Summative Revision Notes
These notes consolidate the seven Morning Rounds in the Rheumatology series. They are written for rapid pre-exam revision, not first-time learning. Each section is self-contained and mirrors the quiz content. Read the debrief panels in the quizzes for full clinical reasoning; use these notes to consolidate what you already know and to cross-reference patterns across diseases.
Rheumatology is examined through two lenses in NEET-PG and UPSC CMS: clinical vignette recognition (which disease fits this presentation) and antibody-to-disease mapping (which antibody predicts which complication). Both are covered here.
Score ≥6/10 classifies as RA. Domains: joint involvement (1 large joint = 0; 2–10 large joints = 1; 1–3 small joints = 2; 4–10 small joints = 3; >10 joints including at least one small = 5); serology (negative RF and anti-CCP = 0; low-positive = 2; high-positive ≥3×ULN = 3); acute-phase reactants (normal CRP and ESR = 0; abnormal = 1); duration (<6 weeks = 0; ≥6 weeks = 1).
Rheumatoid factor (RF): IgM anti-IgG. Sensitivity ~70%, specificity ~85%. Also positive in: Sjogren's, SLE, cryoglobulinaemia, chronic infections, elderly normals. Anti-CCP (anti-citrullinated protein antibody): specificity >95% for RA; predicts erosive disease and poor prognosis; can precede symptoms by years. High titre of either = poor prognostic marker.
Treat-to-target: aim DAS28 remission (<2.6) or low disease activity (<3.2). Step 1: methotrexate (MTX) ± short-term glucocorticoids as bridge. Step 2 (poor prognosis markers present): add biologic DMARD (TNF inhibitor preferred) to MTX. Poor prognostic markers: high RF/anti-CCP titre, elevated CRP/ESR, early erosions, high DAS28, functional limitation. cDMARD triple therapy (MTX + HCQ + sulfasalazine) is an alternative when biologics are unavailable.
| System | Feature | Key Point |
|---|---|---|
| Pulmonary | ILD (UIP/NSIP); pleural effusion; Caplan's | Pleural fluid: exudate, very low glucose, low complement |
| Cardiac | Pericarditis (most common); accelerated atherosclerosis | CV risk management is part of RA care |
| Ocular | Episcleritis; scleritis; secondary Sjogren's (30%) | Scleritis = severe systemic disease; sight-threatening |
| Haematological | Felty's (RA + splenomegaly + neutropaenia) | LGL leukaemia must be excluded; G-CSF for infections |
| Neurological | C1–C2 atlantoaxial subluxation; peripheral neuropathy | Lateral cervical X-ray before any GA/intubation in RA |
| Vasculitis | Digital infarcts; leg ulcers; mononeuritis multiplex | High RF titre + long disease duration |
Anti-CCP: >95% specific DAS28 target <2.6 Biologics need TB screen C1–C2 subluxation pre-GA
Positive ANA (≥1:80) is the mandatory entry criterion. Seven weighted domains follow: constitutional, haematological, neuropsychiatric, mucocutaneous, serosal, musculoskeletal, and renal. Plus immunological domain (anti-dsDNA, anti-Sm, antiphospholipid antibodies, complement, direct Coombs). Score ≥10 = SLE. Each domain counts only its highest-scoring item.
| Antibody | Significance | Tracks Activity? |
|---|---|---|
| Anti-dsDNA | Specific for SLE; correlates with nephritis | Yes — rises with flares |
| Anti-Sm | Most specific for SLE (>99%) | No |
| Anti-histone | Drug-induced lupus (anti-dsDNA absent in DIL) | No |
| Anti-SSA (Ro) | Neonatal lupus; congenital heart block; subacute cutaneous LE | No |
| Anti-SSB (La) | Sjogren's overlap; neonatal lupus (with anti-SSA) | No |
| C3/C4 low | Classical pathway consumption; active nephritis | Yes — fall with flares |
Class I: minimal mesangial. Class II: mesangial proliferative. Class III: focal proliferative (<50% glomeruli). Class IV: diffuse proliferative (>50% glomeruli) — worst prognosis; low C3/C4 reflects classical pathway consumption. Class V: membranous (heavy proteinuria; complement may be normal). Class VI: advanced sclerosis. Classes III and IV: induction with MMF (2–3 g/day) or IV cyclophosphamide + high-dose corticosteroids.
Diagnosis: thrombosis or pregnancy morbidity (recurrent miscarriage ≥3 <10 weeks; one loss ≥10 weeks; premature birth <34 weeks) PLUS positive antiphospholipid antibody on two occasions ≥12 weeks apart. Tests: lupus anticoagulant; anti-cardiolipin IgG/IgM >40 GPL/MPL units; anti-β2-GPI IgG/IgM >99th centile. Triple positivity (all three positive) = highest thrombosis risk. Treatment: venous thrombosis → warfarin INR 2–3. Avoid DOACs in triple-positive APS. Arterial thrombosis → warfarin INR 2–3 ± aspirin. Obstetric APS → aspirin + LMWH.
Anti-SSA (Ro) crosses placenta → congenital heart block (CHB), risk ~2% (rises to 15–20% after previously affected pregnancy). Surveillance: fetal echocardiography weekly/fortnightly from 16–26 weeks. Transient neonatal rash, cytopaenias resolve as maternal antibodies clear. CHB often requires permanent pacing; mortality 15–20%.
Anti-dsDNA tracks activity Anti-Sm most specific APS: 12 weeks apart CHB: echo 16–26 weeks HCQ: continue in pregnancy
Radiological criterion: bilateral sacroiliitis grade ≥2 OR unilateral grade ≥3. Plus at least one clinical criterion: inflammatory back pain ≥3 months; limitation of lumbar motion in both planes; reduced chest expansion. Radiological criterion alone is insufficient. Schober's test: increase <5 cm on forward flexion indicates lumbar restriction.
BASDAI ≥4 (0–10 scale) + assessor agrees disease is active + failure of two NSAIDs at maximum tolerated dose for ≥4 weeks each. No requirement for elevated CRP or MRI evidence (though supportive). cDMARDs are not a required bridge step — go directly to biologic after NSAID failure.
BASDAI ≥4 → biologic No cDMARDs for axial SpA HLA-B27: 90% in AS IL-17-i: avoid in Crohn's
| Feature | MSU (Gout) | CPPD (Pseudogout) | BCP/Hydroxyapatite |
|---|---|---|---|
| Crystal shape | Needle | Rhomboid | Non-crystalline aggregates |
| Birefringence | Negative (strong) | Weakly positive | None — invisible on PLM |
| Colour parallel to slow axis | Yellow | Blue | Not applicable |
| Commonest joint | MTP1 (podagra) | Knee | Shoulder (rotator cuff) |
| Identification | Polarised light microscopy | Polarised light microscopy | Alizarin red S stain; EM |
| X-ray | Punched-out erosions; tophi | Chondrocalcinosis | Calcific tendinitis; joint destruction |
| Associations | Hyperuricaemia; thiazides; low-dose aspirin | HATCH: Hyperparathyroidism, Ageing, Thyroid (hypo), Chondrocalcinosis hereditary, Haemochromatosis | Elderly women; rotator cuff tear |
Acute attack: NSAIDs, colchicine, or corticosteroids (all equally effective). Do not start or stop ULT during an acute attack. ULT indication: ≥2 attacks/year; tophi; urate nephropathy; uric acid stones. Target SUA: <6 mg/dL (<360 μmol/L); <5 mg/dL in tophaceous gout. Allopurinol: start at 50–100 mg/day; titrate slowly; can uptitrate in CKD with monitoring (old dose-cap guidelines are outdated). Prophylaxis: colchicine 0.5 mg/day for first 3–6 months of ULT to cover mobilisation flares.
| Raise SUA | Lower SUA |
|---|---|
| Thiazides; loop diuretics; low-dose aspirin; ciclosporin; pyrazinamide; ethambutol; nicotinic acid | Losartan; fenofibrate; SGLT2 inhibitors; high-dose aspirin (>3 g/day); allopurinol; febuxostat; probenecid |
Normal SUA does not exclude gout ULT: start 2–4 wks post-attack Milwaukee: alizarin red S Losartan is uricosuric
| Size | Disease | Key Distinguishing Features |
|---|---|---|
| Large | Takayasu arteritis | Women <40; aorta + branches; BP asymmetry; MRA/CTA; prednisolone |
| Large | Giant cell arteritis (GCA) | Age >50; temporal artery; halo sign on USS; PMR overlap; visual threat → prednisolone 60 mg immediately |
| Medium | Polyarteritis nodosa (PAN) | No GN; no lung; ANCA negative; microaneurysms; HBV-associated → antivirals |
| Medium | Kawasaki disease | Children; fever >5 days; coronary aneurysm; IV immunoglobulin + aspirin |
| Small (AAV) | GPA (Wegener's) | c-ANCA/PR3; ENT + lung (cavitating) + kidney; pauci-immune crescentic GN; cyclophosphamide or rituximab |
| Small (AAV) | MPA | p-ANCA/MPO; GN + pulmonary haemorrhage; no ENT; treat as AAV |
| Small (AAV) | EGPA (Churg-Strauss) | p-ANCA/MPO (40%); asthma + eosinophilia + vasculitis; cardiac = leading cause of death; mepolizumab for relapsing disease |
PAN: medium vessels; no glomerulonephritis; no pulmonary involvement; ANCA negative; microaneurysms on angiography; HBV association. MPA: small vessels; pauci-immune crescentic GN; pulmonary capillaritis; p-ANCA/MPO positive. This distinction appears in almost every exam diet.
Any visual symptoms (amaurosis fugax, diplopia, blurring) → start prednisolone 60 mg/day immediately, before biopsy. Temporal artery biopsy remains accurate for 2–4 weeks after steroid initiation. Halo sign on USS (hypoechoic wall thickening) replaces biopsy in experienced centres. Tocilizumab (IL-6 receptor inhibitor): approved for relapsing/refractory GCA; allows faster steroid tapering.
GCA visual Sx → steroids first PAN: no GN, no lung, ANCA-ve EGPA: cardiac = leading death EGPA: mepolizumab (anti-IL-5)
| Antibody | Disease/Syndrome | Key Clinical Point |
|---|---|---|
| Anti-Jo-1 | Antisynthetase syndrome | ILD + myositis + arthritis + mechanic's hands + Raynaud's; ILD = leading cause of death |
| Anti-Mi-2 | Classic dermatomyositis | Florid skin; good steroid response; low ILD risk |
| Anti-MDA5 | Amyopathic DM | Rapidly progressive ILD (fatal within weeks); skin ulceration; CK may be normal |
| Anti-TIF1-γ | Dermatomyositis | Strong malignancy association (adults >40); screen for cancer |
| Anti-SRP | Immune-mediated necrotising myopathy | Very high CK; severe; poor steroid response; statins can trigger |
| Anti-HMGCR | Statin-associated IMNM | Persists after statin withdrawal; needs immunosuppression |
Occurs after ≥4–6 weeks on ≥40 mg/day prednisolone. CK is normal; ESR/CRP are normal; EMG shows no spontaneous activity (no fibrillations). This distinguishes it from a PM/DM flare (which gives elevated CK, elevated CRP, and fibrillations on EMG). Management: reduce the steroid dose — increasing steroids worsens the myopathy. Type II fibre atrophy on biopsy.
| Feature | Limited SSc (lcSSc) | Diffuse SSc (dcSSc) |
|---|---|---|
| Antibody | Anti-centromere (ACA) | Anti-Scl-70 (topoisomerase I); anti-RNA pol III |
| Skin | Distal to elbows/knees; face | Trunk, face, proximal limbs |
| Organs | PAH >> ILD; CREST | ILD (early, severe) >> PAH; renal crisis |
| Leading cause of death | Pulmonary arterial hypertension | ILD (anti-Scl-70); renal crisis (anti-RNA pol III) |
Emergency: acute hypertension + rapidly rising creatinine + microangiopathic haemolytic anaemia (schistocytes, thrombocytopaenia). Occurs in early dcSSc, typically first 4–5 years. Risk factor: prednisolone ≥15 mg/day (precipitates SRC). Treatment: ACE inhibitor (captopril) immediately, regardless of degree of renal impairment. Do not withhold. Up to 50% still require dialysis; 50% of those can discontinue after 1–2 years of continued ACE inhibition.
ACR/EULAR 2016 criteria: positive ANA entry; then scored items including focal lymphocytic sialadenitis (focus score ≥1/4mm²) = 3 points (highest single item); anti-SSA = 3 points; threshold ≥4. Most important long-term complication: NHL (MALT lymphoma) — 15–44× increased risk. Lymphoma risk predictors: persistent parotid enlargement, palpable purpura, cryoglobulinaemia, low C4, monoclonal IgM band. Extraglandular: distal RTA type 1 (urine pH >5.5 despite acidosis; hypokalaemia → paralysis).
Steroid myopathy: normal CK SRC: captopril immediately Prednisolone ≥15 mg precipitates SRC Sjogren's: lymphoma risk
| Disease | Leading Cause of Death | Key Note |
|---|---|---|
| SLE | Infection; cardiovascular disease; renal failure | CV risk from accelerated atherosclerosis + steroids |
| Limited SSc (ACA+) | Pulmonary arterial hypertension | Annual echo surveillance; endothelin antagonists |
| Diffuse SSc (Scl-70+) | Interstitial lung disease | HRCT + PFT at diagnosis; nintedanib/MMF for ILD |
| MCTD (U1-RNP+) | Pulmonary arterial hypertension | Annual echo mandatory in all MCTD patients |
| Antisynthetase (Jo-1+) | Interstitial lung disease | NSIP pattern; aggressive immunosuppression |
| EGPA | Cardiac involvement | Eosinophilic myocarditis; echo at diagnosis |
| GPA/MPA | Infection (treatment era); historically renal failure | Rituximab for maintenance reduces infection risk |
Continue indefinitely in SLE — do not stop in remission. Maximum safe dose: ≤5 mg/kg/day of actual body weight (not ideal body weight — this is the exam trap; old guideline was 6.5 mg/kg ideal). Retinal toxicity risk rises sharply after 5 years. Annual retinal screening from year 5: automated visual fields + SD-OCT. Bull's-eye maculopathy = stop HCQ. Retinal damage is largely irreversible. Safe in pregnancy (reduces flare risk; do not stop).
MTX pneumonitis: idiosyncratic hypersensitivity; any dose; any time; upper-lobe ground glass on HRCT; BAL CD4+ lymphocytosis. Not prevented by folic acid. Stop MTX immediately; corticosteroids for moderate-severe disease; do not restart. RA-ILD: UIP pattern (basal honeycombing); slowly progressive; occurs independent of MTX use.
Primary: young women; symmetric; no ulcers; normal nail-fold capillaroscopy; ANA negative; benign. Secondary: asymmetric; digital ulcers; abnormal nail-fold capillaroscopy (giant capillaries, avascular areas = scleroderma pattern); ANA positive; specific antibodies. Nail-fold capillaroscopy is the single best test to distinguish primary from secondary and predict CTD development. Treatment: CCBs (nifedipine) first-line for both.
HCQ: ≤5 mg/kg actual wt MTX pneumonitis: stop, don't restart Nail-fold cap: best Raynaud's test Anti-centromere → PAH Anti-Scl-70 → ILD
For clinical reasoning practice, return to the seven Morning Rounds quizzes linked in the series index.