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
define and name 2 types of haemotomas (bruises/contrusions)
haemontoma: blood into tissues following an injury
intra muscular
- the pressure within the intact muscle as bleeding continues, limits the amoujnt of bleeding and haemotoma is smaller
intermuscular:
- fascia is torn, blood free access to surrounding spaces, bleeding is more excessive
intramuscualr is more painful
define strains and name 3 types
extensive tensile stress placed through a muscles, leading to rupture MTJ
first degree (mild)
- fewfibres affected, minor discomfort, minimal stength and ROM loss
second degree (moderate)
- greater damage, loss of contraction ability, increased welling/ inflamm
third degree (severe)
- tear over whole muscle, fucntion lost, greater swelling, ROM impacted
name the sections of a muscle injury
Central Zone (CZ)
Regereation zone (RZ)
Survival zone (SZ)
name the phases of muscle injury
destruction
repair + remodelling (happen at same time)
describe the destruction phase
take place in the CZ
injury occurs
haemotoma from torn blood vessels
inflammation occurs
- eg. macrophages and fibroblasts living in tissue release mediators
- attract nuetrophils and monos, begining phagocytosis
- necrosis occurs
describe the repair phase
- fibroblasts, fibronectin, proteoglycan etc. move in
- fibroblasts turn into myofibroblasts and form granulation tissue/early scaring
- provides very weak protection, it should be protected
- it also provides scaffolding for new blood vessels/growth factor release (angeogenesis), and myofibres
- some fibroblast develop contractile protiens and contract the wound
describe the remodelling phase
satelite cells
- live below basement membrane
- await activation following inflammation becuase macrophages release growth factors (satelite cells)
- proliferate into myoblasts which fuse together and lay down new muscle
- Grow in toward the CZ (contraction of the injury)
- pierce into and attach onto the newly formed CT(scar) of the CZ
what should a muscle injury look like at the end of this process
- myoblasts regenerating and scar contracting to a point where we have only a small septum or portion of connective scar tissue intervening
define myositis ossificans
aka: heterotrophic bone formation
- post trauma calcification occuring in muscles
- assciated with contusion injury, intramuscular haemotomas, reoccurring injury, bad management, bad/too early physiotherapy,
what are myotis ossificans characterised by/pathphys?
- local swelling
- local tenderness
- limited ROM/stretch of muscle
- pathophys: unknown, could be activation of osteoblasts in muscle, or lack of o2
