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CVPR > CVPR Week 8: RAAS > Flashcards

CVPR Week 8: RAAS Flashcards

1
Q

Objectives

A
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2
Q

The conversion of angiotensinogen into angiotensin I

A
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3
Q

How large is the angiotensinogen protein?

A

57 kDa

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4
Q

What happens in the conversion of angiotensinogen to angiotensin I?

A

14 amino acids in amino-terminal are cleaved by renin

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5
Q

Where is angiotensinogen produced?

A

It is synthesized by the liver

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6
Q

What determines the rate of angiotensin I formation?

A

concentration is important

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7
Q

What increases the concentration of angiotensinogen?

4 listed

A
  • Corticosteroids
  • Estrogens
  • Thyroid hormone
  • Pregnancy
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8
Q

Identify

A
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9
Q

Identify

A
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10
Q

Where is Renin produced?

A

synthesized by the granular juxtaglomerular cells of the kidney

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11
Q

What releases Renin?

A

Granular Juxtaglomerular cells

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12
Q

What controls the release of Renin?

A

Macula densa cells in the distal tubule control the release of Renin

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13
Q

Factors that control active Renin release from granular juxtaglomerular cells

5 listed

A
  • Macula densa mediators
  • β1-adrenergic receptor activation by NE or Epi
  • granular juxtaglomerular cell stretch
  • Angiotensin II negative feedback effect:
  • ANP-BNP
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14
Q

Macula densa mediators of renin release

A
  • decreased Na+ = increased PGE2 release = increased cAMP = increased Renin
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15
Q

β1-adrenergic receptor activation mediators of renin release

A

increased cAMP = increased renin

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16
Q

Granule juxtaglomerular cell stretch control of renin release

A
  • mediated by increased Ca2+ permeable stretch receptor
  • decreased stretch (vasodilation through α1 block, vasodilators, diuretics, anesthetics) = increased renin
  • Increased stretch (vasoconstriction through α1 receptor activation, angiotensin II = decreased renin
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17
Q

Angiotensin II negative feedback effect control of renin release

A

angiotensin II receptor - increased [Ca2+] = decreased renin

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18
Q

ANP-BNP control of renin release

A

increased cGMP = decreased renin

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19
Q

Describe the conversion of angiotensin I to angiotensin II

A
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20
Q

ACE AKA

A

Angiotensin-converting enzyme

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21
Q

ACE functions

A
  • converts angiotensin I to angiotensin II
  • breaks down bradykinin
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22
Q

Effects of angiotensin II

A
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23
Q

Angiotensin II potency in vasoconstriction

A

40 times more potent than norepinephrine

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24
Q

Angiotensin II vasoconstriction mechanism

A
  • Direct effect via angiotensin II receptor activation of Gq and PLC increasing IP3 levels and release of Ca2+ from intracellular stores.
  • Rho kinase is also activated decreasing myosin light chain phosphatase activity
  • Angiotensin II can also increase peripheral resistance via effects on the CNS by increasing sympathetic tone
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25
Q

Angiotensin II reflex bradycardia

A

there is little to no bradycardia because angiotensin II rests the baroreceptor reflex

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26
Q

Angiotensin II effect on the renal circulation

A

constricts the efferent glomerular arteriole maintaining glomerular filtration rate

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27
Q

Effects of angiotensin II

28
Q

Drug classes that inhibit the renin-angiotensin-aldosterone system

5 listed

A
  • Renin release blockers
  • Renin inhibitors
  • ACE inhibitors
  • Angiotensin II receptor blockers
  • Aldosterone antagonists
29
Q

Renin release blockers

2 listed

A
  • β-blockers
  • centrally acting α2 agonists
30
Q

Renin inhibitors

31
Q

ACE inhibitors

32
Q

Angiotensin II receptor blockers

33
Q

Aldosterone antagonists

A
  • spironolactone
  • eplerenone
34
Q

β-blockers and RAAS

A

counteract the harmful effects of sympathetic and RAAS over-activation

35
Q

β-blockers uses and mechanisms of improving outcomes

A

They are particularly useful in heart failure, cardiomyopathy and coronary artery disease

  • decrease remodeling
  • improve survival
  • decreased incidence of sudden death/arrhythmias
  • use in stable heart failure patients without substantial fluid retention
36
Q

Prototype β-blocker

A

Metoprolol

38
Q

Metoprolol clinical uses

A
  • heart failure
  • cardiomyopathy
  • coronary diseases
39
Q

β-blockers side effects

A
  • bronchospasm
  • bradycardia
  • heart block
  • heart failure (uncompensated patients)
  • sedation
  • sleep disturbances
  • depression
  • impotence
  • mask hypoglycemia
  • dyslipidemia
  • rebound hypertension
  • aggravate peripheral vascular disease
40
Q

Renin inhibitor prototype

41
Q

Aliskiren uses

A

hypertension

42
Q

Aliskiren side effects

A
  • teratogen
  • increased creatinine
  • hyperkalemia
  • hypotension
43
Q

Aliskiren interactions

A
  • prevents increases in plasma renin activity caused by other agents, including diuretics, Ca2+ channel blockers and vasodilators
  • renal impairment, hyperkalemia, hypotension in combination with ARBs or ACEIs
  • renal impairment with NSAID diuretics
44
Q

ACE inhibitors mechanism

45
Q

Mechanisms of cardiac benefits of ACE inhibitors

A
  • Hemodynamic actions (i.e. vasodilation and decrease in intravascular volume)
  • decrease in remodeling
46
Q

Indications for ACE inhibitors

A
  • Heart failure
  • hypertension monotherapy
  • hypertension associated with CHF or diabetes
  • Cardioprotective after acute myocardial infarction
  • Delay the progression of kidney disease, including diabetic nephropathy
47
Q

ACE inhibitors adverse effects and mechanisms

A
  • Cough
  • Angioedema
  • Teratogen
  • Increased creatinine
  • Hyperkalemia
  • Hypotension
48
Q

ACE inhibitors and renal vascular autoregulation

49
Q

ACE inhibitors drug interactions

A
  • K+ sparing diuretics, K+ supplements and K+ iodide = risk of hyperkalemia
  • Increase effects of other anti-hypertensive meds (e.g. hypovolemic patients taking diuretics, also be careful with patients on NaCL restricted diets or with GI disorders)
50
Q

ACE inhibitors prototype

51
Q

Captopril uses

A
  • heart failure
  • hypertension
  • chronic kidney disease
  • diabetic nephropathy
52
Q

Captopril side effects

A
  • cough
  • angioedema
  • teratogen
  • increased creatinine
  • hyperkalemia
  • hypotension
53
Q

Angiotensin II receptor blockers prototype

54
Q

Angiotensin II receptor antagonist mechanism

55
Q

Angiotensin II receptor antagonist in heart failure

56
Q

Losartan uses

A
  • heart failure
  • hypertension
  • chronic kidney disease
  • diabetic nephropathy
57
Q

Losartan side effects

A
  • Angioedema (less common)
  • teratogen
  • increased creatinine
  • hyperkalemia
  • hypotension
58
Q

Losartan interactions

A
  • K+ sparing diuretics, K+ supplements and K+ iodide = risk of hyperkalemia
  • Increase effects of other anti-hypertensive meds (e.g. hypovolemic patients taking diuretics, also be careful with patients on NaCL restricted diets or with GI disorders)
59
Q

Aldosterone antagonists mechanism of action

60
Q

Aldosterone antagonists prototypes

A
  • Spironolactone
  • Eplerenone
61
Q

Aldosterone antagonists clinical uses

62
Q

Aldosterone antagonists toxicity

63
Q

Spironolactone and gynecomastia

64
Q

Overview

CVPR (93 decks)

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