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)
difference between acute and chronic inflammation
period of onset:
acutre: rapid, chronic: gradual
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 ( invloves tissue destruction and repair ( vascular proliferation and fibrosis)
what happens after acute inflamation
- harmful stimulus removed-> anti-inflmmatory mechanism kicks its (to stop inflammation), 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
- vascular phase
- exudative phase
- cellular phase
describe the three phases of acute inflmmation
- vascular phase: 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
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
leukocytes are activated to 1.ingest and kill bacterial at the site of the injury,2. remove dead/dying cells, 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 their functions - phagocytosis
- produce sybstance that destroy phagocytosed microbes and dead tissues (lysosomal enzymes, proteases)
- 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
what are the differrent types of acute inflmmation
1, serous inflmmation
2. fibrinous inflmmation
3.suppurative inflammation
serous inflmmation
outpouring of watery, protein-poor fluid from serum or secretions of mesothelial cells (lining serous cavity-fluid filled space)
eg, burns, blisters
fibrinous inflammation
more severe injury (more than serous) resulting in greater vascular permeability-> large molecules eg fibrinogen accumulates, appearas eosinophillic (opink) meshwork of threats or amirphous coagulum (when fibrinogen becomes fibrin)
suppurative inflmation
presence of pus, large amounts of purulent exudate (yellow/green fluid-think pimple) -consists of neutrophils, necrotic cell,edema fluid
eg ulcers( tissue necrosis and inflmation occuring at/near the surface
absess (eg bac inside tissue-pus inside)
role 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 – attracted to site of injury by chemical mediators (eg cytokines)
describe the process od leukocyte recruitment (neutrophil)
(1) Margination, adhesion, rolling
* Exudation of fluid into extravascular tissues causes RBCs to become more concentrated, blood viscosity increases, circulation slows down (stasis).
* Smaller RBCs move faster than larger leukocytes. Leukocytes are pushed towards the vessel wall due to laminar flow.
* Leukocytes tumble along the vessel wall, transiently sticking along the way.
(2) Firm adhesion to vessel wall
* Chemoattractant cytokines (chemokines) secreted by cells at site of injury activate the leukocytes that are rolling along the
vessel wall.
* Activated leukocytes adhere more firmly to vessel wall near site of injury
(3) Transmigration between endothelial cells
* Leukocytes stop and squeeze through intercellular junctions of endothelial cells.
(4) Migration in extravascular tissues to site of damage
* Leukocytes travel through extravascular tissues until they reach the site of damage.
* Leukocytes are attracted to site of injury by substances produced by bacteria, complement proteins and other
mediators produced in response to tissue damage and immunologic reactions.
systemic effect of acute inflmmation
- increased body temp
(Chemical mediator of inflammation circulating in blood and acting on temperature regulatory centres in brain)
2.Changes in blood
– increased production & release of neutrophils; anaemia
- Neutrophils are the predominant leukocytes activated in acute inflammation.
- Chemical mediators of inflammation can inhibit RBC production by bone
marrow.
3.Pain
- Chemical mediators of inflammation (cytokines) and contents of intracytoplasmic
granules of neutrophils stimulate nerves.
- Fluid accumulation results in pressure on tissue components and nerves.
4.Depression, malaise, anorexia, nausea
Effects of pain or chemical mediators on brain.
5.Muscle pain Chemical mediators breakdown muscles.
6.Weight loss - Effects of chemical mediators on appetite centres of brain.
- Muscle breakdown.
- Loss of appetite due to nausea, anorexia, pain.
i c pd wm ( i see pdiddy liking men and women)
harmful effects of acute inflmation
- excessive tissue damage:Normal tissues surrounding site of injury may be digested by enzymes released by activated
neutrophils (eg. proteases) - severe systemic effects: severe loss of appetite, pain and wight loss
- excessive loss of serum: causes Marked swelling, pain, irritation (self-trauma). May result in shock if fluid loss is severe.
- severe fibrin exudation: Formation of fibrous scar tissue at site of injury can damage or hinder normal
function of organ. - Suppurative exudate
* Suppurative exudate becomes walled off by fibrous tissue, forming an abscess. An
abscess that bursts internally can lead to septic peritonitis/pericarditis/septic shock. - Inflammation of vessel walls
* Cause excessive leakiness of blood vessels, resulting in excessive blood loss,
inappropriate clotting of blood and impair blood supply (ischaemia, infarction)
esssi
outcomes of acute inflmmation depends on
nature and intensity of injury
* Site and tissue affected
* Ability of host to mount a response
