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Cardio > Heart Failure Pharmacology > Flashcards

Heart Failure Pharmacology Flashcards

1
Q

Compensatory mechanisms in congestive heart failure

A

Decreased cardiac output leads to decreased carotid sinus firing and decreased renal blood flow.

Decreased carotid sinus firing causes increased sympathetic discharge which increases force, rate, and preload of contractions.

Decreased renal blood flow causes increased renin release, which causes ang II to increase. Which increases preload, afterload and causes cardiac remodeling.

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2
Q

Vasoactive peptides include what types of drugs?

A 
Ace inhibitors
ARBs
Renin inhibitors
Bradykinin
Natiuretic peptides
Endothelins
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3
Q

RAAS

A

Angiotensinogen is convertin to ANG I by renin.

Ang I is converted into ang II by ACE.

Angiotensin II binds ot Angiotensin receptors (AT1-4)

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4
Q

Where is angiotensinogen made?

A

Liver, secreted into blood stream

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5
Q

Where is renin made?

A

In JG cells in kidney, with low perfusion pressure it is secreted into blood stream. Also with beta activation, also with decreased nacl delivery.

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6
Q

Effects of ANG II

A

Increased sodium retention and therefore fluid retention.
Increased blood volume by thirst.
Systemic vasoconstriction
Increases secretion of aldosterone from adrenals
Increases secretion of ADH from pituitary.

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7
Q

Prorenin

A

Converted to renin in JG cells of the kidney. Higher levels of prorenin in circulation than renin.
Binds to prorenin receptor which activates kinases and TFs associated with fibrosis

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8
Q

(Pro)renin receptor

A

Binds renin and prorenin. Activates kinases and TFs that are associated with fibrosis.

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9
Q

How is renin released?

A

When macula densa cells sense increased delivery of NaCl (meaning increased flow), they inhibit renin release from JG cells. This process is mediated by adenosine.

Decreased delivery of NaCl to JG cells (decreased flow) stimulates renin release. This process is mediated by prostaglandins

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10
Q

What factors inhibit renin release and stimulate renin release?

A

Inhibit: adenosine
Stimulate: prostaglandin

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11
Q

Are there sympathetic receptors in the kidney?

A

Yes, beta receptors on juxtaglomerular cells. Hypotension activates sympathetic system (increase preload, contractility, rate)

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12
Q

Direct feedback loop for renin?

A

AT1 receptor at JG cells. So if high AngII, renin inhibited.

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13
Q

Aliskerin mechanism of action

A

Renin inhibitor that directly inhibits renin. So it decreases BP. However, renin levels INCREASE, though renin activity does not.

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14
Q

What happens to renin levels with aliskerin?

A

Renin levels increase because of loss of negative feedback from ang II.

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15
Q

Is renin necessary for ang II creation?

A

No, there are alternative pathways that utilize cathepsin G.

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16
Q

Aliskerin contraindications

A

Don’t use in hyperkalemic patients because aldosterone decreases, which will cause a further increase of K in blood.

Watch out in patients with increased creatinine. Because decrease in ang II will cause decreased Pgc and decreased GFR.

Teratogenic.

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17
Q

Equation for GFR

A

GFR = Kf * [(Pgc-pi gc) - (Pbs-pi bs)]

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18
Q

ACE inhibitors mechanism of action

A

Competitive inhibitor of ace, which converts ang I to ang II. ACE also breaks down bradykinin, so when inhibited, cough.

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19
Q

ACE inhibitor effect on renin, angiotensin I, and ang II levels?

A

ANG II levels decrease, so renin and ang I levels increase.

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20
Q

5 clinical indications for ace inhibitors?

A

Hypertension

Diabetes Mellitus

Congestive heart failure

Acute MI

Coronary artery disease

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21
Q

Why don’t ace inhibitors cause reflex tachycardia?

A

Because baroreceptors are thought to reset.

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22
Q

Why are ACEI used for hypertension?

A

Because ACEIs inhibit AngII mediated vasoconstriction. Decreased BP without reflex tachycardia.

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23
Q

Why are ACEI used for DM?

A

Renoprotective because of decreased GFR, decrease risk of DM nephropathy, decrease proteinuria.

24
Q

Why are ACEi used for CHF?

A

Prevents progression of heart failure by reducing vasoconstriction, which decreases afterload and increases CO. Also decreased aldosterone which causes less Na reabsorption so preload and edema decrease. Also causes venodilation which decreases preload. Finally, reduces ventricular remodeling.

25
Q

Adverse effects of ACEIs

A

Hypotension, cough, hyperkalemia (due to decreased aldosterone), decreased GFR so avoid in patients with bilateral renal artery stenosis.

Can also cause angioedema (rare) – rapid swelling in oropharynx, lips, tongue. Thought to be bradykinin mediated.

26
Q

Captopril – when used and unique side effect

A

Alteration in taste because it has a sulfhydryl group. Also unique because it has the shortest half life of all the ACEIs (3 hours). Can titrate in CHF patients with low BP, but must be dosed frequently.

27
Q

Enalapril

A

A prodrug that is converted by hepatic esterases to the active drug enalaprilat. Only IV ace inhibitor

28
Q

Enalaprilat

A

Active drug that is created by cleavage of enalapril

29
Q

How are ACEIs metabolized or excreted?

A

Renally cleared.

30
Q

ARB mechanism of action

A

Selective AT1 receptor antagonists (10,000 more than AT2)

31
Q

Losartan and clinical indication

A

ARB that is used for hypertension, CHF, MI, and diabetic nephropathy.

32
Q

Adverse effects of ARBs

A

Can cause hypertension, hyperkalemia, decreased GFR, and is teratogenic.

33
Q

How are ARBs metabolized

A

Hepatically by CYP 3A4 and 2C9

34
Q

How do beta blockers affect the RAAS?

A

Decrease plasma renin concentration and activity, because beta receptors on JG cells release renin.

35
Q

How do ARBs affect plasma renin concentration, plasma renin activity, angiotensinogen levels, angiotensin I and angiotensin II

A

Renin increases because of lower BP, which increases ang I and ang II.

36
Q

ANP and BNP

A

Atrial naturietic peptide. Released from atria when volume overloaded. BNP Secreted by left ventricle when volume overloaded. Can order BNP levels to determine fluid overload status.

37
Q

How do ANP and BNP work?

A

Work by decreasing proximal tubule sodium reabsorption, which causes diuresis. Also causes vasodilation to decrease blood pressure

38
Q

Effect of ANP and BNP on RAAS?

A

Decreases renin, aldosterone and ADH.

39
Q

How do ANP and BNP cause vasodilation

A

By increasing cGMP in vascular smooth muscle. This decreases available calcium for contraction.

40
Q

Nesiritide

A

Synthetic recombinant human BNP. Decreases BP by promoting vasodilation (increases cGMP).

41
Q

Clinical indications for nesiritide?

A

Short term treatment of acute CHF. Improves cardiac output by vasodilating (which decreases afterload), and decreases preload.

42
Q

ET-1

A

Endothelin produced by vascular endothelium. A potent vasoconstrictor.

43
Q

How does ET-1 work?

A

Works by binding to ETb receptor and causing transient vasodilation (by releasing NO), but then binds to ETa and causes direct contraction of vascular smooth muscle.

44
Q

Other major effect of ET-1?

A

Causes pulmonary vascular cells to proliferate, thereby causing pulmonary arterial hypertension.

45
Q

Bosentan

A

An ET receptor antagonist. Indicated for pulmonary arterial hypertension.

46
Q

Digoxin

A

Direct inhibitor of Na, K pump. Prevents Na from exiting cell, accumulates, so Na can’t move in to exchange with Ca. Therefore Ca accumulates in the cell and increases contraction.

47
Q

When to be careful with using digoxin?

A

With hyperkalemia, which increases digoxin’s affinity for Na K pump.

48
Q

Effect of digoxin on nervous system

A

Increases parasympathetic outflow at the baroreceptor level.

49
Q

Electrical effects of digoxin

A

Early prolongation of AP, but then shortening of AP at therapeutic levels. This results from the increased K conductance due to Ca activated K currents. Also reduced resting membrane potentials because decreased intracellular K.

50
Q

Toxic effects of digoxin

A

Calcium stores are overloaded. Delayed after depolarizations occur in ventricles right after action potentials. This causes ventricular bigeminy. At even higher concentrations, ventricles will just fire spontaneously.

51
Q

Clinical indications for digoxin

A

Congestive heart failure – will increase CO

Also used in afib and aflutter. Will control rate.

52
Q

Adverse effects for digoxin

A

Yellow-green halos, blurred vision, nausea.

ST segment sags and looks like dali’s mustache.

Bradycardia

Fatigue.

53
Q

How to treat digoxin overdose

A

Digoxin immune fab (digibind). But before that, stop or reduce dose.

54
Q

Milrinone

A

Phosphodiesterase 3 inhibitor. Causes ionotropy because it increases cAMP (increased PKA, increased SERCA), which increases cardiac contractility. Also vasodilates.

55
Q

Milrinone effect on vascular system

A

Vasodilates because cAMP inhibits MLCK, which normally causes contraction.

56
Q

Clinical indication of milrinone

A

Short term management for acute, severe CHF.

Usually for icu patients.

Cardio (23 decks)

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