Psychological Disorders Flashcards
Major depression has a lifetime prevalence of
10%
Heritability of major depression is
moderate
no genes on their own effect major depression, although multiple genes have been linked
true
Serotonin transporter gene 5-HTT
regulates the ability of axons to reabsorb serotonin and recycle it.
two short forms of 5-HTT + stress
higher probability of depression - not replicated
long and short forms of 5-HTT + stress
moderate probability of depression - not replicated
two long forms of 5-HTT + stress
lower probability of depression - not replicated
postpartum affects 20% of women and is caused in part by
drops in estrogen and progesterone levels
hemispheric asymmetry in brain activity affects depression
less activity in left hemisphere, more activity in right hemisphere
Drugs used to treat depression
Tricyclics, Selective serotonin reuptake inhibitors (SSRIs), Monoamine Oxidase inhibitors (MOAIs), Atypical antidepressants
Tricyclics
block transporter proteins that reuptake of serotonin, dopamine, norepinephrine - thus increasing effects of NTs. negative side effects because they also block histamine and acetylcholine receptors, some sodium channels.
Selective serotonin reuptake inhibitors (SSRIs)
similar to tricyclics, but selective to serotonin. Increase effects of serotonin. milder side effects
Monoamine Oxidase inhibitors (MAOIs)
inhibit enzyme MAO, which breaks down serotonin in the presynaptic terminal. More surviving serotonin for release.
Wellbutrin
blocks reuptake of norepinephrine, dopamine, but not serotonin
St. John’s wort
Not regulated by FDA, same effectiveness as standard antidepressants
BDNF (brain derived neurotrophic factor)
People with major depression have lower levels of BDNF. smaller than average hippocampus, learning. Prolonged use of antidepressants increases BDNF production.
Dysthymia
long-term, lifelong unhappy mood. drugs are more effective than psychotherapy.
Antidepressants are not effective for
survivors of childhood neglect or abuse
Electroconvulsive Therapy (ECT)
last resort or suicidal. electrically induced seizure, applied every other day for two weeks. Memory loss minimized if shock is applied to right hemisphere.
Depressed person sleep
enter REM within 45 minutes. earlier onset.
Unipolar disorder
Alternating states of normalilty and depression
Bipolar disorder
Alternating states of mania and depression
Bipolar I, Bipolar II
full blown mania, milder manic phases (hypomania)
Lithium
medication for bipolar disorder - decreases glutamate receptors in the hippocampus, block synthesis of brain chemical arachidonic acid, produced during inflammation.
Seasonal Affective Disorder (SAD)
reach temperature peak later (delayed onset)
Schizophrenia
deteriorating ability to function in everyday life for at least six months
positive symptoms
behaviours that are present that should be absent. easier to treat
negative symptoms
behaviours that are absent that should be present. harder to treat
Cognitive symptoms of schizophrenia
difficulty using and understanding abstract concepts - abnormal interactions between cortex, thalamus, cerebellum
Schizophrenia stats
effects 1% of the population, 10 - 100 times more common in US and europe than developing countries, cities > rural areas, men : women = 7 : 5
schizophrenia heritability
monozygotic > dyzygotic, dy > siblings - suggests possible prenatal environmental effect
DISC1
Disrupted in schizophrenia 1 - gene common in those with schizophrenia, controls the production of dendritic spines, generation of new neurons in the hippocampus.
New gene mutations
microdeletions, microduplications
Neurodevelopmental hypothesis
abnormalities in prenatal and neonatal development that produce mild abnormalities in brain development. Aggravated later in life by environmental symptoms.
People with schizophrenia have minor brain abnormalities
larger than normal ventricals, smaller than normal thalamus. deficits in left temporal and frontal lobe. dorselateral prefrontal cortex matures slowly. smaller cell bodies. Less activity in left hemisphere.
Two families of drugs used to treat schizophrenia
Phenothiazines (chlorpromazine), Buterophenones (Haldol). Both drugs block dopamine receptors.
Dopamine Hypothesis in Schizophrenia
Twice as many D2 (dopamine) receptors occupied in those with schizophrenia. More dopamine activity at receptors, greater cognitive impairment.
Glutamate hypothesis of schizophrenia
Less glutamate release, fewer receptors in the prefrontal cortex and hippocampus. PCP inhibits glutamate receptors. Low dose - slurred speech, high dose positive and negative symptoms.
Glycine increases effects of glutamate by…
binding to glutamate receptors and increasing surface area for glutamate to bind. Not antipsychotic, but increases effects of antipsychotic drugs.
mesolimbocortical system
neurons that project from the midbrain to the limbic system.
drugs block dopamine in the mesostriatal system, resulting in …
tardive dyskinesia, tremors and involuntary movements.
