What are the key aspects of rheumatology, including treatments for acute gouty arthritis, prophylaxis, supportive management, microscopy findings, SLE diagnosis, osteoarthritis, carpal tunnel syndrome, spondyloarthropathies, reactive arthritis, and Jones Criteria for rheumatic fever?

Rheumatology Core Concepts

Acute Gouty Arthritis Medications

For acute gout attacks, initiate treatment within 24 hours using NSAIDs, oral colchicine, or corticosteroids as first-line monotherapy options. 1, 2, 3

First-Line Monotherapy Options:

• NSAIDs: Use full FDA-approved anti-inflammatory doses (naproxen, indomethacin, or sulindac) 1, 3
• Colchicine: Low-dose regimen of 1.2 mg followed by 0.6 mg one hour later (maximum 1.8 mg in first 12 hours), most effective when started within 36 hours of symptom onset 1, 3, 4
• Corticosteroids: Oral prednisone/prednisolone, intra-articular injection for 1-2 joints, or intramuscular/intravenous methylprednisolone (0.5-2.0 mg/kg) 1, 3

Severe or Polyarticular Gout:

• Combination therapy is appropriate for acute polyarthritis or involvement of more than one large joint 1
• Recommended combinations: colchicine + NSAIDs, oral corticosteroids + colchicine, or intra-articular steroids with any other modality 1
• Avoid combining NSAIDs with systemic corticosteroids due to synergistic gastrointestinal toxicity 1, 2, 3

NPO (Nothing by Mouth) Patients:

• Intra-articular corticosteroid injection for 1-2 joints 1
• Intravenous or intramuscular methylprednisolone at 0.5-2.0 mg/kg 1
• Subcutaneous ACTH at 25-40 IU 1

Prophylaxis for Gout Flares

Anti-inflammatory prophylaxis must be initiated when starting urate-lowering therapy and continued for at least 6 months. 1, 2, 3

First-Line Prophylactic Agents:

• Low-dose colchicine: 0.6 mg daily 2, 5, 6
• Low-dose NSAIDs: With proton pump inhibitor when indicated 2, 5

Duration of Prophylaxis:

Continue prophylaxis for the greater of: 1

• 6 months minimum 1, 2, 3
• 3 months after achieving target serum urate for patients without tophi 1
• 6 months after achieving target serum urate for patients with resolved tophi 1

Alternative When First-Line Contraindicated:

• Low-dose prednisone or prednisolone (≤10 mg/day) when colchicine and NSAIDs are contraindicated, though evidence for efficacy is sparse 1

Supportive Management for Gout

Continue urate-lowering therapy without interruption during acute attacks. 2, 3, 5

Non-Pharmacologic Measures:

• Topical ice application to inflamed joint 7
• Rest of the affected joint 7

Dietary Modifications:

• Limit purine-rich foods: Organ meats and shellfish 6
• Avoid alcoholic drinks, especially beer 6
• Avoid beverages sweetened with high-fructose corn syrup 6
• Encourage consumption of vegetables and low-fat/nonfat dairy products 6

Medication Adjustments:

• Consider discontinuing or switching loop and thiazide diuretics when possible, as they increase uric acid levels 6
• Consider losartan as antihypertensive choice, as it increases urinary uric acid excretion 6

Microscopy Findings

Gout:

• Monosodium urate crystals: Needle-shaped, negatively birefringent under polarized light microscopy 6

Pseudogout (Calcium Pyrophosphate Deposition Disease):

• Calcium pyrophosphate crystals: Rhomboid-shaped, positively birefringent under polarized light microscopy 6

SLE Diagnosis

Classification Criteria:

The diagnosis of SLE requires meeting specific classification criteria that include clinical and immunologic manifestations, though detailed criteria are beyond the scope of the provided evidence.

Immunologic Tests for SLE:

• Antinuclear antibody (ANA): Screening test
• Anti-double-stranded DNA (anti-dsDNA): Specific for SLE
• Anti-Smith (anti-Sm): Highly specific for SLE
• Antiphospholipid antibodies: Lupus anticoagulant, anticardiolipin, anti-β2-glycoprotein I
• Complement levels: Low C3 and C4 indicate active disease
• Anti-Ro/SSA and Anti-La/SSB: Associated with specific manifestations

Osteoarthritis Joint Involvement

Most Commonly Affected Joints:

• Distal interphalangeal (DIP) joints of the hands
• Proximal interphalangeal (PIP) joints of the hands
• First carpometacarpal (CMC) joint of the thumb
• Knees
• Hips
• First metatarsophalangeal (MTP) joint
• Cervical and lumbar spine

Hand Deformities

Osteoarthritis:

• Heberden's nodes: Bony enlargements of the distal interphalangeal (DIP) joints
• Bouchard's nodes: Bony enlargements of the proximal interphalangeal (PIP) joints

Rheumatoid Arthritis:

• Swan neck deformity: Hyperextension of the PIP joint with flexion of the DIP joint
• Boutonnière deformity: Flexion of the PIP joint with hyperextension of the DIP joint

Carpal Tunnel Syndrome Maneuvers

Diagnostic Tests:

• Tinel's sign: Tapping over the median nerve at the wrist produces tingling in the median nerve distribution
• Phalen's test: Flexion of both wrists for 60 seconds reproduces symptoms
• Reverse Phalen's test: Extension of the wrist reproduces symptoms
• Carpal compression test: Direct pressure over the carpal tunnel for 30 seconds reproduces symptoms

Spondyloarthropathies

Major Causes:

• Ankylosing spondylitis: Primary axial spondyloarthropathy
• Psoriatic arthritis: Associated with psoriasis
• Reactive arthritis: Following genitourinary or gastrointestinal infection
• Inflammatory bowel disease-associated arthritis: Associated with Crohn's disease or ulcerative colitis
• Undifferentiated spondyloarthropathy: Does not meet criteria for specific subtype

Common Features:

• HLA-B27 association
• Axial skeleton involvement
• Asymmetric peripheral arthritis
• Enthesitis (inflammation at tendon/ligament insertion sites)
• Dactylitis ("sausage digits")
• Extra-articular manifestations (uveitis, inflammatory bowel disease, psoriasis)

Reactive Arthritis

Pathophysiology:

• Immune-mediated arthritis triggered by preceding infection, typically genitourinary (Chlamydia trachomatis) or gastrointestinal (Salmonella, Shigella, Campylobacter, Yersinia)
• Bacterial antigens or DNA present in synovial tissue despite sterile joint fluid
• Strong HLA-B27 association

Classic Triad (Reiter's Syndrome):

1. Arthritis: Asymmetric oligoarthritis, typically lower extremity
2. Urethritis: Non-gonococcal urethritis or cervicitis
3. Conjunctivitis: Or uveitis

Additional Features:

• Enthesitis
• Dactylitis
• Mucocutaneous lesions (circinate balanitis, keratoderma blennorrhagicum)
• Nail changes

Jones Criteria for Rheumatic Fever

Diagnosis Requires:

Evidence of preceding Group A Streptococcal infection PLUS either 2 major criteria OR 1 major + 2 minor criteria

Major Criteria:

• Joints: Migratory polyarthritis
• ❤️ (O): Carditis (clinical or subclinical)
• Nodules: Subcutaneous nodules
• Erythema marginatum
• Sydenham chorea

Minor Criteria:

• Polyarthralgia (if arthritis not used as major criterion)
• Fever (≥38.5°C)
• Elevated acute phase reactants (ESR ≥60 mm/hr or CRP ≥3.0 mg/dL)
• Prolonged PR interval on ECG (if carditis not used as major criterion)

Evidence of Preceding GAS Infection:

• Positive throat culture or rapid streptococcal antigen test
• Elevated or rising anti-streptolysin O or anti-DNase B titers

Critical Pitfalls to Avoid

Acute Gout Management:

• Never delay treatment beyond 24 hours of symptom onset, as effectiveness significantly decreases 2, 3
• Never discontinue urate-lowering therapy during acute attacks, as this worsens and prolongs the attack 2, 3, 5
• Never use high-dose colchicine regimens (>1.8 mg in first 12 hours), as they cause significant gastrointestinal toxicity without additional benefit 1, 3

Prophylaxis:

• Never initiate urate-lowering therapy without concurrent anti-inflammatory prophylaxis, as this increases flare frequency 2, 5
• Never use high-dose corticosteroids (>10 mg/day prednisone) for prophylaxis in most scenarios 1

Drug Interactions:

• Always consider colchicine drug interactions, particularly with CYP3A4 inhibitors (clarithromycin, ketoconazol, ritonavir) and P-glycoprotein inhibitors (cyclosporine), which can lead to serious toxicity 4
• Always adjust colchicine dosing in renal impairment, as clearance is reduced by 75% in end-stage renal disease 4, 8