Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

951 Block 3 > 8. RAAS and SNS in HF > Flashcards

8. RAAS and SNS in HF Flashcards

1
Q

___ (↑/↓) CO activates the RAAS.

A

Low ↓

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The RAAS cooperates with the _____ to adapt the body to the failing cardiac performance.

A

SNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The RAAS maintains _____ ______.

A

arterial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Activation of the RAAS ______ Na and water.

A

retains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

SNS stimulates ___ adrenergic receptors in the _________ region of the kidney

A
  • β1

- juxtaglomerular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What receptor agonism causes the release of renin?

A

β1 agonism in the juxtaglomerular region of the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Angiotensinogen is cleaved by _____ to form Ang I.

A

renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ang I is converted to Ang II by what enzyme?

A

ACE: angiotensin converting enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Angiotensin II is a potent arterial vasodilator. (T/F)

A

False: vasoconstrictor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Ang II promotes Na and water ______.

A

retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Ang II stimulates the release of what?

A

aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where is aldosterone released from?

A

adrenal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What RAAS hormone contributes to pathologic myocardial hypertrophy?

A

Ang II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In what tissue types is ACE expressed?

A
  • cardiac myocytes
  • fibroblasts
  • vascular smooth muscle cells
  • endothelial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Ang II may also be formed through non-ACE-dependent mechanisms. (T/F)

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a tissue protease that converts Ang I into Ang II?

A

chymase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Both chymase and ACE expression are induced during HF. (T/F)

A

False: only ACE expression is induced in HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

In the heart, which enzyme is primarily responsible for generation of AngII?

A

ACE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the main mechanism by which ACE inhibitors improve HF?

A

reduce pathological remodeling of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the standard treatment in all classes of HF?

A

ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the therapeutic effects of ACE inhibitors in HF?

A
  • inhibits formation of Ang II
  • arterial and venous dilation: ↓ afterload and preload
  • ↓ aldosterone release
  • ↓ LV hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the ACE inhibitors approved for use in HF? (7)

A
  • Captopril
  • Enalapril
  • Ramipril
  • Lisinopril
  • Quinapril
  • Fosinopril
  • Trandolapril
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

ACE inhibitors have been proven to improve what aspects of HF?

A
  • hemodynamics
  • clinical status
  • lessen symptoms
  • reduce mortality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the ADRs of ACE inhibitors?

A
  • hypotension (dizziness, syncope)
  • increases renal insufficiency
  • angioedema / cough
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why do ACE inhibitors increase renal insufficiency?

A
  • Renal perfusion pressure is maintained by Ang II during ↓CO, constricting the efferent arteriole.
  • When ACE-I prevents formation of Ang II, GFR ↓ significantly.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the predominant Ang II receptor in the vasculature?

A

Type 1 (AT1)

27
Q

What Ang II receptors are expressed in human myocardium?

A

AT1 and AT2

28
Q

The ADRs of ↑Ang II are mediated by the activation of what receptor?

A

AT1

29
Q

What are the ADRs associate with ↑Ang II levels?

A
  • vasoconstriction
  • myocyte apoptosis
  • cardiac myocyte growth
  • norepinephrine release
  • aldosterone release
30
Q

What were the findings of the ELITE I trial?

A

Losartan is superior to an ACE inhibitor in elderly patients with HF.

31
Q

What were the findings of the ELITE II trial?

A

ACE inhibitors were equal to or superior to Losartan in the larger heart failure population.

32
Q

What were the findings of the VALIANT trial?

A

ACE inhibitors and ARBs show comparable efficacy after MI

33
Q

What are the ARBs approved for HF when ACE inhibitors are poorly tolerated?

A
  • Valsartan

- Candesartan

34
Q

ACE inhibitors take weeks to months to decrease aldosterone levels. (T/F)

A

False: aldosterone levels decrease early in therapy

35
Q

During chronic treatment of HF, aldosterone returns to normal or elevated levels. (T/F)

A

True

36
Q

What are the physiological effects of aldosterone?

A
  • Na retention

- ↑ preload

37
Q

_______ causes myocardial fibrosis.

A

Aldosterone

38
Q

How does aldosterone cause LV hypertrophy?

A

myocardial fibrosis by stimulating the production of collagen in the heart

39
Q

Aldosterone inhibits the uptake of what NT?

A

norepinephrine

40
Q

Aldosterone __ (↑/↓ ) extracellular concentrations of NE in the heart.

A

increases ↑

41
Q

In what ways does spironolactone show benefit in Class IV HF?

A
  • ↓ incidence of sudden death from arrhythmia

- improves NE uptake

42
Q

In a normal heart there is what level of adrenergic stimulation in the LV during resting state?

A

none

43
Q

What is the normal regulatory mechanism for increasing CO?

A

acute increases in SNS activity

44
Q

What are the consequences of chronically elevated SNS activity?

A
  • ↑ HR
  • ↑ vasoconstriction
  • ↑ retention of Na and water
45
Q

Why do HF patients have chronically elevated SNS activity?

A

SNS activity is stimulated by reduced CO

46
Q

What are the consequences of long term sympathetic stimulation?

A
  • further depressed ventricular function

- ↑ heart’s demand for energy

47
Q

In HF, why is there an increase in circulating NE?

A

reduced uptake

48
Q

What are the consequences of increased circulating NE?

A

Excess NE is toxic to the heart due to excessive stimulation of β1 receptors

49
Q

Which adrenergic receptor is expressed more densely in the heart?

A

β1 > α1

50
Q

In the ventricles, which β subtype is more highly expressed?

A

β1 (80%) vs β2 (20%)

51
Q

During HF, what adrenergic receptor is down regulated?

A

β1

52
Q

What are the 3 classes of β-blocker?

A

1st gen: non selective
2nd gen: β1 selective
3rd gen: antagonize β and α receptors

53
Q

What generation of β-blocker is used for HF?

A

2nd gen: β1 selective

54
Q

What are the consequences of prolonged excessive β stimulation?

A
  • β1 down-regulation
  • ↓ adenylyl cyclase activity and cAMP levels
  • down-regulation of CA uptake in SR
  • hyper-phosphorylation of the CA release channel in SR
55
Q

1st generation β-blockers are most effective in compensated HF. (T/F)

A

False: 1st gen are counterproductive

56
Q

2nd and 3rd generation β-blockers are effective in most patients with mild to moderate HF. (T/F)

A

True

57
Q

What are the therapeutic effects of β-blockers in HF?

A
  • reverses down-regulation of β1 receptors
  • produces more normal cardiac performance
  • restores receptor coupling to adenylyl cyclase
  • reduces remodeling and myocardial death
  • reverses hyper-phosphorylation of the CA release channel in SR
58
Q

What are the 2nd generation β-blocker agents that are used in HF?

A
  • metoprolol succinate

- bisoprolol

59
Q

What are the 3rd generation β-blocker agents that are used in HF?

A

carvedilol

60
Q

What are the beneficial α1 effects of carvedilol?

A
  • reduces afterload

- vasodilation counteracts the negative inotropic effects of β-blockade

61
Q

What are the beneficial effects of antiadrenergics for treating HF?

A
  • reduce the adverse effects of excessive NE
  • stabilize cardiac rhythm
  • reduce HR
62
Q

In HF, decreased HR is associated with progressive reduction in cardiac function. (T/F)

A

False: increased HR

63
Q

What are the potential ADRs of antiadrenergic therapy?

A

immediately after starting, may ↓ EF

951 Block 3 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions