalic Phase: ○ Parasympathetic Pathway: Stimulus: Sight, smell, or thought of food. Action: Vagus nerve activation → increased secretion of saliva, gastric juice, and pancreatic enzymes. ○ Sympathetic Pathway: Stimulus: Stress (e.g., fear, anxiety). Action: Inhibits GI blood flow and secretions to conserve energy for the “fight-or-flight” response. 2. Case Study: Watching a Scary Movie: ○ Symptoms: Increased heart rate, elevated blood glucose. ○ Hormones Involved: Epinephrine: Mobilizes energy by: Stimulating glycogenolysis in the liver. Increasing glucose availability to skeletal muscles and the brain. ○ Mechanism: Glucose is released into the bloodstream to fuel the heightened metabolic demands of the “fight-or-flight” state. 3. Feedback Loop: Baroreceptors and ADH Response to Dehydration: ○ Dehydration: Blood pressure drops → baroreceptors signal the hypothalamus → ADH is released. ADH increases water reabsorption in the kidneys and constricts blood vessels, raising blood volume and pressure. ○ Overhydration: Blood pressure rises → baroreceptors inhibit ADH secretion. Excess water is excreted, lowering blood pressure and restoring balance.