inflammation Flashcards

1
Q

what is inflammation

A

a reaction to living tissue around it, not dead tissue

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2
Q

why must tissue be living an vascularised for inflammation

A

ingredients for inflammation are in circulation

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3
Q

what is fibrinogen

A

clot protein
very useful in body, interstitial space
turns into fibrin

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4
Q

what does inflammation deliver

A

concentrated, activated defensive materials in fluid
- phagocytes
- plasma proteins (opsonins, complement)

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5
Q

what is exudate

A

delivered cells, proteins, fluid

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6
Q

5 cardinal signs of inflammation

A

swelling - universal sign
warmer
painful
redness
loss of function
signs differ depending on setting but are driven by active changes in microvasculature which delivers the exudate

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7
Q

how does inflammation start

A

small vessels and ECM respond to danger signals
- damaged matrix
- stressed/dying tissue cells
- mast cells
- pathogens

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8
Q

second stage of inflammation

A

blood fills capillary and venular bed - redness, warmth
exudate fluid leaves capillaries/venules
interstitial matrix actively hydrates - local swelling
venous outflow becomes sluggish - stasis, congestion

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9
Q

how do cytokines sustain inflammation in substantive injuries

A

perivascular mast cells degranulate and release cytokines through projections into vessels
incoming leukocytes take over

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10
Q

local swelling

A

water uptake into connective tissue matrix (hyaluronan)
relaxed compression - collagen detachment and unfolding, fibroblasts relax

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11
Q

hyaluronan in matrix

A

very hyrophilic
tends to be slightly hydrated as is compressed by surrounding cells so doesnt hold as much water as possible

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12
Q

vascular leak

A

junction breaks between endothelial cells
capillary filtration pressure

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13
Q

passive leak

A

from microvessels
usually less important

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14
Q

what happens to leucocytes and platelets entering venules

A

pushed towards the walls by haemodynamics of normal blood flow

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15
Q

what blocks inflammatory cells from sticking firmly to endothelium

A

thick glycocalyx ‘blanket’

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16
Q

what causes endothelium to shed glycocalyx

A

DAMP and cytokines (TNF, IL-1)

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17
Q

what is exposed once glycocalyx is shed

A

surface adhesion molecules like selectins
they enhance neutrophil and platelet rolling

18
Q

what do platelets boost

A

endothelial activation

19
Q

what recruits more platelets

A

fibrin stands forming on endothelium

20
Q

what happens when crawling neutrophils encounter platelets bound to endothelium

A

they move to endothelial junction to exit using proteases

21
Q

transmigration

A

pericytes guide out transmigrating neutrophils
extravasated neutrophils emerge and screen the perivascular tissue
rigidity of inflamed tissue further activates traversing neutrophils

22
Q

what seals the transmigration site

A

platelets

23
Q

what is chemotaxis

A

directed migration up a concentration gradient
phagocytes need a matrix to crawl over

24
Q

things that attract neutrophils - self

A

coagulation products
complement C5a, C3a
IL-8

25
Q

things that attract neutrophils - non-self

A

bacterial endotoxin
f-met-leu-phe peptides

26
Q

what can minor damage be cloaked by

A

resident macrophages
results in damage being concealed from scanning neutrophils

27
Q

what does inflammation develop in response to

A

DAMP and/or PAMP
pattern recognition receptors recruit and activate immune cells, and prime adaptive immune responses

28
Q

what do changes in small blood vessels deliver

A

an exudate that contains active defenses

29
Q

what is in pus

A

neutrophil and enzyme rich

30
Q

fibrinous exudate

A

fibrin&raquo_space; cells
greyish sticky fibrin coating

31
Q

serous exudate

A

fluid&raquo_space; cells
serum like, lacking fibrinogen and platelets
found in burn blisters, allergic polyps

32
Q

haemorrhagic exudates

A

vascular destruction

33
Q

lymphatics in inflammation

A

draining lymph carries immune cells, inflammatory cytokines, extracellular vesicles, matrix fragments etc. from injury site to local lymph nodes - adaptive immune responses

34
Q

what is nociception through

A

Aẟ and C nociceptor neurones

35
Q

what can influence pain thresholds

A

macrophages

36
Q

is all inflammation painful

A

no - indirect pain from adjacent structures

37
Q

systemic effects of inflammation

A

cytokine effects distant to injury
IL-1β, TNF, IL-6, chemokines

38
Q

systemic effects of inflammation - liver

A

acute phase proteins
fibrinogen, c-reactive proteins, serum amyloid A (IL6, IL1)

39
Q

systemic effects of inflammation - bone marrow

A

accelerated wbc release from marrow (esp neutrophilia)

40
Q

systemic effects of inflammation - CNS

A

fever
sickness behaviours
cytokine induced depression (chronic inflammation or immunotherapy)
cognitive impairment (brain fog, chronic inflammation)