HTN/CHF Drugs

Question 1

ACE Inhibitors

Answer 1

Lisinopril, Enalapril, Captopril, Ramipril
Block conversion of Ang 1–> Ang 2, decreasing GFR by blocking constriction of efferent arterioles. Also slow the breakdown of bradykinin, a potent vasodilator.

Clinical use: HTN, CHF, proteinuria, diabetic renal dz. Great benefit in pt with CKD, DM, and post-MI.

Toxicity: "captopril's CATCHH"
C- cough
A- angioedema
T- teratogen
C- creatinine increase (decrease GFR)
H- hypErKalemia  (don't use with K+ sparing diuretics)
H- hypOtension
* Never use in bilateral renal artery stenosis---further decrease GFR--> renal failure*

Question 2

Angiotensin II Receptor Blockers (ARB’s)

Answer 2

Losartan, Valsartan, Candesartan (-sartans)

Similar effects compared to ACE inhibitors but do NOT increase bradykinin—no cough or angioedema! Direct, reversible blockade of Ang II receptor.

Question 3

Ca2+ Channel Blocker

Answer 3

Nifedipine, Verapamil, Diltiazem, and Amlodipine

Block voltage-dependent Ca2+ ch in cardiac and smooth muscle thereby reducing muscle contractility.

Clinical use: HTN, angina, arrhythmias (except nifed), Raynaud’s

Advantages: no effect on cholesterol, non-sedating, okay to use in pt w/ asthma, v. little sexual dysfunction, safe in pregnancy

Disadvantages: peripheral edema—can lead to proteinuria!
HA/flushing, little effect on diastolic BP

Contracindicated: unstable angina, HF, hypotension, post-infarction, and in aortic stenosis.

Question 4

Nifedipine

Answer 4

Ca2+ Ch Blocker, a Dihydropyridine; acts as a VASODILATOR, with least effect on AV node (not an antiarrhythmic). Always give slow-release formula (except in premature labor can give immediate release)

Question 5

Amlodipine

Answer 5

Ca2+ Ch Blocker, a Dihydropyridine; acts as a VASODILATOR, with least effect on AV node (not an antiarrhythmic). Slow-onset drug with t1/2 of 24 hrs

Question 6

Diuretics

Answer 6

cause net loss of Na+/H20 in the urine. Different classes act on different portions of the nephron. Initially will decrease CO, but overtime Na+ balance and CO regain up to 95%, with that remaining 5% decreasing TPR just enough to keep BP low.

Question 7

Mannitol

Answer 7

Osmotic diuretic that acts on the Thin Descending LOH, increases tubular fluid osmolarity, increases urine flow, decreases intraocular/intracranial pressure.

Clinical uses: drug overdose, intracranial/intraocular pressure

Toxicity: pulmonary edema, dehydradation. Contraindicated in CHF.

Question 8

Acetazolamide

Answer 8

PCT weak diuretic; Carbonic Anhydrase Inhibitor—> increases HCO3 excretion

Clinical Use: Glaucoma, urinary alkinalization, Met Alk, altitude sickness,

Toxicitiy: Can cause Met Acidosis “ACIDazolamide causes ACIDosis”. Also can cause NH3 toxicity, and is a sulfa drug (sulfa allergy)

Question 9

Loop Diuretics

Answer 9

Furosemide (lasix), Bumetanide, Torsemide, Ethacrynic Acid.

NKCC2 Inhibitors along ascending LOH. Promote NaCl and K+ excretion. Impairs kidney’s urine concentrating abilities. Also promotes Ca2+ loss (LOOPS LOSE CALCIUM).

Clinical use: edematous states (CHF, cirrhosis, nephrotic syndrome, pulm edema), HTN, hypErCalcemia. Does NOT prolong life.

Toxicity: OH DANG!
O- otoxocitiy
H- hypOKalemia
D- dehyration
A- Allergy to SULFA (all except ethacrynic acid)
N- nephritis
G- Gout

Question 10

Hydrochlorothiazide

Answer 10

HCTZ–thiazide diuretic, inhibits NaCl reabsorption in early DCT, reducing diluting capacity of the nephron. Decreases Ca2+ Excretion!

Clinical Use: HTN, CHF, hyperCalciUria, nephrogenic DI.

Toxicity: HyperGLUC

• hypOnatremia
• hypErGlycemia
• hypErLipidemia
• hypErUricemia
• hypErCalcemia

Question 11

K+ sparing diuretics

Answer 11

Spironolactone, Eplerenone, Triamterene, and Amiloride.
“K+ take a SEAT”

Clinical uses: Hyperaldosteronism, K+ depletion, CHF.

Question 12

Spironolactone and Eplerenone

Answer 12

K+ sparing weak diuretics. Spironolactone and Eplerenone are competitive Aldo Receptor Antagonists that act in cortical CD, allowing Na+ excretion.

Clinical uses: Hyperaldosteronism, K+ depletion, CHF. DOES prolong life.

Toxicity: Gynecomastia/antiandrogen effects at high doses, HyperKalemia (can lead to arrhythmia).

Question 13

Triamterene and Amiloride

Answer 13

K+ sparing diuretics, block ENaC reabsorption of Na+ in cortical CD.

Clinical uses: Hyperaldosteronism, K+ depletion, CHF.

Toxicity: HyperKalemia (can lead to arrhythmia).

Question 14

Distal Convoluted Tubule Diuretics

Answer 14

HCTZ, Chlorthalidone, Metolazone

Block NCC in the DCT; therefore blocks Na+ reabsorption, decreasing urine diluting capacity in nephron, promotes Ca2+ reabsorption (decreases excretion).

Clinical use: HTN, has longer t1/2 than Loop Diuretics

Toxicity: hypOKalemia, Met. acidosis, and Hyponatremia. HyperGLUC (glycemia, lipidemia, uricemia, calcemia).

Question 15

Beta-adrenergic Blockers

Answer 15

Propanolol, Metoprolol, Carvediolol, Atenolol (-olol’s)

Non-selective vs. cardioselective:
cardioselective (Metoprolol/carvediolol/atenolol) best options to tx HTN, though beta blockers are NOT first line tx for HTN.

Decrease CO, but BP drop slow because of slow-onset vasodilation.

Advantages: best post-MI and in progressive CHF.
*paradoxical tx in CHF: lethal in shorterm use in decompensated pt, but in stable pt’s in the longterm actually improves ventricular responsiveness to adrenergics and improves LV systolic fxn.

Disadvantages: fatigue, lethargy, loss of libido, impotence, memory issues, can’t stop suddenly.

Contraindicated in Olympic athlete.

Question 16

Digoxin

Answer 16

cardiac glycoside, a weak positive inotrope, works best in CHF in pts with worse EF, but of no value in pts with diastolic dysfunction. Doesn’t decrease mortality, but reduces hospitalization rates and reduces sxs so rational to use in CHF.

Question 17

Clonidine

Answer 17

centrally-acting sympatholytic; acts on post-synaptic alpha receptors, decreases out flow of SNS, decreases innervation of CV tissue, decreases BP.

3rd/4th line tx for HTN. Good for pt with anxiety or addiction issues. Causes less postural hypotension compared to other drugs, decreases total cholesterol.

Side effects: sedation, dry mouth, nausea, dizziness, HA, congestion, sexual dysfunction; if suddenly stop get rebound sxs: HTN, sweating, tachycardia.

Question 18

Alpha methyldopa (Aldomet)

Answer 18

centrally acting sympatholytic, safe to use in pregnancy. Side effects include nightmares, lupus like dz, lactation issues.

Question 19

Alpha adrenergic blockers

Answer 19

block action of NE in periphery by competitively blocking alpha-receptors; leads to VASODILATION. Improved efficacy if used with diuretics or beta blocker. Good for pts with BPH.

Side effects: postural hypotension, pseudotolerance (may need to increase dose).

Question 20

Vasodilators

Answer 20

act directly on vascular smooth muscle–> vasodilation. Decreases periph vasc resistance to drop BP.

Hydralazine, minoxidil, diazoxide, sodium nitroprusside.

Question 21

Hydralazine

Answer 21

Arterial vasodilator, reduces afterload. Used to tx severe HTN, CHF.

First line tx for HTN in pregnancy (along with methyldopa).
Frequently given with beta-block to prevent reflex tachycardia.

Toxicity: compensatory tachycardia (contraindicated in CAD/angina), fluid retention, nausea, HA, angina, lupus-like syndrome.

Question 22

Minoxidil

Answer 22

direct arterial vasodilator. Increases permeability of cell to K+–> hyperpolarization and decreased muscle ctxn.

Side effects: Na+/fluid retention, tachycardia, hypertrichosis (hair growth).