Cardiovascular Drugs: Antihypertensives Flashcards

1
Q

LIst drug classes that can be used to decrease preload

A

diuretics
nitroglycerin
RAAS drugs
sodium nitroprusside
PDE inhibitor

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2
Q

List drug classes that can be used to decrease afterload

A

hydralazine
RAAS drugs
dihydropyridines
minoxidil
sodium nitroprusside

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3
Q

list drug classes that can be used to decrease contractility

A

B1 antagonists
calcium channel blockers

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4
Q

list drug classes that can be used to increase contractility

A

digoxin
B1 agonists (dobutamine)
dopamine
PDE inhibitor

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5
Q

list drug classes that can be used to regulate (decrease) heart rate

A

B1 antagonists
calcium channel blockers

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6
Q

Are diuretics used for hypertension?

A

yes

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7
Q

Explain the RAAS

A

angiotensinogen produced in liver

renin produced in kidneys

renin catalyzes angiotensinogen –> ang2

ACE (high concentration in lungs) catalyzes ang1 –> ang2

ang2 = ADH secretion, vasoconstriction, aldosterone increase (Na+/water retention)

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8
Q

Mechanism of action of ACE inhibitors

A

inhibit ACE, thus inhibit ang2 formation.

–> vasodilation, decreased aldosterone, decreased CV remodeling

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9
Q

aldosterone results in:

A

Na+/H2O retention
CV remodeling

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10
Q

list some ACE inhibitors

A

lisinopril
enalopril
captopril
benazepril

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11
Q

route of administration of ACE inhibitors

A

PO except enalopril (IV)

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12
Q

Major adverse effects of ACE inhibitors

A

**dry cough
**angioedema (rare)
first dose hypotension
hyperkalemia

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13
Q

are ACE inhibitors approved for use during pregnancy

A

no

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14
Q

How do ARBs (angiotensin II receptor blockers) work?

A

block the effects of ang2 at the receptor

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15
Q

What are the major differences between ACE inhibitors and ARBs?

A

ARBs don’t result in as much cough/angioedema risk
ARBs don’t result in as much aldosterone suppression (lower hyperK+ risk)
ARBs may not prevent cardiovascular remodeling as well

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16
Q

How do direct renin inhibitors work?

A

inhibit the release of renin and thus block the entire RAAS

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17
Q

What is the first line RAAS drug in prevention of cardiac morbidity and mortality?

A

ACE inhibitors

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18
Q

List a direct renin inhibitor

A

aliskiren

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19
Q

List some ARBs

A

losartan
valsartan
cadesartan

20
Q

How do the aldosterone antagonists work?

A

block the effects of aldosterone = K+ retention, Na+/H2O excretion

21
Q

List some aldosterone antagonists

A

spironolactone
eplerenone

22
Q

Adverse effects of aldosterone antagonists?

A

hyperK+
endocrine effects with spironolactone

23
Q

What are the cardiac outcomes of beta 1 antagonism

A

decreased HR
decreased contractility
decreased AV node conduction

24
Q

What does B1 agonism do in the kidney

A

stimulate renin release (RAAS activation)

25
Q

What do calcium channel blockers do in the heart?

A

same as B1 blockers

decreased HR
decreased AV node conduction
decreased contractility

26
Q

What do calcium channel blockers do in the vasculature?

A

vasodilation

27
Q

Which class of calcium channel blockers work only in the vasculature?

A

Dihydropyridines

28
Q

What is the difference between dihydropyridines and nondihydropyridines?

A

Nondihydropyridines block calcium channels in the heart and vasculature; dihydropyridines block calcium channels in the vasculature only

29
Q

What do you expect to HR & BP after dihydropyridine administration?

A

decrease BP
reflex tachycardia

30
Q

what do you expect to happen to HR & BP after nondihydropyridine administration?

A

decrease BP
decrease HR

31
Q

list some dihydropyridines

A

nifedepine
amlodipine
nicardipine
nimodipine

32
Q

list some nondihydropyridines

A

verapamil
diltiazem

33
Q

What is the effect of arteriole vasodilation

A

decreased afterload

= increased cardiac output, increased tissue perfusion

34
Q

what is the effect of venous vasodilation?

A

decreased preload

= decreased ventricular filling & contractility = decreased cardiac output & decreased tissue perfusion

35
Q

Does venous or arteriole vasodilation result in more orthostatic hypotension?

A

venous

(more pooling in the very large capacitance vessels)

36
Q

Does venous or arteriole vasodilation result in more reflex tachycardia?

A

Arteriole

(baroreceptors are located in the arteries)

37
Q

What does hydralazine result in?

A

Direct arteriole vasodilation
reflex tachycardia
long term use = fluid retention

38
Q

What vasodilator works the FASTEST?

A

sodium nitroprusside

39
Q

Does sodium nitroprusside dilate the veins or the arteries?

A

both

40
Q

What is the maximum length of time recommended for sodium nitroprusside infusion?

A

3 days

41
Q

Do the organic nitrates result in more venous or more arteriole vasodilation?

A

venous

42
Q

List some organic nitrates

A

nitroglycerin
isosorbide mononitrate
isosorbide dinitrate

43
Q

What is the active substance of the organic nitrates?

A

nitric oxide (NO)

44
Q

What is the route of administration of nitroglycerin?

A

IV (continuous infusion d/t short half life)
sublingual
buccal
transdermal
PO

45
Q

What is the route of administration of isosorbides?

A

PO

46
Q

What is the route of administration of sodium nitroprusside?

A

IV (continuous infusion d/t short half life)

47
Q

Points of patient education when administering nitroglycerin transdermal?

A

Show how to measure out the dose
Ensure 8+hrs/day “drug free” (to avoid tolerance development)
- usually at night when angina isn’t provoked