2. CAUSE / ETIOLOGY
Local body defensive response of any
living mammalian tissue to injury by
various agent.
Infective agents
Immunological agents
Physical agents
Chemical agents
Inert materials (such as foreign bodies)
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4. TYPE
ACUTE - sudden in onset, short duration,
immediate body response, neutrophil
mainly
CHRONIC – Insidious onset, longer
duration, late body response
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5. ACUTE
INFLAMMATION
1. Vascular events –
Heamodynamic changes
Change in Vascular permiability
Five (5) Changes in haemodynamic
Vasoconstriction
Vasodilation
Increased local hydrostatic pressure
Stasis
Margination of leucocyte (pavmenting)
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6. 2. Changes in vascular permeability
Contraction of endothelial cell
Retraction of endothelial cell
Direct injury of endothelial wall
Injury mediated by leukocyte cell
Neovascularization
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7. Direct injury –
Increase hemodynamic force
Hypoxia
Chemical poison and bacterial toxin
Detached atherosclerotic plug
Thermal injury and radiation
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8. Disturbance of streamline flow
Rolling of WBCs cell
Cell adhere to junction between two cell
WBCs release proteolytic enzyme
Colligenase damage the collegen fibres
Forming microspore
Exudation process
WBCs moves out due to amoeboid movement
(Diapedasis)
Chemotaxis
Phagocytosis of cell
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9. 2. Cellular Events
Pavmenting
Rolling and Adhesion
Emigration
Exudation of leucocyte
Chemotaxis
Phagocytosis
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10. Phagocytosis
Attachment (opsonization) – chemical which
covers the bacteria and foreign agent and
forming the film
Engulfment (Cytoplasmic pseudopodium)
Secretion (degranulation) – vacules and
granules
Killing by toxin and enzymes due to rupture
of lysosome pockets
Degradation
and digestion
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12. LEWIS EXPERIMENT
Red line – due to local vasodilatation of
capillaries and venules
Flare – bright reddish appearance or flush
surrounding the red line due to
vasodilatation of the adjacent arterioles
Wheal – swelling or oedema due to
transudation of fluid into the extravascular
space
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19. HEALING
Trauma – Injury – Cell death – Tissue
destruction – Restoration – Healing
Repair and regeneration process may be
done by simultaneously
Repair – two process
1. Granulation tissue formation
2. Contraction of wound
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20. Granulation tissue formation
Phase of inflammation
Phase of clearance
Phase of ingrowths of granulation tissue –
Angiogenesis or Neovascularisation and
Fibrogenesis
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21. Contraction of wound
Starts after 2-3 days and completed upto
within 14th day
It facilitates Rapid healing
Dehydration
Contraction of Collagen – 5-6 days,
appearance of myofibroblasts (Myofibrin,
actin, myocin, protein)
Real wound contraction done by
myofibroblast
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22. WOUND HEALING
Primary union (healing by first intention)
– Reepithelization
Secondary union (healing by second
intention) - Fibrosis
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23. Steps of primary and secondary
union
Clean cut
Uninfected area
Surgically incised
wound
Less loss of tissue
Edge of wound
approximate by
surgical suture
90% epithelial and
10% fibrosis
Lacerated wound
Zig –zag margin
Infected wound
Excessive loss of
tissue
Wound is not
approximate by
surgical tissue
30% epithelial and
70% fibrosis
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24. Complication Of Wound Healing
Infection
Hyperpigmentation
Deficient scar – depression and scar
Hypertrophy scar
Keloid – pinkish color skin and high
vascularity
Wound contracture
Incisional Hernia
Cancer
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