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354: Pathobiology > 9. Inflammation and Infection In Stroke > Flashcards

9. Inflammation and Infection In Stroke Flashcards

1
Q

name the two approved treatments aimed to restore blood flow in stroke

A

intravenous recombinant tissue plasminogen activator (rtPA)

mechanical thrombectomy (MT)

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2
Q

what is the acute phase response

A

a group of physiological processes that occur soon after the onset of infection

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3
Q

name an acute phase protein

A

C-reactive protein (CRP)

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4
Q

when is the inflammatory cascade activated in stroke

A

immediately after vessel occlusion

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5
Q

what is first released after stagnant blood flow appears

A

P-selectin

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6
Q

what is the role of P-selectin

A

attracts circulating leukocytes to the endothelial surface

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7
Q

what is the role of E-selectin

A

promotes leukocyte adhesion and transmigration through the vessel wall

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8
Q

what activates inflammation in the brain parenchyma

A

damage-associated molecule patterns (DAMPs)

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9
Q

what produces DAMPs

A

dying neurons

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10
Q

what do activated microglial cells do

A

stimulate the inflammasome to release IL-1beta and TNF-alpha

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11
Q

how do these DAMPs and cytokines get access to systemic circulation

A

via the disrupted BBB or CSF drainage system

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12
Q

what happens when DAMPs and cytokines enter systemic circulation

A

results in systemic inflammation

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13
Q

what are the two main mechanisms for why there is an increased risk of chest infection after stroke

A
  1. Aspiration of food material = by swallowing response
  2. initial depression of the immune system caused by systemic circulation of novel CNS antigens (which stimulate a t-cell response)
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14
Q

what type of cells have a protective function in stroke

A

microglia, monocyte derived macrophages

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15
Q

what type of cells have a damaging function in stroke

A

mast cells and innate lymphocytes

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16
Q

what is the damaging role of mast cells

A

their activation contributes to BBB breakdown and brain oedema

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17
Q

where do mast cells reside

A

in the peri vascular space

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18
Q

what is the effect of IL-10 secretion

A

neuroprotective - it reduces the activity of caspases which have been activated by lipopolysaccharide

this reduces neuronal apoptosis

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19
Q

what is the action of IL-6

A

proinflammatory = increases vascular risk

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20
Q

what did research of a multi-ethnic cohort reveal in terms of hsCRP to IL-6

A

when hsCRP is higher than the IL-6 quartile, ischaemic stroke risk was increased

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21
Q

why does inflammation sometimes cause stroke

A

inflammation is key in destabilising vulnerable plaques with consequent thrombosis and distal thromboembolism

22
Q

how can microembolic signals be detected

A

using a transcranial doppler before surgery

23
Q

what do microembolic signals show

A

these signals show in vivo measures of plaque inflammation

24
Q

what was the first cytokine found to act on the brain

A

interleukin 1

25
Q

what is the associated actions of IL-1

A

induced fever
appetite suppression
weight loss
sleep modulation
altered endocrine, neural and immune function

26
Q

what happens if patients are injected with interleukin-1 receptor antagonist into the occlusion

where is this effect more pronounced

A

after 1 hour, lesion volume decreased

this effect was more apparent when injected into cortical regions unlike subcortical regions

27
Q

what is a further action of intravenous IL-1 receptor antagonist

A

it reduced peripheral markers of inflammation

28
Q

what may explain the seasonal variance in stroke incidence

A

environmental factors are at play - e.g. infections precede the stroke.

winter flu may induce stroke occurrance

29
Q

name 2 types of infections that cause inflammation which can induce stroke

A

chlamydia pneumoniae
helicobacter pylori

30
Q

what type of infection is particularly likely to cause stroke

A

bacterial infection

31
Q

what % of stroke patients have an infection in the week preceding stroke

A

10-35%

32
Q

how can we use this finding of the effect of bacterial infections to reduce stroke risk

A

administer IL-1 receptor antagonist = this blocks bacterial endotoxin LPS from exacerbating brain damage

33
Q

IL-1ra blocks the effects of LPS, what exacerbates it?

A

IL-1 beta

34
Q

what gives the patient resistance to LPS

A

having dysfunctional toll like receptor 4 signalling

35
Q

where are infections in post stroke patients common

A

in the respiratory tract and the urinary tract

36
Q

what percentage of deaths within 30 days of admission is due to pneumonia in stroke patients

A

10%

37
Q

name 3 predictors of post stroke infection

A

older age
total anterior circulation infarction
dysphagia

38
Q

what is pneumonia particularly common in

A

tube fed patients

39
Q

what factors make the individual prone to spontaneous infections post stroke

A

impaired cell-mediated immunity
impaired t-cell activity

40
Q

what tool can be used to target post stroke infections

A

vaccinating vulnerable patients

41
Q

how could SARS-COV2 drive stroke

A

NLRP3 inflammasomes drive production of cytokines PAMPs and DAMPs. this could induce plaque instability by overdriving the response of macrophages and lymphocytes

42
Q

how does nitric oxide deficiency arise and what causes it

A

suppression of nitric oxide synthase = nitric oxide deficiency

results in the loss of vasodilatory effects and promotes the adhesion of platelets and leukocytes to the vessel wall.

43
Q

how is a mechanical thrombectomy conducted

A

a catheter is placed through the blood vessels to reach the clot - the catheter is placed through the groin

44
Q

what is the success rate for mechanical thrombectomy

A

66% success rate

45
Q

name a clot busting drug

A

alteplase

46
Q

who is eligible to receive clot busting drugs

A

only those who arrive at the hospital within 90 minutes of stroke symptoms manifesting

47
Q

what is a limitation of alteplase

A

it is less able to break down blood clots which are rich in von Willebrand factor

48
Q

what % of clots are rich in Von Willebrand Factor

A

50%

49
Q

who has recently developed a new clot busting drug

A

the university of manchester

50
Q

describe the new clot busting drug made by UoM

A

good success rates in mice who are resistant to current drugs

this drug targets von willebrand factor

the drug also prevented neutrophils from invading brain tissue starved of oxygen preventing inflammation

354: Pathobiology (10 decks)

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