NSG 531 Rush Advanced Pharmacology: Exam 3 Questions With Correct Answers Latest Updated 2024/2025 / Graded A+.

NSG 531 Rush Advanced Pharmacology: Exam 3 Questions With Correct Answers Latest Updated 2024/2025 / Graded A+. what is the difference between cardiac myocyte action potential and that of the CNS or ANS? - ANSWER nerve cell action potential is very short cardiac action potential is much longer they are longer to have adequate filling time in order to get a good contraction for a reasonable bolus of blood the only way this can happen is if the action potential is longer this will also mean that the refractory period will be longer What are the 5 phases of the non-pacemaker action potential? - ANSWER 0 - depolarization 1 - partial repolarization 2 - plateau 3 - repolarization 4 - resting membrane potential what happens during phase 0 of the non-pacemaker action potential - ANSWER depolarization voltage gated sodium channels are opening up until we get past threshold what happens during phase 1 of the non-pacemaker action potential - ANSWER partial repolarization NSG 531 Rush Advanced Pharmacology: Exam 3 Questions With Correct Answers Latest Updated 2024/2025 / Graded A+. what happens during phase 2 of the non-pacemaker action potential - ANSWER plateau calcium channels open (L-type because they are long) potassium is still open potassium out and calcium in - they are opposing each other in voltage giving the plateau this is when the ventricles are filling what happens during phase 3 of the non-pacemaker action potential - ANSWER repolarization calcium channels are closed potassium channels are the only thing open taking their positive charge with them making the interior more negative what happens during phase 4 of the non-pacemaker action potential - ANSWER resting membrane potential where we are in between action potentials there is no net change in ovltage inside the cell When does contraction take place? - ANSWER begins towards the end of repolarization and ends at some point during repolarization refractory period - ANSWER during phase 0, 1, 2, and part of phase 3 the cell is refractory to the initiation of new action potentials many antiarrhythmic drugs increase the Refractory period which reduces myocyte excitability what are the benefits of the refractory period - ANSWER limits frequency of cardiac contractions allows for adequate filling time prevents sustained contractions how are pacemaker cells different from non-pacemaker cell - ANSWER no resting membrane potential - no point where it is flat there are very few sodium channels in pacemaker - sodium channels are not driving depolarization - calcium is only 3 phases comprised of cells within the SA node generate regular, spontaneous action potentials what are the phases of pacemaker action potential - ANSWER 0 - rapid depolarization 3 - repolarization 4 - slow depolarization what happens during phase 0 of the pacemaker action potential - ANSWER Rapid depolarization something is coming to open voltage gated calcium channels (L-type) calcium comes rushing in what happens during phase 3 of the pacemaker action potential - ANSWER repolarization potassium channels now open up, potassium rushes out, repolarizes what happens during phase 4 of the pacemaker action potential - ANSWER slow depolarization with potassium rushing out we are all the way down at -60 funny sodium channels open up until voltage reaches -50 T-type (transient) calcium channels open up until voltage reaches -40 L-type calcium channels then open back up Describe how non-pacemaker APs can mimic pacemkaer APs - ANSWER Hypoxia and ischemia when the resting membrane potential is not getting enough oxygen it is going to become more positive because you need oxygen to produce ATP. If we are deficient in ATP then the NA K ATPase pump wont be functioning if someone is hypoxic in a focal area - say they have a resting membrane potential at -45 - the fast sodium channels won't open - they start using calcium to open - so they would convert into action potentials that use calcium (hence how they mimic pacemaker APs) excitation-contraction coupling - ANSWER sequence of events from motor neuron signaling to a skeletal muscle fiber to contraction of the fiber's sarcomeres conversion of depolarizing currents into contractile force L-type calcium channels open up in phase 2 in nonpacemaker - calcium comes flooding into myocytes, so we now have calcium in the cell and a sarcoplasmic recticulum (a resovior for calcium) receptors called RYR (ligand gated calcium channels) calcium then comes out - coming int the cell from the calcium channels and the sarcoplasmic recticulum describe how calcium binds to cause contraction - ANSWER when there is an influx of calcium in the cell there is a myosin head separated by troponin. little binding sites for the myosin exist on the aktin but it can't get to it because of the troponin. calcium therefore binds to the tropinin causing a confirmational change in troponin so it will move and take the tropomyosin with it. the myosin can then bind to the aktin molecules when it binds it activates ATP the ATP will be used to generate the sliding of the aktin and the myosin filaments against each other shortening the muscle cell causing contraction Describe how adrenergic stimulation increases the force of contraction through inotropic effects - ANSWER NE and epi bind to adenylyl cyclase coupled g proteins (beta 1) leads to phosphorylation of Ca channels and opens them increases inward movement of Ca there is also increased release of Ca from the SR increases actin/myosin interaction increases force of contraction Describe how adrenergic stimulation increases the force of contraction through chronotropic effects - ANSWER NE and epi bind to adenylyl cyclase coupled g proteins (beta 1) results in phosphorylation of Ca2 channels and opens them increases inward movement of Ca2 shortens phase 0 by increasing the opening of L-type calcium in pacemaker heightened sympathetic state shortens effective refractory period increases rate of contraction how do catecholamines effect the NaK ATPase Pump - ANSWER epi to beta 1 - g coupled protein receptor increase in cAMP activate protein kinase phosphorylate and increase in ATPase proteins available on the cell surface this is why we give epi during hypoxia - cardiac arrest - so that we can initiate more action potentials how does cholinergic stimulation work to decrease heart rate - ANSWER effects on m2 receptors acetylcholine binds to g coupled, alpha subunit comes off can bind to t-type calcium channel - opens after funny sodium and before L-type - if it binds it will inhibit it which will decrease the heart rate it can also bind to potassium channels increasing intracellular potassium causes repolarization and actually hyperpolarization both will have negative chronotropic effects and decrease the heart rate reduces opening of Ca2 channels on the surface of the nodal cells - Ach opens K+ channels and hyperpolarizes nodal cells moving them further away from threshold heart block - ANSWER one of the main phenomena causing pathological disturbances in rhythms arises from fibrosis or ischemia damage in the conducting system - usually in the AV node ectopic pacemaker - ANSWER one of the main phenomena causing pathological disturbances in rhythms pacemaker activity can arise from other tissue when there is ischemia or increased catecholamines they increase intracellular Ca2 concentration raise resting membrane potential and can close Na channels after depolarizations - ANSWER one of the main phenomena causing pathological disturbances in rhythms -spontaneous depolarizations of nonpacemaker cells during either phase 3 (repolarization) or phase 4 (RMP); occur after ERP what causes after depolarizations - ANSWER most often caused by elevated intracelluar calcium that triggers abnormal action potentials associated with hypercalcemia and excessive catecholamines treated with calcium channel blockers and beta blockers what are the main phenomena causing pathological disturbances in rhythms - ANSWER after-depolarizations heart block ectopic pacemaker re-entry Re-entry - ANSWER one of the main phenomena causing pathological disturbances in rhythms a signle impulse re-enters an area of the heart and repeatedly excites it the impulse circles around and is not extinguished typically impulses run into each other and die out if they have a unidirectional block there is no second impulse coming around to block the other one that will then circle conditions leading to re-entry - ANSWER physiologic ring unidirectional block conduction timeERP what are the two main symptoms we see with re-entry - ANSWER tachycardia and atrial flutter Wolf-Parkinson-White Syndrome - ANSWER ventricular preexcitation syndrome accessory conduction pathway from atria to ventricle (bundle of Kent), bypassing AV node ventricles begin to partially depolarize earlier -- delta wave on EKG can result in reentry current leading to supraventricular tachycardia tx: (type Ia) quinidine, disopyramide, procainamide slows AP conduction in myocardium, helps suppress bundle of Kent also do ablation of kent bundle DO NOT USE types II (beta block), IV (Ca block)...these incr AV node refractoriness and would worsen condition