Introduction to Affective Disorder Flashcards
What are the two main categories of Affective disorder?
Depressed mood and Bi-polar disorder
What are the manuals used to classify disorders and why?
DSM (USA) and ICD (Europe)
To communicate to patients
To communicate to other clinicians
To Communicate to health insurance
What Comorbidities do you see with affective disorders?
Anxiety, substance abuse and impulse control disorders
What impact do mood disorders have on teenagers, dementia and society?
Early onset, hard to diagnose due to teenage behaviour and drug use
Significant effect on individual and family-increases risk of dementia by 2X (60000n meta-analysis)
Burden to individual and society
What is the difference between Causes and Correlates?
Causes: Something that produces an effect
Correlate: Phenomeon that accompanies another Phenomeon, usually in a parallel or related way
What are the approaches we can use to research mood disorders?
Engagement and communications-patients and families
Evaluation of underlying biological approaches:
Patients Blood, Saliva, etc, iPS Cells Post Mortem Material Imagining Techniques Animal Studies
How do animal models aid in our understanding of Affective disorders?
Provide a series of behaviours
Enhance understanding of Biological underpinning as brain and behaviour relationship is elucidated
Identify new pathways for drugs and interventions
What Animal behavioural/environmental models used? And what Internal alterations are used?
Environmental:
Restraint test
Unpredictable stress
Social defeat
Isolation
Maternal or sleep deprivation
Internal:
Permanent: Adrenal or olfactory removal)
Transient: (Manipulation of)
Immune or stress system
Dietary
Genetic:
Transgenic and KO
Extreme types of pop
Use of inbred Line
How do Genes inform research in affective disorders?
Improve prognosis and Diagnosis-predict disease and identify risk groups
Pharmacognetics-Drug efficacy and adverse reactions
Research: Novel targets
What is the heritability of unipolar and bi-polar depression?
Unipolar 30-40%
Bi-polar 80-90%
What did the GWAS of MDD by Ripke reveal?
That there was no single nucleotide polymorphism responsible for depression.
Heterogeneity and sample size remains an issue.
How did the Converge Study deal with the issues of sample size and Heterogeneity?
They streamlined there sample and controls:
Females Recurrent Depression over 5000 cases and controls Only Chinese interviews fro detailed info on environment
What did the Converge study find?
Two loci on chromosome 10 were significant.
How can we use imagining approaches to study affective disorders?
Structurally: MRI, CT/CAT, DTI
Functionally: PET and SPECT: distribution of Neurotransmitters
fMRI: Changes in blood flow due to use
The above functional options are indirect examples
Direct functional examples are:
MEG and EEG
What did the Redilch et al study show us regarding Brain morphology in unipolar and Bi polar disorders?
Bi-polar patients showed reduced Hippocampus and amygdala.
What did Joshi et al find regarding structural plasticity and ECG in MDD?
Patients with MDD all showed lower hippocampal and amygdala volume to start, but increased volume over the course of treatment .
What is NICE?
National Institute for Clinical Excellence
Part of the DEPt of Health
Helps to decide best route for treatment in efficacy and economics.
What 3 facts do the WHO tell us regarding Depression
It’s the leading cause of disability worldwide,
despite the high number of treatments:
High relapse
Low recovery rate
What is the monoamine hypothesis and how did it come about?
It is the theory that depression is caused by the lack of monoamine neurotransmitter levels.
1950’s treatment of TB used the drug iproniazid. This increased mood and was seen to inhibit breakdown of monoamines.
Theory was then that the availability of monoamines was the cause.
What was the previous belief regarding neurons?
That the number of neurons were fixed at birth.
Neuroplasticity was due to synaptic strength not neuronal growth.
Research focused on:
NT release and receptors
Number of synapses
What was the neurogenesis theory?
That the ability to increase neurons in adults can improve depressive symptoms.
Why did the monoamine theory come under fire and what theories have come to rise?
Due to the delayed response of SSRI’s.
HPA dysfunction
Macrophage Theory
Oxidative Stress
How did Jacobs et al show the neurogenesis effect on depression?
By using an animal model they showed:
Stress and raised gluccocorticoids decreased neurons and increased depression
Exercise and Antidepressants:
Depression decreased and neurons increased
What did Boldrini ert al show regarding Antidepressants and neurons?
MDD have low numbers of neurons.
Those on triciylics increased neurons.
Where does the neurogenises tend to take place with antidepressants?
IN the hippocampus, SGZ of Dentate gyrus and SVZ of lateral ventricles.
How does the theory of oxidative stress account for depression?
The imbalance of oxidants to anti-oxidants results in decreased neurogenesis or intercellular communication.
What does the meta-analysis of oxidative stress by Palta tell us?
That most studies show a significant correlation between oxidative stress and depression.
What is the correct way to approach to deal with mood disorders?
In a Holistic way.
