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CHRONIC INFLAMMATION
- 1. CHRONIC INFLAMMATION DR. ABHISHEK ANAND MDPATHOLOGY ASST. PROF. 3rd Class
- 2. CHRONIC INFLAMMATION Chronic inflammationis inflammation of prolonged duration (weeks or months) in which inflammation, tissue injury and attempts at repair coexist. Chronic inflammation is defined as prolonged process in which tissue destruction and inflammation occur at same time.
- 3. CAUSES OF CHRONICINFLAMMATION • CHRONIC INFLAMMATION FOLLOWING ACUTE INFLAMMATION • PERSISTANT INFECTION • HYPERSENSITIVE DISEASES • PROLONGED EXPOSURE TO TOXIC AGENTS OTHERS- • ALZHEIMER DISEASE • METABOLIC SYNDROME • ASSOCIATED TYPE 2 DIABETES
- 4. CAUSES OF CHRONICINFLAMMATION I. ACUTE INFLAMMATION SOMETIMES TERNS INTO PROLONGED INFLAMMATION. II. PERSISTENT INFECTIONS BY MICROORGANISMS (MYCOBACTERIA, VIRUS, PARASITE). III. HYPERSENSITIVITY DISEASES WHICH IS EXCESSIVE AND INAPPROPRIATE ACTIVATION OF THE IMMUNE SYSTEM (AUTOIMMUNE DISEASES)
- 5. IV. PROLONGED EXPOSURETO TOXIC AGENTS. a. Silica results in an inflammatory lung disease called silicosis. b. Atherosclerosis a chronic inflammatory process of the arterial wall induced by excessive production and tissue deposition of endogenous cholesterol and other lipids.
- 6. GENERAL FEATURES MONONUCLEAR CELLINFILTRATION TISSUE DESTRUCTION/NECROSIS PROLIFERATIVE CHANGES FIBROSIS ANGIOGENESIS (FORMATION OF NEW BLOOD VESSELS)
- 7. MORPHOLOGIC FEATURES • Infiltrationwith mononuclear cells which include macrophages, lymphocytes and plasma cells • Tissue destruction induced by the persistent offending agent or by the inflammatory cells • Attempts at healing by connective tissue replacement of damaged tissue by fibrosis & angiogenesis (small blood vessels)
- 8. MEDIATORS OF CHRONICINFLAMMATION • MACROPHAGES • LYMPHOCYTES • EOSINOPHILS • MAST CELLS • NEUTROPHILS
- 10. ROLE OF MACROPHAGES •The dominant cells in chronic inflammatory reactions are macrophages • Contribute to the reaction by secreting cytokines and growth factors That act on various cells by destroying foreign bodies and tissues. • Macrophages are professional phagocytes. • Function as effector cells that eliminate microbes in cellular
- 11. THERE ARE TWOMAJOR PATHWAYS OF MACROPHAGE ACTIVATION • CLASSICAL PATHWAY • ALTERNATIVE PATHWAY
- 12. ROLE OF LYMPHOCYTES •Microbes and other environmental antigens activate T and B lymphocytes which amplify chronic inflammation. • By their ability to secrete cytokines, CD4+ T lymphocytes • Promote inflammation and influence the nature of the inflammatory reaction
- 13. OTHER CELLS INCHRONIC INFLAMMATION EOSINOPHILS- • Abundant in immune reactions mediated by IgE and parasitic infections • Eosinophils have granules that contain major basic protein; that is toxic to parasites • Also injures host epithelial cells.
- 14. MAST CELLS- • Widelydistributed in connective tissues • Participate in both acute and chronic inflammatory reactions Neutrophils are characteristic of acute inflammation but many forms of chronic inflammation lasting for months.
- 15. TYPES OF CHRONICINFLAMMATION 1. CHRONIC GRANULOMATOUS INFLAMMATION it is characterized by formation of granuloma e.g. tuberculosis, syphilis, actinomycosis 2. CHRONIC NON SPECIFIC INFLAMMATION it is characterised by non specific cell infiltration e.g. lung abscess , osteomyelitis
- 16. GRANULOMATOUS INFLAMMATION • Distinctivepattern of chronic inflammation characterized by formation of granulomas. • CHARACTERIZED PRESENCE OF ◦ ACTIVATED MACROPHAGES ◦ LYMPHOCYTES ◦ OCCASIONAL PLASMA CELLS
- 17. • The activatedmacrophages develop abundant cytoplasm and resemble epithelial cells and are called epithelioid cells. • Some activated macrophages may use forming multinucleate giant cells.
- 21. GRANULOMA TYPES: • THEREARE TWO TYPES OF GRANULOMAS: I. Foreign body granuloma: Granuloma forms due to inert foreign bodies like suture material, silica. II. Immune granuloma: Granuloma forms due to agents that are capable of inducing a persistent T cell– mediated immune response. E.g. Granuloma in Tuberculosis.
- 22. WHAT IS CASEOUSNECROSIS • Caseous necrosis is found in tubercular granuloma. • Caseous necrosis is granular, cheesy appearance. • Microscopically caseous necrosis is eosinophilic, amorphous, granular.
- 24. EXAMPLES OF DISEASESWITH GRANULOMATOUS INFLAMMATION I. TUBERCULOSIS (CASEOUS NECROSIS PRESENT). II. SARCOIDOSIS . III. SYPHILIS. IV. CAT SCRATCH DISEASE. V. CROHN’S DISEASE.
- 25. TUBERCULOSIS • TUBERCULOSIS ISCAUSED BY MYCOBACTERIUM TUBERCULOSIS • PRIMARY TUBERCULOSIS ◦ USUALLY SEEN IN CHILDREN ◦ DUE TO INITIAL (FIRST) INFECTION • SECONDARY TUBERCULOSIS ◦ SEEN IN ADULTS ◦ REACTIVATION OF PRIMARY INFECTION
- 26. • FOCUS OFTUBERCULOUS INFLAMMATION ◦ WHITE COLORED LESION ◦ ROUND OR IRREGULAR BORDERS ◦ CENTRAL NECROSIS (CASEATION) ◦ SOFT, GRANULAR, CHEESY MATERIAL
- 28. This section showinga granuloma with central caseation necrosis surrounded of lymphocytes, epithelioid cells and giant cells
- 29. ALL GRANULOMATOUS INFLAMMATIONIS CHRONIC INFLAMMATION BUT ALL CHRONIC INFLAMMATION IS NOT GRANULOMATOUS INFLAMMATION
- 30. GIANT CELLS • GIANTCELLS ARE LARGE CELLS WITH MORE THAN ONE NUCLEUS. • PHYSIOLOGICAL GIANT CELLS: MEGAKARYOCYTES, SYNCYTIOTROPHOBLAST. • PATHOLOGICAL GIANT CELLS: LANGHANS GIANT CELLS (TUBERCULOSIS), FOREIGN BODY GIANT CELLS, TUMOR GIANT CELL (REED-STERNBERG CELL)
- 31. A Langshan's giantcell A foreign body giant cell
- 32. SYSTEMIC EFFECT OFINFLAMMATION • FEVER • ACUTE PHASE PROTEIN: C-REACTIVE PROTEIN (CRP), FIBRINOGEN. • LEUKOCYTOSIS • INCREASED PULSE • INCREASED BLOOD PRESSURE • DECREASED SWEATING • RIGORS (SHIVERING)
- 33.