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Neurology > Depression > Flashcards

Depression Flashcards

1
Q

What factors contributes to mental health and illness?

A

Human behaviour
- Product of brain activity

Brain
- Product of genetics and environment
- Experience (trauma / disease)
- Genetic make-up and experience can interact, making a
person more or less susceptible to future experience

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2
Q

What are the 2 types of treatment available for affective disorders?

A
  1. Cognitive behavioural therapy

2. Pharmacotherapy

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3
Q

Outline the characteristics of affective disorders?

A

Characteristics of Affective Disorders

  • Disorders of mood rather than thought / cognition
  • Most common is depression
  • Major cause of premature death and disability
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4
Q

What are the 2 types of affective disorders?

A
  1. Unipolar depression

2. Bipolar depression

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5
Q

What is unipolar depression

A

Mood swings in one direction
Most common depressive illness

75% cases REACTIVE (induced by environmental factors)
25% cases ENDOGENOUS (genetic)

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6
Q

What is bipolar depression?

A

Oscillation between depression and mania`
Less common
Onset usually in adult life
Strong hereditary tendency (no genes found yet)

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7
Q

What is mania?

A

Mania: excessive exuberance, enthusiasm, self confidence, impulsive actions, aggression, irritability, delusions of grandiose

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8
Q

What is depressive disorder?

A

A low state marked by significant levels of sadness, lack of energy, low self-worth, guilt or related syndromes

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9
Q

What is major depressive disorder?

A

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

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10
Q

What is dysthymia?

A

Dysthymic disorder (dysthymia): similar to major depressive disorder but less severe/disabling and more long-lasting (chronic)

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11
Q

Why is diagnosing depression difficult?

A

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

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12
Q

How is depression diagnosed?

A

Based on interview
and DSM 4 handbook

< 5 symptoms persisting for 2 weeks

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13
Q

What are the emotional symptoms of depression?

A

Emotional symptoms (Q)

  • Apathy, pessimism, negativity
  • Low self esteem, feeling guilty
  • Loss of motivation
  • Indecisiveness
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14
Q

What are the biological symptoms of depression?

A

Biological symptoms (Q)

  • Reduced activity
  • Loss of libido
  • Sleep disturbance
  • Loss of appetite
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15
Q

How does gender affect depression epidemiology?

A

Depression affects around twice as many females as males

Lifetime prevalence of major depression: 10-25 % for women and 5-12 % for men

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16
Q

How does age affect depression

A

1st episode of depression usually late adolescence of early adulthood
Age of onset has been decreasing in recent years
Is life now more stressful?

Are we just diagnosing more people with depression?

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17
Q

What factors are important to consider when diagnosing depression patients?

A

suicide

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

comorbidity
- Depression is often comorbid with other psychiatric conditions (e.g. withdrawal from drugs of abuse)

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18
Q

Which medical conditions are comorbid with depression?

A 
Terminal illness
Chronic illness (e.g. chronic pain)
Thyroid dysfunction
Neurological disease
Stroke
Drug abuse
Parkinson’s disease
Anxiety
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19
Q

Describe the comorbidity between anxiety and depression

A

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

20
Q

What are the genetic predispositions of getting depression?

A

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

21
Q

What environmental factors contribute to depression?

A

Environmental factors?

  • Loss
  • Environmental stressors
  • Social isolation
22
Q

Explain normal 5-HT activity

A

Increase in 5HT in synaptic cleft & somatodendritic area causes 5HT1A autoreceptors to down regulate and therefore to disinhibit the 5HT neuron & ↑ 5HT release.

23
Q

How are 5-HT levels altered during depression

A

↑ synaptic 5-HT ‘normalises’ 5HT post synaptic receptors which are thought to be upregulated in depression as low 5-HT activity

24
Q

Describe the monoamine theory of depression

A

Decreased NA and 5-HT causes depression

25
Q

What is reserpine?

A

Reserpine is a drug that blocks monoamine levels in the brain

26
Q

What is the general mechanism of antidepressants?

A

Antidepressants all elevate monoamines and 5-HT

27
Q

Outline the evidence for the monoamine depression theory

A

Evidence For:
- Overall reduced activity of central noradrenergic and / or
serotonergic systems
- Reserpine depletes brain of NA and 5-HT; induces
depression
- Main antidepressant drugs ↑ [amines] in brain (Q devise
drugs to treat depression)

28
Q

What is the evidence against monoamine depression theory

A

Evidence Against
- Difficult to show deficits in brain [NA] & [5-HT] and
functioning/ (-) results from CSF, plasma in depressed
/individuals respond better to one AD than another

  • Most antidepressant drugs take several weeks for
    therapeutic effect but ↑ in amines acute (secondary
    adaptive changes more important)
  • Some antidepressants weak / no effect on amine uptake
    (e.g trazodone)/no increase in 5HT and NA but
    antidepressants!
  • Cocaine blocks amine uptake but has no antidepressant
    effect
  • Decrease in 5HT in dipolar linked to aggression rather
    than depression
29
Q

Describe the neuroendocrine theory of depression

A

> hyperactivity of the HPA axis

NAergic & 5-HT neurons input to hypothalamus

Hypothalamus releases corticotropin-releasing hormone (CRH)

CRH acts on pituitary – release of adrenocorticotropic hormone (ACTH)

Cortisol release from adrenal cortex in response to ↑ ACTH in blood

30
Q

Describe the neuroendocrine depression theory using the HPA axis

A

↓ hippocampal feedback in depression

↓ glucocorticoid receptors (cortisol receptors) in hippocampus

amygdala hyperactivity
hippocampus underactivity produces cortisol

31
Q

How does tactile stimulation affect mental health?

A

Glucocorticoid receptor gene expression regulated by early experience

Tactile stimulation just after birth activates 5-HT pathways to hippocampus

5-HT triggers long-lasting ↑ in expression of glucocorticoid receptor gene
↑ in glucocorticoid receptors in hippocampus

SSRIs ↑ glucocorticoid receptors in the hippocampus

32
Q

Describe the neuroplasticity and neurogenesis depression theory

A
  • Neuronal loss and ↓ neuronal activity in hippocampus
    and prefrontal cortex (decision making centres)
  • Antidepressants and electroconvulsive therapy (ECT)
    promote neurogenesis in these regions
  • 5-HT promotes neurogenesis during development
    (BDNF) - BDNF induced during exercise
  • Increase in Glutamate in Cx of depressed people; causes
    cytotoxicity causing neuronal damage (NMDA antagonists
    potential for depression treatment e.g. ketamine)
33
Q

Outline how stress causes depression

A

Stress hyperactivates HPA signal; releases cortisol; induces detrimental gene transcription response → neural apoptosis and cell death ⇒ depression symptoms

34
Q

Describe how glutamate NMDA receptor hyperactivity induces depression

A

Inc. glutamate causes hyperactivity of NMDA ; excitotoxicity, neuronal loss leads to depression

35
Q

How does NA/5HT neurotransmitters release cause depression?

A

NA/5-HT activate adrenal receptors (alpha2) inhibits detrimental and activates beneficial gene transcription response inducing neurogenesis - antidepressant

Low 5-HT activates detrimental gene transcription → neuronal apoptosis

36
Q

What are the long term treatments for depression?

A

Electroconvulsive therapy (ECT)

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

Psychotherapy

  • Mild to moderate depression
  • Overcome negative views
37
Q

What are the long term neurochemical effects of antidepressants

A

> all increase 5-HT or NA in brain

  • 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 (α2, 5HT2c, 5HT3)
  • Downregulation α2, 5ΗΤ1Α, β1, β2, 5ΗΤ2Α, 5ΗΤ3
38
Q

Outline the mechanism of monoamine oxidase inhibitors

A

Monoamine oxidases reuptake NA and 5-HT, inhibiting these increases neurogenesis

MAOI s ↑ [NA/5-HT]cytoplasm

↑ [NA/5-HT]cytoplasm ↑ leakage of amine

↑ [NA/5-HT] in synaptic cleft

However there are vascular side effects - hypertension and interacts with other drugs

39
Q

What are the effects of Tricyclic antidepressant TCAs?

A

Main therapeutic effects:

  • NA reuptake inhibitor
  • 5-HT reuptake inhibitor

Initially ↑[NA] & [5-HT] in synaptic cleft

Block serotonin and NA transporter, preventing the neurotransmitter re-entering presynaptic cleft; remains and accumulates in the synaptic cleft

40
Q

How do tricyclic antidepressants treat long term depression?

A

Chronic treatment down regulation of
- (β1) & 5-HT2
⍺2, 5-HT1A/1D (autoR)
Also affect mACh, HR, 5HTR

41
Q

Name some tricyclic antidepressants

A

amitriptylline; imipramine; lofepramine

Good but not ideal as takes a long time to produce effect. Also produces side effects

42
Q

What is the benefit of using SSRIs

A

> safer as don’t block NA transport = less dangerous side effects but side effects still prevail

43
Q

Name some common SSRIs

A

fluoxetine, sertraline, paroxetine, citalopram, escitalopram

44
Q

Outline the main effects of SSRIs

A

Main therapeutic effects:

5-HT reuptake inhibitor

45
Q

What is the chronic effect of SSRIs?

A

Chronic action:
↑ [5-HT] down regulation of 5-HT1A/1D
autoreceptors, disinhibition of 5-HT
neuron, ↑ 5-HT release

↑ 5-HT release down regulates
post synaptic 5-HT receptors
‘Normalising’

46
Q

Summarise the antidepressants administered to depressed patterns

A 
Tricyclic antidepressants (TCA), block reuptake of NA and 5-HT (imipramine) 
Selective serotonin (5-HT) reuptake inhibitors (SSRI) (fluoxetine)
NA-selective reuptake inhibitors (reboxetine) 
Monoamine oxidase inhibitors (MAOI), block degradation of NA and 5-HT (phenelzine)

All elevate monoamine levels but antidepressant effect takes several weeks
MAOIs only inactivates the stores which are going to be released, not the ones which are recycled

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