Antihypertensives Flashcards
What are the first line agents, second line agents and other agents for treatment of HTN?
First-line agents:
- ACE-inhibitors, ARBs, calcium channel blockers, thiazide diuretics
Second-line agents:
- B-blockers, aldosterone antagonists
Other agents:
- Loop diuretics, alpha-blockers, direct vasodilators, central alpha2-agonists, renin inhibitors
ACE inhibitors
Captopril, Enalapril, Lisinopril
MOA: inhibition of ACE enzyme preventing conversion of angiotensin I to angiotensin II (also prevent bradykinin degradation)
CE: Catopril will decrease PVR; Enalapril/Lisinopril decrease Na+ and H2O retention
CA: perserve renal function in diabetic/non-diabetic nephropathy pts; Captopril HTN; Enalapril heart failure; Lisinopril post MI
AE: dry cough, angioedema, hyperkalemia, hypotension, rash, fever, altered taste
TCo: pregnancy, bilateral renal artery stenosis
Angiotensin Receptor Blockers (ARB’s)
Losartan
MOA: block angiotensin II type 1 receptors
CE: decrease PVR, Na+ and H2O retention
CA: HTN, heart failure, post MI
AE: hyperkalemia, hypotension, rash, fever, altered taste
TCo: pregnancy, bilateral renal artery stenosis
Renin Inhibitor
Aliskirin
MOA: renin inhibitor
CE: decrease PVR, Na+ and H2O retention
CA: alternative agent in HTN (3rd line)
AE: hyperkalemia, hypotension, rash, fever, altered taste
TCo: pregnancy, bilateral renal artery stenosis
Calcium Channel Blockers
Amlodipine, Nifedipine; Diltiazem, Verapamil
MOA: inhibit vascular L-type Ca2+ channels; inhibit vascular and cardiac L-type Ca2+ channels
CE: Amlodipine/Nifedipine (Dihydropyridine) decrease PVR; Diltiazem/Verapamil decrease PVR, inotropy, chronotropy
CA: Dihydropyridine HTN, angina; Diltiazem/Verapamil HTN, angina, supraventricular tachyarrhythmias, migraine, cerebral vasospasm
AE: Dihydropyridine reflex tachycardia, peripheral edema, hypotension, gingival hyperplasia, fatigue, flushing; Verapamil constipation, negative inotropic effects
TCo: Verapamil pts taking B-blockers, 2nd/3rd degree heart block, or severe left ventricular dysfunction
Diuretics (in general)
Thizide, Loop, K+ sparing
MOA:
CE: decrease PVR, Na+ and H2O retention
CA: HTN, CHF, edema
AE: hypotension, hyponatremia, hypokalemia (hyperkalemia if K+ sparing)
Beta-Blockers
Propanolol (B1/2), Metoprolol (B1), Atenolol (B1), Pindolol (B1/2P)
MOA: antagonist at B-receptors
CE: decrease inotropy, chronotropy, renin secretion (decrease PVR and Na+ and H2O retention)
CA: HTN, angina, heart failure, arrhythmias
AE: airway constriction (Propanolol), bradycardia, CNS effects (fatigue, sexual dysfunction, ect.), disrupt lipid metabolism decrease in HDL/increase in TAGs, mask signs of hypoglycemia in diabetics
TCo: pt taking CCB, 2nd/3rd degree heart block, or severe left ventricular dysfunction; Propanolol asthmatics and COPD; cant stop abruptly becasue of rebound HTN
Alpha-1 Antagonists
Prazosin, Doxazosin
MOA: antagonist at a1-receptors
CE: decrease PVR
CA: HTN, Benign Prostatic Hyperplasia
AE: orthostatic hypotension (first use), diziness, drowsiness, nausea
Alpha and Beta Blockers
Lavetalol
MOA: antagonists at alpha-1 and beta-1 receptors
CE: decrease in PVR, inotropy, chornotropy
CA: HTN, hypertensive emergencies
AE: orthrostatic hypotension
Central Alpha-2 Agonist
Clonidine, Methyldopa
MOA: agonist at alpha-2 receptors
CE: decrease sympathetic outflow, PVR, inotropy, chronotropy
CA: HTN, hypertensive emergencies
Direct Vasodilators
Hydralazine, Minoxidil
MOA: arterial vasodilators (smooth muscle relaxants)
CE: decrease PVR
CA: HTN, hypertensive emergencies
AE: fluid retention, reflex tachycardia; Hydralazine reversible lupus-like syndrome; Minoxidil hypertrichosis
What are the drugs used to treat pulmonary HTN?
- Prostaglandins (Epoprostenol)
- Enothelin Synthesis and Receptor Blocker (Bosentan)
- Phosphodiesterase 5 Inhibitor (Sildenafil)
Prostaglandins
Epoprostenol
MOA: synthetic PGI2
CE: decrease peripheral pulmonary and coronary resistance
CA: pulmonary HTN
AE: flushing, headache, jaw pain, diarrhea, arthralgias
Endothelin Receptor Blocker
Bosentan
MOA: blocks ETA and ETB responses to endothelin
CE: decrease pulmonary resistance
CA: pulmonary HTN
AE: anemia, hepatotoxicity
TCo: pregnancy (Cat X)
Phosphodiesterase 5 Inhibitor
Sildenafil
MOA: inhibit PDE5 to increase cGMP levels > smooth muscle relaxation
CE: decrease pulmonary resistance
CA: pulmonary HTN, erectile dysfunction
AE: headache, flushing, dyspepsia, cyanopsia
TCo: nitrates
What drugs are used for treatment of hypertensive emergency?
- Sodium Nitroprusside (arterial and venous dilator)
- Labetalol (A1 and B1 blocker)
- Fenoldopam (dopamine agonsit)
- Nicardipine (calcium channel blocker)
- Nitroglycerin (mostly venous vasodilator)
- Diazoxide (potassium channel activator)
- Phentolamine (non-selective alpha agonist)
- Esmolol (beta1 blocker)
- Hydralazine (arteriolar vasodilator)
What are the two nitrates?
Sodium Nitroprusside, Nitroglycerin
Sodium Nitroprusside
MOA: direct vasodilator
CE: peripheral vasodilator (arterial and venous smooth muscle)
CA: hypertensive emergencies
AE: hypotension, reflex tachycardia, cyanide toxicity, abdominal cramping, nausea, vomiting
TCo: hypotension
Nitroglycerin
MOA: direct vasodilator
CE: peripheral vasodilator (mainly venous)
CA: hypertensive emergencies in pts with cardiac ischemia or angina, or after bypass surgery
AE: hypotension
Dopamine Agonist
Fenoldopam
MOA: agonist at D1 receptors
CE: arteriolar dilation, maintains renal perfusions as BP lowers
CA: hypertensive emergencies
AE: hypotension
TCo: glaucoma
Nicardipine
MOA: inhibits vascular L-type Ca2+ channels
CE: decrease in PVR
CA: hypertensive emergencies
AE: hypotension, refelx tachycardia
Potassium Channel Activator
Diazoxide
MOA: opens K+ channels, stabilizes membrane potential preventing smooth muscle contraction
CE: arteriolar dilation
CA: hypertensive emergencies
AE: hypotension, reflex tachycardia, Na+ and H2O retention, inhibiton of insulin relase
Non-selective Alpha Antagonist
Phentolamine
MOA: antagonist of alpha1/2 receptors
CE: decrease PVR
CA: catecholamine-related hypertensive emergencies
AE: orthostatic hypotension, dizziness, drowsiness, nausea
Esmolol
MOA: short acting B1 receptor antagonist
CE: decrease inotropy, chornotropy, renin secretion, PVR, Na+ and H2O retention
CA: aortic dissection or p/o hypertension
AE: bradycardia, CNS effects (fatigue, sexual dysfunction, ect.), mask signs of hypoglycemia in diabetics
TCo: pts taking CCBs, 2nd/3rd degree heart block, or severe left ventricular dysfunction
Cardiac Glycoside
Digoxin
MOA: inhibition of Na+/K+ ATPase and vagal stimulation
CE: increase inotropy, decrease chronotropy
CA: add on therapy to improve heart failure symptoms but not survival; A-fib; 1st line for A-fib + Heart failure
AE: arrhythmias, nausea, vomiting, anorexia, headache ,fatigue, confusion, alteration of color perception (yellow/green hues), blurred vision
TCo: diastolic or right sided heart failure, uncontrolled HTN, bradyarrhythmias, non-responders/interolerant pts, increased toxicity in pts with hypokalemia
What are the 4 inotropic agents used to treat acute heart failure?
- Phosphodiesterase III Inhibitors (Inamrinone, Milrinone)
- Dopamine
- Dobutamine
- Glucagon
Phosphodiesterase III Inhibitors
Inamrinone, Milrinone
MOA: inhibit myocardial cAMP PDE activity > increase cAMP
CE: increase inotropy and chronotropy leading to increase in CO, decrease preload and afterload
CA: short-term therapy for patients with intractable heart failure
AE: arrhythmias, HTN, angiona thrombocytopenia
Dopamine
MOA: activates dopaminergic and adrenergic receptors
CE: increase inotropy and chronotropy leading to increase in CO, renal vasodilation at therapeutic doses
CA: shock (which persists after fluid replacement)
AE: high doses can cause vasoconstriction
Dobutamine
MOA: at therapeutic doses major effects is B1 receptor stimulation
CE: increase inotropy and chronotropy leading to increase in CO
CA: acute managment of heart failure
AE: HTN, angina, arrhythmias
Glucagon
MOA: stimulates adenylyl cyclase > cAMP
CE: increase inotropy and chronotropy > increase CO
CA: B-blockers overdosage
AE: HTN, angina, arrhythmias
