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are the body’s response to injury
inflammation and repair
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elininates injurious agents
contains injuries
heal defects
inflammation
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alteration in the environment causing tissue damage
injury
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examples of injury:
physical, chemical, microoganisms, nutritional, deficiencies
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nonspecific response to injury & occurs in the same manner regardless of nature of injury
inflammation
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Inflammation can be:
- Local – one area
- Systemic – throughout
- Acute – minimal & brief
- Chronic -continued inflammation & longer (weeks or months)
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suffix denoting inflammation (pulpitis, gingivitis, etc.)
itis
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increase in numberof WBC's
leukocytosis
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enlargement of lymph nodes
lymphadenopathy
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small blood vessels, certain WBC’s, & chemical mediators
Microscopic components
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constriction of microcirculation then dilation
1st event
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increase blood flow flooding capillary beds – heat/erythema
active hypermia
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plasma fluids & proteins that leave the blood vessels & enter the surrounding tissues. (Causes pain – sensory nerves in area)
exudate
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mainly plasma fluids/proteins (thin/clear)
serous
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tissue debris/many WBC's and serous (thick/colored)
purulent
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clinical sign of edema (swelling)
wheal
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a formation of a natural drainage passage boring through tissue allowing drainage of exudates (Buccal Parulus)
fistula
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mechanical way of draining exudate
incision and drainage (I/D)
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movement of WBC’s to periphery of vessel walls
margination
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lining of vessel walls with WBC’s
pavementing
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escape of WBC from vessels of plasma fluids that enter tissue
emigration
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what are the casues of emigration:
- -inc bld flow casuing inc pressure
- -opening of juntions of endothelial cells linning bld vessel
- -inc mobility of WBC's
- -chemical mediatiors causing directional movement of WBC's (chemotaxis)
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ingestion of foreign substances by WBC's
phagocytosis
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what are the 6 types of WBC's:
neutrophils, monocytes, lymphocytes, plasma cells, eosinophils, & mast cells
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also called PMN’s (polymorphonuclear leukocyte)
1st cell to migrate and primary cell invoved in acute inflammation
NEUTROPHILS
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also called Macrophage
2nd cell to emigrate
MONOCYTE
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involved in chronic inflammation and immune response
EOSINOPHIL/MAST CELL
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macrophages, lyphocytes, & plasma cells become the predominantes
chronic inflammation
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60 – 70% of WBC pop.
main funtion- phagocytosis then dies
Neutrophils
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become macrophages after emigration
3 – 8% of WBC pop.
lysosomal enzymes to aide in destruction of foreign substances
Monocytes
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start or enhance the inflammatory response
has 3 systems
Chemical mediators
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what are the 3 systems of chemical mediators?
- Kinin system
- complement system
- clotting mechanism
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Mediates inflammation by causing inc dilation of blood vessels at the site increasing permeability of blood vessels by widening gaps between endothelial
Early phase of inflammation
Kinn System
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Production of sequential cascade of plasma proteins that are present in the blood in an activated form
Release of histamine (mast cells)
Complement System
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clots bld and helps with repair
Platelets
Clotting Mechanism
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body temp regulated by?
hypothalamic thermoregulatory center
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fever producing substances
pyrogens
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can reduce fever with medications
acetaminophen (tylenol)
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inc of WBC'
Norm #4 -10,000/mm (infection can casue this to rise to 10-30,000)
leukocytosis
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enlargement of lymph nodes
WILL be able to paplate-enlarged mass in area of inflammation
Lymphadenopathy
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primary cells of immune system
production of lymphocytes in nodes
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inc number of cells
hyperplaisa
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inc size of cells
hypertrophy
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distinctive form of chronic inflammation
Granulomatous inflammation
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microscopic groupings of macrophages surrounded by lymphocytes & plasma cells – example: TB
formation of granulomas
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large macrophages having multiple nuclei
Multinucleated giant cells
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the bodies final defense mechanism in its attempt to restore injured tissue to its orgininal state
repair
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occur in both epithelium and connective tissue
repair usually is completed in 2 weeks
microscopic events
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Day of injury-
consist of fibrin, aggregated RBC's and platelets-clot formation (thrombocytes)
-affected by:hereditary, drug extensive injury, certain diseases.
clot forms
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One day after-
neutrophils
acute inflammation takes place
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2 days after-
- monocytes emigrate
- fibroblast inc in # and start producing new collagen fibers
- the initial tissue formed in CT portion of injury called-granulation tissue
- At end of day2-chronic inflm and immune response begins
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the initial tissue formed in CT portion of injury called
granulation tissue
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7 days after
- fibrin is digested by tissue enzymes & sloughs off
- initial repair is completed
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2 wks after injury-
- tissue has full strength-called scar tissuepaler in color at surface because of increased # of collagen fibers & decreased vascularity
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healing of an injury in which there is little loss of tissue
surgical incision
edges are joined by sutures
less scar tissue
Healing by primary intention
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injury whereby there is loss of tissue & the edges of the injury cannot be joined during healing
inc scar tissue
extraction site
keloid formation – excessive scarring in skin
Healing by secondary intentin
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excessive scarring in skin
keloid formation
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infection occurs at site of surgical incision that is healing by 1° intention, and 2° intention may ensue
* waiting to perform surgical tissue repair until infection is resolved
Healing by 3rd intention
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occurs similar to tissue with exception of osteoblasts
bone tissue repair
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interruption due to:removal of osteoblast-producing tissue
hemorrhage
inc movement of bone
infection
bone tissue repair
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