Reading...
Play button
Play button
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;
62 Cards in this Set
- Front
- Back
|
ISR model of stress
|
Stress is a process with four components and two moderating variables. The four components are objective environment, subjective environment, strain, and illness. The two moderating variables are personal characteristics and coping/social support.
|
|
|
Objective environment (component #1 of ISR stress)
|
Conditions outside the individual that can potentially lead to stress. They can be measured. EX: temperature, deadlines.
|
|
|
Subject environment (component #2 of ISR stress)
|
The person's interpretation of the objective environment. EX: I don't like cold weather, I am worried about my paper. Only the subjective environment can cause strain.
|
|
|
Strain (commponent #3 of ISR stress)
|
Physiological, behavioral, and cognitive responses to a stressor. Physiological response refers to sympathetic stimulation. Behavioral response refers to behavioral modifications (healthy and unhealthy) that people use to cope with stress. Examples include eating junk food, doing yoga, etc. Cognitive response refers to the shift in attention that accompanies stress. Your focus shifts from outward to inward.
|
|
|
Illness (component #4 of ISR stress)
|
Relationship between strain and illness. Chronic strain or overstimulation of strain causes illness. Illness can be physical or psychological.
|
|
|
Personality characteristics (moderating variable #1 of ISR stress)
|
Includes actual abilities, self-confidence, personality, etc. Basically, personality characteristics are responsible for perceived demand and perceived resource.
|
|
|
Two types of coping (ISR)
|
Problem-based coping: deal with the problem. Write the paper. Get rid of the stressor. Emotion-based coping: deal with the emotions surrounding the problem. Exercise, drink, etc. Alleviate the feeling of stress, even though the stressor is still there.
|
|
|
Stress and ulcers
|
Most people w/ ulcers have h. pylori, but not everyone w/ h. pylori has ulcers. Two reasons this might be. 1) Stress shuts down digestion, reducing HCl. When the stress finally goes away, you have a rebound effect and a surge of HCl. This rebound effect causes a stomach condition where h. pylori can thrive and cause ulcers. 2) stress --> drinking --> ulcers
|
|
|
What do glucocorticoids do?
|
1) Make glucose more available so you have more energy to deal with the stressor. 2) reduce inflammation. 3) stimulate the hippocampus, amygdala, and frontal lobes. Reason for #3 - remember the location of a dangerous animal or enemy.
|
|
|
Steroid dementia
|
Caused by chronic stress. Amygdala becomes larger and hippocampus becomes smaller.
|
|
|
Innate immunity
|
All the parts of the immune system that are nonspecific - respond to any invader. Barriers, mucous, certain molecules in secretions. Include macrophages and NK cells.
|
|
|
NK cells and stress
|
In stressful situations → ↓ NK → infections and possibly cancers develop
|
|
|
Adaptive immunity
|
All the parts of the immune system that respond to specific invaders. Include B and T cells.
|
|
|
Cytokines
|
Released by wbcs. Communicate with each other and with the brain. They can pass the blood-brain barrier.
|
|
|
Most well-known cytokine
|
Interleukin
|
|
|
How to cytokines create "sick behavior"?
|
Stimulate hypothalamus, causing an increase in temp (fever). Lateral hypothalamus - decrease appetite. SCN of hypothalamus - increase sleepiness.
|
|
|
Stress and cytokines
|
Stress reduces cytokine activity, making it harder to fight off infections.
|
|
|
Positive symptoms of schizophrenia
|
Disorganized thought, word salad, delusions, hallucinations
|
|
|
Negative sx of schizophrenia
|
Flat affect, social withdrawal, anhedonia
|
|
|
Demographics of schizophrenia
|
Sx start in late teens, early 20s. Females develop schizophrenia earlier than males. Acute vs chronic.
|
|
|
Rule of quarters in schizophrenia
|
1/4 get well on own, 1/4 get well with meds, 1/4 get well enough to live in a group home, 1/4 don't recover
|
|
|
Genetics of schizophrenia
|
Genetic predisposition, not cause. Identical twins have a concordance rate of ~50%
|
|
|
Season of birth effects w/ schizophrenia
|
Higher incidence of schizophrenia in people born in late winter/early spring. This is probably because early in pregnancy is the height of flu season. If the mother gets a fever of 101+ neuronal development is slowed and cytokines pass through the placental barrier.
|
|
|
Viral hypothesis of schizophrenia
|
Season of birth, correlated w/ flu season. "cat scratch fever".
|
|
|
Birth trauma hypothesis of schizophrenia
|
umbilical cord gets twisted, ↓ oxygen delivered to the baby
|
|
|
Mild brain damage in schizophrenics
|
Brains are 3-4% smaller w/ greater ventricles and therefore more open space. Decreased size is most prevalent in prefrontal cortex, temporal cortex, and thalamus. Neurons are also abnormal, with smaller cell bodies and disorganized arrangement.
|
|
|
Dopamine hypothesis of schizophrenia
|
(+) sx are associated with increased dopamine levels. Acutal dopamine concentrations are not higher, rather it has a higher turnover rate, is more active, and has faster reuptake. Evidence for this theory: use IZBM/AMPT to see how many receptors are occupied by dopamine. Treat schizophenia by blocking dopamine. Drugs that increase dopamine induce schizophrenic sx.
|
|
|
IZBM/AMPT
|
IZBM is a drug that binds to dopamine receptors. AMPT is a drug that shuts down all dopamine production. Give subject IZBM, then count # receptors that IZBM occupies, wait a week, give AMPT, then give IZBM again. If there is no dopamine being released (AMPT), IZBM will take up all dopamine receptors. Schizophrenics have more receptors taken up by dopamine and less by IZBM at time 0.
|
|
|
Amphetamine psychosis
|
drugs that ↑ dopamine → psychotic sx, even in non-psychotic patients. These drugs include meth, coke, LSD.
|
|
|
Tardive dyskinesia
|
Result of long-term antipsychotic use. Thorazine shuffle, face and neck tics, serpentine tongue. Probably due to dopamine suppression throughout the brain, non-selectively.
|
|
|
Glutamate hypothesis of schizophrenia
|
Decreased glutamate activity leads to schizophrenia. Support: PCP decreases glutamate and causes (+) and (-) sx. Increased glycine causes increased glutamate decreases schizo sx. Schizophrenics who take PCP have a long-term relapse. Schizophrenics who take amphetamines don’t relapse, indicating that glutamate is a more important player than dopamine
|
|
|
Glycine
|
Neuromodulator that increases the effectiveness of glutamate.
|
|
|
Treatment of schizophrenia
|
Classic antipsychotics block dopamine. Glycine increases the effectiveness of glutamate.
|
|
|
3 types of depressive sx
|
Mood, cognition (decreased focus, rumination, etc.), behaviorv (sleep changes, substance abuse, social isolation).
|
|
|
Concordance rates for depression
|
Not as high as for schizophrenia, but still fairly high.
|
|
|
Genetic predisposition for depression
|
Set of genes involved in serotonin transporters. different alleles - if both are short alleles, you have fewer serotonin transporters, which is correlated w/ depression. (↓ transporters, ↑ serotonin)
|
|
|
Viral hypothesis of depression
|
Borna virus is usually found in farm animals. Animals w/ borna virus show bipolar behavior - periods of agitation alternating w/ periods of depression. Prevalence of borna virus is higher in depressed populations. Having the virus increases probability of getting depressed.
|
|
|
Amine hypothesis of depression
|
Depression is associated in ↓ activity of amines (catecholamines + serotonin).
|
|
|
Catecholamines
|
dopamine, norepinephrine & epinephrine
|
|
|
Problems with amine hypothesis of depression (2)
|
1. depressed people don’t have lower levels of amines 2. drugs immediately (in minutes or hrs) ↑ levels of amines, but it takes a minimum of two weeks, usually 1 month, for antidepressant drugs to start working
|
|
|
Neurotrophins and depresion
|
Neurotrophins are neurochemicals (not neurotransmitters) that promote the survival and activity of neurons. Help neuronal development - guide/stimulate neuronal growth. Not necessary for survival, but contribute to healthier and more active neurons. Brain-derived neurotrophin factor (BDNF) is low in people with major depression, especially in limbic system. After prolonged use of antidepressants, BDNF is elevated.
|
|
|
antidepressant drugs (4)
|
SRI, SSRI, MAOI, tricyclic antidepressants
|
|
|
MAOI drugs
|
monoamineoxidase breaks down amines in the body: dopamine, norepinephrine, & epinephrine (catecholamines) and serotonin
|
|
|
Tricyclic antidepressants
|
inhibit reuptake of serotonin and catecholamines broadly, not selectively.
|
|
|
Lag time for antidepressants
|
Antidepressan drugs immediately (in minutes or hrs) ↑ levels of amines, but it takes a minimum of two weeks, usually 1 month, for antidepressant drugs to start working. It also takes about 2 weeks for BDNF levels to increase, so maybe antidepressants work by increasing BDNF. REM deprivation also takes about 2 weeks to work, so maybe antidepressants impact REM.
|
|
|
ECT for depression
|
ECT reduces REM and helps depression long-term, even after therapy is over. During sleep, a chemical that causes depression builds up, so sleep deprivation alleviates depression by reducing buildup of this chemical
|
|
|
Genetics of bipolar disorder
|
Stronger genetic component to bipolar than depression, higher concordance rates.
|
|
|
Drug therapy for bipolar
|
lithium chloride and antiseizure meds
|
|
|
Lithium chloride mechanism of action
|
Stabilize the Na/K balance in neurons. Dangerous, very small therapeutic window, need constant monitoring.
|
|
|
Biological basis for anxiety disorders
|
biological predisposition to sensitive and heightened arousal of sympathetic system, so even a small stimulus puts them over the top to a panic attack
|
|
|
Treatment of anxiety disorders
|
Benzodiazapenes. Stimulate a certain receptor. Body produces a substance that is similar to benzos. Endogenous substance and benzos modulate GABA activity. Do not stimulate GABA systems directly, but increase the effectiveness of GABA --> greater inhibitory effects
|
|
|
Structural abnormalities in anxiety disorders
|
people who are prone to anxiety disorders have fewer benzodiazepine receptors in the brain, so the inhibitory effects of GABA are lessened and sympathetic system is stimulated
|
|
|
OCD loop
|
Worry (orbitofrontal cortex) → fear (amygdala, cingulate cortex, limbic system) → action (basal ganglia: putamen, caudate nucleus, globus pallidus) → reinforcement/addiction (nucleus accumbens)
|
|
|
OCD treatment
|
SSRIs stop the loop at the "action" part. Serotonin is the primary neurotransmitter in the basal ganglia.
|
|
|
Genetic component of OCD
|
OCD runs in families. OCD is also prevalent in families w/ Tourettes
|
|
|
Basal ganglia
|
Responsible for the "action" part of OCD. 3 sets of nuclei: globulus pallidus, putamen, and caudate nucleus. Putamen and caudate nucleus are responsible for species-typical behavior
|
|
|
ADHD symptoms
|
Hyperactivity, low impulse control, defiance, sloppiness
|
|
|
Prevalence of ADD
|
Boys diagnosed more in childhood, equal distribution in adulthood.
|
|
|
Role of association areas in ADHD
|
in people w/ ADHD, their PC allows their association areas to habituate to the stimuli. This is the opposite of non-ADHD brains, where PC inhibits habituation.
|
|
|
Prefrontal cortex and ADHD
|
Decrease in size and activity of prefrontal cortex
|
|
|
Treatment of ADHD
|
Ritalin, aderall, other stimulants. In ADHD people, the prefrontal cortex isn't active enough so activity isn't inhibited. Stimulants active the PC and therefore allow inhibition of habituation
|
|
|
Reinforcement gradient in ADHD
|
ADHD kids need more instant reinforcement, and more reinforcement. this leads to impulsive behavior.
|
