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
Valproate (depakote)
Anticonvulsant
Hepatitis, pancreatitis
Thrombocytopenia and platelet dysfunction
Increased metabolism of NMBDs
Carbamazepine (tegretol)
Anticonvulsant
Hepatic, strong CYP inducer
Stevens-johnson syndrome (toxic epidermal necrolysis
SIADH (older adults)
Increased metabolism of NMBDs and midazolam/fentanyl/methadone/tramadol
Lamotrigine (lamictal)
Anticonvulsant
Sedation/dizziness
Severe dermatological reactions
Blood disorders
Increased sedation and increased metabolism of NMBDs
Amphetamine MOA/anesthesia considerations
Withdrawal syndrome if stopped abruptly
Unpredictable response to sympathomimetics-give direct acting -eg. vasopressin
May require more sedation
Levodopa
MOA
Kinetics
Anesthesia Implications
It is converted to dopamine within the CNS
Administered with AAAD inhibitor (carbidopa) to prevent dopamine accumulation in periphery
MUST BE CONTINUED during perioperative period, discuss schedule with patient-consider NG-instruct them to bring it with them to hospital
COMT inhibitors
Helps prevent metabolism of levodopa-prolongs action in PD patients
Pramipexole
MOA
Kinetics
Implications
Agonism of dopamine receptors
Excreted in urine up to 90% unchanged
Used as adjunct
No significant implications for anesthesia with a relatively long half-life
MG anticholinesterases evaluation/treatment
Edrophonium may be used for diagnostics due to short half-life
Pyridostigmine most often used to treat due to prolonged half-life
Interfere with NMBDs, prolong succ
Common anti muscarinic adverse effects with antidepressants
Xerostomia (dry mouth)
Urinary hesitancy
Decreased gastric motility
Blurred vision
Common MAOIs
Isocarboxazid
Linezolid
Methylene blue
Moclobemide
Phenelzine
Procarbazine
Rasagiline
SELEGILINE
Tranylcypromine
What states of a receptor can local anesthetics bind?
Open and inactivated states
NOT closed
Tertiary amines are selective for?
Serotonin
Secondary amines are selective for?
Norepinephrine
Which class of psych drugs do you stop 2 weeks before surgery?
Psych!
Don’t stop them work around them
What antiemetic agents do you avoid in Parkinson’s?
Dopamine antagonists!!
Which local is most cardio toxic?
Bupivacaine
Which psych drugs will cause an exaggerated response to ephedrine?
TCAs and MAOIs
Which drugs will cause there to be a blunted response to administration of ephedrine?
Methylphenidate and amphetamines
How many mls of 0.1% Bupivacaine can I give to a 95 kg patient?
Do the math bitch
Considerations in Myasthenia Gravis
-increased sensitivity to non-depolarizing NMBDs
Resistance to succinylcholine
