L11: Digitalis & Theophylline Flashcards

1
Q

Source of Digitalis

A

The roots, leaves and seeds of “Digitalis Purpurea” contain several poisonous glycosides.

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2
Q

Toxic Action of Digitalis

A
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3
Q

Risk factors for Digitalis Toxicity

A
  • Age
  • Renal functions
  • Electrolyte indisturbances
  • Drug Interactions
  • Natural products
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4
Q

Age Risk Factors for Digotalis Toxicity

A

Adyanced age (>80 y) is associated with increased morbidity and mortality.

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5
Q

Renal Function Risk Factors for Digotalis Toxicity

A

Deteriorating renal function, dehydration, electrolyte disturbances or drug interactions, usually precipitates chronic toxicity.

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6
Q

Electrolyte Disturbances Risk Factors for Digotalis Toxicity

A
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7
Q

Drug Interactions Risk Factors for Digotalis Toxicity

A
  • Drug interactions are one of the most common causes of digoxin Toxicity

(e.g., Beta-blockers, Calcium channel blockers, Quinidine, loop diuretics)

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8
Q

Natural Products Risk Factors for Digotalis Toxicity

A

Natural licorice should be avoided as it causes
- Sodium and water retention
- Increases potassium loss.

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9
Q

CP of Digitalis Toxicity

A
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10
Q

what causes yellow-green visual changes with digitalis toxicity?

A

due toxic effects on retinal con than rod cell.

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11
Q

Types of Digitalis Toxicity

A
  • Acute overdose toxicity.
  • Acute versus chronic use toxicity (more common).
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12
Q

Investigations in Digitalis Toxicity

A
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13
Q

TTT of Digitalis Toxicity

A
  • Emergency TTT & Supportive
  • Decontamination
  • Antidote
  • Enhanced Elimination
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14
Q

Emergency TTT of Digitalis Toxicity

A
  • ABC and assist ventilation if necessary.
  • Continuous cardiac monitoring for at least 12-24 hours after significant ingestion due to delayed tissue distribution
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15
Q

Continuous cardiac monitoring for at least 12-24 hours after significant ingestion of digitalis due to ……..

A

due to delayed tissue distribution

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16
Q

Aspects of Emergency TTT in Digitalis Toxicity

A
  • Bradycardia or Heart block
  • Ventricular Arrhythmias
  • Hyperkalemia
  • Hypokalemia
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17
Q

Emergenct TTT of bradycardia & Heart Block in Digitalis Toxicity

A
  • Give atropine 0.5-2mg l.V.
  • Temporary transvenous cardiac pacemaker may be needed
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18
Q

Emergency TTT of Ventricular Arrythmia in Digitalis Toxicity

A
  • Fab is the preferred treatment for life-threatening arrhythmias.
  • Lidocaine is the antiarrhythmic drug of choice.
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19
Q

Emergency TTT of hyperkalemia in Digitalis Toxicity

(VIP)

A
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20
Q

when does hyperkalemia of Digitalis Toxicity need TTT?

A

Needs treatment especially if associated with ECG changes

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21
Q

what to do in a case of Hyperkalemia due to digitalis if no FAB is available?

A

Give triad of
- Sodium bicarbonate (1 mEq/kg)

  • Glucose (0.5 g/kg IV)
  • Given simultaneously with Insulin (0.1 U/kg IV)

or Sodium Polystyrene Sulfonate (Kayexalate, 0.5 g/kg PO)

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21
Q

Types of TTT of Hyperkalemia associated with Digitalis Toxicity

A

Moderate elevation of serum k (>5.5 mEq/L):
- Fab Fragment: It rapidly reverses it

Progressive elevation of serum k (k > 6-7 mEq/ L):
- Bi-Carbonate/Glucose/Insulin

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21
Q

why shouldn’t calcium be used in hyperkalemia of Digitalis Toxicity?

A

may worsen ventricular arrhythmias.

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21
Q

Emergency TTT of hypokalemia of Digitalis Toxicity

A
22
Q

why shouldn’t digoxin-specific Fab administration be used in hypokalemia of Digitalis Toxicity until hypokalemia is corrected?

A

Because reinstitution of Na+-K+-ATPase function may cause profound hypokalemia.

23
Q

Deconatmination in Digitalis Toxicity

A
24
Q

Antidote of Digitalis Toxicity

A

Fab Fragments

25
Q

Indications of Fab fragments

A
26
Q

MOA of Fab fragments

A

It is low molecular weight immunoglobulin fragments that bind to digitalis forming complex, which is cleared by the kidney and reticuloendothelial system.

27
Q

Encanced Elimination in Digitalis Toxicity

A
28
Q

is Digoxin hemodialyzable?

A

not dialyzable due to large volume of distribution

29
Q

is Digitoxin Hemodialyzable?

A

dialyzable and can be eliminated by repeated-dose charcoal

  • due to its enterohepatic circulation
30
Q

Therapeutic index of theophylline

A

Theophylline has an extremely narrow therapeutic index

31
Q

Intro to Theophylline toxicity

A
32
Q

Toxic Action in Theophylline toxicity

A
33
Q

Onset of Acute Theophylline toxicity

A

Manifestations of severe toxicity may be delayed 12-16 hours with sustained-release preparations

34
Q

CP of Acute Theophylline toxicity

A
35
Q

Causes of Chronic Theophylline toxicity

A
  • when excessive doses are administered repeatedly over 24 hours or longer
  • when intercurrent illness or an interacting drug interferes (Eg, erythromycin, cimetidine) with hepatic metabolism of theophylline.
36
Q

Incidence of Chronic Theophylline toxicity

A
  • The usual victims are very young infants and elderly patients, especially those with chronic obstructive lung disease.
37
Q

Differences between Acute & Chronic Theophylline toxicity

A

In chronic toxicity:

  • Vomiting and hypotension are less common than acute.
  • Metabolic effects as hypokalemia and hyperglycemia are not present
  • On the other houd, arrythmia and seizures are common at lower level.
38
Q

Investigations in Theophylline toxicity

A
  • Serum Theophylline Level
  • Other Lab Studies
39
Q

Seum Theophylline level

A
40
Q

Other lab studies in Theophylline toxicity

A

Arterial blood gases (ABG), electrolytes, glucose, creatinine, hepatic function tests and ECG.

41
Q

TTT aspects in Theophylline toxicity

A
  • Emergency & supportive treatment
  • Antidotes
  • Decontamination
  • Enhanced Elimination
42
Q

Emergency & Supportive TTT in Theophylline toxicity

A
43
Q

Is there an antidote for Theophylline toxicity?

A

no

44
Q

Decontamination options in Theophylline toxicity

A
  • Gastric Lavage
  • Activated Charcoal
  • Catharitic
  • WBI
45
Q

Gastic lavage in Theophylline toxicity

A

If no vomiting can be done even 4 hs after ingestion.

46
Q

AC in Theophylline toxicity

A
  • It is important to control nausea and vomiting first.
  • “Ondansteron” is the drug of choice to control emesis in theophylline toxicity.
47
Q

Catharitcs in Theophylline toxicity

A

Sorbitol is used with the activated charcoal.

48
Q

WBI in Theophylline toxicity

A

With sustained-release preparations.

49
Q

Enhanced Elimination options in Theophylline toxicity

A
  • Hemodialysis
  • MDAC
  • Hemoperfusion
50
Q

what is teh definitive Life-Saving Intervention in severe Theophylline toxicity?

A

Hemodialysis

51
Q

Introducation to the use of hemodialysis in Theophylline toxicity

A
  • It is the definitive life-saving intervention in severe theophylline poisoning
  • Highly effective in achieving good clinical outcome if commenced early.
  • Arrangements for urgent hemodialysis are made as soon as potentially life-threatening theophylline toxicity is anticipated.
52
Q

Indications of the use of hemodialysis in Theophylline toxicity

A
53
Q

what is the corner stone in TTT of Theophylline toxicity?

A

Multiple dose activated charcoal

54
Q

uses of MDAC in Theophylline toxicity

A
  • Used for stable patients with levels below 100 mg/L in acute toxicity.
  • It enhances the elimination of theophylline
  • but use of this modality delays effective treatment with hemodialysis in severe cases.
55
Q

what is more effective in Theophylline toxicity, Hemodialysis or Hemoperfusion?

A

Hemoperfusion

56
Q

Indications of Hemoperfusion in Theophylline toxicity?

A

Done in the presence of life-threatening toxicity.

  • Persistent seizures
  • persistent hypotension
  • ventricular dysrhythmias
  • If the serum level is greater than 100 mg/L in acute toxicity (If available).