Inflammation produces localized redness, swelling, heat, and pain (see chapter 5, p. 151). The redness is a result of blood vessel dilation and the consequent increase of blood flow and volume within the affected tissues (hyper-emia). This effect, coupled with an increase in permeability of nearby capillaries and venules, swells tissues (edema). The heat comes from the entry of blood from deeper body parts, which is generally warmer than that near the surface. Pain results from stimulation of nearby pain receptors. Most inflammation is a tissue response to pathogen invasion but alternately can be caused by physical factors (heat, ultraviolet light) or chemical factors (acids, bases).

White blood cells accumulate at the sites of inflammation, where some of them help control pathogens by phagocytosis. In bacterial infections, the resulting mass of white blood cells, bacterial cells, and damaged tissue may form a thick fluid called pus.

Tissue fluids (exudate) also collect in inflamed tissues. These fluids contain fibrinogen and other clotting factors that may stimulate a network of fibrin threads to form within the affected region. Later, fibroblasts may arrive and form fibers around the area until it is enclosed in a sac of connective tissue containing many fibers. This action helps to inhibit the spread of pathogens and toxins to adjacent tissues.

^ Major Actions of an Inflammation Response

Blood vessels dilate.

Capillary and venule permeability increase.

Tissues become red, swollen, warm, and painful. White blood cells invade the region.

Pus may form as white blood cells, bacterial cells, and cellular debris accumulate. Tissue fluids seep into the area.

A clot containing threads of fibrin may form. Fibroblasts arrive.

A connective tissue sac may form around the injured tissues. Phagocytes are active.

Bacteria, dead cells, and other debris are removed. Cells divide.

Newly formed cells replace injured ones.

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