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Year 4 - Toxicology > Lecture 10 - Antidepressants > Flashcards

Lecture 10 - Antidepressants Flashcards

1
Q

MAOIs:

___ weeks before new enzyme is synthesized

A

2

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2
Q

Describe the mechanism of MAO A inhibitor toxicity

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

List the 4 phases of MAOI overdose

A

1) asymptomatic (latent) period
2) neuromuscular excitation and sympathetic hyperactivity
3) CNS depression and possible CV collapse
4) secondary complications for survivors

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4
Q

Describe:

1) Asymptomatic period

A
  • delayed toxicity
  • up to 6-12 hours
  • monitor for 24 hours post ingestion
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5
Q

Describe:

2) Neuromuscular excitation and sympathetic hyperactivity

A
  • hypertension
  • hyperreflexia
  • hyperthermia
  • diaphoresis (sweating)
  • tremor
  • myoclonus
  • seizures
  • rigidity
  • agitation

*when treating HTN, treat with short-acting agents so you can readily reverse if they suddenly become hypotensive

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6
Q

Describe:

3) CNS depression and possible CV collapse

A

hypotension

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7
Q

What is the treatment for MAOi overdose?

A

Severe hypertension: use a short acting agent
Arrhythmias: use standard antiarrhythmics
Hypotension: DIRECT acting vasopressors; start low
Charcoal
Hyperthermia: treat aggressively
Rigidity: benzos, dantrolene, to prevent rhabdomyolysis

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8
Q

What foods do you want to avoid with MAOi inhibitors?

A

Foods with high tyramine content:

  • all aged cheese
  • alcohol
  • fish
  • meat
  • ripe fruit
  • yeast extracts
  • sauerkraut
  • beans
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9
Q

Describe the cheese reaction

A

Hypertensive crisis:

  • indirect acting amines
  • direct acting do not require MAO for their metabolism
  • catabolized by COMT

Tyramine: a major dietary amine; indirect acting agonist

Peripheral effects (doesn’t cross BBB)

Causes NE release from peripheral noradrenergic neurons

Normally, little absorbed
-dietary amine is metabolized by GI MAO-A

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10
Q

How do TCAs work?

A
  • Block serotonin and NE reuptake

- Block histamine, muscarinic, and alpha adrenergic receptors

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11
Q

List some cardiac effects of TCAs

A
  • hypertension, tachycardia
  • slowed cardiac conduction
  • antiarrhythmic properties
  • orthostatic hypotension
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12
Q

What patients are at a higher risk for CV effects when taking TCAs?

A
  • elderly
  • CV disease
  • drug interactions that cause increased levels
  • overdose
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13
Q

What are central anticholinergic side effects of TCAs?

A
  • agitation
  • hallucinations
  • confusion
  • sedation
  • coma
  • seizures
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14
Q

What are some peripheral anticholinergic side effects of TCAs?

A
  • hypertension
  • tachycardia
  • hyperthermia
  • mydriasis (dilated pupils)
  • dry, flushed skin
  • decreased GI motility (constipation)
  • urinary retention
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15
Q

What are CV toxic effects of TCAs?

A
  • intraventricular conduction delay (QRS prolongation)
  • sinus tachycardia
  • ventricular arrhythmias
  • hypotension
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16
Q

What are CNS toxic effects of TCAs?

A
  • coma
  • delerium
  • myoclonus
  • seizures
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17
Q

What are other toxic effects of TCAs?

A
  • hyperthermia
  • ileus (lack of movement in intestines that can lead to blockage which means no food, liquid, or gas can get through)
  • urinary retention
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18
Q

What are risk factors that will increase the risk of TCA toxicity?

A
  • pre-existing heart condition
  • electrolyte abnormalities (particularly K+)
  • hepatic insufficiency
  • stimulant drug use
  • multiple drugs that increase QT intervals
  • increase dosage
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19
Q

Describe the general management of TCA overdose?

A
  • Airway if needed; IV line; cardiac monitoring, EKG
  • Decreased LOC; O2, dextrose, naloxone, thiamine, order ABGs
  • Stomach lavage
  • Charcoal 50-100 g + cathartic
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20
Q

What dose of TCAs are usually considered life-threatening?

A

10-20mg/kg

21
Q

Limit Rx of TCA to ___ if patient is suicidal

A

1 gram

22
Q

symptoms of TCA can occur from as little as ____ times their daily dose

A

3-4 times

23
Q

most common cause of death in TCA overdose?

A

refractory hypotension

24
Q

What is Tx for orthostatic hypotension?

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

How do you treat the confusion, agitation or hallucinations of TCA toxicity?

A
  • supportive therapy

- benzos

26
Q

Coma in TCA toxicity usually resolve in ___ hours

A

24

27
Q

Describe the characteristics and treatment of seizures due to TCA toxicity?

A

Seizures are usually brief but often occur immediately before cardiac arrest.

  • acidemia from seizures may predispose to arrhythmias
  • usually responsive to IV benzos; midazolam infusion
  • refractory: barbiturates or propofol
  • phenytoin no longer recommended; pro arrhythmic, limited efficacy
28
Q

________ are contraindicated in TCA toxicity

A

antiarrhythmics

29
Q

TCAs are highly ______

A

lipophilic

30
Q

How does a lipid rescue or lipid emulsion work in TCA toxicity or local anesthetic poisoning?

A

Lipid sink: sequesters TCA into blood and it doesn’t reach the receptors to produce an effect

31
Q

How long should you treat for in an OD situation?

A

at least 2 half lives

32
Q

Which TCA is the worse for fatal toxicity?

A

Amitriptyline

33
Q

Venlafaxine (SNRI):

What overdose symptoms have been reported?

A
  • seizures (all with seizures ingested equal to or greater than 900mg)
  • hypotension
  • sinus tachycardia
34
Q

compare venlafaxine toxicity to TCA toxicity

A
  • more seizures in Venlafaxine Toxicity
  • Velafaxine NOT less likely to prolong QRS than TCAs
  • coma was less likely with venlafaxine
  • serotonin toxicity more common with venlafaxine
  • TCA overdoses are more likely to be unconscious and require ICU admission
35
Q

List 3 things for safety points regarding venlafaxine

A
  • Seizures in overdoses
  • Serotonin syndrome (MAOIs, SSRIs, triptans)
  • BP increases (dose-dependent and usually reversible)
36
Q

What type of patients is venlafaxine CI in ?

A

Relatively CI in patients:

  • high risk of OD
  • with pre-existing seizures and cardiac disease
37
Q

What type of patients should you watch venlafaxine in?

A
  • subjects who are poor CYP 2D6 metabolizers

- concomitant drugs which inhibit CYP 2D6

38
Q

What is the active metabolize of venlafaxine?

A

desmethylvenlafaxine

39
Q

Describe toxicity of desmethylvenlafaxine (Pristiq)

A
  • minor effects with mild hypertension and tachycardia
  • risk of seizures or serotonin toxicity is low
  • generalized seizures occurred in 5%
  • none had abnormal QT or QRS
40
Q

Signs and symptoms of duloxetine (SNRI) toxicity

A
  • somnolence
  • serotonin syndrome
  • seizures
  • vomiting
  • risk of QRS prolongation + arrhythmias is low
41
Q

What are SSRI toxic effects?

A
  • tremor
  • sinus tachycardia
  • n/v/d
  • obtundation (altered level of consciousness)
  • seizures
  • serotonin syndrome
  • mild bradycardia can occurring OD
42
Q

Treatment of SSRI toxicity

A

charcoal + supportive care

43
Q

Treatment of serotonin syndrome

A
  • supportive care
  • use benzos for neuromuscular symptoms
  • use tylenol and cooling blankets for increased temp
  • dantrolene for severe rigidity

For severe symptoms:

  • cyproheptadine
  • 5-HT antagonism
  • watch anticholinergic and antihistaminic properties
44
Q

Describe the presentation of serotonin syndrome

A
  • agitation
  • confusion
  • hypomania
  • diaphoresis
  • diarrhea
  • fever
  • shivering
  • incoordination
  • tremor
  • hyperreflexia
  • myoclonus
45
Q

Describe the cardiac toxicity related to citalopram

A
  • dose-related QT prolongation (high-risk in metabolic disturbance and pre-existing cardiac disease)
  • potential increased risk of tornadoes de pointes
46
Q

What is the max dose?

A

40mg/day

*20mg/day in elderly or hepatic impairment

47
Q

Bupropion may cause _____ or _______

A

tachycardia or seizures

48
Q

How does mirtazapine work?

A
  • increased serotonin and NE + serotonin blocker
  • mild-moderate anticholinergic
  • antihistamine effects
49
Q

Does mirtazapine cause cardiac probs?

A
  • no cardiac effects
  • no QTc prolongation
  • no seizures
  • no serotonin toxicity

Year 4 - Toxicology (24 decks)

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