Cardiology--Pharmacology Flashcards
What are some dihydropyridine CCBs?
amlodipine, nimodipine, nifedipine
What are some non-DHPR CCBs?
diltiazem, verapamil
greater effects on vascular smooth muscle?
amlodipine =nifedipine
greater effects on heart?
verapamil > diltiazem > amlodipine
subarachnoid hemorrhage
use nimodipine to prevent vasospasm
CCBs side effects?
cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation
hydralazine moA?
increases cGMP–>smooth muscle relaxation, vasodilates arterioles > veins, afterload reduction
first line use for HTN in pregancy
hydralazine with methyldopa
what should be co-administered with hydralazine?
a beta blocker to prevent reflex tachycardia
hydralazine SEs?
reflex tachy, fluid retention, lupus like syndrome
nitroprusside moa?
short acting, increases cGMP via direct release of NO, can cause cyanid toxicity
fenoldopam moa?
D1 receptor agonist–>coronary, peripheral, renal, splanchnic vasodilation, decreases BP and increases natriuresis
nitroglycerin, isosorbide dinitrate moa
vasodilates by increasing NO in vascular smooth muscle, increase in cGMP and smooth muscle relaxation–>Dilates veins»_space;> arteries, decrease preload
b blockers contraindicated in angina?
pindolol and acebutolol–partial B agonists
statin effects on lipids?
— LDL, + HDL, - TGs
Niacin (B3) effects on lipids?
– LDL, ++HDL, - TGs
Bile acid resins lipid effect?
– LDL, slightly increase HDL/TGs
ezetimibe lipid effect?
– LDL, no effect on other lipids,
Fibrates lipid effect?
- LDL, + HDL, —TGs
lipid lowering agent combos that cause rhabdomyolysis?
statin + fibrate; statin + niacin
hepatotoxic lipid lowering agents?
statains and fibrates, ezetimibe
red flushed face, hyperglycemia, hyperuricemia
Niacin, decrease flushing by aspirin, possibly a prostaglandin mediated effect
decrease absorbtion of fat soluble vitamins, lipid lowering agent
bile acid resins
lipid lowering agent that causes cholesterol gall stones
fibrates, esp in conjunction with bile acid resins
niacin moa?
inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthess
fibrate moa?
upregulate LPL–>increase TG clearance, activates PPAR-alpha to induce HDL synthesis
digoxin toxicity?
cholinergic, eKG: increased PR, decreased QT, ST scooping, T wave inversion, arrhythmia, AV block; hyperkalemia–poor prognosis;
factors predisposing to digoxin tox?
renal failure, hypokalemia (permissive for digoxin binding to Na/K ATPase K+ binding site); verapamil, amiodarone, quinidine (decreases clearance)
Class IA antiarrythmics? Moa?
quinidine, procainable, disopyramide; block Na channels, affects phase 0 depolarization and phase 3 repolarization–>increased AP duration, increased effective refractory period, increases QT interval
Class IA use?
both atrial and ventricular arrythmias esp re-entrant and ectopic SVT and VT (like WPW)
Class IA sideeffects?
cinchonism (headache, tinnitus) with quinidine, reversible SLE like syndrome with procainamide, heart failure with disopyramide, thrombocytopenia, torsades de pointes due to prolonged QT
General rules for Class I antiarrhythmics?
All are Na channel blockers. all decrease slope of phase 0 depolarization and increased firing threshold in abnormal pacemaker cells. State dependent. Hyperkalemia increases tox for all class I drugs.
class IB antiarrythmics? moa?
lidocaine, mexiletine; decrease AP duration, blocks Na in very rapidly depolarizing cells, preferentially affects ischemic/depolarized purkinje and ventricular tissue
Class IC antiarrhthymics? moa?
Flecainide, Propafenone; significant prolongs refractory period in AV node, no effect on AP duration
Class IC use?
SVTs including afib
Class IC tox?
pro-arrhythmic, contraindicated post MI or structural heart disease
Class II antiarrhthymics? moa?
B blockers, decrease SA/AV nodal activity by decreasing cAMP/Ca currents. Suppresses abnormal pacemakers by decreasing slope of phase 4; AV node particularly sensitive
Class II use?
SVT, slowing ventricular rate in afib/flutter
B-blocker tox?
exacerbate COPD/asthma, sedation/sleep alteration, may mask signs of hypoglycemia, metoprolol can cause dyslipidemia, propanolol can exacerbate prinzmetals angina, tx overdose w/ glucagon
Class III? moa?
amiodarone, ibutilide, dofetilide, sotalol; blocks K efflux, increases AP length w/out affects Na or Ca–>increases AP duration, prolonged QT; used when other drugs fail
class III use?
afib/flutter; VT (amiodarone, sotalol)
SEs of sotalol?
torsades de points, excessive B blockade
SE of amiodarone? what to always check?
PFTS, LFTs, TFTs; pulmonary fibrosis, liver tox, hyper/po thyroidism, corneal deposits, blue gray skin deposits–>photodermatitis; neurologic effects, constipation, CV effects
amiodarone can be in what classes?
class I, 2, 3, and 4 and affects lipid membrane.
Class IV antiarrthmics? moa?
CCBs, verapamil, diltiazem; decrease conduction velocity, increase ERP/PR interal
Class IV use?
prevention of nodal arrythmias, rate control in afib
Class IV SEs?
constipation, flushing, edema
adenosine MOA?
increases K flux out of cells–>hyperpolarizing cell and decreaseing Ica
adenosine use?
drug of choice in diagnosing/abolishing SVTs, very short half life (15 sec)–can cause hypotension/chest pain
Mg2+ use?
torsades de pointes and digoxin tox
which classes are nodal blockers?
class II (beta blockers), class IV (CCBs)
