First Aid High Yield Cardio Pharmacology Flashcards
What 3 diseases are classified under Antihypertensive therapy?
1) Essential hypertension
2) CHF
3) Diabetes mellitus
What is the antihypertensive therapy regimen used for Essential Hypertension?
Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers
What is the antihypertensive therapy regimen for CHF?
-What is a special indication for ß-blockers?
Diuretics, ACE inhibitors/ARBs, ß-blockers (compensated CHF), K+ sparing diuretics
-ß-blockers must be used cautiously in decompensated CHF, and are contraindicated in cardiogenic shock
What is the antihypertensive therapy regimen for diabetes mellitus?
-What is a special indication for ACE inhibitors?
ACE inhibitors/ARBs, calcium channel blockers, diuretics, ß-blockers, α-blockers
-ACE inhibitors are protective against diabetic nephropathy
Calcium channel blockers
- MOA:
- Clinical Use:
- Toxicity
- Nifedipine, verapamil, diltiazem, amlodipine
- MOA: Block voltage dependent L-type calcium channels of cardiac and smooth muscle and thus reduce muscle contractility.
- Vascular smooth muscle - amlodipine = nifedipine > diltiazem > verapamil.
- Heart - verapamil > diltiazem > amlodipine = nifedipine (VERAPAMIL = VENTRICLE)
- Clinical Use: Hypertension, angina, arrhythmias (not nifedipine), PRINZMETAL’s angina, Raynaud’s
- Toxicity: Cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation
Hydralazine
- MOA:
- Clinical Use:
- Toxicity
- MOA: INC cGMP -> smooth muscle relaxation. Vasodilates arterioles > Veins; afterload reduction
- Clinical Use: Severe hypertension, CHF. First line therapy for HYPERTENSION IN PREGNANCY, with METHYLDOPA. Frequently coadministered with a ß-blocker to prevent reflex tachycardia
- Toxicity: Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina. Lupus-like syndrome.
Malignant hypertension treatment
Commonly used drugs include nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam
Nitroprusside MOA:
MOA: Short acting; INC cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide)
Fenoldopam MOA:
MOA: Dopamine D1 receptor agonist - coronary, peripheral, renal, and splanchnic vasodilation. DEC BP and INC natriuresis
Nitroglycerin, isosorbide dinitrate
- MOA:
- Clinical Use:
- Toxicity
- MOA: Vasodilate by releasing nitric oxide in smooth muscle, causing INC in cGMP and smooth muscle relaxation. Dilate veins»_space; arteries. DEC preload
- Clinical Use: Angina, pulmonary edema
- Toxicity: Reflex tachycardia, hypotension, flushing, headache, “Monday disease” in industrial exposure; development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend results in tachycardia, dizziness, and headache upon reexposure.
Antianginal therapy
Goal: reduction of myocardial O2 consumption (MVO2) by DEC 1 or more of the determinants of MVO2: end-diastolic volume, blood pressure, heart rate, contractility, ejection time.
Cardiac glycosides - digoxin characteristics
Digoxin - 75% bioavailability, 20-40$ protein bound, t1/2 = 40 hours, urinary excretion
Digoxin MOA:
Direct inhibition of Na+/K+ ATPse leads to indirect inhibition of Na+/Ca2+ exchanger/antiport. INC Ca2+i –> positive inotropy. Stimulates vagus nerve -> DEC HR
Digoxin Clinical use:
CHF (INC contractility); atrial fibrillation (DEC conduction at AV node and depression of SA node)
Digoxin toxicity:
Cholinergic - nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh). EKG -> INC PR, DEC QT, ST scooping, T wave inversion, arrhythmia, AV block. Can lead to hyperkalemia, a poor prognostic indicator. Factors predisposing to toxicity - renal failure (DEC excretion), hypokalemia (permissive for digoxin binding at K+-binding site on Na+/K+ ATPase), quinidine (DEC digoxin clearance; displaces digoxin from tissue binding sites!)
