topic 4: inflamation Flashcards
fyi: when does inflammation happen and what is the purpose
purpose: it is a protective response intended to eliminate the initial cause of cell injury and then remove necrotic (dead) cells and tissue resulting from the original insult
how it protects: dilute/destroy or neutralise harmful agents by extending the defence of the blood out into the tissues (blood cells, plasma proteins will come out from teh blood and then go cell injury area)
fyi
definition of inflmation
denoted by -itis
definition: a complex progression of blood vascular and tissue change that deveops in responseto tissue injury
inflammatory reaction and subsequent repair process can cause harm if
- uncontrolled: severe/prolonged inflammatory rn (eg harmful agent resists irradication)
- inappropriate: inflammatory cells and molecules (antibodies, immune cells) target self- antigens
inflammatory and repair process can be excerbated by further tissue damage or introduction of infection (eg self trauma)
difference between acute and chronic inflammation
period of onset:
acutre: rapid, chronic: gradual (persistant inflmmatory response for longer than 10-14 days, up to a yr or more)
cells invloved/visible microscopically:
acute: predominantly neutrophils (in fluid and plasma protein exudate- fluid from blood vessel high conc in plasma protein) chronic inflammmation (predominantly mononucleur cells: plasma cells, lymphocytes and macrophages: they come later after initial (acute) respose)
characteristic appearance:
acute: usually exudative ( protein rich fluid coming from blood to surrounfing damaging tissues)
chronic: usually not exudative (usally no exudative phase) ( invloves tissue destruction and repair ( vascular proliferation and fibrosis)
difference between acute and chronic inflmaation: period of onset
acute: rapid onset
chronic: gradual onset
difference between acute and chronic inflmaation: duration of inflammation
acute: shorter duration (mins-few days)
chronic: longer durations (days-yrs)
difference between acute and chronic inflmaation: cells invloved/visible microscopically
acute: predominantly neutrophils (can be found in fluid and plasma proteins exudate)
chronic: mononuclear cells: plasma cells, lymphocytes, macrphages
difference between acute and chronic inflmaation: characteristic appearance
acute: usually exudative(escape of protein rich fluid from the blood to surrounding damage tissues)
chronic: usually not exudative. involves tissue destruction and repair (vasular proliferation and fibrosis)
aim of acute inflmmation
rapidly contain, dilute and remove harmful stimulus bu delivering immune cells and plasma proteins to site of injury + prepare tissur for repair
fyi
causes of acute inflmmation
bacterial infection
trauma (cuts)
foreign bodies
immune reaction (hypersensitivty, eg autoimmune disease-> can cause chronic inflammation)
tissue necrosis (death due to ischemia/physical/chemical injury)
what happens after acute inflamation
- harmful stimulus removed-> anti-inflmmatory mechanism kicks its (to stop inflammation, no need anymore cos remove alr), acute inflamation subsides and tissue returns to its normal state of function
- harmful stimulus persists-> acute inflmmation progresses to chronic inflammation
what are the five cardinal (most noticable signs) signs of acute inflammation
1.redness
2.heat
3.swelling
these three are due to vascular changes and cellular recruitment
4.pain
5.loss of function
these two is due to mediators of inflammation and leukocyte mediated damage
what are the three phases acute inflamation (local effect)
- vascular phase
- exudative phase
- cellular phase
describe the three phases of acute inflmmation
- vascular phase (changes in blood vessel diameter) : arteriole vasodilation-> locally increased blood flow-> engorgement of downstream capillary bed ( sweeling of capillaries after major arterioles) also known as hyperaemia.
-takes few minutes to days (causes cardinal signs: redness and heat) - exudative phase- escape og fluid from blood surrounding extravascular tissue
direct damage of endothelial cells lining the capillaries or contraction of the endothelial cells of the capillary lining-> causing increased vascular permeability
gaps form in capillary wall between the endothelial cells-> allow escape of protein rich fluid (containing RBC,platelets, plasma protein, water, electrolyte) into the surrounding tissue. - cellular phase- recruitment of leukocyes-primarily neutrophils, to site of injury
4
leukocytes are activated to 1.ingest and kill bacterial at the site of the injury,2. remove dead/dying cells and foreign substances 3. direct other cells of the imflmmatory preocess to the site
they may also injure normal host tissues surrounding the the site of teh injury (releaase enzymes to destroy, nomrla cells near injury also get digested- thats why chronic inflmation, persistant this process cause fibrosis aka scaring)
leukocyts recruited and activated at sites of injry perform these functions:
1. phagocytosis
2. produce sybstance that destroy phagocytosed microbes and dead tissues (lysosomal enzymes, proteases)
3. produce more mediators to amplify the inflmatory reactions (eg cytokines)
fluid exudate may become cellular exudate if more leukocytes migrate to the site of injury
describe the vascular phase of acute inflammation
vascular phase (changes in blood vessel diameter) : arteriole vasodilation-> locally increased blood flow-> engorgement of downstream capillary bed ( sweeling of capillaries after major arterioles) also known as hyperaemia.
-takes few minutes to days (causes cardinal signs: redness and heat)
describe the exudative phase of acute inflammation
exudative phase- escape og fluid from blood surrounding extravascular tissue
-direct damage of endothelial cells lining the capillaries
or
contraction of the endothelial cells of the capillary lining-> causing increased vascular permeability
gaps form in capillary wall between the endothelial cells-> allow escape of protein rich fluid (containing RBC,platelets, plasma protein, water, electrolyte) into the surrounding tissue.
current cardial signs: redness and heat (from vascuar phase), swelling (from exudative phase)
describe the cellular phase of acute inflammation
leukocytes are activated to
1.ingest and kill bacterial at the site of the injury,
2. remove dead/dying cells and foreign substances
3. direct other cells of the imflmmatory preocess to the site
they may also injure normal host tissues surrounding the the site of teh injury (releaase enzymes to destroy, nomrla cells near injury also get digested- thats why chronic inflmation, persistant this process cause fibrosis aka scaring)
leukocyts recruited and activated at sites of injry perform these functions:
1. phagocytosis
2. produce sybstance that destroy phagocytosed microbes and dead tissues (lysosomal enzymes, proteases)
3. produce more mediators to amplify the inflmatory reactions (eg cytokines)
fluid exudate may become cellular exudate if more leukocytes migrate to the site of injury
current cardinal signs: redness, heat (from vascular phase), swelling (from exudative phase) , loss of function and pain (sustances used to destroy phagocytosed microbes and dead tissue also destroying normal cell)
why do endothelial cells contract
inflammatory/immune cell eg mast cells, lukocytes are stimulatedf, they release chemical mediators (histamine) that are stored in intracytoplasmic granules.
these chemical mediators bind to receptors on the endothelial surface and cause them to contract, resulting in gaps between endothelial cells
gaps are so large that proteins (albumin, globulin, fibrinogen) can now escape into the tissues.
what are the differrent types of acute inflmmation
1.serous inflmmation
2. fibrinous inflmmation
3.suppurative inflammation
serous inflmmation
serous effusion in serious cavity
outpouring of watery, protein-poor fluid from serum or secretions of mesothelial cells (lining serous cavity-fluid filled space-eg pleural cavity)
eg, burns, blisters
fibrinous inflammation
more severe injury (more than serous) resulting in greater vascular permeability-> large molecules eg fibrinogen able to pass endothelial lining of capillaries.
extravascular fibrin accumulates, appearas as eosinophillic (opink) meshwork of threats or amirphous (lack definitive shape) coagulum (when fibrinogen becomes fibrin- solidifies)
suppurative inflmation
presence of pus/large amounts of purulent exudate (yellow/green fluid produced by body in response to infection/inflammation-think pimple) –>consists of neutrophils, necrotic cell,edema fluid (fruid due to increase vascular permeability)
eg ulcers( tissue necrosis and inflmation occuring at/near the surface
absess (eg bac inside tissue-pus inside)
review of neutrophil in inflmmation
-Characteristic of acute inflammation.
-Segmented nuclei, intracytoplasmic granules containing antimicrobial factors and enzymes (eg. proteases).
-Short lifespan and dies in the process of attacking bacteria.
-First defence against invading microbes and involved in initial removal of dead tissues.
-Motile (moving to site of injury) – attracted to site of injury by chemical mediators (eg cytokines)
what are the steps for recruitment of leukocytes- mainly neutrophils
- margination, adhesion, rolling
- firm adhesion to vessel wall
- transmigration between endothelial cells
- migration in extravascular tissue to site of damage