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Module 10 > Pharmacological Options in Heart Failure > Flashcards

Pharmacological Options in Heart Failure Flashcards

1
Q

how is the SA node of the heart innervated/controlled

A
  1. B1(B2) adrenergic receptors (increase rate)
  2. M2 cholinergic receptors (decrease rate)
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2
Q

how is the atrial muscle of the heart innervated/controlled

A
  1. B1(B2) adrenergic receptor: increase force
  2. M2 cholinergic receptor: decrease force
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3
Q

how is the AV node of the heart innervated/controlled

A
  1. B1(B2) adrenergic receptor: increase automaticity
  2. M2 cholinergic receptor: decreased conduction velocity

M2 cholinergic receptor: AV block

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4
Q

how is the ventricular muscle of the heart innervated/controlled

A
  1. B1(B2) adrenergic receptor: increase automaticity and increased force
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5
Q

how are blood vessels innervated/controlled (coronary, muscle, viscera, skin, brain, erectile tissue, salivary glands, cerebral) and veins

A
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6
Q

what are the mechanisms to control smooth muscle

A

1. contraction:

  • alpha 1 (G-protein coupled)
  • stimulates phospholipase C and enhances Ca entry and intracellular Ca release
  • causes contraction

2. relaxation:

  • B2 (G-protein) receptor coupled to adenylate cyclase which increases cAMP
  • cAMP stimulates protein kinase A and triggers phosphorylation cascade which will inhibit contraction
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7
Q

how do alpha 1 receptors respond to noradrenaline stimulation in vascular smooth muscle cell

A
  1. stimulation causes direct entry of Ca
  2. increases IP3 which stimulates the sarcoplasmic reticulum to increase more Ca
  3. Ca causes contraction of smooth muscles
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8
Q

how do B2 receptors respond to noradrenaline stimulation in the vascular smooth muscle cells

A
  1. linked to adenylate cyclase which stimulates cAMP
  2. cAMP causes phosphorylation cascade
  3. inhibitory effect on contraction
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9
Q

how do B1 receptors on the cardiac muscle cell respond to noradrenaline

A
  1. linked to adenylate cyclase which stimulates cAMP
  2. cAMP stimulates protein kinase A which will increase intracellular Ca
  3. Ca increases contractility
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10
Q

what does inotropy mean

A

force of contraction of heart

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11
Q

what does chronotropy mean

A

speed of contraction

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12
Q

what does lusitropy mean

A

diastolic relaxation of ventricles

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13
Q

what are the approaches to treatment in heart failure

A
  1. stimulate the heart
  2. offload the heart
  3. inodilators
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14
Q

what are sympathomimetics and what is their function

A

B1-agonists

stimulate adenylate cyclase via a G-protein to:

  1. increase cAMP 2. increased Ca 3. increased contraction
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15
Q

what substances act as sympathomimetics

A
  1. all catecholamines stimulate B-receptors
  2. dobutamine: synthetic B1 agonist
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16
Q

what are the effects of catecholamines and what are they used for

A

stimulate B receptors and also alpha receptors

cause –> vasoconstriction, increased HR, pro-arrhythmic

used in resuscitation, not for heart failure

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17
Q

what is dobutamine, what are its effects and how is it used

A

synthetic B1 agonist

  1. potent positive inotrope, little effect on heart rate, little effect on BP

2. indicated in life threatening heart failure with severly impaired systolic function

  1. short term treatment –> up to 3 days (residual benefit)

down regulates B-receptors

*monitor BP, HR, rhythm

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18
Q

what are diuretics and

A

substance that promotes production of urine (increase excretion of water and (electrolytes))

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19
Q

what is diuresis

A

increased urine flow

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20
Q

what is natriuresis

A

increased Na+ excretion

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21
Q

what are the classes of diuretics (5)

A
  1. loop
  2. thiazide
  3. potassium sparing (aldosterone antagonists, amiloride)
  4. osmotic
  5. carbonic anhydrase inhibitors
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22
Q

when are diuretics used

A

treatment and control of systemic edema from either cardiac, hepatic & renal glomerular disease

all patients with signs of congestive heart failure should receive a diuretic (only exception is cardiac tamponade)

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23
Q

what are the functions of loop diuretics

A

secreted into PCT, act in thick ascending limb loop of Henle

inhibits Na/K/Cl carrier in the lumenal membrane by combining with the Cl binding site –> causing loss of these ions, with water, in the urine

also induce renal prostaglandin synthesis (dilate vessels) –> increase renal blood flow (increase amount of filtration)

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24
Q

what is an example of a loop diuretic

A

furosemide

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25
Q

why are loop diuretics classified as high ceiling

A

Na/K/Cl carrier is responsible for reabsorption of a high proportion of Na in the tubular fluid

capable of causing excretion of 15-20% of filtered Na (normally around 1% excretion)

large increase in urine output

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26
Q

why is dose control essential in loop diuretics

A

because they are so potent

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27
Q

what are the side effects of loop diuretics

A

dehydration, pre-renal azotemia, electrolyte disturbances (esp. K, Na, Mg), ototoxicity (at very high doses or when used in combo with aminoglycosides)

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28
Q

what is the onset of action and duration of action of loop diuretics

A

1-1.5hours PO (well absorbed)

lasts 4-6 hours

onset is 10-20mins

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29
Q

where is the action of thiazides

A

secreted in PCT and DCT

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30
Q

what is the action of thiazides

A

block Na/Cl reabsorption causing loss of Na, H, K, Mg, Cl with water in the urine

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31
Q

what is the mechanism of thiazides dependent on

A

renal PG production

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32
Q

what is the potency of thiazides and what can make them ineffective

A

mild-moderate

ineffective if renal blood flow is low

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33
Q

what is the onset, duration of action and absorption of thiazides

A

slower onset

longer acting than furosemide

good oral absorption

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34
Q

what are the side effects of thiazides

A

as for furosemide

alkalosis

insulin resistance

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35
Q

what class of diuretics is amiloride

A

K sparing diuretic

36
Q

where does amiloride act

A

collecting tubule

37
Q

what is the action of amiloride

A

block lumenal sodium channel

indirectly decrease K loss

38
Q

what is the potency of amiloride and when is it used

A

weak

used in combo with others to help to reduce hypokalemia

39
Q

what class of diuretic is spironolactone

A

K sparing diuretic

40
Q

what is the mechanism of action of spironolactone

A

aldosterone antagonist (competitive)

aldosterone: part of RAAS which acts of distal tubules/collecting ducts to increase reabsorption of ions and water –> conserves Na/secretes K+ –> water retention, increased blood pressure and volume

41
Q

when is spironolactone used

A

weak diuretic –> in combo with others to reduce hypokalemia

to counter aldosterone escape

42
Q

what is the safety profile of spironolactone

A

no apparent adverse effects in dogs (except reversible prostatic atrophy)

skin reactions in cats

43
Q

where do osmotic diuretics act

A

filtered and effective mainly in PCT + loop

44
Q

what is an example of an osmotic diuretics

A

mannitol used as 10-20% solution i.v (poor GI absorption)

45
Q

where do carbonic anhydrase inhibitors act

A

secreted into PCT

46
Q

what is the mechanism of action of carbonic anhydrase inhibitors

A

inhibit tubular production of H+ for Na/H exchange

leads to increased NaHCO3 and water (and K) excretion

47
Q

what are carbonic anhydrase inhibitors used for

A

topically for glaucoma

48
Q

what are the aims of vasodilators

A
  1. decrease preload
  2. decrease afterload
    overall: reduce the cardiac workload (arterio-dilators, balanced vasodilators, venodilators)
49
Q

what are the main classes of vasodilators

A
  1. calcium channel blockers
  2. alpha1 adrenoreceptor antagonists
  3. nitrates
  4. angiotensin inhibitors
50
Q

what is the mechanism of action of calcium channel blockers

A

block L-type calcium channels

voltage operated channels responsible for Ca entry during depolarization

initiates contraction

if blocking will inhibit contraction

51
Q

what is the cardiac sub-type of calcium channel blockers

A

phenylalkylamines (verapamil) –> cardiac effect

52
Q

what are the vascular effect calcium channel blocker

A

dihydropyridines (amlodipine) –> vascular effect, primarilty arteriolar dilation, little cardiac effect

53
Q

what are benzothiazepines

A

ex. diltiazem

calcium channel blocker

54
Q

what are the pharmacokinetics of almodipine (bioavailability, metabolism, half life, Vd, safety)

A
  1. 90% bioavailability
  2. extensive metabolism
  3. long half life (around 30 hours)
  4. high Vd (25L/kg)
  5. good safety profile
55
Q

what is an example of a1-adrenoreceptor antagonists

A

prazosin

56
Q

what is the mechanism of action of prazosin

A

non-selective a1-antagonist

57
Q

what are the pharmokinetics of prazosin (absorption, half life)

A

well absorbed

short half life –> 3-4 hours (give freq)

58
Q

what are the side effects of prazosin

A

hypotensive effect prolonged

syncope

59
Q

when is prazosin indicated

A

anti-hypertensive

60
Q

what are nitrovasodilators and what are they used for

A

nitrates

short term antihypertensive therapy

61
Q

what is the mechanism of action of nitrovasodilators

A

nitrates act as donors of nitric oxide

mimic endogenous system –> endothelium derived nitric oxide (lots of stimuli, shear stress/friction in blood vessels) –> diffuses to underlying vascular smooth muscle cell and activates guanylate cyclase –> cGMP –> relaxation

62
Q

what are the side effects of nitrovasodilators

A

hypotension

63
Q

how is nitrovasodilators given

A

ointment

caution to individual applying (wear gloves)

64
Q

what are angiontensi II inhibitors

A

ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II

angiotensin II inhibitors act on the ATI receptors (AT1 subtype receptor antagonists)

65
Q

what are the effects of angiotensin II

A
  1. vascular growth: hyperplasia, hypertrophy
  2. vasoconstriction: direct, via increased noradrenaline release from sympathetic nerves
  3. salt retention: aldosterone secretion, tubular Na reabsorption
66
Q

what are the pharmocodynamic effects of ACE inhibitors

A
  1. arteriolar and venodilation
  2. decrease plasma aldosterone
  3. enhanced Na and water excretion
  4. reduced edema
  5. enhanced bradykinin vasodilation
67
Q

what are the effects of angiotensin II and the kidney

A

angiotensin II increases glomerular filtration by constrictining the efferent and afferent arterioles (constricts efferent more –> increase the pressure within the glomerulus)

consequence of heart failure –> renal hypertension

ACE inhibitors will negate these effects

68
Q

what are the side effects of ACE inhibitors

A
  1. hypotension
  2. renal impairement: monitor renal function & electrolytes
  3. hyperkalemia
  4. anorexia, diarrhea, vomitting, cough
69
Q

how are ACE inhibitors administered

A

as pro drugs

enalaprin –> enalaprilat

benazepril –> benazeprilat

ramipril –> ramiprilat

imidapril –> imidaprilat

70
Q

how are ACE inhibitors eliminated

A

renal/hepatic

71
Q

what can decrease bioavailability of ACE inhibitors

A

food (enalapril, imidapril)

72
Q

what are angiotensin II receptor antagonists

A

direct action at angiotensin II receptors

used in human cardiology

73
Q

what are the differences between ACE inhibitors and angiotensin II receptor antagonists

A

block all formed by other routes

do not prevent breakdown of bradykinin

74
Q

what is telmisartan (semintra)

A

angiotensin II receptor antagonist

competitive antagonist of the AT1 receptor

75
Q

what does telmisartan (semintra) cause

A
  1. decreased BP
  2. decreased proteinuria
76
Q

what are the side effects of telmisartan (semintra)

A
  1. hypotension
  2. decreased RBC count
77
Q

what are the pharmacokinetics of telmisartan (semintra)

A

oral solution

high ppb

glucuronidation occurs (even in cat) but mainly excreted unchanged in feces

78
Q

what is aldosterone escape

A

aldosterone may increase in incomplete inhibition of ACE

block with concurrent aldosterone antagonism –> spironolactone (beware hyperkalemia)

79
Q

what are mechanism of action of inodilators

A

B1 agonists –> stimulate AC via a G-protein

phosphodiesterase (PDE) III inhibitors prevent breakdown of cAMP

both increase cAMP –> increased Ca –> increased contraction

80
Q

what are examples of bipyridine compounds

A

amrinone, milrinone

81
Q

what is the mechanism of action of bipyridine compounds

A

PDE III inhibitors

positive inotropes and vasodilators –> inodilators

82
Q

what are the side effects of inodilators

A

ventricular arrhythmia

ruptured chordae tendinae

83
Q

what is the mechanism of pimobendan

A

calcium sensitizers: sensitizes myocardium to Ca

inodilator: PDE III inhibitor effects

84
Q

what are the benefits of pimobendan

A

less arrhythmogenic than bipyridine compounds

mild positive chronotropic effect

decreased sympathetic drive

85
Q

what is the absorption of pimobendan impaired by

A

food

86
Q

what are other effects of pimobendan

A
  1. PDE V inhibition (pulmonary)
  2. cytokine modulation
  3. antiplatelet effects
  4. positive lusitropic effect

Module 10 (27 decks)

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