Task 6 Flashcards
(40 cards)
What are the two major mood disoreders?
- Bipolar disorder
2. Depressive disorders
What is the prevalence for mood disorders?
Lifetime: 5.2% - 17.1%
–> Could go up to 20% for men and 30% for woman
Comobidity
Around 60% of people with depression also experience anxiety disorder
DSM-5 criteria for major depressive dirorder
- Five or more f the symptoms have to be pressent during same 2-week period. At least one of the symptoms has to be depressed mood or loss of interest or pleasure
- Symptoms cause clinically significant distress or impairment in scoial, etc areas of functioning
- Not attributable to physiological effects of substances or medication
- Cannot be better explained by schizophrenia spectrum disorders or psychotic disorders
- There has never been a manic or hypomanic episode.
- -> this one doesn’t apply if the episodes appear during effects of substance
What is Persistent Depressive Disorder?
When individual meets diagnostic criteria for major depressive disorder for 2 years
–> Diagnosis requires: poor appetite, insomnia/hypersomnia, low energy, lo self esteem, poor concentration, hopelessmess
DSM-‐5 criteria determine when to diagnose major depressive episode, but depression can take many forms/subtypes.
Name them
- Anxious distress
- Mixed features –> presence of at least 3 manic/hypomanic symptoms but doesn’t meet criteria
- Melancholic features
- Psychotic features
- Catatonic features
- Atypical features
- Seasonal pattern SAD (e.g. depressive episode during winter)
- Peripatum onset (during pregnancy or in the 4 weeks after delivery)
What are the melancholic features?
Inabilityto experience pleasure, distinct depressedmood,depression regularlyworse in morning, early morningawakening, marked psychomotorretardation or agitation, significant anorexiaor weight loss, excessive guilt.
What are the psychotic features?
Presence of mood-congruent or mood-incongruent delucions or hallucinations
What are the catatonic features?
Behaviors: not relating to environment, mutism, posturing, agitation, mimicking another’s speech or movements (remember the Joker)
What is the Premenstrual dysphoric disorder?
considered a separate disorder in DSM-5
Increasesin distress during premenstrual phase of menstrual cycle that some womentend toexperience. Symptoms are often a mixture of depression, anxiety and tension,irritability and anger. These may occurinmood swings, the weekbefore onsetof period. Many women experience this mildly, with only2% meetingthe diagnostic criteria.
What do the Biological theories of depressions include?
Genetics, NT systems, and functional abnormalities in brain and neuroendocrine systems
Genetic factors
- If one of your papis had MD then your are 2-3 times more likely to have it
- MJ that appears early in life has stronger genetic base
- Serotonin transporter gene abonormalities
Neurotransmitter theories (1)
- Sero, nore, and dopa are found in the limbic system, which is associated w/ regulation of sleep, appetite amd emotional processes
• Low serotonin and norepinephrine may account for cognitive, behavioral and motivational deficits
• Low dopamine levels may be responsible for deficits in rewards system –> makes them unmotivated
Neurotransmitter theories (2)
- Sero and nore are released by presypnaptic neuron and then bind to receptors on other neurons. This release process (regulated by serotonin trnasporter gene) may be abnormal in depression.
Or receptors may be less sensitive than normal or malfunction
Neuroendocrine system theory
Lack of inhibitory control over the Hypothalamic-Pituitary-Adrenocortical (HPA) network is associated with depression since this system manages and reacts to stress and triggers secretion of cortisol in response to it.
What does the article from Cowel explain about HPA axis and depression?
It was proven that there is a established link between Cortisol hypersecretion and depression.
—> the elevated secretion of cortisol was also found in patients who recovered from depression —> this suggest that some aspects HPA axis abnormalities are more persistent and may be present before onset of illness (due to genetic factors or adverse experiences)
Also found in people not depressed so it has to do more with VULNERABILITY
If cortisol hypersecretion predisposes to depression, what is the mechanism?
- Neurogenesis (especially in hippocampus) is inhibited by excessive cortisol which leads to hippocampus atrophy —> cognitive impairments in declarative memory
- Cortisol may also facilitate emotional memory (more research needed)
Structural and functional brain abnormalities
—> Decreased activation in PFC which results in failure to anticipate incentives - therefore no means to achieve goals
—> Decreased activation in ACC May reflect in deficit in ‘will to change’
—> Deficits in functioning of hippocampus may result in individual dissociating affective response rom relevant contexts (feel sadness in happy context)
—> Increased activation in amygdala may lead to interpreting threatening info negatively
Behavioral theories to depression
Up to 80% of people with depression report a negative life event prior to onset of depression
- Behavioral theories argue that it results from lack of appropriate reinforcement for positive and constructive behaviors. This leads to behavioral vacuum = person becomes inactive and withdrawn.
- Learned helplessness theory
Cognitive theories to depression
- Negative cognitive triad theory (Beck)
- Reformulated learned helplessness theory/Attribution theory
- Hopelessness theory
- Rumination theory
Negative cognitive triad theory (Beck)
Negative views in self, world and future. Ignore good events and exaggerating negative ones.
Reformulated learned helplessness theory/Attributional theory
They become depressed when they attribute negative life events to factors that cannot be controlled or are unlikely to change. They attribute negative events to internal, stable and global factors.
Hopelessness theory
Develops when make pessimistic attributions about important events and perceive that they cannot cope with consequences.
Rumination theory
Suggests that rumination (reflexion, meditation) predicts onset of depressive episodes, as well as relapses.
