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Cardio Exam 1 > Lec 10 Heart Failure Pharm > Flashcards

Lec 10 Heart Failure Pharm Flashcards

1
Q

What is path of RAAS system?

A
  • angiotensin from liver
  • converted to angiotensin I by renin from kidney
  • converted to angiotensin II by ACE from lungs
  • angiotensin II acts of angiotensin receptors AT1-4
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2
Q

What is action of RAAS system if hypotension?

A
  • kidneys sense decrease blood flow –> release renin –> get angiotensin II which causes:
  • -> systemic vasoconstriction –> higher BP
  • -> increase sympathetic
  • -> aldosterone release from adrenal –> Na and fluid retention
  • -> ADH release from posterior pituitary –> fluid retention
  • -> increase thirst –> increase blood volume
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3
Q

What are the downstream effects of angiotensin II?

A

changes in peripheral resistance by: direct vasoconstriction, increase sympathetic, ADH and aldosterone release

changes in renal function: increase Na reabsorption, increase renal sympathetic tone

structural changes: increase growth factors, increase afterload increase wall tension leading to vascular and cardiac hypertrophy and remodeling

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4
Q

What is prorenin?

A
  • secreted from kidney and extrarenal tissue
  • can be converted to renin in JG cells of kidney
  • binds the same receptor as renin and activates transcription factors associated with fibrosis
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5
Q

Where is renin released from?

A

JG cells in kidney

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6
Q

What is action of renin?

A
  • converts angiotensinogen to angiotensin I

- binds pro-renin receptor to activate fibrosis

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7
Q

How is renin regulated?

A
  1. Na delivery to macula densa: less NaCl to macula densa = more renin release
  2. intrarenal baroreceptor: less renal perfusion pressure = more renin release
  3. B-adrenergic receptor: B1 cell on juxtaglomerular cells; activated by hypotension and as part of sympathetic activationa and cause more renin release
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8
Q

What is feedback loop on renin?

A

Angiotensin II inhibits JG cells from releasing renin

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9
Q

What is action of aldosterone?

A
  • reabsorption Na/Cl and H2O

- excretion of K

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10
Q

What is equation for GFR?

A

GFR = Kf * Net filtration pressure

Kf = filtration coefficietn

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11
Q

What is equation for net filtration pressure?

A

(Pgc - πgc) - (Pbc - πbs)

P = hydrostatic
π = oncotic; πbc = 0 normally
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12
Q

What happens to afferent/efferent arterioles in kidney with angiotensin II? To Pgc/GFR?

A

both constricted by efferent constricted more –> high Pgc –> high GFR

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13
Q

What happens to afferent/efferent arterioles in kidney with renin inhibitor [aliskiren]? To Pgc/GFR? Albumin? Creatinine?

A
  • efferent dilated more than afferent
  • -> decreasd kidney flow –> decrease Pgc –> decrease GFR
    • less glomerular pressure, less albumin/ creatinine excretion
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14
Q

What is mech of action ACE inhibitor? What processes does it inhibit?

A
  • competitively inhibits ACE
    inhibits:
  • conversion AT1 to AT2 [so less AT II]
  • bradykinin inactivation [so more bradykinin]
  • Ac-SDKP stem cell regulator [so more of it]
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15
Q

What happens to afferent/efferent arterioles in kidney with ACE inhibitor [lisonopril]? To Pgc/GFR? Albumin? Creatinine?

A
  • efferent dilated more than afferent
  • -> decreasd kidney flow –> decrease Pgc –> decrease GFR
    • less glomerular pressure, less albumin/ creatinine excretion
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16
Q

What are the 3 ACE inhibitors we should know?

A
  • captopril
  • enalapril
  • lisonopril
17
Q

What is a unique side effect of captopril?

A

changes in taste

18
Q

What are ARBs?

A

angiotensin II reeptor antagonists

selective for AT1 receptor over AT2

19
Q

With beta blockers what happens to:

  • renin activity
  • renin concentration
  • angiotensinogen
  • AT I
  • ATII
A
  • low renin activity
  • low renin concentration
  • no change in angiotensinogen/AT I/ATII
20
Q

With renin inhibitors what happens to:

  • renin activity
  • renin concentration
  • angiotensinogen
  • AT I
  • ATII
A
  • low renin activity = direct inhibition from drug
  • high renin conc = feedback from ATII
  • low ATI/ATII conc
  • no change in angiotensinogen
21
Q

With ACE inhibitors what happens to:

  • renin activity
  • renin concentration
  • angiotensinogen
  • AT I
  • ATII
A
  • high renin activity/conc = feedback from low AT II
  • low angiotensinogen
  • high AT I
  • low AT II = directly inhibited by ACEI
22
Q

With ARBs what happens to:

  • renin activity
  • renin concentration
  • angiotensinogen
  • AT I
  • ATII
A
  • high renin activity/conc = feedback from low AT II activity
  • low angiotensinogen
  • high AT I
  • high AT II conc = but not active since directly blocked by ARB
23
Q

What is action of bradykinin?

A

acts on B1 receptors: vasoconstriction

acts on B2 receptors: vasodilation, NO + prostaglandin production –> inflammation

24
Q

What is ANP?

A

atrial natruiertic peptide

- released from atrial myocytes in CHF when atrial stretch with increase volume to cause kidney to get rid of Na/H2O

25
Q

What is BNP?

A

brain natruiretic peptide

  • released from left ventricular myoacrdium in CHF in response to stretch
  • can order BNP level test
26
Q

What is action of ANP/BNP?

A
  • released in response to stretch/fluid overload and cause:
  • vasodilation –> decrease BP
  • decrease renin/aldosterone/ADH –> more vasodilation + decrease blood volume
  • increase GFR –> decrease proximal tubule Na reabsorption –> natriuresis + diuresis
27
Q

How do ANP/BNP decrease BP?

A
  • increase cGMP in vascular smooth muscle
  • decrease sympathetic tone
  • –> vasodilation
  • –> may prevent cardiac remodeling
28
Q

What is the meh of action of endogenous endothelins?

A
  • potent vasoconstrictor peptide ET-1 produced by vascular endothelium
  • G coupled receptors
  • causes: decrease BP via release PGI2/NO; then prolonged increase BP via constriction vascular smooth muscle; vascular cell proliferation which can pulmonary arterial hypertension
29
Q

What is mech of action by which digoxin increases contractility?

A

Direct inhibition NA/K ATPase → increase intracellular Na → NCX doesn’t work as well → more Ca stays in cell → more Ca goes to SR → more contractility

30
Q

How does digoxin alter AP?

A

at first it causes brief prolongation of AP then shortens AP particularly at plateau phase

likely due to increase K conductance

31
Q

What is affect of high cAMP in heart vs vasculature?

A 
heart = more Ca --> more CO
vasculature = inhibits myosin light chain kinase --> arterial and venous dilation --> hypotension

Cardio Exam 1 (16 decks)

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