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SPR2015 > Angiotensin and Adrenergic Antagonist: PHarmacology > Flashcards

Angiotensin and Adrenergic Antagonist: PHarmacology Flashcards

1
Q

Vicious cycle of HFrEF (cycle 1)

A

1) Myocardial disease
2) decr SV/Cardiac output
3) arteriolar vasoconstriction
4) incr systemic vascular resistance
5) incr afterload

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2
Q

Vicious cycle of HFrEF (cycle 2)

A

1) Myocaridal disease
2) decr SV/CO
3) incr NaCl and H2O retention –> incr renin angiotensin/aldosterone –> incr arterial vasoconstriction
4) incr blood volume –> peripheral edema
5) incr LV preload

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3
Q

Hydralazine action

A

Direct arterial vasodilation (decr afterload)

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4
Q

Side effects of hydralazine

A

drug induced SLE

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5
Q

isosorbide dinitrate

A

NO vasodilator = venous vasodilation

decr preload

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6
Q

Side effects of isosorbide dinitrate

A

hypotension
headache
dizziness

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7
Q

side effects of combined hydralazine and isosorbide dintrate

A

headache

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8
Q

which is better used, ACE inhibitor or hydralazine ISDN combo

A

ACE inhibitor

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9
Q

when do you specifically use hydralazine ISDN combo

A

in african ameicans with NYHA 3-4 HFrEF in combo with beta blocker, ACE inhibitor, and a aldosterone antagonist

OR in HFrEF when can’t take ACE inhibitor or ARB

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10
Q

why do african americans have lots of problems with HF?

A

1) TGFB = incr type 1 and type 2 collagen –> incr fibrosis
2) incr endothelin (vasoconstrictor)
3) decr renin angiotensin system
4) decr in NO (vasodilator)

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11
Q

how do ACE inhibitors function?

A

1) angiotensinogen (zymogen produced in liver)
2) renin (produce in kidney in response to low BP/Na) convert angiotensinogen to angiotensin 1
3) ACE (produce in lungs) convert angiotensin 1 to 2

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12
Q

how is bradykinin produced

A

1) bradykninogen (produced in liver)
2) kallikrenin convert bradykininogen to bradykinin
3) kinase II (ACE II) convert bradykinin to inactive filaments

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13
Q

why does high bradykinin lead to cough

A

bradykinin = pulmonary irritant

potent vasodilator

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14
Q

Effect of angiotensin II in vascular smooth muscle

A

incr arteriolar constriction

incr arterial blood pressure

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15
Q

Effect of angiotensin II in CNS and PNS?

A

facilitate sympathetic activity

incr CO

incr arterial blood pressure

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16
Q

Effect of angiotensin II in adrneal cortex

A

incr aldosterone secretion

incr Na reabsoprtion

incr arterial blood pressure

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17
Q

Effect of angiotensin II in kidney tubules

A

incr Na reabsorption

incr arterial blood pressure

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18
Q

Effect of angiotensin II in kidney arterioles

A

change GFR
incr filtration fraction

incr Na+ and H2O retention
incr arterial blood pressure

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19
Q

Effect of angiotensin II in brain

A

incr ADH
incr thirst
incr H2O absorption/ingestion
incr arterial blood pressure

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20
Q

ACE inhibitors names

A

captopril
enalapril
lisinopril

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21
Q

dosing of captopril

A

shortest half life = 3x /day

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22
Q

dosing of enalapril

A

BID

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23
Q

dosing of lisinopril

A

longest half life

once daily

24
Q

Side effects of ACE inhibitors

A

1) cough
2) hyperkalemia
3) angioedema
4) renal dysfunction
5) neutropenia
6) hypotension

25
Q

Drug interactions with ACE inhibitors

A

1) lithium
2) NSAIDs (incr serum Na affecting afterload and preload)
3) Salt substitute
4) loop diuretics
5) K+ sparing diuretics

26
Q

Contraindications of ACE inhibitors

A 
pregnancy
bilat renal artery stenosis 
renal failure
angioedema
hyperklaemia

CAUTION WITH ELDERLY

27
Q

When is ACE inhibitor good?

A

Good for NYHA good for class 2-4 (more sick)

and starts right away
also can reduce risk of HF

28
Q

Is ACE inhibitors dose dependent?

A

NO SIGNIFICANCE

29
Q

what is the angiotensin escape?

A

aldosterone continues to incr even though you are blocking angiotensin

30
Q

why does angiotensin escape occur with ACE inhibitors?

A

Angiotensinogen can be convert directly to angiotensin II via non-renin (tP factor, cathepsin G and tonin)

Angiotensin 1 can be convert to angiotensin II via non-ACE (chymase, CAGE, cathepsin G)

31
Q

where is angiotensin 1a found

A

lung
smooth muscle
liver
brain kidney

32
Q

where is angiotensin 1b found

A

adrenals

pituitary gland

33
Q

where is angiotensin 2 found

A

midbrain/thalamus
adrenal gland (medulla)
embryonic tissue

34
Q

actions of angiotensin?

A

1) incr aldosterone
2) vasoconstriction
3) renal/inotropic response
4) growth promoting

35
Q

Side effects of angiotensin

A

ACE INHIBITOR WITHOUT COUGH and LESS ANGIOEDEMA

other side effects =
hyperkalemia

36
Q

any precautions/contraindications

A

same as ACE
incl
gout and angioedema

37
Q

Any difference in ACE inhibitors or ARBs?

A

NO DIFFERENCE IN ALL CAUSE MORTALITY

38
Q

benefit of ACE inhibitors + ARBs

A

decr all cause mortality, cardiac arrest, HF hospitalization, or need for inotropes

39
Q

when use ARBs?

A

HFrEF NYHA 2-4

40
Q

what are guidelines for ARBs?

A

1) HFrEF pts who can’t use ACE inhibitors
2) Equal to ACE inhibitors
3) HFrEF patients treated with ACE inhibitor + beta blocker

41
Q

Relationship btwn plasma NE and survival in HF

A

incr in plasma NE due to incr in sensitivity of baroreceptors assoc with incr mortality

42
Q

what happens with adrenergic activation?

A

1) incr CNS sympath outflow
2) incr cardiac, kidney and blood vessel activity
3) activ beta 1, 2 (cardiac), alpha 1 receptor (kidney/blood vessel)
4) myocyte death/incr arrhythmia/decr beta1 receptor

alpha 1 receptor also leads to vasoconstriction/Na retention

43
Q

Beta blockers help how?

A

1) upregulate b1 receptors
2) prevent apoptosis/oxid stress (cell death)
3) decr arrhythmias
4) decr hypertrophy/fibrosis

44
Q

First gen beta blockers

A

not selective for b1/b2

propanolol
timolol

45
Q

examples of first gen beta blockers

A

propanolol

timolol

46
Q

2nd gen beta blockers

A

selective for b1 or b2 block

metoprolol
atenolol
bisoprolol

47
Q

example of second gen beta blockers

A

metoprolol
atenolol
bisoprolol

48
Q

3rd gen beta blockers

A

selective or nonselective with additional property

carvedilol
bucindolol = mostly b1 + alpha 1 block
nebivolol (b1)

49
Q

examples of 3rd gen beta blocker

A

carvedilol
bucindolol = mostly b1 + alpha 1 block
nebivolol (b1)

50
Q

best b1 selective inhibitors (2)

A

1) nebivolol

2) bisoprolol

51
Q

which patients are appropriate candidates for therapy?

A

1) mild to mod heart failure (NYHA 2-4)
2) systolic dysfunction of LV
3) treatment with ACE inhibitor + diuretic
4) CAD or nonischemic dilated cardiomyopathy
5) COPD without reactive airway disease
6) diabetic or nondiabetic

52
Q

When should treatment with beta blocker be started?

A

1) treat with diuretic (to decr fluid retention)
2) with ACE inhibitor for 2 wk+
3) no recent IV vasodilators or positive inotropic agents (acute HF)
4) systolic BP >/ 90 mmHg
5) HR > 60 bpm
5) no end organ failure

53
Q

Effect of metoprolol long lasting form in chronic HF

A

decr all cause mortality and prevents worsening HF

54
Q

When to use beta blockers

A

use of beta blocker recommended for all patient with HFrEF

55
Q

what is neprilysin?

A

inhibitor of BNP degradation

56
Q

BNP effects

A

1) vasodilation
2) decr BP
3) decr symp tone
4) decr aldosterone

57
Q

why is new drug (neprilysin inhibitor so effective)

A

keeps BNP around longer and also block angiotensin II

SPR2015 (23 decks)

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