Antihypertensives Flashcards
what are the ACE (angiotensin converting enzyme) inhibitors
captopril, enalapril, lisinopril
clinical uses of ACE inhibitors
hypertension (first line for primary)
heart failure
myocardial infarction
albuminuria in non pregnant patients
why aren’t ACE inhibitors first line agents for blacks and elderly
because the RAAS system is less active in them
how does ACE inhibitors work?
- it blocks conversion of angiotensin I to angiotensin II hence reducing its vasoconstrictive activity and release of aldosterone
- blocks degradation of bradykinin and stimulates release of vasodilators such as prostacyclin and prostaglandin E2
- increase in renin since no neg feedback from angiotensin II
- slight increase in serum creatinine
- rise in K+ levels in blood if renal insufficiency
how do you dose the ACE inhibitors
enalapril and lisinopril given once a day while captopril given two to three times daily
adverse effects of ACE inhibitors
CATCHH
Cough (due to bradykinin)
Angioedema
Teratogen (fetal renal malformation; renal failure in those with bilateral renal artery stenosis)
Creatinine (increased due to decreased GFR)
Hypotension
Hyperkalemia (due to reduction in aldosterone)
ACE inhibitors are contraindicated in who
bilateral renal artery stenosis (no vasoconstriction by angiotensin II on the efferent arteriole to help maintain glomerular capillary pressure and filtration)
hyperkalemia (due to reduction in aldosterone release hence less sodium absorption so less K excretion)
pregnancy (teratogen – fetal renal malformation)
what are the angiotensin II receptor blockers (ARBs)
Losartan
Valsartan
clinical use of ARBs (angiotensin II receptor blockers)
hypertension and heart failure
when do you switch from an ACE inhibitor to an ARB if they both work almost the same way
when the patient is experiencing the bradykinin mediated dry ass cough
when do ARBs work equally effective in black/oldies as it does in whites/youngings
when combined with calcium channel blockers
mechanism of ARBs
- they block the receptor that mediates the effects of angiotensin II hence no vasoconstriction or release of aldosterone
- don’t block the breakdown of bradykinin so no dry ass cough or angioedema (as seen in ACE Inhibitors)
- since angiotensin II not activating its receptor, no negative feedback on renin release so renin still high
what are the adverse effects of ARBs?
hypotension
hyperkalemia (due to less aldosterone secretion hence less Na absorption so less K excretion)
angioedema
diarrhea
acute renal failure (no vasoconstriction on efferent arterioles from angiotensin II if bilateral renal artery stenosis so reduced glomerular capillary pressure and filtration)
contraindication of ARBs
pregnancy (fetal renal malformation)
bilateral renal artery stenosis
hyperkalemia
what are the calcium channel blockers (CCB)
VAND Verapamil (diphenalkylamine) Amlodipine (dihydropyridine) Nifedipine (dihydropyridine) Diltiazem (benzothiazepine)
clinical use of CCBs
hypertension, angina, arrhythmias
why would you combine CCBs with ARBs or ACE Inhibitors
because it is considered the first line drug treatment for hypertension for blacks/elderly
which one of the CCBs can you safely combine with beta blockers and why?
the dihydropyridines (amlodipine and nifedipine) because of their cardio depressant effects
mechanism of CCBs
- block voltage gated L type calcium channels on vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue thereby stopping calcium from entering these cells
- this leads to smooth muscle relaxation, decreased myocardial force, decreased HR
- the dihydropyridines (in comparison to the non-dihydropyridines) only act on vascular smooth muscle hence evoke a reflex tachycardia
knowing that dihydropyridines only act on vascular smooth muscle while the other work on both vascular SM and cardiac tissue, what do you use each type to treat
dihydropyridines - hypertension
verapamil - angina and cardiac arrhythmias (could be used for hypertension)
diltiazem - hypertension, angina, arrhythmias
adverse effects of CCBs
dihydropyridines - reflex tachycardia, peripheral edema, dizziness, flushing, headache, gingival hyperplasia
non-hydropyridines (verapamil and diltiazem) - cardiac conduction abnormalities, constipation (v), anorexia, nausea, peripheral edema, hypotension
contraindications for CCBs
bradycardia, conduction defects, heart failure
esp don’t give verapamil and diltiazem
alpha 1 antagonists increase the risk for CHF, so what conditions would you save alpha 1 antagonist as the treatment for hypertension
in men with BPH because drugs like tamsulosin are used to treat both BPH and hypertension
why should you give a small first dose to those on alpha 1 antagonist for tx for hypertension
some patients have precipitous (dangerously high) drop in BP after first dose
adverse effects of alpha 1 antagonist
sodium and water retention hence why a diuretic should be given in combination
what are the direct vasodilators
hydralazine
minoxidil
clinical uses of direct vasodilators
hydralazine - moderate to severe hypertension, heart failure, pregnant women with preeclampsia
minoxidil - severe hypertension and alopecia androgenetica
adverse effects of direct vasodilators
hydralazine - hypotension, reflex tachycardia and sodium and H2O retention, reversible lupus like syndrome,
minoxidil - hypotension, reflex tachycardia and sodium and H20 retention
when are beta blocker considered first line as an anti hypertensive
in patients with coronary heart disease, heart failure, or post MI
adverse effects of beta blockers
- drug withdrawal (abrupt cessation of beta blocker causes unstable angina, MI, tachycardia and etc because of upregulation of beta receptors)
- CV effects (bradycardia etc)
- disturbed lipid metabolism
- hypoglycemia
- bronchoconstriction
- CNS effect (reduced sexual function and fatigue)
contraindications for beta blockers
reactive airway disease (asthma and COPD)
pts with sinus bradycardia and partial AV block
