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Psychofarmology - College 6 - Coggle Diagram
Psychofarmology - College 6
Mood disorders
Mania
Hypomania
Normal
Dysthymia
Depression
Bipolar I:
At least 1 manic/mixed episode
Can include major depressive episodes
Bipolar II
:
At least 1 major depressive episode
At least 1 hypomanic episode
Cyclothymic disorder
:
Swings between hypomania and dysthymia.
No full manic of major depressive disorder.
Major depressive disorder (MDD):
Depressed mood/loss of interest
Clinically significant distress/impairment
No previous manic episode or a hypomanic episode
More often with women than men, overall
Related to fluctuations in hormonal changes
4 R's:
Remission
= no or minimal symtoms
Recovery
= 6/9 months in remission
Relapse
= during or before remission
Recurrence
= after recovery
Response = we want complete remission.
Important factors in
treatment
:
Quick = better
Optimal risk-benefit: 25-64 years
Relapse rate increases when more treatments are needed
The longer you take the medication, the better.
Persistent depressive disorder (Dysthymia):
"Mild" chronic depression
Not all the symptoms of depression, for over 2 years.
Biological basis:
Stress & HPA-axis:
Growth factor
Neurodegeneration
BDNF
= growth factor.
Function is to sustain the viability of the neuron.
BDNF gets inhibited by the stress. Then neuronal death. Lowers the levels of serotonin, dopamine and norepinephrine. Leading to disfunctioning in the hippocampus and the prefrontal cortex.
-> HPA-axis gets less inhibited.
Chronic stress:
Hypercortisolisme -> Overinhibition -> Atrophy in the hippocampus.
Stress
: Hypothalamus and Hippocampus are inhibited by cortisol so the body can respond correctly on the stress factor.
Monoamine hypothesis:
Focused on the monoamine transmitter system (dopamine, serotonine, norepinephrine ).
-> Too much is mania
-> too little is depression
Direct evidence of the hypothesis is lacking
Serotonin
is made from the precursor tryptophane.
Tryptophane -> 5HTP
5HTP -> 5HT (serotonin)
Two ways to stop it:
Reuptake by SERT
Extracellular destruction by MAO A/MAO B (only when concentration is high)
Norepinephrine
is made from tyrosine (same as dopamine).
Tyrosine -> TOH -> DOPA
DOPA -> DDC -> Dopamine
Dopamine -> DBH -> Norepinephrine
Two ways to stop it:
Reuptake by NET
Destruction by MAO A, MAO B, COMT (just like dopamine)
Neurotransmitter receptor hypothesis & gene expression:
In addition to the monoamine hypothesis
They state that there is not only a disbalance of the monoamines but ALSO a compensation by receptors. The body is upregulating the receptors. Leading to change in gene expression.
Treatment:
Idea is increase the monoamine levels -> reduce receptor sensitivity -> reduce depressive symptoms (normalize)
SSRI
's:
Most widely used type of antidepressants.
= Reuptake inhibitors
It inhibits SERT -> increase in serotonin in the synaptic cleft -> downregulation receptors (reducing side effects) -> less inhibition -> increased serotonin release -> side effects happen -> postsynaptic receptors make sure side effects are reduced.
MAOI
's:
The least used of these types.
Function = Stop MAO A from destroying.
You have dietary restrictions. For your blood pressure.
TCA
's:
It consits of 3 rings in their chemical structure.
They inhibit NET and SERT.
Very effective, but a lot of side effects.
Not commonly used.