Treatments Quiz 5 (final week) Flashcards
Carvedilol
Selective Beta blocker
Improves survival in CHF
Ethacrynic acid
Loop diuretic that blocks NKCC in ascending loop of Henle.
Same as furosemide.
Apresoline
Arterial Vasodilator
Treatment for Diastolic CHF
Beta-blocker (more time for filling) and ACEI’s (decrease afterload and preload, but still has shown efficacy)
Not diuretics or Nitro
Nesiritide (Natrecor)
MOA: drug form of BNP –> decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis (sodium excretion). Thus, the net effect of BNP is a decrease in blood volume, which lowers systemic blood pressure and afterload, yielding an increase in cardiac output, partly due to a higher ejection fraction.
Needs to be infused IV
For stage IV HF. Improved dyspnea
Side effect - hypotension, cost
Metolazone (Zaroloxyn)
Quinazoline diuretic (similar to thiazides except PCT not DCT)
Inhibits Na/Cl cotransporter in PCT.
Side effects = hypokalemia
Ace Inhibitors (-pril)
MOA: Inhibit conversion of Angiotensin I to Angiotensin II
-Angiotensin II on the VSM results in an increase in intracellular Ca++ leading to vasoconstriction (increased BP)
-Angiotensin II on the proximal tubule results in increased Na+ reabsorption (H2O follows) → increased fluid volume → increased CO → increased BP
-Angiotensin II also results in an increased H+ excretion → increased Bicarbonate reabsorption → increased pH
Angiotensin II also acts on the adrenal cortex to cause an increase in aldosterone → sodium retention and potassium excretion (too much ACEI→ not enough potassium excretion = HYPERKALEMIA)
Angiotensin Receptor Blocker
MOA - Block receptors of Angiotensin II (AT1) on both the Vascular Smooth Muscle and the proximal tubule of the kidney.
- Angiotensin II on the VSM results in an increase in intracellular Ca++ leading to vasoconstriction (increased BP)
- Angiotensin II on the proximal tubule results in increased Na+ reabsorption (H2O follows) → increased fluid volume → increased CO → increased BP
- Angiotensin II also results in an increased H+ excretion → increased Bicarbonate reabsorption → increased pH
Clonidine
MOA: Stimulates alpha 2 receptors à block adenylyl cyclase à decrease norepinephrine release à decrease blood pressure
- Use in hypertensive urgency
- Adverse effects – fatigue, sedation, dry mouth, salt/water retention
Aliskiren
Direct Renin Inhibitor
Rarely used due to its severe side effects but it does exist.
HCTZ (thiazide diuretics)
Blocks Sodium Reabsorption in the DCT of the kidney → decreased water reabsorption
Specifically blocks the Na/Cl co-transporter by competing for the binding of the chloride site
In an unrelated mechanism, thiazides increase Calcium reabsorption
Side effects: hypokalemia
Furosemide
Inhibits the NKCC pump on ascending Loop of Henle→ decreased sodium transport → decreased H2O reabsorption
Side effects: hypokalemia
Spironolacone
MOA: aldosterone receptor antagonist –> decreased sodium resorbtion (increased potassium resorbtion)
Positive effects in treating CHF.
Potassium sparing –> can cause hyperkalemia
Terazosin (-zosins)
Antagonism of alpha receptors leads to decreased constriction of VSM → decreased TPR → decreased BP
*for final just remember the various effects of adrenergic agonists on BP given adrenergic antagonists
Hydralazine
MOA unknown –> arteriolar specific vasodilation.
Used in pregnancy and for African Americans w/ CHF (along w/ isosorbide dinitrate = BiDil)