Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by tissue damage caused by autoantibodies and immune complexes. SLE primarily affects women and has a variety of clinical manifestations that can mimic other conditions, making diagnosis difficult. Both genetic and environmental factors contribute to SLE. The disease involves abnormal apoptosis, impaired clearance of dead cells, and production of autoantibodies that form immune complexes and cause tissue injury. Diagnosis is based on identifying a certain number of clinical criteria.
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Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by tissue damage caused by autoantibodies and immune complexes. SLE primarily affects women and has a variety of clinical manifestations that can mimic other conditions, making diagnosis difficult. Both genetic and environmental factors contribute to SLE. The disease involves abnormal apoptosis, impaired clearance of dead cells, and production of autoantibodies that form immune complexes and cause tissue injury. Diagnosis is based on identifying a certain number of clinical criteria.
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by tissue damage caused by autoantibodies and immune complexes. SLE primarily affects women and has a variety of clinical manifestations that can mimic other conditions, making diagnosis difficult. Both genetic and environmental factors contribute to SLE. The disease involves abnormal apoptosis, impaired clearance of dead cells, and production of autoantibodies that form immune complexes and cause tissue injury. Diagnosis is based on identifying a certain number of clinical criteria.
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Download as PPTX, PDF, TXT or read online from Scribd
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by tissue damage caused by autoantibodies and immune complexes. SLE primarily affects women and has a variety of clinical manifestations that can mimic other conditions, making diagnosis difficult. Both genetic and environmental factors contribute to SLE. The disease involves abnormal apoptosis, impaired clearance of dead cells, and production of autoantibodies that form immune complexes and cause tissue injury. Diagnosis is based on identifying a certain number of clinical criteria.
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SYSTEMIC LUPUS
ERYTHEMATOSUS ARUN A VIII Term General Overview SLE is an autoimmune disease in which organs, tissues, and cells undergo damage mediated by tissue-binding autoantibodies and immune complexes. Characterized by wide variety of clinical features and diverse antibody production. SLE is one of several diseases known as "the great imitators" because it often mimics or is mistaken for other illnesses SLE symptoms vary widely and come and go unpredictably Diagnosis can thus be elusive Aetiology 90% cases are Women with peak in 2nd and 3rd Decade. There is no one specific cause of SLE. There are, however, a number of environmental triggers and a number of genetic susceptibilities. Genetics-HLA region on chromosome 6, IRF5, PTPN22, STAT4[27], CDKN1A,[28] ITGAM, BLK[27], TNFSF4 and BANK1 Environment-Extreme stress, exposure to sunlight,UV radiation, hormones, and infections Drug-induced lupus mimics SLE Procainamide, hydralazine, quinidine, and phenytoin. Non-SLE forms of lupus-Discoid (cutaneous) lupus is limited to skin symptoms and is diagnosed by biopsy of rash on the face, neck, or scalp. Pathophysiology Chronic inflammatory disease believed to be a type III hypersensitivity response with potential type II involvement The exact mechanisms for the development of SLE are still unclear. In SLE, the body's immune system produces antibodies particularly against proteins in the cell nucleus Impaired clearance of dying cells+ increased apoptosis. Pathophysiology Apoptosis- * Apoptosis is increased in monocytes and keratinocytes * Expression of Fas by B cells and T cells is increased Antigens near or in cell surfaces probably released due to apoptosis activate the immune system to produce autoantibodies Steps of Immune Complex mediated tissue destruction (1) sequestration and destruction of Ig- coated circulating cells (2) fixation and cleaving of complement proteins (3) release of chemotaxins, vasoactive peptides, and destructive enzymes into tissues Autoantibodies of SLE ◦ Antinuclear antibodies ◦ Anti-dsDNA ◦ Anti-Sm ◦ Anti-RNP ◦ Anti-histone ◦ Anti-phospholipid ◦ Anti-platelet ◦ Anti-ribosomal ◦ Pathology Skin-Deposition of Ig at the dermal- epidermal junction (DEJ), injury to basal keratinocytes, and inflammation dominated by T lymphocytes in the DEJ and around blood vessels and dermal appendages Lupus nephritis Histologic abnormalities in blood vessels are not specific for SLE: leukocytoclastic vasculitis is most common Lymph node biopsies show nonspecific diffuse chronic inflammation. DIAGNOSTIC CRITERIA
Malar rash Fixed erythema, flat or raised,
Discoid rash over the malarcircular Erythematous eminences raised Photosensitivity patches Exposure with adherent keratotic to ultraviolet light Oral ulcers scaling and oralfollicular causes rash Includes plugging; and nasopharyngeal Arthritis atrophic ulcers, scarring observed Nonerosive may by arthritis ofoccur physician two or more peripheral joints, with tenderness, swelling, or effusion Serositis Pleuritis or pericarditis Renal disorder documented by ECG Proteinuria >0.5 g/d oror≥3+, rub or or Neurologic disorder evidence cellular of psychosis Seizurescasts or effusion without Hematologic disorder other causesanemia or leukopenia Hemolytic Immunologic disorder lymphopenia Anti-dsDNA, or anti-Sm, and/or Antinuclear antibodies thrombocytopenia anti-phospholipid An abnormal titer ofin ANA the absence by of offending drugs in the immunofluorescence absence of drugs known to induce ANAs
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