xibocutie's version from 2017-03-19 09:34


Question Answer
A centrally acting alpha2 agonist that stimulates alpha2 adrenergic receptors in CVS centers of CNS to reduce sympathethic outflow clonidine. lots of bad side effects Clinical use of clonidine rarely used to tx htn anymore. used if refractory to other drugs Section 15 QuestionAnswer Alpha-1 receptor antagonist prazosin MOA prazosin decrease BP due to decreased PVR and venous return Clinical Use of prazosin not first line tx for HTN, however, may be indicated in hypertensive men who also have benign prostatic hyperplasia Section 16 QuestionAnswer Direct (Arteriolar) Vasodilators Hydralazine MOA unknown. acts mainly on smooth muscle cells of arterioles to cause relaxation and vasodilation. Pharmokinetics of Hydralazine Oral, IV, and intramuscular. Absorbed via GI tract, but bioavailability varies on patient's acelytation rate. Acetylation is major route of inactivation. Metabolism complex. Half life is one hr but can last 12 hrs. Adverse effects of hydralazine too much vasodilation, headache, nausea, flushing, hypotension, palpitation, tachycardia, dizziness, angina. If used alone, salt retention with development of CHF. Immune: lupus like, serum sickness, hemolytic anemia, glomerulonephritis Clinical use of hydralazine rarely used, tx chronic htn only when refractory to other drugs. do not use in elderly or pts with CAD. Used in hospital to lower BP while waiting for oral agents to act. Oral hydralazine is used in combo with long-acting nitrates for the tx of systolic HF. Section 17 QuestionAnswer Minoxidil MOA: activates ATP-sensitive K channel in VSMCs. Hyperpolarization, less Ca enters--> relaxation of VSMCs Effect of minoxidil on arteries/venous/capacitance vessels Powerful vasodilator. arteriolar vasodilation. No effect on venous or capacitance vessels. Strong reflex sympathetic activation. Potent stimulator of renin release. Pharmokinetics of minoxidil Oral, GI absorption, peak [plasma] in 1 hr, elimination via liver Adverse effects of minoxidil fluid/salt retention, cardiovascular effects due to baroreceptor stimulation of sympathetic nervous system, hypertrichosis (hair growth) Clinical use of minoxidil 3rd line HTN drug. Severe HTN. never used alone. combo with diuretic/b-blocker to prevent side effects
Sympatholytic Drugs AKA Beta-Adrenergic Antagonists Name the prototype drug for Beta adrenergic antagonists Metoprolol site of action of beta blockers heart, kidney, B1/B2, +/- presence of partial agonist activity (aka intrinsic sympathomimetic activity aka ISA) Drug with NO ISA (no intrinsic sympathomimetic activity) Metoprolol. MOA of metoprolol Decrease CO initially with Inc in PVR. No change in BP. Then, PVR returns to normal (hrs to days). The persistent decrease in CO with normal PVR results in a sustained decrease in BP. Drugs with ISA (don't have to know) pindolol: dec HR, dec CO, long term BP dec due to dec in PVR due to B2 receptors that mediate vasodilation Adverse effects of adrenergic drugs Induction of HF, bradycardia, AV block, dec pulm function, erectile dysfunction Clinical use of Beta Blockers HTN, SVTs, angina, prevention of recurrent MIs

Ca Channel Blockers/ Calcium Channel Antagonist Classes

Question Answer
Name Calcium Channel Antagonist ClassesDihydropyridines and Non-dihydropyridine class
Name the 3 Calcium Channel Antagonists we need to knowNifedipine, Verapamil, and Diltiazem
Name a drug(s) in dihydropyridine class of Ca Channel BlockersNifedipine
Name a drug(s) in the non-dihydropyridine class of Ca Channel BlockersVerapamil and Diltiazem
Drugs that end in "dipine" belong in what class of drugs?Dihydropyrindine class of Ca Channel Blockers. ie amlodipine, felodipine
MOA of Ca Channel BlockersInterfere with the movement of Ca ions thru voltage-gated Ca Channels. Decreased Ca entry causes decreased contractility and tone of VSMC, decrease in peripheral vascular resistance. In addition, verapamil and diltiazem have effects on Ca entry in the heart that cause modest decreases in HR and cardiac contractility.
Effect of Ca Channel Blockers on vascular smooth muscle cells
All Ca channel blockers (dihydropyridines and non-) decrease Ca influx via Voltage dependent Ca channels. The resulting decrease intracellular Ca results in relaxation. Ca channel blockers are all selective for arterial smooth muscle and have little effect on the venous system. These drugs have a mild reflex sympathetic response Effect of Ca Channel Blockers on Cardiac Muscle Only Verapamil and diltiazem (But NOT the dihydropyrindines) have DIRECT effects on the heart at therapeutic concentrations. Direct blockade of Ca channels in cardiac cells causes a modest negative inotropic effect. However, this may be offset by the reflex response due to vasodilation in healthy hearts and thus there is no net change in cardiac contractility. SA and AV nodes depend on Ca for conduction. Thus Ca Channel blocking drugs delay recovery of Ca channells (verapamil and diltiazem) depress the rate of the sinus node pacemaker and slow AV conduction. Transition from inaactivated Ca channel to closed/resting is slowed down by what drugs in the heart? Verapamil and diltiazem (non-dihydropyridines)....slows down reactivation of the Ca channels Specific MOA/effect of Dihydropyridines on arteries and reflexes Nifedipine: acts solely as arteriolar vasodilator. Arterial dilation lowers BP. Inc in CO. Reflex sympathetic respose-> positive inotropic (indirect). HR increased modestly. Long-acting formulation preferred to prevent rapid drop of BP. Look in Anki for specifics of Verapamil/Diltiazem---Table Kinda Complex How are the Ca Channel Antagonists metabolized? Metabolized to inactive products in the liver. Clearance is reduced when hepatic function is compromised Adverse effects of Ca Channel Antagonists Excessive vasodilation, dizziness, hypotension, headache, flushing, nausea, peripheral edema, coughing, wheezing, pulmonary edema. Aggravation of myocardial ischemia w/short acting dihydropyridines but not with lon-acting. Bradycardia, transient asystole, exacerbation of HF with verapamil but usually only if IV or with combo with Beta blockers. Constipation. Clinical use of Ca Channel Blockers HTN, (not used in pts with SA/AV node problems nor CHF), Ca antagonists are also used for the tx of angina and cardiac arrythmias