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24 Cards in this Set

  • Front
  • Back
What is inflammation?
A physiologic response to injury not a pathologic response.
by endogenous agents
exogenous agents
Mechanisms of prevention?
Intact skin 1st defense
Inflammation and nonspecific mechanisms of immunity
Specific immune responses
active and passive
Most common causes of inflammation?
Infection Physical trauma
Chemical injury
Irradiation injury
Mechanical injury
Thermal injury Immune reaction
Pathophysiology of cell injury
Acute: Immediate and early response
Chronic: Later stage if healing does not occur or if causes of inflammation persist
Acute Inflammation
2 phases of responce
Vascular response
Cellular response
What is vascular response?
Vasodilation warmth& redness
Increased capillary permeability
increases blood viscosity
Vasoconstriction post injury
Immediate,brief response. chemical mediators sent now, Serotonin Histamine
Leukotrine Prostaglandins
Cellular response post injury
What is margination?
Adherence of leukocytes to blood vessels during the first stages of inflammation.
What is pavementing?
Leukocytes adhere to capillary lining
What is emmigration?
Passage of leukocytes through the capillaries to the damaged cell.
What is chemotaxis?
Directional movement of leukocytes to the injured area.
Vascular response summary
First step
release of chemical mediators by
Mast cells
Vascular response summary
step 2
immediate vasoconstriction by the nerve reflexes.
Vascular response summary
3rd step
rapid release of chemicals
local vasodilation
increased blood flow to area
Vascular Response #4
Increased vascular permeability
Pain due to pressure on nerves from fluid leaking from capillaries.
Increased Capillary Permeability Response
Plasma protein and more fluid shift into interstitial space
Dilution of toxic materials @ injury site. Globulin serves as antibodies. Fibrinogen localizes the injury agent for phagositosis. Cellular response follows.
Cellular Response
Process that brings leukocytes to the area of inflammation as damaged cells release their contents.
Cellular Elements in Inflammatory response
Neutrophils - Phagocytosis
Basophils - Histamine release
Eosinophils - Allergic response
T Lymphocytes- cell-mediated immunity
B Lymphocytes- Antibody production
Macrocytes- Large Phagocytes
Local Effects of Injury
Redness- Rubor
Warmth- Calor
Swelling- Tumor
Pain- Dolor
Function Loss- Functional Lysis
Systemic Effects of Inflammatory Response
Pyrexia or Fever low grade/mild
Diagnostic Tests for Inflammation
WBC w/ diff- leukocytosis increased WBCs
ESR- increased w/ inflammation
Peripheral blood smear- parasites, fungus, protozoans
Cell enzymes- released by microorganisms
Plasma proteins- increased
Chronic Inflammation
Less swelling More collagen produced More lymphocytes, macrophages, fibroblasts, fibrous scar tissue formation. Granulomas may develop, more tissue destruction
Cell injury and Adaptation
Preparation for survival of the species