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CH 5 INFLAMMATION & HEALING (DIAGNOSTIC TESTS (Erythrocyte…
CH 5 INFLAMMATION & HEALING
REVIEW
1ST Line of Defense
Nonspecific (skin, tears, gastric juices)
2ND Line of Defense
Nonspecific (phagocytosis,
Inflammation
)
3RD Line of Defense
Specific (production of antibodies {humeral} or Cell-mediated)
PHYSOLOGY
Disorders use the ending -itis
Inflammation is a normal defense mechanism
Causes
Ischemia, infarction
Allergic reactions
Chemicals (acid, drain cleaner)
Extreme cold or heat
Physical damage (internal or external)
Foreign items
Infection
Steps 9
Activation of pain receptors by bradykinin
Mast cells and basophils release histamine.
Release of bradykinin from injured cells
Capillary dilation (bradykinin and histamine)
Increased blood flow and capillary permeability
Bacteria or other microbe may enter the tissue.
Neutrophil and monocytes come to injury site.
Neutrophils phagocytize bacteria.
Macrophages leave bloodstream for phagocytosis of microbes.
LOCAL AND SYSTEMIC FACTORS
Local
Exudate
Fibrinous Exudate:
Thick, sticky, high cell and fibrin count
:warning:
Increases risk of scar tissue
:warning:
Purulent Exudate:
Thick, yellow-green, contains more WBC(pus)
Serous Exudate:
watery, consists primarily of WBC and sm amounts of proteins
Hemorrhagic Exudate:
Present when blood vessels are damaged
redness, warmth, swelling, pain, loss of function
Systemic
Fever, Malaise, Fatigued, Headache, Anorexia
Fig 5.4 pg71
ACUTE INFLAMMATION
Chemical mediators affect blood vessels and nerves in the damaged area:
#
Chemotaxis
to attract cells of the immune system
Increase in capillary
permeability
Hyperemia:
Increased blood flow
Vasodilation
CHRONIC INFLAMMATION
Follows acute episode but there is more scar tissue and WBC use
DIAGNOSTIC TESTS
Erythrocyte sedimentation rate
ESR: Elevated Plasma Proteins inc
Differential count:
Proportion of each WBC count altered (helps distinguish between bacteria and virus)rise the rate at which RBC settle
Leukocytosis:
more WBC in blood
Circulating plasma proteins:
Cell enzymes:
Realized from necrotic cells and enter tissue fluids and blood; may indicate site of inflammation
(Isoenzymes may be elevated)
Necrosis
TREATMENT
Drugs
Acetylsalicylic acid (ASA)
or Aspirin is used as an anti-inflammatory agent
:warning:not recommended for
children w/viral infections
because the drug will contribute to
Reye syndrome
:warning:
Acetaminophen
or Tylenol
Diminishes fever and pain but NOT the inflammatory response
#
:warning:
Anti-inflammatory drugs integer with blood clotting by reducing platelet adhesion
:warning:
Nonsteroidal antiinflammatory drugs (NSAIDs)
Ibuprofen (Advil or Motrin) Work very similar to Aspirin
#
Glucocorticoids
are corticosteroids or steroidal anti-inflammatory drugs
Adverse Effects:
Atrophy of lymphoid tissue; reduced hemopoiesis :warning:(Increased risk of infection):warning:
Catabolic effects :warning:(Increased tissue breakdown; decreased protein synthesis):warning:
Delayed healing
Delayed growth in children
Retention of sodium and water (Increased gluconeogenesis :warning:(causes rise in BS):warning:)
Effects:
Decreased capillary permeability
Enhanced effectiveness of epinephrine and norepinephrine
Reduced number of leukocytes and mast cells
Reduces immune response
RICE therapy
(Rest, Ice, Compression, Elevation)
TYPES OF HEALING
Scar Formation
Scar tissue is nonelastic, Can restrict range of movement
#
Hypertrophic scar tissue
(Overgrowth of fibrous tissue)
Ulceration
(Blood supply may be impaired around scar)
Resolution
(Minimal tissue damage)
Regeneration
(Damaged tissue replaced with cells that are functional)
Replacement
(Functional tissue replaced by scar tissue) :!!:(Loss of function):!!:
#
#
Table 5.1 pg69
#
