T3 Inflammation Flashcards
Physical characteristics of acute inflammation
- rubr
- calor
- tumor
- dolor
Exudate
extravascular fluid w/ high prtein concentration + cellular debris
Oedema
Exudate or transudate
Pus
inflammatory exudate
neutrophils, dead cell debris, microbes
Changes in vessel calibre in acute inf.
- initial vasoconstriction
- then vasodilation (within 15 mins)
- x10 blood flow
- heat & redness
Why does fluid exudate form
+++ permeability –> escape of protein rich fluid
Causes of fluid exudate
- chemical mediators
- direct vascular injury
- endothelial injury
effects of fluid exudate
- dilution of toxins
- entry of antibodies
- transport of drugs
- fibrin formation
- delivery on nutrient & oxygen
- stimulation of immune system
- high turnover
how is cellular exudate formed
- fluid loss into tissues
- increased vessel calibre
- stasis of blood
- neutrophils stick to vascular endothelium (periphery) - pavementing —> leave cells
what is neutrophils movement dependent on
hydrostatic pressure
what chemical promotes rolling & adhesion of neutrophils
selectin
what chemical promotes adhesion and transmigration of neutrophils
integrin
what is chemotaxis and what substances are involved
neutrophils polymorphs attraction to chemical substances (usually in injured areas)
- complements & cytokines
summarise chemical mediators of acute inflammation
- vasodilation
- migration of neutrophils
- chemotaxis
- +++ vascular permeabiltiy
what are the cell derived mediators of AI
- hist
- prost
- lysosomal components
- leukotrines
- cytokines
what are the plasma derived mediators of AI
- complement system
- kinin system
- coagulation system
- fibrinolytic system
systemic effects of inflammation
- pyrexia
- lymph node enlargement
- nausea, anorexia
- leukocytosis
what is suppuration
xs exudate –> discharge of pus –> repair –> fibrosis
what are the adaptive immune cells found in chronic inflammation
- macrophages
- lymphocyes
- plasma cells
what process happen in CI
- angiogenesis
- fibrosis
- concmitant tissue destruction & repair
what features can be seen in CI
- amyloidosis (serum amyloid A)
- cachexia (cytokines)
- anaemia
causes of CI
- acute background
- infection/exposure
- autoimmunity
- unknown
key components of CI in connective tissue cells
- mast cells
- fibroblast
- macrophages
key components of CI in vessels
- neutrophils
- lymphocytes
- monocytes
- eosinophils
- basophils
- platelets
- clotting factors
key components of CI in connective tissue matrix
- elastic fibres
- collagen fibres
- proteoglycans
ovarall mechanism of CI
injury –> components attracted by mediators –> adhesion
summary of granulation tissue in CI
- angiogenesis
- fibrosis
granuloma?
collection of activated epithelioid macrophages
characteristics of granuloma
- pink cytoplasm
- indistinct cell membranes
- oval nucleus
- surrounded by mononuclear leucocytes
types of granuloma
- caseous (necrotic centre)
- noncaseous
components of noncaseating granuloma
- fibroblasts
- Langhans-type giant cells
- lymphocytes
- plasma cells
what is a Langhans-type giant cell? (same reason why granulomatous inflammation takes place)
macrophages can’t digest something –> they fuse together
categories of causes of granulomatous inflamamtion
- infection
- inorganic metals
- foreign bodies
- unknown
