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Inflammation and Healing.by Arindam
- 2. INFLAMMATION AND REPAIR DEFINITIONS INFLAMMATION Localresponse of living tissues to any insult, in order to eliminate or limit the spread of the insulting agent , and to remove the resulting dead cells and tissues REPAIR Response of the body to restore normal structure and function 2
- 3. INFLAMMATION & Repair Both occur together, with overlap 3 Inflammation Repai r
- 4. INFLAMMATION AND REPAIR DEFINITIONS EXUDATE rich in proteins & cellular debris specific gravity > 1.020 TRANSUDATE low protein content (mainly albumin) specific gravity < 1.012 4 PUS Purulent inflammatory exudate rich in cell debris & leukocytes
- 5. AGENTS OF INFLAMMATION Physical: Heat, cold, radiation, mechanical Chemical: Organic and inorganic poisons Infective: Bacteria,virus,toxins Immunological: Auto antigens 5
- 7. Signs of inflammation (Celsus , Virchow ) 7 Rubor redness Tumor swelling Calor heat Dolor pain Functio laesa loss of function
- 8. 8 TYPES OF INFLAMMATION ACUTE CHRONIC Short duration Neutrophilic exudate Long duration Monocytic /lymphocytic exudate
- 9. PROCESS OF ACUTE INFLAMMATION Vascular events: Hemodynamic changes Changes in vascular permeability Cellular events: Leucocyte exudation Phagocytosis & relaese of mediators 9
- 10. 10 migration margination stasis Extravasation of fluid & proteins Dilatation of capillary bed & increased permeability INJURY Initial vasoconstriction, then vasodilattion (arterioles) REDNESS, WARMTH VASCULAR EVENTS SWELLING rollingpavementingdiapedesis
- 11. Cellular events 11 margination chemotaxis activation phagocytosis Release of mediators TISSUE INJURY ARDS SEPTIC SHOCK pain
- 12. CELL TYPES IN ACUTE INFLAMMATION Neutrophils 6-24 hrs Monocytes 24-48 hrs Pseudomonas inf. Neutrophils for 2-4 days Viral inf. Lymphocytes seen initially Hypersensitivity Eosinophils predomiate reactions 12
- 13. CHEMICAL MEDIATORS OF INFLAMMATION Examples Histamine, serotonin, cytokines, prostaglandins, leucotrienes Source Cells (platelets, leukocytes, mast cells, macrophages) Plasma (complement, kinin & clotting system) Actions Vasodilatation Increasing vascular permeability Chemotaxis Tissue damage 13
- 14. Mediator Effect VASO DILATIO N PERMEABILIT Y CHEMOTAXI S FEVE R PAIN TISSUE DAMAGE PROSTA GLANDINS LEUCO TRIENES AMINES COMPLEMEN T KININS NITRIC OXIDE OTHERS AMINES CHEMO KINES INTER- LUKINS, TNF LYSOSYMES 14 MEDIATORS AND THEIR EFFECTS
- 15. REGULATORS OF INFLAMMATION Acute phase proteins C-reactive protein Alpha antitrypsin Corticosteroids Suppressor T cells Chemical mediators like prostaglandins 15
- 16. SYSTEMIC EFFECTS OF ACUTE INFLAMMATION 16 Fever Lymphangitis Lymphedinitis Systemic Inflammatory Response Syndrome Multiple Organ Dysfunction Syndrome Multiple System Organ Failure Bacteremia, Pyemia Toxemia
- 17. 17 RESULT OF ACUTE INFLAMMATION ACUTE INFLAMMATION CHRONIC INFLAMMATION INJURY resolution abscess Healing Regeneration / scarring Persistence of agent, interference to normal healing process
- 18. CHRONIC INFLAMMATION Mononuclear infiltrate / tissue destruction /granulation tissue Types: Nonspecific Granulomatous Monocyte / Macrophage is the cell of Chronic inflamation 18
- 19. SITUATIONS LEADING TO CHRONIC INFLAMMATION Persistent infection delayed hyperensitivity, granulomas TB, Syphilis, fungal Prolonged exposure to toxins Silica (exo), atheroma (endo) Autoimmuniy RA, LE 19
- 20. Granuloma Central necrosis / caseation Peripheral epitheloid cells Giant cells (Langhan’s, FB) TYPES: FB granuloma Minimal inflammatory / immune response Inert FB Immune granuloma Insoluble particulate antigens, eg. TB 20
- 21. 21 REPAIR Response of the body to restore normal structure and function
- 22. Types of healing Regeneration: proliferation of parenchymal cells and restoration of original tissues Repair: replacement of injured tissue by fibrous tissue Factors affecting: Nature of tissue Presence of stromal network 22
- 23. TYPE OF CELLS Labile cells : skin,bone marrow, lymph nodes Stable cells : parenchymal cells, mesenchymal cells Permanent cells : neurons, cardiac and skeletal muscle 23
- 24. PROCESSES IN HEALING Acute inflammation Angiogenesis Proliferation of parenchymal cells / fibroblasts Formation of granulation tissue Formation of ECM Wound strengthening Wound contraction 24
- 25. WOUND CONTRACTION CAUSES Dehydration Collagen contraction Myofibroblast activity 25
- 26. CLINICAL TYPES OF HEALING By primary intention By secondary intention 26
- 27. HEALING BY PRIMARY vrs SECONDARY PRIMARY INTENTION SECONDAY INTENTION NATURE OF WOUND Clean cuts, minimal tissue damage / loss Tissue loss, infected INFLAMMATORY REACTION Less intense More intense GRANULATION TISSUE Minimal Larger amounts WOUND CONTRACTION Absent Main feature SCAR Strong Weak 27
- 28. TIME FRAME OF WOUND HEALING immediate Fibrin clot and scab formation 6 hrs Neutrophilic infiltrate 48 hrs Epithelial cells bridge the gap beneath the scab 3rd day Neutrophils replaced by macrophages Thickness of epithelial cover increases Granulation tissue appears Collagen fibres present but do not bridge the gap 28
- 29. TIME FRAME OF WOUND HEALING 5th day Normal epithelial thickness Maximum granulation tissue Collagen fibres begin bridging gap End of 1st week Wound strength 10% of normal 2nd week Cellular infiltrate disappears Blanching starts – vascular channels regress, fibroblast proliferation continues & collagen accumulates 3rd – 4th week Healing complete but wound strength subnormal 29
- 30. WOUND STRENGTH TIME AMOUNT CAUSE End of 1st week 10% of normal Collagen deposition End of 2nd month 50% of normal Collagen deposition End of 3rd month 70-80% of normal Restructuring of collagen fibres 30
- 31. FACTORS AFFECTING REPAIR Protein & vitamin C deficiency Diabetes mellitus Decreased blood supply Glucocorticoid hormones Infection Early movement of part FB Small wound size Rich vascular supply Incised wounds 31
- 32. IMPROPER HEALING EXCESS: Hypertrophic scar Keloid formation Conctracture formation LESS: Deficient scar formation Incisional hernia 32
- 33. ADVERSE SCARS FEATURE HYPERTROHIC SCAR KELOID Genetic predisposition absent present age children Young adults sex equal Female predilection cause Longer remodelling phase Wound infection / dehiscence No definite cause identified In well healed wounds extent Within scar borders Extends beyond 33
- 34. ADVERSE SCARS FEATURE HYPERTROHIC SCAR KELOID site Flexor surfaces Sternum, shoulder, face natural history Subsides within 6 mths Continues to grow Needs treatment appearance Tentacles absent present treatment Pressure dressing intralesional steroids, surgery + interstitial radiation 34
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- 37. Harmful inflammation / healing Hypersensitivity reactions Fibrous adhesions Burn contractures 37
- 38. SOME MEDIATORS & THEIR EFFECTS Vasodilation Prostaglandins, nitric oxide Vascular permeability Amines, complement, leucotrienes, kinins Fever Interleukins, TNF, prostaglandins Pain Prostaglandins, kinins Chemotaxis, leucocyte activation Chemokines, leucotrienes, complement, bacterial products Tissue damage Lysosymes, nitric oxide 38
- 39. FACTORS DETERMINING THE TYPE AND AMOUNT OF INFLAMMATORY RESPONSE Agent factors: Type of stimulus: typhoid/osteomyelitis Virulence of organism Dose Portal of entry Products of organisms: hyaluronidase Host factors: General health and immune status Tissue involved 39
- 40. CLINICAL TYPES OF INFECTION 40 LOCAL SYSTEMIC Superficial Surgical Site Infection sepsis Systemic Inflammatory Response Syndrome Multiple Organ Dysfunction Syndrome Multiple System Organ Failure SIRS Temperature: > 380 C or < 360 C Heart rate > 90/min or Resp. rate > 20/min WBC count > 12000/mm3 or < 4000/mm3
- 41. ROLE OF LYMPH SYSTEM IN INFLAMMATION 41 INFLAMMATION Inflammatory exudate Agent destroyed Agent not destroyed Exudate & debris removed via lymphatics Agent carried to lymphatics &lymph nodes Lymphangitis, lymphedenitis
- 42. 42 Injury Vascular & cellular events Acute inflammatory exudate Stimulus destroyed Stimulus not destroyed No/minimal Cell necrosis Cell necrosis Exudate resolved Exudate organised Restitution of Normal structure Scarring Labile/stable cells Permanent cells Framework intact Framework destroyed Regeneration SUMMARY
- 43. TYPES OF INFLAMMATION Pseudomembranous Ulcerative Suppurative (abscess) Cellulitis Bacteremia / toxemia / pyemia/ septicemia Serous Fibrinous Suppurative Ulcerative 43 CLINICAL PATHOLOGICAL
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