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Pharmacology > Iontrophic Agent > Flashcards

Iontrophic Agent Flashcards

1
Q

how does Digoxin differs from Digitoxin

A
  • Digoxin has a quicker onset via oral and IV
  • Has a quicker peak effect oral and IV
  • has less intestinal absorption bc more water soluble; less protein binding
  • greater volume of distribution
  • shorter half life
  • eliminated vai renal (not hepatic)
  • requires a small therapeutic [ ]
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2
Q

MOA of digitalis glycosides

A

reversible inhibition of Na/K ATPase

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3
Q

digitalis glycosides has a higher affinity for what conformation

A

E2

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4
Q

Na and Mg change the conformation to

A

E2, phosphorylates

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5
Q

K+ changes the conformation to

A

E1, dephosphorylates

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6
Q

digitalis glycosides have what 2 major concurrent actions on the heart

A 
1. mechanical
2 electrical (direct and indirect)
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7
Q

function of mechanical action of DG

A

increase myocardial contractility

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8
Q

what are the direct electrical effects of DG

A

depolarize membrane potential

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9
Q

what are the indirect effect of DG

A

increased vagal tone at SA & AV node

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10
Q

what are the mechanical effects of Digoxin

A

1) increase in Tension development - less time in mechanical systole
2) improvement in cardiac function - greater stroke work at each L ventricular end-diastolic pressure

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11
Q

what is the eqn of efficiency

A

cardiac work/cardiac O2 consumption

-this occurs by increase Ca++ availability

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12
Q

what are the direct electrical effects of digoxin

A

1) increased automaticity
2) decreased conduction velocity
3) shorter duration of the AP

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13
Q

what are the indirect electrical effects of digoxin

A

1) increase vagal (PSN) effects - central vagal nuclei are stimulated, Ach effects are facilitated, increased baroreceptor responsiveness
2) electrophysiological implications
- vagus innervates atrial muscles and nodes
- atrial muscle decreases automaticity
- SA node stimulation –> bradycardia
- AV node stimulation –> heart block

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14
Q

what is the therapeutic window of Digoxin

A

narrow therapeutic window

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15
Q

digoxin toxicity

A
  • altered serum electrolytes ( hypokalemia/hyperkalemia, hypercalcemia, hypomagnesemia)
  • acidosis inhibits Na/K pump
  • altered thyroid status
  • renal disease impairs elimination
  • increased sympathetic tone
  • respiratory disease & hypoxia
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16
Q

digoxin decreases absorption of what drug

A

cholestyramine, bran, etc.

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17
Q

digoxin increases plasma levels of what drugs

A

Quinidine, propafenone, verapamil, amidoarone, etc.

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18
Q

digoxin increases absorption of what drug

A

antibiotic treatments

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19
Q

digoxin increase automaticity due to electrolyte alteration of what drugs

A

furosemide, chlorothiazide, etc

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20
Q

digoxin exacerbate A-V node inhibition of what drugs

A

verapamil, dilitazem

21
Q

what are the neurological and GI symptoms of Digoxin Toxicity

A
  • malaise, dizziness, confusion, delerium
  • anorexia, nausea, vomiting, abdominal pain
  • disturbed color vision
22
Q

what are the early cardiac signs of digoxin toxicity

A
  • sinus bradycardia
  • first degree AV block
  • AV pacemaker or ectopic impulses originating from the AV node
23
Q

what are the serious cardiac signs of digoxin toxicity

A
  • marked sinus bradycardia
  • SA node arrest
  • 2nd or 3rd AV block
24
Q

how do you treat serious cardiac digoxin toxicity

A

give atropine, consider giving K+ and possibly pacing

25
Q

what is the most serious cardiac sign of digoxin toxicity

A

any of the previous signs PLUS premature ventricular arrhythmias (PVC’s)

26
Q

how do you treat the most serious digoxin toxicity

A

DIGIBIND (Fab immunoglobulin against digoxin)

27
Q

MOA of Digoxin

A
  • inhibition of Na/K ATPase results in increased intracellular Ca++
  • enhances vagal tone
28
Q

clinical uses of Digoxin

A
  • CHF
  • AV nodal reentrant arrhythmias
  • atrial fib
29
Q

pharmacokinetics of Digoxin

A
  • oral admin
  • primary renal ecretion
  • half-life of 36 hrs
30
Q

Adverse Effects of Digoxin

A

neurological and GI symptoms

31
Q

early cardiac signs of Digoxin toxicity

A

-sinus bradycardia and/or 1st degree heart block

32
Q

serious cardiac signs of Digoxin toxicity

A
  • SA node arrest and/or complete heart block

- PVCs & ventricular arrhythmias

33
Q

positive inotrophic effect in ventricular m. leads to what clinical/ECF effect

A

improved cardiac function

34
Q

lengthens AP duration in nodes leads to what clinical/ECF effect

A

bradycardia & prolonged PR

35
Q

shortens AP duration in cardiac m leads to what clinical/ECF effect

A

shortened QT interval

36
Q

increases automaticity in ventricular m leads to what clinical/ECF effect

A

increased change of PVC’s

37
Q

MOA of Dopamine

A

stimulates B-1 adrenergic and dopamine receptors

38
Q

pharmacodynamics of dopamine

A
  • positive inotrophic effect

- at low doses, causes dilation of renal vessels via D1 receptors

39
Q

AE of dopamine

A
  • tachycardia

- proarrhythmogenic

40
Q

MOA of dobutamine

A

stimulates B1&B2 -adrenergic receptors

41
Q

pharmacodynamics of dobutamine

A
  • positive inotrophic effect (B-1)

- vasodilation of the vasculature (B-2)

42
Q

AE of dobutamine

A

-tachycardia (but less than Dopamine)
proarrhythmogenic (but less than Dopamine)
-tolerance after several days

43
Q

MOA of inamrione

A

phosphodiesterase inhibitor: selective for isozye III, found in cardiac and vascular smooth m, which causes increased cAMP levels in the cells

44
Q

pharmacodynamics of Inamrione

A
  • positive inotropic effect

- vasodilaion

45
Q

AE of inamrione

A
  • proarrhythmogenic w/ prolonged use (a few days)

- thrombocytopenia & liver damage

46
Q

Heart Failure Diuretic drugs

A

Loops, thiazides, & Spironolactone

47
Q

Heart Failure Vasodilator Drugs

A

ACE Inhibitors (Enalapril, Lisinopril, Ramipril)
A-II receptor blockers (Losartan, Valsartan, Candesartan)
Hydralazine/Isosorbide dinitrate combination

48
Q

Heart Failure Beta Blocker Drugs

A

Carvedilol, Metoprolol

49
Q

Heart Failure Inotrope Drugs

A

Digoxin, Dopamine, Dobutamine, Inamrinone

Pharmacology (23 decks)

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