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Flashcards in acute inflammation Deck (50)
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what is acute inflammation?

it is a common , non-specific response to injury
protective response to injury - essential to survival
it aims to rid the body of the initial cause of injury and the consequences of the injury


what is it under?

it is under complex biochemical control


what is an example of acute inflammation?



what is the duration of acute inflammation?

minutes, hours or days


what is the characteristic cell and describe it?

neutrophil polymorph - it has a multilobed nucleus - around 3


what is the basis of AI?

it delivers white cells or plasma proteins to the site of infection or injury


what are the five characteristics of AI?

dolor, calor, rubor, tumor and loss of function


what are the three major causes of AI?

infections, physical and chemical agents


what is a hypersensitivity reaction?

when the normally protective immune system damages the individual's own tissues. They tend to be persistent and difficult to cure.


why does tissue necrosis occur?

when the extent of damage is too severe for cells to regenerate so they repair using fibrosis


what is meningitis?

it is inflammation of the meningeal lining of the brain - it is pus collecting made of neutrophil polymorphs and dead or dying tissue


what happens in acute cholecystitis?

fibrinogen leaks out of the blood vessels and makes contact with the tissues meaning that fibrin is formed in the fibrinous reaction. this is because gall stones block the exit from the gall bladder and therefore there is fat collection. The condition shows cardinal signs of inflammation.


why would the peritoneal cavity appear red and inflamed?

peritonitis. If the peritoneal cavity is filled with exudate (fluid with a lot of protein) then there is serious inflammation. This is from thin fluid from mesothelial or plasma cell secretions. Accumulation can result in effusion.


what are the three major components of AI?

cellular exudate formation, increased vascular permeability and fluid exudate formation and changes in vessel calibre


how are vessels adapted in AI?

they undergo changes to maximise the movement of plasma proteins and cells to the site of injury


what is exudate?

it is extravascular fluid with a high protein concentration containing cellular debris. it implies inflammation.


what is transudate?

it is a fluid with low protein and little or no cellular component


what is oedema?

when there is excess fluid in the interstital fluid or serous cavities - it can be exudate or transudate and can result from heart failure - pulmonary or peripheral


what is pus?

it is inflammatory exudate that is rich in neutrophils, dead cell debris and microbes


what are the changes in vessel calibre?

there is initial transient vasoconstriction. Then there is vasodilation that is from around 15 minutes to several hours, this is an early change. It increases blood flow by up to ten times, and produces redness and heat from vessels and capillaries close to the surface of the skin. It is mediated by histamine and NO on vascular smooth muscle.


what do skin lesions show?

they show the cardinal signs of inflammation - tumor, dolor, rubor, calor


how is fluid exudate formed?

the increased permeability of microvasculature results in the escape of fluid rich fluid into the tissue. It is caused by chemical mediators (histamine, leukotrienes and NO). injury to vasculature from trauma and injury to endothelium from bacteria and toxins.


what is an example of the difference in susceptibility of different body parts to chemical mediators?

the CNS is insensitive to histamine, but skin, conjunctiva and bronchial mucosa are sensitive to this


why is exudation increased in AI and what is the result?

the hydrostatic pressure of the venous end of the capillaries is higher and therefore fluid is not absorbed. Therefore once plasma proteins escape into extravascular space increasing the colloid osmotic pressure so more fluid follows


what are the effects of fluid exudate?

transport of drugs
AB entry
dilution of toxins
fibrin formation - fibrinogen escape out and fibrin forms network for granulation tissue
delivery of oxygen and nutrients
stimulation of the immune response
high turnover


why does more fluid escape during AI?

there is stasis of blood - the blood is thicker and slower as fluid escapes meaning more time for more fluid to escape - permeability and calibre of vessels


what is the difference between action of neutrophils normally and in AI?

normally neutrophils travel along centre of the vessels in axial stream, in AI the neutrophils will go along edges rolling and bouncing - margination, stick to endothelium - pavementing, and migrate into tissue through gaps - chemically mediated or due to direct trauma


what is diapedesis?

how RBC move through the vessel walls - passive due to hydrostatic pressure - unlikely to happen unless penetrative direct trauma


what chemical mediators are used for rolling and sticking of neutrophils?

selectins for rolling
integrins for sticking


what is chemotaxis for?

to get polymorphs into the right place in tissues / area of injury