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Pathology of inflammation. د هبة احمد غيدان LEC 3. OUTCOMES OF ACUTE INFLAMMATION In general, acute inflammation may have one of three outcomes: 1- Complete resolution 2- Healing by fibrosis 3- Progression to chronic inflammation. 1- Complete resolution
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Pathology of inflammation د هبة احمد غيدان LEC 3
OUTCOMES OF ACUTE INFLAMMATION In general, acute inflammation may have one of three outcomes: 1- Complete resolution 2- Healing by fibrosis 3- Progression to chronic inflammation
1- Complete resolution • The battle between the injurious agent and the host may end with restoration of the site of acute inflammation to normal. This is called resolution and is the usual outcome when a. the injury is limited or short-lived b. there has been little tissue destruction c. the damaged parenchymal cells can regenerate
2- Healing by fibrosis • This occurs a. after extensive tissue destruction b. when the inflammatory injury involves tissues that are incapable of regeneration c. when there is abundant fibrin exudation. • When the fibrinousexudate in tissue or serous cavities (pleural, peritoneal, synovial) cannot be adequately cleared, connective tissue grows into the area of exudate, converting it into a mass of fibrous tissue—a process also called organization.
3- Progression to chronic inflammation • Acute to chronic transition occurs when the acute inflammatory response persists, • owing either to the perseverance of the injurious agent or to some interference with the normal process of healing. For example, failure of acute bacterial pneumonia to resolve may lead to extensive tissue destruction and formation of a cavity in which the inflammation continues, leading eventually to a chronic lung abscess then may lead to a chronic lung abscess.
Chronic inflammation: • It is inflammation of prolonged duration (weeks to months to years) in which active inflammation, tissue injury, & healing proceed ocurr simultaneously & characterized by followings: 1. Infiltration of chronic inflammatory cells (Macrophages, lymphocytes, & plasma cells). 2. Tissue destruction by the inflammatory cells. 3. Repair, involving new blood vessel proliferation (angiogenesis) & fibrosis.
Causes of chronic inflammation: 1.Viral infections: these infections require lymphocytes & macrophages to identify & eradicate. 2. Persistent microbial infections: like T.B, Treponemapallidum (syphilis), & fungi. 3. Prolonged exposure to potentially toxic agents: Like inhaled silica (non degradable exogenous substance) which causes silicosis of lung, & plasma lipid (endogenous substance) which is the important cause of atherosclerosis. 4. Autoimmune diseases: means individual develop immune to self antigens like rheumatoid arthritis.
Types of chronic inflammation: 1.Progression from acute inflammation…. Mainly due to persistent underlying causative cause & abscess formation. 2. Following recurrent attacks of acute inflammation (subacutecholecystitis), which progress to chronic cholecystitis. 3. From beginning it is start as chronic inflammation e.g. Tuberculosis.
Cells of chronic inflammation: 1. Macrophages: • -They are tissue cells that are derived from circulating blood monocytes. • Normally distributed in most of connective tissues & in many organs • IN liver…….. Kupffer cells • In lymph node & spleen ………. Sinus histiocytes, • In CNS…….. called microglial cells • In lungs…….. alveolar macrophages.
At the site of inflammation the main function of macrophages is phagocytosis. while in certain type of chronic inflammation macrophages become activated (become large in size, increased content of lysosomal enzymes, less phagocytosis), this activated macrophages are called Epithelioid macrophages. • Activators of macrophages: Gamma interferon, bacterial toxins, extracellular proteins (fibronectin). Sometime in certain chronic inflammation fusion of epithelioid cells will resultin formation of giant multinucleated cells (like in T.B Sarcoidosis).
2. Lymphocytes: Both T &B lymphocytes migrate into inflammatory sites & then they produced lymphokines & gamma interferon which are the major activator of macrophages. 3. Plasma cells:they produce immunoglobulins. 4. Eosinophils: (in parasitic infections & allergic diseases). 5. Mast cells & basophils: produce histamine (important in both acute & chronic inflammation). 6. Fibroblasts: responsible for fibrosis of chronic inflammation.
Chronic Granulomatous inflammation: • Is a distinctive type of chronic inflammation characterized by formation of Granuloma ( which is aggregates of Epithelioid cells surrounded by a rim of lymphocytes). • Causes of Granuloma: 1. Bacterial causes: Tuberculosis, leprosy, syphilis). 2. Parasitic causes: Schistosomiasis. 3. fungal causes: Histoplasmosis, cryptococccusneoformans. 4. Inorganic metals or dusts: Silicosis, Berylliosis. 5. Foreign body: suture material, breast prosthesis. 6. Unknown:Sarcoidoisis.
Granuloma:Is an aggregation of activated modified macrophages (epithelioid) cells surrounding by a cuff (rim) of lymphocytes & fibroblasts (only in older granulomas) • If the center of granuloma is contain necrotic area , this called caseatinggranuloma ( necrotizing granuloma) • Necrosis within the granuloma is mainly seen in T.B granuloma • Some of granuloma contains multinucleated giant cells by union of epithelioid cells especially in presence of undigested material like suture material & T.B. • Epithelioid cells in usual H & E preparations appear squamous like cells with pink granular cytoplasm with indistinct cell boundaries.
Giant cells are formed by fusion of epithelioid cells & consist of large mass of cytoplasm with multiple nuclei & are of two types: 1. Foreign body giant cells: have irregular distributed nuclei. 2. Langhans giant cells: nuclei are arranged at the periphery of cytoplasm as horse shoe appearance. Types of granulomas: 1. Foreign body granuloma: induces by inert substances. 2. Immune granuloma: induced by type IV hypersensitivity reaction (like in tuberculosis).
