Antihypertensive drugs Flashcards

1
Q

Treatment for pts with chronic kidney disease

A
  • ACE inhibitors

- Angiotensin receptor blocker (ARB)

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2
Q

Treatment for pts without chronic kidney disease

A

Black pts

  • Thiazide diuretic
  • calcium channel blocker

Nonblack

  • Thiazide diuretic
  • ACE inhibitor
  • ARB
  • CCB
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3
Q

Diuretics

A

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
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4
Q

Carbonic anhydrase inhibitors

A

Acetazolamide

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5
Q

Loop diuretics

A

Ethacrynic acid

Furosemide (lasix)

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6
Q

Thiazide diuretics

A

Chlorthalidone

Hydrochlorothiazide

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7
Q

K sparing diuretics

A

Aldosterone antagonists
- Spironolactone

Epithelial Na channel inhibitors
- Amiloride

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8
Q

Acetazolamide

A

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

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9
Q

Furosemide and ethacrynic acid

A

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

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10
Q

Hydrochlorothiazide (HCTZ)

A

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

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11
Q

Spironolactone

A

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

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12
Q

Amiloride

A

K sparing diuretic, blocks the Na channels from absorbing, prevents K secretion

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13
Q

ACE inhibitors

A

Captopril
Enalapril

“pril”

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14
Q

ARBs

A

Losartan
Valsartan

“sartan”

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15
Q

Captropril and analapril

A

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

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16
Q

Benefits of ACE inhibitors

A

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

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17
Q

Adverse effects of AVE inhibitors

A
Cough
Angioedema
Teratogen
Creatinine (increased)
Hyperkalemia- avoid K sparing diuretics
Hypotension
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18
Q

Losartan and valsartan

A

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

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19
Q

Aliskiren

A

Direct renin inhibitor
Does not increase bradykinin

Rise in plasma renin levels but decreased renin activity

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20
Q

Vasodilators: Calcium channel blockers- dihydropyridines

A

Amlodipine

Nifedipine

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21
Q

Vasodilators: Calcium channel blockers- non-dihydropyridines

A

Diltiazem

Verapamil

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22
Q

Vasodilator: Nitrix oxide donors

A

Hydralazine

Nitroprusside

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23
Q

Non-dihydropyridines

A

CCB
Prominent cardiac effects, but also act at vascular tissues.
Causes vasodilation.

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24
Q

Dihydropyridines

A

CCB

Predominantly arteriolar vasodilation effects

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25
Q

Verapamil

A

CCB

May cause constipation and peripheral edema

Use of verapamil with a B-blocker is contraindicated bc of the potential for AV block

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26
Q

Potassium channel openers

A

Increased potassium permeability stabilizes the smooth muscle cell membrane at resting potential, reducing the probability of contraction

  • Diazoxide
  • Minoxidil
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27
Q

Diazoxide

A

K channel opener

  • Arteriolar vasodilation
  • Diminishing use in hypertensive emergencies due to adverse efects
  • Excessive hypotension can cause stroke and Mi
  • Hyperglycemia
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28
Q

Minoxidil

A

K channel opener

  • Arteriolar vasodilation
  • Clinical uses include severe hypertension and baldness
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29
Q

Fenoldopam

A

Dopamine receptor agonist
- Activation increases blood flow to the kidneys

For HTN emergencies and post-operative HTN

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30
Q

Hydralazine

A

releases NO from endothelium- dilates arterioles, but not veins

First line oral therapy for hypertension in pregnancy

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31
Q

Nitroglycerin

A

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
32
Q

Labetalol

A

Selective a1 blocker
Nonselective b1 and b2 blocker
partial agonist

IV for severe hypertension
acceptable option for hypertension during pregnancy

33
Q

Combinations to avoid

A
  1. ACE inhibitors, ARBs, and renin inhibitors (only one at a time)
  2. Beta blockers and non-dihydropyridine CCBs
  3. Potassium-sparing diuretics and ACE inhibitors/ARBs/renin inhibitors
34
Q

The most effective parenteral drug for hypertensive emergencies

A

Sodium nitroprusside

Potential for cyanide toxicity limits prolonged use

35
Q

Acute management of severe hypertension in pregnant women

A
  1. Labetalol
  2. Hydralazine- used extensively in the setting of preclampsia
  3. Calcium channel blockers- sustained release nifedipine or immediate release nicardipine
  4. Nitroglycerin- a good option for HTN associated w pulmonary edema
36
Q

Long term oral therapy for hypertension in pregnant women

A
  1. Methyldopa- sedated effect is bothersome to already fatigued patients. Clonidine is another centrally acting sympatholytic that is considered safe in pregnant women
  2. Labetalol- More rapid onset of action than methyldopa
  3. Nifedipine
  4. Hydralazine- due to reflex tachycardia, monotherapy with oral hydralazine is not recommended
  5. Thiazide diuretics- generally only introduced during pregnancy if pulmonary edema has developed
37
Q

Nonedematous states that are treated with diuretics

A
  1. Hypertension
  2. Nephrolithiasis- kidney stone
  3. Hypercalcemia
  4. Diabetes insipidus
38
Q

MUDPILES

A
Methanol
Uremia
Diabetic ketoacidosis
Paraladehyde
Infection, iron, isoniazide
Lactic acidosis
Ethylene glycol, alcohol
Salicylates, starvation ketoacidosis
39
Q

pH

A

7.4

40
Q

pCO2

A

40

41
Q

HCO3

A

24

42
Q

After MI Agent

A

beta blocker, ACE I

43
Q

After MI caution

A

direct vasodilators- may worsen coronary insufficiency

44
Q

CHF agent

A

ACE I, diuretics; beta blockers (no pulm edema)

45
Q

CHF caution

A

beta blockers, CCB

46
Q

hyptertrophic cariomyopathy agent

A

beta blockers, CCB

47
Q

hyptertrophic cariomyopathy caution

A

diuretics, ACE inhibitors, direct vasodilators

48
Q

bradycardia, heart block caution

A

beta blockers, CCB

49
Q

Tachyarrhythmias agent

A

beta blockers, verapamil

50
Q

angina agent

A

beta blockers, CCB, Nitroglycerin

51
Q

Angina caution

A

direct vasodilators (

52
Q

COPD agent

A

CCB

53
Q

COPD caution

A

beta blockers

54
Q

aortic dissection agent

A

nitroprusside, beta blocker

55
Q

aortic dissection caution

A

drugs that > cardiac output (increased shear stress)

56
Q

B/ renal artery stenosis caution

A

ACE I, angiotensin blockers- may worsen renal function

57
Q

Chronic renal insufficiency agent

A

ACE I (w/ serum creatinin

58
Q

Chronic renal insufficiency caution

A

ACE inhibitors, angiotensin blockers- may worsen renal function

59
Q

Renal transplants caution

A

ACE I

60
Q

migraine headaches agent

A

beta blockers, CCB- may relive migraine symptoms

61
Q

stroke or TIA agent

A

ACE I- may allow reestablishment of cns autregulation

62
Q

stroke or TIA caution

A

vasodilators may increase intracranial pressure

63
Q

Diabetes agent

A

ACE I- delay renal failure; decrease proteinuria

64
Q

Pregnancy- preeclampsia, eclampsia agent

A

methyldopa, hydralazine, beta blockers w caution

65
Q

Pregnancy- preeclampsia, eclampsia caution

A

ACE I, angiotensin blockers- may cause renal agenesis, diuretics

66
Q

Gout caution

A

Diuretics- worse joint pain or precipitate gout

67
Q

Cocaine use agent

A

labetalol, clonidine

68
Q

Cocaine use caution

A

Selective B- blockers- unopposed cocaine induced alpha agonism

69
Q

GI bleed agent

A

non-selective beta blocker- lower portal blood pressure

70
Q

GI bleed caution

A

beta blockers- may mask signs of acute bleeding

71
Q

Pheochromocytoma agent

A

Alpha blocker, then beta blockade

72
Q

Pheochromocytoma caution

A

Selective beta blocker- unopposed alpha agonism

73
Q

BPH agent

A

alpha 1 antagonist

74
Q

BPH caution

A

selective beta blocker- unopposed alpha agonism

75
Q

ARB caution

A

life threatening hyperkalemia