Hypertension Drugs

Question 1

Causes of secondary htn

Answer 1

renal: chronic kidney disease, renal artery stenosis
drugs: alcohol, contraceptives, NSAIDs, appetite suppress, tricyclics, MAOi
Endocrine issues: pheochromocytoma, cushings, hyperaldosteronism, hypo and hyperpara/thyroid
pulmonary: obstructive sleep apnea

Question 2

non-modifiable factors that cause hypertension

Answer 2

genetics, gender, age, race

Question 3

modifiable factors that cause htn

Answer 3

sodium intake, obesity, alcohol intake, medications, sedentary lifestyle, physiologic stress, diets lower in potassium and calcium

Question 4

end organ disease due to HTN

Answer 4

brain, eyes, vascular tree, heart, kidneys. end organ disease related to extent of BP elevation and duration of HTN. risk of end organ disease higher in african americans and in premenopausal women

Question 5

most commonly used HTN drugs

Answer 5

thiazide type diuretics. ACE inhibitors. Angiotensin receptor blockers. Calcium channel blockers.

Question 6

less commonly used HTN drugs

Answer 6

beta and alpha blockers. rarely used are central acting alpha 2 agonists and adrenergic blocking agents

Question 7

high, medium, and low potency diuretics

Answer 7

high: loop. competitively inhibit Na, K, and Cl transporters in the proximal ascending tubule
medium: thiazide. inhibit exchange of Na and Cl in the distal ascending loop.
low: potassium sparing. inhibit Na reabsorption in distal tubule

Question 8

cautions for loop and thiazide diuretics

Answer 8

hypokalemia, hypomagnesemia. impaired glucose tolerence. increased lipids. increased uric acid. erectile dysfunction. volume depletion

Question 9

cautions for potassium sparing diuretics

Answer 9

gynecomastia. menstrual irregularities, menorrhagia, and nipple tenderness. hyperkalemia. especially prevalent in setting of renal failure, diabetes, and ACE inhibitors/ARBs

Question 10

biologic effects of diuretics

Answer 10

diuretics cause volume depletion by enhanced excretion of sodium and water. initially causes BP drop and a drop in cardiac output. over time, CO returns to normal

Question 11

mechanism of ACEi

Answer 11

blocking endothelial ACE from converting angiotensin I to angiotensin II. also inhibits the breakdown of bradykinin which is a potent vasodilator.

Question 12

mechanism of angiotensin receptor blockers (ARBs)

Answer 12

mechanism is competitive receptor binding of angiotensin II to vascular endothelium. Angiotensin II is a very potent vasoconstrictor

Question 13

side effects and cautions for ACEi and ARBs

Answer 13

cough (only with ACEi). hypotension. decreased renal function. rarely angioedema. contraindicated in renal artery stenosis, hyperkalemia, pregnancy. use caution in renal failure

Question 14

what conditions do ACEi/ARBs benefit?

Answer 14

chronic kidney disease and proteinuria. congestive heart failure. LV remodeling post MI. left ventricular hypertrophy. May reduce risk of diabetes in patients at risk.

Question 15

spironolactone/epleronone

Answer 15

aldosterone antagonist. gynecomastia and mennorhagia side effects for spironolactone. hyperkalemia side effects. reserved mostly for patients with concomitant advance heart failure or in derm as an anti-testosterone product or in cirrhosis with ascites

Question 16

two categories of calcium channel blockers

Answer 16

dihydropyridines and non-dihydropyridines

Question 17

other benefits of CCBs

Answer 17

anti-anginal benefits. Dihydropyridines can cause a reflex tachycardia and may worsen angina. Non-dihydro decrease heart rate thus decreasing myocardial oxygen demand. Can help with raynauds syndrome

Question 18

CCB mechanism

Answer 18

inhibit contraction of vascular smooth muscles by blocking calcium entry into the cell leading to reduced systemic vascular resistance

Question 19

side effects of CCBs

Answer 19

constipation, leg edema, heart failure, bradycardia, AV nodal block, reflex tachycardia w/ dihydros. Short acting CCBs have the worst side effects.

Question 20

mechanism of action for beta blockers

Answer 20

reduced cardiac output (primary reason for BP lowering). inhibiting renin release. reducing norepi release from neurons. decreasing central vasomotor activity (less sympathetic tone). overall you should expect very modest BP improvement.

Question 21

propanolol

Answer 21

blockage of B1 and B2 receptors and benefit on BP lowering is primarily in decreasing cardiac output. side effects are decreased exercise capacity, bronchospasm, bradycardia, CHF, mask symptoms of hypoglycemia, depression, worsening symptoms of peripheral vascular disease

Question 22

moderately selective Beta Blockers

Answer 22

cardioselective in that it blocks B1 and very little B2 activity. Less likely to cause bronchospasm, depression, hypoglycemic probs.

Question 23

unique beta blockers

Answer 23

carvedilol, labetalol, esmolol. potent antihypertensives used in ICU and CCU for HTN control. Have additional sympathetic properties. Esmolol used for short half life and AV nodal blocking in unstable patients

Question 24

alpha 1 adrenergic receptor antagonist

Answer 24

reduces vascular resistance by blocking receptors on vascular smooth muscles. Side effects are orthostatic hypotension, fluid retention, worsening angina. helps with BPH, but second tier HTN drug

Question 25

hydralazine and minoxidil

Answer 25

relax smooth muscles of peripheral arterioles. Minoxidil used for refractory HTN and in rogaine. hydralazine used in ICU for acute HYN urgency, or with chronic CHF patients who also have HTN

Question 26

central acting sympathoplegic drugs

Answer 26

mech: stim alpha 2 receptors, causes reduced symp outflow from vasomotor centers in the brainstem. inhibits renin release. clonidine only one used really. alpha methyl dopa still used in pregnancy. sedation, dry mouth, fatigue, rebound HTN

Question 27

ganglion blocking agents

Answer 27

guanethidine reduces BP by blocking release of norepi from post-gang sympathetic nerve terminals