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Antidepressants Flashcards

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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
How do we manage Seizures due to SSRC toxicity/
Bzds
26
How do we manage cardiac abnormalities due to SSRI toxicity?
sodium bicarbonate
27
What is the job of the MAOI?
Degrades the serotonin reuptake neurotransmitters, Allowing for an accumulation of drug.
28
How do we manage torsades de pointes due to SSRI toxicity?
magnesium sulfate
29
How do we manage serotonin sybndrome?
cyproheptadine: competitive binding to serotonin receptor = cooling and treatment of muscular rigidity
30
What time frame can we use SDAC for SSRI toxicity management?
Most benefit within 1-2 hours
31
Which SSRI should we know?
Citalopram, escitalopram
32
Which SNRI should we know ?
Venlafaxine
33
Which TCA should we know?
Amitriptyline
34
Is hemodialysis effective in the management of SSRI toxicity?
No because of the high Plasma-plasma binding and volume of distribution
35
What toxicity can occur due to venlafaxine?
Seizure, tachycardia, ECG abnormalities, and serotonin toxicity
36
Bupropion can be used for smoking cessation true or false?
True
37
What is key in successful management of TCA toxicity?
Early identification
38
Progression of clinical toxicity (Via TCA) is ___ and may be ___
unpredictable, rapid
39
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 ____ ”
life-threatening cardiovascular and CNS toxicity within hours.
40
TCA have ___ on gastric emptying
Anticholinergic effect
41
TCAs wit ha greater anticholinergic effect causes ___Perfusion and ___motility of GIT leading to ___ emptying
hypo, hypo, delayed
42
TCAs are ___philic and ___ distributed
Lipo, widely
43
Do TCAs have a high or low PPB?
High
44
What in general metabolized TCA?
Multiple CYPS
45
What are some other things to consider in terms of antidepressants?
Genetic polymorphisms in the Cyp2D6 metabolite
46
Dose ingested and plasma concentration are a poor predictor of outcome. What are the toxic concentrations thought with regards to TCAs?
5-20mg/kg`
47
What are the S/S of toxicity via TCA
Cardiotoxic symptoms show Rapid progression * Onset often within 2 hours of ingestion
48
What is very important with regards to TCA toxicity/
Early ECG is very important
49
What is the S/S of toxicity relating to respiratory and TCAs?
Aspiration Acute respiratory distress syndrome Hypoexmia
50
How is TCA toxicity diagnoised?
serum TCA levels, ECG * Severity of toxicity is best reflected by ECG, not serum levels*
51
What other labs are measured for TCA toxicity>
Lytes, glucose, arterial blood pH
52
With regards to the QRS interval what should we be watching for with regards to TCA toxicity>?
53
How do we manage dysrhythmias?
Sodium bicarbonate
54
What is the MOA of sodium bicarb for dysrhythmias?
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
If dysrhythmias continue what is the next thing we can treat with?
Lidocaine (lidocaine is a blocker of Na+ and K+ channels) Hypertonic salien Magnesium sulfate
56
What is a no with regards to dysrhythmic management?
57
What do we use for seizure management with regards to TCAS?
Bzds, sodium bicarbonate
58
TCAs block ___
sodium channels leading to Qt prolongation
59
Is hemodialysis effective for managing TCA toxicity?
No because high Vd, and and protein bound
60
What may be a an antidote for TCAs?
Intravenous lipid emulsion (ILE)
61
Cardiotoxicity occurs at QRS levels of greater than
>160ms
62
What do we give for QRS increase?
Sodium bicarbonate

Toxicology (3 decks)

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