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Pharm Final Exam > Cardio Pharm > Flashcards

Cardio Pharm Flashcards

1
Q

What is heart failure?

A

inability to provide required physiological needs

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2
Q

What is congestive heart failure?

A
  • retention of fluid secondary to heart failure
  • Na+ retention, H20 follows
  • “diastolic failure”
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3
Q

What neurohumoral factors are increased in response to decreased perfusion of tissues in heart failure?

A
  • SNS
  • RAAS
  • ADH
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4
Q

What are the adaptive responses that occur after an increase in neurohumoral factors?

A
  • vasoconstriction
  • Na/H2O retention
  • increased inotropy
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5
Q

What maladaptive responses occur in heart failure?

A
  • increased afterload
  • increased cardiac work
  • decreased cardiac efficiency
  • fibrosis
  • altered signaling
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6
Q

What is the goal of cardio pharm?

A

blunt maladaptive responses the best we can

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7
Q

What are 2 consequences of maladaptive responses in heart failure?

A
  • decreased ventricular compliance
  • decreased systolic function
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8
Q

What are the three types of CHF?

A
  • left sided CHF: pulmonary edema
  • right sided CHF: ascites
  • biventricular failure: ascites, pleural effusion
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9
Q

How do you progress from heart failure to CHF?

A
  • reduction in compliance of ventricle
  • diseased heart fills at elevated pressure
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10
Q

What are the three goals of pharmacologic therapy for CHF

A
  • resolve/prevent retention of fluid
  • improve quality of life
  • improve prognosis
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11
Q

How will cardio pharm improve the quality of life in CHF patients?

A
  • improve hemodynamic parameters
  • increase exercise capacity
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12
Q

How will cardio pharm improve prognosis in CHF patients?

A

decreased morbidity and mortality

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13
Q

What is preload?

A

end diastolic pressure

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14
Q

What is afterload

A

end systolic pressure

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15
Q

What drugs decrease preload?

A
  • diuretics
  • venous vasodilators
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16
Q

How do diuretics decrease preload to treat heart failure?

A

decrease plasma volume

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17
Q

How do venous vasodilators decrease preload to treat heart failure?

A

increase vascular volume

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18
Q

What drugs decrease afterload to treat heart failure?

A

arterial vasodilators

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19
Q

How do arterial vasodilators decrease afterload to treat heart failure?

A

decrease systemic vascular resistance

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20
Q

What drugs increase pumping strength/efficiency (positive inotropy) in treatment of heart failure?

A
  • catecholamines (epi and norepi)
  • phosphodiesterase inhibitors
  • calcium sensitizers
  • cardiac glycosides
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21
Q

Where are loop diuretics secreted?

A

into the tubular lumen

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22
Q

What is the MOA of loop diuretics?

A
  • inhibition of Na/K/2CL symporter in the thick ascending LOH
  • Na/K/ Cl remain in tubule, disrupting countercurrent multiplication
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23
Q

What is the onset of action of loop diuretics?

A

rapid

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24
Q

What is the duration of action of loop diuretics?

A

relatively short

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25
Q

Because loop diuretics can secrete lots of Na, it is considered potent or what?

A

high ceiling

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26
Q

Describe the potency of torsemide compared to furosemide

A

10x more potent, lasts longer –> be cautious of dehydration

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27
Q

When does peak diuresis occur after oral administration of furosemide?

A

1-2 hours

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28
Q

When does furosemide effect begin to dissipate?

A

6 hours

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29
Q

When does diuretic resistance begin to develop in healthy dogs after beginning furosemide therapy?

A

14 days

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30
Q

What factors contribute to furosemide resistance?

A
  • increased expression of co-transporters in response to aldosterone like substance
  • high ceiling diuretic
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31
Q

What effect does furosemide have when administered IV?

A

venodilation prior to onset of diuretic action

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32
Q

What are the adverse effects of furosemide?

A
  • hypokalemia, hypochloremic metabolic alkalosis
  • dehydration
  • ototoxicity in humans
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33
Q

Furosemide also induces notable excretion of what two compounds?

A

Ca and Mg

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34
Q

What substances may blunt the furosemide response?

A

NSAIDs and steroids

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35
Q

What class of loop diuretics is torsemide in?

A

pyridine-3-sulfonylurea

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36
Q

When does peak diuresis occur with torsemide?

A

1-2 hours after oral administration

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37
Q

When does torsemide begin to dissipate?

A

12 hours

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38
Q

When is torsemide used?

A

when furosemide resistance develops

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39
Q

What are the adverse effects of torsemide?

A
  • hypokalemia, hypochloremic metabolic alkalosis
  • dehydration
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40
Q

Explain the activity of torsemide in regards to aldosterone.

A

anti-aldosterone activity

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41
Q

What is the MOA of thiazide diuretics?

A
  • directly inhibit Na/Cl cotransporter in DCT
  • Na, Cl, and H2O remain in tubule
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42
Q

Are thiazide diuretics considered high or low ceiling?

A

low

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43
Q

When does peak diuresis and dissipation occur with thiazide diuretics?

A
  • rapid GI absorption
  • peak diuresis 1-2 hours after oral admin.
  • dissipates over 6-12 hours
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44
Q

Thiazide diuretics can be used synergistically with what other type of diuretic?

A

loop diuretics

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45
Q

What are the adverse effects of thiazide diuretics (more likely when used with loop diuretics)?

A
  • hypokalemia
  • dehydration
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46
Q

What effect do thiazide diuretics have on Ca?

A

relative Ca-sparing effect

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47
Q

What two drugs are thiazide diuretics?

A
  • hydrochlorothiazide
  • chlothiazide
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48
Q

What is the K sparing diuretic?

A

spiranolactone

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49
Q

What is the MOA of spiranolactone?

A
  • antagonized effects of aldosterone
  • decrease Na/H2O resorption in DCT/CT
  • reduction in luminal Na channel
  • reduction in Na/K ATPase pump at basolateral membrane
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50
Q

Is spironolactone a weak or strong diuretic?

A

weak

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51
Q

Spironolactone is used in combination with other diuretics, why?

A
  • never used for substantial diuresis alone
  • can help obviate hypokalemia from other diuretics
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52
Q

Explain the anti-mitogenic properties of spironolactone?

A
  • hypertrophy (cardiac and smooth muscle)
  • fibrosis (myocardial and vascular)
  • aldosterone-escape with ACE
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53
Q

Why is CHF therapy with diuretics alone should be limited to acute, relative short episodes?

A
  • further reduction in CO and azotemia
  • AKI risk
  • activation of neurohumoral systems and maladaptive responses
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54
Q

How does diuretic therapy induce reduction in CO and pre- or intra-renal azotemia?

A

overaggressive diuresis without other drugs to improve cardiac performance

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55
Q

How does diuretic therapy induce AKI?

A

aggressive therapy with ace –> why you should avoid ace

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56
Q

How does diuretic therapy induce neurohumoral systems and maladaptive responses?

A

chronic administration of even the modest diuretic doses results in activation of these systems

57
Q

What are the effects of arterial vasodilators?

A

afterload reduction

58
Q

What is the effect of venous vasodilators?

A

preload reduction

59
Q

What type of vasodilators can be used in heart failure?

A
  • venous
  • arterial
  • mixed/balanced
60
Q

What is the MOA of venodilators?

A
  • dilation of capacitance veins (intra-abdominal)
  • increased potential vascular volume
  • “pulls” blood away from the left atrium/ventricle
  • reduces volume of blood in left atrium/ventricle
  • reduces filling pressure, relieving extravasation of fluid from vascular space to interstitial space
61
Q

What drug is a venodilator?

A

nitroglycerin

62
Q

What form does nitroglycerin come in?

A

2% ointment - topical

63
Q

What is the MOA of nitroglycerin?

A
  • bioconversion within the mitochondria
  • aldehyde dehydrogenase –> release of NO
  • NO activates smooth muscle soluble guanylyl cyclase (GC) to form cGMP –> inhibits Ca entry into cell –> smooth muscle relaxation
  • NO also activates K channels –> hyperpolarization and relaxation
64
Q

What is the onset of action for nitroglycerin?

A

rapid –> debate over clinical effect

65
Q

What are the adverse effects of nitroglycerin?

A

hypotension with excessive preload reduction

66
Q

Tolerance to nitroglycerin develops rapidly within days depending on frequency of dosing due to what?

A
  • depletion of sulfhydryl group
  • inactive aldehyde dehydrogenase
  • production of peroxynitrite –> blocks conversion of GTP-cGMP
67
Q

What are the effects of arterial vasodilation?

A
  • arterial vasodilation reduces systemic vascular resistance
  • reduced cardiac work
  • reduced activation of neurohumoral systems
68
Q

What are the effects of arterial vasodilation reducing systemic vascular resistance?

A
  • easier for left ventricle to empty volume of blood
  • increase in forward stroke volume/CO
  • smaller end-systolic volume
  • lower end-diastolic pressure
69
Q

What is the goal of arterial vasodilation?

A

~10-20% reduction in SBP (10-20 mmHg) in CHF
should not use in patients with SBP <90 mmHg

70
Q

What are the adverse effects of arterial vasodilation

A
  • hypotension (weakness, collapse)
  • reflex tachycardia (increase cardiac work)
71
Q

What drugs are arterial vasodilators?

A
  • sodium nitroprusside
  • amlodipine (Novasc)
  • ACE inhibitors
  • angiotensin receptor blockers (ARB) - Telmisartan
  • Hydralazine
  • Prosozin
72
Q

Sodium nitroprusside summary

A
  • organic nitrate
  • spontaneous release of NO
  • ultra rapid effect: 1-2 min onset, 1-2 min offset
  • ideal for acute L-CHF
73
Q

What are the special handling requirements for sodium nitroprusside?

A
  • protect from sunlight
  • diluents
74
Q

What are the adverse effects of sodium nitroprusside?

A
  • hypotension
  • converted to cyanide in RBC’s: metabolized to thiocyanate in liver, excreted by kidneys in 7 days
75
Q

Amlodipine summary

A
  • Ca L-channel blocker
  • dihydropyridine class
  • distinctly different than diltiazem
  • peripheral arterial vasodilation –> minimal myocardial/EP effects
76
Q

What is the onset of action of amlodipine?

A
  • within a few hours
  • half life is 24-36 hours
  • 5-7 days to get maximal effect
77
Q

What are the adverse effects of amlodipine?

A
  • hypotension
  • gingival hyperplasia (dogs)
78
Q

What does ACE stand for?

A

angiotensin-converting enzyme

79
Q

What does ACE do?

A

conversion of angiotensin 1 to angiotensin 2

80
Q

What are the effects of angiotensin 2?

A
  • vasoconstriction
  • Na retention
  • aldosterone release
  • mitogenic effects
  • activates sympathetic nervous system
81
Q

What converts angiotensinogen to angiotensin I?

A

renin

82
Q

What are ACE inhibitors not particularly effective for?

A

systemic hypertension –> most commonly hyporeninemic

83
Q

What allows for continued angiotensin II production with ACE inhibitors?

A

tissue chymases

84
Q

How do ace inhibitors prolong survival in dogs and cats with CHF?

A

neurohumoral modulating agent

85
Q

Ace inhibitors are prodrugs metabolized and excreted where?

A

metabolized in liver to active form and excreted by the kidney

86
Q

What is the problem with ace inhibitors?

A

lose ability for renal autoregulation

87
Q

What effects are associated with renal autoregulation?

A
  • reduced glomerular efferent arterial vasoconstriction with reduced renal perfusion
  • common clinical scenario during CHF tx
  • exacerbated by NSAIDs
  • AKI
88
Q

What drugs are considered ACE inhibitors?

A
  • Enalapril
  • Benazepril
  • Lisinopril
89
Q

What is the onset, duration, and distribution of enalapril?

A
  • prodrug
  • onset: 2-4 hours
  • duration: 12-14 hours
  • distribution: all tissues except CNS
90
Q

How is enalapril excreted?

A

renal and hepatic

91
Q

How often should enalapril be administered?

A

BID

92
Q

How is enalaprilat excreted?

A

renal

93
Q

What is the worry with toxicity and enalapril?

A

even at clinical doses you can end up with AKI

94
Q

What is the onset, duration, and distribution of benazepril?

A
  • prodrug
  • onset: 2-4 hours
  • duration: 12-24 hours
  • distribution: all tissues except CNS, placenta
95
Q

How is benazeprilat excreted?

A

renal and hepatic excretion

96
Q

T/F: You must be more cautious with enalapril in kidney failure, not as cautious with benazepril.

A

True

97
Q

What is the excretion, onset, and duration of lisinopril?

A
  • not a prodrug
  • renal excretion
  • onset: 2-4 hour
  • duration: 12-24 hour
98
Q

What is the MOA of angiotensin receptor blockers (ARB)?

A
  • antagonizes angiotensin II binding to angiotensin I receptor
  • downstream antagonism from ACE
  • not subject to tissue chymase limitations
  • preclude some of the ACE issues –> does not induce cough
99
Q

What are the uses of telmisartan (an ARB)?

A
  • only approved drug in vet med
  • only approved for tx of systemic hypertension in cats
  • off label use for proteinuria dogs
  • off label use for refractory systemic hypertension in dogs
100
Q

Describe the oral absorption, metabolism, and excretion of telmisartan?

A
  • relatively rapid oral absorption
  • highly protein bound
  • metabolized and excreted by the liver
101
Q

What are two other arterial vasodilation drugs that are rarely used?

A
  • hydralazine
  • prosozin
102
Q

What drugs are positive inotropes that are sympathomimetics in the drug class of catecholamines?

A
  • epinephrine
  • norepinephrine
  • dobutamine
  • dopamine
103
Q

What is the effect of catecholamines on the body?

A

activation of adrenergic receptors

104
Q

What are the effects of catecholamines on alpha 1 receptors?

A

precapillary vasoconstriction in organs

105
Q

What are the effects of catecholamines on alpha 2 adrenergic receptors?

A

vasoconstriction

106
Q

What are the effects of catecholamines on beta 1 adrenergic receptors?

A
  • positive inotrope
  • positive chronotrope
  • positive lusitrope
  • positive dromotrope
107
Q

What are the catecholamine effects on beta 2 adrenergic receptors?

A

precapillary vasodilation to skeletal muscle

108
Q

Why is dobutamine an excellent choice for CHF tx?

A
  • B1: ++++
  • B2: ++
  • A1: +
109
Q

Describe the drug form, onset, offset, adverse effects, and tolerance of dobutamine

A
  • only available IV (CRI)
  • onset: 2 min (peak at 10 min)
  • offset: 1-2 min
  • adverse effects: arrhythmias
  • develops tolerance within 72 hour
110
Q

Is dopamine use for CHF tx?

A

nope

111
Q

Describe the drug form, onset, offset, and adverse effects of dopamine.

A
  • only available IV (CRI)
  • onset: 5 min
  • offset: 2-5 min
  • adverse effects: tachycardia, arrhythmias
112
Q

What is the MOA of phosphodiesterase inhibitors and their positive inotrope effect?

A
  • increase cAMP
113
Q

What do phosphodiesterases do?

A
  • degrade nucleic acids –> reducing cAMP
114
Q

What drugs are considered phosphodiesterases inhibitors?

A

amrinone and milrinone

115
Q

Describe the type of inhibitor and drug form of phosphodiesterase inhibitors (amrinone, milrinone)

A
  • type III PDE inhibitors
  • IV administration only
116
Q

What is the use of phosphodiesterase inhibitors?

A

short term therapy for severe myocardial failiure

117
Q

What are the adverse effects of amrinone and milrinone?

A
  • arrhythmias
  • hypotension
  • thrombocytopenia
118
Q

How is pimobendan a calcium sensitizer?

A
  • increased Ca effect for given [Ca]
  • no Ca loading
  • positive inotropic
119
Q

How is pimobendan a phosphodiesterase III inhibitor?

A
  • positive inotrope
  • vasodilation
120
Q

What is pimobendan labeled for in dogs?

A
  • dilated cardiomyopathy
  • mitral valve disease (DMVD)
121
Q

Describe how pimobendan undergoes hepatic demethylation

A
  • converted to ODMP
  • 100x more potent than pimobendan
  • predominantly PDEIII inhibition
122
Q

Which drug lasts longer: pimobendan or ODMP?

A

ODMP

123
Q

T/F: pimobendan pharmacodynamics do not persist longer than Cmax.

A

False - persists longer than Cmax

124
Q

What are the adverse effects of pimobendan?

A
  • generally considered low frequency
  • ventricular arrhythmias
  • increases AVN conduction velocity –> consideration for atrial fibrillation
125
Q

What are digitalis glycosides derived from?

A
  • oleander
  • lily of the valley
  • milkweed
126
Q

What are digitalis glycosides used for?

A

treatment of “dropsy” since the Greeks and Romans

127
Q

What is the MOA of the positive inotrope digitalis glycosides?

A
  • inhibit Na/K ATPase –> increases [Na]
  • induces “reverse mode” of Na/Ca exchanger –> increase [Ca], increase release of Ca from SR, increase Ca interaction with TnC
128
Q

How do digitalis glycosides increase density of Na/K ATPase in heart failure?

A
  • baroreceptor dysfunction
  • contributor to increase SNS tone in heart failure
129
Q

How do digitalis glycosides act as positive inotropes?

A
  • Ca loading
  • “neutral” effect on vascular tone
130
Q

What are the electrophysiologic effects of digitalis glycosides?

A
  • through vagal effects
  • direct effects when toxic
131
Q

Describe the absorption and excretion for the positive inotrope digoxin

A
  • rapid absorption with high bioavailability
  • renal excretion
  • establishes steady state within 1 week
132
Q

Describe the toxicity of digoxin

A
  • relatively narrow therapeutic:toxic ratio
  • reduced renal function
  • decreased K, decreased Mg, increased Ca
  • major interactions with almost 300 medications
133
Q

What happens in low level digoxin toxicity?

A
  • GI
  • arrhythmias
134
Q

What happens in moderate level digoxin toxicity?

A

arrhythmias

135
Q

What happens in high level digoxin toxicity?

A
  • arrhythmias
  • neurologic
136
Q

What are the two types of digoxin toxicity related arrhythmias?

A
  • vagal associated
  • direct
137
Q

What happens in vagal associated digoxin toxicity related arrhythmias?

A
  • sinus bradycardia
  • AV block
138
Q

What happens in direct arrhythmias associated with digoxin toxicity?

A
  • ventricular ectopics/tachycardia –> Ca loading (early after depolarization)
  • atrial fibrillation
139
Q

How do you treat digoxin toxicity?

A
  • remove the drug
  • address underlying risk factors
  • treat arrhythmias if necessary

Pharm Final Exam (2 decks)

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