Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
57 Cards in this Set
- Front
- Back
why is the name schizophrenia misleading |
it literally means split mind, but the condition does not involve multiple personalities |
|
when is the typical onset of schizophrenia |
its onset is around 20, abit later for females |
|
what are the types of symptoms that can arise in the order that they arise |
negative, cognitive, positive |
|
what are negative symptoms |
these are traits where the patient lacks compared to normal ppl: social withdrawel, lack of affect |
|
what are cognitive symptoms |
difficulty learning |
|
what are positive symptoms |
positive symptoms are additional traits the individual has that differ from an ordinary person hallucinations (seeing things that arent really there) delusions (believing things that arent real: everyone is out to get you, imagining ppl have control over you, vice versa irrational thinking (no logic to thought process |
|
are schizos aware of their condition |
no they think they are the normal ones and everyone else is crazy! |
|
what causes it genetics or the environmental factors |
both! |
|
why is believed that both genes and environment are responsible for the development of schizophrenia |
bc monozygotic twins (identical gentic info) have more of chance of both having schizo, if they grow up in womb in the same placenta (monochorionic) (60% vs 10% for diochiorionic) |
|
what does monochrionic mean |
one placenta |
|
are there any for telling signs that predict the onset of schizo |
as children they will be socially withdrawn, have webbed toes |
|
what are other environmental factors other than growing up in same/different placenta that effects the risk of developing schizophrenia |
being born in regions of high viruses, high population, parental substance abuse, viatmin D defiency, parental smoking |
|
what is a possible explanation for the seasonal effect (likely hood that child born in feb, march, april may is more likely to develop schizo) |
because parent was pregant during winter where they are more inside, exposed to viruses, high mother immune response effects fetus development and may lead to schizo) |
|
is schizo a degenerative disease |
no!!! its a disease caused by misfiring of neurons |
|
whats different in the anatomy of a schizo |
after onset they appear to have less brain tissue, bigger ventricles compared to individuals who are lossing brain tissue simply due to aging |
|
what are possible treatments for schizo |
antispychotic drugs that block dopamine receptors (D2) and address the positive symptoms of schizo |
|
describe the dopamine hypothesis of schizo |
a) drugs like cocaine that increase the release of dopamine significantly have been shown to produce similar effects to positive symptoms of schizo b) high activity of dopamine in brain (amygdala and VTA/nucleus accumbens of basal ganglia-responsible for rational thinking) are seen to produce the positive symptoms of schizo low activity in the PFC (specifically dorsal lateral prefrontal cortex) are seen to produce the cognitive, negative effects of schizo |
|
what is hypofrontality |
it is the assumed cause of negative, cognitive symptoms of schizo (low dopamine activity) |
|
what is the solution to too much dopamine in amygdala, mesolimbic system, while too little dopamine in PFC |
atypical antypsychotic drugs (these act as partial agonist) |
|
how do partial agonist work |
they a specific to a particular receptor (act as an antagonist in regions of high dopamine activity/address positive symptoms of schizo and agonist in low dopamine regions aka in PFC/addressing cognitive negative symptoms |
|
name an example of atypical antipsychotic drug that addresses the positive symptoms of schizo |
ariprazole |
|
what are the symptoms of being autistic |
impaired social interaction, doesnt like affection (look at faces), slow language (repeats what others say to them, refers to self in 3rd person) and cognitive development, lack of imagination, repetitive movement |
|
what is meant by autism is a disorder on a spectrum |
this means it cant be categorized, the symptoms of the disorder lies on a spectrum that can vary from mild to severe (metal retardation) |
|
what gender is more susceptible to autism |
males |
|
what is an example of a mild form of autism |
aspergers syndrome, characterized by lack of social skills, but not cognitive impairments, also very obsessive about objects |
|
why is Retts disorder no longer considered an example of autism |
bc we know the specific genetic cause that leads to it, while the cause of autism is still unknown |
|
describe childhood disintegration disorder |
this is when the child develops normally, until an age between 2-10 wherein they start to regress cognitively |
|
is autism heritable? |
YES 90% concordance rate between monozygotic twins 20% of autistic cases can be linked back to a biological cause (ie mother being exposed to virus during pregnancy elevating her immune response) |
|
what is different in terms of the brain of autistic people |
they have rapid brain growth between ages 2-3, afterwards it slows down so that their brain is the same size of everyone elses during teens brain activation in response to stimuli is also different in autistic people |
|
what is an example wherein the brain response to stimuli was different for someone with autism |
fusiform doesnt become as activated when autistic person sees a face this is because as a child they didnt dedicate much time to looking at faces (neurons didnt have a need to specialize), also region for deciphering social relationships did not become activated when they saw a shapes interacting eachother (just occipital lobe) |
|
what is a possible treatment for autism |
behaviour reinforcement therapy, shape their behaviours so that they are similar to normal peoples |
|
what are 2 types of affective disorder (mood disorders) |
depression and bipolar |
|
describe bipolar disorder and its treatment |
bipolar disorder is characterized by periods of many (unrealistic happiness) followed by periods of depression, Lithium salts have been effective in reducing mania symptoms thus reducing depressive symptoms as well (no mania=no depression), lithium effects ion channels in brain, its effects are immediate although the mechanism is unclear |
|
are affective disorders hereditary? |
yes, monozygotic concordance>dizygotic results from a combination of mutations on chromosomes that result in individuals being predisposed to depression |
|
what months of birth are said to be greatest predictors of suicide |
april to august |
|
what are the various treatments for depression |
1) Monoamine enzyme inhibitors (block enzymes that break down, reuptake nonrepinephrine, serotonin) 2) ECT (electroconvulsion therapy)-->inducing a brain wide seizure 3) deep brain stimulation (stimulates one specific region of brain) 4) sleep deprivation 5)light therapy |
|
describe the monoamine hypothesis for depression |
hypothesis that depression is caused by inbalance (lack of ) mono amine in the brain (nonrepinephrine, serotonin), this is believed bc drugs like SSRI, SNR, Trycyclic antipressants that increase mono amines in the brain synapses have been shown to decrease depression, similarly reducing serotonin levels in individuals who are predisposed to depression will induce a depressive episode (tested this by elimintating Tryptophan from diet) |
|
what is a possible way to reduce serotonin levels in the brain |
eliminate tryptophan from diet |
|
what are some examples of antidepressant drugs how long does it take to see results |
results are not immediate, requires weeks for drugs to work, ex are SSRI (serotonin, specific reuptake inhibitor, SNRI (serotonin, nonrepinephrine inhibitor), trycyclic antidepressants |
|
describe how ECT (electroconvulsion therapy is used) |
by inducing a high stimulation of neurons in brain (seizure), effects of depression in certain individuals seem to be alieviated, results are immediate after just a few sessions see improvement! |
|
what indicator did scientist have on there being a specific region of the brain that may be the cause of depression |
scientists noted through brain imaging that a region in the brain (area 25) became less activated in individuals who have has successful depression treatment, indicating that maybe this area should be targeted via ECT |
|
what part of the brain was area 25 located in, what were the results of the trial |
area 25 was associated with the limbic system (region for reward, pleasure of the brain), in the frontal lobe (subgenual anterior angulate cortex), too much variance in results of population meaning that not deemed a successful hypothesis |
|
other than area 25 where else could DBS be applied |
nucleus accumbens (basal ganglia) Vagus cranial nerve |
|
what difference is observed between individuals with depression in terms of their sleep |
they have shallow sleep, interrupted sleep, and REM is more concentrated near the begining of the night, similarly, depressed people do not go through phases 2-4 of sleep cycle, just 1& REM |
|
given difference in depressed person sleep cycle, what hypothesis arouse about depression |
maybe it is caused by sleep, maybe REM causes predisposed individuals to be more depressed |
|
what 2 sleep treatments exist, how long does it take for results to appear |
total sleep deprivation (if you make person stay up for 24 hours depression decreases, however once they sleep depression is restored), immediate results partial sleep deprivation, attach them to an ECG everytime they enter REM wake em up, not immediate like SSRI's (antidepressants), it takes awhile fore depression to go down |
|
why did sleep therapy come about |
because it was observed that during winter months some individuals are predisposed to depression because of change in circadian rhytmn (shorter days), therefore to solve this problem exposure to bright light was seen as a solution, works for some people |
|
what is the role of neurogenesis in depression |
proposed that depression leads to decrease neurogenesis in hippocampus and that antidepressants increase neurogenesis so maybe thats why they work in decreasing depression |
|
what is an anxiety disorder |
anxiety disorder is caused by unfounded (no reason for), unrealistic (out of proportion) expectation for disaster, resulting in different physiological responses via autonomic nerve system (sweating, increased HR) that emphasizes unsettling feeling |
|
what is a panic disorder, what gender has them more |
type of anxiety disorder, periods of intense fear accompagnied by autonomic symptoms, more in women |
|
describe anticipatory anxiety |
its the fear of having a panic attack it can lead to agoraphobia |
|
what is agoraphobia |
fear of leaving house |
|
what is a social anxiety disorder, what is a possible cause of it |
targeted anxiety disorder related to the fear of being socially scrutinized by others, results in people avoiding social situations, BDNF mutation (BDNF usually responsible for neuron growth and survival) |
|
what brain activity patterns can be associated with anxiety disorder |
high activity in amygdala, low activity in the PFC |
|
what is a possible treatment for a anxiety disorder |
benzodiazepine, its a sedative that increases GABA inhibition in brain |
|
what is stress |
stress is the arousal of the bodies natural fight or flight response (via autonomic nerve system) in response to something threatening, the extent of the response, duration can lead to a stress disorder |
|
define stress disorder |
its the symptoms undergone by individuals whose response to stress doesnt dissipate once stressor is gone, body doesnt react well to prolongues periods of stress |