Chapter 15: psych Flashcards
which receptors are blocked by antipsychotics
cholinergic
muscarinic
histamine
dopamine
antipsychotic action
comes from blocking of CNS dopamine receptors in the mesocorttical/mesolimbal systems in the brain
EPS is the result of
dopamine blocking in other parts of the body
EPS
parkinson-like syndrome usually occuring with both classes of antipsychotics as a result of years of exposure
symptoms of EPS
dystonia usually occurs within first 5-30 days
tardive dyskkinesia after 6 months (can be reversible)
rhythmic tongue protrusion, puffing cheeks, puckering of mouth
neuroleptic malignant syndrome (NMS)
life-threatening
starts months after therapy begins but rapidly progresses
treatment of NS
rapid d/cof agent and administration of dantrolene to relax muscles
how should antipsychotic therapy be discontinued
slowly reduce dose over 2-3 weeks
first generation antipsychotics (typical)
phenothiazines
examples of phenothiazines
haloperidol (Haldol)
trifluoperazine (Stelazine)
chlorpromazine (Thorazine)
second generation antipsychotics (atypicals)
aripiprazole (Abilify)
risperidone (Risperdal)
Olanzapine (Zyprexa)
largest group of psychotropic agents
phenothiazines
phenothiazine mechanism of action
unknown
theorized that it is a result of dopamine blockage in certain areas of CNS
effects of long term phenothiazine usage
cardiac arrythmia
hyperlexia (life-threatening)
HTN
rigidity
tardive dyskinesia
clinical uses of phenothiazines
acute, idiopathic psychotic illness marked by agitation
manic phase of bipolar disorder
schizophrenia
phenothiazines interactions
- alcohol (CNS depression)
- anticholinergics (increased anticholinergic effects)
- amphetamines (decrease antipsychotic effect)
- antiparkinson drugs (antagonize antipsychotic effect)
- hypoglycemics (weaken control of diabetes)
- lithium (decreases antisychotic effect)
phenothiazines contraindications
parkinsonism
blood dyscrasia
severe liver impairment, cardiac disease, or CNS depression
Reye’s syndrome
overdose of phenothiazines
fairly common but not fatal
symptoms: worsening CNS depression, hypotension, worsening of EPS
why are atypical antipsychotics considered atypical
hey do not cause EPS, tardive dyskinesia, or elevate prolactin levels
what is the only atypical antipsychotic with clear evidence of efficacy in treatment-resistant schizophrenia
clozapine (Clozaril)
black box warning for all antipsychotics
may increase mortality in elderly with dementia-related psychosis
Clozaril places at increased risk for
agranulocytosis, aeizures, and myocarditis
clinical uses for atypical antipsychotics
psychosis in patients with schizophrenia
depression or mania with psychotic features
bipolar disorder
severe agitation and delusions in dementia patients
when are antipsychotic medications used
psychotic episodes when tranquilizing effect is needed
Tourette’s (pimozide)
examples of atypical antipsychotics
- aripiprazole (Abilify)
- asenapine (Sapris)
- clozapine (Clozaril)
- iloperidone (Fanapt)
- lurasidone (Latuda)
- olanzpine (Zyprexa)
- olanzapine/fluoxetine (Symbyax)
- palpiperidone (Invega)
- quetiapine (Seroquel)
- risperidone (risperdal)
- ziprasidone (Geodon)
atypical antipsychotic interactions
any drug requiring liver metabolism (including alcohol)
atypical antipsychotic contraindications
liver impairment
drug classes used for depression
MAOIs (Monoamine oxidase inhibitors)
TCAs (tricyclic antidepressants)
SSRIs (selective serotonin reuptake inhibitors)
non-TCA Antidepressants
examples of third line MAOIs
tranylcypromine (parnate)
selegiline (Emsam)
phenylamine (Nardil)
RARELY USED ANYMORE
MAOI mechanism of action
irreversible, non-selective inhibitors of MAO in its CNS storage sites
depression relief immediately or within 1 week
HTN crisis with MAOIs can be precipitated by
foods rich in tyramine (alcohol, aged cheese)
sympathomimetic drugs (cough meds containing ephedrin)
tricyclic antidepressants
what herb can cause life-threatening serotonin syndrome when taken with MAOI
St. John’s wort
MAOI contraindication
liver impairment
wash out period when witching from MAOI to SSRI
2 weeks
foods high in tyramine
aged cheese, beer, wine, pickled products, liver, raisins, bananas, figs, avocados, chocolate, yogurt, meat tenderizer
second line tricyclic antidepressants (TCAs)
mechanism of action
blocks neuronal reuptake of norepinephrine and serotonin at presynaptic terminus
has anticholinergic properties
ability to increase mood poorly understood as they do not stimulate the CNS
how long to clinical effect of TCAs
2-8 weeks
clinical uses of TCAs
endogenous depression
reactive depression
depression r/t alcohol/cocaine withdrawal, anxiety, neuropathic pain, enuresis, OCD
examples of TCAs
- amitriptyline (Elavil)
- clomipramine (Anafril)
- doxepine (Silenor)
- imipramine (Tofranil)
- trimipramine (Surmontil)
- amoxapine (Asendin)
- desipramine (Norpramin)
- nortriptyline (Pamelor)
- protriptyline (Vivactil)
TCA interactions
any anticholinergic or barbituate, chlorpropamide, cimetidine, clinodine, epinephrine, ethanol, fluoxetine, neuroleptics, norepinephrine, propoxyphene, quinidine, and SSRIs