Week 1.1: Introduction to the Complex World of Mood Flashcards

1
Q

They are also known commonly as mood disorders

A

Affective Disorders

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2
Q

They are a group of conditions where a disturbance in an individual’s mood is the main characteristic.

A

Affective Disorders

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3
Q

Clinicians and researchers currently use two main systems for the classification of affective
disorders.

A

1) The Diagnostic and Statistical Manual of Mental Disorders (DSM) published by the APA

2) The International Classification of Diseases (ICD) produced by the WHO

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4
Q

Affective Disorders are very complex
neuropsychiatric conditions, and traditionally and broadly, they have been divided into two:

A

1) Depressed Mood (Major Depressive Disorder, Clinical Depression, Unipolar Depression, or Major Depression)

2) Bipolar Disorder (Manic Depression)

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5
Q

Both classifications offer a common language and standard criteria and they allow medical health
professionals to determine and to help communicate the patient’s diagnosis after an evaluation, and they
also allow to categorize patients using the criteria for research purposes.

A

DSM & ICD

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6
Q

Is the most popular diagnostic system for the mental health disorders in the USA

A

DSM

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7
Q

Is a classificaiton system used more widely in Europe and in other parts of the world.

A

ICD

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8
Q

What are the latest editions of the DSM and ICD?

A

DSM-5 and ICD-10

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9
Q

The additional diseases or disorders that are co-occurring with main
effective disorder, are very common.

A

Comorbidities

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10
Q

A group of mental health conditions where individuals experience physical symptoms that cannot be fully explained by a medical condition.

These symptoms are often caused or worsened by psychological factors like stress, anxiety, or emotional distress

A

Somatoform Disorders

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11
Q

They’re very serious conditions that cause a lot of suffering to the patients and their families, and they can start at
early age, and they are hard to diagnose in the youth, because they are sometimes confused with
normal teenage behaviour, with drug use or with other psychiatric illnesses.

A

Mood Disorders

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12
Q

What is the difference between Cause and Correlate?

A

So a cause is something that produces an effect, a result of a condition,
while a correlate is a phenomenon that accompanies another phenomenon, and is usually parallel to it, and is
related to it in some way, but it’s not necessarily the one causing it.

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13
Q

What are some approaches to understanding Affective Disorders?

A

1) Clinical Interviews (Patient OR Family)
2) Biological Sampling (Bodily Fluids, Genetic Factors, Biomarkers)
3) Brain Imagine
4) Post-Morten Sampling
5) Induced Pluripotent Stem Cells (iPSC)
6) Animal Models

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14
Q

They are useful to identify new underlying pathways and new drug targets and also to test possible
protective interventions.

A

Animal Models

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15
Q

What are common environmental manipulations in animal models?

A
  • Social Isolation
  • Unpredictable chronic mild stress
  • Social Defeat
  • Physical Manipulation/Restraint Stress
  • Maternal Deprivation
  • Sleep Deprivation
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16
Q

What internal alterations can be done for animal models?

A

Permanent
- Olfactory Bulbectomy
- Adrenalectomy

Transient
- Manipulation of the immune or stress systems
- Disruptions induced by changing the dietary composition

Genetic Modifications
- Transgenic and knock-out animals
- Selection of extreme types (aggression or anxiety)
- Inbred stains

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17
Q

Diagnosis VS Prognosis

A

Diagnosis: Identifies what the problem is.
Prognosis: Predicts how the problem will likely unfold.

A diagnosis must be made before a prognosis can be determined.
Prognoses are not always certain and can change based on the patient’s response to treatment and other factors.

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18
Q

Aims to understand how an individual’s genetic makeup influences their response to medications.

A

Pharmacogenetics

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19
Q

Genetic Studies: Unipolar Disorder VS Bipolar Disorder

A

The genetic contribution to unipolar depression is around 40% while the one for bipolar disorders are much higher and are between 80 and 90%

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20
Q

Why is identifying genes related to affective disorders crucial for improving treatment and understanding these conditions?

A
  • To improve diagnosis and prognosis
  • Pharmacogenetics
  • Research (new drug targets)
21
Q

What are the different Structural Neuroimaging Techniques?

A

MRI (Magnetic Resonance Imaging)
CT Scans (Computerized Tomography)
DTI (Diffusor Tensor Imaging)

22
Q

Creates detailed images of brain structures.

A

MRI (Magnetic Resonance Imaging)

23
Q

X-ray imaging technique providing detailed cross-sectional views.

A

CT Scans (Computed Tomography Scans)

24
Q

A specialized MRI technique that reveals information about white matter tracts and brain connectivity.

A

DTI (Diffusion Tensor Imaging)

25
Q

What are the different Functional Neuroimaging Techniques?

A

PET (Positron Emission Tomography)

SPECT (Single-Photon Emission Computed Tomography)

fMRI (Functional Magnetic Resonance Imaging)

MEG (Magnetoencephalography)

EEG (Electroencephalography)

26
Q

PET (Positron Emission Tomography)

A

Uses radioactive tracers to measure glucose metabolism

27
Q

SPECT (Single-Photon Emission Computed Tomography)

A

Similar to PET but uses different radiotracers.

28
Q

fMRI (Functional Magnetic Resonance Imaging)

A

Measures brain activity indirectly by detecting changes in blood flow and oxygen levels.

29
Q

MEG (Magnetoencephalography)

A

Measures electrical activity of the brain with high temporal resolution.

30
Q

EEG (Electroencephalography)

A

Measures electrical activity of the brain with lower temporal resolution but higher portability.

31
Q

The leading cause of disability
worldwide according to the WHO

A

Depression

32
Q

What are the main neurotransmitters?

A

Serotonin
Dopamine
Norepinephrine

33
Q

Neurotransmitter that regulates mood, sleep, and appetite.

A

Serotonin

34
Q

Neurotransmitter that is involved in reward and pleasure systems.

A

Dopamine

35
Q

Neurotransmitter that affects stress response and alertness.

A

Noripinephrine (adrenaline)

36
Q

The formation of new neurons in the brain

A

Neurogenesis

37
Q

The idea that there are fixed neurons in the adult brain and that neural plasticity is achieved by strengthening synapses without adding new neurons.

A

Monoamine Theory

38
Q

This theory suggests that impaired neurogenesis (production of new neurons) in the hippocampus may contribute to depression

A

Neurogenesis Theory

39
Q

Dysfunction in the HPA axis, which regulates the body’s stress response, may contribute to depression

A

Hypothalamic Pituitary Adrenal (HPA) Axis Dysfunction

40
Q

Alterations in the inflammatory response, particularly involving macrophages (immune cells), may play a role in depression

A

Macrophage Theory

41
Q

They are unstable molecules that have unpaired electrons and seek out other molecules to pair with, which can cause damage to cells in the process.

A

Free Radicals

42
Q

An imbalance between oxidants and antioxidants that can lead to a loss of control or certain intercellular
signalling pathways. This imbalance can lead to cell and tissue damage

A

Oxidative Stress

43
Q

Molecules that can neutralize free radicals by donating an electron, thus preventing them from causing damage to cells

A

Antioxidants

44
Q

These are stress hormones.

Increased levels of such would decrease neurogenesis in animal models.

Reduced neurogenesis is associated with an increase in depressive-like behaviors.

A

Glucocorticoids

45
Q

Confirmed that depressed individuals have fewer new neurons in their brains.

However, those who had been treated with tricyclic antidepressants showed an increase in new neuron levels, supporting the idea that neurogenesis plays a role in depression and its treatment.

A

Post-Mortem Studies (Depressed Individuals)

46
Q

Medications that treat depression can increase neurogenesis

A

Antidepressants

47
Q

A treatment for severe depression that also boosts neurogenesis

A

Electroconvulsive Therapy (ECT)

48
Q

Physical activity is known to enhance neurogenesis

A

Exercise

49
Q

Is there a timeline for mood improvement after engaging in therapies increasing neurogenesis?

A

Patients typically feel better after several weeks, likely due to the time it takes for new neurons to grow and form connections