Mer Scott
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PHCY320 (Psychiatry) Quiz on PSY4 Depression, created by Mer Scott on 12/10/2019.

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PSY4 Depression

Question 1 of 12

1

Epidemiology of major depressive disorder:
• 1 in primary care patients present with depressive symptoms.
• Lifetime risk of depression is 15% and 12 month prevalence is 4.1%.
• NZ - 17.9% of and 10.4% of
• Highest rates in (21%)
• Mean age of onset is 27 years with 40% having a first episode by the age of 20
• 54% recover within 6 months, 70% within one year, 12–15% fail to recover and develop a chronic unremitting illness
• Economic cost in NZ > $2 billion/year

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    10
    women
    men
    women 35 – 44 years

Explanation

Question 2 of 12

1

Match the symptoms/performances affected with their associated regions:
PFC, concentration, interest, pleasure, mental fatigue, guilt, worthlessness, suicidality, mood
S, striatum;
NA, nucleus accumbens;
HY, hypothalamus;
A, amygdala;
C, cerebellum;

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    prefrontal cortex;
    physical fatigue
    pleasure, interest, energy
    sleep, appetite
    guilt, worthlessness, suicidality, mood
    psychomotor

Explanation

Question 3 of 12

1

Select from this list of depression symptoms those that overlap with anxiety.

Select one or more of the following:

  • Sleep issues

  • Concentration issues

  • Fatigue

  • Psychomotor arousal (restlessness)

  • Anhedonia

  • Apathy

  • Worthlessness

  • Appetite and weight changes

  • Suicidality

Explanation

Question 4 of 12

1

Diagnosis of depression requires ONE of: .
Also requires at least of: appetite/weight change, sleep disturbances, cognitive , agitation/restlessness, fatigue, suicidal ideation, worthlessness.

Major depressive disorder is the most mood disorder, defined by occurrence of at least a single major depressive episode - most people experience episodes.

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    apathy/anhedonia OR depressed mood
    4
    dysfunction
    common
    recurrent

Explanation

Question 5 of 12

1

Pathophysiology:
• Inefficient/dysfunctional projections to amygdala and VMPFC are linked to depression
• Poor information processing in the and NAc (NA, 5HT and DA projections) linked to psychomotor /retardation
-active monoaminergic projections from the brain stem to the hypothalamus, basal forebrain and PFC linked to disturbances
• Feelings of guilt/worthlessness regulated by amygdala and VMPFC - inefficient or dysfunctional projections
• Suicidal ideation regulated by control of the amygdala, VMPFC and cortex (OFC)
• Weight and appetite 5-HT projections in the

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    5-HT, NA and/or DA
    cerebellum, striatum
    agitation
    Hypo
    sleep
    5-HT
    serotonergic
    orbital frontal
    hypothalamus

Explanation

Question 6 of 12

1

Why might the clinical effect of SSRIs and SNRIs take several weeks to develop?

Select one of the following:

  • Secondary adaptive changes such as downregulation of 5-HT2, α2, β binding sites and the functional response to agonists

  • DA neurotransmission is decreased in the mesolimbic pathway at first

  • Blockade or release of a particular neurotransmitter is slow

Explanation

Question 7 of 12

1

Monoamine receptor hypothesis of depression:
There is no clear convincing that monoamine deficiency accounts for depression – i.e., there is no “real” monoamine deficit, but increasing monoamines as a treatment is effective. The monoamine hypothesis of depression extends the classic monoamine hypothesis of depression, positing that activity of monoamine causes regulation of synaptic monoamine neurotransmitter which leads to depression.

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    evidence
    receptor
    deficient
    neurotransmitters
    up
    post-
    receptors

Explanation

Question 8 of 12

1

SSRI mechanisms:
- Block 5-HT pump ()
- Increase (initially)
- Desensitize somatodendritic
- Turn on and increase 5-HT from terminals
- Finally desensitize receptors

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    reuptake
    SERT
    somatodendritic 5-HT
    5-HT1A autoreceptors
    neuronal impulse flow
    release
    axon
    postsynaptic 5-HT

Explanation

Question 9 of 12

1

Mirtazepine - α2 - noradrenergic & specific serotonergic antidepressant (also blocks a couple receptors).
• α2-adrenergic receptors are mostly autoreceptors and heteroreceptors which enhance adrenergic and serotonergic neurotransmission. This:
a) stops turning off its own release ( feedback) so is increased
b) blocks synaptic α2 i.e. the “brakes” on neurons, so there is enhanced
• SEs - somnolence(excess ), sedation, mouth, weight , increased , and fatigue.

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    antagonist
    5-HT
    NA
    negative
    NA release
    pre-
    heteroreceptors
    serotonergic
    serotonergic transmission
    sleepiness
    dry
    gain
    appetite
    dizziness

Explanation

Question 10 of 12

1

Agomelatine acts as a MT1 and MT2 receptor (involved in ) and 5HT(2C) antagonist.
- Stimulation of receptors helps depression-altered circadian rhythms, which potentially can optimize these changes in monoamines
- Binds to receptors on interneurons, prevents 5-HT from and prevents of NA and DA release in the cortex - ie facilitates their releases.

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    sleep
    MT1 and MT2
    resynchronize
    5HT2C
    GABA
    binding
    inhibition
    prefrontal
    agonist

Explanation

Question 11 of 12

1

Venlafaxine (SNRI)
- Inhibits at low doses and also at increased doses
- Converted to active , desvenlafaxine, by 2D6
- Desvenlafaxine also inhibits SERT and NAT but its effects are greater than venlafaxine - new drug...

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    5-HT reuptake
    NA reuptake
    metabolite
    CYP
    noradrenergic

Explanation

Question 12 of 12

1

All TCAs:

Select one of the following:

  • Block NA reuptake (NAT) and voltage-sensitive sodium channels (VSCCs), and are antagonists at H1, α1, and muscarinic cholinergic receptors.

  • Block 5-HT reuptake (SERT) and voltage-sensitive sodium channels (VSCCs), and are angonists at H1, α1, and muscarinic cholinergic receptors.

Explanation