MEDICAL PHYSIOLOGY Electrophysiology Conference Quiz 2A September 18, 2001 1. How does hyperthyroidism enhance susceptibility to insulin-induced flaccid paralysis? By increasing the number of sodium-potassium pumps in cell membranes. 2. By what mechanism does hypokalemia produce flaccid paralysis? Increased sodium channel inactivation due to depolarization of the resting potential of skeletal muscle. 3. Why does hypokalemia widen the QRS complex? Slows conduction velocity of ventricular action potential due to reduction of rate of phase 0 depolarization. 4. What effect does hypokalemia have on the maximum diastolic potential of SA-node cells? Causes maximum diastolic potential to be less negative. 5. How and by what mechanism does exercise affect the susceptibility to hypokalemia-induced flaccid paralysis? Reduces susceptibility by shifting potassium out of the cell; increased potassium efflux associated with increased action potential firing. ------------------------------------------------------------------------ MEDICAL PHYSIOLOGY Electrophysiology Conference Quiz 2B September 20, 2001 1. How is the transmembrane flux of potassium affected by insulin? Increased potassium influx due to enhanced sodium-potassium pump activity 2. What role does membrane resting potential play in hypokalemia-induced flaccid paralysis? Resting potential depolarization decreases excitability by increasing sodium channel inactivation; reduced number of resting sodium channels 3. Why does hypokalemia increase the QT interval? Decreased potassium conductance reduces delayed rectifier potassium current thereby increasing the duration of the ventricular action potential. 4. What effect does hypokalemia have on the rate of phase 4 depolarization of SA-node cells? Speeds phase 4 depolarization 5. How and by what mechanism does inhibition of beta2-adrenergic receptors affect the susceptibility of the hyperthyroid patient to attacks of flaccid paralysis? Reduces susceptibility by reducing sodium-potassium pump activity.