24_Rhumatologie

Main ideas, concepts, and lessons (rheumatology “review tour” for exams)

Overall purpose and exam strategy

• The speaker (an intern) presents a TACFA-style review tour in rheumatology to help students refine revisions for written exams (ODN/EDN-type).
• The focus is not exhaustive; it targets high-yield, recurrent knowledge.
• Exam questions often test:
  • Pain characterization (core reasoning element)
  • Classic disease patterns (clinical presentation + imaging + key labs)
  • Recognition of destructive vs non-destructive arthropathies
  • Diagnostic algorithms and first-line management

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1) Pain rhythm & rheumatologic pain types

Key categorization

• Nociceptive pain (emphasized first), versus:
  • Neuropathic
  • Nociplastic
• Within nociceptive pain, distinguish:
  • Inflammatory pain
  • Mechanical pain

Inflammatory vs mechanical pain (high-yield markers)

• Mechanical pain

  • Worse with end-of-day use / maximal effort
  • May cause night awakening, typically positional
  • Morning stiffness: generally < 30 minutes

• Inflammatory pain

  • The “opposite” pattern:
  • More prominent morning stiffness and inflammatory features

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2) Symmetry, distal distribution, and radiographic destructiveness (polyarthritis focus)

Multiple-choice themes

• Diseases classically causing symmetrical distal involvement
• Diseases causing destructive changes on radiography
  • Examples given in the review:
    • Rheumatoid polyarthritis
    • Psoriatic rheumatism

Joint count language

• Monoarthritis: 1 joint
• Oligoarthritis: about 3–3 joints
• Polyarthritis: ≥ 4 joints

A “small algorithm” for expected clinical/radiologic patterns

Typical distribution patterns in polyarthritis

• Symmetrical proximal lesions (referenced as PPR) → described as something you “control.”

• Rheumatoid polyarthritis (RA)

  • Elderly onset possible
  • Typically symmetrical
  • Destructive on imaging (erosions)
  • Often small joints
  • Spare DIP joints (key contrast vs lupus)

• Microcrystalline rheumatism

  • Example: hydroxyapatite
  • Often described as proximal asymmetric
  • Distal symmetric patterns may occur depending on subtype

• “Controlled” patterns mentioned as examples:

  • Rheumatoid arthritis, lupus, sarcoid arthritis, distal asymmetric arthritis (e.g., psoriasis, spondylitis, microcrystalline)

Radiographic approach: destructive vs non-destructive

• Split diseases into:
  • Destructive
  • Non-destructive

If destructive: reconstructive vs non-reconstructive logic

• Memory anchor: RA = rheumatoid arthritis
• Reconstructive destructive types (examples given)
  • Psoriasis
  • Spondylitis
  • Gout (chronic arthropathy progressing toward secondary osteoarthritis)

Radiographic hallmarks emphasized

• Rheumatoid arthritis (RA) typical findings:

  • Erosions
    • e.g., at 1st MTP head
    • Erosion at base/head of the 5th metatarsal
    • Head of the 5th metatarsal as a “most important memory”
  • Tarsal condensation, possible fusing tarsals
  • Subluxations

• Additional reconstructive examples mentioned:

  • Syndesmophytes
  • Enthesophytes (peripheral/axial context)
  • Osteophytes
  • Hemochromatosis → “hook-like” osteophytes

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3) Quick overview of polyarthritis syndromes (classification by pattern)

Rheumatoid arthritis (RA)

• Symmetrical destructive
• Small joints
• Spare DIP joints
• (Also reiterated later in the review: ACPA-positive; cervical involvement late, etc.)

Lupus arthritis

• Symmetrical
• Non-destructive
• Migratory
• Deformation can resemble destructive disease but is often reducible subluxations
• Mentioned classic wording similar to “Jaccoud” arthropathy

Psoriasis

• Asymmetric polyarthritis
• Erosive-reconstructive (as stated)

Spondyloarthritis (spectrum)

• Included but details deferred later

RS3PE

• Acute polyarthritis in the elderly
• Often men > 65
• Acral/distal, bilateral and symmetrical
• Typically negative for:
  • Rheumatoid factor
  • Anti-CCP
• Can be benign or malignant (paraneoplastic possibility)
• EDN testing not deeply detailed; corticosteroids noted (short/long duration)

Sarcoidosis-related polyarthritis

• Symmetrical
• Mentions ankle involvement
• Linked to a Fever–lymph nodes–arthritis type syndrome (FIGA)

Hemochromatosis arthropathy

• Iron metabolism disorder
• Destructive and reconstructive

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4) Rheumatoid polyarthritis (RA) details: diagnosis & monitoring

Typical RA presentation (clinical pattern)

• Predominantly women ~50
• Smoking as a risk factor
• Peripheral, symmetrical polyarthritis
• Duration: > 6 weeks
• Spare DIP joints
• Possible cervical involvement (C1–C2) → risk of serious dislocations
• No sacroiliac or thoracolumbar involvement described (with shoulders/hips possibly later)
• Tenosynovitis/tenovitis mentioned
• “Evolved forms” described (concept: progressive disease)

Extra-articular manifestations listed

• Rheumatoid nodules
• Pulmonary and cardiac involvement
• Dry eye syndrome; possible ocular involvement (e.g., ceritis/scleritis)
• Felty’s syndrome (important, severe RA variant)
  • Women 30–50
  • Very destructive RA with low/no joint inflammation
  • Triad: splenomegaly + neutropenia + severe RA activity
  • Consequence: recurrent bacterial infections

Biology (diagnostic tests)

• Inflammatory syndrome (not always)
• ACPA / anti-CCP
  • “Very specific” for RA
• Rheumatoid factor (RF)
  • May be specific but not sufficient alone
  • Negative does not rule out RA

Imaging / workup emphasized

• Standard radiographic assessment includes:
  • Chest X-ray
  • Hand X-ray (front view)
  • Foot X-ray (front 3/4 view) (to visualize the 5th ray metatarsal head)
  • X-rays of painful joints (excluding feet/hands if already done)
• Ultrasound can supplement but is stated as not essential for diagnosis in this teaching context

Prognosis / severity factors

• Poor prognostic factors:
  • ACPA+, RF+
  • Early erosions
  • High inflammation
  • Extra-articular involvement
  • Major functional impact
• DAS28 used to assess severity and monitor disease activity

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5) RA treatment methodology (stepwise decision structure)

Pre-treatment baseline tests (systematic evaluation)

Before starting methotrexate (first-line), include:

• CRP
• CBC (NFS) (also flags connective tissue disease/hematologic issues)
• Kidney function (creatinine/BUN)
• Liver function tests
  • to detect cytolysis (important due to methotrexate risk)
• ANA/ENAs
  • positivity should prompt search for associated connective tissue disease

Chest X-ray considerations:

• Exclude infection before immunosuppression (e.g., tuberculosis)
• Assess for pleuritis/pericarditis
• Look for diffuse interstitial lung disease (therapy selection may change)

Methotrexate: contraindications to check

• Allergy
• Severe liver dysfunction
• Alcoholism
• Severe renal impairment
• Neutropenia
• Severe anemia
• Severe thrombocytopenia
• Infection
• Pregnancy
• In young women: do beta-hCG before methotrexate

Treatment timeline & escalation logic

• Start methotrexate, often with corticosteroids depending on severity
• Reassess at 3 months
  • Improved at 3 months?
  • Goal achieved by 6 months?
• If working → continue
• If poor response / high risk (e.g., erosions, ACPA/RF+, high activity, prior failures) → targeted therapy
  • If still on methotrexate → switch csDMARD (examples given):
    • leflunomide or sulfasalazine
  • If on leflunomide → switch to sulfasalazine or similar
• Continue reassessment at 3 months and 6 months
• If still not working → change targeted therapy stepwise

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6) Polymyalgia rheumatica (PMR/PPR): recognition and key “don’t miss”

Core clinical pattern

• Generally affects women > 50
• Peak described: 70–80
• Bilateral symmetrical inflammatory pain
  • shoulder/waist “girdle” areas
• Duration: evolution > 4 weeks
• Marked morning stiffness
• Peripheral joints involved in ~20% (warning against diagnostic trap)

Diagnostic must-not-miss: Giant cell arteritis (Horton disease)

• Look for recent cephalic features:
  • scalp hypersensitivity
  • “comb sign”
  • jaw claudication
  • visual disturbances
• Requires urgent action due to risk (especially vision/functonal prognosis)

PMR biology & imaging

• Inflammatory syndrome (e.g., CRP elevated)
• RF/anti-CCP negative (contrasts with RA)
• Liver tests may show cytolysis (not always)
• CPK generally normal
• Imaging teaching points:
  • No erosions
  • Shoulder/hip ultrasound may show bursitis and tenosynovitis

Treatment methodology

• Corticosteroids
  • Example dosing: 0.3 mg/kg
  • Gradual taper after remission over 12–24 months
• Corticosteroid-dependent/refractory forms:
  • If flare while tapering:
    • return to effective dose, or
    • introduce methotrexate / “anti-IL” drug (as stated)
• Response speed:
  • improvement within 24–72 hours is described as a diagnostic clue
• Steroids may be started once suspected/after diagnostic evaluation

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7) Spondyloarthritis (SPA) spectrum: axial vs peripheral & diagnostic criteria

Classification

• Axial involvement
  • may be radiographic or non-radiographic
• Peripheral involvement
  • split into:
    • joint involvement
    • enthesitis

Enthesis definition

• Enthesis = insertion zone of tendon/capsule/ligament into bone

Typical patient profile

• Usually < 35 years
• Slight male predominance
• HLA-B27 associated but not sufficient alone

Diagnostic logic (2009 axial classification described)

• Mandatory entry criteria:
  • Low back pain > 3 months
  • onset before age 45
• Additional criteria:
  • If MRI shows sacroiliitis → add 1 sign from listed features
  • If clinical branch with HLA-B27 positive → add 2 signs

Key clinical features emphasized

• Inflammatory back pain:
  • buttock pain
  • gradual spinal “re-expansion”
  • assessed via mobility measures (garbled in subtitles)
• Peripheral:
  • large joint involvement (ankles, knees, hips; possible coxitis)
  • dactylitis (“sausage finger”):
    • enthesitis + teno-synovial component (described)
    • tenosynovitis also mentioned
  • plantar heel pain
• Extra-articular:
  • uveitis
  • psoriasis
  • “other extra-articular features” (garbled text; concept retained)

Treatment methodology (algorithmic)

• First line: NSAIDs
  • only if no contraindications (ulcers, cardiovascular risk, renal insufficiency)
• “Failure” rule:
  • don’t label failure until trying two different NSAIDs over ~4 weeks
• If accessible peripheral inflamed joint → consider infiltration
• If persistent severe symptoms:
  • differentiate:
    • Purely peripheral (no axial/pelvic-spinal syndrome)
      • consider csDMARD (e.g., methotrexate)
      • reassess at 12 weeks
      • if no improvement → targeted therapy
    • Peripheral with enthesitis/dactylitis OR axial involvement
      • go directly to targeted therapy (no methotrexate role in this teaching)

Prognosis / poor response factors

• Significant inflammatory syndrome
• Smoking
• Poor NSAID response

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8) Septic arthritis & spondylodiscitis (infectious differentiation & procedures)

Septic arthritis (peripheral, often acute monoarthritis)

• Often monoarthritis with:
  • sudden onset
  • severe inflammatory pain
  • major functional impairment
• Fever not required
  • absence of fever does not exclude septic arthritis

Workup and procedure list (step-by-step)

1. Blood tests (CRP, CBC, etc.)
2. Obtain ≥ 2 sets of blood cultures, ideally before antibiotics
3. Imaging
   • X-ray of affected joint and consider differential diagnoses
   • ultrasound can guide puncture
4. Joint aspiration (puncture):
   • mandatory for direct examination and culture
   • culture essential even if crystals are present

Crystals rule

• Presence of crystals does not exclude septic arthritis.

Antibiotics timing logic

• If patient unstable:
  • start antibiotics and perform puncture/cultures as possible (urgent)
• If not unstable:
  • timing can allow exam/culture depending on protocol
• If synovial WBC threshold suggests high probability (garbled in text):
  • antibiotics after at least 2 blood cultures when threshold ≥ 2
  • (core concept: culture first when feasible)

Antibiotic duration by diagnosis (as stated)

• Septic arthritis: 4–6 weeks
• Spondylodiscitis: 6 weeks
• Osteomyelitis: 3 months
• Tuberculosis: up to 12 months

Spondylodiscitis: diagnostic approach

• Not just “infection”:
  • clinical pattern: inflammatory back pain + major multidirectional pain
• Best test:
  • MRI of the spine
  • X-ray may be normal early; delayed changes occur later
• Additional tests:
  • blood cultures
  • consider CT if suspect endocarditis/bacteremia; check murmur
  • possible vertebral biopsy

Decision logic

• If MRI suspected and blood cultures positive:
  • treat assuming same germ in blood and spine
• If MRI suspected and blood cultures negative:
  • perform disc-vertebral biopsy to identify organism

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9) Gout and other microcrystalline diseases: key teaching points

Gout (uric acid / monosodium urate)

• Microcrystalline arthropathy from monosodium urate crystals
• Typical: acute intermittent inflammatory arthritis

Risk terrain categories

• Primary (metabolic) terrain:
  • middle-aged man; smoking, alcohol, overweight, diabetes, hypertension, heart failure
• Secondary terrain:
  • renal insufficiency, blood disorders
• Drugs:
  • diuretics (e.g., furosemide, thiazide-like), etc.

Clinical features

• Sudden onset arthritis ± fever
• Fever cannot confirm or exclude infection (do not prematurely exclude septic arthritis)
• Common location:
  • first MTP (podagra)
• More attacks → higher risk of spread to other joints (knee, wrists, elbows, etc.)
• Extra-articular:
  • skin involvement
  • renal urate stones

Diagnosis (method)

• Blood tests:
  • inflammatory syndrome may be present
  • measure uric acid
• Urinary evaluation:
  • urinalysis/urinary function assessment for therapy planning
• Joint aspiration:
  • visualize crystals
  • culture remains relevant if infection is a concern

Management methodology

• Separate:
  • acute attack treatment
  • long-term urate-lowering

Acute attack treatment principles

• Kidney function determines options
• Example colchicine regimen (as stated):
  • 1 mg then 0.5 mg later, then stop