Inflammation and Depression - Hunter Flashcards

1
Q

Depression may be caused by infammation due to the release of which three cytokines from the acute phase response?

A

TNF-a
IL-1b
IL6

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2
Q

one third of people with depression have high levels of (CRP/SEDR)

A

CRP

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3
Q

Compared to autoimmune and infectious dz, how do the increased levels of inflammatory markers in depression look?

A

not as high as autoimmune but comparable to CVD, stroke, and diabetes

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4
Q

Which two inflammatory mediators serve as biomarkers and prognostic indicators of depression?

A

CRP and IL-1b

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5
Q

T/F: t/f: inflammation is both necessary and sufficient to cause depression

A

false

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6
Q

T/f: inflammation as a feature of depression is a feature only in a subset of patients

A

true

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7
Q

There is evidence for what two to other factors that may cause depression/

A

genetic and environmental

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8
Q

What other mental illnesses have shown a disruption in the immune and inflammatory response?

A

schizophrenia

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9
Q

Depression occurs in 5-10x higher in people with what types of dz?

A

peripheral inflammatory diseases
psoriasis
rheumatoid arthritis
IBS

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10
Q

MS has a lifetime prevalence of depression of (blank) %

A

50%, suicide 15%

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11
Q

T/F: cancer, stroke, CAD, and epilepsy are risk factors for depression

A

true

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12
Q

Patients treated with inflammatory cytokines have a high rate of (blank)

A

depression

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13
Q

Which two cytokines that cause a cytokine storm are used for immunotherapy in hept C and cancer?

A

IFN-a

IL2

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14
Q

the prevalence of pts treated with IFN-a was (blank)%

A

30%

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15
Q

Pts with Crohn’s disease and depression had sig. remission from depression after treatment with (blank) an anti-TNF-a antibody

A

infliximab

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16
Q

55% of pts with psoriasis and depression were treated with (blank), a soluble TNF-a receptor improved compared to antidepressants

A

etanercept

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17
Q

T/f: anti-inflammatory tx have been associated with antidepressant effects

A

true

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18
Q

Addition of celecoxib, a COX-2 inhibitor that inhibits the production of (blank), added to reboxetine a SNRI, showed increased improvement compared to reboxetine alone

A

PGE2

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19
Q

t/F: Tx with antidepressants cuases a decrease in inflammatory mediators and depression

A

true

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20
Q

T/f: IL1b, IL6, and TNF-a levels all decrease in response to antidepressants

A

FALSE, NOT TNFa

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21
Q

Decrease in inflammatory markers was specific to Tx with (SSRI/SNRI)

22
Q

T/F: antidepressants may block the action of inflammatory cytokines in the brain

23
Q

Inflammation plays a role in depression only in a subset of (blank) susceptible individuals

A

genetically

24
Q

Inflammation may act as a (blank) factor pushing someone into depression or a (blank) factor that is an obstacle for recovery

A

precipitating and perpetuating

25
t/F: inflammatory mediators may aid in diagnosis and prognosis of depression
true
26
Cytokines are produced by which three brain cell types?
neurons microglia astrocytes
27
T/f: the cells that produce cytokines in the brain also have cytokine receptors
true
28
Is the brain immunologicaly priveleged or can peripheral cytokines signal the brain?
peripheral cytokines can signal the brain
29
What are the four pathways through which cyotkines may access the brain?
1. neural pathway 2. humoral pathway 3. cytokine transporters 4. Secondary messengers via the BBB
30
Cytokines produced in the periphery trigger sensory afferents of which two cranial nerves? What pathway is this called?
vagal glossopharyngeal neural pathway (CNs then stimulate other neurons in the CNS to stim glial cells to release cytokines)
31
volume diffusion of cyotkines from leaky circumventricular ogans that are outside the bbb is which pathway?
humoral
32
T/F: direct cytokine transporters exist in the blood brain barrier
true
33
Secretion of which two secondary messengers via the cells of the BBB allow peripheral cytokines to cause creation of cytokines within the brain?
PGE2 and NO
34
Infection and tissue damage, aka PAMPs and DAMPs, are recognized by what receptor that stimulates the release of NF-kB
TLR-4
35
Release of NF-kB causes the production and rlease of which three proinflammatory mediators
TNF-a IL1b IL6
36
Cytokines that gain access to the brain or signal the brain to make cytokines act via which three hormone pathways?
1. Serotonergic and dopaminergic signaling 2. activation of CRH and engagement of HPA axis (cortisol production) 3. disruption of synaptic plasticity (BDNF)
37
Activation of CRH causes the HPA axis to produce what stress hormone?
cortisol
38
Cytokines cause the disruption of synaptic plasticity via the downregulation of which neurotrophic factor?
BDNF
39
Environmental stressors activate (sympathetic/parasymp) neurons that synapse on mac's
sympathetic
40
Which neurotransmitter is used in the synapses with macrophages?
norepi
41
synapses on macrophages trigger the release of what transcription factor?
NF-kB
42
Stressors cause an (inc/dec) on inhibitory motor vagal input which prevents the formation of NF-kB
decreases the inhibition therefore more NF-kB is produced therefore more inflamm
43
ACh released from inhibitory motor vagal afferents bind to which receptor?
a7nAChR
44
activation of the mitogen activated protein kinase pathway inhibits the function of which receptor?
glucocorticoid receptor
45
Inhibition of the glucocorticoid receptors (inc./dec,) NF-kb release
increases NF-kB release from negative regulation
46
With functioning receptors, glucocorticoids will (inc/dec.) inflammation
decrease, that's why we give you steroids when you have asthma
47
The reason why the CHRONIC stimulation of CRH in the brain by peripheral cytokines doesn't lead to inflammatory down regulation via glucocoriticoid is....
GLUCOCORTICOID RESISTANCE, that's why chronic stress leads to diabetes and shit
48
Which cell has the a7nAChR on it?
macrophages
49
What cell type are the sympathetic, and motor vagal inputs synapsing on?
macrophages
50
T/F: release of NF-kB causes an increase in adhesion moecules
true
51
T/F: sympathetic input to macrophages only stimulates a1 adrenergic receptors
false; stimulates both a and b adrenergic