Practice 5 structured short- and long-answer medical questions on Weekly Year 1: Physiology Exam - August 7, 2026 (Sections B & C). Review model answers for...
Answer: 1. Sarcolemmal depolarization: An action potential travels along the sarcolemma and down the T-tubules. 2. Calcium release: T-tubule depolarization opens voltage-gated Ca2+ channels (DHP receptors), which are mechanically coupled to ryanodine receptors on the sarcoplasmic reticulum (SR). 3. SR Ca2+ release: Ryanodine receptors open, releasing Ca2+ from the SR into the sarcoplasm. 4. Troponin-tropomyosin complex: Ca2+ binds to troponin. 5. Tropomyosin shift: Ca2+-troponin binding causes a conformational change in the troponin-tropomyosin complex, exposing the myosin-binding sites on actin. 6. Cross-bridge formation: Myosin heads (energized by ATP hydrolysis) bind to actin, forming cross-bridges. 7. Power stroke: The power stroke occurs as myosin heads pivot, pulling actin filaments towards the M-line, shortening the sarcomere. ADP is released. 8. ATP binding and detachment: ATP binds to the myosin head, causing detachment from actin. ATP is hydrolyzed to ADP and Pi, re-energizing the myosin head for the next cycle.
Answer: 1. Location of reabsorption: Primarily occurs in the proximal convoluted tubule (PCT). 2. Glucose reabsorption: Occurs via secondary active transport. Sodium-glucose cotransporters (SGLT2 and SGLT1) in the apical membrane of PCT cells use the electrochemical gradient of Na+ (maintained by Na+/K+-ATPase on the basolateral membrane) to transport glucose into the cell. Glucose then exits the cell into the interstitial fluid via facilitated diffusion through GLUT1 and GLUT2 transporters on the basolateral membrane. 3. Amino acid reabsorption: Similar to glucose, amino acids are reabsorbed via secondary active transport using Na+-amino acid cotransporters in the apical membrane. Different transporters exist for different types of amino acids. Like glucose, they exit the PCT cells via facilitated diffusion on the basolateral membrane. 4. Hormonal regulation: While generally reabsorbed to completion under normal physiological conditions, the capacity for reabsorption is finite (transport maximum, Tm). In conditions like diabetes mellitus, where plasma glucose levels exceed the Tm, glucose appears in the urine (glucosuria). Hormonal regulation is less direct for glucose and amino acid reabsorption compared to other substances like Na+ or water, but conditions affecting overall renal function can indirectly impact their handling.
Answer: 1. SA node: The primary pacemaker of the heart, located in the right atrium. It possesses intrinsic automaticity due to 'funny' channels (If) that allow slow inward Na+ and K+ flow, leading to spontaneous depolarization to threshold. 2. Depolarization: Once threshold is reached, voltage-gated Ca2+ channels open, causing rapid depolarization and the action potential. 3. Conduction to atria: The SA node impulse spreads rapidly across both atria via gap junctions, causing atrial contraction. 4. AV node: Located in the interatrial septum, near the tricuspid valve. It receives the impulse from the atria. 5. AV nodal delay: The AV node has slower conduction velocity due to fewer gap junctions and smaller cell size. This delay is crucial as it allows complete atrial emptying into the ventricles before ventricular contraction begins. 6. Conduction to ventricles: After the delay, the impulse passes rapidly through the Bundle of His, bundle branches, and Purkinje fibers, ensuring coordinated ventricular depolarization and contraction.
Answer: 1. Definition: The Bohr effect describes the observation that hemoglobin's affinity for oxygen decreases as the partial pressure of carbon dioxide (PCO2) increases, and/or the pH decreases. Conversely, hemoglobin's affinity for oxygen increases as PCO2 decreases and/or pH increases. 2. Mechanism: Increased PCO2 in tissues leads to the formation of carbonic acid (H2CO3), which dissociates into H+ and bicarbonate ions. The increased H+ concentration binds to specific amino acid residues on hemoglobin, stabilizing the deoxygenated T-state, thus reducing oxygen affinity. 3. Physiological Significance: a. Tissues: In metabolically active tissues, PCO2 is high and pH is low due to cellular respiration. This shifts the oxygen dissociation curve to the right, facilitating the release of oxygen from hemoglobin to the tissues where it is needed most. b. Lungs: In the lungs, PCO2 is low and pH is high. This shifts the oxygen dissociation curve to the left, promoting the uptake of oxygen by hemoglobin from the inhaled air.
Answer: 1. Introduction to Blood Pressure Regulation: Arterial blood pressure (BP) is a critical physiological parameter maintained by a complex interplay of short-term and long-term regulatory mechanisms to ensure adequate perfusion of vital organs. Key determinants of BP are cardiac output (CO) and systemic vascular resistance (SVR), where BP = CO x SVR. 2. Neural Regulation (Short-Term): a. Baroreceptor Reflex: Stretch receptors (baroreceptors) in the carotid sinuses and aortic arch monitor BP. - High BP: Increased stretch stimulates baroreceptors, sending signals via glossopharyngeal and vagus nerves to the medulla oblongata. This leads to increased parasympathetic outflow (vagal stimulation of the heart, decreasing HR) and decreased sympathetic outflow (reducing HR, contractility, and vasoconstriction). - Low BP: Decreased stretch reduces baroreceptor firing, leading to decreased parasympathetic and increased sympathetic outflow, resulting in increased HR, contractility, and vasoconstriction. b. Chemoreceptor Reflex: Primarily sensitive to changes in blood oxygen and carbon dioxide levels, and pH. Low O2 or high CO2/low pH can stimulate chemoreceptors, leading to increased sympathetic outflow and vasoconstriction, thus raising BP. c. Central Nervous System Ischemic Response: A potent vasoconstrictor response triggered by severe hypotension and reduced blood flow to the brainstem. Vasoconstriction is extreme, leading to a significant rise in BP. 3. Hormonal Regulation (Intermediate to Long-Term): a. Renin-Angiotensin-Aldosterone System (RAAS): - Renin Release: Decreased renal perfusion pressure, decreased Na+ delivery to the distal tubule, or sympathetic stimulation triggers renin release from the juxtaglomerular apparatus. - Angiotensin II: Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by ACE (angiotensin-converting enzyme). - Vasoconstriction: Angiotensin II is a potent vasoconstrictor, directly increasing SVR. - Aldosterone Release: Stimulates the adrenal cortex to release aldosterone. - ADH Release: Stimulates the posterior pituitary to release antidiuretic hormone (ADH). - Sodium and Water Reabsorption: Increases Na+ and water reabsorption in the PCT of the kidney. - Aldosterone: Promotes Na+ and water reabsorption in the distal tubules and collecting ducts, increasing blood volume. - ADH (Vasopressin): Increases water reabsorption in the collecting ducts, further increasing blood volume. b. Antidiuretic Hormone (ADH): Primarily regulated by plasma osmolality and, to a lesser extent, by baroreceptors. Released when osmolality rises or BP falls significantly. Increases water reabsorption by the kidneys, concentrating urine and expanding extracellular fluid volume. c. Atrial Natriuretic Peptide (ANP) & Brain Natriuretic Peptide (BNP): Released by atrial and ventricular myocytes, respectively, in response to atrial stretch (high BP and volume). ANP/BNP cause vasodilation, promote Na+ and water excretion, and inhibit renin and aldosterone release, thereby reducing BP and blood volume. d. Epinephrine and Norepinephrine: Released from the adrenal medulla in response to sympathetic stimulation. Epinephrine generally causes vasodilation in skeletal muscle and heart (beta-2 effects) while increasing HR and contractility (beta-1 effects). Norepinephrine causes vasoconstriction (alpha-1 effects) and increases HR and contractility. 4. Intrinsic Regulation (Local/Tissue Level): a. Myogenic Response: Smooth muscle in the walls of arterioles constricts in response to increased transmural pressure (stretch) and relaxes in response to decreased pressure. This helps maintain stable blood flow to organs despite fluctuations in systemic BP. b. Local Metabolic Regulation: Metabolites (e.g., adenosine, lactate, K+, CO2) produced by active tissues lead to vasodilation, increasing blood flow to meet metabolic demands. Lack of oxygen also causes vasodilation. c. Endothelial Factors: The endothelium produces vasodilators (e.g., nitric oxide, prostacyclin) and vasoconstrictors (e.g., endothelin), contributing to local BP control. 5. Pathological Conditions: a. Hypertension (High Blood Pressure): Can result from overactivity of the RAAS, sympathetic nervous system, impaired baroreceptor function, excessive salt and water retention, or endothelial dysfunction. Chronic hypertension damages blood vessels, leading to increased risk of stroke, heart attack, kidney disease, and heart failure. b. Hypotension (Low Blood Pressure): Can result from hypovolemia (e.g., hemorrhage, dehydration), impaired cardiac function (cardiogenic shock), vasodilation (e.g., septic shock, anaphylaxis), or autonomic dysfunction. Inadequate tissue perfusion can lead to organ damage and failure. c. Heart Failure: Often associated with complex dysregulation of BP mechanisms. Initially, compensatory mechanisms like RAAS and sympathetic activation aim to maintain CO, but chronic activation can be detrimental, leading to fluid overload, excessive vasoconstriction, and further cardiac damage. d. Atherosclerosis: Chronic elevation of BP contributes to the development and progression of atherosclerosis, a condition characterized by plaque buildup in arteries, which further exacerbates hypertension and cardiovascular risk.