Depression and bipolar disorder
12 important questions on Depression and bipolar disorder
What are affective disorders?
Mood is psychiatric condition.
What are the main affective disorders? And what medication do you give them?
•Major Depressive Disorder (MDD) (Unipolar) Treatment: Anti-depressants
• Bipolar Disorder (Alterations between depression and mania) Treatment: Anti-depressants + Mood stabilisers
What is the prevalence of MDD? (4 facts)
•Highly prevalent disorder: 21% of world population affected
•
• > 300,000 people in Republic of Ireland suffer from depression
• Depression is currently the leading cause disability as measured by Years Lived with Disability (YLDs).
More females
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What are symptoms of MDD and what can we see in a fMRI?
Is depression an underactive or more active state of disease?
- Increase in cerebral blood flow
Amygdala, medial orbital
What is a monoamine? And three which types do we have?
connected to an aromatic ring by a two-carbon chain.
•Catecholamines: Derived from tyrosine Examples: Dopamine, Noradrenaline (NA), Adrenaline (A)
•Tryptamines: Derived from tryptophan
•Examples: Serotonin (5-hydroxytryptamine; 5HT), Melatonin
•Histamine: Derived from histidine (in our diet)
Top down stress model. What does it mean? (preserved stress) Belongs to the neuroendocrine mechanisms.
Cortical releasing factor (hypothalamus) -> adreno cortical thyroid (pituitary) -> cortisol
--> noradrenalin and 5HT
--> symptoms
What is the anti-depressive pathway?
Feedback and switch of neurons.
Whole picture is the linking between neurotransmission and actual stress that causes depression.
So, what is included in the neuroendocrine mechanism?
•Stress causes an upregulation in the hypothalamic-pituitary-adrenal (HPA) axis.
•Excessive release of cortisol into the circulation has a number of effects, including elevation of blood glucose.
•The negative feedback of cortisol to the hypothalamus, pituitary and immune system is impaired. This leads to continual activation of the HPA axis and excess cortisol release.
•Cortisol receptors become desensitized leading to increased activity of the pro-inflammatory immune mediators and disturbances in neurotransmitter transmission.
•Increased activation can lead to hippocampal cell loss and shrinkage >20 years > alzheimers
What does the theory about reduced neuroplasticity mean?
(i) Lower levels of BDNF (brain derived neurotrophic factor)
(ii) Malfunction of BDNF receptor, TrkB
(iii) Excessive glutamate damages neurons in the brain (glutamate is in general for studying; too much is not good)
BDNF = growth factor. Binds to TrkB (tyrosine kinase B receptor). Less binding = potential cause of depression.
Do we know the full pathway of the medicines against depression?
Which MAO is an reversible inhibitor?
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