Acute inflammation Flashcards
Give the signs of inflammation
redness pain loss of function heat swelling
Describe the changes in blood flow
transient vasoconstriction from the contraction of smooth muscls in arterioles
vasodilation from relaxation of arteriolar smooth muscle and distention of capillaries
increased blood flow = red and warm appearance
allows increased deliverity of molecules and cells
following increased blood flow there is gradual slowing of circulation = dilation of capillaries, altered vascular permeability as capillary endothelium becomes more permeable to plasma proteins = oedema
describe the formation of oedema
increased flow though arterioles causes an increase in hydrostatic pressure at the arterial end of the tissue microcirculation
with increased capillary permeability this causes an increase in fluid moving from within the blood vessels to the tissue spaces
fluid is rich in protein = loss of normal osmotic gradient which opposes the accumulation of tissue fluid.
Describe the main mechanism for increased vascular permeability
depends on the type of injury main method is endothelial contraction mainly in venules response to histamine, leukotrienes rapdi and short lived
Describe other mechanism of increased vascular permeability depending on the tissue injury
1 direct endothelial injury
if vascular damage occurs e.g. in burns and some bac infections there is some delay between injury and leakage of protein rich exudate to allow the development of the full process of cell death and detachment form vessel wall.
affects all of micro vessels, arterioles, capillaries and venules.
the exudate is leaked until the vessels either become occluded with thrombus or repaired
Describe other mechanism of increased vascular permeability depending on the tissue injury
when leucocyte mediated injury to vessels occurs when WBC release of cytotoxic agents causes endothelial damage - vasculitis
leakage of exudate occurs from the time of endothelial loss and is sustained thoughout the diesease as new endothelail cells become targets for leucocyte mediate damge
in neoangiogeneiss - exudate is lost
Give the properties of the vascular phase
formation of protein rich exudate
tissue oedema
increased blood viscosity coupled with reduced flow leading to stasis
NB the exudate contains immunoglobulins, complement components, coagulation factors and kinins which contributed to inflammatory response
Describe the margination and adhesion of the cellular phase of acute inflammation
the slowing of blood allows for WBC move from axial position to peripheral.
WBC roll on the endothelial surface - margination - and become more adherent to the surface - caused by selectins interacting with specific carb groups on neutrophils and macrophages
adhesion increased by interaction of integrins on leucocytes and immunoglobulin supergene family on endothelia surface
the activation of endothelial cells is controlled e.g. histamine
can be leucocyte adhesion deficiencies = recurrent bac infections with extensive tissue damage
Describe leucocyte migration
after attachment leucocytes pass between endothelial cells, pass though endothelial basement membrane by enzymatic degradation fo the extracellular matrix
migrate towards site of injury by chemotaxis (chemotaxins e.g. C3a and C5a components of complement)
move by the extension of an anteriro pseudopod with attachment to extracellular matrix e.g. fibronectin - cell pulled forwrd by action of actin and myosin
Describe phagocytosis
recognition of neutrophil for bacteria - coated by opsonins (immunoglobulins, complement and carb molecules) and bind to antigens on bac
englufment cytoplasmci extension or pseudopods flow aroudn bac till complete enclosure = phagosome
secretion of granule contents into phagolysosome
describe bacterial killing
oxygen dependent - reactive oxygen metabolites generated drugin phagocytosis because fo activation of NADPH oxidase on NADPH = produces superoxide which is converted to hydrogen peroxide (produced in a lysosome and released by metabolic burst
hydrogen peroxide may also be converted to HOCl-
hydrogen peroxide is detoxed by catalase
oxygen independent - lysozyme degrades the glycopeptide coat of bacteria, lactoferrin
can have deficiency disease
Give both good and bad outcomes of inflammatory response
protective: ingress of phagocytes, oedema formation tilute toxic substances, antibodies are delivered to site of infection and fibrin forms a substratum for cell migration
harmful: diestion of adjacent vaible tissue local swelling (esp in epiglottitis)
loss of function and increasedvascular permeability can case shock e.g. anaphylaxis
give some sequelae of actue inflammation
resolution - following short lived tissue injury where there is little tissue damage
abscess formation - localised collection of pus forms, surroudned by granulation tissue and fibrosis - pyogenci organisms e.g. staphylococci
healing by fibrosis and scar formation - substatial tissue destruction and unable to regenerate
chronic inflammation
Give the causes of acute inflammation
bacterial infection hypersensitivity reactions chemical reagents including toxins physical agents such as radiation tissue necrosis from infarction
