Angiotensin and Adrenergic Antagonist: PHarmacology Flashcards Preview

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Flashcards in Angiotensin and Adrenergic Antagonist: PHarmacology Deck (57)
1

Vicious cycle of HFrEF (cycle 1)

1) Myocardial disease

2) decr SV/Cardiac output

3) arteriolar vasoconstriction

4) incr systemic vascular resistance

5) incr afterload

2

Vicious cycle of HFrEF (cycle 2)

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

3

Hydralazine action

Direct arterial vasodilation (decr afterload)

4

Side effects of hydralazine

drug induced SLE

5

isosorbide dinitrate

NO vasodilator = venous vasodilation

(decr preload)

6

Side effects of isosorbide dinitrate

hypotension
headache
dizziness

7

side effects of combined hydralazine and isosorbide dintrate

headache

8

which is better used, ACE inhibitor or hydralazine ISDN combo

ACE inhibitor

9

when do you specifically use hydralazine ISDN combo

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

10

why do african americans have lots of problems with HF?

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)

11

how do ACE inhibitors function?

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

12

how is bradykinin produced

1) bradykninogen (produced in liver)

2) kallikrenin convert bradykininogen to bradykinin

3) kinase II (ACE II) convert bradykinin to inactive filaments

13

why does high bradykinin lead to cough

bradykinin = pulmonary irritant

potent vasodilator

14

Effect of angiotensin II in vascular smooth muscle

incr arteriolar constriction
incr arterial blood pressure

15

Effect of angiotensin II in CNS and PNS?

facilitate sympathetic activity

incr CO

incr arterial blood pressure

16

Effect of angiotensin II in adrneal cortex

incr aldosterone secretion

incr Na reabsoprtion

incr arterial blood pressure

17

Effect of angiotensin II in kidney tubules

incr Na reabsorption
incr arterial blood pressure

18

Effect of angiotensin II in kidney arterioles

change GFR
incr filtration fraction

incr Na+ and H2O retention
incr arterial blood pressure

19

Effect of angiotensin II in brain

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

20

ACE inhibitors names

captopril
enalapril
lisinopril

21

dosing of captopril

shortest half life = 3x /day

22

dosing of enalapril

BID

23

dosing of lisinopril

longest half life
once daily

24

Side effects of ACE inhibitors

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

25

Drug interactions with ACE inhibitors

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

26

Contraindications of ACE inhibitors

pregnancy
bilat renal artery stenosis
renal failure
angioedema
hyperklaemia

CAUTION WITH ELDERLY

27

When is ACE inhibitor good?

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

and starts right away
also can reduce risk of HF

28

Is ACE inhibitors dose dependent?

NO SIGNIFICANCE

29

what is the angiotensin escape?

aldosterone continues to incr even though you are blocking angiotensin

30

why does angiotensin escape occur with ACE inhibitors?

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

where is angiotensin 1a found

lung
smooth muscle
liver
brain kidney

32

where is angiotensin 1b found

adrenals
pituitary gland

33

where is angiotensin 2 found

midbrain/thalamus
adrenal gland (medulla)
embryonic tissue

34

actions of angiotensin?

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

35

Side effects of angiotensin

ACE INHIBITOR WITHOUT COUGH and LESS ANGIOEDEMA

other side effects =
hyperkalemia

36

any precautions/contraindications

same as ACE
incl
gout and angioedema

37

Any difference in ACE inhibitors or ARBs?

NO DIFFERENCE IN ALL CAUSE MORTALITY

38

benefit of ACE inhibitors + ARBs

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

39

when use ARBs?

HFrEF NYHA 2-4

40

what are guidelines for ARBs?

1) HFrEF pts who can't use ACE inhibitors

2) Equal to ACE inhibitors

3) HFrEF patients treated with ACE inhibitor + beta blocker

41

Relationship btwn plasma NE and survival in HF

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

42

what happens with adrenergic activation?

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

Beta blockers help how?

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

44

First gen beta blockers

not selective for b1/b2

propanolol
timolol

45

examples of first gen beta blockers

propanolol
timolol

46

2nd gen beta blockers

selective for b1 or b2 block

metoprolol
atenolol
bisoprolol

47

example of second gen beta blockers


metoprolol
atenolol
bisoprolol

48

3rd gen beta blockers

selective or nonselective with additional property

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

49

examples of 3rd gen beta blocker

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

50

best b1 selective inhibitors (2)

1) nebivolol
2) bisoprolol

51

which patients are appropriate candidates for therapy?

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

When should treatment with beta blocker be started?

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

Effect of metoprolol long lasting form in chronic HF

decr all cause mortality and prevents worsening HF

54

When to use beta blockers

use of beta blocker recommended for all patient with HFrEF

55

what is neprilysin?

inhibitor of BNP degradation

56

BNP effects

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

57

why is new drug (neprilysin inhibitor so effective)

keeps BNP around longer and also block angiotensin II