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Toxicology Final > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

____ weeks before new MOA A and B are synthesized

A

2 weeks

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2
Q

What is the mechanism of MOA A inhibitor toxicity

A
  • decreased amine degradation
  • amphetamine like effect and increased catecholamine release from intracellular vesicles
  • decreased amine reuptake
  • increased amine release
  • tranylcypromine; GABA antagonism; metabolized to amphetamine
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3
Q

What are the 4 phases of MOA A overdose

A
  1. asymptomatic (latent)
    - up to 6-12 hours
  2. neuromuscular excitation and sympathetic hyperactivity
    - hypertension
    - tremor
    - hyperreflexia
    - hyperthermia
    - diaphoresis
    - seizures
    - rigidity
  3. CNS depression and possible CV collapse
    - hypotension
  4. secondary complications for survivors
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4
Q

What is the tx of severe hypertension with MAO overdose

A

a short acting agent

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5
Q

What is the tx of arrhythmias associated with MAO overdose

A

standard antiarrhythmics

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6
Q

What is the tx of hypotension associated with MAO overdose?

A
  • direct acting vasopressors- start low
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7
Q

What is the tx of rigidity associated with MAO overdose

A

benzos, dantrolene, to prevent rhabdomyolysis

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8
Q

What foods should be avoided with MAO inhibitors

A
  • cheese
  • alcoholic beverages
  • fish
  • meat
  • fruit (overripe, banana peels)
  • yeast extracts
  • sauerkraut
  • beans
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9
Q

What is the cheese reaction?

A
  • hypertensive crisis (indirect acting amines, direct acting do not require MAO for their metabolism; catabolized by COMT)
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10
Q

What is tyramine?

A
  • a major dietary amine

- indirect acting agonists

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11
Q

Does tyramine cross the BBB

A
  • no
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12
Q

What is the effect of tyramine?

A
  • causes NE release from peripheral noradrenaline neurons
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13
Q

What is the mechanism of action of TCAs?

A

blocks 5HT and NE reuptake

- also reputes histamine, muscarinic and alpha adrenergic receptors

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14
Q

In usual doses, what is the cardiac effects of TCAs?

A
  • hypertension, tachycardia
  • slowed cardiac conduction
  • antiarrhythmic properties
  • orthostatic hypotension
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15
Q

What are the high risk patients for TCA overdose?

A
  • elderly
  • cardiovascular disease
  • drug interactions
  • overdose cases
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16
Q

What are the central anticholinergic effects of TCAs?

A
  • agitation
  • hallucinations
  • confusion
  • sedation
  • coma
  • seizures
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17
Q

What are the peripheral anticholinergic effects of TCAs?

A
  • hypertension
  • tachycardia
  • hyperthermia
  • mydriasis
  • dry, flushed skin
  • decreased GI motility
  • urinary retention
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18
Q

What are the cardiovascular specific effects of TCAs?

A
  • intraventricular conduction delay
  • sinus tachycardia
  • ventricular arrhythmias
  • hypotension
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19
Q

What are the CNS effects of TCAs?

A
  • coma
  • delirium
  • myoclonus
  • seizures
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20
Q

What are the risk factors that increase the risk of toxicity of TCAs?

A
  • pre-existing heart condition
  • electrolyte abnormalities
  • hepatic insufficiency
  • stimulant drug use (concomitant stimulant drug use)
  • multiple drugs that increase QT intervals
  • increase drug dosage
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21
Q

What is the general management strategies for TCA overdose?

A
  • support airways
  • cardiac monitoring
  • EKG
  • if decreased LOC: O2, dextrose, naloxone, thiamine, ABGs
  • stomach lavage
  • charcoal 50-100 g + cathartic
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22
Q

What is the life threatening dose of TCAs?

A
  • 10-20 mg/kg is considered life threatening
  • limit rx to 1 g if pt is suicidal
  • sx from as little as 3-4 times daily dose
23
Q

What is the most common cause of death with TCAs?

A
  • refractory hypotension (due to vasodilation or impaired cardiac contractility)
24
Q

What is the tx of orthostatic hypotension?

A
  • intravascular volume expansion
  • sodium bicarbonate, vasopressors or ionotropes (dopamine)
  • correct hyperthermia, acidosis, seizures
25
Q

What is given as tx for CNS toxic effects?

A
  • supportive tx

- benzos

26
Q

Coma usually resolves in ______

A

24 hours

27
Q

Acidemia from seizures may predispose to _______

A

arrhythmias

28
Q

What are seizures usually treated by?

A
  • IV benzos, midazolam infusion(if patients are actively seizing)
29
Q

What is used for refractory seizures?

A
  • barbiturates or propofol
30
Q

Are drug levels a good predictor of whether or not someone will have a seizure

A

NO

31
Q

What is the most common mechanism of death with cardiac toxicity?

A
  • myocardial depression, ventricular tachycardia, or ventricular fibrillation
32
Q

What is a good predictor of arrhythmias?

A
  • QRS duration (should be >0.10 s)
33
Q

_________ has a dramatic effect on narrowing QRS

A

sodium bicarbonate

this reduces arrhythmias and hypotension

34
Q

What is the mechanism of cardiac toxicity?

A
  • reductions of extracellular K or increase in extracellular Na
  • improves membrane responsiveness and increase conduction velocity
  • increase in serum pH may result in reductio of free TCA
  • unbound drug correlates with tissue uptake
35
Q

Describe a lipid rescue- lipid emulsion

A
  • TCAs= highly lipophilic
  • indication: refractory cardiotoxicity for overdoses of lipophilic medications
  • (TCAs, local anesthetic poisoning)
36
Q

How long should someone be monitored for in the ICU post TCA OD?

A
  • in the ICU for 12-24 hours after all sx are resolved
37
Q

What are the s/s of overdose with venlafaxine?

A
  • seizures, hypotension, sinus tachycardia
38
Q

Serotonin toxicity was _____ common with venlafaxine compared to TCAs

A

more

39
Q

Is blood pressure increases dose dependant with venlafaxine?

A
  • YES IT IS (risk increases with increased age)
40
Q

When is venlafaxine CI’ed in patients?

A

pre-existing seizures and cardiac diseases

41
Q

What is the normal half life of venlafaxine, and what can it be extended up to in overdose?

A

5 hours normally, 15 hours with toxicity

42
Q

What are the s/s associated with duloxetine overdose?

A
  • somnolence
  • serotonin syndrome
  • seizures
  • vomiting
43
Q

What is the risk of QRS prolongation and arrhythmias with duloxetine?

A
  • LOW
44
Q

What are the toxic effects of SSRIs?

A
  • tremor
  • sinus tachycardia
  • n/v, diarrhea
  • obtundation
  • seizures
  • serotonin syndrome
  • mild bradycardia may occur in OD as well
45
Q

What is the tx of antidepressant overdose?

A
  • charcoal and supportive care
46
Q

What are some of the causes of serotonin syndrome?

A
  • inhibition of breakdown of 5HT (MAO inhibitors)
  • blocking reuptake of 5HT (SSRIs, clomipramine, DM, meperidine, cocaine, venlafaxine)
  • 5HT precursors or agonists (lithium, bispirone, LSD)
  • enhance 5HT release (MDMA)
47
Q

What is the treatment 5HT syndrome?

A
  • supportive care
  • neuromuscular symptoms (benzos)
  • increased temp (tylenol, cooling blankets)
  • severe rigidity (dantrolene)
  • severe sx: cyproheptadine 4 mg po q4h
48
Q

What are the s/s of serotonin syndrome?

A
  • agitation
  • mental status changes (confusion, hypomania)
  • diaphoresis
  • diarrhea
  • fever
  • shivering
  • incorporation
  • myoclonus
  • tremor
  • hyperreflexia
49
Q

When should only 20 mg of citalopram be used?

A
  • 20 mg should only be used in the elderly and in those with hepatic impairment
50
Q

What is the safety profile of buproprion?

A
  • may cause sinus tachycardia but not usually associated with conduction abnormalities
51
Q

What is the MOA of mitazipine toxicity?

A
  • increased 5HT and NE + serotonin blocker
  • mild-moderate anticholineric
  • antihistamine effects
52
Q

Watch for ________ and ______ effects in overdose of mirtazapine

A

anticholineric and serotonergic

53
Q

What are the usual s/s of mirtazapine toxicity?

A
  • decreased LOC
  • tachycardia
  • hypertension
  • no QTc prolongation; no arrhythmias
  • NO seizures or serotonin toxicity

Toxicology Final (14 decks)

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