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Toxicology > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

Depressed patients are more likely to develop

A

Type 2 diabetes and
cardiovascular disease.

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2
Q

Depression is thought to involve

A

changes in receptor-neurotransmitter relationships

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3
Q

Neurotransmitters involved in depression?

A

Serotonin, norepinephrine, dopamine

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4
Q

What are the classes of anti-depressant drugs (5)

A
  1. Selective Serotonin Re-uptake Inhibitors (SSRI)
  2. Serotonin/Norepinephrine Reuptake Inhibitors (SNRI)
  3. Tricyclic Antidepressants (TCA)
  4. Monoamine Oxidase Inhibitors (MAOI)
  5. Atypical Antidepressants
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5
Q

What is the MOA of SSRI:

A

Selective Serotonin Re-uptake Inhibitors (SSRI)
Mechanism of action

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6
Q

What are the SSRIs? (6)

A
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7
Q

What are the SNRIs? (4)

A
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8
Q

What are the TCAs?

A
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9
Q

What are the MAOI? (3)

A
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10
Q

What is the issue with MAOI?

A

Drug interactions and drug food interactions. Can induce serotonin syndrome

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11
Q

There is a functional imbalance in which neurotransmitters?

A

Dopamine, Serotonin, Norepinephrine

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12
Q

What is the MOA of bupropion?

A

inhibits DAT and NET.
* Enhances both noradrenergic and dopaminergic
neurotransmission via reuptake inhibition of the
norepinephrine/noradrenalin and dopamine.

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13
Q

What is the bupropion toxicity? (3 major points)

A
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14
Q

What are the benefits for SSRI?

A
  • Fewer significant adverse effects and less problematic in overdose than TCAs and MAOIs
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15
Q

What is the therapeutic window of SSRIs?

A

Very high (50-75x)

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16
Q

What is the SSRI Absorption?

A

tmax 4-8 hours

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17
Q

What are SSRIs mainly metabolized by?

A

Cyp2D6

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18
Q

What is the distribution of SSRIs?

A

High volume of distribution

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19
Q

What is the elimination of SSRI?

A

Mostly renally excreted

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20
Q

What are the two SSRi that may be more toxic in overdose?

A

Citalopram, escitalpram

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21
Q

SNRI such as ____ are associated with greater risk of significant toxicity and mortality in overdose

A

venlafaxine

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22
Q

What is serotonin syndrome?

A

Diaphoresis, diarrhea, hyperthermia, mental status
changes, myoclonus.

Inducible or ocular clonus, agitation, diaphoresis,
hypertonicity, hyperthermia

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23
Q

Serotonin toxicity occurs most frequently after use of____ of serotonergic xenobiotics

A

combination

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24
Q

How is SSRI diagnosis performed?

A

ECG, SCr, LFT, myoglobin, rhabdomyolysis. Creatinine kinase

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25
Q

How do we manage Seizures due to SSRC toxicity/

A

Bzds

26
Q

How do we manage cardiac abnormalities due to SSRI toxicity?

A

sodium bicarbonate

27
Q

What is the job of the MAOI?

A

Degrades the serotonin reuptake neurotransmitters, Allowing for an accumulation of drug.

28
Q

How do we manage torsades de pointes due to SSRI toxicity?

A

magnesium sulfate

29
Q

How do we manage serotonin sybndrome?

A

cyproheptadine: competitive binding to serotonin receptor = cooling and treatment of muscular rigidity

30
Q

What time frame can we use SDAC for SSRI toxicity management?

A

Most benefit within 1-2 hours

31
Q

Which SSRI should we know?

A

Citalopram, escitalopram

32
Q

Which SNRI should we know ?

A

Venlafaxine

33
Q

Which TCA should we know?

A

Amitriptyline

34
Q

Is hemodialysis effective in the management of SSRI toxicity?

A

No because of the high Plasma-plasma binding and volume of distribution

35
Q

What toxicity can occur due to venlafaxine?

A

Seizure, tachycardia, ECG abnormalities, and
serotonin toxicity

36
Q

Bupropion can be used for smoking cessation true or false?

A

True

37
Q

What is key in successful management of TCA toxicity?

A

Early identification

38
Q

Progression of clinical toxicity (Via TCA) is ___ and may be ___

A

unpredictable, rapid

39
Q

The progression of clinical toxicity is unpredictable and may be rapid. Patients commonly present to the emergency department (ED) with minimal apparent clinical abnormalities only to develop ____
”

A

life-threatening
cardiovascular and CNS toxicity within hours.

40
Q

TCA have ___ on gastric emptying

A

Anticholinergic effect

41
Q

TCAs wit ha greater anticholinergic effect causes ___Perfusion and ___motility of GIT leading to ___ emptying

A

hypo, hypo, delayed

42
Q

TCAs are ___philic and ___ distributed

A

Lipo, widely

43
Q

Do TCAs have a high or low PPB?

A

High

44
Q

What in general metabolized TCA?

A

Multiple CYPS

45
Q

What are some other things to consider in terms of antidepressants?

A

Genetic polymorphisms in the Cyp2D6 metabolite

46
Q

Dose ingested and plasma concentration are a poor predictor of outcome. What are the toxic concentrations thought with regards to TCAs?

A

5-20mg/kg`

47
Q

What are the S/S of toxicity via TCA

A

Cardiotoxic symptoms show Rapid progression
* Onset often within 2 hours of ingestion

48
Q

What is very important with regards to TCA toxicity/

A

Early ECG is very important

49
Q

What is the S/S of toxicity relating to respiratory and TCAs?

A

Aspiration
Acute respiratory distress syndrome
Hypoexmia

50
Q

How is TCA toxicity diagnoised?

A

serum TCA levels,
ECG *

Severity of toxicity is best reflected by ECG, not serum levels*

51
Q

What other labs are measured for TCA toxicity>

A

Lytes, glucose, arterial blood pH

52
Q

With regards to the QRS interval what should we be watching for with regards to TCA toxicity>?

A
53
Q

How do we manage dysrhythmias?

A

Sodium bicarbonate

54
Q

What is the MOA of sodium bicarb for dysrhythmias?

A

increase in serum pH and the increase in extracellular sodium.

Alkalinization of arterial blood pH: inhibits binding of TCA to myocardial Na+ channel as drug is not
ionised

55
Q

If dysrhythmias continue what is the next thing we can treat with?

A

Lidocaine (lidocaine is a blocker of Na+ and K+ channels)

Hypertonic salien

Magnesium sulfate

56
Q

What is a no with regards to dysrhythmic management?

A
57
Q

What do we use for seizure management with regards to TCAS?

A

Bzds, sodium bicarbonate

58
Q

TCAs block ___

A

sodium channels leading to Qt prolongation

59
Q

Is hemodialysis effective for managing TCA toxicity?

A

No because high Vd, and and protein bound

60
Q

What may be a an antidote for TCAs?

A

Intravenous lipid emulsion (ILE)

61
Q

Cardiotoxicity occurs at QRS levels of greater than

A

> 160ms

62
Q

What do we give for QRS increase?

A

Sodium bicarbonate

Toxicology (3 decks)

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