inflammation

Acute and chronic inflammation: 

Acute and chronic inflammation RAVINDER NAIK DHARAVATH PHARMACOLOGY AND TOXICOLOGY NIPER-AHMEDABAD

INFLAMMATION :: 

INFLAMMATION : Immediate and early response to tissue injury (physical, chemical, microbiologic, etc. ) It is body defence reaction in order to eliminate or limit the spread of injurious agent as well as to remove the consequent necrotised cells and tissues

Types of inflammation: 

Types of inflammation Acute inflammation Chronic inflammation

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Functions of Inflammation 1. Destroy and remove pathogens 2. If destruction is not possible, to limit effects by confining the pathogen and its products. 3. Repair and replace tissue damaged by pathogen and its products.

Beneficial effects :: 

Beneficial effects : Dilution of toxins Entry of antibodies Transport of drug to the site of action Fibrin formation Delivery of nutrients and oxygen Stimulation of immune response

Causative Agents :: 

Causative Agents : Physical agents : - heat, cold, radiation, mechanical trauma Chemical agents : -Organic & Inorganic poisons Infective agents : -Bacteria, Viruses, and Toxins Immunological agents : -Cell mediated &antigen-antibody reactions

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LOCAL MANIFESTATIONS

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Fever Chills Myalgia Malaise ACUTE INFLAMMATION SYSTEMIC MANIFESTATIONS

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Vasoconstriction Vasodilation Increased vascular permeability Hemoconcentration and stasis Leukocyte Adhesion Transmigration Chemotaxis Aggregation Phagocytosis ACUTE INFLAMMATION STEPS INVOLVED IN INFLAMMATION

Process of Inflammation: 

Process of Inflammation

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ACUTE INFLAMMATION VASODILATION

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Normal flow Stasis ACUTE INFLAMMATION HEMOCONCENTRATION AND STASIS

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ACUTE INFLAMMATION LEUKOCYTE ADHESION

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ACUTE INFLAMMATION EMIGRATION ( TRANSMIGRATION )

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ACUTE INFLAMMATION CHEMOTAXIS

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ACUTE INFLAMMATION AGGREGATION

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ACUTE INFLAMMATION PHAGOCYTOSIS - ENGULFMENT

Chemical mediators of inflammation: 

Chemical mediators of inflammation Cell derived chemical mediators -Mast cells, Basophils , platelets 1.Lysosomal enzymes - tissue damage 2.platelet activate factors - Permeability 3.Prostaglandins – Vasodilatation 4.Leukotrienes – increased Permeability 5.Cytokines - fever 6.Nitric oxide &oxygen metabolites –tissue damage

Contd….: 

Contd …. Plasma derived Clotting & fibrinolytic system 2. Kinin system Complement system

Fate of A.I.: 

Fate of A.I. Resolution Healing by scarring Suppuration Chronic inflammation

Chronic inflammation: 

Chronic inflammation reasons: persisting infection or prolonged exposure to irritants (intracell. surviving of agents - TBC) repeated acute inflamations (otitis, rhinitis) primary chronic inflammation - low virulence, sterile inflammations (silicosis) autoimmune reactions (rheumatoid arthritis, glomerulonephritis, multiple sclerosis)

Causes :: 

Causes : Followed by A.I. Ex: Osteomylities,pneumonia Recurrent attack of A.I. Ex: A.I. of gall bladder C.I. Starting de novo Ex : tuberculosis

Cells involved :: 

Cells involved : Lymphocytes Plasma cells Eosinophils Mast cells

SYMPTOMS :: 

SYMPTOMS : Fever Anaemia Leucocytosis ESR Amyloiclosins

Types of C.I. : 

Types of C.I. Non specific Ex:chronic osteomylitis , chronic ulcer Specific Ex: T.B. Syphilis

DIAGNOSIS :: 

DIAGNOSIS : Blood test X – ray Laproscopy Endoscopy Morphological changes of perticular body part

Complications : 

Complications A.I. can be lead to C.I. Surrounding tissue damage Pain persisting for long time

Treatment : 

Treatment NSAIDS STEROIDAL DRUGS

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