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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 ↓

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2
Q

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

A

SNS

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3
Q

The RAAS maintains _____ ______.

A

arterial pressure

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4
Q

Activation of the RAAS ______ Na and water.

A

retains

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5
Q

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

A
  • β1

- juxtaglomerular

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6
Q

What receptor agonism causes the release of renin?

A

β1 agonism in the juxtaglomerular region of the kidney

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7
Q

Angiotensinogen is cleaved by _____ to form Ang I.

A

renin

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8
Q

Ang I is converted to Ang II by what enzyme?

A

ACE: angiotensin converting enzyme

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9
Q

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

A

False: vasoconstrictor

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10
Q

Ang II promotes Na and water ______.

A

retention

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11
Q

Ang II stimulates the release of what?

A

aldosterone

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12
Q

Where is aldosterone released from?

A

adrenal cortex

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13
Q

What RAAS hormone contributes to pathologic myocardial hypertrophy?

A

Ang II

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14
Q

In what tissue types is ACE expressed?

A
  • cardiac myocytes
  • fibroblasts
  • vascular smooth muscle cells
  • endothelial cells
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15
Q

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

A

True

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16
Q

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

A

chymase

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17
Q

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

A

False: only ACE expression is induced in HF

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18
Q

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

A

ACE

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19
Q

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

A

reduce pathological remodeling of the heart

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20
Q

What is the standard treatment in all classes of HF?

A

ACE inhibitors

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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
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22
Q

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

A
  • Captopril
  • Enalapril
  • Ramipril
  • Lisinopril
  • Quinapril
  • Fosinopril
  • Trandolapril
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23
Q

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

A
  • hemodynamics
  • clinical status
  • lessen symptoms
  • reduce mortality
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24
Q

What are the ADRs of ACE inhibitors?

A
  • hypotension (dizziness, syncope)
  • increases renal insufficiency
  • angioedema / cough
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25
Why do ACE inhibitors increase renal insufficiency?
- Renal perfusion pressure is maintained by Ang II during ↓CO, constricting the efferent arteriole. - When ACE-I prevents formation of Ang II, GFR ↓ significantly.
26
What is the predominant Ang II receptor in the vasculature?
Type 1 (AT1)
27
What Ang II receptors are expressed in human myocardium?
AT1 and AT2
28
The ADRs of ↑Ang II are mediated by the activation of what receptor?
AT1
29
What are the ADRs associate with ↑Ang II levels?
- vasoconstriction - myocyte apoptosis - cardiac myocyte growth - norepinephrine release - aldosterone release
30
What were the findings of the ELITE I trial?
Losartan is superior to an ACE inhibitor in elderly patients with HF.
31
What were the findings of the ELITE II trial?
ACE inhibitors were equal to or superior to Losartan in the larger heart failure population.
32
What were the findings of the VALIANT trial?
ACE inhibitors and ARBs show comparable efficacy after MI
33
What are the ARBs approved for HF when ACE inhibitors are poorly tolerated?
- Valsartan | - Candesartan
34
ACE inhibitors take weeks to months to decrease aldosterone levels. (T/F)
False: aldosterone levels decrease early in therapy
35
During chronic treatment of HF, aldosterone returns to normal or elevated levels. (T/F)
True
36
What are the physiological effects of aldosterone?
- Na retention | - ↑ preload
37
_______ causes myocardial fibrosis.
Aldosterone
38
How does aldosterone cause LV hypertrophy?
myocardial fibrosis by stimulating the production of collagen in the heart
39
Aldosterone inhibits the uptake of what NT?
norepinephrine
40
Aldosterone __ (↑/↓ ) extracellular concentrations of NE in the heart.
increases ↑
41
In what ways does spironolactone show benefit in Class IV HF?
- ↓ incidence of sudden death from arrhythmia | - improves NE uptake
42
In a normal heart there is what level of adrenergic stimulation in the LV during resting state?
none
43
What is the normal regulatory mechanism for increasing CO?
acute increases in SNS activity
44
What are the consequences of chronically elevated SNS activity?
- ↑ HR - ↑ vasoconstriction - ↑ retention of Na and water
45
Why do HF patients have chronically elevated SNS activity?
SNS activity is stimulated by reduced CO
46
What are the consequences of long term sympathetic stimulation?
- further depressed ventricular function | - ↑ heart's demand for energy
47
In HF, why is there an increase in circulating NE?
reduced uptake
48
What are the consequences of increased circulating NE?
Excess NE is toxic to the heart due to excessive stimulation of β1 receptors
49
Which adrenergic receptor is expressed more densely in the heart?
β1 > α1
50
In the ventricles, which β subtype is more highly expressed?
β1 (80%) vs β2 (20%)
51
During HF, what adrenergic receptor is down regulated?
β1
52
What are the 3 classes of β-blocker?
1st gen: non selective 2nd gen: β1 selective 3rd gen: antagonize β and α receptors
53
What generation of β-blocker is used for HF?
2nd gen: β1 selective
54
What are the consequences of prolonged excessive β stimulation?
- 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
1st generation β-blockers are most effective in compensated HF. (T/F)
False: 1st gen are counterproductive
56
2nd and 3rd generation β-blockers are effective in most patients with mild to moderate HF. (T/F)
True
57
What are the therapeutic effects of β-blockers in HF?
- 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
What are the 2nd generation β-blocker agents that are used in HF?
- metoprolol succinate | - bisoprolol
59
What are the 3rd generation β-blocker agents that are used in HF?
carvedilol
60
What are the beneficial α1 effects of carvedilol?
- reduces afterload | - vasodilation counteracts the negative inotropic effects of β-blockade
61
What are the beneficial effects of antiadrenergics for treating HF?
- reduce the adverse effects of excessive NE - stabilize cardiac rhythm - reduce HR
62
In HF, decreased HR is associated with progressive reduction in cardiac function. (T/F)
False: increased HR
63
What are the potential ADRs of antiadrenergic therapy?
immediately after starting, may ↓ EF

951 Block 3 (10 decks)

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