Depression and Treatment Pt 1 Flashcards
T/F: there is a discrimination between endogenous and nonendogenous depression
false. There used to be. But there is no longer an emphasis on the difference between the two. Both have typical treatment: drug therapy + some sort of alternative therapy for everyone, regardless of type of depression.
which “type” (end vs nonend) is more likely to respond better to therapy, CBT and exercise?
nonendogenous depression.
____ depression is biologically derived, where as _____ depression is environmentally/reactively derived.
ENDOGENOUS depression is biologically derived, where as NON-ENDOGENOUS depression is environmentally/reactively derived.
Symptoms (sleep and neurobiological) of endogenous depression.
- early morning waking
- depressed in the morning
- psychomotor retardation
- increased ventricular size
- THALAMIC ENLARGEMENT
- hippocampal brain reduction after multiple depressive episodes.
- more weightloss.
- biologically derived with no triggering issue (environment could be good, but person could still be depressed)
Non-endogenous depressive symptoms
- initial insomnia
- depressed in the PM
- often weight GAIN
non-endogenous depression is characterized by depression at ___, where as endogenous depression is characterized by depression in the ____
non-endogenous depression is characterized by depression at NIGHT, where as endogenous depression is characterized by depression in the MORNING
____ ___ waking is the most significant predictor of the severity of depression. Why?
Early morning waking is the most significant predictor of severity of depression. It is related to hypothalamic activity and REM.
Young (2008) proposed that an enlargement of the ____ may predispose someone to depression. What were his findings?
thalamus enlargemnet.
- related to 5HT (genetic variant controlling 5HT transporter)
- he saw that thalamic volume was REDUCED to more normal levels with antidepressant treatment.
- noticed that developmental stress and trauma exacerbate thalamic enlargement through effects on the 5HT transporter.
___l stress and ___ exacerbate thalamic enlargement through effects on the ____ transporter, which may predispose someone to depression
developmental stress and trauma exacerbate thalamic enlargement through effects on the 5HT transporter.
What were the implications of young (2008)’s work about how depressive episodes are related to thalamic enlargement? What “kind” of depression is implicated?
the discovery of thalamic enlargement has led to the belief that ENDOGENOUS depression is related to a NEUROBIOLOGICAL ETIOLOGY (genetic predisposition) that can be triggered by environmental factors. –> Diathesis stress.
treatment implications: some suggest there is a role for PROPHYLACTIC (PREVENTATIVE) treatment of ENDOGENOUS depression, related to issues of recurrent episodes of depression.
T/F: there is an increased susceptibility to depression with subsequent episodes
True. depression results from a sensitization process to the state of depression. This is known as the Kindling effect: depression is related to the number of prior episodes– presence of a stressful life event and genetic risk.
depression results from a sensitization process to the state of depression. This is known as the ____ ____:
Kindling effect: depression is related to the number of prior episodes– presence of a stressful life event and genetic risk.
difference in brain structure from the first depressive episode compared to later episodes?
brain hippocampal volume reduction is NOT present in the first depressive episode, but becomes increasingly evident with multiple episodes.
treatment implications of the kindling effects and the findings of subsequent hippocampal brain volume loss
implications: treatment should continue until full remission. Anything less can increase the risk of relapse.
depression is now seen as a __- and ___ condition
recurrent and chronic condition
- 15-20% show a chronic couse
- up to 80% show recurrences
- if discontinued treatment early, the risk of relapse is 50%
____ symptoms strongly predict relapse (70%). How does this affect treatment implications?
RESIDUAL SYMPTOMS strongly predict relapse. If the person is not in complete remission, the risk of relapse is higher. Once in remission, continue treatment for 6-12 months at the same dose, and then titrate.
3 reasons to focus on studying neuroendocrine abnormalities and challenge tests in relation to depression
1) allows you to understand neuroendocrine abnormalities in depression
2) allows one to understand the relationship to endogenous depression
3) allows one to predict antidepressant response.
TRH pathway
TRH: thyrotropin/thyroid releasing hormone, a hypothalamic peptide which functions to stimulate the release of TSH from the pituitary.
TSH: thyroid stimulating hormone, which is released from the pituitary gland. stimualtes release of thyroid hormone from the thyroid.
Pathway:
Hypothalamus (TRH) –> Pituitary gland (TSH) –> Thyroid
TRH challenge test:
the normal response to TRH is the production of TSH. BUT in depressed people, there is a BLUNTED response to TRH. This indicates that there is A DEFECT IN THE HYPOTHALAMUS, not in the control organs. This is consistent with the monoamine theory of depression (deficiency of catecholamine activity plays a role in depressive symptoms)
- This is the opposite of other textbooks for TRH challenge tests, so I am confused.
IN textbooks:
An increase in the serum TSH level following TRH administration means that the cause of the HYPOthyroidism is in the hypothalamus (tertiary hypothyroidism), i.e. the hypothalamus is not producing TRH. Therefore, when TRH is given exogenously, TSH levels increase.
If the increase in serum TSH level following TRH administration is absent or very slight, then the cause of the hypothyroidism is in the anterior pituitary gland, i.e. the pituitary is not secreting TSH. Therefore, even when TRH is given exogenously, TSH levels do not rise as the pituitary is diseased.
DST
dexamethasone suppression test. Dexamethasone is a synthetic hormone similar to cortisole, which regulates BP, use of proteins and fats and increases in secretion in response to stress. Cortisol is normally made in the adrenal glands.
After injecting dexamethasone, a normal person should see a decrease in cortisol because of negative feedback. But in a depressed person, there is no cortisol supression, resulting in plasma cortisol levels staying high.
Cortisol pathway
Hypothalamus (CRH) –> Pituitary Gland (ACTH) – adrenal gland (Cortisol)
In normal person, what happens when cortisol is too high (or when dexamethasone is injected)? What about in a depressed person?
negative feedback occurs. too much cortisol results in less CRH being released by the hypothalamus, which prevents more cortisol from being released by the adrenal glands.
In a depressed person, pts fail to show this negative feedback mechanism of supression. Plasma cortisol levels remain hgih, and cortisol is elevated and resistant to suppression.
- this could provide a differential diagnosis re. endogenous depression.
High cortisol levels in the ____ are related to depressive vulnerability (endogenous)
high cortisol levels in the MORNING is a marker for the predisposition to depression. Increased cortisol levels in the morning is a marker for major depression in teen boys.
recurrent depressive episodes is associated with enlargement of ___ and atrophy of ____ mainly, as well as two other parts:
recurrent depressive episodes is associated with enlargement of THALAMUS and atrophy of HC/AMYGDALA/PFC.
- damage isn’t seen in the first episode, but after recurrent episodes, atrophy becomes more evident. atrophy to brain regions during recurrent episodes may produce cumulative brain damage.
What REM sleep differences are noticed in people with depression
1) decreased REM latency: therefore, a shorter time is elpased to get to REM
2) increased REM density: there is more time spent in REM sleep with increased intensity in dreams.
These two factors contribute to overall more REM sleep and less slow wave sleep
