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PSY4 Depression

Deleted user 12 questions Updated 14 Oct 2019

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  1. 1Epidemiology of major depressive disorder:
    • 1 in [blank_start]10[blank_end] primary care patients present with depressive symptoms.
    • Lifetime risk of depression is 15% and 12 month prevalence is 4.1%.
    • NZ - 17.9% of [blank_start]women[blank_end] and 10.4% of [blank_start]men[blank_end]
    • Highest rates in [blank_start]women 35 – 44 years[blank_end] (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
    1. A10
    2. Bwomen
    3. Cmen
    4. Dwomen 35 – 44 years
  2. 2Match the symptoms/performances affected with their associated regions:
    PFC, [blank_start]prefrontal cortex;[blank_end] concentration, interest, pleasure, mental fatigue, guilt, worthlessness, suicidality, mood
    S, striatum; [blank_start]physical fatigue,[blank_end]
    NA, nucleus accumbens; [blank_start]pleasure, interest, energy[blank_end]
    HY, hypothalamus; [blank_start]sleep, appetite[blank_end]
    A, amygdala; [blank_start]guilt, worthlessness, suicidality, mood[blank_end]
    C, cerebellum; [blank_start]psychomotor[blank_end]
    1. Aprefrontal cortex;
    2. Bphysical fatigue
    3. Cpleasure, interest, energy
    4. Dsleep, appetite
    5. Eguilt, worthlessness, suicidality, mood
    6. Fpsychomotor
  3. 3Select from this list of depression symptoms those that overlap with anxiety.
    1. ASleep issues
    2. BConcentration issues
    3. CFatigue
    4. DPsychomotor arousal (restlessness)
    5. EAnhedonia
    6. FApathy
    7. GWorthlessness
    8. HAppetite and weight changes
    9. ISuicidality
  4. 4Diagnosis of depression requires ONE of: [blank_start]apathy/anhedonia OR depressed mood[blank_end].
    Also requires at least [blank_start]4[blank_end] of: appetite/weight change, sleep disturbances, cognitive [blank_start]dysfunction[blank_end], agitation/restlessness, fatigue, suicidal ideation, worthlessness.

    Major depressive disorder is the most [blank_start]common[blank_end] mood disorder, defined by occurrence of at least a single major depressive episode - most people experience [blank_start]recurrent[blank_end] episodes.
    1. Aapathy/anhedonia OR depressed mood
    2. B4
    3. Cdysfunction
    4. Dcommon
    5. Erecurrent
  5. 5Pathophysiology:
    • Inefficient/dysfunctional [blank_start]5-HT, NA and/or DA[blank_end] projections to amygdala and VMPFC are linked to depression
    • Poor information processing in the [blank_start]cerebellum, striatum[blank_end] and NAc (NA, 5HT and DA projections) linked to psychomotor [blank_start]agitation[blank_end]/retardation
    • [blank_start]Hypo[blank_end]-active monoaminergic projections from the brain stem to the hypothalamus, basal forebrain and PFC linked to [blank_start]sleep[blank_end] disturbances
    • Feelings of guilt/worthlessness regulated by amygdala and VMPFC - inefficient or dysfunctional [blank_start]5-HT[blank_end] projections
    • Suicidal ideation regulated by [blank_start]serotonergic[blank_end] control of the amygdala, VMPFC and [blank_start]orbital frontal[blank_end] cortex (OFC)
    • Weight and appetite 5-HT projections in the [blank_start]hypothalamus[blank_end]
    1. A5-HT, NA and/or DA
    2. Bcerebellum, striatum
    3. Cagitation
    4. DHypo
    5. Esleep
    6. F5-HT
    7. Gserotonergic
    8. Horbital frontal
    9. Ihypothalamus
  6. 6Why might the clinical effect of SSRIs and SNRIs take several weeks to develop?
    1. ASecondary adaptive changes such as downregulation of 5-HT2, α2, β binding sites and the functional response to agonists
    2. BDA neurotransmission is decreased in the mesolimbic pathway at first
    3. CBlockade or release of a particular neurotransmitter is slow
  7. 7Monoamine receptor hypothesis of depression:
    There is no clear convincing [blank_start]evidence[blank_end] that monoamine deficiency accounts for depression – i.e., there is no “real” monoamine deficit, but increasing monoamines as a treatment is effective. The monoamine [blank_start]receptor[blank_end] hypothesis of depression extends the classic monoamine hypothesis of depression, positing that [blank_start]deficient[blank_end] activity of monoamine [blank_start]neurotransmitters[blank_end] causes [blank_start]up[blank_end]regulation of [blank_start]post[blank_end]synaptic monoamine neurotransmitter [blank_start]receptors[blank_end] which leads to depression.
    1. Aevidence
    2. Breceptor
    3. Cdeficient
    4. Dneurotransmitters
    5. Eup
    6. Fpost-
    7. Greceptors
  8. 8SSRI mechanisms:
    - Block 5-HT [blank_start]reuptake[blank_end] pump ([blank_start]SERT[blank_end])
    - Increase [blank_start]somatodendritic 5-HT[blank_end] (initially)
    - Desensitize somatodendritic [blank_start]5-HT1A autoreceptors[blank_end]
    - Turn on [blank_start]neuronal impulse flow[blank_end] and increase 5-HT [blank_start]release[blank_end] from [blank_start]axon[blank_end] terminals
    - Finally desensitize [blank_start]postsynaptic 5-HT[blank_end] receptors
    1. Areuptake
    2. BSERT
    3. Csomatodendritic 5-HT
    4. D5-HT1A autoreceptors
    5. Eneuronal impulse flow
    6. Frelease
    7. Gaxon
    8. Hpostsynaptic 5-HT
  9. 9Mirtazepine - α2 [blank_start]antagonist[blank_end] - noradrenergic & specific serotonergic antidepressant (also blocks a couple [blank_start]5-HT[blank_end] receptors).
    • α2-adrenergic receptors are mostly autoreceptors and heteroreceptors which enhance adrenergic and serotonergic neurotransmission. This:
    a) stops [blank_start]NA[blank_end] turning off its own release ([blank_start]negative[blank_end] feedback) so [blank_start]NA release[blank_end] is increased
    b) blocks [blank_start]pre[blank_end]synaptic α2 [blank_start]heteroreceptors[blank_end] i.e. the “brakes” on [blank_start]serotonergic[blank_end] neurons, so there is enhanced [blank_start]serotonergic transmission[blank_end]
    • SEs - somnolence(excess [blank_start]sleepiness[blank_end]), sedation, [blank_start]dry[blank_end] mouth, weight [blank_start]gain[blank_end], increased [blank_start]appetite[blank_end], [blank_start]dizziness[blank_end] and fatigue.
    1. Aantagonist
    2. B5-HT
    3. CNA
    4. Dnegative
    5. ENA release
    6. Fpre-
    7. Gheteroreceptors
    8. Hserotonergic
    9. Iserotonergic transmission
    10. Jsleepiness
    11. Kdry
    12. Lgain
    13. Mappetite
    14. Ndizziness
  10. 10Agomelatine acts as a MT1 and MT2 receptor [blank_start]antagonist[blank_end] (involved in [blank_start]sleep[blank_end]) and 5HT(2C) antagonist.
    - Stimulation of [blank_start]MT1 and MT2[blank_end] receptors helps [blank_start]resynchronize[blank_end] depression-altered circadian rhythms, which potentially can optimize these changes in monoamines
    - Binds to [blank_start]5HT2C[blank_end] receptors on [blank_start]GABA[blank_end] interneurons, prevents 5-HT from [blank_start]binding[blank_end] and prevents [blank_start]inhibition[blank_end] of NA and DA release in the [blank_start]prefrontal[blank_end] cortex - ie facilitates their releases.
    1. Asleep
    2. BMT1 and MT2
    3. Cresynchronize
    4. D5HT2C
    5. EGABA
    6. Fbinding
    7. Ginhibition
    8. Hprefrontal
    9. Iagonist

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User has deleted their subject information Quiz on PSY4 Depression, created by Deleted user on 14/10/2019.
Author
Deleted user
Language
English
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Created on 14 Oct 2019 · updated on 14 Oct 2019
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