schizophrenia and anxiety disorders

OCD, PTSD, SCHIZOPHRENIA

how is schizophrenia defined

severe psychopathology characterized by negative symptoms and positive symptoms

what are the major symptom categories of schizophrenia

auditory hallucinations, personalized delusions, changes in emotion (affect), cognitive impairments

what are delusions defined as

false beliefs

what are the major divisions of schizophrenic symptoms distinguish by in psychiatry? are there any other categories schizophrenic symptoms may fall under

negative and positive symptoms; cognitive symptoms

what are positive symptoms (define)

symptoms that are PRESENT but SHOULD NOT BE; behavioral states that have been gained

what are negative symptoms (define)

characteristics of an individual that r ABSENT but SHOULD BE PRESENT'; behavioral states that have been lost

what are examples of positive symptoms—name @ least 2

hallucinations, delusions, excited motor behavior, disorganized thought and speech; psychosis

what are examples of negative symptoms—name @ least 2

emotional dysregulation: lack of emotion expression, reduced face express, inability to experience pleasure in daily activities, emotional withdraw

impaired movement: social withdraw, slow and impoverished thought and speech

what is schizophrenia considered if both individuals of twin pair have schizophrenia (trait)

concordant

what is schizophrenia considered if only one individual of twin pair exhibits schizophrenia (trait)

discordent

what does concordant mean

refers to any trait that is been in both individual pair of twins

what does discordant mean

refers to any trait that is seen in only one individual of a pair of twins

what is an endophenotype

a group of behavioral/physical characteristics that accompany an inherited susceptibility to a particular disorder

twins who develop schizophrenia were more abnormal; this suggests that schizophrenia may have an associated endophenotype. what are examples of findings that would suggest this?

weighed less @ birth; more submissive, tearful, sensitive than identical sibling; during dev may have more instances of physiological distress; inability to use smooth eye movements, disordered motor coordination

what do cognitive symptoms of schizophrenia refer to (define)

problems w processing and acting on external information

what are examples of cognitive symptoms

memory problems, poor attention spans, difficulty making plans, reduced decision-making capacity, abnormal movement patterns, poor social cognition (neurocognitive impairments)

what are the 2 categories within negative symptoms

emotional dysregulation and impaired motivation

what are the many genes that increase the risk of schizophrenia also known to be involved in?

synaptic rearrangement

what are the genes that participate in synaptic signaling and myelination, and implied in synaptic plasticity found to be in some schizophrenia cases

abnormal

what does the emerge of schizophrenia depend on

the interaction of genes that make a person vulnerable to environmental stressors

are genes necessary, sufficient, both, or neither for schizophrenia? explain

neither. not sufficient as it is the interaction between genes and the environment that may increase susceptibility but won’t cause it. not necessary as it is not entirely hereditary, ppl can dev without having the history of it—there is a risk inc if you do have a family history w it tho!

what is different abt ppl w schizophrenia compared to ppl w/o schizophrenia in the cerebral ventricles

enlarged ventricles, esp. the lateral ventricles to well counterparts w compared w normal sized ventricles

what is different abt ppl w schizophrenia compared to ppl w/o schizophrenia in the limbic system

ppl with schizophrenia have disorganized looking hippocampal pyramidal cells, abnormal activity in limbic networks from hippocampus to other structures, and their hippocampus and amygdala is smaller comp. to normal

what may cause the seen cellular disorganization of schizophrenia? when?

early cell development from abnormal synaptic rearrangement of input/output of the cell and abnormal neurogenesis/disordered integration of newborn cells

what are the cortical abnormalities seen w ppl w schizophrenia compared to ppl w/o schizophrenia

structure differences and diff functional activity of corpus callosum; those w schizophrenia have accelerated loss of gray matter @ adolescence

what may the accelerated loss (thinning) of gray matter in adolescence of those with schizophrenia reflect

loss of synapse during dev

what is different abt ppl w schizophrenia compared to ppl w/o schizophrenia in brain activation

ppl w schizophrenia frontal lobes r less active, reduced frontal blood flow seen, gray matter changes compared to those w/o

what may contribute to the seen less active frontal cortex in individuals w schizophrenia

neurons in frontal cortext have dendrites w reduced density of synaptic spines compared to control group

what is the genetic factor of schizophrenia: is there a specific gene that may cause it

no! many genes contribute to the risk of it rather than a single gene determining it all

what is a lobotomy

the surgical separation of a portion of the frontal lobe from the rest of the brain; once used as treatment for schizophrenia and other mental disorders

what are antipsychotics

a class of drugs that alleviate symptoms of schizophrenia via blocking post synaptic dopamine receptors (D₂)

what the 2 two major classes of antipsychotics

first generation and second generation

what are first generation antipsychotics

D₂ receptor antagonists (block D₂ dopamine receptors)

what are second generation antipsychotics

D₂ receptor antagonists AND 5-HT receptors (serotonin) among others—blocks

what may cause tardive dyskinesia

prolonged use of antipsychotics

what is tardive dyskinesia

disorder characterized by repetitive involuntary movements involving face, mouth, lips, and tongue

uncontrollable movement of tongue, sucking or smacking of lips, sudden jerking movement of arms/legs are examples of what?

tardive dyskinesia

what do the biochemical theories of schizophrenia emphasize?

dopamine, glutamate, and serotonin receptors

what is the side effect of second-generation antipsychotics that is not seen for first generation antipsychotics

weight gain

what is the dopamine hypothesis

ppl with schizophrenia have an excess of either: dopamine release OR dopamine receptors

amphetamine promotes the release of dopamine and prolongs the action by blocking reuptake when high doses are taken to get high. the resulting high is comparable to the positive symptoms of schizophrenia. antipsychotics are able to rapidly reverse amphetamine psychosis. does this support the dopamine hyp? explain :3

ya, bc the inc and prolonged release of dopamine results in schizophrenia (pos) symptoms which reflects the idea that schizophrenic individuals have excess dopamine release that causes these symptoms to occur.

treating ppl who have parkinsons disease w a metabolic precursor of dopamine (L-dopa) may induce schizophrenic symptoms via boosting synaptic availability of dopamine. does this support the dopamine hyp? explain :3

ya, bc the inc of sypanic availability of dopamine results in schizophrenic symptoms—reflecting the idea that excess dopamine release is a component to schizophrenia

what is the glutamate hypothesis

schizophrenia results from under activation (stimulation) of ALL glutamate receptors, accounting for reduction in activity of frontal cortex

what is phencyclidine (PCP, angel dust)

a potent drug that induces a state that resembles schizophrenia positive AND negative symptoms

what does PCP act as that prevents glutamate from its usual activities

PCP acts as an NMDA receptor antagonist, blocking NMDA Ca2+ channel

how does PCP support the glutamate hypothesis

it produces phenomena that resembles pos and neg symptoms of schizophrenia by acting on NMDA receptor by blocking the Ca2+ channel, in reuslt prevents glutamate from its excitatory events

when ppl deal w physical, emotional, and lifestyle changes—what may this increase the risk of

schizophrenia

what is an anxiety disorder classified as

any class of psychological disorder that includes recurrent panic states and generalized anxiety disorder

what may an individual with an anxiety disorder experience

irrational fears, sense of terror, dizziness, difficulty breathing, shaking, feeling loss of control

what are benzodiapines

a class of antianxiety drugs that have high affinity to receptor molecules in CNS—favored drug in treating anxiety

what are anxiolytics

drugs that combat anxiety such as alcohol, opiates, and benzodiazepine to name a few

what do anxiolytic benzodiazepines bind to? competitive or non? agonist, antagonist, inverse agonist?

GABA receptors, acting as a noncompetitive agonist

what does the ^- cause the effect of

increase GABA inhibitory effect

what is the “ult” of benzodiazepine-GABA A receptors? why is that so?

regulate the permeability of neuron membrane to Cl-; opens Cl-, hyperpolarize, inhibit neuron from firing

how may SSRIs be a sort of effective treatment for anxiety disorders? explain what they do and why that helps!

increases stimulation of serotonin receptors—density is abnormal so stimulating helps and provides relief from anxiety

what is post traumatic stress disorder (PTSD)

disorder in which memories on an unpleasant experience repeatedly plagues a person—inability to forget an unpleasant/horrible experience

what does PTSD induce in individuals who have the disorder (what it produces, what it activates in the body)

prod. same intensive arousal—fear, trembling, and general autonomic activation

what may cause the activation of fear in PSTD

stressful circumstances + mild stimuli that prompt recollection of og even somehow

combat related PSTD shows memory changes (ex. amnesia), flashbacks, and deficits in short term memory. what do structure do these findings imply that may play a role in PTSD? what is found in the volume of the structure in combat vets. v. controls that supports this?

the hippocampus—vol of right hippocampus is smaller in combat vets. compared to controls

in PTSD, what lobe experiences decay

temporal lobe

what may cause the decay of the temporal lobe

exposure to stress hormones and prolonged sensitivity to these hormones (ex. cortisol)

what are the 2 pathways that are activated that are proposed to underline PTSD

brainstem system and the amygdala

what does the brain stem system do

sensitizes the person ro related stimuli of experience in future

what is sensitization

the occurrence of PTSD behavior becoming stronger every time it is activated (exposed to stimuli that relates to og experience)

what is the brain stem system to the brain

the general alarm system—arousal system and brain alarm response

what causes the activation of the brain stem system

subsequent stressors

what are the acute neurochemical responses that occur from subsequent stressor

locus coeruleus floods the brain with norepinephrine, ventral tegmental area alter dopamine, endogenous opioids (r there), and corticotrophin releases hormones causing fight or flight response

what causes PTSD to become WORSE overtime? how?

the sensitization from the brain stem system—every subsequent stressor increases various behavioral responses

what causes the activation of the amygdala system

sensory and cognitive associations to the original trauma

what does the amygdala system condition in a person w PTSD

conditions a long-lasting fear reaction—traumatic remembrance (basically fear conditioning)

what is considered the learn/predict system? why?

amygdala system as it learns to predict danger; learn relations between what happened → stressor

what are the things that the amygdala system learns

sound, sight, smell, thoughts (among other things) that are associated with stressor

how do you target the amygdala system

exposure therapy to target the fear conditioning

in exposure therapy to target the amygdala system what relationship do you want to break

conditioned stimulus to unconditioned stimulus: CS -/→ US

what do we call the breaking of the relationship between the conditioned stimulus from the unconditioned stimulus

extinction

does the breaking of CS to the US erase the memory that causes PTSD? if not, what is occurring instead in the amygdala system?

NO. just dissociates—new learning, amygdala no longer predicting

what are the involved structures in extinction of CS to US in amygdala system

vmPFC and the hippocampus

what does the ventro medial prefrontal cortex do for extinction?

stores extinction memory and acts as a brake system

what does the hippocampus do for extinction?

provides broader context, preventing generalizations; stores extinction memory; acts as a brake system

why is the function of preventing generalizations of the hippocampus so important

w/o it, an individual would apply fear stimulus to ANYTHING and EVERYTHING

are the brainstem system and the amygdala system reciprocal?

yas

what do the brainstem system and the amygdala system reciprocal interactions facilitate

encoding and retrieval of traumatic memories

norepinephrine strengthens cues linked w fear conditioning in amygdala, causing flashbacks and vivid recall in experience. what is this reflecting in the PTSD pathway

the reciprocal interactions of the brain stem system and the amygdala

abnormal cortisol lvls are seen w those w PTSD. this is caused by stressful stimuli from feeling stress hormones more strongly than others in which it may be harder for them to forget stressful events. what PTSD pathway would this reflect.

the brain stem pathway

what is obsessive-compulsive disorder (ocd)

syndrome in which the affected individual engages in recurring repetitive acts that r carried out w/o reason or ability to stop

how is OCD characterized

by changes in basil ganglia and the frontal cortex—linked to serotonin

what do the routine acts individuals with OCD become

compulsions—acts that r repeated over and over

what effective drugs that help OCD

any that inhibit the reuptake of serotonin @ synapse and increase synaptic availability of serotonin

what may underlie OCD

the overactivity of a circuit from prefrontal cortex to strontium to thalamus and back to cortex

genes may affect serotonergic, dopaminergic, and glutamatergic systems—what does this suggest about what also underlies OCD

there may be a heritable component to it

torettes syndrom and OCD are part of a spectrum of related disorders, both involve abnormalities in basil ganglia. what is the relationship of torettes syndrom and OCD called

comorbid

what does comorbid refer to

the tendency of certain diseases/disorders to occur together in individuals

what are anxiety states characterized by

functional changes in temporal lobes—particularly amygdala

what do benzodiazepines enhance

inhibitory effect of receptor for GABA