Rheumatology

150591010

RheumatologyAll New Content, Including 96 Multiple-Choice Questions

14 AMA PRA Category 1 Credits™

available until July 31, 2015.

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Medical Knowledge Self -Assessment Program®

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Table of Contents

Hormones. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16Antibodies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16Environmental Factors. . . . . . . . . . . . . . . . . . . . . 16

Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16Clinical Manifestations. . . . . . . . . . . . . . . . . . . . . 16Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16

Complications and Extra-Articular Manifestations. . . . 18Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

NSAIDs and Corticosteroids . . . . . . . . . . . . . . . . 20Disease-Modifying Antirheumatic Drugs . . . . . . . 20Surgical Therapy . . . . . . . . . . . . . . . . . . . . . . . . . 21Nonpharmacologic Management. . . . . . . . . . . . . 21

Rheumatoid Arthritis and Pregnancy . . . . . . . . . . . . . 21

OsteoarthritisPathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22Clinical Features and Classification . . . . . . . . . . . . . . . 22

Primary Osteoarthritis . . . . . . . . . . . . . . . . . . . . . 23Secondary Osteoarthritis . . . . . . . . . . . . . . . . . . . 23Erosive Osteoarthritis . . . . . . . . . . . . . . . . . . . . . 23Diffuse Idiopathic Skeletal Hyperostosis. . . . . . . . 23

Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24Imaging Studies. . . . . . . . . . . . . . . . . . . . . . . . . . 24

Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24Nonpharmacologic Interventions. . . . . . . . . . . . . 24Pharmacologic Therapy . . . . . . . . . . . . . . . . . . . . 25Intra-articular Injection . . . . . . . . . . . . . . . . . . . . 25Surgical Intervention . . . . . . . . . . . . . . . . . . . . . . 25

FibromyalgiaEpidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26Evaluation and Diagnosis . . . . . . . . . . . . . . . . . . . . . . 26Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27

Nonpharmacologic Therapy . . . . . . . . . . . . . . . . 27Pharmacologic Therapy . . . . . . . . . . . . . . . . . . . . 27

SpondyloarthritisPathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28

Genetic Predisposition . . . . . . . . . . . . . . . . . . . . . 28Environmental Triggers . . . . . . . . . . . . . . . . . . . . 28

Classification. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28Ankylosing Spondylitis. . . . . . . . . . . . . . . . . . . . . 29

Approach to the Patient with Rheumatic DiseaseInflammatory Versus Noninflammatory Pain. . . . . . . . . 1The Musculoskeletal Examination. . . . . . . . . . . . . . . . . 1Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Monoarticular Arthritis . . . . . . . . . . . . . . . . . . . . . 2Oligoarthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2Polyarthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Extra-Articular Manifestations of Rheumatic Disease. . . 3Dermatologic Manifestations . . . . . . . . . . . . . . . . . 3Fever . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3Inflammatory Eye Disease . . . . . . . . . . . . . . . . . . . 3Lung Disease. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4Diarrhea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5Musculoskeletal and Rheumatic Manifestations . . . 5

Laboratory Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6Tests That Measure Inflammation . . . . . . . . . . . . . 6Antibody Tests. . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

Imaging Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7Radiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7CT and MRI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8Ultrasonography . . . . . . . . . . . . . . . . . . . . . . . . . . 8

Joint Aspiration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8

Principles of TherapeuticsEvaluation of Disease Progression . . . . . . . . . . . . . . . . . 9Anti-Inflammatory Agents . . . . . . . . . . . . . . . . . . . . . . 9

NSAIDs. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9Analgesics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10Colchicine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10Corticosteroids . . . . . . . . . . . . . . . . . . . . . . . . . . 10

Disease-Modifying Antirheumatic Drugs . . . . . . . . . . 11Nonbiologic Disease-Modifying Antirheumatic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11Biologic Disease-Modifying Antirheumatic Drugs. . 12

Urate-Lowering Therapy . . . . . . . . . . . . . . . . . . . . . . 14Allopurinol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15Febuxostat. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15Probenecid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15Uricase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

Rheumatoid ArthritisPathophysiology and Risk Factors . . . . . . . . . . . . . . . . 15

Genetic Factors . . . . . . . . . . . . . . . . . . . . . . . . . . 15

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Psoriatic Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . 30Inflammatory Bowel Disease–Associated Arthritis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30Reactive Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . 30

Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31Laboratory Studies . . . . . . . . . . . . . . . . . . . . . . . 32Imaging Studies. . . . . . . . . . . . . . . . . . . . . . . . . . 32

Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33Axial Involvement . . . . . . . . . . . . . . . . . . . . . . . . 33Peripheral Involvement . . . . . . . . . . . . . . . . . . . . 34Reactive Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . 34

Systemic Lupus ErythematosusPathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35Clinical Manifestations . . . . . . . . . . . . . . . . . . . . . . . . 35

Mucocutaneous Manifestations . . . . . . . . . . . . . . 35Musculoskeletal Manifestations . . . . . . . . . . . . . . 35Kidney Manifestations . . . . . . . . . . . . . . . . . . . . . 36Neurologic Manifestations . . . . . . . . . . . . . . . . . . 36Cardiovascular Manifestations . . . . . . . . . . . . . . . 37Pulmonary Manifestations . . . . . . . . . . . . . . . . . . 37Hematologic Manifestations . . . . . . . . . . . . . . . . 37Gastrointestinal Manifestations . . . . . . . . . . . . . . 37Malignancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38Differential Diagnosis . . . . . . . . . . . . . . . . . . . . . 39

Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40Reproductive Issues . . . . . . . . . . . . . . . . . . . . . . . . . . 40Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

Systemic SclerosisPathophysiology and Epidemiology . . . . . . . . . . . . . . 41Classification. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41Clinical Manifestations and Management . . . . . . . . . . 42

Cutaneous Manifestations . . . . . . . . . . . . . . . . . . 42Musculoskeletal Manifestations . . . . . . . . . . . . . . 43Vascular Manifestations . . . . . . . . . . . . . . . . . . . . 43Gastrointestinal Manifestations . . . . . . . . . . . . . . 43Kidney Manifestations . . . . . . . . . . . . . . . . . . . . . 43Pulmonary Manifestations . . . . . . . . . . . . . . . . . . 44Cardiac Manifestations. . . . . . . . . . . . . . . . . . . . . 44Scleroderma Spectrum Disorders . . . . . . . . . . . . . 45

Pregnancy and Systemic Sclerosis . . . . . . . . . . . . . . . . 45

Sjögren SyndromeEpidemiology and Pathophysiology . . . . . . . . . . . . . . 46Clinical Manifestations . . . . . . . . . . . . . . . . . . . . . . . . 46Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47

Mixed Connective Tissue DiseaseClinical Manifestations . . . . . . . . . . . . . . . . . . . . . . . . 47Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48Treatment and Prognosis . . . . . . . . . . . . . . . . . . . . . . 48

Crystal-Induced ArthropathiesGout. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 48Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . 48Clinical Manifestations. . . . . . . . . . . . . . . . . . . . . 50Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51

Calcium Pyrophosphate Deposition Disease . . . . . . . . 52Epidemiology and Pathophysiology . . . . . . . . . . . 52Clinical Manifestations. . . . . . . . . . . . . . . . . . . . . 53Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53

Basic Calcium Phosphate Deposition Disease . . . . . . . 54

Infectious ArthritisDiagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54

Clinical Manifestations and Physical Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54Laboratory and Radiographic Studies. . . . . . . . . . 54

Common Causes . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55Infection with Gram-Positive Organisms . . . . . . . 55Infection with Gram-Negative Organisms . . . . . . 55Lyme Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . 56Mycobacterial Infections . . . . . . . . . . . . . . . . . . . 56Fungal Infections. . . . . . . . . . . . . . . . . . . . . . . . . 56Viral Infections . . . . . . . . . . . . . . . . . . . . . . . . . . 56Prosthetic Joint Infections . . . . . . . . . . . . . . . . . . 57Infections in Previously Damaged Joints . . . . . . . 57

Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57Pharmacologic Therapy . . . . . . . . . . . . . . . . . . . . 57Surgical Management . . . . . . . . . . . . . . . . . . . . . 58

Idiopathic Inflammatory MyopathiesPathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58Clinical Manifestations . . . . . . . . . . . . . . . . . . . . . . . . 59

Muscular Manifestations . . . . . . . . . . . . . . . . . . . 59Cutaneous Manifestations . . . . . . . . . . . . . . . . . . 59Extramuscular Manifestations . . . . . . . . . . . . . . . 59Cardiopulmonary Manifestations . . . . . . . . . . . . . 60Gastrointestinal Manifestations . . . . . . . . . . . . . . 60

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Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60Muscle-Related Enzymes . . . . . . . . . . . . . . . . . . . 60Autoantibodies . . . . . . . . . . . . . . . . . . . . . . . . . . 60Imaging Studies. . . . . . . . . . . . . . . . . . . . . . . . . . 61Electromyography . . . . . . . . . . . . . . . . . . . . . . . . 61Muscle Biopsy . . . . . . . . . . . . . . . . . . . . . . . . . . . 61

Differential Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . 61Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62Association with Malignancy. . . . . . . . . . . . . . . . . . . . 62Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62

Systemic VasculitisLarge-Vessel Vasculitis. . . . . . . . . . . . . . . . . . . . . . . . . 64

Giant Cell Arteritis. . . . . . . . . . . . . . . . . . . . . . . . 64Polymyalgia Rheumatica . . . . . . . . . . . . . . . . . . . 65Takayasu Arteritis . . . . . . . . . . . . . . . . . . . . . . . . 65

Medium-Sized Vessel Vasculitis . . . . . . . . . . . . . . . . . . 66Polyarteritis Nodosa . . . . . . . . . . . . . . . . . . . . . . 66Kawasaki Disease . . . . . . . . . . . . . . . . . . . . . . . . . 66

Small-Vessel Vasculitis . . . . . . . . . . . . . . . . . . . . . . . . . 67Antineutrophil Cytoplasmic Antibodies and Associated Vasculitis. . . . . . . . . . . . . . . . . . . . . . . 67Cryoglobulinemic Vasculitis. . . . . . . . . . . . . . . . . 69Henoch-Schönlein Purpura . . . . . . . . . . . . . . . . . 69Cutaneous Leukocytoclastic Vasculitis . . . . . . . . . 69

Other Systemic Inflammatory DiseasesBehçet Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70

Clinical Manifestations and Diagnosis . . . . . . . . . 71Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71

Relapsing Polychondritis. . . . . . . . . . . . . . . . . . . . . . . 71Clinical Manifestations. . . . . . . . . . . . . . . . . . . . . 71Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72

Adult-Onset Still Disease . . . . . . . . . . . . . . . . . . . . . . 72Clinical Manifestations. . . . . . . . . . . . . . . . . . . . . 72Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73

Familial Autoinflammatory Diseases . . . . . . . . . . . . . . 73Diseases of Collagen . . . . . . . . . . . . . . . . . . . . . . . . . . 73

Osteogenesis Imperfecta . . . . . . . . . . . . . . . . . . . 73Ehlers-Danlos Syndrome . . . . . . . . . . . . . . . . . . . 73Marfan Syndrome . . . . . . . . . . . . . . . . . . . . . . . . 74

Sarcoidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74Clinical Manifestations. . . . . . . . . . . . . . . . . . . . . 75Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75

Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75

Self-Assessment Test . . . . . . . . . . . . . . . . . . . . . . 79

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151

Rheumatology

The MusculoskeletalExaminationIdentifying the source of pain is essential when determiningthe cause of musculoskeletal symptoms. Patients may fre-quently refer to their symptoms as “joint pain” (for example,shoulder or hip), although the source may be periarticular (forexample, rotator cuff or trochanteric bursa).

Palpation of the joint can determine the presence of ten-derness, warmth, or swelling. Pain associated with direct pal-pation of the joint line suggests arthritis or a joint-associatedpathology (for example, meniscal injury). Pain associated withthe surrounding soft tissues can suggest other pathology (forexample, bursitis, ligamentous strain, or tendinitis).Examination for the presence of swelling can be difficult. Thecapsule from many joints extends beyond the immediate jointline. The suprapatellar bursa, which is a reflection of the trueknee joint capsule along the distal femur, is perhaps the bestknown example. To examine for a knee effusion, palpate thispotential space while compressing the suprapatellar bursa.Similarly with other joints (for example, metacarpophalangealjoints), it is important to envelop the potential joint space(support the palmar aspect of the joint) while compressing themedial and lateral joint lines.

Examination of the joint for passive and active range ofmotion is also important. Pain with passive range of motion(in which the joint is rotated but the tendons are not activelyengaged) suggests an arthritic condition. Pain with activeresisted range of motion (in which the joint is immobilizedwhile the patient tries to move the extremity) suggests tendonpathology. Overuse of a tendon or excessive strain across a

Approach to the Patientwith Rheumatic DiseaseInflammatory VersusNoninflammatory PainDistinguishing between inflammatory and noninflammatoryjoint pain is critical in evaluating patients with musculoskele-tal conditions (Table 1). Inflammation may be the only symp-tom that distinguishes psoriatic arthritis from osteoarthritis orsystemic lupus erythematosus (SLE) from fibromyalgia.

Joint pain is associated with loss of function. Non -inflammatory pain arises from sources such as prostaglandins,cathepsin, chemokines, and growth factors. Cytokines (inter-leukin [IL]-1, IL-6, and tumor necrosis factor [TNF]) areincreasingly recognized sources of inflammatory pain.

Inflammatory pain can be distinguished from noninflam-matory pain by the presence of redness, heat, and/or swelling.Subjective manifestations of joint inflammation include morn-ing stiffness for more than 60 minutes as well as constitutionalsymptoms such as fatigue and malaise; objective findingsinclude soft-tissue swelling around the joint, joint effusions,joint erythema, and warmth.

K E Y P O I N T S

• Inflammatory joint pain can be distinguished fromnoninflammatory pain by the presence of redness,heat, and/or swelling of the joint.

• Patients with joint inflammation typically have morn-ing stiffness, fatigue, and malaise.

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TABLE 1 . Features of Inflammatory Versus Noninflammatory Pain

Feature Inflammatory Pain Noninflammatory Pain

Physical examination findings Synovitis; erythema; warmth; soft-tissue swelling No synovitis; bony enlargement may occur in osteoarthritis

Morning stiffness >60 min <30 min

Constitutional symptoms Fever; fatigue Generally absent

Synovial fluid Leukocyte count >2000/µL (2.0 × 109/L), Leukocyte count <2000/µL (2.0 × 109/L), less predominantly neutrophils than 50% neutrophils

Other laboratory findings Elevated inflammatory markers (ESR, CRP); Inflammatory markers usually normal or anemia of chronic disease minimally elevated

Arthritis imaging studies Symmetric joint-space narrowing; periarticular Asymmetric joint-space narrowing; osteopenia; erosions osteophytes; subchondral sclerosis

CRP = C-reactive protein; ESR = erythrocyte sedimentation rate.

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deconditioned muscle may lead to localized pain syndromes(Table 2).

K E Y P O I N T S

• Pain associated with direct palpation of the joint linesuggests arthritis or a joint-associated pathology.

• Pain associated with passive range of motion suggestsan arthritic condition; pain with active resisted rangeof motion suggests tendon pathology.

ArthritisDiagnosing arthritis relies on pattern recognition. The type ofarthritis can be established by determining the duration ofsymptoms (acute versus chronic), number of affected joints,whether symptoms and signs point to an inflammatory ornoninflammatory condition, and whether joint involvementis symmetric or asymmetric.

Monoarticular ArthritisMonoarticular arthritis is classified as acute or chronic. Acutemonoarticular arthritis can be noninflammatory (traumatichemarthrosis, internal derangement) or inflammatory (crystallineor septic). In the setting of acute monoarticular arthritis, joint

Approach to the Patient with Rheumatic Disease

aspiration is needed to evaluate for infectious arthritis (see JointAspiration). Suspicion for infectious arthritis should be guided byclinical presentation and examination. Hematogenous sources forinfection or local skin breaks should be sought.

Chronic inflammatory monoarticular arthritis (signs ofinflammation present 26 weeks) should raise concern formycobacterial, fungal, or Borrelia burgdorferi infection.Synovial fluid analysis alone may be inadequate for diagnosis;therefore, systemic evidence of infection (serologies or otherlaboratory tests) or synovial biopsy may be required to estab-lish the diagnosis. Chronic noninflammatory monoarticulararthritis is usually caused by osteoarthritis.

OligoarthritisAcute inflammatory oligoarthritis (involvement of two tofour joints) may be caused by gonorrhea or rheumatic fever.Chronic inflammatory oligoarthritis can be caused by spondy-loarthritis or a connective tissue disease. Chronic noninflam-matory oligoarthritis is usually caused by osteoarthritis.

PolyarthritisAcute polyarthritis (involvement of more than four joints) canbe caused by viral infections (parvovirus B19, HIV, hepatitisB, rubella) or may be an early manifestation of a chronic

TABLE 2 . Common Overuse Syndromes

Region Etiology Symptoms Examination Findings

Shoulder Rotator cuff tendinitis Pain in upper outer arm; pain Pain on abducting arm between with overhead activities or 30 and150 degrees; less pain on reaching behind the back passive motion of shoulder

Biceps tendinitis Pain in anterior shoulder; pain Pain on palpation of biceps tendonworsens when lifting heavy objects

Elbow Lateral epicondylitis Pain at lateral epicondyle; pain Tender lateral epicondylewhen carrying briefcase/purse or gripping steering wheel

Wrist de Quervain tenosynovitis Pain along radial aspect of wrist Positive Finkelstein test (pain grabbing thumb and stretching abducenstendon) or pain palpating the tendon

Carpal tunnel syndrome Pain and paresthesia in palmar Positive Tinel sign (symptoms aspect of first three digits and radial reproduced by tapping palmar aspect of the fourth aspect of wrist with flat end of

reflex hammer)

Hand Trigger finger Locking of finger on flexion; pain and Flexor tendon nodule on palmar crepitus on palpation of tendon sheath aspect of metacarpophalangeal joint

Buttocks Ischial bursitis Pain in buttocks, worsens when Pain on palpation of ischium(weaver’s bottom) sitting

Piriformis syndrome Pain in buttocks with symptoms Pain on deep palpation of buttocks inof sciatica region of sciatic notch

Hip Trochanteric bursitis Pain in lateral hip, worsens when Pain on palpation over lateral lying on that side trochanter of the hip

Knee Pes anserine bursitis Pain just below knee at Tenderness at anteromedial aspect of anteromedial aspect of the tibia the tibia just below the kneewhen exercising or climbing stairs

Foot Plantar fasciitis Pain on bottom of the heel when Tenderness along medial aspect of the walking base of the heel

Self-

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Rheumatology Self-Assessment TestThis self-assessment test contains one-best-answer multiple-choice questions. Please read these directions carefullybefore answering the questions. Answers, critiques, and bibliographies immediately follow these multiple-choicequestions. The American College of Physicians is accredited by the Accreditation Council for Continuing MedicalEducation (ACCME) to provide continuing medical education for physicians.

The American College of Physicians designates MKSAP 16 Rheumatology for a maximum of 14 AMA PRACategory 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participationin the activity.

Earn “Same-Day” CME Credits OnlineFor the first time, print subscribers can enter their answers online to earn CME credits in 24 hours or less. You cansubmit your answers using online answer sheets that are provided at mksap.acponline.org, where a record of yourMKSAP 16 credits will be available. To earn CME credits, you need to answer all of the questions in a test andearn a score of at least 50% correct (number of correct answers divided by the total number of questions). Takeany of the following approaches:

➢ Use the printed answer sheet at the back of this book to record your answers. Go to mksap.acponline.org,access the appropriate online answer sheet, transcribe your answers, and submit your test for same-dayCME credits. There is no additional fee for this service.

➢ Go to mksap.acponline.org, access the appropriate online answer sheet, directly enter your answers, andsubmit your test for same-day CME credits. There is no additional fee for this service.

➢ Pay a $10 processing fee per answer sheet and submit the printed answer sheet at the back of this book bymail or fax, as instructed on the answer sheet. Make sure you calculate your score and fax the answer sheetto 215-351-2799 or mail the answer sheet to Member and Customer Service, American College of Physi-cians, 190 N. Independence Mall West, Philadelphia, PA 19106-1572, using the courtesy envelope pro-vided in your MKSAP 16 slipcase. You will need your 10-digit order number and 8-digit ACP ID number,which are printed on your packing slip. Please allow 4 to 6 weeks for your score report to be emailed backto you. Be sure to include your email address for a response.

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CME credit is available from the publication date of July 31, 2012, until July 31, 2015. You may submit youranswer sheets at any time during this period.

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Item 1A 52-year-old man is evaluated in the emergency departmentfor a 2-week history of progressive fever and malaise withgradual onset of shortness of breath, pleuritic chest pain,myalgia, arthralgia, and rash. He reports no cough. He has a15-year history of rheumatoid arthritis, which is well con-trolled with methotrexate and etanercept; his last flare was 1year ago. Other medications are naproxen and folic acid.

On physical examination, temperature is 39.0 °C(102.2 °F), blood pressure is 148/94 mm Hg, pulse rate is90/min, and respiration rate is 22/min. Cardiac examina-tion is normal. Pulmonary examination reveals a left pleuralfriction rub. There is synovial thickening of the wrists andmetacarpophalangeal and proximal interphalangeal jointsbilaterally as well as small bilateral knee effusions. A non-blanching purpuric rash is noted over the distal lowerextremities.Laboratory studies: Hemoglobin 9.8 g/dL (98 g/L)Leukocyte count 2600/µL (2.6 × 109/L)Platelet count 128,000/µL (128 × 109/L)Erythrocyte 86 mm/h

sedimentation rateUrinalysis 1+ protein; 2-5 erythrocytes/

hpf; 5-10 leukocytes/hpf

Chest radiograph reveals blunted costophrenic anglesbilaterally without infiltrate.

Blood and urine culture results are pending.

Which of the following is the most appropriate diag-nostic test to perform next?

(A) Antinuclear antibody and anti–double-stranded DNAantibody assay

(B) Bone marrow aspiration and biopsy(C) CT of the chest, abdomen, and pelvis(D) Rheumatoid factor and anti–cyclic citrullinated pep-

tide antibody assay

Item 2A 42-year-old woman is evaluated for recurring pain andswelling of the left knee and right ankle that began 5 monthsago. At that time, she also had an episode of conjunctivitis aswell as dysuria, both of which resolved spontaneously. Thejoint pain and swelling persisted, and aspiration of the leftknee was performed, which revealed leukocytosis withoutevidence of crystals or bacteria. She started naproxen, whichprovided some relief; 1 month later, she switched toindomethacin, but there was no improvement. She thenbegan corticosteroid joint injections, which initially providedrelief, but now the pain and swelling have recurred. Sixmonths ago she also had an episode of nonbloody diarrheaof 5 days’ duration that resolved spontaneously.

On physical examination, vital signs are normal.Cutaneous examination is normal. There is no evidence ofconjunctivitis or iritis. Musculoskeletal examination

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reveals swelling, tenderness, and warmth of the left kneeand right ankle.

Rheumatoid factor, antinuclear antibody, andanti–cyclic citrullinated peptide antibody testing is negative.Lyme disease serology results are negative. Chlamydia tra-chomatis and Neisseria gonorrhoeae test results are negative.

Radiographs of the left knee and right ankle arenormal.

Which of the following is the most appropriate treat-ment for this patient?

(A) Colchicine(B) Glucosamine(C) Nitrofurantoin(D) Sulfasalazine

Item 3A 52-year-old man is evaluated for a 5-year history of grad-ually progressive left knee pain. He has 20 minutes of morn-ing stiffness, which returns after prolonged inactivity. Hehas minimal to no pain at rest. He reports no clicking orlocking of the knee. Over the past several months, the painhas limited his ambulation to no more than a few blocks.

On physical examination, vital signs are normal. BMIis 25. The left knee has a small effusion and some fullness atthe back of the knee; the knee is not erythematous or warm.Range of motion of the knee elicits crepitus. There is medialjoint line tenderness to palpation, bony hypertrophy, and amoderate varus deformity. There is no evidence of jointinstability on stress testing.

Radiographs of the knee reveal bone-on-bone joint-space loss and numerous osteophytes.

Which of the following is the most appropriate nextdiagnostic step for this patient?

(A) CT of the knee(B) Joint aspiration(C) MRI of the knee(D) No diagnostic testing

Item 4A 72-year-old woman is evaluated in the emergency depart-ment for severe right shoulder pain and swelling. Threeweeks ago, she injured her shoulder when falling from astepladder and went to the emergency department; radio -graphs of the shoulder revealed soft-tissue swelling. She par-tially improved, but the pain and swelling recurred after sev-eral days and gradually worsened. She has been takingacetaminophen for the pain, with no relief.

On physical examination, temperature is 37.1 °C(98.8 °F), blood pressure is 116/76 mm Hg, pulse rate is78/min, and respiration rate is 14/min. BMI is 23. Theright shoulder is swollen, erythematous, warm, and tender,particularly over the anterior surface. Range of motion ofthe shoulder elicits pain and is limited.

Item 1 Answer: A

Educational Objective: Diagnose drug-inducedlupus erythematosus.

Testing for antinuclear antibodies (ANA), as well asanti–double-stranded DNA antibodies and complementlevels, is indicated for this patient with suspected drug-induced lupus erythematosus (DILE) caused by thetumor necrosis factor (TNF)-α inhibitor etanercept. Hehas new-onset fever, arthralgia, myalgia, nonblanchingpurpuric rash, pleuritis, pancytopenia, and proteinuriawith active urine sediment, all of which are suggestive ofa clinical diagnosis of systemic lupus erythematosus(SLE). Although these findings might also be compati-ble with an infection, he has no focal symptoms or find-ings to suggest sepsis and has been appropriately testedwith blood and urine cultures.

Most patients with DILE caused by TNF-αinhibitors have fever, rash, arthritis, and hematologicabnormalities in the presence of positive ANA as wellas anti–double-stranded DNA antibodies. This clinicaland serologic profile is in contrast to DILE induced byother medications, which is characterized by positiveANA, antihistone antibodies, and anti–single-strandedDNA antibodies. Nephritis is not common but hasbeen reported in patients with DILE caused by TNF-α inhibitors.

If DILE and infection are both ruled out, bone mar-row aspiration and biopsy to evaluate for the presence of aprimary hematologic diagnosis or CT of the chest,abdomen, and pelvis to evaluate for lymphadenopathy sug-gestive of underlying lymphoma would be indicated.

Testing of rheumatoid factor and anti–cyclic citrulli-nated peptide (CCP) antibodies is not appropriate,because the patient has had a clear diagnosis of rheuma-toid arthritis, and, even if a flare were present, rheuma-toid factor and anti-CCP antibodies would not necessar-ily increase.

K E Y P O I N T

• Drug-induced lupus erythematosus caused bytumor necrosis factor α inhibitors is character-ized by fever, rash, arthritis, and hematologicabnormalities in the presence of positive anti-nuclear antibodies and anti–double-strandedDNA antibodies.

BibliographyWilliams EL, Gadola S, Edwards CJ. Anti-TNF-induced lupus.Rheumatology. 2009;48(7):716-720. [PMID: 19416947]

Item 2 Answer: DEducational Objective: Manage reactive arthritiswith sulfasalazine.

Treatment with sulfasalazine is appropriate for this patientwith reactive arthritis. Reactive arthritis is characterized bythe presence of inflammatory arthritis that manifests within2 months of an episode of bacterial gastroenteritis or non-gonococcal urethritis or cervicitis in a genetically predisposedpatient. Approximately one third of patients manifest theclassic triad of arthritis, urethritis, and conjunctivitis. Reactivearthritis is usually self-limited and remits within 6 monthswithout causing erosive damage; approximately 25% ofpatients develop a chronic persistent arthritis that can berefractory to treatment with NSAIDs. This patient hasreactive arthritis related to an episode of gastroenteritis.NSAIDs and corticosteroids have been ineffective in improv-ing her condition. Data on the use of disease-modifyingantirheumatic drugs in reactive arthritis are limited; however,sulfasalazine has been shown to have some efficacy in patientswith chronic reactive arthritis and may be beneficial for thispatient. The benefits of sulfasalazine in peripheral muscu-loskeletal manifestations of other forms of spondylo -arthritis, including psoriatic arthritis, inflammatory boweldisease–associated arthritis, and ankylosing spondylitis, alsosupport the use of sulfasalazine in reactive arthritis.

Colchicine is used to control inflammation in patientswith crystal-associated arthritis as well as some autoinflam-matory syndromes but is not used for patients with reactivearthritis.

Glucosamine may have a limited role in pain relief insome patients with osteoarthritis but has not been studiedor suggested for use in patients with reactive arthritis.

Despite the association between reactive arthritis andbacterial infection, antibiotics are indicated primarily foracute infection and generally are of dubious benefit forreactive joint disease. In some studies, a 3-month trial ofminocycline or a similar agent was shown to improve theclinical course of reactive arthritis, particularly when thiscondition was associated with Chlamydia trachomatisinfection. There is no role for nitrofurantoin in the treat-ment of this patient.

K E Y P O I N T

• Treatment with sulfasalazine is appropriate for apatient with chronic reactive arthritis who doesnot respond to NSAIDs or corticosteroids.

BibliographyCarter JD, Hudson AP. Reactive arthritis: clinical aspects and medicalmanagement. Rheum Dis Clin North Am. 2009;35(1):21-44.[PMID: 19480995]

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