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Episode 110
DIP Episode 110 - ABIM/Medicine ITE/USMLE Step 3 Review Series 8 (Rheumatology 2)
ImmunologyMedium4 - HighHas Q&A
Step 1Step 2Step 3COMLEXMedicineUSMLEStep 1Step 2Step 3
Topic
Seronegative spondyloarthropathies; Diffuse idiopathic skeletal hyperostosis (DISH); Crystal arthropathies (Gout); HLA associations.
Key Takeaway
The diagnosis and management of seronegative spondyloarthropathies require distinguishing between axial involvement (NSAIDs/TNF inhibitors) and peripheral involvement (DMARDs), while acute gout flares must be treated empirically without measuring serum uric acid levels.
Runtime: 48.6 min
Published: 2019-06-08
Completed audio: Yes
Completed notes: Yes
Anki made: Yes
Section: —
Episode Notes
Source / episode info
- Episode: 110
- Title: Divine Intervention Episode 110 – ABIM/Medicine ITE/USMLE Step 3 Review Series 8 (Rheumatology 2)
- Published: 2019-06-08
- Source: Episode page
One-liner
This episode reviews seronegative spondyloarthropathies (PsA, As, IBD-As, RA), the diagnostic criteria and management of Diffuse Idiopathic Skeletal Hyperostosis (DISH), and the pathophysiology, diagnosis, and treatment strategies for gout, emphasizing key HLA associations.
High-yield summary
- Seronegative Spondyloarthropathies: Characterized by enthesitis and axial involvement; the four core diseases are Psoriatic Arthritis, Ankylosing Spondylitis, IBD-associated arthritis, and Reactive Arthritis (formerly Reiter's syndrome).
- Gout Pathophysiology: Caused by monosodium urate crystals (needle-shaped, negatively birefringent) depositing in joints; most cases result from under-excretion of uric acid.
- Acute Gout Management: Initial treatment is empirical (NSAI Ds, Corticosteroids, Colchicine); never measure serum uric acid levels during an acute flare.
- Chronic Gout Therapy: First-line agents are Xanthine Oxidase Inhibitors (Allopurinol, Febuxostat), aiming for a target uric acid level of < 6 mg/dL (or < 5 mg/dL if tophaceous).
- DISH vs. AS: DISH is characterized by ossification of the anterior longitudinal ligament and multiple bridging osteophytes, crucially lacking sacroiliac joint inflammation or sclerosis.
- HLA Associations: Remember HLA-B27 for seronegative SpA; check for HLA-B57:01 before Abacavir; be aware of HLA-B58:01 in Asians regarding Allopurinol risk.
Learning objectives
- Differentiate the clinical presentation and imaging findings among the four seronegative spondyloarthropathies (PsA, As, IBD-As, ReA).
- Master the acute vs. chronic management principles for gout, including appropriate drug selection and contraindications.
- Recognize the key features of Diffuse Idiopathic Skeletal Hyperostosis (DISH) versus inflammatory sacroiliitis.
- Understand the clinical significance of specific HLA alleles in rheumatology and anti-infective therapy.
- Apply knowledge of differential diagnosis for acute arthritis, distinguishing crystal deposition from septic or infectious causes.
Board exam buzzwords
| Condition | Key Finding | Association | Board Exam Tip |
| Seronegative Spondyloarthropathies (SpA) | Enthesitis; Axial involvement | HLA-B27; Psoriasis/GI disease | Remember the mnemonic: Ps, As, IBD, Re. |
| Gout | Needle-shaped, negatively birefringent crystals | Monosodium urate; Uric acid under-excretion | Never measure uric acid in the acute flare. |
| Diffuse Idiopathic Skeletal Hyperostosis (DISH) | Bridging osteophytes; Anterior longitudinal ligament ossification | Metabolic syndrome/Age | The absence of sacroiliac joint inflammation is key to diagnosis. |
| Allopurinol Therapy | Hypersensitivity reaction | HLA-B58:01 (especially in Asian descent) | Always check for this allele before starting XOI drugs in high-risk populations. |
Rapid review table
| Topic | Key Point | Context | Exam Relevance |
| Seronegative SpA | Axial involvement is often symmetric; Peripheral involvement is often asymmetric. | As/IBD-As tend to have more axial focus; PsA/ReA involve peripheral joints. | Helps differentiate the pattern of joint damage and guides treatment (axial vs. peripheral). |
| Gout Diagnosis | Synovial fluid analysis must be performed for definitive diagnosis. | Acute monoarticular arthritis, especially in the MTP joint. | The gold standard is crystal identification; look for negative birefringence. |
| DISH | Ossification of the anterior longitudinal ligament with bridging osteophytes. | Often seen in older men with metabolic risk factors. | If SI joints are normal/unaffected, think DISH instead of AS. |
| Chronic Gout Tx | Xanthine Oxidase Inhibitors (XOI) reduce uric acid production. | Goal: Uric acid < 6 mg/dL; if tophaceous, target < 5 mg/dL. | Know the drug interactions (e.g., XOI drugs and Azathioprine). |
Board-speak -> diagnosis
| Board-speak / Vignette phrase | Diagnosis / Concept | Why it fits |
| Young man with morning low back pain, improving significantly after physical activity; bilateral sacroiliitis on imaging. | Ankylosing Spondylitis (As) | Classic presentation of inflammatory axial arthritis in young males. |
| A patient presenting with polyarthralgia and skin findings like pitting/sausage digits, along with evidence of nail psoriasis. | Psoriatic Arthritis (PsA) | Combines classic psoriatic skin manifestations with peripheral joint involvement. |
| Acute monoarticular arthritis that started at night in the big toe, accompanied by a history of heavy alcohol use and metabolic syndrome. | Gout | Classic presentation of hyperuricemia crystal deposition; often affects MTP joint (podagra). |
| Imaging shows calcifications along the anterior longitudinal ligament with multiple bridging osteophytes, but no sacroiliac joint involvement. | Diffuse Idiopathic Skeletal Hyperostosis (DISH) | The key differentiator from AS is the absence of SI joint inflammation/sclerosis. |
| A patient taking Abacavir who develops a fever and rash; testing reveals positive HLA-B57:01. | Hypersensitivity Reaction to Abacavir | This specific HLA allele predicts a life-threatening reaction, requiring drug avoidance. |
| A young person with bloody diarrhea following Campylobacter infection, weeks later developing asymmetric arthritis of the knee and conjunctivitis. | Reactive Arthritis (ReA) | Classic triad: urethritis/conjunctivitis/arthritis; triggered by recent GI or GU infection. |
Differential diagnosis / distinguishing features
Acute Arthritis: Gout vs. Septic Arthritis
| Key Features | Distinguishing Findings | Next Step |
| Gout (Crystal) | Needle-shaped, negatively birefringent crystals in synovial fluid; Often associated with hyperuricemia/metabolic syndrome. | Synovial Fluid Analysis (Polarized light microscopy). |
| Septic Arthritis | High WBC count (>50,000); Positive culture; Usually rapidly destructive joint damage. | Synovial Fluid Culture and Gram stain; Urgent antibiotics. |
Chronic Gout Management: XOI vs. Uricosuric Agents
| Key Features | Distinguishing Findings | Next Step |
| Xanthine Oxidase Inhibitors (Allopurinol, Febuxostat) | Decrease uric acid production. First-line agents for most patients. | Monitor renal function and perform HLA screening before starting. |
| Uricosuric Agents (Probenecid) | Increase uric acid excretion via the kidneys. Highly restricted use. | Only used if patient is an under-excreter, has no renal failure, and no history of nephrolithiasis/gout stones. |
Management pearls
- Acute Gout Flare: Treat empirically with NSAI Ds (e.g., Naproxen), IV Corticosteroids, or Colchicine. Do not initiate chronic therapy or measure uric acid levels until the flare resolves.
- Seronegative SpA Treatment Strategy: For axial involvement, start with NSAI Ds/PT; escalate to TNF inhibitors (e.g., Adalimumab); if refractory, consider IL-17/IL-23 inhibitors.
- DISH Workup: If a patient presents with spinal ossification and the sacroiliac joints are normal, DISH is highly suspected. Imaging should confirm bridging osteophytes without inflammatory signs in the SI joint.
- XOI Drug Interactions: Be vigilant about drug interactions; XOI drugs inhibit the metabolism of Azathioprine, leading to elevated levels and potential bone marrow suppression.
Don't miss
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Anterior Uveitis: The most common uveitis associated with seronegative spondyloarthropathies (e.g., As, PsA).
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Posterior Uveitis: If posterior uveitis is suspected on an exam, think of Sarcoidosis first.
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HLA-B 58:01: This allele in Asian populations predisposes to a life-threatening hypersensitivity reaction to Allopurinol.
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DISH Hallmark: The defining feature is the bridging osteophytes and ossification of the anterior longitudinal ligament, without sacroiliitis.
Integration & clinical reasoning
- Rheumatology & GI: IBD-associated arthritis often presents with axial involvement, but peripheral joint inflammation correlates strongly with gut inflammation (unlike AS).
- Pharmacology & Genetics: The use of XOI drugs requires genetic screening for HLA-B*58:01 and careful monitoring of drug metabolism pathways (e.g., Azathioprine) due to enzyme inhibition.
- Rheumatology & Orthopedics: Before any extensive spinal manipulation or surgery in patients with SpA, obtain cervical spine X-rays in flexion/extension views to rule out atlantoaxial instability.
OMM / COMLEX integration
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For COMLEX: know these viscerosomatics / Chapman points, but don't let OMM distract from emergent diagnosis and management.
- Acute Flare Management: In any acute inflammatory crisis (MI, sepsis, etc.), standard emergency management takes priority over OMT. Anti-inflammatory agents like NSAI Ds and corticosteroids are used adjunctively to manage symptoms but do not replace core life support measures.
- Spinal Instability: The need for flexion/extension X-rays in SpA patients highlights the importance of assessing spinal stability before invasive procedures, a principle applicable across many orthopedic emergencies.
Concept connections / cross-references
- For detailed information on the pathophysiology and management of Inflammatory Bowel Disease (IBD), see Episode 105.
- For general principles of rheumatology and inflammatory markers, review Episode 98.
High-yield association table
| Condition | Association | Mechanism | Clinical Significance |
| Ankylosing Spondylitis | Aortic regurgitation; Sacroiliitis | Chronic inflammation/vascular damage | Increased risk for aortic dissection and requires careful cardiac monitoring. |
| Psoriatic Arthritis | Nail pitting, dactylitis ("sausage digits"), onycholysis | Skin barrier dysfunction; Immune dysregulation | These skin findings are highly specific markers that help differentiate PsA from other arthritides. |
| Gout | Thiazide diuretics, low-dose aspirin, alcohol consumption | Impaired renal excretion of uric acid (under-excretion) | Lifestyle and medication modifications are crucial for prevention; these drugs increase risk. |
| HLA-B27 | Seronegative Spondyloarthropathies | Genetic predisposition to inflammatory axial arthritis | Suggests a diagnosis but is not diagnostic; requires clinical correlation. |
Key terms glossary
| Term | Definition | Context | Example |
| Enthesitis | Inflammation at the site where a tendon or ligament attaches to bone. | Common finding in seronegative spondyloarthropathies. | Tendon inflammation at the Achilles insertion point. |
| Negatively Birefringent Crystals | Crystal structure that appears yellow when viewed under polarized light against a green background. | Diagnostic hallmark of gout (Monosodium urate). | Identifying needle-shaped crystals in synovial fluid. |
| Bridging Osteophytes | Bone spurs that connect multiple adjacent vertebral bodies, forming a continuous bony bridge. | Characteristic finding in DISH or advanced AS. | Seen on plain film X-ray of the spine. |
| Uricase Analogs (e.g., Rasburicase) | Medications designed to convert uric acid into allantoin, which is highly water-soluble and easily excreted. | Used for severe hyperuricemia/gout; alternative to traditional XOI drugs. | Administered intravenously in a hospital setting. |
Study optimization
| Topic | Study Approach | Priority | Resources |
| Seronegative SpA | Use the mnemonic (Ps, As, IBD, Re) and focus on differentiating axial vs. peripheral involvement patterns. | High | Review clinical vignettes comparing joint symmetry/location. |
| Gout Management | Master the acute vs. chronic treatment paradigm; memorize contraindications for all drugs. | Critical | Create a flow chart: Acute Flare -> Chronic Tx (XOI) -> Alternative Agents. |
| DISH/Spine Imaging | Focus on the absence of SI joint inflammation to distinguish DISH from AS. | Medium-High | Practice identifying bridging osteophytes vs. normal degenerative changes. |
Question pattern recognition
- The "Best Answer" Trap: In gout, the most common trap is asking for a lab value (e.g., serum uric acid) during an acute flare; always choose empirical treatment first.
- Differential Diagnosis Overlap: Be prepared to distinguish between similar conditions like DISH and AS based on specific imaging findings (SI joint status).
- Drug Interaction/Hypersensitivity: Always consider HLA typing when starting drugs like Allopurinol or Abacavir, as these are high-yield safety questions.
Test yourself
Common mistakes to avoid
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Mistake 1: Confusing DISH and AS. Do not assume calcification of the anterior longitudinal ligament means Ankylosing Spondylitis; confirm the absence of SI joint inflammation to diagnose DISH.
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Mistake 2: Acute Gout Lab Workup. Never measure serum uric acid levels during an acute flare, as this is a common test trap. Treat empirically first.
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Mistake 3: Probenecid Use. Do not use Probenecid unless the patient meets all criteria (under-excreter, no renal failure, no nephrolithiasis, no history of gout stones).
Common traps
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Trap 1 (Gout): The question asks for the best initial treatment for acute gout. Choosing a chronic agent or measuring uric acid is incorrect; empirical anti-inflammatories are required.
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Trap 2 (SpA): A patient has sacroiliitis and back pain, leading to suspicion of AS. If SI joint inflammation is absent, DISH must be considered instead.
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Trap 3 (HLA): When given a drug like Allopurinol, the test may try to distract you with other HLA associations (e.g., Abacavir/B 57:01), but remember B 58:01 is specific for XOI drugs in Asians.