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25 Cards in this Set
- Front
- Back
what are the major actions of drugs used to treat heart failure? |
preservation or recovery of cardiac function and reduction of symptomatic edema |
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what does the heart do during heart failure that makes it selfish?
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suppress requests of periphery, augment heart function, reverse fluid retention |
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how do you determine right heart failure? left heart failure? |
right- systemic edema left- pulmonary edema |
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what are the four effects of cardiovascular adaptation during heart failure? what are the negative effects of each? |
increase preload, arterial constriction, tachycardia and inotropy, ventricular hypertrophy preload- pulmonary and systemic edema, increased myocardial o2 consumption constriction- increased after load, decrease stroke volume, increase mv02 tachy ino- short filling, increased mv02, down regulation of b receptors hypertrophy- diastolic and systolic dysfunctin, risk of cell death and arrythmia |
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what part of the above dose digoxin work? |
on tachycardia and inotropy |
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how does hypertrophy effect look if you have systolic failure? dystiolic failure? |
systolic- thin chambers dystolic- thick chambers |
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MOA of thiazide diuretic? MOA of loop diurectic? |
inhibit the sodium chloride symporter in the DVT loop- na,k,cl symporter in ascending loop of henele |
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how do diuretics reduce symptoms of heart failure? |
reduce preload which results in reduced capillary overload and ventricular wall stress (prevents remodeling) |
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why are loops perferred over thiazides? |
more efficacious in fluid reduction |
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MOA of aldosterone antagonist? effects on electolytes? |
inhibits the sodium reabsorption in the collecting duct by preventing synthesis of sodium channels decrease na increase k and mg |
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what do the aldosterone antagonist directly effect on the heart? why is this good to prevent? |
prevents myocardial fibrosis and fibroblast formation, these increase risk of arrythmia since conduction becomes blocked |
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main benefit of the aldonsterone antagonsits? |
improve survival |
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what are the detrimental effects of angiotensin 2? |
vascular hypertrophy, arteriolar constriction, peripheral NE release, catecholamine release from adrenal medulla, sodium reasorption, aldosterone release, adh release |
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MOA of hydralazine? does it increase venous capcitance? what does this mean? |
direct arteriolar vasodilator which reduces afterload does not increase venous capcitance so combine with isosrbide dinitrate to prevent more edema |
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why are beta adrenergic agonists bad during heart failure? what did the beta antagonists show? |
contributing to viscious cycle, more stimulation is toxic to the myocardium reversal of myocardial damage, improved ejection fraction |
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how long does it take to see benefit of beta blockers in heart failure |
at least 3 months |
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what is digoxin dosed on? why? |
lean body mass, does not go into fat |
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describe the MOA of cardiac glycoside like digoxin? start with normal phsiology |
action potential stimulates na entry this stimulates calcium entry via L type channel in the transverse tubule this activates the ryanodine receptor to release more ca this causes contraction reversed by removal of ca into sr or by na/ca exchanger which uses atp digoxin inhibits the na/k atpase pump to prevent sodium leaving, decreasing electrochemical gradient this decreases the function of the na/ca exchanger and ca remains in the cell this extra ca is pumped into sr and greater ca release leading to inotropy |
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what do the cardiac glycosides to contractility of the atrium and ventricle? AV and SA node? on conductivity? on refractory period? |
increase both no effect on either c- decrease both r- increase both |
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why do cardiac glycoside have no effect on av and sa node? |
the nodes are sensitized to vagal nerve and depend on stimulation form there |
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what can cardiac glycosides do at therapetuic levels? toxic levels? |
decrease SNS increase SNS |
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where is digoxin abosrbed? what does it depend on? how is eliminated? |
intestine, P-gp activity renally |
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where are the p-gp transporters found? generally what does inhibiting it cause? |
renal, liver, gi blocking it prevents removal of things, and things remain in the body longer |
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what drugs result in digoxin toxcity? what are each of there effects? |
quinidine tox, verapamil tox, rifampin lower levels, loop and thiazide diuretics or anything that deplets potassium tox |
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