Week 15 Neuro Flashcards
symptoms of serotonin syndrome
Mild - HTN, tachycardia, shivering, tremor, hyperreflexia
Moderate - all + hypothermia, hyperactive bowels, mild agitation
Severe - all+ hyperthermia, dramatic swings in HR/BP, delirium, muscle rigidity
how long does it take to see physical improvements with antidepressants?
2 weeks
how long does it take to see emotional improvements with antidepressants?
6-8 weeks
can you stop antidepressants at any time?
no, need to be tapered off to avoid withdrawal symptoms
what should be monitored with antidepressants?
DDI, anticholinergic effects, suicide risk
selective serotonin reuptake inhibitor (SSRI) MOA
inhibit reuptake of serotonin in CNS
selective serotonin reuptake inhibitor (SSRI) AE
HA, N/V/D, insomnia, sexual side effects
- less anticholinergic and CV effects
serotonin/NE reuptake inhibitor (SNRI) MOA
inhibit reuptake of serotonin and NE in CNS
serotonin/NE reuptake inhibitor (SNRI) AE
HA, nausea, dry mouth, sweating, sexual dysfunction, insomnia
SSRI drugs
Citalopram (Celexa) and Escitalopram (Lexapro)
SNRI drugs
Venlafaxine (Effexor) and Duloxetine (Cymbalta)
Bupropion MOA
inhibit NE and dopamine reuptake
Bupropion AE
HA, nausea, significant insomnia, tremor, dry mouth, decrease appetite
- risk of seizures
TCA MOA
inhibit reuptake of serotonin and NE in CNS
TCA AE
anticholinergic effects, weight gain, sexual dysfunction, sedation, hypotension
- serious risk of OD - monitor CV
MAO inhibitors MOA
increase serotonin, NE and dopamine by inhibiting MAO enzyme
MAO AE
OH, weight gain, sexual dysfunction
- high risk for serotonin syndrome
Benzos/Xanax MOA
bind BZD receptors on GABA channels to enhance GABA inhibitory effects
Benzos/Xanax AE
sedation, ataxia, memory issues
Buspar AE
dizziness
benefits to buspar over xanax
no risk of abuse, no withdrawal symptoms
disadvantages to buspar
dizziness
~ 3 weeks to see improvement, metobilized by CYP 3A4 so potential DDI
difference between 1st generation and 2nd generation antipsychotics
FGA - typical, before 1990, neuroleptics due to more frequent neurologic AE
SGA - atypical, after 1990, less extrapyramidal symptoms and tardive dyskinesia
FGA MOA
block D2 receptors in mesolimbic tract where excess dopamine may contribute to positive sx
SGA MOA
block D2 receptors but less than FGA; more affinity for histamine
D2 receptor blockade AE
akathisia, tremor, rigidity, bradykinesia, tardive dyskinesia
H1 receptor blockade
sedation, weight gain
muscarinic receptor blockade
anticholinergic
a1 receptor blockade
hypotension, dizziness, syncope, reflux tachycardia
rehab concerns for FGA agents
patient at risk for cardiac abnormalities, tachycardia, arrhythmia
rehab concerns for SGA agents
significant weight gain, hyperglycemia, and lipid abnormalities
Lithium AE
GI (N/V/D), weight gain, polydipsia (thirsty), polyuria, decrease memory, concentration, CNS issues
- toxicity
