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74 Cards in this Set

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drug class that prevents renin release
Beta blockers
drug class that blocks renin actions
ACE-inhibitors
drug class that blocks the increase in preload with angiotensin II
diuretics
drug class that blocks the increase in afterload with angiotensin II
vasodilators
class and adverse side effects of this antihypertensive drug: hydrochlorothiazide
diuretic- hypokalemia, mild hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia
class andadverse side effects of this antihypertensive drug: loop diuretics
diuretic- potassium wasting, metabolic alkalosis, hypotension, ototoxicity
class andadverse side effects of this antihypertensive drug: clonidine
sympathoplegics- dry mouth, sedation, severe rebound HTN
class andadverse side effects of this antihypertensive drug: methyldopa
sympathoplegics- sedation, + coombs test
class andadverse side effects of this antihypertensive drug: hexamethonium
sympathoplegics- severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction
class andadverse side effects of this antihypertensive drug: reserpine
sympathoplegics- sedation, depression, nasal stuffiness, diarrhea
class andadverse side effects of this antihypertensive drug: guanethidine
sympathoplegics- ortho/exercise hypotension, sexual dysfunction, headache
class andadverse side effects of this antihypertensive drug: prazosin
sympathoplegics- 1st dose ortho hypotension, dizziness, headache
class andadverse side effects of this antihypertensive drug: beta blockers
sympathoplegics- impotence, asthma, CV effects, CNS effects
class andadverse side effects of this antihypertensive drug: hydralazine
vasodilators- N, headache, lupus-like syndrome, reflex tachy, angina, salt retention
class andadverse side effects of this antihypertensive drug: minoxidil
vasodilators- hypertrichosis, pericardial effusion, reflex tachy, angina, salt retention
class andadverse side effects of this antihypertensive drug: nifedipine, verapamil
vasodilators- dizziness, flushing, nausea, constipation (verapamil), AV block (verapamil)
class andadverse side effects of this antihypertensive drug: nitroprusside
vasodilators- dcyanide toxicity (releases CN)
class andadverse side effects of this antihypertensive drug: diazoxide
vasodilators- hyperglycemia (reduces insulin releas, hypotension)
class andadverse side effects of this antihypertensive drug: captopril, enalapril, fosinopril
ACE-inhibitors- hyperkalemia, cough, angioedema, taste changes, hypotension, pregnancy problems (fetal renal damage), rash, increase renin
class andadverse side effects of this antihypertensive drug: losartan
fetal renal toxicity, hyperkalemia
MOA and AE's for hydralazine
increase cGMP--> smooth muscle relaxation---> vasodilates arterioles> veins--> decreases afterload Aes- compensatory tachy, fluid retention, lupus-like syndrome
MOA and AE's for minoxidil
K+ channel opener--> hyperpolarizes and relaxes vascular smooth muscle AE's = hypertrichosis, pericardial effusion
MOA and AE's for calcium channel blockers as antihypertensive
block voltage-dependant L-type channels of cardiac and smooth muscle --> reduce muscle contractility. AE's = cardiac depression, peripheral edema, flushing, dizziness, and constipation
MOA and AE's for nitroglycerin, isosorbide dinitrate
vasodilate by releasing NO in smooth muscle, causing increase in cGMP and smooth muscle relaxation- dilates veins>>>arterioles decreases preload. AE's tachycardia, hypotension, flushing, headache. "Monday disease"
3 drugs for malignant HTN treatment:
nitroprusside (NO cGMP), fenoldapam (D1 agonist relaxes renal smooth muscle), diazoxide(K+ channel opener- hyperpolarizes and relaxes smooth muscle)
goal of antianginal therapy:
reduce myocardial O2 consumption via decreaseing one of the following: EDV, BP, HR, contractility, ejection time
of the Ca+ channel blockers, which ones work more at vascular smooth muscle vs heart
vascular smooth muscle- nifedipine>diltiazam>verapamil heart verapamil>diltiazam>nifedipine
as an antianginal agent, nitrates primarily work to affect _____
preload- thereby reducing EDV, BP, ejection time, and MVO2 consumption
as an antianginal agent, beta blockers primarily work to affect _____
afterload- thereby reducing BP, contractility, HR, and MVO2
combined effect of nitrates and beta blockers on EDV, BP, HR, contractility, ejection time, MVO2:
no effect or decreased EDV, decreased BP, decreased HR, little or no effect on contractility, little or no effect ejection time, big decrease in MVO2 consumption!!!! Yeah!!!!
best drug at lowering LDL
statins- HMG-CoA reductase inhibitors
Side effects of statins
expensive, reversible increase in LFTs, myositis
MOA of niacin as a lipid lowering agent
inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation
what do you coadminister with niacin to reduce side effect?
ASA- reduces facial flushing
MOA of cholestyramine, colestipol
(bile acid resins) prevent intestinal reabsorption of bile acids- liver must use cholesterol to make more
Adverse effects of cholestryamine, colestipol
bile acid resins tast like- well, yeah- GI discomofrt, decreased absoprtion of fat soluble vitamins
ezetimibe MOA
prevents cholesterol reabsortion at small intestine brush border- only effects LDL
gemfibrozil, clofibrate, bezafibrate, fenofibrate MOA
upregulate Liproprotein lipase LPL to induce TG clearance- good at lowering triglycerides
gemfibrozil, clofibrate, bezafibrate, fenofibrate side effects
myositis, increas LFTs
MOA of cardiac glycosides
digoxin- direct inhibitor of Na/K/ATPase leads to indirect inhibition of Na/Ca+ exchanger/intipor--> increase inctracellular Ca = positive inotropy
uses of digoxin
CHF (increases contractility), atrial fib- decreases conduction at AV node and depression of SA node)
ECG side effects of digoxin
increase PR interval, decreased QT interval, scooping of ST segment, T-wave inversion
non ECG side effects of digoxin
increased parasympathetic activity: N, V, D, blurry yellow vision. Arrythmia. Toxicities increased by renal failure, hypokalemia potentiates effects, and quinidine (decreases clearance, displaces from tissue binding sites)
digoxin OD antidote
slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg++
class I antiarrhythmics are all ____ channel blockers
Na+
common MOA of all Class I antiarrhythmics
Na+ channel blockers- slow/block conduction. Decrease the slope of phase 4 depolarization and increase the threshold for firing in abnormal pacemaker cells. (state dependent)
what are the class IA antiarrhythmics?
Quinidine, Amiodarone (also class III), procainamide, disopyramide Queen Amy Proclaims Diso's Pyramide
Class IA antiarrhythmics ___ AP duration, ____ effective refractory period, and ___ QT interval
increase, increase, increase
which class IA antiarrhythmic has a reversible SLE-like side effect?
procainamide
which class IA antiarrhythmic can produce cinchonism- headache, tinitis; thrombocytopenia, torsades de pointes (increased QT interval)?
quinidine
what are the class IB antiarrhythmics?
Lidocaine, mexiletine, tocainide I'd Buy Lidy's Mexican tacos (phenytoin also fits this)
what are the class IC antiarrhythmics?
flecainide, encainide, propafenone
what are the class II antiarrhythmics?
propranolol, esmolol, metoprolol, atenolol, timolol (beta blockers)
what are the class III antiarrhythmics?
sotalol, ibutilide, bretylium, amiodarone (also class IA)
what are the class IV antiarrhythmics?
verapamil, diltiazem
class IB antiarrhythmics ____ AP duration
decrease- affect ischemic or depolarized purkinje and ventricular tissue
uses for class IB antiarrhythmics
acute ventricular antiarrhythmias -especially post MI- and digitalis induces arrythmias
side effects for class IB antiarrhythmics
local anesthetic- CNS stimulation/depression, CV depression
class IC antiarrhythmics ____ AP duration
have no change on
class IC antiarrhythmics are used as a last resort in refractory ____ and intractable ____.
Vtachs that progress to Vfib, SVT
toxicity of class IC antiarrhythmics:
proaarhythmic- especially post MI (contracindicated)- significantly prolongs refractory perios in AV node
common toxicity for all class I drugs-
hyperkalemia
MOA for class II antiarrhythmics
beta blockers-decrease cAMP leads to decrease Ca++ currents- suppress abnormal pacemakers by decreasing slope phase 4. AV node esp. Increase PR interval.
clinical use of class II antiarrhythmics
V-tach, SVT, slowing ventricular rate during a-fib and atrial flutter
toxicity of class II antiarrhythmics
impotence, exacerbation of asthma, bradycardia, AV block, CGF, sedation, sleep alteration. May mask signs of hypoglycemia- metoprolol can cause dysliidemia
MOA for class III antiarrhythmics
K+ channel blocker increase AP duration, increase ERP- used when other antiarrhythmics fail. Increased QT interval
sotalol (class III antiarrhythmic) side effects:
torsades de pintes, excessice beta block
amiodarone (class IA/III antiarrhythmic)
pulmonary fibrosis, conreal deposits, hepatotoxicity, skin deposits in photodermatitis, neuro effects, bradycardia, heart block, CHF, hypothyroidism/hyperthyroidism
wolff--parkinson-white syndrome (class III antiarrhythmic)
amiodarone
what labs need to be checked when on amiodarone?
PFTs, LFTs, TFTs (thyroid)
MOA of class IV antiarrhythmics
Ca ++ channel blockers affect AV nodal cells-- decreasing conduction velocity, increasing ERP, PR interval. Used in prevention of nodal arrythmias
AE's of class IV antiarrhythmics
constipation, flushing, edema, CHF, AV block, sinus node depression, torsades de pointes (bepridil)
MOA of adenosine on heart
increase K+ out of cell hyperpolarizes it. Drug of choice in diagnosing/abolishing AV nodal arrhythmias. Very short acting- flushing, hypotension, chest pain
Mg++ is effective as an antiarrhythmic in treating ______ and _____ toxicity
torsades de pointes, digoxin