Cardio I Drugs Flashcards
(31 cards)
Lovastatin
MECH - struct sim to HMG CoA intermed
-rev competive inhib for active site of HMGCoA reductase
KINETICS: metab by CYP3A4;prodrug
SE: myopathy/rhabdomyolysis
CONTRAINDICATIONS: hypersens; active liver dz; elev of serum transaminases; preg; breast feeding
LP profile: TG decrease; HDL increase; LDL decrease
USE: first line for pt at high risk for MI due to hypercholesterolemia
Simvastatin
MECH: binds active site of HMGCoA reductase –> upreg LDL R
-prodrug
SE: same as other statins
LP profile: TG decrease; HDL increase; LDL decrease
USE: same as other statins
Atorvastatin
MECH: inhib active site of HMGCoA reductase
-active admin
Same as other statins
Cholestyramine
MECH: binds bile acids; increase bile acid excretion in feces –> liver makes more LDL R
KINETICS: time delay before effect (1-2wks)
SE: poor pt compliance
LP profile: TG INCREASE transiently, signif increase if > 250; HDL increase; LDL decrease
USE: hypercholesterolemia NOT when w/increased TG
Ezetimibe
MECH: binds NPC1L1 - inhib cholesterol transfer form intestine to cell; increased exp of LDL R
Metab to active metabolite
SE: do not use w/ bile acid sequestrants - will inhib absorp of drug
LP Profile: TG reduced; LDL reduced; HDL increased
USE: hypercholesterolemia when pt resistant to statins
* comb w/ simvastatin = 60% reduction of LDL but increased risk myopathy
Niacin
KINETICS: immed release - quick absorp; or long ax rel (increased risk hepatotox); extended rel - less SE
SE: intense cutaneous flush and pruritis (decrease w/ aspirin)
CONTRAINDICATION: peptic ulcer; gout; hepatic dysfx; caution w/ diabetics
*use w/ statins –> increased risk myopathy
LP profile: TG decrease (4-7d) ; LDL decrease (3-6 wks); HDL increase; REDUCES LPa
USE: hypertriglyceridemia, elev LDL (Esp in pts w/ low HDL)
Gemfibrozil
MECH: bind PPARaplpha - inhib de novo FA syn
SE: gen well tolerated
**this + statin = increase creatine kinase = renal failure
LP profile: TG decrease; LDL decrease (variable); HDL increase
USE: HIGH serum TG (>750); pt w/ high TG, low HDL (metabolic syn, T2DM)
Fenofibrate
MECH: binds PPARalpha
Same everything as gemfibrozil
Alirocumab
MECH: PCSK9 inhib - med of hepatic LDL R degredation –> increase avail of LDL R
Lomitapide
MECH: microsomal triglyceride transfer protein inhibitor: prevents assemb of apoB containing lipoproteins; inhib syn of chylomicrons and VLDL
Metab by CYP3A4
SE: risk of hepatotox; reduced absop of fat solub vitamins
USE: homozygous familial hypercholesterolemia
Mipomersen
MECH: apoB100 inhib
LDL decrease; ApoB decrease; Lpa decrease; tot cholesterol decrease
What to use in acute episodes of ischemic heart dz?
Fast acting nitrates
Drug classes used in prevention of MI
- beta adrenergic receptor blockers
- Ca channel blockers (dihydropyridines and non)
- Long acting nitrates
Beta adrenergic receptor blockers
Non Selective – Propranolol, Timolol, Carvedilol
Selective antag – Metoprolol, Atenolol
-reduce oxygen demand: decrease ventricular contraction; HR; BP
Contraindication: heart failure, diabetes, obstructive airway dz
Ca channel blockers
**block voltage gated L type Ca channels
Dihydropyridines –> Amlodipine; Nifedipine
-potent arterial vasodilator
-relieve ischemia by: decreasing oxygen demand (vasodilator-decrease afterload - red wall stress); increase oxygen supply by coronary vasodilation
Non-Dihydropyridines –> verapamil, diltiazem
- decrease contractility; bradycardia - less potent vasodilator - relieve ischemia by: decrease oxygen demand by red force of contraction and HR
SE: headache, flushing, edema, constipation
Long acting nitrates
Vasodilator - much greater effect on VENOUS bv
MECH: enz de nitrated in SM – free nitrate –> NO –> *guanylyl Cyclase = increase cGMP –> *PKG –> phos targets = decrease Ca, dephos of myocin
- *decreases preload
- lg 1st pass metab in liver = low oral bioavail
Acute therapy – nitroglycerin
Chronic therapy – isosorbide dinitrate; isosorbide mononitrate; nitroglycerin patch
*complete tolerance devel if used cont for more than few hours
Ranolazine
DOES not AFFECT HR or vasodilator
MECH: inhib late Na current in myocytes
Decrease freq angina episodes; decrease nitroglycerin consumption; increase exercise capacity
**prod dose depend increase in QT interval
USE: sub if other anti angina agents ineffective; add to traditional tx if relief of sx not achieved
Aspirin
MECH: irrev acetylates COX1 of platelet – block prod of TXA
USE: give to all pts Acute coronary syn (chew and swallow); low dose for coronary artery dz
CONTRA: hypersens; GI bleeding; Gout
Clopidogrel
MECH: inhib ADP activation of platelets; irrev
METAB BY CYP2C19
USE: comb w/ aspirin = increased benefit (increased bleeding risk)
Prasugrel
MECH: inhib ADP med activation of platelets
Irrev
Prodrug
Ticagrelor
MECH: inhib ADP med activation of platelets
REVERSIBLE = advantage if pt req surgery bc no waiting period necessary
What drug has SE of severe neutropenia and thrombocytic purpura?
Ticlopidine
Abciximab
MECH: block access of fibrinogen, vWF and other adhesive factors to GPIIb/IIIa R
IV; monoAb
USE: pt undergoing PCI; in comb w/ heparin or aspirin; w/alteplase for thrombolysis
Epifibatide
MECH: binds to GPIIb/IIIa R
Renal clearance
USE: pt undergoing PCI; pt w/unstable angina and MI, often + LMWH
