GAD and Schizophrenia Flashcards
what are anxiety disorders
fear = response threat,
anxiety = anticipiation of threat
what is GAD?
+ diagnostics
intense worry about everyday things
worries interfere with functioning, long-lasting, +physical symptoms
relapsing
excessive anxiety most of time for 6+ months
cant control worry
+ 4 physical symptoms (fatigue, muscle tension etc)
deszcribe a bit about aetiology of GAD
30& heritability
correlated with neuroticism
SNP in BDNF gene
environment = separation, overprotection, family dysfunction
gene x env = inc methylation glucocorticoid receptor
GABA and anxiety
inhibitor
ionotropic GABAa (benzodiazepines), metaboropic GABAb
dec binding benzo in GAD, panic disorder + pTSD
dec GABA linked w anxiety
infusion of gaba antagonists can induce anxiety
monoamines in anxiety
disrupted serotonin signalling
serotonin agonist exacerbates anxiety in GAD
low receptor binding 1A = highler anxiety (low in anterior cingulate)
inc release norepinephrine
NE + MHPG inc in blood + saliva =? correlates with symptoms
brain circulatory patho anxiety
inc activity amygdala + prefrontal cortex => correlates with symptoms
act anterior cingulate cortex inc during decision making in GAD
endocrinology patho anxiety
overactive HPA = inc waking cortisol,
inc CRF = greater startle response
overactivity in amygdala =? overstim HPA axis => HRC loss => loss of stop break
pharm treaments anxiety serotonin
serotonin => block serotonin uptake, balance
HT1a implicated
\prsynaptic serotonin dec firing
postsynaptic limbic system + frontal cortices, regulated by glucocorticoids
pharm treatments anxiety gaba
GABA => benzo eg valium
allosteric site GABA a, inc open prob, inc gaba transmission in aygdala
pharm treatments anxiety - cannabidiol
endocannabinoid system
act cbir receptor is anxiolytic
signalling in hippo + amygala = red following chronic stress
stimulates 51a
psychotic disorders diagnosis
+ what is schiz
positive, negative + cognitive symptoms
two or more (delusions, hallucinations, disorganised speech) + more
low level functioning
symptoms present for 6 months
aetiologyu of schizo
80% heritability
dopamine d2 receptor, subunits NMDA, ERBB4
env = paternal age, drug abuse, maternal vit D deficiency
ntsm patho schizo
dopamine hypothesis
interacts with D1 excit and D2 inhib
d2 antagonists improve psychosis
dopamine agonists = induce psychosis
=> high levels dopamine => schizo
antipsych can improve pos symptoms bu t not gneg/cog
hypothesis refines => mesolimbic pathway = overactive =? dop synth is increasedd2 stim
mesocortical pathway = underactive =? red dopamine in prefrontal cortex + low d1 in pFC
glut hypothesis schizo
nmda receptors induce symptoms of schizo
also, nmdar antagonists inc firing neurons for excessive dopamine release
=? inc glut in schizo
schizo could be disinhibition
brain structure patho schizo
global dec grey white matter, brain V, cortical thickness (prefrontal cortex)
inc ventricular V