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42 Cards in this Set

  • Front
  • Back
inflammation is characterized by what (what is in it, where does it go first, second)
interstital accumulation of fluid
accumulation of leukocytes
- first around injury
then within injury
characteristics of acute inflammation
short duration
increases vascular permeability
neutrophil infiltration
characteristics of chronic inflammation
long duration
mononuclear cell infiltration (monocyte, macrophage, lymphocyte)
associated with tissue REPAIR (fibrosis)
what are the cells involved in acute inflammation? chronic?
acute- neutrophil infiltration
chronic- monocyte, macrophage, lymphocyte
what are the cardinal signs of inflammation
rubor- redness (erythema)
tumor- swelling (edema)
calor- heat (pyrexia)
dolor- pain (hyperalgesia)
functio laesa- tissue injury/dysfunction
what does ITIS mean
inflammation!
what are the UNDERLYING settings of ACUTE inflammation
tissue necrosis (trauma)
bacterial infection
immune (type 1 2 and 3 hypersensititvites)
acute inflammation- hemodynamic alterations?
blood flow/pressure increase = erythema
acute inflammation- effects on venules?
increase in vascular permeability
(leaky postcapillary venules)
= edema
what causes erythema?
vasodilation of PREcapillary arterioles
swelling= edema or accumulation of water in tissues
acute inflammation- what cells infiltrate? where do they emigrate through?
neutrophil infiltration (PMN)
emigrate through POSTcapillary venules
*pmn= polymorphonuclear leukocyte
what are the underlying settings of chronic inflammation
persistent tissue insult or injury
repeated bouts of acute inflammation
infection by intracellular parasites
immune- type 4 hypersensitivity, autoimmunity
foreign bodies
what cells are in the interstitial fluid of chronic inflammation
lymphocytes, monocytes/macrophages and possible plasma cells
maybe diffuse or focal with perivascular cuffing (around the venule)
*eosinophils= parasitic infection
what is a granuloma?
what is granulomatous?
granuloma- filled with mononucleated giant cells, epitheliod histeocytes and lymphocytes
granulomatous- adj. describing a granuloma
chronic inflammation- describe granulomatous
spherical mononuclear cells, central necrosis
epitheliod histeocytes (macrophages) in center
multinucleated ginat cells
outer rim contains lymphocytes, plasma cells and fibrosis
what are the morphologic patterns of inflammation
serous
fibrinous
suppurative
hemorrhagic
ulcerative
mixed
what are the steps (pathophysiology) of inflammation
injury
mediator release
target cell receptors
signal transduction
target cell activation
target cell response
pathophys respons
cardinal signs of inflammation
what types of injuries are leukocyte mediated
apoptosis
necrosis
inflammatory tissue injury/dysfunction includes
obstruction
leukocyte injury
systemic
fibrosis
hemodynamic response involves
erythema and increases vascular permeability
define 4 modes of target cell activation
autocrine- same target cell
paracrine- different target cells in immediate proximity
endocrine- different target cells at distant locations
juxtacrine- two target cells after their adherence to each other
what are the sources of inflammatory mediators
cell derived- 7
plasma derived- 4
cell- PMN, lymphocytes, monocyte/macrophage, platelets, endothelial cells, mast cells, parenchymal cells
plasma- complement, kallikrein-kinin, coagulation, fibrinolytic
describe bradykinin formation
activators-> prekallikrein-->kallikrein-->kininogen-->bradykinin
describe characteristics of bradykinin
vasodilation
increased vascular permeability
pain
endothelial cell stimulation
c3b, c3bi--->opsonins
c3b, c3bi--> opsonins
what are cyclooxygenase AA (arachidonic acid) products
PGE2, PGI2, TXA2
what are effects of PGE2
vasodilation, hyperalgesia (pain), fever, potentiates edema
how do NSAIDS work (in regards to AA, COX1,2)
nsaids block COX1,2 which blocks PGE2 and all the other pg's
how do steroids work?
they block PLA2 and AA and cut off allll the stuff
what are the cell classifications in regards to proliferative capacity
permanent cells- dont divide
stable cells- not continuously dividing but can be stimulated to do so
labile cells- continuously cycling
stem cells- pluripotent precurosrs
give examples of different types of proliferating cells
labile- epithelial
stable- hepatocytes
permanent- neuron, cardiac
what is the difference between cell necrosis and apoptosis
necrosis- breakdown of plasma membrane organelles and nucleus, leakage of contents
apoptosis- cell is fragmented into apoptotic bodies and phagocytosized
describe the steps of apoptosis
cell shrinkage
chromatin condensation
cytoplasmic blebbing
apoptotic body formation
phagocytosis of bodies
= cell death with no inflammation
in what instances would be see cell apoptosis (or programmed cell death)
morphogenesis/metamorphosis
normal cell aging
hormone growth factor stimulation or withdrawal
mitochondrial cytochrom c release
failed dna repair
tumor regression
cytotoxic ddrugs, ionizing radiation
what are some leukocyte responses to inflammation
margination and pavementing on vascular endothelium
transendothelial migration (diapedesis, emigration)
chemotaxis through interstitium
phagocytosis, intracellular killing and digestion
define tissue regeneration
replacement of lost tissue by tissue of same type
define tissue REPAIR
replacement of lost tissue bye FIBROUS CONNECTIVE TISSUE SCAR
examples of growth cells
labile- epithelial and hematopoietic cells
stable cells- liver and connective tissue
permanent- neurons cardiac skeletal
what are the requisite factors of tissue regeneration
must be comprised of labile and or stable cells
must be preservation of at least some portion of original tissue
must be preservation of scaffolding of original tissue (extracell matrix)
what are the requisite factors of tissue repair
always in necrotic tissue containing permanent cells
when there has been extensive tissue necrosis
tissue scaffolding destroyed
chronic inflammation
what is granulation tissue
highly vascularized loose connective tissue formed during tissue repair that produces typ1 collagen scar
what is the sequence of scar formation by granulation tissue
type 1 collagen biosynthesis by fibroblasts
extracell secretion of collagen and formation of collagen fibrils
resoprtion of granulation tissue by apoptosis
covalent cross linking of type 1 collagen froming the mature scar