Antihypertensive drugs Flashcards
Treatment for pts with chronic kidney disease
- ACE inhibitors
- Angiotensin receptor blocker (ARB)
Treatment for pts without chronic kidney disease
Black pts
- Thiazide diuretic
- calcium channel blocker
Nonblack
- Thiazide diuretic
- ACE inhibitor
- ARB
- CCB
Diuretics
Increase the rate of urine flow and Na excretion
- Used to adjust the volume and/or composition of body fluids in a variety of clinical situations
Carbonic anhydrase inhibitors
Acetazolamide
Loop diuretics
Ethacrynic acid
Furosemide (lasix)
Thiazide diuretics
Chlorthalidone
Hydrochlorothiazide
K sparing diuretics
Aldosterone antagonists
- Spironolactone
Epithelial Na channel inhibitors
- Amiloride
Acetazolamide
Inhibits carbonic anhydrase enzyme
Results in
- Decreased H formation inside PCT cell
- Decreased Na/H antiport
- Increased Na and HCO3 in lumen
Increased diuresis
Urine pH increased, body pH decreased
CI: glaucoma, altitude sickness, metabolic alkalosis
Furosemide and ethacrynic acid
Loop diuretics- inhibit the luminal Na/K/2Cl cotransporter in the TAL of henle
results in
- Decreased intracellular Na, K, Cl, in TAL
- Decrease back diffusion of K and positive potential
- Decreased reabsorption of Ca and Mg
Ion transport is virtually nonexistent, making it the most efficacious.
Increased diuresis.
Half-life correlated to kidney function.
Used for edematous states
Hydrochlorothiazide (HCTZ)
Thiazide diuretic- causes inhibition of the Na/Cl cotransporter
Results in
- Increased luminal Na and Cl in DCT
- Enhances the reabsorption of Ca in both DCT and PCT, why it is sometimes used for renal stones
Adverse effects- hyperGLUC
Mess with the body’s ability to regulate glucose levels
Spironolactone
K sparing diuretic, aldosterone receptor antagonist.
Can’t reabsorb Na and secrete K.
Uses: hyperaldosteronism, K depletion, HF
Do not require access to the tubular lumen to induce diuresis
Amiloride
K sparing diuretic, blocks the Na channels from absorbing, prevents K secretion
ACE inhibitors
Captopril
Enalapril
“pril”
ARBs
Losartan
Valsartan
“sartan”
Captropril and analapril
ACE inhibitors
Inhibit the conversion of ANG I to the more active ANG II. Also prevents degradation of bradykinin-vasodilator
Vasodilate the efferent arteriole- reduces back pressure on the glomerulus and reduces protein excretion
Benefits of ACE inhibitors
Cardiac function in pts w uncomplicated hypertension is little changed. Lowers TPR and mean, diastolic, and systolic BP
Baroreceptor function and cardiovascular reflexes are not compromised
Adverse effects of AVE inhibitors
Cough Angioedema Teratogen Creatinine (increased) Hyperkalemia- avoid K sparing diuretics Hypotension
Losartan and valsartan
Angiotensin II receptor blockers (AT1)
Selective block ANG II receptors, leads to
- Decreased contraction of vascular smooth muscle
- Decreased aldosterone secretion
- Decreased pressor responses
- Decreased cardiac cellular hypertrophy and hyperplasia
Effects similar to ACE inhibitors, but ARBs do not increase bradykinin
Aliskiren
Direct renin inhibitor
Does not increase bradykinin
Rise in plasma renin levels but decreased renin activity
Vasodilators: Calcium channel blockers- dihydropyridines
Amlodipine
Nifedipine
Vasodilators: Calcium channel blockers- non-dihydropyridines
Diltiazem
Verapamil
Vasodilator: Nitrix oxide donors
Hydralazine
Nitroprusside
Non-dihydropyridines
CCB
Prominent cardiac effects, but also act at vascular tissues.
Causes vasodilation.
Dihydropyridines
CCB
Predominantly arteriolar vasodilation effects
Verapamil
CCB
May cause constipation and peripheral edema
Use of verapamil with a B-blocker is contraindicated bc of the potential for AV block
Potassium channel openers
Increased potassium permeability stabilizes the smooth muscle cell membrane at resting potential, reducing the probability of contraction
- Diazoxide
- Minoxidil
Diazoxide
K channel opener
- Arteriolar vasodilation
- Diminishing use in hypertensive emergencies due to adverse efects
- Excessive hypotension can cause stroke and Mi
- Hyperglycemia
Minoxidil
K channel opener
- Arteriolar vasodilation
- Clinical uses include severe hypertension and baldness
Fenoldopam
Dopamine receptor agonist
- Activation increases blood flow to the kidneys
For HTN emergencies and post-operative HTN
Hydralazine
releases NO from endothelium- dilates arterioles, but not veins
First line oral therapy for hypertension in pregnancy
Nitroglycerin
Used to treat hypertensive emergencies, heart failure, and angina
- Dilates both arterial and venous vessels- decreases TPR and venous return
- Decreases both preload and afterload
Labetalol
Selective a1 blocker
Nonselective b1 and b2 blocker
partial agonist
IV for severe hypertension
acceptable option for hypertension during pregnancy
Combinations to avoid
- ACE inhibitors, ARBs, and renin inhibitors (only one at a time)
- Beta blockers and non-dihydropyridine CCBs
- Potassium-sparing diuretics and ACE inhibitors/ARBs/renin inhibitors
The most effective parenteral drug for hypertensive emergencies
Sodium nitroprusside
Potential for cyanide toxicity limits prolonged use
Acute management of severe hypertension in pregnant women
- Labetalol
- Hydralazine- used extensively in the setting of preclampsia
- Calcium channel blockers- sustained release nifedipine or immediate release nicardipine
- Nitroglycerin- a good option for HTN associated w pulmonary edema
Long term oral therapy for hypertension in pregnant women
- Methyldopa- sedated effect is bothersome to already fatigued patients. Clonidine is another centrally acting sympatholytic that is considered safe in pregnant women
- Labetalol- More rapid onset of action than methyldopa
- Nifedipine
- Hydralazine- due to reflex tachycardia, monotherapy with oral hydralazine is not recommended
- Thiazide diuretics- generally only introduced during pregnancy if pulmonary edema has developed
Nonedematous states that are treated with diuretics
- Hypertension
- Nephrolithiasis- kidney stone
- Hypercalcemia
- Diabetes insipidus
MUDPILES
Methanol Uremia Diabetic ketoacidosis Paraladehyde Infection, iron, isoniazide Lactic acidosis Ethylene glycol, alcohol Salicylates, starvation ketoacidosis
pH
7.4
pCO2
40
HCO3
24
After MI Agent
beta blocker, ACE I
After MI caution
direct vasodilators- may worsen coronary insufficiency
CHF agent
ACE I, diuretics; beta blockers (no pulm edema)
CHF caution
beta blockers, CCB
hyptertrophic cariomyopathy agent
beta blockers, CCB
hyptertrophic cariomyopathy caution
diuretics, ACE inhibitors, direct vasodilators
bradycardia, heart block caution
beta blockers, CCB
Tachyarrhythmias agent
beta blockers, verapamil
angina agent
beta blockers, CCB, Nitroglycerin
Angina caution
direct vasodilators (
COPD agent
CCB
COPD caution
beta blockers
aortic dissection agent
nitroprusside, beta blocker
aortic dissection caution
drugs that > cardiac output (increased shear stress)
B/ renal artery stenosis caution
ACE I, angiotensin blockers- may worsen renal function
Chronic renal insufficiency agent
ACE I (w/ serum creatinin
Chronic renal insufficiency caution
ACE inhibitors, angiotensin blockers- may worsen renal function
Renal transplants caution
ACE I
migraine headaches agent
beta blockers, CCB- may relive migraine symptoms
stroke or TIA agent
ACE I- may allow reestablishment of cns autregulation
stroke or TIA caution
vasodilators may increase intracranial pressure
Diabetes agent
ACE I- delay renal failure; decrease proteinuria
Pregnancy- preeclampsia, eclampsia agent
methyldopa, hydralazine, beta blockers w caution
Pregnancy- preeclampsia, eclampsia caution
ACE I, angiotensin blockers- may cause renal agenesis, diuretics
Gout caution
Diuretics- worse joint pain or precipitate gout
Cocaine use agent
labetalol, clonidine
Cocaine use caution
Selective B- blockers- unopposed cocaine induced alpha agonism
GI bleed agent
non-selective beta blocker- lower portal blood pressure
GI bleed caution
beta blockers- may mask signs of acute bleeding
Pheochromocytoma agent
Alpha blocker, then beta blockade
Pheochromocytoma caution
Selective beta blocker- unopposed alpha agonism
BPH agent
alpha 1 antagonist
BPH caution
selective beta blocker- unopposed alpha agonism
ARB caution
life threatening hyperkalemia
