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Pharmacology II > HF3 > Flashcards

HF3 Flashcards

1
Q

what is the mechanism of action of clonidine

a. direct dilation of arterioles
b. selectively block alpha1 receptors
c. reduce sympathetic outflow from vasomotor centers in the brainstem
d. prevent the release of NE from peripheral postganglionic sympathetic neurons

A

c. reduce sympathetic outflow

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2
Q

which are the predominant initial effects of B1 antagonists

a. decrease HR and decrease FOC
b. decrease HR and decrease PVR
c. decrease PVR and decrease preload
d. decrease preload and decrease CO

A

a. decrease in HR and decrease in FOC

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3
Q

what is the most likely adverse effect of a drug that causes direct vasodilation of arterioles

A

tachycardia

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4
Q

list 4 groups known as preload reducers

A
  1. diuretics
  2. aquaretics
  3. aldosterone antagonists
  4. venodilators
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5
Q

what are diuretics effects on symptoms of HF and hypertrophy

A

decreases symptoms and decreases hypertrophy

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6
Q

which is an antidiuretic hormone antagonist:

a. acetazolamide
b. conivaptan
c. eplerenone
d. triamterene

A

b. conivaptan

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7
Q

name two aquaretics

A

conivaptan (IV)

tolvaptan (PO)

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8
Q

what are the effects of auqaretics?

A

increase urine output, increase sodium concentration, decrease HF symptom,s, and effect BP

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9
Q

list two aldosterone antagonists that decrease preload

A

spironolactone and eplerenone

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10
Q

what is the MOA of aldosterone antagonists

A

decrease Na/ K exchange in collecting duct;

decreasing sodium and water reabsorption

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11
Q

what should be monitored when taking spironolactone?

A

potassium

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12
Q

list the venodilators.

what is there MOA

A

NTG
sodium nitroprusside
increase venous capacitance

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13
Q

what do venodilators do to venous return to heart and O2 demand

A

decrease venous return

decrease O2 demand

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14
Q

does sodium nitroprusside effect the arterial side or venous side more in a normal heart?
in HF?

A

in normal heart venouse side

in HF arterial side

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15
Q

list 3 afterload reducing groups

A

ACEI/ ARB
Beta blocker
Vasodilators

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16
Q

what is the MOA of ACEIs and ARBs on preload side?

A

blocks aldosterone

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17
Q

what is the MOA of ACEIs and ARBs on afterload side

A

blocks angio II’s vasoconstriction

18
Q

how does angio II have a slow pressor response

A

aldosterone release

19
Q

how does angio II have a rapid pressor response

A

altered SVR

20
Q

other than decrease afterload and preload what hemodynamic effect does ACEI’s and ARBs have?

A

decrease remodeling and decrease hypertrophy

21
Q

why does BB use seem paradoxical in HF?

A

they can cause drop in CO initially (bad).

over long term, have decreased mortality do to

22
Q

what all is decreased by BBs in HF?

A 
decreased:
HR
renin
apoptosis
tachyarrhythmias
23
Q

BBs stop tachycardia caused from what in HF

A

neurohumoral mechanism

24
Q

when should BB’s not be used for HF

A

acute situation

25
Q

list two vasodilators used in afterload reduction

A

Nesiritide

BiDil

26
Q

what is in BiDil

A

hydralazine and ISDN

27
Q

name a synthetic brain natriuretic peptide?

what is it’s MOA

A

Nesiritide

MOA = vasodilation by binds to GC receptor on vascular smooth muscle

28
Q

what is brain naturetic peptide

A

a marker of HF

29
Q

what does nesiritide do by binding to GC receptor?

A

increase cGMP leading to relaxation

also gives diuresis

30
Q

what needs to be monitored with nesiritide

A

renal fxn and BP

31
Q

where does BiDil work? arterial or venous

A

both
hydralazine = arterial
ISDN = venous

32
Q

what is beneficial about BiDil

A

decreases mortality (especially in AA pts)

33
Q

what is a problem with BiDil

A

TID

34
Q

what are the inotropic agents for HF

A

cardiac glycosides
beta agonists
PDE inhibitors

35
Q

what is digoxins effects on electrolytes

A

increases Na at Na/K ATPase pump, increases Ca at Na/Ca exchanger

36
Q

how does digoxin increase FOC

A

increases intracellular Ca

37
Q

how is digoxin eliminated

A

renally

38
Q

at what crcl is digoxin contraindicated

A

ClCr less than 50

39
Q

which should have a lower renin level of digoxin: for HF or for arrhythmia

A

for HF

40
Q

what happens to ejection fraction with digoxin tx?

A

increases (more blood flow to organs)

41
Q

what is a conduction problem with digoxin

A

slows conduction to AV node; can cause arrhythmias

Pharmacology II (15 decks)

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