GLOSSARY SECTION I PART C Flashcards
5-30 min after exposure-resolves in 30-60 min
vasodilation, vascular leakage, sm contraction
immediate response of type I hypersensitivity
type III hypersensitivity is this type of reaction
immune complex
for cell repair to happen you must have an increase in cell death and also an increase in cell proliferation
increased collagen deposition is required for scar formation and wound healing
increased
recognizes dead cell product, uric acid, extracellular ATP, crystals
activates caspase-1 (leads to recruitment of WBC)
inflammasome
immediate and early response to injury or infection
vascular and cellular components
characterized by exudate and emigration
acute inflammation
tissue destruction-repair and fibrosis with infiltration of mononuclear cells
chronic inflammation
important for WBC recruitment, fibroblast proliferation, chemotaxis, collagen synthesis and collagenase synthesis
cytokine
interleukin-1
invisible nucleus because dissolved into fine particles
karyolysis
extends beyond site of original wound doesn’t regress spontaneously
keloid
heterotrimeric and cross shaped structure that spans the basal lamina
most abundant glycoprotein in basement membrane
laminin
de novo synthesis of secondary mediators
2-8 hours after exposure can last for days
inflammation and tissue destruction
late phase hypersensitivity reaction
increase in the number of WBC
leukocytosis
reduction in the number of WBC
leukopenia
causes chemotaxis
leukotriene B4
type of pre-mortem thrombus
lines on vessel endothelium from blood actively flowing during clot formation
lines of Zahn
seen in brain and infection due to neutrophil release
cheesy
liquefactive necrosis
infection, mechanical problems, foreign bodies, aberrations of cell growth
local factors that influence repair
cell adhesion molecule found on lymphocytes
L-selectin
primary cell of chronic inflammation
produces products that control inflammation processes
produces products that control inflammatory processes
good for chronic inflammation because they are longer lived cells and they make GFs that cause repair process to begin through the classically activated pathway
macrophage
release histamine due to:
physical agent IgE reaction anaphylactoxins neuropeptide cytokine
mast cell
endogenous cause of glycogen accumulation
melanin
degrade collagen and other ECM components
dependent on zinc ions to work
produces by fibroblasts, macrophages, neutrophils, synovial cells, epithelial cells
metalloproteinases
reversible change that replaces one adult cell type with another cell type
loses function
replaces with cell better able to withstand stress
metaplasia
mitochondrial dysfunction is irreversible and causes profound disturbances in membrane function
mitochondrial enzymes help to protect against free radicals
mitochondrial
determines by the permeability of mitochondria (physiologic)
mitochondrial pathway of apoptosis
cytotoxic lymphocyte that is part of the innate immune system
viruses, tumors
natural killer cells
include the Fc portion of the IgG, C3b, and collectins
mark cell for recognition and destruction by phagocytosis
opsonin
destruction or disappearance of bone tissue
leads to hypercalcemia
osteolysis
effect on nearby cells
paracrine
WBCs attack foreign material of dead tissue
steps: recognition and attachment, engulfment, killing or degradation
phagocytosis
phospholipid derived mediator
acts to aggregate platelets, cause bronchoconstriction, vasodilate and increase vascular permeability
platelet activating factor
protein core that’s linked to polysaccharide
proteoglycan
excessive granulation
protrudes above the surface of the skin and blocks re-epithelialization
proudflesh
ghost nucleus (dense, shrunken, dark)
pyknosis
