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Pathopysiology of Sle
Pathopysiology of Sle
Disordered T-cell function (cellular immune response) Hyperactivity of B cells (humora response) Production of a large variety of autiantibodies against normal body components (nucleic acid, erythrocytes, coagulation protein, lymphocytes & platelets) SLE auto-antibodies react with corresponding antigen forming immune complex
SLE auto-antibodies deposited in the connective tissues of blood vessels, lymphatic and other tissues The deposits trigger inflammatory response leading to local tissue damage
Affects kidneys, MS system, brain, heart, spleen, lungs, GI, skin and peritoneum
Manifestations: mimics RA: fever, anorexia, malaise, weight loss, multiple arthralgias and symmetric polyarthritis; butterfly rash, photosensitivity, discoid lesion, hives, alopecia, mucous membrane ulceration, enlarged glands, edema in the legs and around the eyes, pale cyanotic fingers and toes Other Effects: Kidneys: proteinuria, cellular casts Nephrotic Syndrome & Renal Failure Hematologic: Leukopenia, Anemia and thrombocytopenia Cardiovascular: Pericarditis, vascilitis & Raynauds phenomenon Pulmonary: Pleurisy, Pleural Effusion & Lupus Pneumonitis