L9- anxiety and depression Flashcards
disorder related to limbic system
anxiety, depression and bipolar
what is anxiety
excessive worry and fear repsonse to stressor
what is secreted in response to anxiety
corticosteriods- cortisol
types of anxiety dirsorders
general
phobic
panic
features of general anxiety disorder
SNS and ANS effects
restlessness, tachycardia, sweating
components of the brain and other body parts involved in generatign normal anxiety
cortex> amygdala and hippocamus> HPA axis releasing cortisol
what is suggested about the brain and HPA causing excessive anxiety
overactivity of HPA
changes in synaspes and connectivity
treatment for anxiety
Benzidiazepines (benzo)
-5-HT partial agonists
B adrencoreceptor antagonists
-anti depressants like SSRIs
mechanism of benzo
bind to allosteric sites on GABA receptor
-increase GABA affinity and Cl entry for inhibition and hyperrepolarisation
eg of benzo
diazepam
nitrazepam
kinds of benzo
anxiolytic
hypnotic
problems with benzo
sedation, acute overdose, built up tolernace, dependance - wthdrawal issues
pros of using 5-HT partial agonists
no sedation
non addicitve
no withdrawal effects
symtpoms of depression
misery, despair, losso of motivation, suidicial thoughts
what is monoamine (MA) theory of depression and evidence for it
- due to hypoactivity of MA synsapes in the brain
- antidepressants (ADD) increase MA activity in the brain
evidence against MA theory
Antidepressants takes weeks to work
-Amphetamine and cocain work even thought they arent antidepressants
treatment for depression
psychotherapy
ECT
antidepressant drugs
classes of ADD
MA oxidase inhibtiors
tricyclic ADsants
SSRI- selective re uptake inhibtors
what is MA oxidase (MAO)
enzyme in mitochondria that breaks down MAs
mechanism of MAO inhibitors
prevents MA from being broken down so more stimukation of MA neurons
mechanism of SSRI
prevents recycling of NTs so more in the synapse celft
effects of MAOI and negative effects
- immediate effect of euphoria
- AD action
negative
-antimuscarnic affects
alpha 1 receptor antgaonism
negaitve effects of TCAs
slow-
anti muscarinic
sedative
overdose
network theory of depression
increase of CRF (cortisol releasinf factor) and cortisol in CSF
- hyperactivity og neuroendocrine stress response > depression
