GAD and Schizophrenia Flashcards

1
Q

what are anxiety disorders

A

fear = response threat,
anxiety = anticipiation of threat

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2
Q

what is GAD?
+ diagnostics

A

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)

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3
Q

deszcribe a bit about aetiology of GAD

A

30& heritability
correlated with neuroticism
SNP in BDNF gene
environment = separation, overprotection, family dysfunction
gene x env = inc methylation glucocorticoid receptor

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4
Q

GABA and anxiety

A

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

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5
Q

monoamines in anxiety

A

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

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6
Q

brain circulatory patho anxiety

A

inc activity amygdala + prefrontal cortex => correlates with symptoms
act anterior cingulate cortex inc during decision making in GAD

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7
Q

endocrinology patho anxiety

A

overactive HPA = inc waking cortisol,
inc CRF = greater startle response
overactivity in amygdala =? overstim HPA axis => HRC loss => loss of stop break

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8
Q

pharm treaments anxiety serotonin

A

serotonin => block serotonin uptake, balance
HT1a implicated
\prsynaptic serotonin dec firing
postsynaptic limbic system + frontal cortices, regulated by glucocorticoids

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9
Q

pharm treatments anxiety gaba

A

GABA => benzo eg valium
allosteric site GABA a, inc open prob, inc gaba transmission in aygdala

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10
Q

pharm treatments anxiety - cannabidiol

A

endocannabinoid system
act cbir receptor is anxiolytic
signalling in hippo + amygala = red following chronic stress
stimulates 51a

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11
Q

psychotic disorders diagnosis
+ what is schiz

A

positive, negative + cognitive symptoms
two or more (delusions, hallucinations, disorganised speech) + more
low level functioning
symptoms present for 6 months

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12
Q

aetiologyu of schizo

A

80% heritability
dopamine d2 receptor, subunits NMDA, ERBB4
env = paternal age, drug abuse, maternal vit D deficiency

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13
Q

ntsm patho schizo

A

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

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14
Q

glut hypothesis schizo

A

nmda receptors induce symptoms of schizo
also, nmdar antagonists inc firing neurons for excessive dopamine release
=? inc glut in schizo
schizo could be disinhibition

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15
Q

brain structure patho schizo

A

global dec grey white matter, brain V, cortical thickness (prefrontal cortex)
inc ventricular V

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16
Q

brain activity patho schizo

A

inc act midbrain salience processing (hallucinations + delusions)
inc auditory speech processing
dec amygdala to respond to emotional stim
dec act dorsolateral prefrontal cortex during executive functioning task

17
Q

1st and 2nd gen schizo pharm treatment

A

1st => d2 receptor antagonist anaesthetic improves symptoms + drugs with similar structure, but side effects = involuntary mvm
2nd => clozapine = . d2 + 5Ht, less motor side effects
minimal to no relief from cog and neg symptoms
looking at red glut release