Schizophrenia Flashcards
Schizophrenia dx
2 or more of sx in significant percent of 1 month time period (less if treated) or only 1 sx if bizarre delusions or hallucinations
- social /occ dysfunction at least 6 months, incl 1 month of sx (unless txd)
Duration of sx for schizophreniform vs brief psychotic episode
Brief psychotic episode 1 day to 1 month (with return to preempt of function)
Schizophreniform disorder 1 month to 6 months
Schizoaffective disorder dx
Sx similar to schizophrenia
Plus underlying affective component to disorder - either mania depression or mixed episode
- residual sx may be less severe and less chronic than in schizophrenia
- must be mood episode concurrent with sx meeting criterion A for schizophrenia
Schizophreniform disorder dx
Sx similar to schizophrenia but duration of illness is at least 1 month to max of 6 months
- therefore social or Occupational functioning impairment is not a dx requirement (6 month req)
Onset sx of schizophrenia
Can be abrupt or insidious but
Prodromal phase usually characterize by NEGATIVE sx
Pathophysiology of schizophrenia - dopamine
Dopamine - hyperactivity in limbic system leading to positive sx
Dopamine - hypo functioning in prefrontal cortex leading to negative sx
Pathophysiology of schizophrenia - serotonin 5-HT
Serotonin -increase in serotonin transporter density in subcortical regions no change in cortical regions
Use of 5-HT antagonists leads to increased dopamine release in prefrontal cortex
Pathophysiology of schizophrenia - glutamate and NDMA
Glutamate corticostriatal pathway inhibits dopamine function in ventral striatum - deficiencies in glutamate produce sx similar to dopamine hyperactivity
NMDA - receptor dysfunction may play a role - use of NMDA antagonists leads to positive sx by increasing dopamine release in limbic areas and reducing dopamine release from ventral tegumental area leading to negative sx
ACT
Non pharm tx of schizophrenia
Assertive Community Treatment
**shiwn to reduce hospitalizations and homelessness among schizo pt
System of care with multidisciplinary team for persons at risk (repeated hospitalizations, homelessness)
Other non Pharm tx of schizo
Supported employment, skills training,
Cognitive behavioral therapy - may benefit but sustained relapse benefit has been difficult to sho
Token economy - involve particular behavioral interventions for patients based on social learning principles to address personal hygiene , social interactions, other issues
Family services- for both pt and family, shown to reduce relapse and re hospitalization in some pts,
Non pharm medical interventions for schizophrenia
Repetitive transcranial magnetic stimulation (rTMS)
- effective for acute tx of refractory auditory hallucinations - effects last 8-12 weeks - se include seizure and syncope
Electroconvulsive therapy (ECT)
- insufficient evidence for tx of core symptoms of schizophrenia - most efficacy may be seen if pt is catatonic or has depressive sx - se include anterograde and retrograde amnesia, status epilepticus, laryngospasm and peripheral nerve palsy
First gen high potency antipsychotics
Fluphenazine Haloperidol Pimozide (only FDA for Tourette's ) Trifluoperazine Thiothixene
Low potency antipsychotics
Chlorpromazine
Thioridazine
Chlo and Thio = Low
Mid potency antipsychotics FGA
Loxapine
Perphenazine
Dopamine tract effect when blocked: mesocortical (aka prefrontal cortex)
Worsening negative sx
Dopamine tract effect when blocked: Mesolimbic (basal ganglia)
Relief of positive sx
Dopamine tract effect when blocked: nigrostriatal (substantia nigra)
Extra pyramidal sx
Dopamine tract effect when blocked: tuberoinfundibular (hypothalamus)
Increase prolactin release
Antipsychotic effect mediated by what dopamine mechanism
Decrease in central dopaminergic transmission, likely related to blockade of post synaptic D2 receptors in Mesolimbic area and possibly mesocortical area
Maximal D2 blockade with how much haloperidol ?
2 to 5 mg
