Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
65 Cards in this Set
- Front
- Back
|
evaluation of hypertension |
over 140/90 mmHg |
|
|
prehypertensive |
systolic 120-140 - do lifestyle modifications |
|
|
short-term goal of HTN Rx |
reduce blood pressure - acute/emergency HTN, primary/essential HTN, secondary HTN |
|
|
long-term goal of HTN Rx |
reduce mortality due to CV-disease related events - MI, stroke, HF, nephropathy, atherosclerosis, retinopathy |
|
|
what systems control BP? |
sympathetic nervous system, renin/angiotensin/aldosterone system |
|
|
general mechanisms of lowering BP |
reduce CO, reduce peripheral vascular resistance, reduce plasma volume |
|
|
Primary drugs |
thiazide diuretics, renin angiotensin system blockers, calcium channel blockers |
|
|
Secondary drugs |
adrenergic receptor blockers, sympathetic nerve blockers, direct vasodilators |
|
|
Thiazide site of action |
distal convoluted tubule of kidney |
|
|
Thiazide MOA |
block the Na/Cl transporter = decrease Na reabsorption = reduce plasma volume and reduce total body Na+ |
|
|
Thiazide indications |
monotherapy for mild-moderate HTN, combo w/ other anti-HTN drugs, reduced risk of other CV disease related events most efficacious in "low renin" or volume-expanded forms of HTN |
|
|
Drugs that reduce cardiac output |
CCB, beta-blockers, sympatholytics, ACEIs, ARBs, renin inhibitors, centrally acting sympatholytics, alpha-2-adrenoceptor agonists |
|
|
Drugs that reduce peripheral vascular resistance |
vasodilators, CCBs, alpha-1 blockers, alpha-2 agonists, beta blockers, ACEIs, ARBs, renin inhibitors |
|
|
Drugs that reduce plasma volume |
diuretics, ACEIs, ARBs, renin inhibitors |
|
|
Thiazide diuretic name |
end in "zide" or "one" (hydrochlorothiazide) |
|
|
Thiazide considerations |
Na+ reabsorption is coupled to K+ excretion => hypokalemia can result |
|
|
prevent hypokalemia with thiazide |
add potassium supplementation or a K-sparing diuretic to the patient's regime |
|
|
Spironolactone |
inhibits Na+ reabsorption in the collecting tubules; decreases K+ excretion (blocks aldosterone R in kidney) |
|
|
Drugs affecting the renin-angiotensin system |
Angiotensin converting enzyme (ACE) inhibitors, Angiotensin receptor blockers (ARB), renin inhibitor |
|
|
Renin/Angiotensin system |
Angiotensinogen -> Renin -> Angiotensin I -> ACE -> Angiotensin II -> Angiotensin II Type 1 receptor |
|
|
effects of Angiotensin II |
increase pressure/volume: vasoconstriction in vessels and kidneys, incr. aldosterone, incr. Na+ reabsorption in kidneys, hypertrophy and fibrosis in heart, incr. sympathetic activity, incr. infl. and atherosclerosis |
|
|
Bradykinin |
vasodilator that increases capillary permeability to cause local edema and swelling - metabolized by ACE |
|
|
ACE inhibitors |
end in "pril" = lisinopril (active drug), enalapril (prodrug) |
|
|
ACE inhibitor MOA |
inhibit ACE = reduce circulating and local tissue AT II |
|
|
effects of ACE inhibitors |
reduce systemic arteriolar resistance, systolic, diastolic and mean arterial pressures increased regional blood flow, increased large artery compliance, aldosterone secretion reduced, reduced CV remodeling |
|
|
ACE inhibitors in HTN |
first line drug for monotherapy of mild to moderate HTN also patients w/ CHF - post MI recommended in patients with diabetes, chronic kidney disease, stroke history |
|
|
ACE inhibitors are less effective in... |
black patients |
|
|
primary drug for CHF |
ACE inhibitors |
|
|
ACE inhibitor adverse effects |
excessive hypoT initially, dry cough and angioedema (bradykinin increase), hyperkalemia (from aldosterone inhibition), renal failure, teratogen, ageusia |
|
|
Angiotensin II Receptor Blockers/Antagonists (ARBs) |
end in "sartan" = Losartan, Valsartan |
|
|
ARB MOA |
competitive or non-competitive antagonism of type 1 AT-II receptors (prevent incr. BP and other CV effects) direct antihypertensive effect, reduced CV remodeling |
|
|
ARB S/E |
little cough, angioedema excessive hypoT initially, hyperkalemia, renal failure, teratogen few generics |
|
|
ARB uses |
hypertension, congestive heart failure, post MI |
|
|
Renin inhibitor |
Aliskiren |
|
|
Aliskiren MOA |
inhibits renin, the rate limiting step in angiotensin II formation |
|
|
Aliskiren indication |
treats primary HTN (once daily administration) in combo with other (non-renin angiotensin) drug classes |
|
|
Aliskiren S/E |
excessive hypoT, hyperkalemia, diarrhea, contraindicated in pregnancy, renal failure |
|
|
Beta-adrenoceptor blockers |
names end in "olol" non-selective and cardioselective types are equally effective in reducing BP |
|
|
non-selective beta blockers |
block Beta1 and Beta2 = propranolol |
|
|
cardioselective beta blockers |
block Beta1 only = metoprolol, atenolol |
|
|
Mixed receptor blockers |
block Beta1, Beta2, Alpha1 = carvedilol (useful for heart failure) |
|
|
primary use for beta blockers |
prevent angina |
|
|
beta-adrenoceptor antagonist effects in HTN |
decr. CO and decr. renin release from the kidney to lower BP |
|
|
beta-blocker uses |
HTN with compelling indications: angina pectoris, heart failure, previous MI less effective in preventing some CVD events, not a first line drug for HTN |
|
|
beta blocker S/E |
CNS - fatigue, sleep problems; enhanced bronchospasm in asthma, bradycardia, worsens heart failure and heart block in high doses withdrawal effects rise in TGs, decr. in HDL, prolonged hypoglycemia |
|
|
Calcium channel blockers (CCBs) |
end in "dipine" = Nifedipine, amlodipine Diltiazem, verapamil |
|
|
Nifedipine and amlodipine MOA |
block "L" type calcium channels in vascular smooth muscle |
|
|
Diltiazem and verapamil MOA |
block "L" type calcium channels in vascular smooth muscle and in the heart |
|
|
CCBs indication |
first line drugs for monotherapy of mild to moderate HTN |
|
|
most commonly used CCB in HTN |
dihydropyridines |
|
|
CCBs are best in |
low renin HTN (effective in African americans and elderly) |
|
|
CCB S/E |
excessive hypoT = facial flushing, H/A, dizziness, peripheral edema, reflex tachycardia bradycardia, AV nodal block, cardiac depression (verapamil, diltiazem) |
|
|
Verapamil and diltiazem do NOT cause... |
reflex tachycardia |
|
|
Alpha-adrenergic receptor blockers: non-selective |
alpha 1 and alpha 2 blockers; phentolamine |
|
|
Alpha-adrenergic receptor blockers: selective |
alpha 1 blocker; prazosin |
|
|
alpha-adrenergic blocker MOA |
block vascular alpha-adrenoceptors that cause vasoconstriction = decrease peripheral vascular resistance |
|
|
Non-selective alpha blocker usage |
hypertensive crisis of pheochromocytoma |
|
|
Selective alpha blocker use |
monotherapy and adjunct therapy for HTN (NOT first line drug) benign prostatic hyperplasia use |
|
|
alpha blocker S/E |
first dose phenomenon - postural hypoT, dizziness, fainting reflex tachycardia, sodium and water retention |
|
|
Direct vasodilators |
Hydralazine, Minoxidil |
|
|
Hydralazine MOA |
inhibits calcium release, stimulates the NO/cGMP pathway in vascular smooth muscle => marked vascular relaxation |
|
|
hydralazine use |
secondary drug, in combo with a diuretic and beta-blocker, used in refractory HTN CHF!!! |
|
|
Minoxidil MOA |
potassium channel opener, causes cell membrane hyperpolarization which causes substantial vascular relaxation |
|
|
Minoxidil use |
refractory hypertension only lasts 24 hours |
|
|
Minoxidil S/E |
marked fluid retention and edema, marked tachycardia and palpitations, causes hypertrichosis give diuretic and beta-blocker!! |
