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Psychofarmology - College 7 - Coggle Diagram
Psychofarmology - College 7
Anxiety disorder
2 key components of this disorder:
Fear (anxiety) -> Amygdala
Worry -> CSTC (portico-striatal-thalamic-cortical)
Generalized Anxiety Disorder
=
Excessive anxiety and worry (apprehensive expectation) about different situations /activities -> general and pervasive.
Symptoms
are restlessness (tense), difficulty concentrating, muscle tension, easily fatigued, irritability, difficulties sleeping
Amygdala pathways:
All pathways show overactivity.
(Fear)
Difference with 'worry' is that the HPA axis is involved here.
1.
Affect of fear
:
From amygdala to ACC and OFC (front of the brain).
Lead to the feeling of fear.
Avoidance
(due to affect of fear; it's a reaction of the fear feeling)
From amygdala to the PAG. Leads to the fear response (freeze, flight, fight).
Breathing output
:
From amygdala to PBN (in brainstem)
Increase in breathing fastness, shortness of breath, astma.
Endocrine output
:
From amygdala to hypothalamus
Increase in cortisol, increased risk in stroke, increased risk of coronary diseases.
Autonomic output
:
From amygdala to LC (also in brainstem)
Bodily reaction to increase in blood pressure. Can lead to damage to the heart etc.
CSTC circuit
(Worry/obsessions):
A negative feedback loop of overactivation.
Difference with 'fear' is that dopamine is involved here.
Biological basis
COMT theory
- 'Warriors & Worriers':
Dopamine
is important in processing information in the DLPFC
Normal situation:
Met variant -> lower activity COMT
More dopamine, so better information processing.
Val variant -> higher activity COMT
Less dopamine, poorer information processing
Worriers group
: stressor leads to increase in dopamine. With
met
variant you will have too much dopamine, so less proficient information processing.
Warriors group
: stressor leads to increase in dopamine. With
val
variant you will have a normal level of dopamine. 'Some people need stress for better functioning.'
GABA synthesis
:
GABA is made from glutamate, by the enzyme GAD.
Stopping GABA:
Reuptake by GAT
Destroyed by GABA-T
3 groups receptors
:
GABA-A = Ligand-gated ion channel
-> 4 transmembrane regions = 1 subunit
5 subunits = receptor
Important: Chloride channel; open -> more influx -> inhibition neuron
GABA-B = G-protein linked
GABA-C = Ligand-gated ion channel
GABA-A receptor
:
Benzodiazepine insensitive (alpha & delta) -> tonic inhibition
Benzodiazepine sensitive (beta, gamma & alpha) -> basic inhibition (fases of inhibition)
Benzodiazepine
= PAM (positive; stimulating action)
Allosteric modulator
: The primary neurotransmitter has to be present for the second one to have an effect.
Benzodiazepine
= lowers anxiety (calming), muscle relaxation (anticonvulsant)
Side effects:
'Hangover'
Amnesia
Depression
Motor/coordination difficulties
Overdose -> neuseau, confusion, headache, vomiting
Antidote ->
Flumazenil
Conditioning
: linking stimulus (situation) to fear. Difficult to reverse.
Extinction
: New link stimulus - (not) fear. Old link remains, new is stronger.
Reconsolidation
: Recall old link + weaken/destroy. Combi psychotherapy + psychopharmacology
OCD
:
Obsessions = thoughts, urges, images (internal), cause marked anxiety or distress
Compulsion = repetitive behaviors or mental acts. (internal & external), first goal-oriented, later conditioned response.
Probably serotonin imbalance.
Exposure and response prevention (ERP) works the best and longest.