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FTK III- Gen Path > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Cardinal signs of inflammation

A

rubor (redness)
calor (warmth)
tumor (swelling)
dolor (pain)
functio laesa (loss of function)

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2
Q

Acute Inflammation

A

several hours to several days
exogenous and endogenous triggers
3 phases: fluidic, cellular, reparative
failure to clear stimulus –> chronic inflammation

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3
Q

Acute inflamm.- fluidic phase

A

vasodilation- due to histamines and nitric oxide; causes hyperemia (increased blood flow–> calor and rubor)
endothelial cell activation (increased vascular permeability–> fluid, protein, fibrinogen exudation –> edema (tumor))
increased blood viscosity (slower blood flow allows leukocytes to accumulate along endothelium)
leukocyte adhesion cascade begins

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4
Q

fibrinogen

A

important plasma protein floating in blood
** in tissues= fibrin

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5
Q

acute inflamm.- cellular phase

A

margination
rolling
stable adhesion
transendothelial cell migration

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6
Q

margination

A

bridge between fluidic and cellular phases of acute inflammation
due to vasodilation (reduced flow and increased viscosity) WBCs line up along endothelial surface

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7
Q

rolling

A

transient, weak binding between endothelial cell and leukocyte
**Selectins on both endothelial cells and WBCs interact and facilitate rolling

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8
Q

stable adhesion

A

WBCs strongly bind to endothelium
cytokines (**IL-1, IL-6, IL-8, TNF), complement factors, and other inflammatory mediators activate WBCs and endothelial cells
** Integrins on WBC surface facilitate stable adhesion

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9
Q

Transendothelial cell migration

A

WBCs move across endothelial cell layer into tissue
** Facilitated by PECAM-1 (CD31)

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10
Q

variations of acute inflammation

A

serous inflammation
catarrhal inflammation
fibrinous inflammation
suppurative inflammation

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11
Q

serous inflammation

A

low plasma proteins, little or NO WBCs
thermal injury –> blister
acute allergic response–> watery eyes and runny nose

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12
Q

catarrhal inflammation

A

thick gelatinous fluid containing abundant mucus
ex. chronic inflammation of airways –> asthma

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13
Q

fibrinous inflammation

A

due to endothelial cell activation/injury leading to leakage of fibrinogen
leads to formation of fibrin
occurs in body cavities, synovial membranes of joints, and meninges

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14
Q

suppurative inflammation

A

inflammation with high plasma protein and high number of leukocytes (predominantly neutrophils)–> pus
due to pyogenic bacteria

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15
Q

how long do neutrophils take to respond in inflammation?

A

6-24 hours
predominate in acute inflammation

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16
Q

how long do monocytes take to respond to inflammation?

A

24 hours and beyond
** become macrophages in tissue

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17
Q

how long do lymphocytes and plasma cells take to respond to inflammation?

A

greater than 48 hours and beyond
part of adaptive immune response

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18
Q

main histologic features of acute inflammation

A

neutrophils (first) then macrophages

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19
Q

main pathologic features of acute inflammation

A

plasma/fluid leakage–> edema +/- fibrin

20
Q

when does progression to chronic inflammation occur?

A

acute response is unresolved/inciting cause isn’t cleared
repeated episodes of acute inflammation with extensive injury and necrosis
establishment of an autoimmune response

21
Q

histologic changes in progression to chronic inflammation

A

shift of cellular elements from neutrophils to lymphocytes, macrophages, and plasma cells
also eosinophils and mast cells

22
Q

pathologic changes in progression to chronic inflammation

A

tissue destruction is one of the hallmarks of chronic inflammation

23
Q

lymphocytes role in chronic inflammation

A

antibody and cell-mediated immune reactions

24
Q

plasma cells role in chronic inflammation

A

develop from activated B lymphocytes, produce antibody against antigens or altered tissue components

25
Q

macrophages role in chronic inflammation

A

responsible for much of the tissue injury in chronic inflammation (ROS, extracellular matrix proteases)
important role in healing- induce fibroblast activation and formation which leads to collagen deposition and angiogenesis

26
Q

types of chronic inflammation

A

granulomatous inflammation
pyogranulomatous inflammation
abscess formation

27
Q

granulomatous inflammation

A

activated epithelioid macrophages, multinucleated giant cells mainly
some lymphocytes and plasma cells
surrounded by fibrosis (deposition of collagen)

28
Q

granuloma

A

one or more isolated foci of granulomatous inflammation

29
Q

pyogranulomatous inflammation

A

epitheliod macrophages forming granulomas with admixed neutrophils and necrosis
typical with fungi

30
Q

abscess formation

A

occurs when acute inflammatory response fails to rapidly eliminate inciting stimulus
enzymes and inflammatory mediators from neutrophils liquefy tissue to form pus
seen grossly as pus circumscribed by a fibrous capsule

31
Q

acute vs chronic inflammation

A

acute: rapid onset, short duration, fluid and plasma proteins leak into tissues (edema), fibrinogen –> fibrin, neutrophils migrate into tissues, leads to chronic inflammation if unresolved
chronic: long time frame (days to weeks to years), lymphocytes, plasma cells, and macrophages, fibrous connective tissue deposition, tissue necrosis

32
Q

outcomes of acute inflammation

A

progression to chronic inflam.

complete resolution leads to regeneration

healing by fibrosis

33
Q

complete resolution of acute injury

A

typical outcome to limited injury
mediators decay quickly, vascular permeability returns to normal, leukocytes die, edema, proteins removed by macrophages
tissue regeneration= 100% normal when resolved

34
Q

regeneration

A

replacement of cells of the same type

requires an intact framework

occurs by compensatory growth–> organ becomes functional due to cell hyperplasia and hypertrophy

35
Q

what determines whether or not a tissue will undergo regeneration or healing

A

type of tissue damaged
damage to ECM
extent of wound
blood supply, nutrition

36
Q

continuously dividing (labile) tissues

A

cells that proliferate throughout life
ex: gut epithelium

37
Q

quiscent (stable) tissues

A

low level of replication; may undergo division in response to stimuli
ex; cells of liver, kidney, and pancreas

38
Q

post-mitotic (permanent/terminally differentiated) tissues

A

cannot undergo mitotic division in postnatal life
ex: neurons, cardiac muscle cells

39
Q

healing by fibrosis

A

restoration of integrity to injured tissue; typically involves collagen deposition and scar formation

40
Q

4 temporal phases of wound repair/healing

A

hemostasis (vascular phase)
acute inflammation (cellular phase)
proliferation (granulation tissue)
remodeling (maturation phase, contraction)

41
Q

inflammation phase of wound repair/healing

A

24 hour after injury
macrophages are necessary for tissue repair- remove cell debris and degrade ECM and release GF and fibroblasts necessary for proliferation phase
fibrin is a loose gel-like matrix to serve as scaffold for granulation tissue

42
Q

proliferation phase of wound repair/healing

A

lasts up to 3-4 weeks (depends on size of wound)
granulation tissue= proliferation of new blood vessels, fibroblasts, and deposition of early collagen (necessary for re-epithelialization and sometimes called “wound bed”)

42
Q

remodeling/maturation pahse of wound repair/healing

A

begins ~3-4 weeks after injury but only after previous phases are complete
can last years
granualtion tissue (BV and immature CT) is converted to mature CT (fibrosis)
TGF-B mediates fibrosis (pro-fibrosis and anti-inflammatory)
Extracellular Collagen formation (ECM restored)
contraction of tissues by fibroblasts and myofibroblasts
** Tissues do not return to 100% normal structure and function

42
Q

Disruptors of repair

A

bacterial infection
poor nutrition
glucocorticoid therapy (inhibits TGF-B)
mechanical factors
poor apposition/dehiscence
poor perfusion
amount of tissue injured
tissue type

42
Q

abnormalities in tissue repair

A

inadequate granulation tissue repair
excessive formation
aberrations of cell growth and ECM production (exuberant granulation tissue is common in distal limbs of horses)
contraction

FTK III- Gen Path (5 decks)

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