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Systemic Lupus Erythematosus (SLE) - Coggle Diagram
Systemic Lupus Erythematosus (SLE)
Altered Physiology
Genetic & Environmental Factors
contributes to loss of immune self-tolerance
Genetic Predispositions
HLA gene variants
Compliment deficiencies (C1q, C2, C4)
Environmental Triggers
UV radiation
Infection
Drugs
Hormonal influences (estrogen)
Immune System Dysregulation
Impaired Clearance of apoptotic cells
Accumulation of nuclear antigens
B-cell hyperactivity
Production of autoantibodies
Anti-dsDNA
Anti-Smith
ANA
T-cell dysfunction
Abnormal immune signalling
Immune Complex Formation
Antibodies and self-antigens
Immune complexes
Immune complexes deposit in tissues
Activates the compliment system
Inflammatory cytokine release
Chronic Inflammation
Compliment activation
Recruitment of neutrophils and macrophages
Inflammatory mediators
tissue injury and organ damage
Multi-System Tissue Damage
Vasculitis
Connective tissue destruction
Organ dysfunction
Multi-System Alterations in Function
Skin
Immune complex deposition in dermis leads to inflammation of small vessels resulting in:
Malar (butterfly) rash
Photosensitivity
Discoid lesions
Musculoskeletal System
Autoimmune inflammation of synovium resulting in:
Joint pain
Non-erosive arthritis
Joint stiffness
Renal System
Immune complexes deposit in glomeruli leading to compliment activation resulting in:
Lupus nephritis
Proteinuria
Hematuria
Reduced kidney function
Cardiovascular System
Chronic inflammation of blood vessels and heart tissue resulting in:
Pericarditis
Accelerated atherosclerosis
Increased cardiovascular risk
Nervous System
Autoantibodies and vascular injury resulting in:
Seizures
Cognitive dysfunction
Mood disorders
Headaches
Hematologic System
Autoantibodies target blood cells resulting in:
Hemolytic Anemia
Leukopenia
Thrombocytopenia
Clinical Manifestations
Constitutional Symptoms
Inflammation and immune activation
Fatigue
Fever
Weight loss
Dermatologic Manifestations
Immune complex deposition in skin
Malar Rash
Photosensitivity
Discoid lesions
Musculoskeletal Manifestations
Joint pain
Joint swelling
Morning stiffness
Renal Manifestations
Proteinuria
Hypertension
Edema
Progressive kidney damage
Neurologic Manifestations
Headaches
Seizures
Cognitive impairment
Depression and anxiety
Hematologic Manifestations
Anemia
Leukopenia
Thrombocytopenia
Treatment Modalities
Goal: Reduce immune activation, control inflammation, and prevent organ damage
Anti-Inflammatory Therapy: NSAIDs
Mechanism
Inhibits prostaglandin synthesis
Reduces pain and inflammation
Used for mild joint and musculoskeletal symptoms
Antimalarial Drugs: Hydroxychloroquine
Mechanism
Modulates immune signaling
Reduces autoantibody production
Benefits
Decreases disease flares
Protects organs
Corticosteroids
Mechanism
Suppresses inflammatory cytokines
Reduce immune activity
Used for: Moderate to severe disease and acute flares
Immunosuppressive Therapy
Examples: Methotrexate, Azathioprine, Mycophenolate
Mechanism: Suppresses B- and T-cell activity
Used for: Organ-threatening disease (kidney, CNS)
Biologic Therapy
Example: Belimumab
Mechanism: Inhibits B-cell activating factor (BAFF)
Result: Decreased autoantibody production
Supportive Management
Lifestyle and prevention strategies
Sun protection
Cardiovascular risk reduction
Monitoring kidney function
Infection prevention