Internal Medicine EOR: Rheumatologic / Musculoskeletal (2026) (Smarty PANCE)

What is Avascular Necrosis (AVN)?

Death of bone tissue due to disrupted blood supply, leading to bone collapse, most commonly affecting the femoral head.

What are the most common risk factors for AVN?

Corticosteroid use and chronic alcohol use (account for the majority of nontraumatic cases); also trauma, sickle cell disease, SLE, and the bends (dysbarism).

What is the most common site of avascular necrosis?

The femoral head, due to its tenuous retrograde blood supply.

What is the imaging study of choice for early AVN?

MRI, which detects changes before plain radiographs (earliest finding is the "double-line sign"); the crescent sign on X-ray indicates subchondral collapse.

What is the classic presentation of femoral head AVN?

Insidious groin pain worsened by weight-bearing and motion, with limited internal rotation and abduction.

What is the definitive treatment for advanced AVN of the hip?

Total hip arthroplasty; core decompression may be used in early (pre-collapse) disease.

What is Osteomyelitis?

Infection of bone, usually bacterial, that can be acute or chronic and arise from hematogenous spread, contiguous spread, or direct inoculation.

What is the most common causative organism of osteomyelitis overall?

Staphylococcus aureus (including MRSA).

Which organism is classically associated with osteomyelitis in sickle cell disease?

Salmonella species (though S. aureus remains common even in sickle cell patients).

Which organism is associated with osteomyelitis from puncture wounds through a shoe sole?

Pseudomonas aeruginosa.

What is the gold standard for diagnosing osteomyelitis?

Bone biopsy with culture; MRI is the most sensitive imaging study, while early plain films are often normal (changes lag 1-2 weeks).

What laboratory markers are useful in osteomyelitis?

Elevated ESR and CRP (CRP useful for tracking treatment response); blood cultures may be positive in hematogenous cases.

What is the treatment for osteomyelitis?

Prolonged culture-directed IV antibiotics (typically 4-6 weeks) plus surgical debridement of necrotic bone when indicated.

What is Septic Arthritis?

Infection within a joint space causing acute inflammatory monoarthritis that is a medical emergency requiring urgent drainage.

What is the most common cause of septic arthritis in adults?

Staphylococcus aureus; Neisseria gonorrhoeae is the most common cause in young, sexually active adults.

What is the most common cause of septic arthritis overall and the most commonly affected joint?

S. aureus, and the knee is the most commonly affected joint.

What is the diagnostic test of choice for septic arthritis?

Arthrocentesis with synovial fluid analysis showing WBC typically >50,000/µL (often >100,000) with neutrophil predominance, plus Gram stain and culture.

How does gonococcal arthritis classically present?

Triad of migratory polyarthralgia, tenosynovitis, and dermatitis (pustular skin lesions), often in a young sexually active patient.

What is the treatment for nongonococcal septic arthritis?

Urgent joint drainage (arthrocentesis or surgical washout) plus empiric IV antibiotics (vancomycin for MRSA coverage, adjusted by culture).

What is Bursitis?

Inflammation of a bursa (fluid-filled sac that cushions bony prominences), causing localized pain and swelling.

What are the most commonly affected bursae?

Subacromial, olecranon, prepatellar ("housemaid's knee"), and trochanteric bursae.

What distinguishes septic from aseptic bursitis?

Septic bursitis presents with warmth, erythema, fever, and is most often caused by S. aureus; aspiration is required to differentiate.

What is the treatment for aseptic bursitis?

Rest, ice, NSAIDs, and activity modification; aspiration and corticosteroid injection for refractory cases (avoid steroids if infection suspected).

What is Costochondritis?

Benign inflammation of the costochondral or costosternal cartilage causing anterior chest wall pain.

How does costochondritis present and how is it diagnosed?

Reproducible, localized chest wall tenderness on palpation; it is a clinical diagnosis of exclusion after ruling out cardiac and pulmonary causes.

How is costochondritis distinguished from Tietze syndrome?

Tietze syndrome involves visible swelling of the costochondral junction, whereas costochondritis lacks swelling.

What is the treatment for costochondritis?

Reassurance, NSAIDs, and activity modification; it is self-limited.

What is Tendonitis / Tenosynovitis?

Inflammation of a tendon (tendonitis) or of a tendon and its surrounding synovial sheath (tenosynovitis), usually from overuse.

What is De Quervain tenosynovitis and how is it tested?

Inflammation of the abductor pollicis longus and extensor pollicis brevis tendons at the wrist; positive Finkelstein test (pain with ulnar deviation while thumb is clasped in fist).

What is the cause and presentation of stenosing tenosynovitis (trigger finger)?

Inflammation causing the finger to catch or lock in flexion, with a palpable nodule at the A1 pulley.

What organism causes infectious tenosynovitis from a cat or human bite?

Pasteurella multocida (cat/dog bites); Eikenella corrodens (human bites).

What are Kanavel signs of infectious flexor tenosynovitis?

Finger held in flexion, fusiform swelling, tenderness along the tendon sheath, and pain with passive extension; a surgical emergency.

What is the general treatment for overuse tendonitis?

Rest, ice, NSAIDs, activity modification, and splinting; corticosteroid injection for refractory cases.

What are Bone Tumors (Benign & Malignant)?

Neoplasms arising from bone that may be benign (e.g., osteochondroma) or malignant (primary like osteosarcoma, or metastatic).

What is the most common benign bone tumor?

Osteochondroma, typically presenting in adolescents/young adults at the metaphysis of long bones.

What is the most common primary malignant bone tumor and its classic radiographic finding?

Osteosarcoma, with a "sunburst" pattern and Codman triangle (periosteal elevation), occurring in adolescents around the knee.

What is the classic radiographic finding of Ewing sarcoma?

"Onion-skin" periosteal reaction; it occurs in children/adolescents and is associated with the t(11;22) translocation.

What benign bone tumor presents with night pain relieved by NSAIDs/aspirin?

Osteoid osteoma, showing a small radiolucent nidus with surrounding sclerosis.

What are the most common sources of metastatic bone disease?

Breast, prostate, lung, thyroid, and kidney cancers; metastases are far more common than primary bone tumors in adults.

What is Osgood-Schlatter Disease?

Traction apophysitis of the tibial tubercle from repetitive quadriceps stress, common in adolescent athletes during growth spurts.

How does Osgood-Schlatter disease present?

Anterior knee pain and swelling over the tibial tubercle, worsened by activity (running, jumping) and relieved by rest.

How is Osgood-Schlatter disease diagnosed?

Clinically; X-ray may show tibial tubercle irregularity/fragmentation but is not required.

What is the treatment for Osgood-Schlatter disease?

Rest, activity modification, ice, NSAIDs, and stretching; it is self-limited and usually resolves with skeletal maturity.

What is Slipped Capital Femoral Epiphysis (SCFE)?

Displacement of the femoral head through the growth plate (physis), occurring in adolescents, classically obese males.

How does SCFE classically present?

Hip, groin, or referred knee pain with a limp in an obese adolescent; the affected leg is often externally rotated.

What is the diagnostic imaging for SCFE and its classic finding?

Bilateral hip X-rays (AP and frog-leg lateral) showing the femoral head slipping posteriorly/inferiorly, like "ice cream slipping off the cone"; Klein line.

What is the treatment for SCFE?

Urgent surgical fixation with in-situ screw placement; the patient should be made non-weight-bearing immediately to prevent AVN.

What is Osteoarthritis?

A degenerative joint disease characterized by progressive cartilage loss and bony remodeling, the most common form of arthritis.

How does osteoarthritis present clinically?

Joint pain worse with activity and relieved by rest, brief morning stiffness (

What are the characteristic exam findings in hand osteoarthritis?

Heberden nodes (DIP joints) and Bouchard nodes (PIP joints).

What are the classic radiographic findings of osteoarthritis?

Joint space narrowing, osteophytes, subchondral sclerosis, and subchondral cysts.

What is the first-line treatment for osteoarthritis?

Exercise, weight loss, and acetaminophen or topical/oral NSAIDs; intra-articular corticosteroid injections and joint replacement for advanced disease.

What is Osteoporosis?

A skeletal disorder of reduced bone mass and microarchitectural deterioration leading to increased fracture risk.

How is osteoporosis diagnosed by bone density?

DEXA scan with a T-score ≤ -2.5; a T-score between -1.0 and -2.5 indicates osteopenia.

Who should be screened for osteoporosis?

All women age 65 and older, and younger postmenopausal women with risk factors.

What are the most common fracture sites in osteoporosis?

Vertebrae (most common), hip, and distal radius (Colles fracture).

What is the first-line pharmacologic treatment for osteoporosis?

Bisphosphonates (e.g., alendronate), plus calcium and vitamin D supplementation and weight-bearing exercise.

What patient counseling is important for oral bisphosphonates?

Take on an empty stomach with water and remain upright for 30-60 minutes to prevent esophagitis.

What is Paget Disease of Bone?

A disorder of excessive, disorganized bone remodeling (increased osteoclastic then osteoblastic activity) producing weak, enlarged bone.

How does Paget disease classically present?

Often asymptomatic; may cause bone pain, skull enlargement (increasing hat size), hearing loss, and bowing of long bones.

What is the characteristic laboratory finding in Paget disease?

Markedly elevated alkaline phosphatase with normal calcium and phosphate.

What is the treatment for symptomatic Paget disease?

Bisphosphonates (first-line); calcitonin as an alternative.

What serious complication can arise from Paget disease?

Osteosarcoma (rare but feared malignant transformation), and high-output heart failure from increased bone vascularity.

What are Connective Tissue Diseases?

A group of autoimmune disorders that target connective tissue, including SLE, scleroderma, Sjögren, and inflammatory myopathies, often with positive ANA.

What is the best initial screening test for connective tissue diseases?

Antinuclear antibody (ANA), which is sensitive but not specific; specific autoantibodies help identify the particular disease.

What is mixed connective tissue disease (MCTD)?

An overlap syndrome with features of SLE, scleroderma, and polymyositis, associated with high-titer anti-U1 RNP antibodies.

What general symptom overlap is common across connective tissue diseases?

Raynaud phenomenon, arthralgias, fatigue, and constitutional symptoms.

What is Gout / Pseudogout?

Crystal-induced arthritis caused by monosodium urate crystals (gout) or calcium pyrophosphate dihydrate crystals (pseudogout).

What is the classic presentation of acute gout?

Sudden, severe monoarticular arthritis, often the first MTP joint (podagra), with warmth, erythema, and exquisite tenderness.

What does synovial fluid analysis show in gout versus pseudogout?

Gout: needle-shaped, negatively birefringent crystals (yellow when parallel to light); Pseudogout: rhomboid-shaped, positively birefringent crystals.

What radiographic finding suggests pseudogout?

Chondrocalcinosis (calcification of cartilage), commonly in the knee or wrist.

What is the treatment for acute gout flares?

NSAIDs, colchicine, or corticosteroids; do not start or stop urate-lowering therapy during an acute flare (but continue if already on it).

What is the urate-lowering therapy for chronic gout?

Allopurinol (xanthine oxidase inhibitor), first-line for prevention; avoid initiating during acute attacks.

What is Polyarteritis Nodosa (PAN)?

A systemic necrotizing vasculitis of medium-sized arteries that spares the lungs and is associated with hepatitis B.

How does PAN present?

Fever, weight loss, abdominal pain, mononeuritis multiplex, hypertension, renal involvement, and skin lesions (livedo reticularis); spares the lungs.

What infection is associated with PAN?

Hepatitis B virus.

How is PAN diagnosed?

Biopsy of affected tissue showing necrotizing vasculitis, or angiography showing microaneurysms ("beads on a string"); PAN is typically ANCA-negative.

What is the treatment for PAN?

High-dose corticosteroids, often with cyclophosphamide for severe disease; antivirals if hepatitis B-associated.

What is Polymyalgia Rheumatica (PMR)?

An inflammatory condition causing pain and stiffness of the shoulder and hip girdles in patients over age 50.

How does PMR present?

Bilateral aching and morning stiffness of the shoulders, neck, and hips lasting >30 minutes, without true muscle weakness.

What laboratory finding is characteristic of PMR?

Markedly elevated ESR (often >50 mm/hr) and elevated CRP; creatine kinase is normal.

What condition is strongly associated with PMR?

Giant cell (temporal) arteritis; up to 15-20% of PMR patients develop it.

What is the treatment for PMR?

Low-dose corticosteroids (prednisone ~15 mg/day) with rapid, dramatic symptom improvement.

What is Polymyositis / Dermatomyositis?

Idiopathic inflammatory myopathies causing symmetric proximal muscle weakness; dermatomyositis adds characteristic skin findings.

How do polymyositis and dermatomyositis present?

Progressive, symmetric proximal muscle weakness (difficulty climbing stairs, rising from a chair); dermatomyositis adds skin findings.

What are the classic skin findings of dermatomyositis?

Gottron papules (over knuckles), heliotrope rash (purple eyelid discoloration), and shawl sign.

What laboratory and antibody findings support these diagnoses?

Elevated creatine kinase and aldolase; anti-Jo-1 and anti-Mi-2 antibodies; positive ANA.

What malignancy association is important in dermatomyositis?

An increased risk of underlying malignancy, warranting age-appropriate cancer screening.

What is the treatment for polymyositis/dermatomyositis?

High-dose corticosteroids first-line, with steroid-sparing immunosuppressants (methotrexate, azathioprine) for maintenance.

What is Reactive Arthritis?

A seronegative spondyloarthropathy triggered by a preceding GI or genitourinary infection, formerly called Reiter syndrome.

What is the classic triad of reactive arthritis?

"Can't see, can't pee, can't climb a tree" — conjunctivitis/uveitis, urethritis, and arthritis.

What infections classically trigger reactive arthritis?

Chlamydia trachomatis (GU), and enteric pathogens (Salmonella, Shigella, Campylobacter, Yersinia).

What HLA association is seen in reactive arthritis?

HLA-B27 positivity.

What is the treatment for reactive arthritis?

NSAIDs first-line; treat underlying infection; most cases are self-limited though some become chronic.

What is Rheumatoid Arthritis (RA)?

A chronic systemic autoimmune disease causing symmetric inflammatory polyarthritis with synovial proliferation and joint destruction.

How does RA present?

Symmetric polyarthritis of the small joints (MCP, PIP, wrists) with prolonged morning stiffness (>1 hour) that improves with use.

What are the characteristic hand deformities of RA?

Ulnar deviation, swan-neck deformity, boutonnière deformity, and MCP/PIP involvement that spares the DIP joints.

What antibodies and labs support RA?

Anti-CCP (most specific) and rheumatoid factor; elevated ESR and CRP.

What are the radiographic findings of RA?

Periarticular osteopenia, joint space narrowing, and marginal erosions.

What is the first-line disease-modifying treatment for RA?

Methotrexate (DMARD), started early; biologics (e.g., TNF inhibitors) for inadequate response; NSAIDs/steroids for symptom control.