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Neurobiology of Disease > Depression and Bipolar > Flashcards

Depression and Bipolar Flashcards

1
Q

What are the 2 main symptoms of depression?

A
  • Persistent low mood
  • Loss of interest or pleasure
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2
Q

What are other symptoms of depression?

A
  • Low energy/fatigue
  • Worthlessness/excessive or inapp guilt
  • Sucidal thoughts/plans etc
  • Poor concentration
  • Restlessness, agitation or slowed down in movt and thinking
  • Change in sleep
  • Change in appetie
  • Concern over impeding death
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3
Q

Explain on the neuroanatomy of depression

A
  • ↓ in patients suffering from severe depression (imaging studies)
  • Prefrontal cortex
  • Amygdala
  • Hippocampus
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4
Q

What monoamine hypothesis of depression?

A
  • Tricyclic antidepressants (Tacs) and monoamine oxidase inhibitors (MAOIs) heralded as 1st generation antidepressants
  • Act by impacting NA and 5-HT neurotransmission
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5
Q

Why is the monoamine hypothesis of depression a poor hypothesis?

A
  • Doesn’t meet all the other complexities associated with depression
  • Limited in its link to depression
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6
Q

How is the HPA axis involved in depression?

A

Depressed patients displayed HPA hyperactivation:
* ^ Cortisol in saliva, plasma and urine
* ^ CRH in CSF and in limbic brain region
* ^ Size (as well as activity) of pituitary and adrenal glands

  • Impaired negative feedback loop
  • Antidepressants enhance the negative feedback and ↓ HPA axis hyperactivity
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7
Q

What is BDNF?

A
  • Brain Derived Neurotrophic Factor:
  • Regulates neurogenesis, development, dendritic growth, survival and maturation
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8
Q

What does the neurotrophic hypothesis of depression state?

A
  • Proposes that depression is associated with reduced brain BDNF levels
  • Antidepressants treatments alleviate depressive behaviour and ^ BDNF levels
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9
Q

What Neurotransmitters are involved in depression?

A
  1. 5-HT - Anxiety, obsessions, compulsions
    * Depression due to ↓ 5-HT

2.NA - Alertness, anxiety, interest in life
* Role in reward and stress

3.DA - Attention, motivation, reward
* ↓ tyrosine (precursor to DA)

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10
Q

What are non-pharmacological managements of depression?

A
  • CBT - Objective is to stop cycle of negative thinking that influences emotion and behaviour
  • E.g.
    1. Feeling: I feel anxious
    2. Thoughts: I cant do this, whats wrong with me etc
    3. Behaviour: Get away from the situation, avoid it in future

These can all interact back and forth with eachother.

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11
Q

What are the negatives of pharmacological managements of depression?

A
  • Adverse effect profile
  • Toxicity in overdose
  • Interaction with other treatments
  • Cost
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12
Q

What are 3 main modes of action antidepressants?

A
  1. Reuptake
  2. Receptor blockade
  3. MAO enzyme inhibition
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13
Q

What are the main classes of antidepressants?

A
  1. Tricyclic (TCA) antidepressant
  2. Monoamine Oxidase Inhibitor
  3. SSRIs
  4. Serotonin-Noradrenaline reuptake inhibitor
  5. Noradrenaline Reuptake inhibitor
  6. Mirtazapine
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14
Q

What are Tricyclic (TCA) antidepressants?

A
  • Inhibit serotonin and noradrenaline reuptake
  • E.g. Amitripyline
  • Sedative properties
  • Anticholinergic side effects (dry mouth, blurred vision etc)
  • CV effects can be fatal on overdose
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15
Q

What are MAO?

A

E.g. Phenelzine

  • Cheese reaction - tyramine displaces noradrenaline from vesical storage
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16
Q

What are SSRIs?

A
  • First line option
  • E.g. Fluoxetine, Paroxetine
  • Favourable ‘side effects’ profile and less toxic in overdose
17
Q

What are SNRIs?

A
  • E.g. Venlafaxine
  • Similar to SSRIs
18
Q

What are Noradrenaline reuptake inhibitors?

A

E.g. Reoxetine

19
Q

What is Mirtazapine?

A
  • Enhances NA and 5-HT transmission
  • Presyn a2-adrenoceptors responsible for inhib noradrenaline release
  • Presyn 5-HT2 responsible for inhib 5-HT release are also blocked
20
Q

How do you treat mild depression in < 18Yo?

A
  • Psychologcal therapy e.g. CBT
21
Q

How do you treat moderate-severe depression in < 18Yo?

A
  • Psychological therapy
  • Combined therapy i.e. psyho+Fluoxetine (SSRI)
  • If unresponsive to combined therapy - consider alternative psychological therapy
  • If experiencing side effects to fluoxetine –> Sertaline or citalopram
22
Q

Explain the delay of clinical effects

A
  • The main theory of delayed response to antidepressants: increasing neurotransmitters will increase activation of autoreceptors
  • Which will cause less neurotransmitter to be released
  • However, as a person continues to take the drug, the autoreceptors will become desensitised, so more neurotransmitters will be released
23
Q

What is Bipolar disorder?

A
  • Cycle between depressed mood and mania

Diagnosis:
* Eliminate misdiagnosis of bipolar disorder –> Differential diagnosis
* Confirmed by a specialist mental health professional

24
Q

What are pharmacological interventions for bipolar?

A

Managing Mania
Acute:
* Antipsychotics - Haloperidol
* Longer term: Lithium

Managing Bipolar depression
* SSRI Fluoxetine combined with olanzapine
* Quetiapine alone
* Olanzapine alone
* Lamotrignine alone

25
Q

What are the problems of Lithium?

A
  • Narrow therapeutic window
  • Must be tightly regulated
26
Q

What are experimental treatments?

A

Ketamine (NMDA antagonist): Dysfunction of glutamatergic neurotransmission is found in patients with MDD

BDNF target: Recent findings demonstrated that TRKB was a target for antidep

Neurobiology of Disease (22 decks)

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