Random Pharm Flashcards
Which type of antihypertensive must be used cautiously in decompensated CHF patients + is contraindicated in cardiogenic shock?
beta-blockers
First-line antihypertensive in T2DM pts
ACEi/ARBs (protective against diabetic nephropathy)
vasoselective Ca2+ channel blockers
amlodipine, nifedipine
dihydropyridine
cardioselective Ca2+ channel blockers
verapamil > diltiazem
(“Verapamil = Ventricle”)
non-dihydopyridine
how do Ca2+ channel blockers lower blood pressure
block L-type Ca2+ channels of cardiac and smooth muscle –> decreased muscle contractility
(decreased risk of vasospasm, hence used in prinzmetal angina and raynaud’s)
which drug can be used to prevent cerebral vasospasm following subarachnoid hemorrhage?
nimodipine (dihydropyridine Ca2+ channel blocker)
Finding Nimo in the see of blood that is a subarachnoid hemorrhage
antihypertensives used in pregnancy
hydralazine (can cause lupus-like syndrome) + methyldopa (can cause hemolytic anemia)
how does hydralazine work?
inceases cGMP –> smooth muscle relax’n (arterioles > veins; afterload reducer)
what drug is commonly given with hydralazine? why?
beta-blocker, to prevent reflex tachycardia
which drug given in hypertensive emergencies is the only IV agent that increases renal perfusion and decreases BP (ie, is good for pts with renal failure)?
fenoldopam (D1 receptor agonist)
feared side effect of nitroprusside (given in hypertensive emergency)
cyanide toxicity (treat with sodium thiosulfate)
goal of antianginal therapy
reduce myocardial O2 consumption
main effect of nitrates in treating angina (nitroglycerin, isosorbide, dinitrate)
reduce preload
main effect of beta-blockers in treating angina
reduce afterload
partial beta-agonists contraindicated in angina
pindolol and acebutolol
mechanism of statins
HMG-CoA reductase inhibitors
main effect of statins
reduce LDL
statin side effects
hepatotoxicity and rhabdo (esp when used with fibrates and niacin/B3)
main effect of niacin/B3
decrease LDL and increase HDL
mechanism of niacin/B3
reduce VLDL synthesis and release by hepatocyte; inhibit lypolysis in adipocytes
side effects of niacin/B3
flushing, hyperglycemia, hyperuricemia
cholestyramine, colestipol, colesevelam
bile acid resins
mechanism and effect of bile acid resins (“chol”, “col”)
prevent intestinal reabsorption of BILE ACIDS –> lower LDL
side effects of bile acid resins
cholesterol gallstones, GI upset, decreased abs of fat soluble vits
mechanism and effect of ezetimibe
prevent absorption of CHOLESTEROL from small intestinal brush border –> lower LDL
effect of fibrates
decrease TGs
mechanism of fibrates
upregulate LPL (lipoprotein lipase) --> increased TG clearance activate PPAR-alpha to induce HDL synthesis
side effects of fibrates
myositis (esp w/ statins);
hepatotox;
cholest gallstones (esp w/ bile acid resins, “chol” “col”)
mechanism of digoxin
direct inhibition of Na/K ATPase --> indirect inhib of Na/Ca exchanger --> increased intracellular Ca --> increased contractility; stimulates vagus (how???) --> decreased HR
RFs for digoxin toxicity
renal failure (decreased excretion), hypokalemia, tx w/ verapamil, amiodarone, quinidine [–> decreased dig clearance]
digoxin: class of drug
cardiac glycoside
digoxin: use
CHF, A Fib
Nasty Bets Kill Cats
Class I: Na+-channel blocker (slow depolar’n, phase 0)
Class II: Beta-blocker (slow SA/AV conduction rates, ie phase 4)
Class III: K+-channel blocker (slow repol’n)
Class IV: Ca2+-channel blocker (slows conduction velocity)
Double Quarter Pounder
Class IA: disopyramide, quinidine, procainamide
Lettuce, Tomato, Mayo
Class IB: lidocaine, tocainide, mexilitine (, +/- phenytoin)
Can i have More Fries Please?
Class IC: Moricizine, Flecainide, Propafenone
AIDS Kills
K = K+-channel blocker (class III antiarrhythmics) Amiodarone Ibutilide Dofetilide Sotalol
Class IB is Best for ???
post-MI, dig-induced arrhythmia
Class IC is Contraindicated in ???
structural and ischemic heart dz (eg, post-MI…pro-arrhythmic)
Which class II antiarrhythmic is very short acting?
Esmolol
Which class of antiarrhythmics may mask hypoglycemia?
class II (beta-blockers)
I bet(a) you don’t know I’m low on sugar!
Remember to check ??? (x3) when using amiadorone
PFTs, LFTs, TFTs
Drug of choice when diagnosing/abolishing SVTs
adenosine, very short acting (~15s)
First-gen H1-blockers
names contain “en/ine” or “en/ate”
diphenhydramine, dimenhydrinate, chlorpheniramine
Second-gen H1-blockers
names usually end in “adine” (eg loratadine) + cetrizine
used for allergy; far less sedating than first gen b/c decreased entry into CNS
Which asthma drug is rarely used due to its narrow therapeutic index?
theophylline (PDE inhibitor) –> cardiotox, neurotox
Which class of drugs is considered 1st-line therapy for chronic asthma?
corticosteroids (beclomethasone, fluticasone)
What drug is used in an acute asthma exacerbation?
albulterol (beta-agonist)
Examples of LABA
salmeterol, formoterol
What drug is used to diagnose asthma?
methacholine (muscarinic receptor agonist –> provocation challenge)
What drug is used to tx pulmonary arterial HTN?
bosentan (competitively antagonizes endothelin-1 receptors –> decreased pulm vasc resistance)
What diuretic is used to tx drug overdose?
mannitol (osmotic diuretic –> flush that shit out)
OH DANG
side effects of loop diuretics Ototoxicity Hypokalemia Dehydration Allergy (sulfa) Nephritis (interstitial) Gout
examples of loop diuretics
Furosemide, torsemide, bumetanide, ethacrynic acid
loop diuretic for pts w/ sulfa allergy
ethacrynic acid (phenoxyacetic acid deriv)
examples of thiazides
HCTZ, chlorthalidone, indapamine, metolazone
CHIMe
HyperGLUC
some side effects of HCTZ
HyperGlycemia, Lipidemia, Uricemia, Calcemia
[also causes hypoK, metabolic alKalosis]
The K+ STAys
K+-sparing diuretics: Spironolactone, eplerenone [aldo antagonists]; triamterene, amiloride [ENaC blockers]
Which diuretic causes gynecomastia, antiandrogen effects?
spironolactone (used to treat hirsutism)
Diuretic effects: Urine NaCl
increased (all except acetazolamide)
Diuretic effects: Urine K+
up in loop and thiazides
down in K+-sparing
Diuretic effects: blood pH
down (acidemia) in CAHi’s, K+-sparing
up (alkalemia) in loops and thiazides
Diuretic effects: Urine Ca2+
up in loops
down in thiazides (used to prevent nephrolithiasis)
CATCHH
ACEi’s side effects: cough, angioedemia (contraindicated in C1 esterase inhibitor defic), teratogen (fetal renal malform), elevated Cr (secondary to decreased GFR), hyperK, hypoTN
ACEi’s = contraindicated in ???
bilateral renal artery stenosis; further decline in GFR can precipitate renal failure
