36- Depression Flashcards
name the two types of depression
unipolar
bipolar
describe characteristics & symptoms of unipolar depression
most common depressive disorder
environmental and genetic factors at play
associated with stressful life events
symptoms: range from mild to severe
- depressive mood swings
- hallucinations and delusions in severe cases, psychotic symptoms
describe characteristics & traits of bipolar depression
strong genetic factors, can be triggered by stress in adult life
oscillations between depressive and manic episodes
two types - type I and II
- type I = major manic episodes with/ without depression
- type II = hypomania, a less severe form of mania, with major depressive episodes
symptoms:
- manic episodes = self-confidence, excessive enthusiasm, impulsivity, aggression and irritability
- oscillations between depressive and manic episodes
criteria for diagnosis
according to DSM-V, person must exhibit 5 or more symptoms within a 2-week period
- depressed mood
- appetite and weigh changes
- loss of interest or pleasure
- psychomotor changes - slowing down of thoughts, reduced physical movement
- fatigue
- feeling worthless, inappropriate guilt
- suicidal thoughts = recurrent thoughts of death, suicidal ideation, a suicide attempt
- cognitive impairment
division of symptomology into emotional and biological
emotional symptoms
- apathy, pessimism, negativity
- low self-esteem and feeling guilty
- loss of motivation
- indecisiveness
biological symptoms
- reduced activity
- loss of libido
- sleep disturbances
- loss of appetite
describe co-morbidity associated with depression
medical conditions associated with depression such as - drug abuse, anxiety, Parkinson’s, thyroid dysfunction and neurological disease
define the two theories that may explain the biological basis of depression
monoamine theory = downregulation of noradrenaline, 5-HT and their post-synaptic receptors
neuroendocrine theory = an extension of the monoamine theory and dysregulation of the HPA axis
describe the monoamine theory
decrease in NA and 5-HT release - brain should respond through neuroplasticity and increase post-synaptic receptors, increasing sensitivity and responsiveness to NTs
in depression - downregulation of 5-HT, NA and their post-synaptic receptors
imbalances cause long-term changes in gene expression, growth factors, neuronal loss and monoamine regulation
evidence for and against the monoamine theory
evidence for:
- reserpine decrease 5-HT and noradrenaline, induces depression
- some antidepressants work by increasing monoamine levels, relieving depressive symptoms
evidence against:
- individual responses towards antidepressants - some don’t experience relief of depressive symptoms despite monoamine increase
- plasma and CSF levels of NA and 5-HT are normal between depressed and healthy individuals
- delayed onset of therapeutic effects of antidepressants = suggests secondary adaptive changes in the brain (neuroplasticity) may be needed
describe the neuroendocrine theory behind depression
extension of the monoamine theory with dysfunction of the HPA axis - two aspects of it are increased plasma cortisol and neuronal loss
increased plasma cortisol:
- 5-HT and noradrenaline released from neurons and act on the hypothalamus
- hypothalamus release CRH
- anterior pituitary releases ACTH
- ACTH acts on the adrenal cortex = cortisol released
- increased plasma cortisol and CSF CRH in depressed individuals
neuronal loss:
- neuronal loss = decreased neural activity especially in hippocampus and pre-frontal cortex due to decrease in 5-HT levels
- 5-HT along with BDNF mediates/promotes neurogenesis and synaptic plasticity
- excess glutamate levels also associated = can cause excitotoxicity and neuronal cell death
describe glutamate’s role in depression
excess glutamate can alter neurotransmission and induce excitotoxicity - neuronal cell death and damage
NMDA receptor antagonists like ketamine can relieve depressive symptoms by decreasing glutamate activity
evidence supporting the neuroendocrine theory
- decreased BDNF in depressed patients
- observed neuronal loss and decreased neural activity in the hippocampus and prefrontal cortex = explains emotional dysregulation and indecisiveness in depression. antidepressants promote neurogenesis in these areas
- ketamine-like drugs can modulate glutamate, have fast-acting anti-depressive effects
describe the psychological treatments available for treating depression
cognitive behavioural therapy - improving behaviours and mood by helping patients change negative cognitive processes
interpersonal therapy - assume depression is multi-factorial and interpersonal difficulties play a role in maintaining depressive symptoms
name the three main types of antidepressants
tricyclic antidepressants (TCAs)
monoamine oxidase inhibitors
SSRIs/ selective serotonin reuptake inhibitors
mechanism of action of tricyclic antidepressants?
block serotonin and NA reuptake, increasing their conc the synaptic cleft
downregulates alpha and beta adrenoreceptors, histamine receptors, muscarinic Ach receptors, and 5-HT 1A-D and 2A receptor subtypes
