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Linde's Sets > Pharm II - CVS drugs > Flashcards

Pharm II - CVS drugs Flashcards

1
Q

What are the CVS effects of cardiac glycosides (CGs)? (6)

A
  1. increase contractility/excitability
  2. increase CO
  3. Diuresis
  4. Reduces edema
  5. Decrease HR
  6. Decrease venous Pressure
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2
Q

Is diuresis a prominent feature of Digitalis?

A

No. It is 2ry to circulatory improvement

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3
Q

How does Digitalis cause diuresis (2)?

A
  1. Increases renal blood flow

2. Decreases aldosterone secretion

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4
Q

Will Digitalis induce diuresis if the edema is not cardiogenic in nature?

A

No

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5
Q

CO depends on what 3 things?

A
  1. Intrinsic response of cardiac mm. to change in myofiber length
  2. HR
  3. Contraction force of heart
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6
Q

Compensatory mechanisms of the the CVS? (4)

A
  1. Activation of Sympathetic NS
  2. Renin-andiotensin-aldosterone system
  3. Myocardial hypertrophy
  4. CHF
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7
Q

CGs are a ____ compound linked by an _____ atom to one or more ____ molecules.

A

neutral
oxygen
sugar

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8
Q

What are Ionotrophic drugs generally used for?

A
  1. increase myocardial contractile force

2. TX CHF

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9
Q

What are the iontropic drugs (6)?

A 
Digitalis 
Inamrinone
Milrinone
Pimbendan
Dobutamine
Aminophylline
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10
Q

Digitalis collectively refers to what 3 drugs?

A

Digoxin
Digitoxin
Ouabain

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11
Q

Where does the cardioactivity of CGs reside?

A

principally in the aglycone moiety & sugar molecules attached to aglycone

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12
Q

How does digitalis affect cardiac rate & rhythm?

A

stimulates vagal afferents & directly depresses SA node conduction = decrease HR

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13
Q

How does digitalis affect cardiac excitability?

A

reduces the diastolic potential to threshold level, enhancing excitability

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14
Q

Higher bioavailability

(75-95%) is achieved when digoxin is administered in what form?

A

elixir form

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15
Q

Which species are CGs poorly absorbed? Why?

A

Ruminants

due to metabolism by ruminal micro-organisms

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16
Q

Does digoxin bind to PP?

A

Yes, poorly (25%)

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17
Q

What BW should be used to calculate digoxin dosage?

A

Lean BW (not well distributed to fat)

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18
Q

Does digitalis undergo enterohepatic circulation?

A

yes, gives it a long 1/2 life

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19
Q

List the half life for a single IV dose of digitalis by species shortest to longest. (6)

A 
sheep- 7.2 hrs
Cattle- 7.8 hrs
Horses- 23 hrs
Dogs- 28 hrs
Cats- 35 hrs
Humans - 39+ hrs
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20
Q

How can digitalis be administered for maintenance therapy?

A

PO or parenteral

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21
Q

What is digitalization?

A

involves initial admin of a large amt of digitalis (loading dose) in several divided doses over 24-48 hrs followed by a daily maintenance dose to maintain therapeutic efficacy

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22
Q

What is the main aim of digitalis therapy?

A

to determine the smallest amt of CG that will effectively maintain cardiac compensation w/o signs of toxicity

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23
Q

What is the slow method of oral digitalization?

A

Admin loading dose in 5 equal parts over 48 hrs

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24
Q

What is the rapid method of oral digitalization?

A

Admin loading dose in 3 equal parts every 6 hrs

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25
Q

What is the intensive method of digitalization?

A

ER!!

  1. Give 1/2 loading dose
  2. Give 1/4 loading dose 6 hrs later
  3. Give 1/8 loading dose at 4-6 hr intervals
  4. Use maintenance dose
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26
Q

When is the steady state conc. of digitalis attained? What do you do then?

A

6th to 8th day of maintenance therapy

assess for response to TX

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27
Q

Which 2 organ fxns should be assessed before beginning digitalis tx?

A

Liver & kidneys

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28
Q

What should you do with the digitalis dose in patients w/ renal & hepatic dz?

A

Reduce the dose levels

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29
Q

When is IV admin of digitalis recommended?

A

animal does not retain oral meds or has acute cardiac decompensation or respiratory distress

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30
Q

Why is careful monitoring required after giving digitalis IV?

A

It can induce toxic arrhythmias

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31
Q

Can you give digitalis IM?

A

Not recommended, causes pain & swelling

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32
Q

What is the MOA of CGs?

A

Inhibits Na/K ATPase –> increases INTRAcellular Ca –> excess Na is exchanged for Ca by the Na/Ca pump (3:1) –> increases [Ca] –> activates inotropic action

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33
Q

What is digoxin safety margin?

A

Narrow

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34
Q

Should steady state plasma [digoxin] be done?

A

yes

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35
Q

How do you monitor digitalis toxicity? (3)

A
  1. ECG
  2. [plasma/serum]
  3. serum [K]
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36
Q

Serum ___ & ____ influence myocardial sensitivity to digitalis action?

A

K & Ca

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37
Q

K+ ______ digitalis binding to Na/K ATPase?

A

inhibits

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38
Q

____kalemia increase digitalis binding w/ Na/K ATPase & toxicity?

A

Hypokalemia

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39
Q

How does Quinidine increase digitalis steady state concentration?

A
  1. displaces digitalis from its tissue binding site

2. inhibits P-glycoprotein in GIT & Kidney –> increases absorption & decreases excretion of digitalis

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40
Q

Increased ____ may enhance the toxic effect by increasing intracellular Ca stores?

A

Ca

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41
Q

How does Cholestyramine resin TX digitalis toxicity?

A

binds glycoside w/in GIT & inhibits enterohepatic circulation = increases elimination of digitalis

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42
Q

When is digitalis contraindicated?

A

in case of AV block!

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43
Q

What should you do when administering digitalis & Quinidine together?

A

Reduce digitalis dose by 1/2 6-8 days prior to therapy w/ Quinidine

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44
Q

What adjunct therapy should be used along with CGs?

A

Diuretics –> reduces cardiac preload

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45
Q

Furosemide is a ____ diuretic? Where does it act?

A

Loop-acting

Ascending LoH

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46
Q

MOA of Furosemide?

A

inhibits Na/K/Cl co-transport mechanism

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47
Q

Which animals show decreased response to furosemide?

A

animals w/ low CO & poor renal perfusion

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48
Q

List the diuretics (3) used in CVS therapy.

A

Furosemide
Thiazide diuretics
K sparing diuretics

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49
Q

MOA of thiazide diuretics

A

inhibit Na/Cl symport in DCT–> increasing K excretion & enhancing Ca reabsorption

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50
Q

Which diuretic increases the risks of digitalis toxicity?

A

Thiazide diuretics due to effects on serum [K] & [Ca]

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51
Q

What is the preferred diuretic to use in CVS therapy?

A

K sparing diuretics –> decreases K in urine

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52
Q

MOA of K sparing diuretics?

A

interferes w/ Na/K exchange mechanism in renal collecting tubules

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53
Q

What is the problem w/ K sparing diuretics?

A

slow onset of action

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54
Q

What oral combo produces diuresis w/o delayed onset of action or excessive urinary excretion of K?

A

equal portions of Hydryoflumethiazide & Spironolactone

55
Q

Which CGs are phosphodiesterase inhibitors? (4)

A

Inamrinone
Milrinone
Pimobendan
Aminophylline

56
Q

Which CG is a beta-adrenergic agonist? Which receptor?

A

Dobutamine

Beta 1 receptor

57
Q

What is the 1/2 life of Dobutamine?

A

2-4 min

very short; requires constant admin

58
Q

Why does dobutamine have a rapid 1/2 life?

A

due to biotransformation of the drug by catechol O-methyltransferase (in tissues)

59
Q

Aminophylline is a ____ complex & _____ soluble.

A

theophylline-etylenediamine

water

60
Q

Is Aminophylline indicated for the management of CHF?

61
Q

Vasodilators (VDs) relax & dilate the smooth mm of ____ & thereby _____.

A

arterioles

reduce systemic vascular resistance

62
Q

The compensatory response elicited by VDs is mediated by ____ & _____.

A

baroreceptors

sympathetic NS

63
Q

VDs can selectively dilate ___, ____ or ____

A

arteries
veins
both

64
Q

VDs that dilate both arteries & veins are called?

A

balance vasodilators

65
Q

Which VDs decrease systemic vascular resistance & afterload

A

arteriolar dilators

66
Q

Which vasodilation diverts blood volume from pulmonary to systemic circulation?

A

Peripheral venous vasodilation

67
Q

Peripheral venodilation does what 2 things?

A
  1. reduces ventricular preload & filling pressure

2. reduces pulmonary edema

68
Q

VDs can be used in combo w/ ____ &/or ____ for effective TX of hypertension?

A

antihypertensive drugs

diuretics

69
Q

Which drugs are preferred for the management of CHF?

A

Vasodilators –> decrease workload & are safer than inotropic agents

70
Q

What is the total amount of Na nitroprusside that can be infused w/in a 2 hr period?

71
Q

How is Hydralazine administered?

72
Q

How is Hydralazine metabolized?

A

extensive hepatic metabolism

73
Q

List the vasodilators. (8)

A 
Na nitroprusside
Hydralazine
Minoxidil
Prazosin
Nitroglycerin
Isoxsuprine
Amlodipine
Sildenafil
74
Q

What drugs are Ca channel blockers? (4)

A

Nifedipine
Verapamil
Diltiazem
Amlodipine

75
Q

Which drugs stimulate the release of Renin?

A 
Vasodilators
Beta-adrenoceptor agonists
Alpha1-adrenoceptor ANTagonists
Phosphodiesterase inhibitors
Diuretics
Anaesthetic agents
76
Q

Can ACE inhibitors be used in ischaemic heart dz?

A

yes, do not activate the Sympathetic NS

77
Q

What is the active form of the prodrug Enalapril maleate?

A

Enalaprilat

78
Q

What is the active form of the prodrug Benazepril hydrochloride?

A

Benazeprilat

79
Q

MOA of ACE inhibitors. (2)

A

Inhibit peptidyl dipeptidase (hydrolyses Angiotensin I –> Angiotensin II)

Inhibits Bradykinin degradation

80
Q

Is it necessary to monitor renal fxn before & during TX w/ ACE inhibitors?

81
Q

The dose of ACE inhibitors should be _____ in renal insufficiency cases?

82
Q

What is the dosage regimen of ACE inhibitors?

A

Admin Furosemide first followed by Enalapril

diuretic then ACE inhibitor

83
Q

Will increasing the size of the ACE inhibitor dose increase the therapeutic effect once maximal inhibition of ACE is achieved?

84
Q

Which drug should you avoid using while on ACE inhibitors?

A

NSAIDs

can decrease the hypotensive effect

85
Q

ACE inhibitors produce a ______ & ______ effect.

A

mild netriuretic

K sparing

86
Q

What are the fixed-dose preparations of ACE inhibitors contain?

A

ACE inhibitor + Thiazide diuretic

87
Q

List the 2 fixed-dose preparations containing ACE inhibitors & thiazide diuretics that can effectively manage hypertension in dogs & cats.

A

Captopril hydrochlorothiazide

Enalapril hydorchlorothiazide

88
Q

What are the 3 main goals of TXing Left Ventricular Failure

A
  1. improve gas exchange
  2. enhance myocardial contractility
  3. reduce workload of the left ventricle
89
Q

How does IV Furosemide INCREASE venous capacitance?

A

by redistributing venous blood from lung to peripheral circulation –> alleviates pulmonary congestion

90
Q

What are the benefits of Morphine sulphate? (2)

A
  1. decreases peripheral resistance (hypotensive effect)

2. decreases responsiveness of medullary respiratory center

91
Q

Is Epinephrine indicated for acute left ventricular heart failure?

A

NO!!

causes peripheral vascoconstriction & is arrhythmogenic

92
Q

What are the classifications of Antiarrhythmic (AA) drugs?

A

Class I-IV

93
Q

MOA of Class I AA drugs

A

membrane stabilizers/local anaesthetics

decrease Na influx & decrease phase 0 (max. depol rate)

Inhibits phase 4 (spontaneous depol) in automatic cells

94
Q

MOA of Class II AA drugs.

A

Beta adrenergic ANTagonists

beta blockers

95
Q

MOA of Class III AA drugs

A

prolong the refractory period

96
Q

MOA of Class IV AA drugs

A

Ca channel blockers

97
Q

How do Beta blockers work? (5)

A 
reduce sympathetic input 
depress automaticity 
prolong AV conduction
Decrease HR & contractility
Shorten duration of AP
98
Q

Which drug is better at suppression of ventricular ectopic depolarization? (beta blocker or Class IA AA drugs)

A

Class IA AA drugs

99
Q

Which class of AA drugs produce “pure” prolongation of the AP & extend the refractory period?

A

Class III AA drugs

100
Q

What does Amiodarone block/inhibit? (3)

A

Blocks K & Ca channels in heart

Non-competitive inhibitor of Beta-adrenoceptors

101
Q

Class IV AA drugs have specific inhibitory effects on ____.

A

Ca dependent SLOW response –> slows AV conduction & prolongs refractory period

102
Q

What enhances the efficacy of Ca channel blockers?

A

Beta blockers

103
Q

What will predispose the patient to the development of AV block?

A

Ca channel blockers + beta blockers (use w/ extreme caution)

104
Q

What are the primary considerations when approaching AA drug therapy?

A

characterize the arrhythmia

decide whether or not AA therapy is required

105
Q

Should you monitor steady state plasma [AA]?

A

yes, advised

106
Q

What is the PD interaction between Diltiazem & propranolol/atenolol; Quinidine & a beta-blocker?

A

Quinidine inhibits oxidative metabolism of beta blocker

107
Q

What is the PK interaction between Digoxin & Quinidine/Diltiazem?

A

Quinidine displaces digoxin from its tissue binding site

Diltiazem completely inhibits renal tubular excretion of digoxin

108
Q

What are the effects of Quinidine on cardiac rhythmicity?

A

Direct & indirect

Direct- prolongs refractory period

Indirect-lengthens refractory period by its anticholinergic action

109
Q

Quinidine has ____ like vagolytic effects.

110
Q

To avoid the acceleration of ventricular rate, always precede Quinidine with what?

111
Q

Is Quinidine very effective in TXing atrial fibrillation in small breeds of dogs?

A

No, better on large breeds of dogs

112
Q

Is Quinidine recommended to TX AV or Interventricular block?

A

No, contraindicated

113
Q

What type of arrhythmia is Procainamide better at controlling?

A

Ventricular arrhythmias

114
Q

What are the reason Disopyramide has limited use in Vet Med? (3)

A

Requires repeated administration

Has pronounced Atropine-like side effects

Exerts (-) inotropic effects on the heart

115
Q

Which drug is used to control ventricular arrhythmias in dogs resistant to standard therapy?

A

Aprinidine –> last resort

116
Q

What is a new aprindine congener that possesses 6xs the potency of Aprindine w/ few side effects?

A

Indecainide

117
Q

_____ slows the rate of spontaneous discharge of the SA & ectopic pacemakers.

A

Propranolol

118
Q

Propranolol slows both ___ & ____ conduction.

A

antegrade & retrograde

119
Q

What is the metabolism of Propranolol?

A

well absorbed through GIT, undergoes 1st Pass effect

120
Q

If given oral, what must one do to the dose of Propranolol?

A

Increase the IV dose by 6-10 times

121
Q

Can you use Propranolol in animals with obstructive airway dz? Why or why not?

A

No beta blockade causes airway obstruction

122
Q

Can you use beta blockers in patients w/ reduced cardiac reserve (CHF)? Why?

A

WITH CAUTION b/c sympathetic activity is more pronounced in these patients w/ CHF

123
Q

MOA of Bretylium

A

adrenergic neuronal blocking agent –> inhibits release of NE from adrenergic nerve endings

124
Q

Will Bretylium prolong AP duration and refractory period in the atria?

A

No, only effects ventricles

125
Q

T/F Administration of Bretylium to animals anaesthetized w/ halogenated hydrocarbon anaesthetics is contradicted.

126
Q

How are ventricular arrhythmias produced by Bretylium?

A

as a 2ry effect to the initial catecholamine release

127
Q

How can you gain steady state [Amiodarone]?

A

with oral admin

128
Q

T/F: Ca channel blockers are used safely in cardiac failure patients.

A

False, use w/ caution

129
Q

What are the contraindications of Epinephrine use in cardiac patients?

A

Acute left ventricular failure

Cardiac emergencies during anaesthesia

130
Q

What is Epinephrine reversal?

A

Administration of epinephrine to an animal w/ blocked ALPHA1-adrenoceptors results in a DEPRESSOR response

131
Q

At LOW IV infusion rate, Dopamine causes what?

A

decreased peripheral resistance (vasodilation) in renal & splanchnic arterial beds

132
Q

At INTERMEDIATE IV infusion rate, Dopamine causes what? (2)

A

stimulates Beta1-adrenocerptors in the heart –> (+) inotropic action

decreased peripheral resistance

133
Q

Dopamine can be used as adjunctive therapy for what?

A

Oliguric renal failure

134
Q

What drug increases the efficacy of Furosemide by increasing renal blood flow?

Linde's Sets (16 decks)

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