Acute Inflammation Flashcards
Vasodilation
the blood vessels get wider
Vascular Changes
first involves arterioles and then capillary beds, is mediated by histamine and nitric oxide, resulting in increased calor and rubor in localised area.
Normal Flow
blood flows centrally within a vessel
White Cell Margination
with vascular dilation, the rate of flow slows and cells begin to move peripherally - especially larger white cells.
Adhesions
normal vessel walls are slippy and blood cells don’t stick, in inflammation the vessels express proteins on the luminal surface that have a matching protein on white cell surface (key and lock)
Selectins
expressed on various cells (endothelial and white cells). Cellular Adhesion Molecules
Integrin/Selectin Interaction with their Ligand
is of low affinity and binding on is fast and binding off is fast
Inflammatory Cells
histamine and thrombin form inflammatory cells increase selectin expression. Tumour necrosis factor (TNF) and interleukin-1 (IL-1) increase endothelial cell expression of VCAM and ICAM.
VCAM
Vascular Cell Adhesion Molecule
ICAM
Intercellular Adhesion Molecule
Increased Avidity
chemokines from site of injury bind to proteoglycans on endothelial cell surface. Proteoglycans then increase the affinity of VCAMs and ICAMs for integrins, making things more attractive.
Vascular Permeability
white cells have to go from inside to outside the vessels, so go leaky. Loss of proteins causes change in osmotic pressure as water follows the protein resulting in swelling (tumour).
Rubor
redness
increased perfusion, slow flow, increased permeability of vessels.
Calor
heat
increased perfusion, slow flow rate, increased vascular permeability
Tumor
swelling
due to vascular changes
