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Drugs and diseases-2106 > Depression > Flashcards

Depression Flashcards

1
Q

What is depression?

A
  • Complex and difficult to classify
  • Lots of proximal causes of depression:
    1. Pain
    2. Trauma
    3. Grief
    4. Genetic predisposition
  • Long-term, intractable depression categorised as major depressive disorder (MDD) or clinical depression
  • Lifetime prevalence in US population is 14%
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2
Q

What are the symptoms of depression?

A
  1. Psychological
  2. Physiological
  3. Social
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3
Q

What are the psychological symptoms of depression?

A
  • Anhedonia (lack of pleasure and motivation, apathy)
  • Negative affect (fear, anxiety, suicidal thoughts)
  • Despair (Hoplessness, helplessness, pessimism
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4
Q

What are the Physiological symptoms of depression?

A
  • Sleep disruption (insomnia or hyposomnia)
  • Loss of apetite, libido, energy
  • Unexplained aches or pains
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5
Q

What are the social symptoms of depression?

A
  • Neglected self-care
  • Loss of interest on hobbies or activities
  • Unable to function in wok, social or domestic setting
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6
Q

What are the treatment approaches to depression?

A

Lifestyle changes:
* Sleep
* Excercise
* Diet

Talking therapies:
* Cognitive behavioural therapy
* Rapport with therapist seems critical

Antidepressants:
* Often used in conjunction with other methods
* Can take a few weeks to become effective

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7
Q

What is the neurochemical approach to depression?

A

Obvious starting point for treatment is mood regulation. So systems linked to pleasure, motivation, energy and optimism.

  • Dopamine–Reward and motivation
  • 5-HT–Mood and status
  • Noradrenaline–Arousal
  • Monoamine hypothesis–for depression
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8
Q

What are SSRIs?

A
  • Inhibit serotonin reuptake transporters (SERTs)
  • Prolong 5-HT synaptic transients
  • Increase tonic extracellular 5-HT concentration
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9
Q

What is Citalopram?

A
  • SSRIs bind to ‘central site’ that locks transporter in outward-facing configuration
  • Citalopram can also occupy a second allosteric site that prevents dissociation from central site
  • Causes prolonged inhibition
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10
Q

What are the unpredictable effects of SSRIs?

A
  • Generalised Inc in 5-HT has distinct short-term & long-term effects
  • 5-HT1a and 5-HT5a autoreceptors depress 5-HT release
  • Desensitisation/adaption in longer term reduces this effect
  • Breadth of roles 5-HT leads to complex outcomes
  • Side effects:
    1. Anxiety
    2. Dizziness, nausea
    3. Sexual dysfunction
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11
Q

How has the current view of depression changed?

A
  • 5-HT cannot be the whole story
  • Functional and anatomical changes in frontal cortex and subcortical systems
  • Hypothalamic-pituitary-adrenal axis(HPA)
  • Cause or consequences
  • Glutamate hypothesis
  • Neuroplasticity hypothesis
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12
Q

What is the Glutamate hypothesis?

A
  • Glutamate is the core excitatory transmitter
  • Receptors (especially mGluR and NMDA( linked to synaptic plasticity
  • Ketamine found to work rapidly as antidepressant
  • Changes in plasma and CSF levels of glutamate and glutamine in depressed patients
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13
Q

What is glutamate signalling?

A
  • Tripartite synapse
  • Multiple classes of receptors and transporters
  • Astrocyte uptake and recycling of glutamate to glutamine
  • NMDA receptor linked to synaptic plasticity
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14
Q

What is Ketamine?

A
  • Pore-blocker for NMDA receptor
  • Devloped as anisthetic and tranquiliser
  • Difficult to use
  • Risk of abuse
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15
Q

What is the neuroplasticity hypothesis?

A
  • Changes in regional volume, connectivity and neurogenesis lead to the onset of depression
  • Multiple regions implicated
  • ENIGMA–Major depressive disorder working group
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16
Q

What are the neurological changes correlated with MDD?

A
17
Q

What is BDNF signalling?

A
  • Key regulator of these processes is brain derived neurotrophic factor
  • BDNF is coupled to multiple intacellular signalling cascades
  • Regulates many forms of neuroplasticity
18
Q

How does BDNF interact with neuroplasticity?

A
  • BDNF regultes changes in synaptic strength and connectivity
  • BDNF upregulates hippocampul neurogenesis
19
Q

How can SSRIs effect neuroplasticity?

A
  • Evidence accumulating that SSRI treatment can reverse changes in brain volumes, connectivity and fucntion
  • Changes to levels of glutamate and glutamine also reduced
  • Cause for optimism-the structural changes linked to depression can be reversed
  • 5-HT receptor activation is linked to upregulation of BDNF
20
Q

Summarise Depression.

A
  • Clinical depression has many causes and symptoms
  • 3 leading hypotheses for the disease mechanism:
    1. Monoamine
    2. Glutamate
    3. Neuroplasticity
  • Multiple classes of antidepressants (MAOIs, TCA, SSRIs, atypical)
  • SSRIs work by inhib SERTs and reducing 5-HT reuptake
  • SSRIs can also reverse changes in brain volume, connectivity and fucntion associated with depression.

Drugs and diseases-2106 (38 decks)

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