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Pharm Final Exam > Cardio Pharm > Flashcards

Cardio Pharm Flashcards

(139 cards)

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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
Because loop diuretics can secrete lots of Na, it is considered potent or what?
high ceiling
26
Describe the potency of torsemide compared to furosemide
10x more potent, lasts longer --> be cautious of dehydration
27
When does peak diuresis occur after oral administration of furosemide?
1-2 hours
28
When does furosemide effect begin to dissipate?
6 hours
29
When does diuretic resistance begin to develop in healthy dogs after beginning furosemide therapy?
14 days
30
What factors contribute to furosemide resistance?
- increased expression of co-transporters in response to aldosterone like substance - high ceiling diuretic
31
What effect does furosemide have when administered IV?
venodilation prior to onset of diuretic action
32
What are the adverse effects of furosemide?
- hypokalemia, hypochloremic metabolic alkalosis - dehydration - ototoxicity in humans
33
Furosemide also induces notable excretion of what two compounds?
Ca and Mg
34
What substances may blunt the furosemide response?
NSAIDs and steroids
35
What class of loop diuretics is torsemide in?
pyridine-3-sulfonylurea
36
When does peak diuresis occur with torsemide?
1-2 hours after oral administration
37
When does torsemide begin to dissipate?
12 hours
38
When is torsemide used?
when furosemide resistance develops
39
What are the adverse effects of torsemide?
- hypokalemia, hypochloremic metabolic alkalosis - dehydration
40
Explain the activity of torsemide in regards to aldosterone.
anti-aldosterone activity
41
What is the MOA of thiazide diuretics?
- directly inhibit Na/Cl cotransporter in DCT - Na, Cl, and H2O remain in tubule
42
Are thiazide diuretics considered high or low ceiling?
low
43
When does peak diuresis and dissipation occur with thiazide diuretics?
- rapid GI absorption - peak diuresis 1-2 hours after oral admin. - dissipates over 6-12 hours
44
Thiazide diuretics can be used synergistically with what other type of diuretic?
loop diuretics
45
What are the adverse effects of thiazide diuretics (more likely when used with loop diuretics)?
- hypokalemia - dehydration
46
What effect do thiazide diuretics have on Ca?
relative Ca-sparing effect
47
What two drugs are thiazide diuretics?
- hydrochlorothiazide - chlothiazide
48
What is the K sparing diuretic?
spiranolactone
49
What is the MOA of spiranolactone?
- 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
50
Is spironolactone a weak or strong diuretic?
weak
51
Spironolactone is used in combination with other diuretics, why?
- never used for substantial diuresis alone - can help obviate hypokalemia from other diuretics
52
Explain the anti-mitogenic properties of spironolactone?
- hypertrophy (cardiac and smooth muscle) - fibrosis (myocardial and vascular) - aldosterone-escape with ACE
53
Why is CHF therapy with diuretics alone should be limited to acute, relative short episodes?
- further reduction in CO and azotemia - AKI risk - activation of neurohumoral systems and maladaptive responses
54
How does diuretic therapy induce reduction in CO and pre- or intra-renal azotemia?
overaggressive diuresis without other drugs to improve cardiac performance
55
How does diuretic therapy induce AKI?
aggressive therapy with ace --> why you should avoid ace
56
How does diuretic therapy induce neurohumoral systems and maladaptive responses?
chronic administration of even the modest diuretic doses results in activation of these systems
57
What are the effects of arterial vasodilators?
afterload reduction
58
What is the effect of venous vasodilators?
preload reduction
59
What type of vasodilators can be used in heart failure?
- venous - arterial - mixed/balanced
60
What is the MOA of venodilators?
- 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
What drug is a venodilator?
nitroglycerin
62
What form does nitroglycerin come in?
2% ointment - topical
63
What is the MOA of nitroglycerin?
- 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
What is the onset of action for nitroglycerin?
rapid --> debate over clinical effect
65
What are the adverse effects of nitroglycerin?
hypotension with excessive preload reduction
66
Tolerance to nitroglycerin develops rapidly within days depending on frequency of dosing due to what?
- depletion of sulfhydryl group - inactive aldehyde dehydrogenase - production of peroxynitrite --> blocks conversion of GTP-cGMP
67
What are the effects of arterial vasodilation?
- arterial vasodilation reduces systemic vascular resistance - reduced cardiac work - reduced activation of neurohumoral systems
68
What are the effects of arterial vasodilation reducing systemic vascular resistance?
- easier for left ventricle to empty volume of blood - increase in forward stroke volume/CO - smaller end-systolic volume - lower end-diastolic pressure
69
What is the goal of arterial vasodilation?
~10-20% reduction in SBP (10-20 mmHg) in CHF should not use in patients with SBP <90 mmHg
70
What are the adverse effects of arterial vasodilation
- hypotension (weakness, collapse) - reflex tachycardia (increase cardiac work)
71
What drugs are arterial vasodilators?
- sodium nitroprusside - amlodipine (Novasc) - ACE inhibitors - angiotensin receptor blockers (ARB) - Telmisartan - Hydralazine - Prosozin
72
Sodium nitroprusside summary
- organic nitrate - spontaneous release of NO - ultra rapid effect: 1-2 min onset, 1-2 min offset - ideal for acute L-CHF
73
What are the special handling requirements for sodium nitroprusside?
- protect from sunlight - diluents
74
What are the adverse effects of sodium nitroprusside?
- hypotension - converted to cyanide in RBC's: metabolized to thiocyanate in liver, excreted by kidneys in 7 days
75
Amlodipine summary
- Ca L-channel blocker - dihydropyridine class - distinctly different than diltiazem - peripheral arterial vasodilation --> minimal myocardial/EP effects
76
What is the onset of action of amlodipine?
- within a few hours - half life is 24-36 hours - 5-7 days to get maximal effect
77
What are the adverse effects of amlodipine?
- hypotension - gingival hyperplasia (dogs)
78
What does ACE stand for?
angiotensin-converting enzyme
79
What does ACE do?
conversion of angiotensin 1 to angiotensin 2
80
What are the effects of angiotensin 2?
- vasoconstriction - Na retention - aldosterone release - mitogenic effects - activates sympathetic nervous system
81
What converts angiotensinogen to angiotensin I?
renin
82
What are ACE inhibitors not particularly effective for?
systemic hypertension --> most commonly hyporeninemic
83
What allows for continued angiotensin II production with ACE inhibitors?
tissue chymases
84
How do ace inhibitors prolong survival in dogs and cats with CHF?
neurohumoral modulating agent
85
Ace inhibitors are prodrugs metabolized and excreted where?
metabolized in liver to active form and excreted by the kidney
86
What is the problem with ace inhibitors?
lose ability for renal autoregulation
87
What effects are associated with renal autoregulation?
- reduced glomerular efferent arterial vasoconstriction with reduced renal perfusion - common clinical scenario during CHF tx - exacerbated by NSAIDs - AKI
88
What drugs are considered ACE inhibitors?
- Enalapril - Benazepril - Lisinopril
89
What is the onset, duration, and distribution of enalapril?
- prodrug - onset: 2-4 hours - duration: 12-14 hours - distribution: all tissues except CNS
90
How is enalapril excreted?
renal and hepatic
91
How often should enalapril be administered?
BID
92
How is enalaprilat excreted?
renal
93
What is the worry with toxicity and enalapril?
even at clinical doses you can end up with AKI
94
What is the onset, duration, and distribution of benazepril?
- prodrug - onset: 2-4 hours - duration: 12-24 hours - distribution: all tissues except CNS, placenta
95
How is benazeprilat excreted?
renal and hepatic excretion
96
T/F: You must be more cautious with enalapril in kidney failure, not as cautious with benazepril.
True
97
What is the excretion, onset, and duration of lisinopril?
- not a prodrug - renal excretion - onset: 2-4 hour - duration: 12-24 hour
98
What is the MOA of angiotensin receptor blockers (ARB)?
- 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
What are the uses of telmisartan (an ARB)?
- 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
Describe the oral absorption, metabolism, and excretion of telmisartan?
- relatively rapid oral absorption - highly protein bound - metabolized and excreted by the liver
101
What are two other arterial vasodilation drugs that are rarely used?
- hydralazine - prosozin
102
What drugs are positive inotropes that are sympathomimetics in the drug class of catecholamines?
- epinephrine - norepinephrine - dobutamine - dopamine
103
What is the effect of catecholamines on the body?
activation of adrenergic receptors
104
What are the effects of catecholamines on alpha 1 receptors?
precapillary vasoconstriction in organs
105
What are the effects of catecholamines on alpha 2 adrenergic receptors?
vasoconstriction
106
What are the effects of catecholamines on beta 1 adrenergic receptors?
- positive inotrope - positive chronotrope - positive lusitrope - positive dromotrope
107
What are the catecholamine effects on beta 2 adrenergic receptors?
precapillary vasodilation to skeletal muscle
108
Why is dobutamine an excellent choice for CHF tx?
- B1: ++++ - B2: ++ - A1: +
109
Describe the drug form, onset, offset, adverse effects, and tolerance of dobutamine
- only available IV (CRI) - onset: 2 min (peak at 10 min) - offset: 1-2 min - adverse effects: arrhythmias - develops tolerance within 72 hour
110
Is dopamine use for CHF tx?
nope
111
Describe the drug form, onset, offset, and adverse effects of dopamine.
- only available IV (CRI) - onset: 5 min - offset: 2-5 min - adverse effects: tachycardia, arrhythmias
112
What is the MOA of phosphodiesterase inhibitors and their positive inotrope effect?
- increase cAMP
113
What do phosphodiesterases do?
- degrade nucleic acids --> reducing cAMP
114
What drugs are considered phosphodiesterases inhibitors?
amrinone and milrinone
115
Describe the type of inhibitor and drug form of phosphodiesterase inhibitors (amrinone, milrinone)
- type III PDE inhibitors - IV administration only
116
What is the use of phosphodiesterase inhibitors?
short term therapy for severe myocardial failiure
117
What are the adverse effects of amrinone and milrinone?
- arrhythmias - hypotension - thrombocytopenia
118
How is pimobendan a calcium sensitizer?
- increased Ca effect for given [Ca] - no Ca loading - positive inotropic
119
How is pimobendan a phosphodiesterase III inhibitor?
- positive inotrope - vasodilation
120
What is pimobendan labeled for in dogs?
- dilated cardiomyopathy - mitral valve disease (DMVD)
121
Describe how pimobendan undergoes hepatic demethylation
- converted to ODMP - 100x more potent than pimobendan - predominantly PDEIII inhibition
122
Which drug lasts longer: pimobendan or ODMP?
ODMP
123
T/F: pimobendan pharmacodynamics do not persist longer than Cmax.
False - persists longer than Cmax
124
What are the adverse effects of pimobendan?
- generally considered low frequency - ventricular arrhythmias - increases AVN conduction velocity --> consideration for atrial fibrillation
125
What are digitalis glycosides derived from?
- oleander - lily of the valley - milkweed
126
What are digitalis glycosides used for?
treatment of "dropsy" since the Greeks and Romans
127
What is the MOA of the positive inotrope digitalis glycosides?
- 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
How do digitalis glycosides increase density of Na/K ATPase in heart failure?
- baroreceptor dysfunction - contributor to increase SNS tone in heart failure
129
How do digitalis glycosides act as positive inotropes?
- Ca loading - "neutral" effect on vascular tone
130
What are the electrophysiologic effects of digitalis glycosides?
- through vagal effects - direct effects when toxic
131
Describe the absorption and excretion for the positive inotrope digoxin
- rapid absorption with high bioavailability - renal excretion - establishes steady state within 1 week
132
Describe the toxicity of digoxin
- relatively narrow therapeutic:toxic ratio - reduced renal function - decreased K, decreased Mg, increased Ca - major interactions with almost 300 medications
133
What happens in low level digoxin toxicity?
- GI - arrhythmias
134
What happens in moderate level digoxin toxicity?
arrhythmias
135
What happens in high level digoxin toxicity?
- arrhythmias - neurologic
136
What are the two types of digoxin toxicity related arrhythmias?
- vagal associated - direct
137
What happens in vagal associated digoxin toxicity related arrhythmias?
- sinus bradycardia - AV block
138
What happens in direct arrhythmias associated with digoxin toxicity?
- ventricular ectopics/tachycardia --> Ca loading (early after depolarization) - atrial fibrillation
139
How do you treat digoxin toxicity?
- remove the drug - address underlying risk factors - treat arrhythmias if necessary

Pharm Final Exam (2 decks)

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