psychiatric disorders

what are the conceptions of mental illness

statistical rarity, subjective distress, impairement, societal disapproval, bio dysfunction

what is statistical rarity of mental illness and an example

small number of the population has it, ex. schizophrenia and bipolar

which mental illnesses are statistical rarity

schizophrenia and bipolar

which mental illnesses are not statistical rarity

depression + anxiety

what kinds of impairment can happen due to mental illness

personal or professional

what does DSM 5 do differently and an ex.

warn about physical issues that may cause symptoms and treat those first ex. kidney issues can cause depressive symptoms

what approach does DSM take

biopsychosocial

what percent of US has serious mental illness

4 and half%

which gender has more prevalence of mental illness

female

which age has more prevalence of mental illness

18-25 age range

what are the reasons this age range have more prevalence of mental illness

symptoms appear after brain finishes developing + undergo more stress than other age bracket

what is unique about mental illness over age brackets

less prevalence

which races have higher prevalence of mental illness

biracial and then white

which disorders have higher lifetime prevalence for US population

affective disorders + anxiety: depression, bipolar and anxiety disorders

which disorder has lowest lifetime prevalence for US population

schizophrenia

what does concordance rate tell us

what % of pop has a disorder through gene

what are two ways to get concordance rate

compare twins (MZ and DZ) and adopted kids

what is disconcordance

one member of the pair doesn't have the disorder

what is concordance rate

% of pairs that have the disease / 100 %

what are monozygotic twins

identical twins + one zygote

what are dizygotic twins

fraternal twins + two sperm and two eggs fertilized

why are higher concordance rate rarer

few disorders are only gene related

how does twins show concordance rate

higher MZ and lower DZ shows more support for gene

what does higher adoptive parent similarity to child show

more environmental reasons

how many US experience affective disorders in lifetime

20%

what is the most common affective disorder

major depressive disorder

what is MDD prevalence

17%

which population is MDD most prevalent in

30s female

how is MDD different from bipolar

MDD is unipolar in that it doesn't have mania, only has depression

what is the mild form of MDD

dysthymia = disregulated mood

which of the MDD form is more common

dysthymia = disregulated mood

what is the opposite of mild form of MDD

MDD

how is MDD different from mild for patients

mild can participate in life functioning while MDD cannot at all + treatment resistant disorder

what does treatment resistant disorder mean

normal meds for mild don't work to treat it

how many symptoms on DSM need to be experienced to be diagnosed

not all

what is the prevalence rate of bipolar

1.6%

what are symptoms of depression

feelings of unworth/guilt, less energy, pace restless, cry often, apetite for previous hobbies, disturbed sleep, risk for suicide

how many times more likely are people with affective disorders to have a relative with affective disorder

10 times

what is concordance rate of affective disorders in MZ

60% regardless if reared together or not

what is concordance rate of affective disorders in DZ

20%

what are the four brain changes in depression

1. less blood flow in two cortex parts
2. right hemisphere cortex is thinner
3. smaller hippocampus volume
4. more activity in PFC (prefrontal cortex) + amygdala

which parts of the cortex have less blood flow

parietal + posterior temporal cortex and anterior cingulate

what are the parts of the cortex that have less blood flow during depression function related to

attention

which two brain changes are we not sure causes depression or are caused by depression

right hemisphere cortex thinning and smaller hippocampus volume

what could be two reasons as to why does the right hemisphere cortex thin

less cell bodies or compressed cell bodies

how does more activity in PFC relate to depression symptoms

PFC = planning + decision making, ruminating behavior

how does more activity in amygdala relate to depression symptoms

emotion of fear + worry

what is the monoamine hypothesis

depression comes due to insufficient monoaminergic neuron activity, specifically NE + 5HT

which was a long accepted hypothesis, not as valid now

monoamine hypothesis

what give the evidences for monoamine hypothesis

1. monoamine antagonist
2. 5HTIAA studies
3. tryptophan depletion studies

give an example of monoamine antagonist and how does it relate to depression

reserpine; depressive symptoms induced by monoamine antagonists

is reserpine in studies harmful

no since short path life so no long term affects

what is 5HTIAA

a metabolite of serotonin in cerebrospinal fluid

how does 5HTIAA studies show monoamine hypothesis

MDD patients have lower 5HTIAA in cerebrospinal fluid which in turn means less serotonin

which of the three evidences for monoamine hypothesis is most unusual to happen in real life and why

tryptophan because it's caused by depletion and it's an amino acid so depletion is hard to cause

what is tryptophan

amino acid precursor to serotonin

how does tryptophan relate to evidence for monoamine hypothesis

brief depletion of tryptophan for the transporters in blood brain barrier cause symptoms of depression

what are the antidepressants based on

monoanime hypothesis

what are the anti depressant basically

monoaminergic agonist

what are the different monoaminergic agonist

MAOI + TCA + SSRI + SNRI

how do MAOI/Monoamine oxygenase inhibitors work

prevent breakdown of monoamine nts in presynaptic neuron because inhibition of monoamino oxygenase enzyme causes increased nts as they aren't broken down by enzyme

how do TCA/Tricyclics work

inhibit 5HT, DA, NE reuptake transporters

what is wrong with TCA

they aren't very specific, dirty drug

which of the depression treatments are not as safe and which ones are safe

safe- SSRI + SNRI
not safe- MAOI + TCA

what are reasons why side effects happen

1. dirty drugs bind to several things 2. nts such as serotonin have several functions

how is SSRI different to TCA

more specific than TCA

how are SSRI + TCA similar

both reuptake related

what is the placebo effect rate in depression treatments

20%

what is the drug efficacy in depression treatments

30%

what percent of patients feel better after med depression treatments

5%

what are the issues with monoamine hypothesis

placebo effect with less efficacy + patients feel better after 4-6 weeks even though the drugs work/ increase 5ht +NE right away

what can explain why patients feel better 4-6 weeks after drug usage

lag time

what is SNRI related to

serotonin + NE

what is SSRI related to

serotonin

what is SNRI similar to SSRI for

placebo and efficacy

what are the side effects of SSRI depression med treatments

higher risk of suicide in adolescents

what are the alternative to meds in depression

ECT, deep brain stimulation, sleep deprivation, repetitive transcranial magnetic stimulation, vagus nerve stimulation, therapy

when is ECT used for depression treatment

used as a last resort

how effective is ECT

very effective

in which type of MDD is ECT used

MDD- treatment resistant disorder/ depression

how does ECT work to help depression

electric shocks --> seizure --> more glutamate --> higher LTP by restoring brain's ability to rewire itself (plasticity)

what hypothesis is ECT based on

plasticity

what idea is ECT working on for depression

that brain is locked into certain firing connections that maintain depression and unlock those through LTP

what are side effects of ECT

adverse memory effects

when is deep brain stimulation used in depression and why

as a last resort since requires implantation in brain

how does deep brain stimulation work

induce LTD in mood parts of brain such as limbic system

where are successes of deep brain stimulation seen

clinical trials

how are sleep patterns different for depressed people

1. long periods of awake before sleep 2. several awakenings at night 3. don't get to stage 3 (sws)

how do sleep deprivation studies help with depression treatment

cause deprivation to allow long sleep of SWS for rest

are repetitive transcranial magnetic stimulation, vagus nerve stimulation invasive or non invasive

non invasive

are repetitive transcranial magnetic stimulation effective

not sure

how do repetitive transcranial magnetic stimulation work

hover magnets over brain to stimulate activity in brain

what is vagus nerve

cranial nerve that stimulates stress

what are the types of therapy used for depression

cbt + behavior therapy

how effective and widespread are therapy for depression

very effective, due to insurance not as accessible

which of the disorders can be cured

depression

can depression again after having it once

may or may not

what are the newer ideas about depression

inflammation and stress - BDNF

what are the alternative to meds in depression based on

plasticity hypothesis

how does HPA axis work during stress

hypo release crh--> pitiuary release acth--> adrenal gland release glucocoricoids + cortisol