Lecture 11: Anti-depressants Flashcards
Outline of depression and treatments
See figure
Types of depressive disorders
Reactive (secondary) depression
Bipolar disorder
Major depression
Reactive (secondary) depression
Temporary reaction to real stimuli such as grief or illness
Treatment is largely by psychotherapy
Bipolar disorder
Recurrent major depressive episodes with intervening manic, or mixed episodes
Major depression
One or more major depressive episodes free of manic, mixed or hypomanic episodes
Defined by DSM-V
Prevalence of major depressoin
Males: 9.6 %
Females: 16.2 %
3-5% of the population is experiencing a major depressive episode at any given time
30-50% have a single episode, recurrent episodes in 50-70%
Onset of major depression
25-44 years of age
Genetic component of major depression
1st degree relatives 1.5-3 times more likely to have MD
Risk by inheritance: 39%
Symptoms of major depression
Emotional: persistent diminished ability to experience pleasure, loss of interest in usual actives, pessimistic outlook, anxiety
Physical: chronic fatigue, insomnia, appetite disturbances
Cognitive: Poor concentration, slow thinking, poor short-term memory, confusion
Psychomotor: slowed physical movements and speech, agitation
Therapies for major depression
Non-pharmacologic: psychotherapy, ECT (electroconvulsive therapy)
Pharmacologic: 50-60 % of patients are responsive, newer drugs are well tolerated, all drugs have similar efficacy
Amine hypotesis II
Most antidepressant drugs appear to work by enhancing synaptic monoamines
Block normal neurotransmitter reuptake processes
Therapeutic lag of anti-depressants
Drugs increase neurotransmitter levels right away but efficacy is delayed 1-4 weeks
Phases of amine hypothesis
Phase 1: amine enhancement - short term (min-hours) uptake inhibition
Phase 2: amine enhancement - long term (weeks) effects of phase 1 enhancement. Produces further enhanced amine levels to reach therapeutic significance
What happens in normal receptors without antidepressants?
Pre-synaptic receptors will create a feedback inhibition to stop amine release
Phase 1 causes down regulation of receptors to maintain normal agonist: receptor levels
This leads to reduced negative feedback and phase 2 amine increase
What does pre-synaptic receptor down regulation correlate with?
Mood
Less pre-synaptic receptors = better mood
