T3 Inflammation Flashcards

1
Q

Physical characteristics of acute inflammation

A
  • rubr
  • calor
  • tumor
  • dolor
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2
Q

Exudate

A

extravascular fluid w/ high prtein concentration + cellular debris

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3
Q

Oedema

A

Exudate or transudate

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4
Q

Pus

A

inflammatory exudate

neutrophils, dead cell debris, microbes

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5
Q

Changes in vessel calibre in acute inf.

A
  • initial vasoconstriction
  • then vasodilation (within 15 mins)
  • x10 blood flow
  • heat & redness
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6
Q

Why does fluid exudate form

A

+++ permeability –> escape of protein rich fluid

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7
Q

Causes of fluid exudate

A
  • chemical mediators
  • direct vascular injury
  • endothelial injury
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8
Q

effects of fluid exudate

A
  • dilution of toxins
  • entry of antibodies
  • transport of drugs
  • fibrin formation
  • delivery on nutrient & oxygen
  • stimulation of immune system
  • high turnover
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9
Q

how is cellular exudate formed

A
  • fluid loss into tissues
  • increased vessel calibre
  • stasis of blood
  • neutrophils stick to vascular endothelium (periphery) - pavementing —> leave cells
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10
Q

what is neutrophils movement dependent on

A

hydrostatic pressure

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11
Q

what chemical promotes rolling & adhesion of neutrophils

A

selectin

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12
Q

what chemical promotes adhesion and transmigration of neutrophils

A

integrin

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13
Q

what is chemotaxis and what substances are involved

A

neutrophils polymorphs attraction to chemical substances (usually in injured areas)
- complements & cytokines

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14
Q

summarise chemical mediators of acute inflammation

A
  • vasodilation
  • migration of neutrophils
  • chemotaxis
  • +++ vascular permeabiltiy
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15
Q

what are the cell derived mediators of AI

A
  • hist
  • prost
  • lysosomal components
  • leukotrines
  • cytokines
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16
Q

what are the plasma derived mediators of AI

A
  • complement system
  • kinin system
  • coagulation system
  • fibrinolytic system
17
Q

systemic effects of inflammation

A
  • pyrexia
  • lymph node enlargement
  • nausea, anorexia
  • leukocytosis
18
Q

what is suppuration

A

xs exudate –> discharge of pus –> repair –> fibrosis

19
Q

what are the adaptive immune cells found in chronic inflammation

A
  • macrophages
  • lymphocyes
  • plasma cells
20
Q

what process happen in CI

A
  • angiogenesis
  • fibrosis
  • concmitant tissue destruction & repair
21
Q

what features can be seen in CI

A
  • amyloidosis (serum amyloid A)
  • cachexia (cytokines)
  • anaemia
22
Q

causes of CI

A
  • acute background
  • infection/exposure
  • autoimmunity
  • unknown
23
Q

key components of CI in connective tissue cells

A
  • mast cells
  • fibroblast
  • macrophages
24
Q

key components of CI in vessels

A
  • neutrophils
  • lymphocytes
  • monocytes
  • eosinophils
  • basophils
  • platelets
  • clotting factors
25
Q

key components of CI in connective tissue matrix

A
  • elastic fibres
  • collagen fibres
  • proteoglycans
26
Q

ovarall mechanism of CI

A

injury –> components attracted by mediators –> adhesion

27
Q

summary of granulation tissue in CI

A
  • angiogenesis

- fibrosis

28
Q

granuloma?

A

collection of activated epithelioid macrophages

29
Q

characteristics of granuloma

A
  • pink cytoplasm
  • indistinct cell membranes
  • oval nucleus
  • surrounded by mononuclear leucocytes
30
Q

types of granuloma

A
  • caseous (necrotic centre)

- noncaseous

31
Q

components of noncaseating granuloma

A
  • fibroblasts
  • Langhans-type giant cells
  • lymphocytes
  • plasma cells
32
Q

what is a Langhans-type giant cell? (same reason why granulomatous inflammation takes place)

A

macrophages can’t digest something –> they fuse together

33
Q

categories of causes of granulomatous inflamamtion

A
  • infection
  • inorganic metals
  • foreign bodies
  • unknown