Notes Case

Study Guide for Psychopharmacology Test 4

Schizophrenia

* Hallucinations

* Catatonia

* Multiple Personality Disorder (Different from Schizophrenia)

* Person vs. reality (Main difference for MPD)

* Paranoia

* Compulsions

* Delusions

* Often not harmful, more personal distress than public danger break with reality → usually auditory hallucinations, same visual.

* Positive and negative symptoms

* Positive- having something "normal" people don't have (ex. catatonia)

* Negative- missing something "normal" people have (ex. absence of emotions)

* Acute vs. Chronic Schizophrenia

* Acute- bad experience (ex. Trauma)

* Chronic- starts in childhood as personality disorder

* Onset for acute schizophrenia is late teens to early 20's

* Combination of 6 different disorders chronic and acute symptoms

* diathesis-stress

○ combination of genetic and the environment

○ causes of schizophrenia

● excess of dopamine

* Dopamine Hypothesis

○ L-dopa overdose can cause schizophrenia symptoms (positive schizophrenia). Adding l-dopa precursor to dopamine much in synaptic gap makes receptors habituate and need more and more

○ Excess cocaine  blocks dopamine reuptake, increases dopamine. Psychosis.

○ Amphetamine induced psychosis

■ More dopamine in amphetamine because pump dopamine out of neuron in cleft.

○ Decrease dopamine symptoms- D2 receptor blocker, 5 categories of dopamine receptors. Decrease dopamine decreases schizophrenia

* Dopamine hypothesis is incorrect... Therapeutic delay in Thorazine

○ 2-3 weeks for symptoms to decrease

○ ADHD- too much dopamine reuptake, not enough dopamine schizophrenia not due to dopamine neurotransmitter

○ Takes too long, delay can mean something else may be going on

○ Not because of dopamine itself but more to do with receptors

* Dopamine receptor hypothesis

○ Too much dopamine in cleft  post synaptic receptors down regulate (desensitize) block same D2 receptors, rest of receptors up-regulate (increase sensitivity)  change due to genetic expression changes new receptors, proteins have higher affinity for dopamine.

○ A decrease in glutamate can cause positive symptoms of schizophrenia

○ Induced abnormality of low sensitivity

○ Adaptation- solution for local problem (not necessarily good)

○ Not just dopamine levels, receptors change glutamate blockers can cause symptoms, PCP induced symptoms. *PCP is a glutamate blocker*

○ Receptor reaction from high dopamine levels damage to glutamate neurons from environmental stress.

* Mechanism for ADHD

○ Low dopamine in frontal lobes, lead to hypodopamine  lack of inhibition, hypofrontality

○ Negative symptoms form cell death

* Mass of the human head is made up of:

○ Ventricles- cerebrospinal fluid filled with cushion and buoyancy

○ Head= Brain matter + ventricles

○ VERY BAD to have large ventricles  less brain cell death in negative schizophrenia positive and negative symptoms

○ Large ventricles of cell death in frontal lobes, high level of dopamine cause of frontal lobe cell death?

* Types of Schizophrenic Drugs

○ Thorazine- binds to fat cells, orally, 2 day half-life, slow, not high abuse potential, anti-fun, people less reinforceable, no withdrawal, no addiction

○ Tardive dyskinesia- late appearing movement disorder. Side Effect for some treatments of schizophrenia. Post-synaptic receptors upregualate too much. Hypersensitive in motor systems, NO TREATMENT

○ Haldol- rapid, shorter therapeutic delay, for acute schizophrenia, briefer treatment, excelevates everything (tardive dyskinesia develops faster)- compresses EVERYTHING  timing wise, helps treat symptoms quickly but also speeds up TD.

○ Atypical anitpsychosis- (ex. Clorapine, Clozaril)- blocks D4 receptors instead of D2, blocks same serotonin receptors, treats both positive and negative symptoms, doesn't cause tardivive dyskinesia.

○ Thocazine blocks Ach. Receptors (deals with muscles.. Makes sense) This is a side effect of atypical antipsychotic

○ Agranulocytosis-death of white blood cells from clozapine, damages immune system.

○ There are two choices when using these drugs; either have a musucle disorder or no immune system.

○ Risperidone (Risperdal)  blocks D4, antipsychotic, causes heart problems, weight gain, don't cause agranulocytosis

Depression

* Lasts for a very long time, and interrupts your life

* Identical twins are more likely to have it so there is a strong belief in concordance

○ The probability that if you find something in one person you find it in another person. Usually suggests that depression is genetic

* Monoamine Hypothesis

○ Not enough serotonin and or not enough nonephrienphrene

○ If we deplete someone's serotonin  the person gets depressed

* Neurotransmitters that deal directly