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10. inflammation

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10. inflammation

  1. 1. Introduction O Local response of living tissues to injury. O Causes: O Infective agents – bacteria, virus, fungi, toxins, parasites. O Immunological agents O Physical agents – heat, cold, radiation, mechanical trauma O Inert materials like foreign bodies. O Prefix –itis (except – boils, abscess, pneumonia, etc)
  2. 2. Signs of inflammation O Cardinal signs (celsus in 1st century AD) O Rubor (redness) O Tumor (swelling) O Calor (heat) O Dolor (pain) O Functio laesa (loss of function) – virchow Purpose of inflammation O To dilute, localize and to destroy the injurious agent. O To limit tissue injury O To restore the tissue towards normality.
  3. 3. Types O Acute – O Short duration (<2 weeks) O Early body reaction (exudative lesion) O Resolves quickly O Usually followed by healing O Fulminant acute inflammation (severe form) O Chronic – O Longer duration O Occurs if the cause of acute inflammation persists for a long time. (proliferative lesion) O Subacute inflammation – phase between acute and chronic inflammation O Chronic active inflammation (acute exacerbation)
  4. 4. Acute vs. Chronic Inflammation Feature Acute chronic Common cause Pyogenic organism Tubercle bacilli, lepra bacilli, etc Duration Hours to days Weeks to months to years Character Exudative Proliferative Vascular phenomenon Prominent Non prominent Fluid exudates Marked Scanty Cellular exudates Earl PMN then macrophages Mononuclear cells in most cases Repair process Follows it Starts concurrently
  5. 5. Acute inflammation O Aetiology: O Infection O Physical injury O Chemical injury O Immunologic injury O Necrosis associated injury O Idiopathic O Events: O Vascular events O Cellular events
  6. 6. Vascular events 1. Haemodynamic changes O Immediate transient vasoconstriction O Persistent progressive vasodialation O Increased local hydrostatic pressure  transudation of fluid (edema) O Stasis  leucocytic margination (cellular events) 2. Altered vascular permeability Mechanisms: O Contraction of endothelium O Retraction of endothelium O Direct injury to endothelium O Leucocyte mediated endothelial injury O Leakiness and neovascularization
  7. 7. Lewis’ experiment of triple response 1. Red line within few seconds (local vasodilation of capillaries and venules) 2. Flare (bright reddish appearance/ flush) d/t vasodilation of adjacent arterioles. 3. Wheal (swelling/ oedema) d/t transudation
  8. 8. Cellular events O Change in formed elements of blood  margination O Rolling and adhesions O Selectins, integrins and Ig gene superfamily adhesion molecules O Emigration O WBC + RBC escape (diapedesis) O Chemotaxis O Chemokines (leukotrine, complements, cytokines, soluble bacterial products) O Phagocytosis O Recognition and attachment (opsonins) O Engulfment (via cytoplasmic pseudopods) O Killing and degradation
  9. 9. Outcomes of acute inflammation O Resolution O Abscess formation (suppuration) O Healing (regeneration/ scarring) O Chronic inflammation
  10. 10. Chemical mediators O Cell derived mediators O Vasoactive amines O Histamine O 5-HT / serotonin O Neuropeptides O Arachidonic acid metabolites (eicosanoids) O Via cyclo-oxygenase pathway – PGs, TXA2, prostacyclin, resolvins O Via lip-oxygenase pathway – 5 HETE, LT (leukotrienes), LX (lipoxins) O Lysosomal components O Granules of neutrophils O Granules of monocytes & tissue macrophages O Platelet activating factor (PAF) O Cytokines O Free radicals O Plasma derived mediators (plasma proteases) O The kinin system O The clotting system O The fibrinolytic system O The complement system
  11. 11. O Platelet activating factor (PAF) O Released from IgE sensitised basophils or mast cells, leucocytes, endothelium and platelets Actions of PAF: • Increased vascular permeability • Vasodilation in low concentration; otherwise constriction • Bronchoconstriction • Adhesions of leucocytes to endothelium • chemotaxis O Cytokines O Polypeptides produced by lymphocytes and monocytes (activated) O IL-1, TNF-alpha and beta, IFN- gamma and chemokines O Free radicals O Oxygen derived metabolites O Nitric oxide
  12. 12. Plasma derived mediators (plasma proteases) O The kinin system O Activation by factor XIIa generated bradykinin from kallikrein. Actions: • Smooth muscle contraction • Vasodilation • Increased permeability • pain O The clotting system O Factor XIIa fibrinogen  fibrin and fibropeptides. Actions: • Increased vascular permeability • Chemotaxis for WBC • Anticoagulant activity O The fibrinolytic system O Activated by plasminogen activator Actions: • Activation of factor XII • Complement C3 C3a (permeability factor) • Degradation of fibrin to degradation products  chemotaxis + permeability O The complement system O C3a, 5a,4a (anaphylatoxins); C3b (opsonin); C5a (chemotaxis), C5b- C9 (membrane attack complex – MAC)
  13. 13. Regulators of inflammation 1. Acute phase reactants: O Cellular protection – Alpha 1 antitrypsin, alpha 1 chymotrypsin, alpha 2 antiplasmin O Coagulation proteins – Fibrinogen, plasminogen, VW factor, Factor VIII O Transport proteins (ceruloplasmin, haptoglobin) O Immune agents (sr amyloid A and P, CRP) O Stress proteins (HSP) O Antioxidants (ceruloplasmin) 2. Glucosteroids: O Anti inflammatory action 3. Free cytokine receptors 4. Anti-inflammatory chemical mediators O PGE2, prostacyclin
  14. 14. Giant cells O Multinucleate giant cells formed when macrophages fail to deal with the particles to be removed. O Giant cells in inflammation: • Foreign body giant cells – chronic infective granulomas, TB and leprosy. • Langhan’s giant cells – tuberculosis and sarcoidosis • Touton giant cells – xanthoma • Aschoff giant cells – rheumatic nodules O Giant cells in tumors: • Anaplastic cancer GC – carcinoma of liver, soft tissue sarcoma, etc. • Reed-stenberg cells – Hodgkin’s lymphoma • Ginat- cell tumor of bone – osteoclastic giant cells
  15. 15. Chronic inflammation O Prolonged process of tissue destruction, inflammation and repair occur simultaneously. Causes: 1. Following acute inflammation 2. Recurrent attacks of acute inflammation (recurrent UTI  chronic pyelonephritis) 3. Chronic de novo (e.g. in TB)
  16. 16. General features
  17. 17. Systemic effects O Fever O Anaemia O Leucocytosis O ESR elevated O Amyloidosis (group of diseases/ disorders characterised by extracellular deposition of fibrillar proteinaceous substance called amyloid)
  18. 18. THANK YOU