Learning Issue: Pathophysiology of Inflammation: Upper Respiratory System
Inflammation is the result of a complex reaction in the vascularized connective tissue involving 1)
phagocytosis of the injurious agent, 2) entrapment of the irritant by specialized cells that ingest it, 3)
neutralization of the noxious stimuli by hypertrophy of the cell or one of its organelles and 4)
reaction of blood vessels, leading to the accumulation of fluid and leukocytes in extravascular tissues.
It serves to destroy, dilute, or wall off the injurious agent, but also, in turn, sets in motion the event of
healing/repair of damaged tissue.
Inflammation is a fundamentally protective response that serves to rid the organism (in this case
Brianne) of both the initial cause of cell injury (e.g., microbes, toxins) and the consequences of such
injury – necrotic cells and tissues and cellular byproducts of injury to dead/dying cells and tissues.
Without the inflammatory response, infection would go unchecked and wounds would never heal.
The response occurs in the vascularized connective tissues, including plasma, circulating cells
(neutrophils, monocytes, eosinophils, lymphocytes, basophils and platelets), blood vessels, and cellular
(mast cells, fibroblasts, resident macrophages and lymphocytes) and extra-cellular constituents (e.g.,
structural (collagen, elastin) and, adhesive glycoproteins (fibronectin, laminin, nonvibrillar collagen,
entactin, tenascin and so forth)) of connective tissue.
Inflammation is divided into acute and chronic patterns.
Acute inflammation is of relatively short
duration, lasting for minutes, several hours, or a few days and its main characteristics are the exudation
of fluid and plasma proteins (edema) and the emigration of leukocytes, mostly neutrophils. Chronic
inflammation is of longer duration and is associated histologically with the presence of lymphocytes