Chapter 15: Psychological Disorders Flashcards
Major depression
- Feeling sad and helpless for weeks at a time
- 2X common in women
- Little energy
- Feelings of worthlessness
- Suicidal thoughts
- Difficulty sleeping, concentrating
- Experience little pleasure
Biological risk factors (major depression)
- Twin studies suggest heritability
- Short form of SHTT gene (related to stress reactivity)
- Borna disease: viral infection which may predispose to depression
Brain activity
- Prefrontal cortex
- Decreased activity in left PFC, increased activity in right PFC
Antidepressants
- Tricyclics
- SSRIs
- MAOIs
- Atypical antidepressants
- Most effective for people with severe depression
- Children: tend to be ineffective
- Ineffective with early childhood trauma
Tricyclics
- Block transporter proteins that reabsorb seratonin, dopamine and noepinephrine into presynaptic neuron after release
- Block histamine and acetylcholine receptors and certain sodium channels
- Many side effects (dry mouth, heart irregularities)
SSRIs
- Block reuptake of seratonin
- Milder side effects than tricyclics
MAOIs
- Block enzyme monoamine oxidase that metabolizes catecholimines and seratonin
- Results in more transmitters in presynaptic terminal available for release
- Prescibed after SSRIs and MAOIs don’t work
Atypical
-Misc. group of drugs with antidepressant effects and mild side effects
Schizophrenia
- Characterized by deteriorating ability to function in every day life and some combination of the following:
1. Hallucinations
2. Delusions
3. Thought disorder
4. Movement disorder
5. Inappropriate emotional expression
Acute
-Sudden onset and good prospect for recovery
Chronic
-Gradual onset and long-term recovery
Positive symptoms
- Behaviors present that should be absent
1. Psychotic. - Delusions: unfounded beliefs
- Hallucinations: abnormal sensory experiences associated with increased activity in the thalamus, hippocampus and cortex
2. Disorganized - Inappropriate emotional displays, bizarre behaviors and thought disorders
Negative symptoms
- Behaviors absent that should be present
1. Weak social interaction
2. Emotional expression
3. Speech
4. Working memory - Usually stable over time and difficult to treat
Neurodevelopment hypothesis
- Abnormalities in the prenatal or neonatal development of the nervous system
- Supporting evidence:
1. Several kinds of prenatal or neonatal difficulties are linked to later schizophrenia
2. People with schizophrenia have minor brain abnormalities that originate early in life
3. Abnormalities of early development could impair behavior in adulthood
Risk factors for schizophrenia
- Poor nutrition of the mother during pregnancy
- Premature birth
- Low birth weight
- Complications during delivery
- Head injuries in early childhood
- Extreme stress of mother during pregnancy
Season of birth effect
- People born in winter to have a slightly greater probability of developing schizophrenia
- More pronounced in latitudes far from the equator
- Might be explained by complications of delivery, nutritional factors, or increased likelihood of viral infection in mother
Brain abnormalities
- Strongest deficits found in the left temporal and frontal lobe of the cortex
- Thalamus smaller than average
- Larger than normal ventricles
- Dorsolateral prefrontal cortex
Antipsychotic/neuroleptic drugs
-Tend to relieve schizophrenia
Chlorpromazine
- Used to treat schizophrenia that relieves the positive symptoms
- Relief usually experienced in 2-3 weeks
Chemical families of drugs
- Phenothiazines - includes chlorpromazine
- Butyrophenones - includes halperidol (Haldol)
- Both drugs block dopamine synapses
Dopamine hypothesis
-Schizophrenia results from excess activity at dopamine synapses in certain areas of the brain
Substance induced psychotic disorder
- Characterized by hallucinations and delusions resulting from repeated large doses of amphetamines, methamphetamines, or cocaine
- Each prolongs activity of dopamine at the synapse, providing further evidence for dopamine hypothesis
Glutamate hypothesis
- Suggests the problem relates partially to deficient activity at glutamate receptors
- Especially in prefrontal cortex
- In many brain areas, dopamine inhibits glutamate release or glutamate stimulates neurons that inhibit dopamine release
- Increased dopamine produces the same effects as decreased glutamate
Second generation antipsychotics
- Used to treat schizophrenia but seldom produce movement problems
- More effective at treating negative symptoms