PHGY 216 MIDTERM EXAM (NEWEST UPDATE 2026/2027) QUESTION BANK | HIGH-YIELD QUESTIONS WITH ACCURATE, VERIFIED ANSWERS | A+ GRADE GUARANTEED.

PHGY 216 MIDTERM EXAM (NEWEST UPDATE 2026/2027) QUESTION BANK | HIGH-YIELD QUESTIONS WITH ACCURATE, VERIFIED ANSWERS | A+ GRADE GUARANTEED. 1. Calculate the Nernst potential for K⁺ at 37°C if [K⁺]ₒ = 5 mM and [K⁺]ᵢ = 150 mM. • Answer: Eₖ = (61.5/z) log([K⁺]ₒ/[K⁺]ᵢ) = 61.5 log(5/150) = 61.5 log(0.0333) = 61.5 × (-1.48) = -91 mV 2. Why is the resting membrane potential (-70 mV) slightly less negative than Eₖ (-91 mV)? • Answer: Because the membrane has a small but significant permeability to Na⁺ at rest. Na⁺ influx slightly depolarizes the cell from the K⁺ equilibrium potential. 3. Describe two mechanisms that could cause hyperpolarization of a neuron. • Answer: 1) Increased K⁺ efflux (opening of K⁺ channels). 2) Increased Cl⁻ influx (opening of Cl⁻ channels, if E_cl is negative to RMP). 3) Decreased Na⁺ or Ca²⁺ influx. Neurophysiology & Synapses 4. How does tetrodotoxin (TTX) affect the action potential? • • Answer: TTX blocks voltage-gated Na⁺ channels. This prevents the rapid upstroke/ depolarization phase of the action potential, leading to a complete block of signal conduction. Muscle Physiology 5. What is the role of troponin in skeletal muscle contraction? • Answer: Troponin (specifically Tn-C) is the Ca²⁺-binding subunit. When Ca²⁺ binds, it induces a conformational change in the troponin-tropomyosin complex, moving tropomyosin away from the myosin-binding sites on actin, allowing cross-bridge formation. 6. Why does a muscle twitch have a longer duration than an action potential? • Answer: The action potential is over in 1-2 ms. The muscle twitch (~100 ms) includes the entire excitation-contraction coupling process (Ca²⁺ release, cross-bridge cycling, and Ca²⁺ reuptake by the SR), which is much slower than the electrical event. 7. What is the primary source of the cytosolic Ca²⁺ for skeletal vs. cardiac muscle contraction? • Answer: Skeletal: Almost entirely from the Sarcoplasmic Reticulum (SR). Cardiac: A small but critical influx of extracellular Ca²⁺ via L-type channels triggers the release of a larger amount from the SR (CICR). Cardiovascular Physiology 8. If stroke volume is 70 mL and heart rate is 72 bpm, what is the cardiac output? • Answer: CO = SV × HR = 0.070 L × 72 bpm = 5.04 L/min 9. What is the physiological significance of the AV nodal delay? • Answer: It ensures that the atria have completed their contraction and emptied blood into the ventricles before ventricular contraction (systole) begins. This optimizes ventricular filling. 10. On an ECG, what does a widened QRS complex indicate? • Answer: It typically indicates a conduction abnormality within the ventricles, such as a bundle branch block, where one ventricle depolarizes later than the other, prolonging the total ventricular depolarization time. 11. What is an IPSP and how is it generated? Answer: An Inhibitory Post-Synaptic Potential is a local hyperpolarization that moves the membrane potential away from threshold. It is typically generated by neurotransmitters (e.g., GABA, glycine) that open Cl⁻ or K⁺ channels. 12. Explain the concept of spatial summation. • Answer: The additive effect of multiple excitatory postsynaptic potentials (EPSPs) from different synaptic inputs occurring simultaneously on a neuron. If their combined depolarization reaches threshold, an action potential is triggered. 13. A patient has a heart rate of 120 bpm and a systolic/diastolic BP of 115/75 mmHg. Estimate their MAP. • Answer: MAP ≈ Diastolic + 1/3(Pulse Pressure). PP = SBP - DBP = 115 - 75 = 40. MAP ≈ 75 + (40/3) ≈ 75 + 13.3 = 88.3 mmHg • 14. According to the Frank-Starling curve, what happens to stroke volume if venous return increases? • Answer: Increased venous return increases end-diastolic volume (EDV/preload). This stretches the ventricular myocardium, increasing the force of contraction and thereby increasing stroke volume. Integration & Application 15. Describe the baroreceptor reflex response to acute hemorrhage. Answer: Hemorrhage → ↓ Blood volume → ↓ MAP → ↓ Baroreceptor firing → ↑ Sympathetic outflow & ↓ Parasympathetic outflow → Results: ↑ HR, ↑ contractility, ↑ TPR (vasoconstriction) → All act to ↑ MAP back toward normal. more SR Ca²⁺ release. Both lead to more forceful contraction. 16. What is autoregulation of blood flow and what are two proposed mechanisms? • Answer: The ability of an organ to maintain a relatively constant blood flow despite changes in perfusion pressure. Mechanisms: Myogenic theory (vascular smooth muscle contracts in response to stretch). Metabolic theory (decreased O₂ or increased metabolites like CO₂, H⁺, adenosine cause vasodilation). 17. Contrast the effects of epinephrine on alpha vs. beta-2 receptors in the vasculature. • Answer: Alpha-1 receptors: Cause potent vasoconstriction (in skin, splanchnic circulation). Beta-2 receptors: Cause vasodilation (in skeletal muscle, coronary arteries). At low [Epi], beta-2 effect may dominate; at high [Epi], alpha-1 effect dominates. 18. Explain why ventricular pressure rises dramatically during isovolumetric contraction. • Answer: During this phase, the ventricles are contracting but all valves are closed (AV and semilunar). The contraction is against a fixed volume of blood (end-diastolic volume), causing a rapid, steep increase in pressure without a change in volume. 19. Why does increasing heart rate too much (e.g., 180 bpm) actually decrease cardiac output? • Answer: At very high heart rates, the time for ventricular filling (diastole) is drastically reduced. This severely decreases enddiastolic volume (preload), which decreases stroke volume (via Frank-Starling). The drop in SV can outweigh the increase in HR, leading to a net decrease in CO.