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2 Cards in this Set

  • Front
  • Back
ACE inhibitors (Lisinopril)
1. EFFECTS:
- decrease systemic arterial pressure by decreasing vasoconstriction, facilitate natriuresis by decreasing aldosterone production and reducing Na reabsorption from distal nephron, and reducing adverse ventricular remodeling

2. CLINICAL USES
- in hypertensive pts: lower BP without change in CO. effective in most pt irregardless of renin levels. inc GFR by dilating afferent and efferent glomerular arterioles. do not affect glucose or lipid levels. do not result in hypokalemia. USED IN DIABETIC HYPERTENSIVE PT because of decreased diabetic nephropathy
- pts with heart failure: reduce peripheral vascular resistance (afterload), reduce cardiac filling pressures (preload), and inc CO. BP DOES NOT FALL BECAUSE OF INC CO.

3. ADVERSE:
-should be reduced in patients with renal failure
- hypotension: especially in pts with heart failure whose BP is heavily dependent upon AII facilitated vasoconstriction
- hyperkalemia: because of reduced aldosterone, renal insufficiency, DM, and use of K-sparring diuretics may cause dangerous hyperkalemia
- renal insufficiency: may results in hypotension with decreased renal perfusion and azotemia. in pts with bilateral renal artery stenois, renal failure may be precipitated by ACEi facilitated vasodilation of efferent arteriole (efferent vasoconstriction dependent upon AII)
- cough: probably by increased bradykinin
- not to be used in pregnancy. may result in fetal injury during 2nd and 3rd trimester
ARB (Losartan)
1. MECHANISM:
- block the AT1 receptor (AT2 receptor found in fetus)
- block actions of AII. more effective than ACEi, because ACEi does not completely block all AI to AII conversion
- enhanced by concomitant use of thiazide diuretic
- recommended in heart failure pts who are intolerant of ACEi

2. ADVERSE:
- hypotension and hyperkalemia
- no cough produced