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29 Cards in this Set

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What are the 7 categories of anti-hypertensive drugs?
(1) diuretics
(2) drugs that alter SNS activity
(3) vasodilators
(4) calcium channel blockers
(5) ACE inhibitors
(6) angiotensin II receptor blockers
(7) renin inhibitor
Recall there are 5 classes of diuretics. Which of these 5 are anti-hypertensive?
(1) thiazides : hydrochlorothiazide, chlorthalidone, metolazone

(2) loop diuretics : furosemide, bumetanide, torsemide, ethacrynic acid

(3) K-sparing diuretics : amiloride, triamterene, spironolactone
What are the 3 sub-classes of anti-HTN drugs that alter SNS activity?
(1) drugs that have CNS action

(2) drugs that act on postganglionic nerve endings

(3) adrenergic receptor blockers
Which 2 anti-HTN drugs act at postganglionic sympathetic nerve endings?
(1) reserpine
(2) guanethidine
How do alpha-1 blockers lower BP?

Describe the first dose phenomenon associated with the alpha-1 blockers.

What is the prototype alpha blocking drug?
Alpha-1 receptor blockers block the postsynaptic receptors, leading to decreased SNS activity.

The first dose phenomenon refers to teh symptomatic orthostatic hypoTN & possibly syncope that may occur in a patient who is starting an alpha blocker.

Prototype: prazosin
How do non-selective beta blockers lower BP?

What is the prototype non-selective beta blocker drug?
Beta blockers decrease HR and contractility, leading to decreased cardiac output. They also decrease renal renin release.

Prototype: propanolol
What are some adverse effects of propanolol?
(1) dec myocardial contractility
(2) bradyarrhythmias
(3) bronchospasm
(4) prolonged hypoglycemia in pts taking insulin
(5) sedation
(6) beta blocker withdrawal
Describe the pathogenesis of beta blocker withdrawal.
Chronic beta receptor blockade causes upregulation of the beta receptors... This upregulation is of no real consequence while the patient is still on the beta blocker meds.

However, sudden discontinuation of the medicine may result in adverse effects like angina exacerbation and even myocardial infarctions.
Which 2 drugs are alpha AND beta blockers?
(1) labetalol
(2) carvedilol

They are alpha-1 selective & beta non-selective.
Which 2 drugs have their principal effect in the CNS?

What are their respective adverse effects?
(1) clonidine

(2) methyldopa

Common adverse effects: sedation, dry mouth, orthostatic hypotension

Clonidine adverse effects: HTN crisis w/ sudden withdrawal

Methyldopa adverse effects: dec mental concentration, hepatotoxicity, positive Coombs test & hemolytic anemia
Describe how clonidine & methyldopa lower BP.
Clonidine: stimulates alpha-2 receptors in brainstem to dec SNS outflow from CNS

Methyldopa: stimulate CNS alpha receptors by active metabolite to dec SNS outflow
What are the adverse effects of reserpine?

What are the adverse effects of guanethidine?
Reserpine adverse effects: sedation, depression

Guanethidine: orthostatic hypotension, drug interactions that block transport of drug into nerve ending
List the anti-hypertensive arterial dilators.

Which of these are administered in the case of hypertensive emergencies?
(1) Hydralazine
(2) Minoxidil
(3) Fenoldopam : IV drug for HTN emergency
(4) Diazoxide : IV drug for HTN emergency
A patient who is a slow acetylator and taking hydralazine is at risk of forming this...
drug induced lupus
What is the route of administration for each of the following...

(1) hydralazine
(2) minoxidil
(3) fenoldopam
(4) diazoxide
(5) Na nitroprusside
(1) hydralazine : oral & IV
(2) minoxidil : oral
(3) fenoldopam : IV
(4) diazoxide: IV
(5) Na nitroprusside: IV
What is the mechanism of action for each of the following dilators...


(1) hydralazine
(2) minoxidil
(3) fenoldopam
(4) diazoxide
(5) Na nitroprusside
(1) hydralazine : dec PVR & dec BP by causing NO release

(2) minoxidil : opens K+ channels to induce hyperpolarization of smooth muscle cells, making contraction less likely

(3) fenoldopam : stimulates DA-1 receptors, leading to vasodilation

(4) diazoxide : opens K+ channels

(5) Na nitroprusside : stimulates guanylyl cyclase, leading to increased cGMP and relaxation
Name the dilator drug that is associated with the following unique adverse effects...

(1) cyanide toxicity
(2) hypertrichosis
(3) drug-induced lupus
(4) pericardial effusion
(5) inc intraocular pressure
(1) cyanide toxicity // Na nitroprusside

(2) hypertrichosis // minoxidil

(3) drug-induced lupus // hydralazine

(4) pericardial effusion // minoxidil

(5) inc intraocular presure // fenoldopam
Sodium nitroprusside, fenoldopam & diazoxide are all administered for the treatment of hypertensive emergencies.

How do their mechanisms differ?
What are their time courses of action?
Na NITROPRUSSIDE: arterial & venous dilator; stimulate guanylyl cyclase & increase cGMP; rapid onset & offset

FENOLDOPAM: stimulate DA-1 receptors; rapidly metabolized & given via continuous IV infusion

DIAZOXIDE: open potassium channels & cause hyperpolarization; duration of action is 4-12hrs
Name the 3 dilator drugs that can be administered during a hypertensive emergency.

What are the adverse effects associated with each drug?
Na NITROPRUSSIDE: hypotension, cyanide or thiocyanate toxicity

FENOLDOPAM: inc HR, inc intraocular pressure

DIAZOXIDE: excessive lowering of BP & reflex SNS stimulation; latter can cause angina, cardiac failure; fluid retention; hyperglycemia
How is angiotensin II formed?

What are its 3 main functions?
1)Kidney releases renin which converts angiotensinogen to angiotensin I.
2) Angiotensin I concerted to angiotensin II by ACE.

3 main functions of A-II...
a) Resistance: peripheral vasoconstriction
b) Renal: inc Na reabsorption in proximal tubule; causes release of aldosterone
c) Cardio structure: inc afterload; inc wall tension
List the 2 ACE inhibitors.

What is their mechanism of action?

What are their "downstream" effects due to their mechanism of action?
(1) captopril
(2) enalapril

They inhibit conversion of A-I to A-II, which leads to these downstream effects...
1) inc plasma renin activity
2) dec vasoconstriction
3) dec aldosterone
4) dec bradykinin breakdown
Your patient is taking captopril.

What would be this patient's hypertensive response to an A-II injection?

A-I injection?
If a person is not any medication, both an A-I and A-II injection would cause a pressor effect. A-I would be converted to A-II by ACE and vasoconstriction would occur.

However, if this patient -- who is on an ACE-I -- gets an A-I injection. there will not be a pressor response because captopril is inhibiting the conversion of A-I to A-II.

The patient would, however, experience a pressor response (just like a non-medicated person) following an A-II injection.
Your patient has bilateral renal artery stenosis. How would her GFR change with adminstration of captopril?

What if your patient had a chronic renal disease, like diabetic nephropathy. How would administration of captropril affect this patient's renal function?
Pt with B/L renal artery stenosis: captopril, an ACE-I, would decrease the GFR, leading to an increased BUN: Cr ratio (bad news bears)

Pt with diabetic nephropathy: captopril would decrease albuminuria and stabilize renal function
What are some adverse effects shared by ACE inhibitors & A-II receptor blockers?
--hypotension
--hyperkalemia
--angioedema (ACE-I >> ARB)
--cough (ACE-I >> ARB)
--decreased renal function in those patients w/ bilateral renal artery stenosis
--fetal toxicity
Compare how ACE inhibitors and A-II receptor blockers lower BP.

Under which circumstance (ACE-I or ARB) would a patient's renin activity be increased? A-II levels be increased?
ACE inhibitors: inhibit conversion of angiotensin I to angiotensin II.. no A-II means lower BP

ARB: inhibits type1 A-II receptors but does not inhibit A-II formation...no A-II action means lower BP

Both drugs would cause an increased plasma renin activity.

Patients taking an ARB would have an increased plasma A-II level.
Describe the mechanism of action of aliskiren.

Does aliskiren affect renin activity or renin concentration? or both?
Aliskiren inhibits renin activity, which then leads to decreased A-II levels.

Aliskiren affects both renin levels & activity. Aliskiren decreases renin activity and causes an increased plasma renin concentration.
What are some adverse effects associated with aliskiren?
(1) diarrhea
(2) angioedema
(3) cough
(4) hyperkalemia
For each of the following effects, decide if it is an effect of ACE inhibitors, ARB's or aliskiren..

1) increased plasma renin concentration

2) increase A-II levels

3) increased plasma renin activity

4) angioedema and cough adverse effects
1) increased plasma renin concentration : aliskiren

2) increase A-II levels : aliskiren and ARB's

3) increased plasma renin activity : ACE inhibitors, ARB's

4) angioedema and cough : all three
Recall the various category names of anti-hypertensive drugs (vasodilator, adrenergic antagonist, etc)... Match the following drugs with its respective category.

(1) Na nitroprusside
(2) fenoldopam
(3) labetalol
(4) captopril
(5) aliskiren
(6) losartan
(7) prazosin
(8) metoprolol
(9) verapamil
(10) clonidine
(11) propanolol
(1) Na nitroprusside = arterial and venous dilator

(2) fenoldopam = arterial dilator

(3) labetalol = alpha and beta blocker

(4) captopril = ACE inhibitor

(5) aliskiren = renin inhibitor

(6) losartan = A-II receptor blocker

(7) prazosin = alpha1-selective blocker

(8) metoprolol = beta1-selective blocker

(9) verapamil = Ca channel blocker

(10) clonidine = principal CNS effect; alpha2 agonist

(11) propanolol = non-selective beta blocker