Lecture 10 - Antidepressants Flashcards
(49 cards)
MAOIs:
___ weeks before new enzyme is synthesized
2
Describe the mechanism of MAO A inhibitor toxicity
- decreased amine degradation
- amphetamine-like effect + increased catecholamine release from intracellular vesicles
- decreased amine reuptake
- increased amine release
- tranylcypromine; GABA antagonism; metabolized to amphetamine
List the 4 phases of MAOI overdose
1) asymptomatic (latent) period
2) neuromuscular excitation and sympathetic hyperactivity
3) CNS depression and possible CV collapse
4) secondary complications for survivors
Describe:
1) Asymptomatic period
- delayed toxicity
- up to 6-12 hours
- monitor for 24 hours post ingestion
Describe:
2) Neuromuscular excitation and sympathetic hyperactivity
- 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
Describe:
3) CNS depression and possible CV collapse
hypotension
What is the treatment for MAOi overdose?
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
What foods do you want to avoid with MAOi inhibitors?
Foods with high tyramine content:
- all aged cheese
- alcohol
- fish
- meat
- ripe fruit
- yeast extracts
- sauerkraut
- beans
Describe the cheese reaction
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
How do TCAs work?
- Block serotonin and NE reuptake
- Block histamine, muscarinic, and alpha adrenergic receptors
List some cardiac effects of TCAs
- hypertension, tachycardia
- slowed cardiac conduction
- antiarrhythmic properties
- orthostatic hypotension
What patients are at a higher risk for CV effects when taking TCAs?
- elderly
- CV disease
- drug interactions that cause increased levels
- overdose
What are central anticholinergic side effects of TCAs?
- agitation
- hallucinations
- confusion
- sedation
- coma
- seizures
What are some peripheral anticholinergic side effects of TCAs?
- hypertension
- tachycardia
- hyperthermia
- mydriasis (dilated pupils)
- dry, flushed skin
- decreased GI motility (constipation)
- urinary retention
What are CV toxic effects of TCAs?
- intraventricular conduction delay (QRS prolongation)
- sinus tachycardia
- ventricular arrhythmias
- hypotension
What are CNS toxic effects of TCAs?
- coma
- delerium
- myoclonus
- seizures
What are other toxic effects of TCAs?
- hyperthermia
- ileus (lack of movement in intestines that can lead to blockage which means no food, liquid, or gas can get through)
- urinary retention
What are risk factors that will increase the risk of TCA toxicity?
- pre-existing heart condition
- electrolyte abnormalities (particularly K+)
- hepatic insufficiency
- stimulant drug use
- multiple drugs that increase QT intervals
- increase dosage
Describe the general management of TCA overdose?
- Airway if needed; IV line; cardiac monitoring, EKG
- Decreased LOC; O2, dextrose, naloxone, thiamine, order ABGs
- Stomach lavage
- Charcoal 50-100 g + cathartic
What dose of TCAs are usually considered life-threatening?
10-20mg/kg
Limit Rx of TCA to ___ if patient is suicidal
1 gram
symptoms of TCA can occur from as little as ____ times their daily dose
3-4 times
most common cause of death in TCA overdose?
refractory hypotension
What is Tx for orthostatic hypotension?
- intravascular volume expansion
- sodium bicarbonate, vasopressors (NE) or isotropes (dopamine)
- correct hyperthermia, acidosis, seizures
