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5BBM0218 Physiology and Pharmacology of CNS > L11: Depression > Flashcards

L11: Depression Flashcards

1
Q

What is SAD (seasonal affective disorder) and how is it treated?

A
  • SAD is a type of depression with seasonal patterns, affecting more females than males.
  • Treatment: Light therapy is used to compensate for reduced natural sunlight during the winter
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2
Q

What is bipolar depression, and how is it treated?

A
  • Bipolar depression involves oscillations between depressive and manic episodes.
  • Treatment: Mood stabilizers help manage mood swings between depression and mania.
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3
Q

What is unipolar depression, and what are some common characteristics?

A
  • Unipolar depression = most common form, more prevalent in females.
  • Common characteristics: Persistent depressed mood, lack of interest in pleasurable activities.
  • Treatment: Psychotherapy, antidepressants, and ECT for severe cases
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4
Q

What are the criteria for a major depressive episode?

A
  • Major depressive episode: Depressed mood, lack of interest in activities for ≥2 weeks.
  • Additional symptoms: Changes in appetite, sleep disturbances, fatigue, worthlessness, difficulty concentrating, thoughts of death or suicide
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5
Q

What are the neurochemical factors associated with depression?

A
  1. Noradrenaline - found in locus coeruleus & Raphe nucleus, plays a role in motivation.
  2. Serotonin: located in the dorsal & ventral raphe, influences mood, anxiety & sleep.
  3. HPA axis: Involves the hypothalamus, cortisol levels are elevated in individuals with depression, affecting growth and prolactin levels.
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6
Q

What is the monoamine hypothesis of depression?

A
  • Monoamine hypothesis: Depression results from a deficiency of monoamine neurotransmitters, while mania is caused by an excess of the same neurotransmitters
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7
Q

How does the malfunction of the neurotrophic pathway relate to depression?

A
  • evidence suggests reduced BDNF levels OR malfunction of TrkB (BDNF receptor) in depression - affecting the neurotrophic pathway
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8
Q

How do antidepressants affect neurochemistry and brain structure in depression?

A
  • Antidepressants reduce NMDA receptor activation & glutamate release
  • can both depress & facilitate the depressive mood
  • Antidepressants may prevent long-term changes in the brain by stimulating neurogenesis & ↑ BDNF levels.
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9
Q

what are TCAs?

A
  • Tricyclic Antidepressants
    -one of the oldest classes of antidepressants.
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10
Q

what are SSRIs?

A
  • Selective serotonin reuptake inhibitor
  • most commonly prescribed antidepressants
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11
Q

what are SNRIs?

A

Serotonin-Norepinephrine Reuptake Inhibitors

SNRIs target both serotonin and norepinephrine reuptake

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12
Q

What are NaSSAs?

A

Noradrenaline-Serotonin Specific Antidepressants (NaSSAs):

NaSSAs enhance noradrenaline and serotonin neurotransmission

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13
Q

What is the mechanism of action of TCAs?

A
  • Block reuptake of serotonin and norepinephrine
  • increasing their availability in synapses
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14
Q

Name some TCAs

A

Amitriptyline, Imipramine, Nortriptyline

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15
Q

How long does it typically take for TCAs to show improvement in symptoms?

A

2-4 weeks

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16
Q

What are some common side effects of TCAs?

A
  • Dry mouth
  • constipation
  • blurred vision
  • drowsiness
  • potential for cardiac side effects
17
Q

How do SSRIs work to alleviate depression? Discuss their mechanism of action

A
  • SSRIs inhibit the serotonin reuptake process, allowing more serotonin to remain in the synapse
  • increase in serotonin levels in synapse enhances serotonin signalling & transmission between nerve cells.
  • prolonged presence of serotonin in the synapse= improved communication between nerve cells involved in mood regulation
18
Q

name some SSRIs

A

Fluoxetine (Prozac), Sertraline (Zoloft), Escitalopram (Lexapro)

19
Q

How long does it usually take for SSRIs to show significant improvement?

A

Typically takes 2-6 weeks

20
Q

What are some common side effects associated with SSRIs?

A
  • Nausea
  • sexual dysfunction
    insomnia
  • potential for serotonin syndrome
21
Q

What neurotransmitters do SNRIs target and how?

A

Block the reuptake of both serotonin AND norepinephrine

22
Q

Name some SNRIs used as antidepressants

A

Venlafaxine (Effexor), Duloxetine (Cymbalta), Desvenlafaxine (Pristiq)

23
Q

How long does it take for SNRIs to demonstrate noticeable effects?

A
  • may take 2-6 weeks
24
Q

What are some potential side effects of SNRIs?

A
  • Nausea, headache, increased blood pressure, and potential for withdrawal symptoms
25
Q

How do NaSSAs work to treat depression?

A
  • enhance noradrenaline & serotonin neurotransmission by blocking specific receptors
26
Q

name some NaSSAs used as antidepressants

A

Mirtazapine (Remeron), Mianserin (Lantanon)

27
Q

How long does it typically take for NaSSAs to take effect?

A

may take several weeks

28
Q

What are some common side effects associated with NaSSAs?

A
  • Sedation, weight gain, dry mouth, and potential for agranulocytosis (rare)
29
Q

What are some common side effects of antidepressants?

A

include nausea, dry mouth, dizziness, and headache

30
Q

What unwanted effect is commonly associated with antidepressants?

A
  • Some antidepressants may cause sexual dysfunction
  • leading to decreased libido and difficulties achieving orgasm
31
Q

According to the monoamine hypothesis, what is the cause of depression?

A
  • caused by a functional deficit of monoamine transmitters (serotonin, norepinephrine, dopamine)
32
Q

What is believed to cause mania, as per the monoamine hypothesis?

A

caused by a functional excess of the same monoamine NTs

33
Q

How do antidepressants work to alleviate depression based on this monamine hypothesis?

A
  • Antidepressants aim to restore the balance of these neurotransmitters in the brain to alleviate symptoms of depression
34
Q

What is the Neuroendocrine Theory of Depression?

A
  • suggests that abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis - which regulates body’s stress response - play role in development of depression
  • theory highlights the dysregulation of cortisol (a stress hormone) and other neuroendocrine factors in depression
35
Q

What is the Neuroplasticity Theory of Depression?

A
  • proposes that depression is linked to impaired neuroplasticity
  • which refers to the brain’s ability to reorganize and form new neural connections in response to experiences and learning
  • suggests that depression may result from reduced neurogenesis (formation of new neurons) and synaptic plasticity in specific brain regions

5BBM0218 Physiology and Pharmacology of CNS (17 decks)

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