week 2: chronic inflammation Flashcards
what is chronic inflammation
it is when acute inflammation does not get rid of ofending agen and inflammation becomes prolonged, and collateral damge will occur
difference between acute and chronic inflammation
cell profile
- accute inflammation cell profile is mainly nuetrofils, with later attention from macrophages, chronic inflamm is more macropahes, T/B cells, it is more hypercellular
destruction and repair
- chronic inflammation is a process of destuction and repair
process of destruction in chronic inflammation
acute vascular and cellular process takes place
macrophages proliferate
phagocytose
- release growth factors (encourage repair process)
- lysosomal enzyme release (degrade cell material, has some specificity)
-causes respiritory bursts (non-specific, free radicals)
- release cytokines, MMP’s (dissolve cell material and are non-specific and damaging)
release of cytokines:
- activate surrounding cells
- activate B cells
- activate T cells
- activate endothelial cells (more adhesion)
- cause more cyokine release
- activate nuetrophils
- attract fibroplasts
what are the 2 types of healing that might take place after destruction
- regenration: of parenchymal cells of same type
- replacement: by connective tissue (scar) that si not functional and not as good
most of the time both take place
define labile cell
proliferate throughout life, cells are continuallly destroyed
define stable cells
low normal level of replication of tissue
- parenchymal cells (liver, kidney, pacreas)
define permenant cells
cannot be replaced
- nerve cells - CNS nuerons replaced with scar
- cardiac muscles: connective tissue scar
what are the 3 main phases of tissue healing
- inflammation (chronic)
- prolifferative (producing ganulation tissue
- remodelling
descibe the proliferative phase
granulation tissue is formed
fibroplasia (fibroblasts laying down collagenous tissue)
- fibroblast drawn to wound
- macrophages release cytokines
- fibroblasts turn into myofibroblasts that proliferate into wound and “pull” it together
- produce fibronectin, collagen and ground substance
- type 3 collagen first appears 48-72 hours post injury
angiogenesis (development of new blood supply to area)
- growth factors and local cytokine release
- endothelial cell sprouting
- growth of new blood vessels into area
**granulation process
**- early stage=type 3 collagen
- late=type 1
- myfibroblast contract the granulation tissue and wound becomes smaller
- increase of collagen
- decrease of active fibroblasts and new vessels
- decrease pink colour
- more scar tissue
describe the remodelling stage
- achive a balance between tissue synthesis and degradation
- collagen conversion type 3 to type 1, by MMP’s and acc to stress
- wound contracts (myofibroblasts)
- scar formation
- driven by weight bearing
what does healing by primary intention mean
when there is a defect int he skins/tissue and it is surgically dealt with
- there is minimal loss of tissue, it is aeseptic
- we see limited number of granulation tissue, less epithelial and connective tissues killed, less scaring
healing by secondary intention?
- lareg tissue defect that must be filled with granulation tissue
- more fibrin, necrotic debris, exudate
- more intense inflammation process
- no regeneration process, it reults in conversion to a scar
what are some general factors that affect healing
- age
- cortiosterioids (anti-inflamm effect)
- nutirtion (zinc, vit c)
- blood dearrangments (defect in nuetros )
- chronic conditions (decrease in nuetos)
local factors that affect healing
- blood supply
- nerve supply
- type of tissue
- infection
- foreighn bodies
name 3 types of muscle injury
contusions (bruise)
strains or tears
lascerations