Usmle Recall Antihypertensive Drugs

Front 1

Hydralazine: MOA

Back 1

direct vasodilator (arterial) to treat HTN

Front 2

Hydralazine : Clincal uses

Back 2

severe HTN, CHF

Front 3

Hydralazine: toxicity

Back 3

reflex (compensatory) tachycardia, lupus-like syndrome

Front 4

What are some calcium channel blockers (CCBs)?

Back 4

nifedipine, verapamil, diltiazem

Front 5

What is the MOA of CCBs?

Back 5

blocks voltage-dependent L-type (long-acting) calcium channels of cardiac and smooth muscle and therefore reduces muscle contractility

Front 6

What are the clinical uses of CCBs?

Back 6

1. hypertension: CCBs decrease vascular resistance; obtains arteriolar smooth muscle relaxation
2. angina: angina is due to oxygen supply not meeting oxygen demand, CCBs help decrease the work of the heart by causing peripheral dilation (decreases afterload)
3 atrial arrhythmias: AV node conduction depends on Ca2+ channel action potentials. CCBs increase AV node refractory period

Front 7

Why should you NOT use nifedipine for arrhythmias?

Back 7

Nifedipine is very potent on smooth muscle. In fact you'd kill the patient with massive vasodilatation before you got to the dosage that affected the heart; so just used to vasodilate (angina or HTN), but not arrhythmias (not affect cardiac muscle as normal doses)

Front 8

What are the effects of the 3 CCBs on vascular smooth muscle and cardiac muscle?

Back 8

vascular smooth muscle: nifedipine>diltiazem>verapamil

heart:
verapamil>diltiazem>nifedpine

Front 9

CCBs (nondihydropyridine): diltiazem and verapamil
CCBs (dihydropyridine): amlodipine and nifedipine
What is the main difference?

Back 9

Diltiazem and verapamil decrease peripheral resistance and decrease cardiac output
(main toxicities are bradycardia and AV block)
Amlodipine and nifedipine decrease peripheral resistance (more specific for vascular smooth muscle than heart) - main toxicity is reflex tachycardia

Front 10

What is the MOA of ACE inhibitors?

Back 10

Inhibitis angiotensin-converting enzyme (which converts angiotensin I to angiotensin II), reducing levels of angiotensin II
Also prevents inactivation of bradykinin (a potent vasodilator)

1. decreases ATII production
2. decreases aldosterone secretion (via decreasing ATII production)
3. decreases peripheral resistance (again decreasing ATII production)

Front 11

What does angiotensin II do?

Back 11

1. stimulates release of ADH from pituitary to act on the collecting duct on kidney to absorb water
2. stimulates release of aldosterone from adrenal cortex, aldostersone causes reabsorption of Na+/Cl- and H20 and excretion of K+ and H+
3. arteriolar vasconstriction
4. increases sympathetic activity

Front 12

What are the names of some ACE inhibitors?

Back 12

Captopril, Lisinopril, Quinapril, Benazepril

Front 13

What are the side effects of ACE inhibitors?

Back 13

1. dry cough (due to accumulation of bradykinin)
2. hyperkalemia (due to preventing effects of aldosterone, namely excretion of potassium)
3. angioedema
4. renal failure -proteinuria (why?)
5. increased renin (since you're blocking production of ATII, the renal-angiotensin cascade has no feedback inhibition, so the body makes MORE renin, renin tries to make more angiotensin II, but this is prevented by the ACEi)
6. pregnancy problems - fetal renal damage

Front 14

What is the MOA of angiotensin II receptor blocks (ARBs)?

Back 14

blocks the receptor of angiotensin II so angiotensin II is MADE, but cannot exert its effects (vs. ACEi, which actually block the production of angiotensin II by inhibitor ACE, the enzyme that makes angiotensin II)

Front 15

What are the adverse effects of ARBs?

Back 15

fetal renal toxicity
hyperkalemia
but better side effect profile than ACE ihibitors

Front 16

What are the names of some ARBs?

Back 16

Losartan, Valsartan

Front 17

What is the MOA of clonidine and methyldopa?

Back 17

alpha2-receptor agonists (at the pre-synaptic junction) - when you stimulate these receptors, they inhibit the release of NE, so they are centrally-acting HYPOtensive drugs - they decrease CNS sympathetic outflow

Note: if you activated alpha1-receptors at the post-synaptic junction, you get alpha-1 affects, which are generally excitatory exception for in the GI tract (GI relaxation, vasoconstriction, lipolysis, inhibition of insulin release, mydriasis - (dilation of pupil)

Front 18

What are the main side effects of clonidine?

Back 18

sedation/depression; and hypertensive crisis (on withdrawal of clonidine) - severe rebound hypertension

Front 19

What is the MOA of prazosin, terazosin and doxazosin?

Back 19

they are alpha1-receptor antagonists (alpha-1 receptor = vasconstriction, except for in the GI), so if you block this, you get vasodilation and decreased peripheral resistance

Front 20

What is the adverse effects of prazosin?

Back 20

1st-dose orthostatic hypotension (postural hypotension because of blockage of vasoconstriction)

Front 21

What is the MOA of propranolol

Back 21

nonselective-beta blocker
(B1 - stimulates heart muscle, increased heart rate and heart contraction
B2 - vasodilation, bronchial smooth muscle relaxation, intestinal smooth muscle relaxation)
so, if you block these effects, you get negative chronotropic and inotropic effects, reducing cardiac output
- you get decreased AV conduction (blocking B1 receptors) and increased peripheral resistance (because you block B2 receptors)

Front 22

What are the selective beta1-receptor blockers?

Back 22

B1>B2 - Acebutolo, Betaxolol, Esmolol (short acting), Atenolo, Metoprolol

Front 23

What are the non-selective beta-receptor blockers?

Back 23

propranolol, timolol, pindolol, nadolol, and labetalol (also blocks alpha1-receptors)

Front 24

What are the adverse effects of beta-blockers?

Back 24

-bronchospasm, bradycardia, AV block and sexual dysfunction
-you can exacerbate asthma because you block B2 (bronchodilation); if you block B1, you can also get cardiovascular adverse effects of bradycardia, AV block and CHF

Front 25

You must use beta-blockers with caution in diabetics and asthmatics! Why?

Back 25

1. asthmatics, if you block B2 and bronchodilation, you could get get bronchospasm
2. diabetics (you can block effects of hypoglycemia - which generally activates the sympathetic nervous system. If a diabetic takes beta-blockers, then, they will NOT get an increased heart rate, but will probably still get sweaty since sweat glands use ACh (and not NE, which is what beta-blockers block)

Front 26

How can beta-blockers worsen peripheral artery disease?

Back 26

You block B2, which is used in vasodilation

Front 27

What class of drugs are labetalol and carvedilol (Coreg)?

Back 27

combined alpha1 and beta-blockers

Front 28

What is the mechanism of nitroglycerin and isosorbide dinitrate?

Back 28

vasodilate by releasing nitric oxide in smooth muscle, causing increase in cGMP and smooth muscle relaxation (dilates veins>>arteries) vs. CCBG, which dilate arteries and not veins

Front 29

What is the clinical use of nitroglycerin?

Back 29

angina

Front 30

What are the adverse effects of nitroglycerin?

Back 30

tachycardia, hypotension, headache

Front 31

In mild heart failure, which choice of drugs should you use?

Back 31

1. ACEi
-decreases preload by venous dilation/pooling, decreases filling pressure
-decreases afterload by arteriolar dilation; reduction in vascular tone decreases work and oxygen demand of failing heart
2. add diuretic: increase Na+ excretion, decreases blood volume and decreases preload
3. add digoxin: increase force of cardiac muscle contraction