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Block 8 Week 1 Colt > Inflammation and Depression - Hunter > Flashcards

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)

A

SSRI

22
Q

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

A

true

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
Q

t/F: inflammatory mediators may aid in diagnosis and prognosis of depression

A

true

26
Q

Cytokines are produced by which three brain cell types?

A

neurons
microglia
astrocytes

27
Q

T/f: the cells that produce cytokines in the brain also have cytokine receptors

A

true

28
Q

Is the brain immunologicaly priveleged or can peripheral cytokines signal the brain?

A

peripheral cytokines can signal the brain

29
Q

What are the four pathways through which cyotkines may access the brain?

A
  1. neural pathway
  2. humoral pathway
  3. cytokine transporters
  4. Secondary messengers via the BBB
30
Q

Cytokines produced in the periphery trigger sensory afferents of which two cranial nerves? What pathway is this called?

A

vagal
glossopharyngeal
neural pathway
(CNs then stimulate other neurons in the CNS to stim glial cells to release cytokines)

31
Q

volume diffusion of cyotkines from leaky circumventricular ogans that are outside the bbb is which pathway?

A

humoral

32
Q

T/F: direct cytokine transporters exist in the blood brain barrier

A

true

33
Q

Secretion of which two secondary messengers via the cells of the BBB allow peripheral cytokines to cause creation of cytokines within the brain?

A

PGE2 and NO

34
Q

Infection and tissue damage, aka PAMPs and DAMPs, are recognized by what receptor that stimulates the release of NF-kB

A

TLR-4

35
Q

Release of NF-kB causes the production and rlease of which three proinflammatory mediators

A

TNF-a
IL1b
IL6

36
Q

Cytokines that gain access to the brain or signal the brain to make cytokines act via which three hormone pathways?

A
  1. Serotonergic and dopaminergic signaling
  2. activation of CRH and engagement of HPA axis (cortisol production)
  3. disruption of synaptic plasticity (BDNF)
37
Q

Activation of CRH causes the HPA axis to produce what stress hormone?

A

cortisol

38
Q

Cytokines cause the disruption of synaptic plasticity via the downregulation of which neurotrophic factor?

A

BDNF

39
Q

Environmental stressors activate (sympathetic/parasymp) neurons that synapse on mac’s

A

sympathetic

40
Q

Which neurotransmitter is used in the synapses with macrophages?

A

norepi

41
Q

synapses on macrophages trigger the release of what transcription factor?

A

NF-kB

42
Q

Stressors cause an (inc/dec) on inhibitory motor vagal input which prevents the formation of NF-kB

A

decreases the inhibition therefore more NF-kB is produced therefore more inflamm

43
Q

ACh released from inhibitory motor vagal afferents bind to which receptor?

A

a7nAChR

44
Q

activation of the mitogen activated protein kinase pathway inhibits the function of which receptor?

A

glucocorticoid receptor

45
Q

Inhibition of the glucocorticoid receptors (inc./dec,) NF-kb release

A

increases NF-kB release from negative regulation

46
Q

With functioning receptors, glucocorticoids will (inc/dec.) inflammation

A

decrease, that’s why we give you steroids when you have asthma

47
Q

The reason why the CHRONIC stimulation of CRH in the brain by peripheral cytokines doesn’t lead to inflammatory down regulation via glucocoriticoid is….

A

GLUCOCORTICOID RESISTANCE, that’s why chronic stress leads to diabetes and shit

48
Q

Which cell has the a7nAChR on it?

A

macrophages

49
Q

What cell type are the sympathetic, and motor vagal inputs synapsing on?

A

macrophages

50
Q

T/F: release of NF-kB causes an increase in adhesion moecules

A

true

51
Q

T/F: sympathetic input to macrophages only stimulates a1 adrenergic receptors

A

false; stimulates both a and b adrenergic

Block 8 Week 1 Colt (10 decks)

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