Cardio Drugs Flashcards
ACE inhibitors (Angiotensin Converting Enzyme)
lisinopril, captopril, enalapril, ramipril
ACE inhibitors MOA, use, AE
MOA - inhibit ACE -> decreased AT II -> decreased vasoconstriction, decreased GFR by preventing constriction of efferent arterioles
Use - HTN, HF (decreases mortality), proteinuria, diabetic nephropathy, post MI
AE - cough, angioedema (C/I in C1 esterase inhibitor deficiency), teratogen, increased Creatinine, hyperkalemia, and hypotension
Angiotensin receptor blockers
losartan, candesartan, valsartan
Angiotensin receptor blocker MOA, use, AE
MOA - selectively block binding of angiotensin II to AT1 receptor; do not increase bradykinin
Use - HTN, HF (decreases mortality), proteinuria, chronic kidney disease
AE - hyperkalemia, decreased GFR, hypotension, teratogen, angioedema
Aliskiren
direct renin inhibitor; blocks conversion of angiotensinogen
Calcium Channel Blockers
Dihydropyridine (-dipine)
- amlodipine, felodipine, nicardipine, nifedipine, nisoldipine
Nonhydropyridine
-diltiazem, verapamil
MOA, use, AE of dihydropyridine CCB
MOA: act on vascular smooth muscle to cause vasodilation
Use: HTN, angina, vasospasm, esophageal spasm, migraine prophylaxis
AE: peripheral edema, flushing, dizziness, constipation, reflex tachycardia
MOA, use, AE of nondihydropyridine CCB
MOA - block calcium channels at pacemaker cells
Use - HTN, angina, arrhythmia
AE - cardiac depression (avoid with CHF), AV block, flushing, dizziness, constipation
Minoxidil MOA, use, AE
MOA: opens K+ channels and hyperpolarizes smooth muscle (Ca2+ channels stay closed), resulting in relaxation of vascular smooth muscle
Use: severe HTN, topical application for hair loss
AE: hypertrichosis, hypotension, reflex tachycardia, fluid retention/edema
Hydralazine MOA, use, AE
MOA - increase cGMP (activate myosin phosphatase -> vasodilation) -> smooth muscle relaxation; vasoldilates arterioles > veins; reduces afterload
Use - severe HTN, HF, safe to use during pregnancy (frequently coadministered with a beta blocker to prevent reflex tachycardia)
AE - compensatory tachycardia (C/I with angina/CAD), fluid retention, HA, angina, lupus-like syndrome
What Abs are found with drug-induced lupus?
anti-histone Abs
Nitrates MOA, Use, AE
Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate
MOA - vasodilator by increasing NO in vascular smooth muscle -> increase cGMP and smooth muscle relaxation; dilate veins > arteries; decrease preload
Use - angina, acute coronary syndrome, pulmonary edema (pools blood in periphery)
AE - reflex tachycardia, hypotension, flushing, HA
Nitroprusside - cyanide toxicity
What antihypertensive medications should be used in CKD patients?
ACE inhibitors or ARBs
What antihypertensive medications should be used in black patients without CKD?
thiazide diuretics, CCB
What antihypertensive medications should be used in non-black patients without CKD?
thiazide diuretics, CCB, ACE inhibitor or ARB
What antihypertensives should be used in CHF? What should be avoided?
Give: ACE inhibitor/ARB, beta blocker, aldosterone antagonist
Avoid: CCB (cause edema), beta blocker (in acute decompensated)
What antihypertensive medications should be used in DM? What should be avoided?
Give: ACE inhibitor/ARB (protect against diabetic nephropathy)
Avoid: beta blocker (raise blood sugar)
What antihypertensive medications should be used in post-MI/CAD?
thiazide, beta blocker, ACE inhibitor/ARB, CCB (as needed for angina), nitrates (as needed for angina)
What antihypertensive medications should be used in atrial fibrillation?
beta blocker, diltiazem/verapamil (control HR)
What antihypertensive medications should be AVOIDED in bradycardia?
beta blocker, diltiazem/verapamil (decrease HR)
What antihypertensive medications should be used in BPH?
alpha-blocker
What antihypertensive medications should be used in pregnancy? What should be avoided?
Use: hydralazine, methyldopa, labetalol, dihydropyridines
Avoid: ACE inhibitors, ARBs
Want antihypertensive medications should be used for migraines?
CCB, beta blocker
What antihypertensive medications should be used for essential tremor?
propranolol
HMG-CoA reductase inhibitors
statins
lovastatin, pravastain, atrovastatin
HMG-CoA reductase inhibitors MOA, effects on LDL, HDL, triglycerides, AE
MOA - inhibit conversion of HMG-CoA reductase -> inability to produce de novo cholesterol; increase cell surface LDL receptors LDL: big decrease HDL: slight increase Triglycerides: slight decrease AE - heptatotoxicity, myopathy
Bile acid resins
cholestyramine, colestipol, colesevelam
Bile acid resin MOA, effects on LDL, HDL, triglycerides, AE
MOA: prevent intestinal reabsorption of bile acids
LDL: moderate decrease
HDL: slight increase
Triglycerides: slight increase
AE - GI upset, decreased absorption of fat-soluble vitamins, development of cholesterol gallstones
Ezetimibe MOA, effects on LDL, HDL, triglycerides, AE
MOA - prevent cholesterol absorption at small intestine brush border
LDL: moderate decrease
HDL: slight decrease/no effect
triglycerides: slight decrease/no effect
AE - rare increase in liver function tests, diarrhea
Fibrates
Gemfibrozil, Bezafibrate, fenofibrate
Fibrate MOA, effect on LDL, HDL, triglycerides, AE
MOA - up regulate LPL -> increase triglyceride clearance
LDL - slight decrease
HDL - slight increase
Triglycerides - big decrease
AE - myopathy, cholesterol gallstones, hepatotoxicity
Niacin (Vit B3) MOA, effect on LDL, HDL, triglycerides, AE
MOA - inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis
LDL - moderate decrease
HDL - moderate increase (most of all drugs)
Triglycerides - slight decrease
AE - flushing (decreased by aspirin before or long-term use), hyperglycemia, hyperuricemia
What is the effect of Nitrates on EDV (preload), BP, HR, contractility, and myocardial O2 demand?
decrease preload/EDV, decrease BP, increase HR (compensatory), no effect on contractility, decrease myocardial O2 demand
What is the effect of beta blockers on EDV (preload), BP, HR, contractility, and myocardial O2 demand?
no effect on preload/EDV, decrease BP, decrease HR, decrease contractility, decrease myocardial O2 demand
What is the goal in treating angina?
reducing myocardial O2 demand
Ranolazine MOA, use, AE
MOA - inhibits the late phase of sodium current -> reduce diastolic wall tension and O2 consumption (no effect on HR or contractility)
Use - angina refractor to other meds
AE - constipation, dizziness, HA, N, QT prolongation
Na+ channel blockers IA, IB, IC
IA - disopyramide, quinine, procainamide (double quarter pounder)
IB - mexiletine, lidocaine, tocainide (mayo, lettuce, tomato)
IC - flecainide, propafenone (fries, please)
Na+ channel blockers MOA, effects
MOA - decrease slope of phase 0 in mycoytes
Effects - increase effective refractory period (ERP), QT interval, and AP duration
Procainamide uses and SE
Wolffe-Parkinson-White (WPW)
SE: drug-induced lupus
Quinidine SE
cinchonism, thrombocytopenia, TdP
General Uses of Class IA Na+ Channel Blockers
atrial and ventricular arrhythmias, especially re-entrant SVT and VT
General Uses of Class IB Na+ Channel Blockers
acute ventricular arrhythmias (esp post MI), digitalis-induced arrhythmias
General Uses of Class IC Na+ Channel Blockers
SVTs, including atrial fibrillation (last resort for VT)
AE and C/I for Class IC Na+ channel blockers
C/I post MI and ischemic heart disease
AE - proarrhythmic, esp post-MI; toxicity is worse with hyperkalemia
Ivabradine MOA, Use, AE
MOA - inhibits funny sodium channels (If)
Effects - prolongs phase 4, decreased SA node firing
Use - chronic stable angina (when can’t take beta blockers), chronic HF
AE - luminous phenomena/visual brightness, HTN, bradycardia
Beta blockers
metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol
Beta blockers MOA
decrease cAMP, decrease Ca2+ current -> suppress abnormal pacemakers by decreasing the slope of phase 4 of the pacemaker cells
Beta blockers use in arrhythmias
SVT, ventricular rate control for a fib and a flutter, V tach
Beta Blockers AE
exacerbation of COPD and asthma, CV effects (bradycardia, AV block, HF); may mask Sx of hypoglycemia
Tx Beta blocker overdose with glucagon
Potassium Channel Blockers
Amiodarone, ibutilide, dofetilide, sotalol, bretylium
Potassium Channel Blocker MOA & effect
MOA - inhibit phase 3 of the myocyte
Effect - increase AP duration, increase ERP, increase QT interval
Clinical Use and AE of Potassium Channel Blockers
Use - a fib, a flutter, V tach; amiodarone can be used for WPW
AE - TdP for all
AE of amiodarone
pulmonary fibrosis, hepatotoxicity, hyper or hypothyroidism, photo dermatitis, CV effects (bradycardia, heart block, HF)
Calcium Channel Blockers
Nondihydropyridine (dihydropyridine have no effect on heart - only blood vessel; use for HTN)
Verapamil
Diltiazem
MOA & effects of CCB
MOA - inhibit phase 0 of pacemaker
Effects - decrease conduction velocity of AV node, increase ERP, increase PR interval
Use, AE, and C/I of CCB
Use - prevention of SVT, rate control in a fib
AE - constipation, flushing, edema, CV effects (HF, AV block, sinus node depression)
C/I - HF, DO NOT combine with beta blockers
Adenosine MOA, use, AE
MOA - increase K+ out of cell -> hyper polarizes cell and decreases intracellular calcium -> decreases AV node conduction -> stops heart
Use - diagnosing/treating SVT
(Effects blunted by theophylline - used for COPD and severe asthma)
AE - flushing, hypotension, chest pain
When is Mg2+ useful in regards to arrhythmias?
TdP and digoxin toxicity
What antihypertensive drug causes first-dose orthostatic hypotension?
alpha 1 blockers (-zosin), clonidine (alpha 2 agonist)
What antihypertensive drug causes hypertrichosis?
milnoxidil
What antihypertensive drug causes cyanide toxicity?
nitroprusside
What antihypertensive drug causes dry mouth, sedation, and severe rebound HTN?
clonidine (alpha 2 agonist)
