psychopathology Flashcards
how much of the population does schizophrenia affect?
1 percent
what is the key symptom of schizophrenia?
impaired logical thought
what are positive symptoms?
abnormal symptoms that are gained which are usually acute and more likely to respond to antipsychotic mediations
what are negative symptoms?
lost functions
what are positive symptoms of schizophrenia
hallucinations, delusions, excited motor behavior
what are negative symptoms of schizophrenia
slow thought and speech, emotional and social withdrawal, and blunted affect of emotional expression
what are cognitive symptoms of schizophrenia
disorganized thoughts, difficulty concentrating and following instruction
schizophrenia is partially what?
heritable
what are the causes of schizophrenia
environmental exposure combined with genetics will cause illness if threshold is exceeded
environmental factors do what
up regulate and down regulate gene function
what is the characteristic of epigenetics
people with the same genome can have different outcomes
the pyramidal neurons in the hippocampus are what
disorganized in schizophrenia
what parts of the brain are smaller in people with schizophrenia
hippocampus and the amygdala
what is hypofrontality schizophrenia
underactivity of temporal and frontal lobes
where do we see loss of gray matter and less metabolic activity
frontal and temporal lopes along with accelerated aging and neuron loss
schizophrenia results from excess what
synaptic dopamine or increased post synaptic sensitivity to it
what are examples of the dopamine hypothesis of schizophrenia
- neuroleptics are DA antagonist
- chronic amphetamine use produces schizophrenia like syndrome
- L-dopa treatment of Parkinson may produce psychosis
- D2 levels in auditory thalamus are higher in schizophrenics
All current antipsychotic drugs do what?
control function of dopamine D2 receptor
what are some neuroleptic drugs
risperidone and abilify
what do neuroleptic drugs do
block serotonin and D2 receptors - some increase dopamine in frontal cortex
what is the glutamate hypothesis
schizophrenia is due to underactivation of glutamate receptors
PCP is a what
NMDA receptor antagonist which means it prevents glutamate from acting normally
what are symptoms of acute schizophrenia
prolonged NMDA receptor underactivation
endocannabinoids act on what
CB1 receptors
CB1 inhibits what
other neurotransmitters
where are EC levels elevated
In CSF of schizophrenics
depression is what
the most common mood disorder
symptoms of depression
sad mood, feeling worthless or guilty, loss of interest or pleasure in activities, increased or decreased appetite and weight, changes in sleep pattern, and suicidal thoughts or plans
what is normal depression
normal reaction to life events (death of a loved one)
what is clinical depression
chemical imbalance-genetic
what are symptoms of normal depression
- mood described as “blue”
- short duration
- little if any impairment
what are symptoms of clinical depression
- mood described as “ black”
- long duration
- significant impairment in function
what activity (blood flow) increases during depression
emotional orbitofrontal cortex and amygdala
what activity (blood flow) decreases during depression
areas involving attention and language
what is the monoamine hypothesis
depression is due to reduced synaptic activity of norepinephrine and serotonin
MAO inactivated what
monoamines
treatment with MAO inhibitors does what?
raises level of monoamines at the synapse, and improve depression
what does reserpine do
reduced monoamines and can cause depression
what are the first ways antidepressants work
- inhibiting reuptake of 5-HT (serotonin or NE)
what is the second way antidepressants could work
- Binding to presynaptic 5-HT or NE autoreceptors, thus enhancing neurotransmitter release
what is the third way antidepressants could work
inhibiting monoamine oxidase thereby reducing neurotransmitter breakdown
what do overactive serotonin autoreceptors do
impair serotonin release which causes depression
what does autoreceptor activation do
decrease 5HT release
depressed patients have what
overactive autoreceptors
what happens after weeks of SSRI use
autoreceptor function and number declines over weeks increasing neuronal firing and serotonin release
what are the early findings of electroconvulsive shock therapy
drug-induced seizures alleviate depression
ECT raises what
monoamine levels
ECT is now used in what
severe depression
-suicidal ideation that requires immediate alleviation
what are some brain stimulations treatment for affective disorders
fast TMS, deep brain stimulation, and stimulation of the vagus nerve
what is fast TMS(transcranial magnetic stimulation)
produces effects similar to traditional ECT
what does deep brain stimulation do
anterior cingulate gyrus and median forebrain bundle produce immediate effects
what does the stimulation of the vagus nerve do
gradually relieves depression
what are the main antidepressant pills
SSRI, SNRI, RCA, and MAO inhibitors
why are SSRIs the usual first choice
they are less severe adverse effects and less danger with overdose
depression is the imbalance of the what
immune system, stress system, and gut microbiota
ketamine causes an upsurge of what
glutamate, restoring synaptic functioning
ketamine will likely replace what
ECT for treatment of severe acute depression
what is disturbed in depression
sleep
what is bipolar disorder
individuals alternate between depression and mania
what are bipolar psychotic symptoms
delusions, hallucinations, paranoia, bizarre behavior-similar to schizophrenia
what is mania
excess energy, confidence, grandiose thinking, little need to sleep, hypersexual drive, drug abuse
how is the cycling in bipolar disorder
unpredictable, varies from days to months
what varies with ventral prefrontal cortex
activity varies with mood state
how is the ventromedial cortex affected in people who are depressed
it is smaller, neuron number is normal, but glial cells are much reduced
what increases at the start of a manic period
subgenual prefrontal cortex
what is cylcothymia
mild form of bipolar disorder-patients cycle between dysthymia and hypomania
what is dysthymia
mild depression
what is hypomania
increased energy
what are phobic disorders
intense irrational fear centered on a object, activity, or situation
what are some anxiety disorders
panic disorder- recurrent attacks of fearfulness
generalized anxiety- persistent, excessive worry
OCD- incontrollable irrational thoughts and compulsions(need to preform task over and over)
what helps with OCD
antidepressants, reducing serotonin autoreceptors sensitivity, antipsychotics, and glutamate blockers
what do OCD patients activate more than normal during the stroop test
dorsolateral prefrontal cortex
where do OCD patients have more activity
orbital frontal cortex and caudate nuclei(basal ganglia)
what produces long lasting effects for OCD
surgery to disconnect orbitofrontal cortex
what is serotonin supported by
effectiveness of SSRIs
what are the 2 major nuclei
MRN and DRN
what is the MRN
limbic/prefrontal cortex
-mediates fear/anxiety
what is the DRN
prefrontal cortex, basal ganglia, PAG
- modulates cognitive/behavioral components
what treats anxiety
benzodiazepines
how do benzodiazepines treat anxiety
bind GABA receptors to enhance GABA inhibitory actions
what is related to OCD
Tourette’s syndrome
what was done to people with all sorts of psychiatric disorders
frontal lobotomy
