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INFLAMMATION and
HEALING
Presented by
Dr. YOGITA CHANDRAKAR
B.A.M.S., M.D.
Assist. Professor
Department of Rog Nidan Avum Vikriti Vigyan
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)
4/22/2020 2DR.YOGITA CHANDRAKAR
INFLAMMATION
 RUBOR
 TUMOR
 CALOR
 DOLOR
 FUNCTIONLOSSIA
4/22/2020 3DR.YOGITA CHANDRAKAR
TYPE
 ACUTE - sudden in onset, short duration,
immediate body response, neutrophil
mainly
 CHRONIC – Insidious onset, longer
duration, late body response
4/22/2020 4DR.YOGITA CHANDRAKAR
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)
4/22/2020 5DR.YOGITA CHANDRAKAR
2. Changes in vascular permeability
Contraction of endothelial cell
Retraction of endothelial cell
Direct injury of endothelial wall
Injury mediated by leukocyte cell
Neovascularization
4/22/2020 6DR.YOGITA CHANDRAKAR
Direct injury –
Increase hemodynamic force
Hypoxia
Chemical poison and bacterial toxin
Detached atherosclerotic plug
Thermal injury and radiation
4/22/2020 7DR.YOGITA CHANDRAKAR
 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
4/22/2020 8DR.YOGITA CHANDRAKAR
2. Cellular Events
 Pavmenting
 Rolling and Adhesion
 Emigration
 Exudation of leucocyte
 Chemotaxis
 Phagocytosis
4/22/2020 9DR.YOGITA CHANDRAKAR
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
4/22/2020 10DR.YOGITA CHANDRAKAR
Chemotaxis
 Leucotrine
 Complimentary system
 Cytokines
 Soluble bacterial product
 Tumour Nacrotic factor (TNF)
4/22/2020 11DR.YOGITA CHANDRAKAR
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
4/22/2020 12DR.YOGITA CHANDRAKAR
MORPHOLOGY
 Pseudo membranous inflammation (eg.
Diptheria)
 Ulcer (mouth ulcer or stomatitis)
 Suppuration (Abcess)
 Cellulitis (eg.Mumps)
4/22/2020 13DR.YOGITA CHANDRAKAR
CLINICAL FEATURE
 Fever
 Leucocytosis
 Lymphangitis and lymphadenitis
 Shock
4/22/2020 14DR.YOGITA CHANDRAKAR
Fate Of Acute Inflammation
 Resolution (Restoration)
 Healing by scaring
 Progression to Suppuration – cavity
formed
 Progression to Chronic inflammation
4/22/2020 15DR.YOGITA CHANDRAKAR
CHRONIC INFLAMMATION
 Mononuclear cell infiltration
 Tissue destruction or necrosis
 Proliferative changes
4/22/2020 16DR.YOGITA CHANDRAKAR
SYSTEMIC EFFECTS
 Fever
 Anaemia
 High ESR
 Amyloidosis
4/22/2020 17DR.YOGITA CHANDRAKAR
TYPE
 Specific
 Nonspecific
4/22/2020 18DR.YOGITA CHANDRAKAR
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
4/22/2020 19DR.YOGITA CHANDRAKAR
Granulation tissue formation
 Phase of inflammation
 Phase of clearance
 Phase of ingrowths of granulation tissue –
Angiogenesis or Neovascularisation and
Fibrogenesis
4/22/2020 20DR.YOGITA CHANDRAKAR
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
4/22/2020 21DR.YOGITA CHANDRAKAR
WOUND HEALING
 Primary union (healing by first intention)
– Reepithelization
 Secondary union (healing by second
intention) - Fibrosis
4/22/2020 22DR.YOGITA CHANDRAKAR
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
4/22/2020 23DR.YOGITA CHANDRAKAR
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
4/22/2020 24DR.YOGITA CHANDRAKAR
THANK
YOU

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Inflammation and Healing

  • 1. INFLAMMATION and HEALING Presented by Dr. YOGITA CHANDRAKAR B.A.M.S., M.D. Assist. Professor Department of Rog Nidan Avum Vikriti Vigyan
  • 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) 4/22/2020 2DR.YOGITA CHANDRAKAR
  • 3. INFLAMMATION  RUBOR  TUMOR  CALOR  DOLOR  FUNCTIONLOSSIA 4/22/2020 3DR.YOGITA CHANDRAKAR
  • 4. TYPE  ACUTE - sudden in onset, short duration, immediate body response, neutrophil mainly  CHRONIC – Insidious onset, longer duration, late body response 4/22/2020 4DR.YOGITA CHANDRAKAR
  • 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) 4/22/2020 5DR.YOGITA CHANDRAKAR
  • 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 4/22/2020 6DR.YOGITA CHANDRAKAR
  • 7. Direct injury – Increase hemodynamic force Hypoxia Chemical poison and bacterial toxin Detached atherosclerotic plug Thermal injury and radiation 4/22/2020 7DR.YOGITA CHANDRAKAR
  • 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 4/22/2020 8DR.YOGITA CHANDRAKAR
  • 9. 2. Cellular Events  Pavmenting  Rolling and Adhesion  Emigration  Exudation of leucocyte  Chemotaxis  Phagocytosis 4/22/2020 9DR.YOGITA CHANDRAKAR
  • 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 4/22/2020 10DR.YOGITA CHANDRAKAR
  • 11. Chemotaxis  Leucotrine  Complimentary system  Cytokines  Soluble bacterial product  Tumour Nacrotic factor (TNF) 4/22/2020 11DR.YOGITA CHANDRAKAR
  • 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 4/22/2020 12DR.YOGITA CHANDRAKAR
  • 13. MORPHOLOGY  Pseudo membranous inflammation (eg. Diptheria)  Ulcer (mouth ulcer or stomatitis)  Suppuration (Abcess)  Cellulitis (eg.Mumps) 4/22/2020 13DR.YOGITA CHANDRAKAR
  • 14. CLINICAL FEATURE  Fever  Leucocytosis  Lymphangitis and lymphadenitis  Shock 4/22/2020 14DR.YOGITA CHANDRAKAR
  • 15. Fate Of Acute Inflammation  Resolution (Restoration)  Healing by scaring  Progression to Suppuration – cavity formed  Progression to Chronic inflammation 4/22/2020 15DR.YOGITA CHANDRAKAR
  • 16. CHRONIC INFLAMMATION  Mononuclear cell infiltration  Tissue destruction or necrosis  Proliferative changes 4/22/2020 16DR.YOGITA CHANDRAKAR
  • 17. SYSTEMIC EFFECTS  Fever  Anaemia  High ESR  Amyloidosis 4/22/2020 17DR.YOGITA CHANDRAKAR
  • 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 4/22/2020 19DR.YOGITA CHANDRAKAR
  • 20. Granulation tissue formation  Phase of inflammation  Phase of clearance  Phase of ingrowths of granulation tissue – Angiogenesis or Neovascularisation and Fibrogenesis 4/22/2020 20DR.YOGITA CHANDRAKAR
  • 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 4/22/2020 21DR.YOGITA CHANDRAKAR
  • 22. WOUND HEALING  Primary union (healing by first intention) – Reepithelization  Secondary union (healing by second intention) - Fibrosis 4/22/2020 22DR.YOGITA CHANDRAKAR
  • 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 4/22/2020 23DR.YOGITA CHANDRAKAR
  • 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 4/22/2020 24DR.YOGITA CHANDRAKAR