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
• rubor
• calor
• tumor
• dolor
• functio laesa
• 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
