Rheumatology

A

• Acute Gout Flare - Treatment Algorithm

  Treat acute gout with monotherapy at appropriate anti inflammatory doses using NSAID, colchicine, or steroid; avoid starting urate lowering therapy during the flare unless already on it.
• Adult‑Onset Still Disease — Treatment Escalation (IL‑1/IL‑6)

  Inflammatory syndrome with quotidian fevers, evanescent salmon rash, and arthritis; ferritin often very high. Treat with NSAIDs/steroids; early IL‑1/IL‑6 inhibitors for steroid‑sparing; monitor for MAS.
• ANCA Vasculitis - Pulmonary Renal Syndrome Initial Management

  ANCA-associated vasculitis with pulmonary-renal syndrome is an organ-threatening emergency characterized by rapidly progressive glomerulonephritis with or without diffuse alveolar hemorrhage. Immediate care requires confirmation of kidney and lung involvement, exclusion of infection and anti-GBM disease, and prompt induction immunosuppression with glucocorticoids plus rituximab or cyclophosphamide. Plasma exchange is reserved for selected high-risk situations rather than routine use in every patient.
• Antiphospholipid Syndrome — Diagnosis & Anticoagulation

  APS requires clinical events (thrombosis or pregnancy morbidity) plus persistent aPL antibodies ≥12 weeks apart. Treat with anticoagulation (warfarin preferred for high‑risk) and manage pregnancy with LMWH + aspirin.

C

• Calcium Pyrophosphate Disease - Acute Arthritis Management

  Acute calcium pyrophosphate crystal arthritis causes abrupt inflammatory monoarthritis or oligoarthritis, often of the knee or wrist, and can closely mimic gout or septic arthritis. Arthrocentesis with crystal analysis and culture is the key diagnostic test when infection is possible. Acute therapy uses joint aspiration, intra-articular glucocorticoid, NSAID, colchicine, or short systemic glucocorticoid treatment chosen according to comorbidity.

G

• Giant Cell Arteritis - High Dose Steroids and Vision Protection

  Giant cell arteritis is a large-vessel vasculitis in adults older than 50 that can cause irreversible visual loss, stroke, and aortic complications. New visual symptoms, amaurosis fugax, diplopia, or ischemic optic neuropathy require immediate glucocorticoid treatment before diagnostic confirmation. Diagnosis integrates inflammatory markers, temporal artery biopsy and/or vascular imaging, and clinical features such as new headache, scalp tenderness, jaw claudication, polymyalgia rheumatica, and constitution
• Giant Cell Arteritis — High-Dose Glucocorticoids, Temporal Artery Biopsy, and Steroid-Sparing

  Age ≥50 with new headache, scalp tenderness, jaw claudication, or visual symptoms. Start high‑dose glucocorticoids immediately to prevent vision loss; confirm with temporal artery biopsy or vascular imaging; consider tocilizumab or methotrexate as steroid‑sparing agents and monitor for large‑vessel involvement.
• Giant Cell Arteritis — Immediate High‑Dose Steroids, Biopsy/Imaging, and Vision Protection

  In patients ≥50 with headache, scalp tenderness, jaw claudication, or visual symptoms, start high‑dose glucocorticoids immediately to prevent vision loss, then confirm with temporal artery biopsy (within 1–2 weeks) or vascular imaging. Consider steroid‑sparing tocilizumab in relapsing disease.
• Giant Cell Arteritis — Rapid Steroids, Imaging/Biopsy, and Vision Protection

  Age ≥50 with new headache, scalp tenderness, jaw claudication, or vision symptoms. Start high‑dose glucocorticoids immediately to protect vision; obtain temporal artery biopsy within 1–2 weeks and consider vascular imaging; add tocilizumab in selected patients.
• Gout - Urate Lowering Therapy Initiation and Titration

  Urate-lowering therapy prevents recurrent gout by maintaining serum urate below the crystallization threshold. Allopurinol is preferred first-line for most patients, including many with chronic kidney disease, and should be started low then titrated to a serum urate target below 6 mg/dL. Anti-inflammatory prophylaxis with colchicine, NSAID, or glucocorticoid is used during initiation because mobilization flares are common.
• Gout — Treat‑to‑Target Urate‑Lowering Therapy

  Chronic gout requires urate‑lowering therapy to a serum urate target <6 mg/dL (<5 if tophaceous). Allopurinol is first‑line for all CKD stages; use prophylaxis during initiation and escalate doses as needed.
• Gout Flare — ED Treatment

  An acute gout flare is intense crystal-driven inflammatory arthritis that is treated rapidly with an NSAID, colchicine, or glucocorticoid selected for the patient's comorbidities. The main emergency diagnostic challenge is not mistaking septic arthritis for gout; atypical or first presentations often require arthrocentesis, and chronic urate-lowering therapy should generally be continued rather than stopped during a flare.

H

• Hypermobility Spectrum Disorders — Evaluation & Management

  Generalized joint hypermobility becomes a disorder when it causes pain, instability, injury, or functional limitation. Confirm the pattern clinically, exclude alternative heritable or inflammatory disease when indicated, and emphasize progressive strength, proprioception, pacing, and joint protection rather than repeated immobilization or end-range manipulation.

I

• IgG4‑Related Disease — Multiorgan Presentation & Management

  Systemic fibroinflammatory condition affecting pancreas, biliary tree, salivary glands, kidneys, etc. Characterized by tumefactive lesions, storiform fibrosis, and elevated IgG4+ plasma cells. Treat with glucocorticoids and consider rituximab for relapse or maintenance.
• Inflammatory Myositis - Initial Workup

  Idiopathic inflammatory myopathy presents with subacute symmetric proximal weakness, often with elevated muscle enzymes and characteristic autoantibodies, MRI, EMG, biopsy, or dermatomyositis skin findings. Initial workup must identify dysphagia, respiratory muscle weakness, interstitial lung disease, myocarditis, and cancer risk. Treatment generally begins with glucocorticoids plus an early steroid-sparing immunosuppressant, tailored to subtype and organ involvement.

P

• Polymyalgia Rheumatica - Initial Management

  Polymyalgia rheumatica causes bilateral shoulder and often hip-girdle pain with prominent morning stiffness in adults over 50, usually with elevated inflammatory markers. Diagnosis is clinical after excluding mimics and screening for giant cell arteritis. Treatment is low-to-moderate-dose oral glucocorticoid with an individualized taper, while recurrent relapse or high steroid-toxicity risk may justify steroid-sparing therapy and rheumatology involvement.
• Polymyositis & Dermatomyositis — Diagnosis & Treatment

  Idiopathic inflammatory myopathies cause proximal weakness (± rash in DM). Confirm with muscle enzymes, myositis antibodies, MRI/EMG, and biopsy when needed. Treat with glucocorticoids plus steroid‑sparing agents; screen for malignancy and ILD.

R

• Relapsing Polychondritis — Recognition & Treatment

  Autoimmune inflammation of cartilaginous structures (ears, nose, laryngotracheal tree). Diagnose clinically; treat with NSAIDs/steroids and disease‑modifying agents; airway involvement is life‑threatening.
• Rheumatoid Arthritis - Initial DMARD Strategy

  Early rheumatoid arthritis treatment aims for remission or low disease activity before irreversible joint damage accumulates. Methotrexate is the preferred initial conventional synthetic DMARD for most patients with moderate-to-high activity, with folic acid supplementation and treat-to-target reassessment. Hydroxychloroquine or sulfasalazine may be appropriate for lower activity or when methotrexate is unsuitable. Long-term glucocorticoids should be avoided whenever possible.

S

• Sarcoidosis — Extrapulmonary Manifestations & Care

  Beyond pulmonary disease, sarcoidosis affects eyes, heart, skin, liver, and nervous system. Screen key organs and treat when organ‑threatening or symptomatic; use steroid‑sparing agents for chronic disease.
• Scleroderma (Systemic Sclerosis) — Organ Screening & Management

  Multisystem autoimmune disease; early organ screening is essential (ILD, PAH, renal crisis). Manage with targeted therapies: mycophenolate for ILD/skin, vasodilators for PAH/Raynaud, ACE inhibitors for renal crisis.
• Scleroderma Renal Crisis - ACE Inhibitor Urgency

  Scleroderma renal crisis is an emergency of systemic sclerosis characterized by abrupt hypertension and rapidly progressive kidney injury, often with microangiopathic hemolytic anemia and thrombocytopenia. An ACE inhibitor, classically captopril because it can be rapidly titrated, should be started immediately when renal crisis is diagnosed, even if creatinine is rising. Glucocorticoid exposure, especially higher doses, increases risk and should be minimized.
• Systemic Lupus Flare - Evaluation and Initial Treatment

  A systemic lupus erythematosus flare requires rapid distinction between inflammatory disease activity, infection, thrombosis, medication toxicity, and irreversible damage. Initial assessment is organ-based: renal, neurologic, cardiopulmonary, hematologic, and vasculitic manifestations can be organ- or life-threatening and warrant urgent immunosuppression and specialty care, while mild mucocutaneous or musculoskeletal flares are managed with lower-intensity therapy. Hydroxychloroquine is foundational for mos

V

• Vasculitis — Large Vessel Imaging & Steroid‑Sparing Agents

  Large‑vessel vasculitis (GCA/Takayasu): use vascular imaging (US, CTA/MRA, PET) and prompt glucocorticoids; add steroid‑sparing agents (tocilizumab) to reduce relapse and exposure.