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50 Cards in this Set
- Front
- Back
Anti-Hypertensive
Sites of Action |
- nervous system
-renal system |
|
Sympatholytics
|
suppress sympathetic action
1. beta-adrenergic blockers 2. alpha1 –adrenergic receptor blockers 3. alpha2 - agonists |
|
Calcium channel blockers
|
(nervous system)
affect vascular smooth muscle, heart. |
|
Direct-acting Vasodilators
|
(nervous system)
relax vascular smooth muscle |
|
Angiotensin Converting Enzyme
Inhibitors (ACE Inhibitors) |
(renal system)
prevent conversion of angiotensin I into angiotensin II. |
|
Angiotensin II Receptors (ARB)
|
(renal system)
block angiotensin II receptors so prevents action of angiotensin II. |
|
Diuretics
|
(renal system)
acts on renal tubules to promote Na and water excretion |
|
Anti-Hypertensive Meds
|
-Beta-Adrenergic Blockers
-Alpha 1 -Adrenergic Receptor Blockers -Alpha2-agonists -Calcium Channel Blockers (CCB) |
|
dihydropyridines
|
class of CCB
end in “dipine” – potent vasodilators ONLY, no effects in heart. amiodipine/norvasc felodipine/plendil nifedipine/adalat isradipine/dynacirc |
|
other – nondihydropyridines
|
class of CCB
vasodilators and affects the heart diltiazem/cardizem (used a lot) verapamil/isoptin, calan |
|
Beta-Adrenergic Blockers
MOA |
block Beta1 receptors in heart, blocks site and decreases sympathetic effects on heart.
Blocks Beta1 receptors in the kidney causing decrease in renin. 1. decrease heart rate 2. decrease force of contraction 3. reduced velocity of impulse conduction |
|
Beta-Adrenergic Blockers
IN |
HTN, angina, CHF, MI, dysrythmias
|
|
Beta-Adrenergic Blockers
AE |
bronchoconstriction
bradycardia reduced CO AV heart block b/c impulses of node slowed down |
|
Beta-Adrenergic Blockers
TYPES |
end in “LOL”
atenolol/tenormin bisoprolol/zabeta carvediolol/coreg labetalol/normodyne metoprolol/lopressor nadolol/corgard propanolol/inderal |
|
Alpha 1 -Adrenergic
Receptor Blockers MOA |
block the effects of alpha 1 receptors.
Results in: 1. dilated blood vessels: decrease BP 2. cardiac output decrease Blocks sympathetic system effects |
|
Alpha 1 -Adrenergic
Receptor Blockers IND |
HTN
|
|
Alpha 1 -Adrenergic
Receptor Blockers AE |
orthostatic hypotension
reflux tachycardia Na retention and increased blood volume (b/c of decreased CO) |
|
Calcium Channel Blockers
(CCB) MOA |
Blocks entry of Ca into cells – blood vessels and heart.
|
|
Calcium Channel Blockers
(CCB) IND |
HTN, angina, migraines, dysrythmias
|
|
Calcium Channel Blockers
(CCB) DI |
others:
digoxin- problems with liver: should avoid Beta-blockers |
|
Calcium Channel Blockers
(CCB) AE |
both types: flushing, peripheral edema, gingival hyperplasia, HA
dihydropyridines: reflex tachycardia others: bradycardia, AV block |
|
Vasodilators
MOA |
relax smooth muscle in blood vessels
•Arterio-dilators: cause decrease in peripheral vascular resistance, decrease afterload -> decrease work of the heart, increase CO, increase tissue perfusion •Venous–dilators: reduce force with which blood is returned to heart so decrease ventricular filling, decrease preload -> decrease force of contraction •Result: decrease CO |
|
Vasodilators
IND |
HTN, angina, heart failure, MI, peripheral vascular disease.
Types: hydralazine/apresoline: arterio–dilator minoxidil/loniten: arterio–dilator, more potent, more severe SE reactions sodium nitroprusside /Nitropress- arterio and venous; works rapidly, IV infusion, cardiac emergencies, potent |
|
Vasodilators
AE |
postural hypotension
reflex tachycardia expansion of blood/increased blood volume |
|
Vasodilators
DI |
other antihypertensive meds
|
|
Angiotensin Converting
Enzyme Inhibitors (ACE Inhibitors) MOA |
Blocks the enzyme (angiotensin converting enzyme, kinase II) that converts angiotensin I to angiotensin II -> therefore decrease vasoconstriction and aldosterone
production. Results in: 1. vasodilation 2. decrease blood volume/BP 3. prevent or reverse pathological changes in heart, vessels |
|
Angiotensin Converting
Enzyme Inhibitors (ACE Inhibitors) IND |
HTN, CHF, MI, left ventricular dysfunction, nephropathy
TYPES: end in “PRIL” benazepril/lotensin captopril/capoten enalapril/vasotec lisinopril/zestril ramipril/altace fosinopril/monopril |
|
Angiotensin Converting
Enzyme Inhibitors (ACE Inhibitors) AE |
cough
first dose syncope- b/c BP drops rapidly hyperkalemia- don’t give with potassium renal failure angioedema |
|
Angiotensin Converting
Enzyme Inhibitors (ACE Inhibitors) DI |
other anti HTN
potassium sparing diuretics or drugs that raise K diuretics |
|
Angiotensin II Receptor
Blockers (ARBs) MOA |
Angiotensin II receptor blocker competes with angiotensin II at tissue binding sites: blocks effects of angiotensin II.
Effects similar to ACE inhibitors: 1. vasodilation 2. reduces blood volume/BP 3. reverses pathological changes in the heart |
|
Alpha2-agonists
MOA |
Centrally acting
– reduces firing of sympathetic neurons – suppresses sympathetic activity to heart and blood vessels. Decreases vasoconstriction – decrease BP |
|
Alpha2-agonists
IND |
HTN, severe pain
Ex: clonidine/catapres |
|
Alpha2-agonists
AE |
rebound hypertension
drowsiness xerostomia (dry mouth) |
|
Angiotensin II Receptor Blockers
(ARBs) MOA |
Angiotensin II receptor blocker competes with angiotensin II at tissue binding sites: blocks effects of angiotensin II.
Effects similar to ACE inhibitors: 1. vasodilation 2. reduces blood volume/BP 3. reverses pathological changes in the heart |
|
Angiotensin II Receptor Blockers
(ARBs) TYPES |
Types: end in ‘sartan”
losartan/cozaar valsartan/diovan irbesartan/avapro candesartan/atacand |
|
Angiotensin II Receptor Blockers
(ARBs) AE |
renal failure
hyperkalemia (but less than ACEI) |
|
Diuretics
definition |
Drugs that increase renal excretion of water, Na, and other e-lytes
– results in an increase in urine output. |
|
Diuretics
Indications |
HTN
remove edematous fluid prevent renal failure- to stimulate renal output |
|
Diuretics
Classifications |
1. High – ceiling: Loop
2. Thiazides 3. Potassium – Sparing diuretics 4. Osmotic diuretics |
|
High – ceiling: Loop
MOA |
inhibits Na and Cl reabsorption in ascending loop of Henle, getting more fluid out
|
|
High – ceiling: Loop
IN |
multiple uses – HTN, heart failure, pulmonary edema, renal disease
Ex: Furosemide/Lasix |
|
High – ceiling: Loop
AE DI |
dehydration,
electrolyte imbalances esp K (hypokalemia) and Na, hypotension, ototoxicity (ear toxicity, temporary and can be reversed) DI: digoxin |
|
Thiazides
MOA |
decrease reabsorption of Na, H2O, Cl, bicarbonate in distal convoluted tubule.
•Most common diuretic and HTN medication given |
|
Thiazides
IND |
HTN, edematous states, diabetes insipidus
Ex: HCTZ – hydrochlorothiazide |
|
Thiazides
AE DI |
AE: similar to loop diuretic, risk for hypokalemia, no ototoxicity
DI: similar to loop diuretics |
|
Potassium – Sparing diuretics
MOA |
blocks aldosterone in distal nephron – decrease Na reabsorption and K excretion
|
|
Potassium – Sparing diuretics
IND |
HTN, edema, severe heart failure, cirrhosis
Ex: spironolactone/aldactone |
|
Potassium – Sparing diuretics
AE DI |
AE: hyperkalemia
DI: do not take with other agents that increase K levels, or with other potassium sparing diuretics; foods high in K; watch IV fluids |
|
Osmotic diuretics
MOA |
creates osmotic forces in lumen of nephron – draws water into renal tubule.
Not metabolized; rapid acting, very strong, used in emergencies |
|
Osmotic diuretics
IND DI |
prophylaxis of renal failure, reduction of intracranial pressure with cerebral edema, reduction of intraocular pressure
Ex: mannitol/osmitrol DI: edema |