Depression Flashcards
what is psychiatry
branch of medicine which focuses on the prevention, assessment, and treatment of mental, emotional and behavioural disorders
what is delusion?
a belief that is clearly false and indicates an abnormality in content of thought, the belief is held despite being presented with evidence against it
what is hallucination?
a sensory preception in the absence of a corresponding external or somatic stimulus and described according to the sensory domain in which it occurs
what is psychosis
hallcination, delusion OR hallucination and deluision
- loss of contact with external reality
what is the central component of psychosis
impaired reality testing
what is delirium
acute, fluctuating change in attention and consciousness including disorganized thoughts
what is a depressive episode
experience of low or depressed mood, loss of interest in most activities
what are the characteristics of someone with mania
increased talkativeness, rapid speech, decreased need for sleep, racing thoughts, distractibility, increase in goal-direct activity, elevated mood, impulsivity, irritability
what is the duration of mania?
1 week or more Or if severity of symptoms warrants hospitalization
how long is hypomania
at least 4 days, shorter than mania
hypomania does not cause what?
does not cause major deficit in social or occupational functioning
what are the two components that must be present in the DSM-5 for Major Depressive Disorders
- depressed mood
- anhedonia
what is anhedonia?
loss of interest/pleasure in almost all activities
what are the leading biomedical theories for MDD
- monoamine hypothesis
- stress-induced depression hypothesis
- neurotrophic/neuroplasticity hypothesis
- cytokine hypothesis/neuroinflammation hypothesis
- circadian hypothesis of depression
- GABA-glutamate-mediated depression hypothesis
what is the monoamine hypothesis?
altered levels of monoamine neurotransmitters,, specifically serotonin, noradrenaline, and dopamine cause depression
what is the critique for the monoamine hypothesis?
critiqued in that abruptly decreasing serotonin and/or dopamine doesn’t cause depression in a healthy person
what is stress-induced depression hypothesis
chronic stress leads to dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis
what does chronic HPA activation lead to?
excess cortisol secretion and pro-inflammatory agents that damage glia and neurons, interfere with neurogenesis and reduce glutamate and GABA
what is the critique for stress-induced depression hypothesis
hypercortisolism is not a feature of all MDD cases AND not clear what causes HPA dysregulation (i.e. loss of GR sensitivity)
explain the neurotrophic and neuroplasticity hypothesis for depression
Brain-derived neurotrophic factor (BDNF) promotes neurogenesis, regulates differentiation and growth of neurons
Decreased BDNF gene expression, decreased BDNF levels and receptors in MDD patients
Increased cortisol can inhibit BDNF
Same triggers that elevated cortisol appear to block neurogenesis
what do antidepressants do?
have been demonstrated to stimulate neurogenesis in adult hippocampus (animal studies)
explain cytokine and neuroinflammation hypothesis for depression
MDD patients have increased levels of pro-inflammatory markers and increased levels of macrophage/monocyte activation
explain the circadian physiology in a healthy state
- light inhibits pineal gland from producing melatonin by activating neurons with suprachiasmatic nucleus of the hypothalamus
- SCN regulates production of melatonin throughout the body
- melatonin production increases at night during conditions of dark
explain the circadian hypothesis for depression
genes controlling circadian rhythms in anterior cingulate cortex are dysregulated in depression
- phase advance in cortisol rhythm and reduced amount of melatonin production seen in some patients with MDD
explain the excitatory neurotransmitters hypothesis for depression
- Glutamate may cause excitotoxicity resulting in neuronal atrophy and reduced synaptic connectivity
○ Stress induced changes may be accelerated in the presence of elevated Glu
○ Reduced GABA in CSF of MDD px – may be d/t change in serotonin which modulates GABA, which in turn modulates glutamate
explain glutamate excitotoxicity for depression
excessive accumulation of glutamate within synaptic cleft results in over stimulation of postsynaptic glutamate receptors
- Via NMDA receptor glutamate promotes calcium influx
describe bipolar 1
At least 1 manic episode and usually depressive episodes
describe bipolar 2
Major depressive episodes with at least 1 hypomanic episode
what are the pathophysiology of bipolar disorders
- Circadian Rhythm Dysfunction
- Metabolic Dysfunction
- Mitochondria Dysfunction
- Glutamate Excitotoxicity
explain the aspect of circadian rhythm dysfunction for bipolar disorder
- During mania there is a reduced need for sleep
- Observations in patients with bipolar disorders:
○ Changes in melatonin levels
○ Changes in melatonin receptor expression with CNS
○ Changes in cortisol profiles (patterns of release)
○ Sleep deprivation as well as light therapy have been effective as adjunct in some cases of bipolar disorder
explain the aspect of metabolic dysfunction for bipolar disorder
- Various metabolic abnormalities have been found in patients with bipolar disorder such as:
○ Increased risk of obesity, type 2 diabetes, and reduced longevity due to increased cardiovascular problems
○ Increased amount of leptin secreted in obese patients with bipolar compared to obesity alone
§ Leptin regulated appetite AND sleep duration - A hypothesis suggests that the body is forced to compensate for the high metabolic demand of the brain during manic states:
○ Reduced appetite
○ Reduced sleep
○ Increased energy expenditure
explain the aspect of mitochondria dysfunction for bipolar disorder
Impairment in mitochondrial function resulting brain metabolism shifting towards glycolysis
- Polymorphisms within mitochondrial DNA linked to BD
- Reduced levels of phosphocreatine within frontal cortex
- Evidence of impaired oxidative phosphorylation
- Reduced expression of genes coding for various complexes of the electron transport chain in hippocampus
explain the aspect of glutamate excitotoxicity for bipolar disorder
increased glutamate in frontal cortex of px with BD
- increased levels of excitatory glutamate appear to result an increased energy demand on the neuron,
increased glucose consumption in areas of high glutamate synaptic activity
