Test
PSY4 Depression
Este test tiene tipos de pregunta que se abren en el reproductor de siempre.
Preguntas del test (12)
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- A10
- Bwomen
- Cmen
- Dwomen 35 – 44 years
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]- Aprefrontal cortex;
- Bphysical fatigue
- Cpleasure, interest, energy
- Dsleep, appetite
- Eguilt, worthlessness, suicidality, mood
- Fpsychomotor
3Select from this list of depression symptoms those that overlap with anxiety.
- ASleep issues
- BConcentration issues
- CFatigue
- DPsychomotor arousal (restlessness)
- EAnhedonia
- FApathy
- GWorthlessness
- HAppetite and weight changes
- ISuicidality
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.- Aapathy/anhedonia OR depressed mood
- B4
- Cdysfunction
- Dcommon
- Erecurrent
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]- A5-HT, NA and/or DA
- Bcerebellum, striatum
- Cagitation
- DHypo
- Esleep
- F5-HT
- Gserotonergic
- Horbital frontal
- Ihypothalamus
6Why might the clinical effect of SSRIs and SNRIs take several weeks to develop?
- ASecondary adaptive changes such as downregulation of 5-HT2, α2, β binding sites and the functional response to agonists
- BDA neurotransmission is decreased in the mesolimbic pathway at first
- CBlockade or release of a particular neurotransmitter is slow
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.- Aevidence
- Breceptor
- Cdeficient
- Dneurotransmitters
- Eup
- Fpost-
- Greceptors
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- Areuptake
- BSERT
- Csomatodendritic 5-HT
- D5-HT1A autoreceptors
- Eneuronal impulse flow
- Frelease
- Gaxon
- Hpostsynaptic 5-HT
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.- Aantagonist
- B5-HT
- CNA
- Dnegative
- ENA release
- Fpre-
- Gheteroreceptors
- Hserotonergic
- Iserotonergic transmission
- Jsleepiness
- Kdry
- Lgain
- Mappetite
- Ndizziness
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.- Asleep
- BMT1 and MT2
- Cresynchronize
- D5HT2C
- EGABA
- Fbinding
- Ginhibition
- Hprefrontal
- Iagonist
11Venlafaxine (SNRI)
- Inhibits [blank_start]5-HT reuptake[blank_end] at low doses and also [blank_start]NA reuptake[blank_end] at increased doses
- Converted to active [blank_start]metabolite[blank_end], desvenlafaxine, by [blank_start]CYP[blank_end]2D6
- Desvenlafaxine also inhibits SERT and NAT but its [blank_start]noradrenergic[blank_end] effects are greater than venlafaxine - new drug...- A5-HT reuptake
- BNA reuptake
- Cmetabolite
- DCYP
- Enoradrenergic
12All TCAs:
- ABlock NA reuptake (NAT) and voltage-sensitive sodium channels (VSCCs), and are antagonists at H1, α1, and muscarinic cholinergic receptors.
- BBlock 5-HT reuptake (SERT) and voltage-sensitive sodium channels (VSCCs), and are angonists at H1, α1, and muscarinic cholinergic receptors.
Información
- Descripción
- El usuario ha eliminado su información de asignaturas Test sobre PSY4 Depression, creado por Usuario eliminado el 14/10/2019.
- Autor
- Usuario eliminado
- Idioma
- English
- Visitas
- 64
- Historial
- Creado el 14 oct 2019 · actualizado el 14 oct 2019
- Etiquetas
- Valoración
- Aún sin valoraciones Valora este test