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Systemic lupus erythematosus - Coggle Diagram
Systemic lupus erythematosus
Multi-system alterations
Type 3 hypersensitivity: primary pathway: antibodies bind to antigens, creating a complex that deposits in vessel walls and activating the complement system.
These complexes depositing into vessel walls trigger neutrophils to degrannulate which causes tissue damage and further inflammation. This process happens all over the body, causing irritation and inflammation system wide
Complexes deposit in kidneys, joints, and blood vessels most commonly, causing inflammation, scarring, damage, and loss of function in affected tissues
Type 2 and 4 hypersensitivities: concurrently active but less engaged. Type 2 causes hemolytic anemia and thrombocytopenia. Type 4 uses T cells to amplify organ inflammation and damage
Clinical Manifestations
Cardiovascular: increased atherosclerosis, increased clotting, anemia, leukopenia, thrombocytopenia, endocarditis, myocarditis, pericarditis, vasculitis, raynaud's syndrome
Lungs: pleuritis, pulmonary effusions, pulmonary hypertension, pneumonitis, interstitial lung disease
Neurologic: brain fog, confusion, trouble concentrating, fatigue, memory loss, trouble expressing thoughts, carpal tunnel syndrome, loss of vision, tinnitus, dizziness, facial droop, numbness, tingling, myelitis, stoke, seizures
Skin: butterfly rash, hair loss, mouth/nose sores
Kidneys: lupus nephritis, kidney failure, lupus cystitis, frequent UTIs
Musculoskeletal: arthritis, joint swelling/pain/stiffness, osteoporosis, osteopenia, myalgia
Treatments
Immunosuppressants/anti-inflammatories: steroids, NSAIDs, antimalarials, ACTH gels
Symptom management: pain medications, antidepressants, meds to counteract symptoms caused by core medication regimen
Damage prevention: aspirin, anticoagulants, anti-hypertensives, statins, calcium, vitamin D supplements
Altered physiology
Risk factors: genetic, hormonal (estrogen), immunological, triggering environmental event (pregnancy, surgery, stress, UV light exposure)
Apoptotic cells not efficiently phagocytized by macrophages
Internal proteins and nuclear material displayed on surface of apoptotic cells
Immune system becomes sensitized and launches a response to unphagocytized apoptotic cells
Inflammation causes more cells to be damaged and undergo apoptosis, continuing the cycle
Inflammation reduces via intrinsic regulation until a trigger causes increased apoptosis, triggering a flare