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

NSG 531 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