Flashcards in Schizo Deck (22):
Schizophrenia is a
chronic debilitating illness associated with deterioration in mental function and behavior (clearly involves a GENE BY ENVIRONMENT interaction, with no known social or environmental cause)
Prevalence of schizo in adults is; over time, patients with it can
undergo downward drift, where they had had psychosocially functional lives but then lost their wives, jobs, support network, etc (lower socioeconomic status)
In schizo, what is a hallmark symptom? You have an___ that could present as
impairment in reality testing;
1. alteration in sensory perceptions (hallucinations, or hearing voices)
2. Abnormalities in thought content (delusions, or fixed, false beliefs)
3. Abnormalities in thought process/organization (thought blocking and loose associations are the worst, with tangential being pretty bad as well)
For schizo, patients have at least; in contrast to delirium or substance abuse
one episode of psychosis with persistent disturbances of thought, behavior, appearance, speech and affect (emotion), along with impairment in occupational and social functioning (a break from reality!!) BAT, SOFA;
patients with no clouding of consciousness (alert and oriented, with memory and attention typically intact WHEN NOT PSYCHOTIC)
Major diagnostic criteria for schizo?
1. Need 2 of delusions, hallucinations, grossly disorganized or catatonic behavior, negative symptoms (flat affect, alogia, or avolition), or disorganized speech during a 1-month period
2. Social/occupational dysfunction (below level achieved prior to onset)
3. Continuous signs of the disturbance persisting for AT LEAST 6 MONTHS (should have at least one month of the active phase symptoms, and periods of prodromal or residual symptoms)
Key positive symptoms and what do they respond to in schizo?
Delusions, hallucinations, agitation, talkativeness, thought disorder; think ATYPICAL antipsychotic agents
Key negative symptoms and what do they respond to?
Amotivated/depressed, social withdrawal, flattened affect/emotion, cognitive disturbances, poor grooming, poor speech;
Residual schizo is; catatonic is
at least one psychotic episode with subsequent NEGATIVE symptoms, but mild positive symptoms if any;
stupor or extreme agitation with bizarre posturing and blank facial expression
Three phases of schizo
1. Prodromal (become antisocial, quiet, passive, or irritable; sudden interest in religion, patient in touch with reality)
2. Psychotic/Active (lose touch with reality and you will see positive symptoms
3. Residual (period b/w psychotic episodes; in touch with reality but still the NEGATIVE SYMPTOMS)
Random facts about etiology and maybe environmental factors?
1. Adoption and twin studies support genetics role
2. Increased risk with advanced paternal age
3. Gender differences (occurs equally in men and women, but men earlier than women)
4. Women respond better to antipsychotic meds, but greater risk of TD with D2 receptor blockade (see choreic movements);
5. Think viral infection and exposure to drugs
6. Think cold-weather months
7. Third-trimester maternal use of diuretics and malignant HTN requiring it
List the main neurological abnormalities associated with schizo:
1. Abnormalities of the frontal lobes (decreased use of glucose in the prefrontal cortex)
2. Ventricles (lateral and third) get larger
3. Changes in brain density (parahippocampal gyrus, amygdala, hippocampus)
4. Abnormalities in eye movement (poor saccadic smooth visual pursuit)
5. Abnormal cerebral symmetry (normally e.g. right frontal lobe > LFL)
What is the DA hypothesis for schizophrenia? Think about the tracts involved:
Excessive DA activity in mesolimbic tract;
Stimulant drugs like amphetamines and cocaine can cause PSYCHOTIC symptoms by amplifying mesolimbic tract, while there is hypoactivity of mesocortical dopamine tract/pathway leading to NEGATIVE symptoms
If one were to try and lower the amount of dopamine activated in the mesolimbic tract, what could occur?
Could have NIGROSTRIATAL issues, since lack of dopamine could now lead to tardive dyskinesia or Parkinsonian issues; without dopamine, that also means you had hypoactive mesocortical pathway to start with!!
How can we conceptualize the glutamate hypothesis?
If you have NMDA receptor protein defects on GABA interneurons (e.g. b/w cortical glutamate pyramidal neuron and its secondary neuron), you don't get inhibition of secondary neuron and you have increased firing in ventral tegmental area (VTA) to send more DA into LIMBIC system
With the mesolimbic system having more DA, one would see more ____ symptoms like; what is the pathway for seeing these symptoms?
positive; hallucinations, delusions, talkativeness, agitation, thought disorders;
Glu-GABA-Glu-DA (GABA interneuron not responding and can't inhibit secondary glutamate neuron, and it keeps firing leading to more DA release)
With the mesocortical system having ____ DA, one would see _____ symptoms in the context of schizo like; what is the pathway for seeing these symptoms?
less; negative; think poor grooming, poor speech, cognitive disturbances, social withdrawal, flattened affect, amotivation;
Glu-GABA-Glu-GABA-DA (Too much inhibition from the secondary GABA and less DA sent to the prefrontal cortex in the mesocortical pathway)
Out of the differential for schizo, list some causes?
1. Psychotic disorder caused by general med condition (B12/folate deficiency, corticosteroid induced, temporal lobe epilepsy)
2. Manic phase of BIPOLAR disorder
3. Substance-induced psychotic disorder (cocaine, ritalin, crystal meth, bath salts)
4. Other psychotic disorders
What are other psychotic disorders that could make one think about schizo?
1. Brief psychotic disorders (1-29 days of schizo symptoms)
2. Schizophreniform disorder (1-6 mos of symptoms)
3. Schizoaffective disorder (schizo + mania and/or depression)
4. Delusional disorder (JUST DELUSIONS)
5. Shared psychotic disorder (2 people share same delusion)
What meds can be used for schizo? SE's?
1. Think antipsychotics that block D2 receptors in mesolimbic DA pathway (usually traditional high- and low-potency TYPICAL FGA like haloperidol, chlorpromazine, etc)
2. However, they bind and stick to D2 receptors better and could cause more side effects in nigrostriatal (TD/Parkinsonism) and tuberoinfundibular (hyperprolactinemia) pathways
What meds are used for first line agents in schizo? Some patients will not take this drug: why and what can help their case?
1. ATYPICAL SGA to block 5HT2a receptors (pines, dones, aripiprazole; they have fewer negative effects like parkinsonism or tardive dyskinesia because 5HT2a blockade allows freer DA in NIGROSTRIATAL pathway)
2. Unpleasant side effects (fatigue, grogginess, sedation) and poor patient insight; so give INJECTABLE DEPOT forms like high potency FGA, or the dones and aripiprazole
Management of schizo includes:
1. Cognitive Behavioral therapy (help with executive dysfunction since mesocortical pathway is afffected so help with memory, concentration, planning, prioritizing)
2. Family therapy (decrease stress and risk of psychosis)
3. Peer and mentor support or social skills group