HTN meds: ACEI, ARB, Renin Inhibitor and Diuretics Flashcards Preview

Pharm: Pre Midterm 1 > HTN meds: ACEI, ARB, Renin Inhibitor and Diuretics > Flashcards

Flashcards in HTN meds: ACEI, ARB, Renin Inhibitor and Diuretics Deck (39)

What is essential HTN?

Cause in elevation of blood pressure in unknown
--likely multifactorial


What is secondary HTN?

Caused by chronic kidney disease or renovascular disease


What are the classifications of HTN for adults?

Normal: 120/80
Pre-HTN: 120-139 over 80-89
HTN, stage 1: 140-159 or 90-99
HTN, stage 2: over 160 over 100


The actual increase in arterial blood pressure is caused by either ?

1. Increase in peripheral vascular resistance (determined by vascular tone)
2. Increase in cardiac output (determined by HR and stroke volume)
3. Kidney also contributes to the maintenance of blood pressure by regulating the volume of intravascular fluid


Cardiac Output and Peripheral vascular resistance are controlled by the baroreceptors, which are mediated by ?

1. Sympathetic nervous system (decreased BP -- baroreflex- increased HR)
2. Renin angiotensin aldosterone system: angiotensin II is a potent vasoconstrictor acting on both arterioles and veins to result in an increase in blood pressure and increase in GFR
---Angiotensin II stimulates secretion of aldosterone from the adrenal cortex ---- aldosterone causes tubules to increase Na and H20 reabsorption


Antihypertensive drugs do what?

Lower blood pressure by actions on
--peripheral resistance
--cardiac output
or both


What drugs are used to treat HTN?

Diuretics (Reduce blood volume)
--thiazide diuretics, loop diuretics, potassium sparing diuretics
Vasodilators (reduce peripheral resistance)
--inhibitors of angiotensin, calcium channel blockers, alpha-adrenoceptor antagonists, direct vasodilators
Cardioinhibitor Drugs (Reduce heart rate and contractility)
--B-blockers, calcium-channel blockers
Centrally acting sympatholytics (reduce systemic vascular resistance and cardiac output)
--central alpha2 agonists


Most patients with stage 1 HTN should initially be treated with what?

1. Thiazide diuretic
2. ACE inhibitor
3. Angiotensin II receptor blocker (ARB)
4. Calcium channel blockers


What is the recommended blood pressure meds for black patients?

Respond well to calcium channel blockers and diuretics but have smaller blood pressure reductions with ACE inhibitors, ARBs and b-blockers


If a patient has heart failure, what meds should be used for HTN?

Diuretic plus ACEI or ARB plus B-blocker
--aldosterone antagonist if severe HF
--Hydralazine/Isosorbide dinitrate (if black)


If a patient has post MI what HTN meds should be used?

B-blocker then add ACEI or ARB
--aldosterone antagonist


If a patient has CAD, what HTN meds should be used?

B blocker than add ACEI or ARB
--CCB, diuretic


if a patient has DM, what HTN meds should be used?

CCR or thiazide


If a patient has Chronic Kidney Disease, what HTN meds should be used?

CCB or thiazide


if a patient has a prior ischemic stroke, what HTN meds should be used?

CCB or thiazide


The last set of cards went through diuretics, what is the best thiazide diuretic to give for HTN?

--in patients with normal renal and cardiac function
--also first line in black/elderly patients who dont respond well to ACEI or ARBs


What is the best loop diuretic to give for HTN?

--prescribed for patients who do not respond well to thiazide diuretics
--preferred over thiazides in patients with severe renal disease or severe HTN


What is the best K sparing diuretics?

Amiloride and Triamterene
--are less efficacious then the previous two diuretics
--used in combo with other diuretics to attenute or correct drug induced K excretion and resultant hypokalemia


What is the best Aldosterone antagonists?

Spironolactone and Eplerenone
--also K sparing diuretics but more potent
--very useful in secondary hypertension caused by hyperaldosteronism


Again the last set of cards went through in detail the mechanism of action of diuretics, how does diuretics help with blood pressure?

Reduction in plasma volume and stroke volume associated with diuresis decreases cardiac output and therefore blood pressure
--however, the decrease in cardiac output stimulates the renin system which leads to volume retention and an increase in peripheral vascular resistance.
--however after about 2 months of treatment the volume and plasma return to pretreatment levels and peripheral vascular resistance falls


What are the pharmokinetics for diuretics?

Thiazide and K sparing: long duration of action
Loop: short duration of action


In treating hypertension, what is the most common adverse effect of diuretics?

--except for K sparing diuretics


Now moving on to the vasodilators, the first class are the inhibitors of angiotensin. Renin release is from the kidney cortex and is controlled by what 4 things?

1. Changes in tension in the afferent arteriolar wall
2. Macula densa detecting changes in NaCl in the distal tubule
3. Circulating angiotensin
4. sympathetic nervous system which stimulates renin secretion mediated by B1 receptors


What are the actions of angiotensin II?

Sodium retaining activity
Stimulates aldosterone release
Regulates blood pressure


There are three classes of drugs that act specifically on the renin system. The first are ACE inhibitors which include Captopril, Enalapril and Lisinopril. What are some of the clinical applications of ACEI?

1. HTN: first line in primary HTN and HTN caused by unilateral renal artery stenosis. Also treatment of nonpregnant patients with albuminuria
2. Heart Failure: chronic
3. MI: following MI -- reduce deleterious remodeling that occurs post infarction. give 24H after MI


In black or elderly patients they have a decreased amount of renin in the body, so they do not respond as well to ACEI or ARBs. So what are first line drugs in these patients?

A thiazide or calcium channel blocker is preferred as a first line agent instead.


What is the mechanism of action of ACEI?

Block the conversion of angiotensin I to angiotensin II
--therefore reducing vasoconstriciton and aldosterone secretion
--creatinine can increase due to decreased vasoconstriction of efferent arterioles leading to a decrease in GFR (reversible and not harmful)
Renin levels increase as well as Angiotensin I levels due to the lack of negative feedback from angiotensin II to renin


ACEI block the degradation of bradykinin and therefore stimulate what?

The secretion of other vasodilating substances
-prostaglandin E2


ACEI are useful in treating patients with chronic kidney disease why?

--Diminish proteinuria and stabilize renal function


What are some adverse effects of ACEI?

1. Hypotension: occurs at onset of therapy
2. Hyperkalemia: not clinically important except in chronic kidney disease patients or diabetics
3. Acute Renal Failure: contraindicated in patients with bilateral renal artery stenosis due to risk of renal failure
--ACEI remove constriction on the efferent arterioles and causes an abrupt fall in GFR
4. Dry cough: due to rise in bradykinin levels
5. Angioedema: increase in bradykinin levels
6. Altered sense of taste, skin rashes, drug fever


What are the contraindications in ACEI?

1. Pregnancy: congenital malformations and neonatal problems (renal failure or death)
2. Bilateral renal artery stenosis
3. Hyperkalemia


The next group of drugs of vasodilators are Angiotensin Receptor Blockers (ARBs), Losartan and Valsartan. What are the clinical applications for these drugs?

Tx of HTN and heart failure
--beneficial effects in patients with left ventricular failure or diabetic nephropathy
--just as good as ACEI
--use in patients who experience the cough with ACEI
--work better in white, Asian or young.


What is the mechanism of action of ARBs?

Block Angiotensin I receptor
---therefore blocking angiotensin II vasoconstriction and aldosterone secretion
--no blockage of bradykinin breakdown so no dry cough or angioedema
--again renin, angiotensin I levels will increase


What are the adverse effects seen in ARBs?

Acute renal failure: rare but serious


What are the contraindications for ARBs?

Pregnancy: again due to congenital and fetal malformations
Bilateral renal artery stenosis


The last drug in this card set will be renin inhibitor, Aliskiren. What are the clinical applications of this drug?

Tx of HTN
--only used as an alternative therapy due to lack of long term studies
--in combo with an ACEI or ARB might increased CVS and renal events in patients with diabetes and should be avoided


What is the mechanism of action of Aliskiren?

Block the renin system at it point of activation which reduces renin activity, vasodilation and a decrease in blood pressure


What are the adverse effects with Aliskiren?

Acute Renal Failure


Finally what are the contraindications for Aliskiren?

Bilateral Renal artery stenosis