Inflammation Flashcards

1
Q

What does inflammation allow?

A

protective response geared towards removing the cause and consequence of the injury
allows potential healing

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2
Q

list the cell types and soluble factors involved?

A

cells = neutrophils, macrophage, lymphocytes, eosinophils, mast cells
soluble factors = cytokines, antibodies, complement system, coagulation system

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3
Q

define acute inflammation

A

rapid non-specific response to cellular injury orchestrated by mediators released by injured cells

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4
Q

what response does acute inflammation involve?

A

leukocyte and vascular

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5
Q

define chronic inflammation

A

persistent inflammatory response that may arise from acute inflammation

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6
Q

name a type of chronic inflammation

A

granulomatous inflammation

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7
Q

what are signs of acute inflammation? what causes them

A

rubor - slow blood flow gives redness
calor - histamine vasodilation
tumor - histamine increased permeability and oedema
dolor - swelling and pain

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8
Q

what are the 3 main components of acute inflammation?

A

alteration in the calibre of blood vessels to increase flow
structural changes to the microvasculature to allow protein and leukocytes to leave circulation
emigration, accumulation and activation of leukocytes at the focus of injury

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9
Q

what does vasodilation cause? what is it induced by? what is it followed by?

A

heat and redness
induced by nitric oxide and histamine
increased permeability of microvasculature (leads to turbulent flow)

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10
Q

summarise the mechanism for increased vascular permeability and causes

A

endothelial cells contract
increase interendothelial spacing
causes = histamine, NO, endothelial injury, leukocyte mediated vascular injuryy

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11
Q

how is histamine released? what does it cause?

A

mast cell degranulation after IgE bind to cell

vasodilation and vascular permeability

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12
Q

define exudate

A

fluid with high protein, cellular debris content and specific gravity which has escaped from blood vessels and has been deposited in tissues due to inflammation

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13
Q

define transudate

A

low protein, cell content and specific gravity caused by disturbances in hydrostatic and colloid osmotic pressure

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14
Q

what is the function of exudate?

A

the fluid dilutes pathogen and allows soluble mediators to spread
the protein e.g. fibrin wall off pathogens to stop it spreading

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15
Q

name and describe the exudate types

A
serous = fluid filled, lower protein content
fibrinous = high fibrin content due to traumatic injury
purulent = pus filled, combo of fibrin, inflammatory cells, debris and fluid
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16
Q

What are the key leukocytes in the initial phase of acute inflammation? why?

A

neutrophil and monocyte/macrophage
kill bacteria and eliminate foreign and necrotic material, produce multiple factors and mediators that interact with other cells (degranulate)

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17
Q

summarise the mechanism by which neutrophils migrate into the tissue site

A

margination, rolling, adhesion to activated endothelium via loose selectin bonds then strong integrin bonds, transmigration across endothelium and migration via chemotaxis

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18
Q

what receptors are activated in a leukocyte response?

A

toll-like receptors - for microbial products
g-protein coupled receptors - bacterial peptides
opsonic receptors - for IgG and C3b
cytokine receptors - for IFN-gamma

19
Q

How is acute inflammatory response terminated?

A

mediators and neutrophils have short half life
macrophages, mast cells and lymphocytes release anti-inflammatory products
injury cause is removed

20
Q

list histological features of acute inflammation

A

many neutrophils, mast cells and eosinophils

21
Q

how does acute inflammation evolve to chronic inflammation?

A

myofibre breakdown, fewer neutrophils, other cells involved

22
Q

list causes of chronic inflammation

A

persistent infection, prolonged exposure to toxins, autoimmunity, foreign body

23
Q

what is chronic inflammation characterised by?

A

mononuclear cell infiltrate (macrophage, lymphocyte, plasma cells)
tissue destruction induces by persistent inflammatory agent of the inflammatory cells
attempts at healing by replacement of damaged tissue with connective tissue FIBROSIS

24
Q

what is the role of macrophages and what does the role depend on?

A

phagocytosis, amplification of inflammation, wound repair and fibrosis, anti-inflammatory
depends on the activation pathways

25
Q

how does the action of macrophages differ in acute and chronic?

A

acute - destroy agent and stimulate others to do the same

chronic - persist and destroy tissue

26
Q

list the cells involved in chronic inflammation

A

T cells, plasma cells, eisonphils, mast cells, neutrophils (if coexisting with acute)

27
Q

what is prominent in chronic inflammation?

A

angiogenesis

28
Q

what is chronic inflammation lacking?

A

exudate, less necrosis

29
Q

list the histological feature of chronic inflammation

A

abundant macrophages, lymphocytes and plasma cells

many fibroblasts producing granulomatous tissue

30
Q

list histological features of granulomatous inflammation

A

macrophages in middle and lymphocytes on outside

fused macrophages seen at later stage

31
Q

list causes of granulomatous inflammation

A

infection, foreign material, reaction to tumours, immune disease

32
Q

list the differences between acute and chronic

A
acute/chronic
neutrophils/monocytes
histamine/cytokine
necrosis/scar tissue
few days/weeks, year, months
33
Q

what is a good outcome of inflammation?

A

removal of agent, cessation of inflammation, healing of tissue

34
Q

what is a local bad outcome of inflammation?

A

excess local tissue and scarring, secondary effects on nearby tissue

35
Q

what is a systemic bad outcome of inflammation?

A

systemic inflammatory reaction, secondary multi organ failure

36
Q

define resolution wound healing

A

regeneration of normal functional parenchymal cells

37
Q

define repair wound healing

A

connective and scar tissue formation

38
Q

how does resolute occur?

A

tissue cells are capable of regeneration and little structural damage done as cells need framework e.g. basement membrane to build on

39
Q

when and how does repair occur?

A

tissue loss is too great and cells can’t regenerate
tissue replaced with fibrous scar tissue
fibroblast produce collagen
collagen is a string scar ye
remodelling - reorganisation of collagen fibres for maximal tensile strength
angiogenesis

40
Q

what hinders repair?

A

poor nutrition, vitD deficiency, mineral deficiency, suppressed inflammation, poor blood supply, persistent foreign body, movement

41
Q

what is keloid formation?

A

XS collagen deposition

42
Q

what are contractures?

A

fibrous scar tissue contacts as it matures and can limit joint mobility

43
Q

how can organ function be impaired?

A

fibrous scars in organs limits function