Studied by 25 people
inflammation reaction purpose:
prevent the spread of damage agents to set the stage for repair
affects of inflammation:
capillary dilation
increases capillary permeability
attraction of leukocytes
systemic effects of inflammation:
fever
feeling ill
severe widespread of inflammatory process
characteristics of inflammation:
heat and redness from dilated blood vessels
swelling like edema
tenderness and pain for irritation or never endings
impairment of function die to any agent that causes cell injury
causes of inflammation:
a nonspecific response to any gent that causes cell injury
dominant cells of acute inflammation:
monocyte
polymorphonuclear leukocyte cell
Polymorphonuclear leukocyte cell
most important cell in acute inflammatory response
neutrophils arrive first
monocyte:
follow water to clean up tissue damage
exudate:
fluid mixture of protein, leukocyte, and tissue debris
benefits of exudate:
dilutes toxins to reduce further damage
Increase pain to prevent additional injury
Brings antibodies into tissue to act against microorganisms
Brings protein into tissues
types of exudates:
Serous: primarily fluid, endothelial cells contract slightly so only fluid escapes like a blister
Purulent: large inflammatory cells of living and dead WBS, like pus or abscess
mild inflammatory process:
self limiting, subsides with tissue resolution
severe inflammatory process:
tissue damage
goals of healing:
restore structure
strength
some function
regeneration healing:
when tissue is replaced from parenchyma
lost cells are replaced by mitosis of adjacent uninjured cells
repair healing:
when fibrous scar tissue fills the gap left by the loss of damage tissue
restore the strength and structural integrity of tissues that can’t regenerate
inflammatory mediators:
chemical agents that intensity the inflammatory process
cell derived mediators:
mast cells
platelets
arachidonic acid derivatives
mast cells:
specialized CT cells with granules filled with histamine and heparin
platelets:
release histamine and serotonin when activated
Arachidonic acid derivatives:
produced by all WBC's
mediators form blood plasma:
Formed following a cascade of activation steps
Bradykinins: activation is triggered by one of the proteins in the blood coagulation cascade
Complement: consists of 20 blood proteins that circulate in inactive form
Roles of lysosomal enzymes with inflammation:
Released from the cytoplasm of phagocytic neutrophils and monocytes that are damaged or destroyed during an inflammatory reaction
Roles of antigen-antibody with inflammation:
Activates complement, generating mediators
Attracts leukocytes
Harmful effects of inflammation:
Tissue injury results in part from the injurious agent and in part from the inflammatory reaction itself
In most cases inflammation is self-limited and subsides when harmful agent has been eliminated
Pain: signals tissue damage and limits use of injured tissue
Swelling: sometime it is so great that it impairs function or blocks passages
Tissue damage: sometimes can leads to damage of healthy tissue
Temperature:
Application of cold or heat
Cold: applied early to limit swelling since it causes vasoconstriction
Heat: applied after to stimulate phagocytosis
Elevation:
limits swelling by slowing blood flow and promoting drainage
Compression:
limits welling by preventing exudate formation due to increased tissue pressure and promoting drainage
Drug therapy;
Directed at chemical mediators that underlies inflammation
Corticosteroids: used to suppress a persistent inflammatory
NSAIDs: block production of prostaglandins
Antihistamines: block the action of histamine at blood vessel receptors
When might chronic inflammation occur:
Inflammation can become chronic when the acute inflammatory response is unable to remove or neutralize an injurious agent
Relatively quiet, smoldering inflammation, associated with repeated attempts of the body healing
Causes damage of normal tissue
Predominant cells:
lymphocytes, plasma cells, and monocytes
