Neuropsych Objectives Deck Flashcards
Serotonergic system
Conversion:
Tryptophan to 5-HT (serotonin)- released via vesicles to 5-HT receptor
Noradrenergic system
Conversion:
Tyrosine to DOPA to DA to Norepinephrine
Packaged in vesicles and released to bind adrenergic receptors_ a-1 a-2 beta-1 and beta-2
NE metabolism in the synapse is via MAO or COMT (catechol-O-mthyltransferase
Dopaminergic System
Dopamine is intermediary in synthesis of norepi- so similar cascade but with dopamine transporters and receptors
Tricyclic antidepressants
MOA
Kinetics
Adverse effects/Anesthesia implications
Pre and post synaptic effects on receptors or serotonin and norepinephrine
Large Vd, 50% first pass, hepatic metabolism
Anticholinergic effects
Increased arrhythmogenicity
Tachycardia/prolonged Qt
Exaggerated response to indirect acting sympathomimetics
Selective Serotonin Reuptake Inhibitors
MOA
Kinetics
Adverse effects/Anesthesia implications
5-HTT inhibition
Hepatic metabolism, all have active metabolites
Half life ~24hrs
QTc prolongation
Inhibit platelet aggregation, increased bleeding
Serotonin syndrome-can mimic MH
Monoamine Oxidase Inhibitors
Irreversible binding to MAO for about 2 weeks
Avoid tyramine
Can cause HTN crisis with ephedrine
Avoid phenylpiperidines (MEPERIDINE) due to weak serotonin reuptake inhibition
First generation antipsychotics
Blockade of D2 receptors
Often used for anti-emetic or sedative effects
Ex.
Prochlorperazine (compazine)
Promethazine (phenergan)
Chlorpromazine (Thorazine)
Haloperidol (haldol)
Droperidol (Inapsine)
Metoclopramide (reglan)
Extrapyramidal symptoms
Movement disorders
Dystonia
Akathesia
TD
Pseudoparkinsonism
Dystonia
Acute head/neck spasms
Single dose
Reversible with Anticholinergic
Akathesia
Restlessness
Single dose
Give Anticholinergic or benzo to quell anxiety
Pseudoparkinsonism
Takes several weeks to develop
Generally responsive to anticholinergics
Don’t give dopamine antagonists in a dopamine disorder!!! Will exacerbate symptoms of Parkinson’s
Tardive dyskinesia
Worm like movement
Typically from long term therapy
Often irreversible and anticholingerics may worsen
Same with D2 antagonists
Neuroleptic Malignant Syndrome
Triggered by first generation antipsychotics
Hyperthermia, muscle rigidity, severe metabolic syndrome (acidosis/hyperkalemia), HTN/tachycardia, AMS
Rhabdo in severe cases
Dantrolene & supportive care
As well as dopamine agonists (bromocriptine)
Neuromalignant Syndrome Vs Serotonin syndrome
NMS- takes time to develop (days instead of hours), diminished reflexes
SS- hyperreflexia
Lithium
Adverse effects
Drug interactions
Anesthesia concerns
Narrow therapeutic index
Weight gain
DI
Nephro/neurotoxic
Increased blood levels of thiazide diuretics, ACEIs, ARBs and NSAIDs
Prolongs all paralytics, avoid NSAIDs