Inflammation

Ac ut e & Ch ron ic In fl amm ati on

BY: DR. ANTOINETTE T. LEUTERIO

Acu te & Ch roni c In fl am ma ti on • Acute inflammation • short duration • edema • neutrophils

• Chronic inflammation • longer duration • fibrosis and tissue necrosis • lymphocytes & macrophages

Acu te In fl am mati on • Cardinal clinical signs • • • • •

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• Morphologic & functional changes • Microcirculatory response (vascular changes) • Cellular events

Micro circ ulat ory Re spo ns e • Active vasodilatation (hyperemia) • Increased permeability – DISTINCT PHASES • immediate transient • prolonged response • delayed response

• Exudation of fluid (transudate & exudate) • Changes in blood flow rate • Changes in lymphatic flow

CELLULAR RESPONSE • • • • • • •

Types of cells involved Margination of neutrophils ( rouleaux ) Pavementing of neutrophils Emigration of neutrophils Chemotactic factors ( C5A & leukotriene B4 ) Movement of other cells ( diapedesis ) Phagocytosis – ) recognition ( opsonization ) – engulfment – microbial killing ( macrophage activating factor

Chemical Mediators of acute inflam • • • • • • • • • • •

Specific Mediators vasoactive amines ( histamine & serotonin ) kinin system ( bradykinin & kallikrein ) coagulation cascade ( Hageman factor ) complement system ( C5a & C3a ) arachidonic acid metabolites ( prostaglandin ) neutrophilic factors ( platelet activating factor ) cytokines & chemokines nitric oxide lysosomal constituents of leukocytes oxygen-derived free radicals

Chemical Mediators of acute inflam • • • • • • • • • •

Triple response (Thomas Lewis) red line red flare wheal Systemic Clinical Signs fever ( pyrogens & prostaglandin ) Changes in peripheral WBC count- neutrophil leukocytosis Changes in plasma protein levels- increased ESR TABLE - Summary for Chemical mediators TABLE - Role of Mediators in diff rexns of inflammation

Course (outcomes) of acute inflammation • Resolution • Repair - regeneration, fibrosis , scar – liquefactive necrosis • suppurative inflam • pus • abscess

• Immune response - chronic inflammation

Differences between exudates & transudates • • • • • • • •

Vascular permeability : T- normal E - increased Protein content : T - 0-1.5 g/dl E - 1.5- 6g/dl Protein types: T- albumin E - albumin, globulins, complements Fibrin: T - no E - yes Specific gravity: T - 1.010 - 1.015 E - 1.015 - 1.027 Cells: T- none E - inflammmatory Causes: T - cirrhosis of the liver, constrictive pericarditis E - bacterial peritonitis , tuberculous peritonitis

Types of Acute Inflammation

• Serous inflammation • F: marked fluid exudation • C: burns, bacterial infections • Fibrinous inflammation • F: excess fibrin formation • C: virulent bacterial infections • Suppurative inflammation • F: exaggerated neutrophil response & liquefactive necrosis • C: pyogenic bacteria as staphylococci • Ulcer • a local defect or excavation of the surface of

Chronic Inflammation • • • •

Causes of chronic inflammation persistent infections prolonged exposure to potentially toxic drugs autoimmunity – chronic inflammatory cells

• • • •

Morphologic features infiltration with mononuclear cells tissue destruction healing by connective tissue replacement of damaged tissues

Morphologic types of chronic inflammation – Granulomatous chronic inflammation • characteristic features: – epitheloid cell granulomas – langhans type giamt cell

• causes: MIF & MAF • changes in affected areas: form large masses

– Nongranulomatous chronic inflammation characteristic features: scattered diffusely causes: chronic viral infxs , chronic autoimmune dse chronic chemical intoxication, chronic nonviral infx , chronic metazoan infx

Chronic Inflammation • CHRONIC INFLAMMATION IN RESPONSE TO NONANTIGENIC INJURIOUS AGENT – FOREIGN BODY GRANULOMA

• FUNCTION & RESULT OF CHRONIC INFLAMMATION – TISSUE NECROSIS ( serious clinical illness ) – ASSOCIATED FIBROSIS ( contribute to the disease )

• MIXED ACUTE & CHRONIC INFLAMMATION – CHRONIC SUPPURATIVE INFLAMMATION – RECURRENT ACUTE INFLAMMATION