Free USMLE Step 2 CK Rheumatology practice questions

This woman has objective dryness: a Schirmer result of 5 mm or less in 5 minutes and an unstimulated salivary flow of 0.1 mL/min or less, each worth 1 point under the 2016 ACR/EULAR classification criteria. The main mimics have been excluded (anticholinergic drugs, radiation, HIV, hepatitis C, IgG4-related disease and sarcoidosis). However, she is seronegative for anti-Ro/SSA, so she has only 2 points. A diagnosis of Sjogren disease requires at least 4, and only two items carry 3 points: anti-Ro/SSA positivity and a labial gland biopsy showing focal lymphocytic sialadenitis. With anti-Ro negative, a labial minor salivary gland biopsy is the decisive test.

The biopsy is done under local anesthesia through a small incision in the inner lower lip, removing several minor glands. A focus score of 1 or more (at least one aggregate of 50 or more lymphocytes per 4 mm² of gland) scores 3 points and would bring her to 5, establishing the diagnosis. Making the diagnosis matters even for a patient with mainly sicca symptoms, because it prompts monitoring for extraglandular disease (renal tubular acidosis, neuropathy, lung disease) and lymphoma.

A. Repeating the antibody test is unlikely to change the result; about a third of patients with Sjogren disease are anti-Ro negative. C. Fine-needle aspiration of the parotid is used for a discrete mass or suspected lymphoma, not for diagnosing Sjogren disease. D. ACE levels are nonspecific, and her chest radiograph already makes sarcoidosis unlikely. E. Sialography is no longer part of the classification criteria and is less specific than histology.

This older woman has knee and first carpometacarpal osteoarthritis with persistent pain despite exercise. The ACR/Arthritis Foundation guideline makes topical NSAIDs the first drug for knee OA and conditionally recommends them for hand OA, and they are especially preferred at age 75 or older or with comorbidity because systemic absorption is minimal. Her CKD with an eGFR of 34, prior peptic ulcer and treatment with both an ACE inhibitor and a thiazide make systemic NSAIDs hazardous, while diclofenac gel applied to the knee and thumb bases gives similar local relief with far less renal, GI and cardiovascular exposure. A thumb-base orthosis is a useful addition.

A. Oral naproxen in a patient on an ACE inhibitor and a diuretic creates the triple whammy combination that can precipitate acute kidney injury, and her prior ulcer and CKD add GI and renal risk. C. Opioids other than tramadol are avoided in OA because of falls, dependence and poor long-term benefit, risks magnified at her age. D. Glucosamine and chondroitin perform no better than placebo and are recommended against. E. Systemic glucocorticoids have no role in osteoarthritis; corticosteroids are given only as intra-articular injections for flares.

Neck pain radiating down the posterior arm with a positive Spurling test indicates a cervical radiculopathy, and the deficits localize the root. C7 supplies the triceps (elbow extension), wrist flexors and finger extensors, carries the triceps reflex, and provides sensation to the middle finger. This patient's weak elbow extension and wrist flexion, isolated triceps hyporeflexia and middle finger numbness therefore indicate a left C7 radiculopathy, the most commonly affected cervical root. Because cervical roots exit above the vertebra of the same number, the usual cause is a C6 to C7 disc herniation or foraminal stenosis. Conservative care is first-line, with MRI reserved for progressive deficits, myelopathy, red flags or persistent symptoms.

A. C6 radiculopathy causes weakness of wrist extension and elbow flexion, a reduced brachioradialis (and biceps) reflex and numbness of the thumb and index finger, all of which are normal here. C. C8 radiculopathy weakens finger flexors and hand intrinsics (grip) and causes numbness of the ring and little fingers and medial forearm, without a reliable reflex change. D. Ulnar neuropathy at the elbow causes weakness of hand intrinsics and numbness of the little finger and half of the ring finger, with no neck pain or triceps changes. E. Carpal tunnel syndrome causes numbness in the thumb, index, middle and part of the ring finger with thenar weakness, but it does not affect the triceps or its reflex or cause pain provoked by neck movement.

A young man with more than 3 months of inflammatory back pain (onset before 40, insidious, nocturnal and morning pain, improvement with exercise but not rest, good NSAID response), prior acute anterior uveitis, elevated CRP, and HLA-B27 has a high probability of axial spondyloarthritis. Radiographic sacroiliitis takes years to develop, so normal pelvic films do not exclude early disease (nonradiographic axial spondyloarthritis). MRI of the sacroiliac joints, including fluid-sensitive (STIR or fat-saturated T2) sequences, detects bone marrow edema of active sacroiliitis before structural damage appears, and current ACR/SAA/SPARTAN guidance recommends it when radiographs are normal or indeterminate. Confirming the diagnosis matters because NSAIDs and physical therapy are first-line, and TNF inhibitors are effective for persistent activity, whereas methotrexate does not treat axial disease.

B. Waiting 2 years for radiographic change delays diagnosis and treatment when MRI can show active inflammation now.

C. Bone scintigraphy is sensitive but nonspecific for sacroiliitis and has been replaced by MRI.

D. CT myelography evaluates spinal canal and nerve root compression; this patient has no radicular or neurologic findings.

E. Rheumatoid factor is negative in spondyloarthropathies by definition and does not help confirm axial disease.

This older man has true weakness of abduction and external rotation and a positive drop-arm test after a fall, with preserved passive motion. That combination indicates a full-thickness rotator cuff tear, most often of the supraspinatus, extending into the infraspinatus. Radiographs, the appropriate first study after shoulder trauma, have already excluded fracture and dislocation. The next step is soft-tissue imaging of the cuff, with MRI (or diagnostic ultrasound where local expertise is available) to confirm the tear and define its size, retraction, and muscle quality.

The timing matters. An acute traumatic full-thickness tear in a patient who was functional before the injury is usually best repaired early, before the tendon retracts and the muscle atrophies, so imaging should not be deferred for a long trial of therapy. This differs from atraumatic tendinopathy with a painful arc and normal strength, in which no imaging is needed at first and conservative care is started.

A. Electromyography would be useful for a suspected axillary or suprascapular nerve injury, but normal sensation and reflexes and a mechanical drop-arm sign point to a tendon tear; it is not the first test. B. CT shows bone well but is poor at demonstrating tendon tears without arthrography. C. MRI of the cervical spine evaluates radiculopathy, which is unlikely with full painless neck motion, a negative Spurling test, and a normal neurologic examination. E. Repeat radiographs are used to look for an occult fracture, such as of the scaphoid; they cannot show a tendon tear and would delay a time-sensitive repair.

This man has a rapidly progressive glomerulonephritis: creatinine has nearly quadrupled over months, the sediment is nephritic (dysmorphic red cells and red cell casts), and the biopsy shows crescents. The immunofluorescence pattern sorts RPGN into three groups: linear IgG (anti-GBM disease), granular deposits (immune complex disease such as lupus, IgA nephropathy, or PSGN), and little or no staining, called pauci-immune, which means ANCA-associated vasculitis. Normal C3 and C4 fit both anti-GBM disease and ANCA vasculitis and argue against immune complex disease.

Within the ANCA vasculitides, the organ pattern names the disease. Granulomatosis with polyangiitis involves the upper airway (chronic refractory sinusitis, bloody crusts, septal perforation that can progress to saddle nose), the lower airway (nodules that often cavitate), and the kidney (pauci-immune crescentic GN). It is usually associated with c-ANCA directed against proteinase 3 (PR3). The pending serology would be expected to show PR3-ANCA, but the clinical and biopsy picture is already diagnostic enough to begin induction therapy with glucocorticoids plus rituximab or cyclophosphamide.

A. Anti-GBM disease also causes lung and kidney involvement, but the hallmark is diffuse alveolar hemorrhage rather than cavitating nodules, there is no destructive sinonasal disease, and the biopsy shows bright linear IgG along the basement membrane, not pauci-immune staining. B. EGPA is a pauci-immune vasculitis, but it occurs with asthma, allergic rhinitis, and peripheral eosinophilia, all absent here. D. Microscopic polyangiitis causes pauci-immune GN and pulmonary capillaritis with MPO-ANCA but lacks granulomatous inflammation, so destructive upper airway disease and cavitating nodules point away from it. E. Class IV lupus nephritis is an immune complex GN with full-house granular immunofluorescence and low C3 and C4, which this patient does not have.

This woman with known high-risk APS developed thrombosis in three or more organs within less than a week: brain (confusion), lungs (hypoxemia and infiltrates), kidneys (acute kidney injury and infarcts), spleen and skin (digital ischemia and livedo), with thrombocytopenia. Classic triggers are present: surgery and interruption of anticoagulation without bridging. This is catastrophic antiphospholipid syndrome (CAPS), a rare, widespread small-vessel thrombotic storm with a mortality of roughly one-third.

The laboratory pattern helps exclude look-alikes: ADAMTS13 activity is preserved, schistocytes are rare, and fibrinogen and INR are normal. Treatment should start immediately without waiting for biopsy confirmation: triple therapy with therapeutic heparin, high-dose glucocorticoids, and plasma exchange and/or IVIG, plus treatment of any trigger. Rituximab or eculizumab is considered for refractory disease.

A. TTP also causes thrombocytopenia, neurologic and renal involvement, but it is defined by severely reduced ADAMTS13 activity (below 10%) with abundant schistocytes and hemolysis; her ADAMTS13 is normal. B. HIT requires heparin exposure 5 to 10 days earlier; she received only mechanical prophylaxis and no heparin. D. DIC consumes clotting factors, so fibrinogen falls and the INR rises; both are normal here. E. Septic emboli from endocarditis can cause renal and splenic infarcts and digital lesions, but she has only low-grade fever, no murmur is described, and the setting of APS with interrupted anticoagulation and diffuse livedo points to CAPS; blood cultures should still be drawn.

In an older adult, chronic symmetric wrist and MCP synovitis that is seronegative and accompanied by chondrocalcinosis of the triangular fibrocartilage and menisci, plus a recent self-limited acute knee attack, suggests calcium pyrophosphate deposition disease presenting as pseudo-RA. Because this mimic is common in the elderly and is managed differently from RA, the accessible effusion should be aspirated before any DMARD is started. Synovial fluid examined under compensated polarized light shows rhomboid, weakly positively birefringent CPP crystals, which confirms the diagnosis; the fluid should also go for cell count, Gram stain, and culture. Treatment of CPPD focuses on NSAIDs, colchicine, or intra-articular glucocorticoid for flares, low-dose colchicine for prophylaxis, and screening for associated conditions (hyperparathyroidism, hemochromatosis, hypomagnesemia, hypothyroidism).

A. Methotrexate may eventually be considered for refractory chronic CPP arthritis, but starting it before establishing the diagnosis treats this patient as having RA when the radiographs point elsewhere.

B. Allopurinol lowers urate in gout; CPPD has no equivalent crystal-dissolving therapy, and the uric acid level is normal.

C. MRI of the wrists would show synovitis and edema but does not identify crystals and is less informative and more costly than a simple aspiration.

D. Synovial biopsy is invasive and reserved for unexplained chronic monoarthritis, such as suspected tuberculosis or pigmented villonodular synovitis; fluid analysis comes first.