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clinical depression
affects 10% of the population and can last several months
c = uncontrolled stress (dysregulation of HPA), genetic predisposition expressed via environmental factors
major depressive episode
must meet 5/9 symptoms that are persistent for at least 2 weeks from DSM-V
effects of high cortisol
low 5-HT, DA, and NE in synapse (monoamine hypothesis of depression)
leads to decreased 5-HT1A, 5-HT2, beta, alpha 2A, and D1
low production of BDNF
depression in the brain
increased amygdala activity
increased activity in frontal lobe
thinning of cortex of R hemisphere
decreased hippocampal volume
decreased blood flow to ares involved in attention
major depressive disorder (MDD)
intense sadness alternates with mania
congenital
types:
bipolar I
bipolar II
rapid-cycling
t = antidepressants + modd stabilizer
postpartum depression
depression after childbirth
1/8 women
c = drop in estrogen/progesterone after childbirth
lack of treatment causes postpartum psychosis
postpartum psychosis
caused by untreated postpartum depression
s = hallucinations, delusions, paranoia
seasonal effective disorder (SAD)
seasonal depression
c = increased 5-HT transporters, increased melatonin
t = antidepressants + light therapy
monoamine oxidase inhibitor (MAOI)
reduce degradation of 5-HT
side = hypertension with food/drugs
hardil
tricyclic antidepressants (TCA)
blocks reuptake of 5-HT, NE, DA
side = dizzy, hypotension
elavil
serotonin-specific reuptake inhibitors (SSRI)
reduces 5-HT reuptake by binding to SERT
side = weight gain, sexual dysfunction
prozac, zoloft, paxil
serotonin norepinephrine reuptake inhibitors (SNRI)
reduce reuptake of 5-HT and NE
side = nausea
effexor
norepinephrine dopamine reuptake inhibitor (NDRI)
reduce reuptake of NE and DA
side = tremors, dizzy, insomnia
wellbutrin, zyban
electroconvulsive shock therapy (ECT)
electrical current induces seizure
repetitive transcranial magnetic stimulation (rTMS)
alters cortical electrical activity
deep brain stimulation
implant electrode to stim cingulate cortex
ED50
effective dose in 50% of patients
TD50
toxic dose in 50% of patients
LD50
lethal dose in 50% of patients
anxiety in the brain
prefrontal cortex shuts down
anterior cingulate cortex hyperactive
amygdala enlarges (boosts signal)
GABA in anxiety
decreased → not effective in inhibiting release of NE and 5-HT
NE and 5-HT in anxiety
increased release of NE and 5-HT to synapse (5-HT hypothesis of anxiety)
generalized anxiety disorder (GAD)
persistent anxiety for long time without identification of true source
t = cognitive behavioral therapy + meds
phobias
intense irrational fears centered in specific thing
t = exposure and response therapy (ERT)
obsessive compulsive disorder (OCD)
recurrent uncontrolled thoughts (obsessions) cause anxiety and repetitive acts (compulsions)
c = exposure to strep as a child produces antibodies that attack brain proteins
t = cognitive behavioral therapy + meds
post-traumatic stress disorder (PTSD)
memories of unpleasant event causes intense anxiety
s = repeated flashbacks, nightmares, sporadic behaviors
c = deficit in STM, overactive adrenergic system, small hippocampus, reduced neurogenesis
t = propanolol
benzodiazapenes (BZD)
binds to GABA → increases binding to GABAA → increase inhibition of 5-HT and NE release
s = habit forming, drowsy, memory impairment
valium, xanax, ativan
buspar
5-HT1A agonist
beta-blockers
propanolol
antidepressants
prozac, paxil, effexor
schizophrenia
involves breakdown of relation between thought, emotion, and behavior (split mind)
positive symptoms
not present under normal conditions
positive symptoms of schizo
psychosis
negative symptoms
should be present under normal conditions
negative symptoms of schizo
emotional dysregulation
flat effect
anhedonia
impaired motivation
algonia
social withdrawal
cognitive symptoms of schizo
neurocognitive impairment
risk factors for schizo
genetic predisposition
mutation of DISC1 gene
environmental factors
older paternal age
virus in vivo
erythroblastosis fetalis
hypoxic during birth
stress associated with city living and pollution
schizo in the brain
hypofrontality hypothesis: decreased blood flow to frontal lobes due to decreased metabolic activity there
enlargement of lateral ventricles
NT in schizo
increased DA
increased 5-HT
decreased G
first-generation antipsychotics (FGA)
D2 agonists
reduce positive symptoms, worsen negative symptoms
long term use leads to movement disorders
only used as a last resort
side = akathisia, dystonia, neuroleptic-induced parkinsonism, tardive dyskinesia (TD)
chlorpromazine, haloperidol (halodol)
second-generation antipsychotics (SGA)
agonists for D2 and 5-HT2A
reduces positive and negative symptoms
side = weight gain, diabetes, heart issues
risperidone, olansopine, zyprexa, ablify
atypical antipsychotic
NMDA agonist, 5-HT2A antagonist, balances DA levels
side = sleepy, nausea, dizzy, dry mouth
caplypta
glutamate hypothesis
dysfunction of G leads to underactivation of G receptors, leading to decreased activity in frontal cortex
brain-derived neurotropic factor (BDNF)
helps in neural connections, prevents neurodegeneration, promotes plasticity
lithium
mood stabilizer
reduce NMDA to reduce G activity
increase GABAB to increase GABA activity
increase BDNF
side = weight gain, fatigue, kidney damage
depakote
mood stabilizer
increases GABA activity
dose response curve
graph that shows effective dose of drug
prefrontal cortex function
dampens anxiety under normal conditions
anterior cingulate cortex function
amplifies signals from amygdala under normal conditions
amygdala function
responds to scary stimulation under normal conditions
social cognition
understanding social cues
akathisia
feelings of anxiety, restlessness, pacing, repetitive and purposeless actions
dystonia
involuntary muscle contractions and abnormal postures
neuroleptic-induced parkinsonism
tremor at rest and slowing of limbs
tardive dyskinesia (TD)
irreversible movement disorder, involuntary hyperkinetic movements of face/tongue/limbs/trunk