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Pathophysiology of Sle: Precipitating Factors: Environmental Drug-Induced Infection
Pathophysiology of Sle: Precipitating Factors: Environmental Drug-Induced Infection
Female producing estrogen First generation familial possession of Infectious agents n the body
influencing SLE DNA
Spontaneous
occurrence of SLE
activation.
Defective B-cell
Impaired membrane integrity of dendritic Presented to T-cells activation by
cells autoantigens
Various
Autoantibody Autoreactive cytotoxic T-cell activation Negative abnormal B-
productions cell contribution to
already deficient
immune system.
Inflammation of the affected system
Production of Anti-Nuclear Systemic Lupus Erythematosus
Antibodies (ANA) in renal
Serositis
Elevated intracranial pressure
Management and If not treated: Management and If not treated:
treatment: -Further inflammation treatment: -Progressive
-Immunosuppressive -Infection and -Immunosuppressive intracranial
drugs deterioration of drugs pressure.
-Non-steroidal anti- myocardial and -Non-steroidal anti- -Deterioration of
inflammatory drugs. pleural linings. inflammatory drugs. cerebral functions
-Lung Collapse -Multiple system
-Cardiac tamponade failure.
-Chronic constrictive
pericarditis.
-Congestive Heart
Failure.
Production of specific ANA in gastric cells Inflammatory response around the liver cells
Non-neurologic sites of damage include the renal glomeruli, joints, pleural or pericardial
serosa, integument, cardiac or vascular endothelium, cardiac valves, and the oral and
conjunctival mucosa. Multiple sites may be involved within the nervous system.