depression Flashcards
2 ways of treating depression?
CBT or pharmacotherapy
-side effects to drugs
what can cause depression?
- premature death
- disability
2 types of depression?
unipolar or bipolar
explain unipolar depression
most common type, mood swings in 1 direction
75% of cases are reactive/environmental
25% of cases are genetic
explain bipolar depression
less common, oscillation between depression and mania, mood swings in 2 directions
- mania is excessive exuberance, self confidence, aggression, irritability
- more based on genetics
depressive disorder
low state, feelings of guilt, sadness, low self worth
major depressive disorder
severe pattern of depression that is disabling, not caused by factors like drugs/general medical condition
what is the name of major depressive disorder that is chronic?
dysthymic disorder
is diagnosing depression easy?
no
you can do a clinical interview and ask questions, and use the book
what is DSM IV?
what psychiatrists use to diagnose a person with any mental illness
- need 5 or more of the symptoms present in the same 2 week period
eg. significant weight loss, insomnia, feeling of low self worth, recurrent thoughts of death, low energy, not able to concentrate
how can the symptoms of depression be categorised?
emotional symptoms
-pessimism, loss of motivation, low self esteem, indecisiveness
biological symptoms
-decreased appetite, sleep disturbance, loss of libido
how does depression differ between males and females?
affects twice as many females
how does depression differ between age groups?
1st episode of depression usually late adolescence/early adulthood
suicide
20% of depressed patients attempt suicide
depression and comorbidity
depression is often comorbid with other psychiatric conditions
-eg. cancer, pain
name some medical conditions where you would find depression:
- terminal illness
- chronic illness
- neurological disease
- stroke
- drug abuse
- parkinsons disease
- anxiety
what are comorbid?
depression and anxiety
is there a genetic predisposition to depression, and how do we know this?
yes there is, we know this because of twin studies
-the environment also plays a role
explain the monoamine theory of depression
depression is caused by monoamine deficiencies
- reduced activity of noradrenergic/serotonergic systems
- antidepressant drugs increase amine concentration in the brain
explain the neuroendocrine theory of depression
depression is caused by hypersensitivity of the HPA axis
- stress activates the hypothalamus to release CRH, ant pit releases ACTH, adrenal cortex (zona fasiculata) releases cortisol
- HPA activated in situations which normally wouldn’t even be considered stressful
- results in increased basal cortisol levels
- increased CRH levels have been found in cerebrospinal fluid, and increased plasma cortisol levels in depressed patients
- decreased hippocampal glucocorticoid receptors
what controls the HPA?
HPA releases cortisol, which acts positively on the hippocampus
-hippocampus inhibits the HPA
-amygdala stimulates the HP
so, hyperactive amygdala or hypoactive hippocampus can cause depression
role of tactile stimulation?
tactile stimulation after birth activates 5-HT pathways to the hippocampus
-5-HT triggers long lasting increase in the expression of glucocorticoid receptor gene
-therefore, increase in glucocorticoid receptors in hippocampus
this is why abused/neglected babies can end up with mental illnesses
how do SSRIs affect glucocorticoid receptors?
they increase glucocorticoid receptors in hippocampus
hippocampus and pre frontal cortex
neuronal loss and decreased neuronal activity in depression
what does 5-HT promote?
neurogenesis during development (BDNF)
BDNF promotes survival of cells in the brain
how does exercise have an anti-depressant effect?
increased BDNF levels, therefore increased neurogenesis
chronic stress consequences
- increased cortisol levels will stimulate the detrimental gene transcription response
- increase glutamate release, hyper activation of NMDA receptors, causing excitotoxicity neuronal death and depression
what inhibits the detrimental gene transcription response?
activation of alpha 2 or 5HT-1A
-ie high levels of NA or serotonin
treatments for affective disorders?
- ECT
- Psychotherapy (CBT)
ECT
electroconvulsive therapy,
- localised electrical stimulation
- evidence of neurogenesis but side effect of MEMORY LOSS
psychotherapy
treats mild-moderate depression
- overcome negative views
- based on the idea that social interaction has a big anti-depressant effect
all drugs that treat depression work by….
increasing NA or serotonin levels
-neurons get activated, NA released and binds to post-synaptic receptors, gets back inside the neurones via NA transporter
drugs treatments
Monoamine Oxidase Inhibitors (MAOIs) Tricyclic Antidepressant Drugs (TCAs) Selective Serotonin Re-uptake Inhibitors (SSRIs) mixed 5HT/NA reuptake inhibitors (SNRIs) NA reuptake inhibitors
Tricyclic antidepressants (TCAs)
- block reuptake of 5HT and NA, increase levels of these 2 in the synaptic cleft
- down regulation of presynaptic receptors and therefore increase in transmitter release
- long time to produce effects
- good but not ideal
- cardiovascular effects
- also affects other receptors eg. muscarinic
Monoamine Oxidase Inhibitors (MAOIs)
- increased cytoplasm levels of 5HT/NA, increased leakage of these 2 monoamines
- increased levels in the synaptic cleft
Selective Serotonin Re-uptake Inhibitors (SSRIs)
5-HT reuptake inhibitor
- Increase in 5HT in synaptic cleft
- autoreceptors down regulated
benefits and consequences of Selective Serotonin Re-uptake Inhibitors (SSRIs):
no cardiovascular problems because they don’t affect NA, but side effects include:
- insomnia and sexual dysfunction due to activation of 5-HT2A receptor
- nausea, diarrhoea and headache due to 5-HT3 receptor activation
how long does the anti-depressant effect take?
antidepressant effect takes several weeks
how do anti-depressants dampen down the HPA hyperactivity?
Increased hippocampal glucocorticoid receptor expression
