Cardiology Drugs Flashcards

Question

Prazosin

Answer 1

Alpha 1 antagonist arterial and venous vasodilation, prostate smooth muscle relaxation Use: PTSD, BPH, HTN Adverse effects: orthostatic hypotension, reflex tachycardia

Answer 2

Alpha 1 antagonist arterial and venous vasodilation, prostate smooth muscle relaxation USE: BPH, HTN

Answer 3

Alpha 1 antagonist arterial and venous vasodilation, prostate smooth muscle relaxation USE: BPH, HTN

Answer 4

Alpha 1 antagonist arterial and venous vasodilation, prostate smooth muscle relaxation USE: BPH (best osin drug for this)

Answer 5

Irreversible A1+A2 antagonist Decreased PVR and BP USES: pheochromocytoma (preoperatively - so volume replenishes first)

Answer 6

Reversible A1 + A2 antagonist Decreased PVR and BP USES: Cocaine induced HTN (NO beta blockers), patients on MAOIs who ate tyramine containing foods, Pheochromocytoma intraoperatively if needed.

Answer 7

A2 antagonist works in CNS to increase SNS outflow to periphery USE: ED CI: CVD

Answer 8

Carvedilol, labetolol (have alpha adrenergic antagonist activity), nicardipine, clevdipine, nitroprusside, fenoldopam

Answer 9

PDE3 inhibitor. increases cAMP in cardiomyocytes by preventing degredation--> Ca influx-->increased inotropy and chronotropy. Also general vasodilation because Ca inhibits MLCK activty Use: Short term in decompensated HF Adverse effects: arrhythmias, hypotension

Answer 10

Inhibits late phase of Na current --> decreased diastolic wall tension and O2 consumption. No affect on HR and contractility USES: angina refractory to other therapy Adverse Effects: constipation, dizziness, headache, nausea, QT prolongation

Answer 11

HMG CoA reductase inhibitors inhibits HMG-CoA conversion to mevalonate (cholesterol precursor). Increases LDL-R due to increased SBREP activity Decreases LDL a ton and TAGs slightly USE: dyslipidemia, hypercholesterolemia Adverse effects: Hepatotoxicty, myopthy, rhabdomyolysis, myoglobinuria CI: pregnant, lactating, interaction with OAT inhibitors (gemfibrozil and cyclosporine) and red yeast rice **atorvastatin and rosuvastin have longer half lives so typically used

Answer 12

PCSK9 Inhibitor Monoclonal Abs target PCSK9 which prevents degredation of LDL-R Decreases LDL a ton and TAGs slightly Adverse effects: neurocognitive effects (dementia, delirium), myalgias

Answer 13

PCSK9 Inhibitor Monoclonal Abs target PCSK9 which prevents degredation of LDL-R Decreases LDL a ton and TAGs slightly Adverse effects: neurocognitive effects (dementia, delirium), myalgias

Answer 14

Prevent cholesterol absorption at SI brush border by blocking NPC1L1 transporter LDL-R increases (SREBP activity increases), LDL decreases but more modest because HMG-CoA reductase upregulation via SREBP *Synergistic with statins (prevent directy cholesterol and endogenous cholesterol) Adverse effects: diarrhea, rare increase in LFTs

Answer 15

Bile acid resin + charged so bind - charged bile acids. Prevent intestinal reabsorption of bile acids. Liver than uses cholesterol to make more. this also increases LDL-R production via SREBP and upregulates HMG-CoA reductase. LDL decreases but slightly attenuated by upregulated HMG-CoA R USE: lower LDL, remov digitalis from GI tract, trt bile salt accumulation in cholestasis Adverse effects: GI upset, decreased absorption of some drugs, fat soluble vitamins CI: pts with hypertriglyceridemia - increased bile acid production leads to icnreased hepatic TAG synthesis

Answer 16

Bile acid resin + charged so bind - charged bile acids. Prevent intestinal reabsorption of bile acids. Liver than uses cholesterol to make more. this also increases LDL-R production via SREBP and upregulates HMG-CoA reductase. LDL decreases but slightly attenuated by upregulated HMG-CoA R USE: lower LDL, remov digitalis from GI tract, trt bile salt accumulation in cholestasis Adverse effects: GI upset, decreased absorption of some drugs, fat soluble vitamins CI: pts with hypertriglyceridemia - increased bile acid production leads to icnreased hepatic TAG synthesis

Answer 17

Bile acid resin + charged so bind - charged bile acids. Prevent intestinal reabsorption of bile acids. Liver than uses cholesterol to make more. this also increases LDL-R production via SREBP and upregulates HMG-CoA reductase. LDL decreases but slightly attenuated by upregulated HMG-CoA R USE: lower LDL, remov digitalis from GI tract, trt bile salt accumulation in cholestasis Adverse effects: GI upset, decreased absorption of some drugs, fat soluble vitamins CI: pts with hypertriglyceridemia - increased bile acid production leads to icnreased hepatic TAG synthesis

Answer 18

Fibric Acid Derivatives Upregulates LPL, which results in icnreased TAG clearance. Also activates PPAR-alpha to induce HDL synthesis USE: hypertriglyceridemia Adverse effects: cholesterol gallstones (cholesterol alpha hydroxylase inhibition), oral anticoagulant potentiation, GI symptoms, *myopathy* CI: renal failure, pregnancy, hepatic dysfunciton, children

Answer 19

Fibric Acid Derivatives Upregulates LPL, which results in icnreased TAG clearance. Also activates PPAR-alpha to induce HDL synthesis USE: hypertriglyceridemia Adverse effects: cholesterol gallstones (cholesterol alpha hydroxylase inhibition), oral anticoagulant potentiation, GI symptoms, *myopathy* CI: renal failure, pregnancy, hepatic dysfunciton, children

Answer 20

Fibric Acid Derivatives Upregulates LPL, which results in icnreased TAG clearance. Also activates PPAR-alpha to induce HDL synthesis USE: hypertriglyceridemia Adverse effects: cholesterol gallstones (cholesterol alpha hydroxylase inhibition), oral anticoagulant potentiation, GI symptoms, *myopathy* CI: renal failure, pregnancy, hepatic dysfunciton, children

Answer 21

inhibits lipolysios (Hormone sensitive lipase) in adipose tissue which decreases VLDL synthesis and thus decreases LDL. Also decreases TAGs because decreased transport of FFAs to liver. LPL enhanced. HDL icnreases Adverse effects: Red flushed face (tr this with NSAIDs), pruritus, rashes, dry skin, hyperglycemia, hyperuricemia, hepatotoxicity Not really used anymore due to side effects

Answer 22

Drugs: Procainamide, Quinidine, Disopyramide Mech: sodium channel block, some K+ block AP change: slow upstroke, prolonged AP, QT prolongation, prolonged ERP (why its good for reentry) Use: Artia and ventricualr arrhythmias. reentrant/ectopic SVT + VT. can terminate a Fib given IV CI: Long QT syndrome Adverse effects: ALL: torsades, thrombocytopenia -Qunidine: cinchonism (headache, tinnitus) -Procainamide: decreased PVR, reversible SLE syndrome, torsades de pointe (NAPA accumulation -Disopyramide: HF, atropine like - urinary retention, dry mouth, blurred vision, constipation

Answer 23

Drugs: Lidocaine, Mexetiline - phenytoin can fall into this category Mech: sodium channel block. preferentially effect ischemic or depolarized ventricular tissue (because bind channels in open or inactive state -ventricles have longer AP so more likely depolarized and ischemic tissue have higher RMP that prevent transition from inactive to resting as quick) AP change: decreased slope ) upstroke (but most modest of Class 1). shortened AP duration Use: Post MI ventricualr arrhythmias, VT termination, prevention of V fib following cardioversion in ischemia setting, digitalis induced arrhythmias mexelitine also used for diabetic neuropathy pain + nerve injury NOT affective for SVT, or anything atrial CI: Adverse effects: CNS stimualiton/depression -->PARESTHESIA, tremor, slurred speech, convulsions

Answer 24

Drugs: Flecanide, Propafenone Mech: sodium channel block. tightest bind. prolong ERP in AV node and bypass tracts. No effect on ERP in purkinje and ventricular tissue AP change: Largest decrease in slope of phase 0. minimal effect on duration Use: Supraventricualr arrhythmias, A fib + flutter cardioversion CI: post MI, in structural heart disease Adverse effects: proarrhythmatic - especially post MI - ventricular arrhythmias

Answer 25

Class 3 antiarrhythmatic Mech: phase 2 K+ block AP change: increase AP duration, increase ERP, increase QT interval Use: a fib, a flutter, VT CI: Adverse effects: torsades, excessive beta blockade (asthma, bradycardia

Answer 26

Class 3 antiarrhythmatic Mech: phase 2 K+ block. also some Na blocking - has effects of all the classes AP change: prolongs AP duration, decreases slope of phase 0 Use: A fib, A flutter, VT CI: Adverse effects: pulmonary fibrosis, hypo/hyperthyroidism (drug is 40% iodine), acts as a hapten resulting in corneal deposits and blue/gray skin deposits - results in photodermatitis, neuro effects, constipation

Answer 27

Class 3 antiarrhythmatic Mech: phase 2 K+ block. so effect ability to respond to tachyarrhythmias, but DO NOT effect conduction velocity. reverse use dependence (so AP prolongation is most marked at slower rates rather than fast which is what is wanted) AP change: increas AP duration, increase ERP, increase QT interval Use: A fib, A flutter CI: long QT syndrome Adverse effects: Torsades de pointe (drug action is most potent at slower rates, which is when this is more likely to happen to begin with)

Answer 28

Beta blockers - metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol Mech: sympatholytic. decrease cAMP and calcium current --> decreased SA and AV node activity. AV node is particularly sensitive (increased PR interval). AP change: decreased phase 4 slope Use: SVT (terminate as well as prevent by suppressing pvcs), rate control in A fib and flutter CI: WPW (uncontrolled firing in accessory path) Adverse effects: bradycardia, AV block, HF, unopposed alpha in cocaine overdose or pheochromocytoma (except nonselective ones with some alpha effects -labetolol, carvedilol) Overdose: trt with saline, atropine, glucagon

Answer 29

CCB: verapamil, diltiazem Mech: calcium current blockade, slowed AP rise, and prolonged repoalrization. slows conduction in the AV (mainly) and SA node. drugs also peripheral dilate AP change: slows conduction, increases ERP, increases PR Use: AVNRT (SVT) rate control in A fib + flutter, CI:WPW Adverse effects:

Answer 30

Mech:increases K+ exit out of cell (IKr), and inhibits Ca2+ and funny current. causes hyperpolarization and suppresion of Ca dependent APs. MAJORLY effects AV node specifically. Very short acting Use: #1 for terminating SVTs. CI: Adverse effects:

Answer 31

Cofactor for Na/K ATPase. antagonist of Ca channels. hypomagnesia contributes to many arrhythmias. treats torsades de pointe

Answer 32

Mech: inhibits Na/K ATPase, which indirectly inhibits NCX and allows Ca to stay in the cell. ALso stimulates the vagus N End effect: increased inotropy (Ca), decrased HR (vagus) Use: HF, A fib (decrease conduction at AV node) CI: renal failure, hypokalemia (allows extra drug binding), verapamil, quinidine, amiodarone Adverse effects: cholinergic (nausea, vomiting, diarrhea, blurry yellow vision- van Gogh , arrhythmias, AV block. can cause hyperkalemia,

Answer 33

use dependent. blocks funny current in SA node and reduces HR without affecting myocardial contractility, ventricular repolarization, or intracardiac conduction. so may be good for patients with low EF