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
Verapamil
CCB May cause constipation and peripheral edema Use of verapamil with a B-blocker is contraindicated bc of the potential for AV block
26
Potassium channel openers
Increased potassium permeability stabilizes the smooth muscle cell membrane at resting potential, reducing the probability of contraction - Diazoxide - Minoxidil
27
Diazoxide
K channel opener - Arteriolar vasodilation - Diminishing use in hypertensive emergencies due to adverse efects - Excessive hypotension can cause stroke and Mi - Hyperglycemia
28
Minoxidil
K channel opener - Arteriolar vasodilation - Clinical uses include severe hypertension and baldness
29
Fenoldopam
Dopamine receptor agonist - Activation increases blood flow to the kidneys For HTN emergencies and post-operative HTN
30
Hydralazine
releases NO from endothelium- dilates arterioles, but not veins First line oral therapy for hypertension in pregnancy
31
Nitroglycerin
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
Labetalol
Selective a1 blocker Nonselective b1 and b2 blocker partial agonist IV for severe hypertension acceptable option for hypertension during pregnancy
33
Combinations to avoid
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
The most effective parenteral drug for hypertensive emergencies
Sodium nitroprusside Potential for cyanide toxicity limits prolonged use
35
Acute management of severe hypertension in pregnant women
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
Long term oral therapy for hypertension in pregnant women
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
Nonedematous states that are treated with diuretics
1. Hypertension 2. Nephrolithiasis- kidney stone 3. Hypercalcemia 4. Diabetes insipidus
38
MUDPILES
``` Methanol Uremia Diabetic ketoacidosis Paraladehyde Infection, iron, isoniazide Lactic acidosis Ethylene glycol, alcohol Salicylates, starvation ketoacidosis ```
39
pH
7.4
40
pCO2
40
41
HCO3
24
42
After MI Agent
beta blocker, ACE I
43
After MI caution
direct vasodilators- may worsen coronary insufficiency
44
CHF agent
ACE I, diuretics; beta blockers (no pulm edema)
45
CHF caution
beta blockers, CCB
46
hyptertrophic cariomyopathy agent
beta blockers, CCB
47
hyptertrophic cariomyopathy caution
diuretics, ACE inhibitors, direct vasodilators
48
bradycardia, heart block caution
beta blockers, CCB
49
Tachyarrhythmias agent
beta blockers, verapamil
50
angina agent
beta blockers, CCB, Nitroglycerin
51
Angina caution
direct vasodilators (
52
COPD agent
CCB
53
COPD caution
beta blockers
54
aortic dissection agent
nitroprusside, beta blocker
55
aortic dissection caution
drugs that > cardiac output (increased shear stress)
56
B/ renal artery stenosis caution
ACE I, angiotensin blockers- may worsen renal function
57
Chronic renal insufficiency agent
ACE I (w/ serum creatinin
58
Chronic renal insufficiency caution
ACE inhibitors, angiotensin blockers- may worsen renal function
59
Renal transplants caution
ACE I
60
migraine headaches agent
beta blockers, CCB- may relive migraine symptoms
61
stroke or TIA agent
ACE I- may allow reestablishment of cns autregulation
62
stroke or TIA caution
vasodilators may increase intracranial pressure
63
Diabetes agent
ACE I- delay renal failure; decrease proteinuria
64
Pregnancy- preeclampsia, eclampsia agent
methyldopa, hydralazine, beta blockers w caution
65
Pregnancy- preeclampsia, eclampsia caution
ACE I, angiotensin blockers- may cause renal agenesis, diuretics
66
Gout caution
Diuretics- worse joint pain or precipitate gout
67
Cocaine use agent
labetalol, clonidine
68
Cocaine use caution
Selective B- blockers- unopposed cocaine induced alpha agonism
69
GI bleed agent
non-selective beta blocker- lower portal blood pressure
70
GI bleed caution
beta blockers- may mask signs of acute bleeding
71
Pheochromocytoma agent
Alpha blocker, then beta blockade
72
Pheochromocytoma caution
Selective beta blocker- unopposed alpha agonism
73
BPH agent
alpha 1 antagonist
74
BPH caution
selective beta blocker- unopposed alpha agonism
75
ARB caution
life threatening hyperkalemia