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Physiology 2: Sem 3 > NEURO: Depression > Flashcards

NEURO: Depression Flashcards

1
Q

Neurology

Psychiatry

What are psychiatric conditions caused by?

A

branch of medicine, diagnosis & treatment of nervous system disorders (e.g. MS, paralysis)

branch of medicine, diagnosis & treatment of disorders that affect the mind (or psyche)

an imbalance in neurotransmitters/chemical changes in the brain

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2
Q

What is depression?

A

There are multiple ways to define it:
DEPRESSIVE DISORDER: a low state marked by significant levels of sadness, lack of energy, low self-worth, guilt or related syndromes

MAJOR DEPRESSIVE DISORDER: severe pattern of depression that is disabling and is not caused by factors such as drugs or a general medical condition

DYSTHYMIC DISORDER (DYSTHYMIA): similar to major depressive disorder but less severe/disabling and more long-lasting (chronic)

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3
Q

What type of disorder is depression?

Treatments of depression

A

affective (mood) disorder

Non-pharmacological Treatment
-e.g. cognitive behavioural therapy
Pharmacotherapy
-antidepressants

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4
Q

Types of depression

A 
Unipolar Depression:
· Mood swings in one direction
· Most common depressive illness
· 75% cases REACTIVE (induced by environmental factors)
· 25% cases ENDOGENOUS (genetic)

Bipolar Depression:
· Oscillation between depression and mania
· Mania: excessive exuberance, enthusiasm, self-confidence, impulsive actions, aggression, irritability, delusions of grandiose
· Less common
· Onset usually in adult life
· Strong hereditary tendency (no genes found yet)

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5
Q

Diagnosing depression

A

Diagnosis is difficult

  • Wide variety of symptoms that patients can report
  • Difficult to know when a normal fluctuation in mood becomes depression
  • No single objective test to establish diagnosis

The diagnosis of depression is based on the interview with the patient, and if these patients are exhibiting 5 of the following symptoms during the same 2 week period. At least one of the symptoms is either:

  • Depressed mood
  • Loss of interest or pleasure
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6
Q

What are some symptoms of depression?

A

EMOTIONAL SYMPTOMS (Q):

  • negativity
  • low self-esteem
  • loss of motivation
  • indecisiveness

BIOLOGICAL SYMPTOMS (Q):

  • reduced activity
  • loss of libido
  • sleep disturbance
  • loss of appetite
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7
Q

Who gets depression?

A

GENDER:

  • depression affects around twice as many females as males
  • lifetime prevalence of major depression: 10-25 % for women, 5-12 % for men

AGE:

  • 1st episode of depression is usually late adolescence or early adulthood
  • age of onset has been decreasing in recent years
  • is life now more stressful?
  • are we just diagnosing more people with depression?

Suicide

  • Suicidal thoughts are common among depressed patients
  • 20% of depressed individuals will attempt suicide
  • 10% of severe depressives will commit suicide

Co-morbidity
- depression is often comorbid with other psychiatric conditions (e.g. withdrawal from drugs of abuse)

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8
Q

Co-morbidity of Depression

A

Depression has co-morbidity with many other conditions:

  • terminal illness
  • chronic illness (e.g. chronic pain)
  • thyroid dysfunction (hypothyroidism)
  • neurological disease
  • stroke
  • drug abuse
  • Parkinson’s disease
  • Anxiety

Depression and anxiety are often co-morbid.
>Manifest more severe symptoms
>Less responsive to treatment
>Higher risk of suicide

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9
Q

Causes of depression

A

Genetic Predisposition

Environmental Factors

  • loss
  • social isolation
  • environmental stressors
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10
Q

Monoamine Theory of Depression

Evidence supporting monoamine theory of depression

A

According to the monoamine theory of depression, depression is caused by low levels of noradrenaline and serotonin (5-HT) in the brain.

  • Reserpine (depletes noradrenaline and serotonin from brain) induces depression when injected into mouse brain
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11
Q

Evidence against monoamine theory of depression

A
  • Difficult to show deficits and functioning of noradrenaline and serotonin in the brain
  • Most antidepressant drugs take several weeks for therapeutic effect but increase in monoamines is acute (secondary adaptive changes more important)
  • Some antidepressants are weak/no effect on monoamine uptake (e.g. trazodone), with no increase in serotonin and noradrenaline
  • Cocaine blocks monoamine uptake but has no antidepressant effect
  • Decrease in serotonin in bipolar linked to aggression rather than depression
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12
Q

Neuroendocrine theory of depression

A

According to the neuroendocrine theory of depression, depression is caused due to a hyperactivity of the hypothalamic-pituitary-adrenal axis (HPA axis).

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13
Q

What activates the HPA axis?

A

stressful stimuli:

  • noradrenergic and serotonergic neurones input to the hypothalamus
  • hypothalamus release corticotropin-releasing hormone (CRH)
  • CRH acts on pituitary- release of adrenocorticotrophic hormone (ACTH)
  • cortisol release from the adrenal cortex in response to an increase in ACTH in blood
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14
Q

Evidence to suggest the neuroendocrine theory of depression is correct

A
  • CRH has behavioural effects which mimic depression symptoms
  • Increased cortisol in plasma in depressed patients
  • Increased CRH in CSF
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15
Q

HPA axis in depression

A

If you suffer from depression, the HPA axis is hyperactive. Therefore, the basal cortisol levels will be higher.

There is also reduced hippocampal feedback in depressed patients, evidently by:
- Reduced hippocampal glucocorticoid (cortisol) receptors

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16
Q

What causes the hyperactivity of the HPA axis?

A

genes and environment

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17
Q

What can cause depression?

A

GENETIC PREDISPOSITION?

  • General population: 3.2%
  • First degree relatives of patients: 20%
  • Monozygotic twins: 40-50%

ENVIRONMENTAL FACTORS?

  • Loss
  • Environmental stressors
  • Social isolation
18
Q

Amygdala and HPA Axis

A

Activation of the amygdala induces the activation of the HPA axis to induce cortisol release.

*hyperactivity of amygdala causes increased HPA activity and an increase in cortisol, causing depression.

19
Q

Hippocampus and HPA Axis

A

· Glucocorticoid receptors in the hippocampus detect increased cortisol levels. Activation of these receptors sends a signal to the HPA axis to inhibit CRH neurones in the hypothalamus, and therefore inhibit cortisol release.

*hypo-activity of the hippocampus causes increased activity of the HPA axis, and subsequently an increase in cortisol (check with Vanessa)

20
Q

Glucocorticoid receptor gene expression

A

Regulated by early sensory experience:
· Tactile stimulation (e.g. hugging babies) just after birth activates 5-HT (serotonergic) pathways to the hippocampus.
· 5-HT triggers long-lasting increase in expression of glucocorticoid receptor gene
· Increase in glucocorticoid receptors in the hippocampus.
· Glucocorticoid receptors negatively regulate cortisol release by inhibiting CRH neurones in the hypothalamus
· Increased inhibition of HPA axis, decreasing cortisol
· Decreased cortisol means babies don’t get stressed (because increased cortisol causes depression)

21
Q

Environmental stressor which affects glucocorticoid receptor expression

A
  • Trauma at an early developmental age will reduce glucocorticoid receptor expression, reducing levels of glucocorticoid receptors in the hippocampus.
  • This results in decreased hippocampal feedback, less activation of the hippocampus, and as a result less inhibition of the HPA axis (less inhibition of CRH neurones).
  • HPA axis, therefore, increases levels of cortisol, which causes detrimental gene transcription response and subsequently causes mental health conditions later in life
22
Q

How does trauma decrease glucocorticoid receptors?

A

via epigenetic modulations

-environment and genetics are therefore interacting to cause depression

23
Q

Effect of SSRIs on glucocorticoid receptors

A

SSRIs increase glucocorticoid receptors in the hippocampus, and therefore SSRIs reduce depression by enhancing the inhibition of the HPA axis by the hippocampus.

24
Q

What is the neuroplasticity & neurogenesis theory of depression?

A

Depression is caused by neuronal apoptosis (excitotoxicity) and decreased neuronal activity in the hippocampus and prefrontal cortex (decision-making centres)

Neurones are killed by the excess release of glutamate, which causes excitotoxicity and cell death, resulting in depression.

*evidence showed there is less neuronal loss with antidepressant drugs

25
Q

What promotes neurogenesis?

A

· Antidepressants and electroconvulsive therapy (ECT) promote neurogenesis in the hippocampus and prefrontal cortex
· 5-HT and BDNF (brain-derived neurotrophin factor) promote neurogenesis in the hippocampus during development

*therefore these have antidepressant effects

26
Q

BDNF is increased in response to…

A

exercise

-promotes beneficial gene transcription and inhibits detrimental gene transcription, increasing neurogenesis and hence decreasing depressive symptoms

27
Q

Why does increased cortisol cause depression?

A

The increase in cortisol causes a detrimental gene transcription response, which promotes neural apoptosis (excitotoxicity), causing depressive symptoms.

28
Q

Effect of noradrenaline and serotonin (5-HT1A receptors) on depression

A

Noradrenaline (alpha 2 receptors) and serotonin (5-HT1A receptors) inhibit the detrimental gene transcription but activate beneficial gene transcription. This will activate neurogenesis, which decreases depressive symptoms.

> therefore, low levels of noradrenaline and serotonin promote detrimental gene transcription, neural apoptosis and therefore increase depression

29
Q

Non-pharmacological treatments of affective disorders

A

Electroconvulsive Therapy

  • Localised electrical stimulation
  • Some evidence of neurogenesis, the possible involvement of the hippocampus
  • Adverse effect: memory loss

Psychotherapy (e.g. CBT)

  • Mild to moderate depression
  • Overcome negative views
30
Q

What do antidepressants do?

Antidepressants include…

A

increase levels of noradrenaline or serotonin in synapses

· Monoamine Oxidase Inhibitors (MAOIs)
· Tricyclic Antidepressant Drugs (TCAs)
· Selective Serotonin Reuptake Inhibitors (SSRIs)
· Other mixed 5HT/NA reuptake inhibitors (SNRIs)
· NA Reuptake inhibitors
· Monoamine receptor antagonists (a2, 5HT2C, 5HT3)
· Downregulation of a2, 5HT1A, b1, b2, 5HT2A, 5HT3

31
Q

Monoamine Oxidase Inhibitors (MAOIs)

Example of an MAOIs

A

If you suffer from depression, there are low levels of monoamines. Therefore, monoamine oxidase inhibitors prevent the metabolic breakdown of monoamines and therefore increase monoamine concentration at the synaptic bouton which will eventually leak out into the synaptic cleft.

Phelezine

32
Q

Disadvantages of Monoamine oxidase inhibitors (MAOIs)

A

accompanied by many side effects, most of them due to the increase in noradrenaline causing cardiovascular side effects (e.g. hypertension).

33
Q

Tricyclic Antidepressants (TCAs)

A

block reuptake of serotonin and noradrenaline by blocking the transporters, increasing their concentration at synaptic cleft

34
Q

Chronic action of TCAs

Disadvantage of TCAs

A
  • Downregulation of β1 and 5HT2
  • Downregulation of ⍺2 and 5HT1A/1D autoreceptors
  • Also affect mACh, HR, 5HTR
  • very long time to produce a biological effect
  • many side effects
35
Q

Examples of TCAs

What drugs are predominantly used for depression?

A

· Amitriptyline
· Imipramine
· Iofepramine

SSRIs

36
Q

Selective Serotonin Reuptake Inhibitors (SSRIs)

A

SSRIs block the serotonin transport (5-HT re-uptake inhibitor)

As a result, there is no re-uptake of serotonin in the presynaptic membrane, increasing its concentration at the synapse.

*may also promote neurogenesis, reducing depressive symptoms

37
Q

Chronic Action of SSRIs

Examples of SSRIs

A

increased serotonin concentration causes:
-down regulation of 5-HT1A/1D autoreceptors
-disinhibition of 5-HT neurones
both increase serotonin release

· Fluoxetine
· Sertraline
· Paroxetine
· Citalopram
· Escitalopram
38
Q

Why are SSRIs used over MAOIs and TCAs?

A

because they do not increase noradrenaline (causes cardiovascular side effects).

*however they take 2-3 weeks to have any positive effect (very long)

39
Q

By increasing monoamine levels, what do antidepressants essentially promote?

A

hippocampal glucocorticoid receptor gene expression, causing for:

  • increased hippocampal feedback AND neurogenesis in hippocampus and prefrontal cortex
  • increased HPA axis inhibition
  • less cortisol
  • less detrimental gene transcription response
  • less neural apoptosis
  • reduced depressive symptoms
40
Q

Bipolar depression treatment

A

Lithium

  • Stabilises mood (mania and depression)
  • Inhibits enzymes involved in signal transduction

Physiology 2: Sem 3 (39 decks)

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