Inflammation
non-specifc response to injury and occurs in the same manner, regardless of the nature of the injury
inflammation
increased blood flow that fills capillary beds in injured tissue and is responsible for2 local signs of inflammation- erythema and heat
hyperemia
fluid that contains cells and a higher concentration of protein molecules that flows into injured tissue as the result of inflammation
exudate
biochemically mediates inflammation by causing increased dilation and increased permeability of the blood vessels at the site of injury. Components of this system also induce pain
cells and associated tissues that have undergone necrosis are replaced with live cells and new tissue components
repair
5 Localized signs of inflammation
redness
heat
swelling
pain
loss of the usual level of tissue function
plasma fluid with a low protein content without any cells leaving entering the tissue outside of the blood vessel
transudate
directed movement of WBCs towards the site of injury
chemotaxis
primarily function is stopping bleeding at the site of injury
causes local vascular dilation and important in tissue repair because it forms the future frame work for the repair process
clotting mechanism
Most favorable resolution of acute inflammation when there is slight tissue damage, the inflamed area may return completely to its usual structure and usual level of function
regeneration
4 systemic signs of inflammation
fever
leukocytosis
lymphadenopathy
elevated C-reactive protein
movement of WBCs to the periphery in a blood vessel
margination
WBCs trying to remove foreign substances from the site by ingesting and digesting them
phagocytosis
series of plasma proteins that are activated in a cascading fashion, functions in the process of inflammation and immunity
complement system
if the source of the injury is removed, the repair process for regeneration and formation of scar tissue is how long
2 weeks
first microscopic event of the inflammatory response
brief vasoconstriction
the lining of the walls of injured blood vessels by WBCs
pavementing
first WBC to site of injury
neutrophil
complement proteins can attach to the surface of bacteria stimulating WBCs to phagocytize them
opsonization
healing of an injury in which little loss of tissue takes place
-clean edges of the incision
-small clot forms
-very little granulation tissue
healing by primary intention
what two local clinical signs of inflammation is hyperemia responsible for?
erythema (redness)
heat
process of WBCs escaping the blood vessel
emigration
2nd WBC to site of injury
monocyte emigrate from blood vessels into the injured tissue to become a macrophage
programmed cell death
apoptsis
healing after significant tissue loss
edges of injury cannot be joined during healing
large clot forms resulting in increased formation of granulation tissue
healing by second intention