acute and chronic inflammation Flashcards
Rapid in onset (minutes)
Short duration (hours or a few days)
Exudation of fluid and plasma proteins (edema)
Emigration of leukocytes (neutrophils)
acute inflammation
May follow acute inflammation May be insidious in onset Longer duration Presence of lymphocytes and macrophages Proliferation of blood vessels and fibrosis Tissue destruction
chronic inflammation
3 major components of acute inflammation
Alterations in vascular caliber
Structural changes in the microvasculature
Emigration of the leukocytes
what are causes of acute inflammation?
infections
tissue necrosis
foreign bodies
immune reactions
what is exudate?
Inflammatory extravascular fluid
High protein concentration
Specific gravity > 1.020
Usually due to permeability
what is transudate?
Fluid with low protein concentration (albumin)
Specific gravity < 1.012
Permeability usually not increased (due to a pressure response)
what is the earliest manifestation of acute inflammation?
vasodilation
what is the hallmark of acute inflammation?
increased vascular permeability
what is the most common mechanism for vascular leakage?
contraction of endothelial cells
what is called the immediate transient response?
contraction of endothelial cells
contraction of endothelial cells are mediated by…
histamine
bradykinin
leukotriene
neuropeptide substance P
what are the different mechanisms of increased vascular permeability?
contraction of endothelial cells (minutes)
endothelial injury (hours to days)
leukocyte mediated vascular injury (late stages of inflammation. hours)
transcytosis (occurs in venules and induced by VEGF)
what is lymphangitis?
lymphatics secondarily inflammed
what is lymphadenitis?
draining lymph nodes may be inflamed
what are the stages of recruitment of leukocytes?
extravasation
margination
rolling
adhesion
what kind of cells predominate during the first 6-24 hours of acute inflammation?
neutrophils
except if infected with peudomonas bacteria. In which case will be neutrophils for days
except if infected with viral infections. in which case lymphocytes would be first to arrive
what kind of cells predominate during hours 24-48 of acute inflammation?
monocytes
how is microbial killing done??
reactive oxygen species reactive nitrogen species can also occur from other stuff in granules - elastase - defensins - cathelicidins - lysozyme -lactoferrin - major basic protein - bacteriacidal/permeability protein
what are some functional responses of activated leukocytes?
stimulate proliferation of endothelial cells and fibroblasts
stimulate synthesis of collagen
stimulate enzymes that remodel connective tissues
drive the process of repair after tissue injury
what happens in chediak higashi syndrome?
defective fusion of phagosomes and lysosomes causing susceptibility to infections
Abnormalities in melanocytes (leading to albinism)
Cells of the nervous system (associated with nerve defects)
Platelets (causing bleeding disorders)
Leukocyte abnormalities
Neutropenia (decreased numbers of neutrophils)
Defective degranulation
Delayed microbial killing
what happens with chronic granulomatous disease?
Defects in bacterial killing
Render patients susceptible to recurrent bacterial infection
Inherited defects in the genes encoding components of phagocyte oxidase
Initial neutrophil defense is inadequate
Collections of activated macrophages that wall off the microbes
Aggregates called granulomas
what are 2 major vasoactive amines?
histamine and serotonin
among the first mediators to be released during inflammation
where can you find serotonin?
present in platelets
- stimulated when platelets aggregate
present in certain neuroendocrine cells in the GI tract
what are the arachodonic acid metabolites?
prostaglandins
leukotrienes
lipoxins
derived from linoleic acid
