Family Medicine EOR (Rheumatologic/Musculoskeletal): New for 2026 Topic List (Smarty PANCE)

What is Developmental Dysplasia of the Hip (DDH)?

A spectrum of hip joint abnormalities in infants ranging from acetabular dysplasia to complete dislocation due to abnormal development of the femoral head and acetabulum.

What two physical exam maneuvers screen for DDH in newborns?

Ortolani (reduction - hip is dislocated and you relocate it with abduction) and Barlow (provocation - hip is reduced and you dislocate it posteriorly with adduction).

What is the preferred imaging study for DDH in infants under 4-6 months?

Hip ultrasound (femoral head not yet ossified); after 4-6 months use AP pelvis X-ray.

What is the first-line treatment for DDH in infants under 6 months?

Pavlik harness (maintains hips in flexion and abduction) for 6-12 weeks.

What are the major risk factors for DDH (mnemonic: 6 F's)?

Female, Firstborn, Frank breech, Family history, Fluid (oligohydramnios), Foot (left hip more common).

What is a Ganglion Cyst?

A benign, fluid-filled synovial cyst most commonly arising from a joint capsule or tendon sheath, often on the dorsal wrist.

What is the most common location of a ganglion cyst?

Dorsal wrist (scapholunate ligament, 60-70%), followed by volar wrist and flexor tendon sheath of the fingers.

What is the classic appearance of a ganglion cyst on transillumination?

Transilluminates brightly (fluid-filled) - helps distinguish from solid masses.

What is the first-line treatment for an asymptomatic ganglion cyst?

Observation/reassurance - up to 50% resolve spontaneously; avoid the traditional "Bible therapy" (smashing with a book).

What is the definitive treatment for a symptomatic or recurrent ganglion cyst?

Surgical excision; aspiration alone has high recurrence rate (~50%).

What is Bursitis?

Inflammation of a bursa (fluid-filled sac that cushions joints), causing localized pain, swelling, and decreased range of motion.

What is the most common cause of olecranon bursitis?

Repetitive trauma/pressure (student's elbow); also gout, infection (septic bursitis - often Staph aureus), and RA.

How do you differentiate septic from aseptic bursitis?

Aspirate bursal fluid - septic shows WBC >2,000/mm³ with predominant PMNs, positive Gram stain/culture; warmth, erythema, fever suggest infection.

What is the treatment for non-septic bursitis?

RICE (Rest, Ice, Compression, Elevation), NSAIDs, activity modification; aspiration ± corticosteroid injection if persistent.

What is the most common site of trochanteric bursitis and its presentation?

Lateral hip pain at greater trochanter, worse with lying on affected side and stair climbing; tenderness to palpation over greater trochanter.

What is Costochondritis?

Self-limited inflammation of the costochondral or costosternal junctions causing anterior chest wall pain reproducible with palpation.

What is the hallmark physical exam finding in costochondritis?

Reproducible chest wall tenderness with palpation of costochondral junctions (typically 2nd-5th).

How do you distinguish costochondritis from Tietze syndrome?

Costochondritis: multiple levels, no swelling | Tietze syndrome: single level (usually 2nd or 3rd costochondral junction), visible swelling.

What is the treatment for costochondritis?

NSAIDs, heat/ice, activity modification, reassurance; self-limited (resolves in weeks to months).

What is the key diagnostic principle when costochondritis is suspected in adults?

Costochondritis is a diagnosis of exclusion - must rule out cardiac causes (ACS), PE, and aortic dissection first in appropriate patients.

What is Tendonitis?

Inflammation of a tendon, usually from overuse, repetitive motion, or acute injury, causing pain, swelling, and decreased function.

What is the classic presentation of De Quervain tenosynovitis?

Radial wrist pain with thumb movement, positive Finkelstein test (pain with ulnar deviation of wrist while thumb flexed in palm); affects abductor pollicis longus and extensor pollicis brevis.

What special test is used to diagnose lateral epicondylitis (tennis elbow)?

Cozen test - pain over lateral epicondyle with resisted wrist extension; affects extensor carpi radialis brevis tendon.

What is the first-line treatment for tendonitis?

Rest, ice, NSAIDs, activity modification, eccentric strengthening exercises; corticosteroid injections for refractory cases.

What tendon ruptures cause a positive Thompson test and what does it indicate?

Achilles tendon rupture - squeezing calf with patient prone does NOT produce plantarflexion (normally would).

What is Osgood-Schlatter Disease?

Traction apophysitis (osteochondrosis) of the tibial tubercle caused by repetitive quadriceps strain in adolescents during growth spurts.

What is the classic patient demographic and presentation for Osgood-Schlatter?

Active adolescents (boys 12-15, girls 8-12) with anterior knee pain and prominent/tender tibial tubercle, worse with running/jumping.

What X-ray findings are seen in Osgood-Schlatter disease?

Soft tissue swelling, fragmentation/irregularity of tibial tubercle apophysis (often clinical diagnosis - imaging not required).

What is the treatment for Osgood-Schlatter disease?

RICE, NSAIDs, activity modification, quadriceps stretching; self-limited - resolves with skeletal maturity (physeal closure).

What complication can occur from Osgood-Schlatter disease?

Persistent tibial tubercle prominence (cosmetic), rarely tibial tubercle avulsion fracture; some adults retain a painful ossicle requiring excision.

What is Osteoarthritis?

A degenerative joint disease characterized by progressive cartilage loss, subchondral bone changes, and osteophyte formation, causing pain and stiffness.

What are the classic joints affected by primary osteoarthritis?

DIPs (Heberden nodes), PIPs (Bouchard nodes), 1st CMC, hips, knees, lumbar/cervical spine; SPARES MCPs and wrists (suggests RA).

What are the classic radiographic findings in osteoarthritis (mnemonic: LOSS)?

Loss of joint space (asymmetric), Osteophytes, Subchondral sclerosis, Subchondral cysts.

What is the morning stiffness duration in OA vs RA?

OA: <30 minutes, worse with activity, better with rest | RA: >1 hour, better with activity.

What is the first-line pharmacologic treatment for OA?

Topical NSAIDs (knee/hand) and acetaminophen; then oral NSAIDs; intra-articular corticosteroid or hyaluronic acid injections; joint replacement for refractory disease.

What is Osteoporosis?

A systemic skeletal disease characterized by low bone mass and microarchitectural deterioration leading to increased fracture risk.

What T-score on DEXA scan defines osteoporosis vs osteopenia?

Osteoporosis: T-score ≤ -2.5 | Osteopenia: T-score between -1.0 and -2.5 | Normal: T-score ≥ -1.0.

Who should be screened for osteoporosis with DEXA scan?

All women ≥65 years, postmenopausal women <65 with risk factors, men ≥70 years, or anyone with fragility fracture.

What is the first-line pharmacologic treatment for osteoporosis?

Bisphosphonates (alendronate, risedronate, zoledronic acid) PLUS calcium 1200 mg/day and vitamin D 800-1000 IU/day.

What is the proper administration of oral bisphosphonates?

Take on empty stomach with full glass of water, remain upright for 30-60 minutes; reduces risk of esophagitis and ensures absorption.

What is Plantar Fasciitis?

Inflammation/degeneration of the plantar fascia at its calcaneal insertion, causing inferomedial heel pain.

What is the classic presentation of plantar fasciitis?

Sharp inferomedial heel pain with first steps in the morning or after rest, improves with activity but worsens with prolonged standing.

What physical exam finding confirms plantar fasciitis?

Point tenderness at medial calcaneal tubercle (origin of plantar fascia); pain reproduced with dorsiflexion of toes (windlass mechanism).

What is the first-line treatment for plantar fasciitis?

Rest, ice, NSAIDs, plantar fascia/calf stretching, supportive footwear with arch supports, night splints; corticosteroid injection for refractory cases.

What is the risk of corticosteroid injection in plantar fasciitis?

Plantar fascia rupture and fat pad atrophy - use sparingly and avoid multiple injections.

What are Connective Tissue Diseases?

A group of autoimmune disorders that affect connective tissues including joints, skin, muscles, and internal organs (e.g., SLE, scleroderma, Sjögren, dermatomyositis, mixed connective tissue disease).

What is the classic triad of Sjögren syndrome?

Dry eyes (keratoconjunctivitis sicca), dry mouth (xerostomia), and arthritis; associated with anti-Ro (SS-A) and anti-La (SS-B) antibodies.

What antibody is specific for limited cutaneous systemic sclerosis (CREST syndrome)?

Anti-centromere antibody; CREST = Calcinosis, Raynaud, Esophageal dysmotility, Sclerodactyly, Telangiectasias.

What antibody is associated with diffuse systemic sclerosis and what is the most feared complication?

Anti-Scl-70 (anti-topoisomerase I); scleroderma renal crisis - treat with ACE inhibitors (NEVER use steroids - precipitates renal crisis).

What is the classic skin finding and antibody in dermatomyositis?

Gottron papules (over MCPs/PIPs) and heliotrope rash (purple eyelid discoloration); anti-Jo-1 antibody (associated with interstitial lung disease); proximal muscle weakness with elevated CK.

What is Fibromyalgia?

A chronic widespread pain syndrome characterized by diffuse musculoskeletal pain, fatigue, sleep disturbance, and cognitive symptoms ("fibro fog") without inflammation or structural pathology.

What are the diagnostic criteria for fibromyalgia (2016 ACR)?

Widespread pain index (WPI) ≥7 and symptom severity (SS) score ≥5, OR WPI 4-6 and SS ≥9; symptoms present ≥3 months; no other explanation.

What are typical lab findings in fibromyalgia?

NORMAL labs (CBC, ESR, CRP, CK, TSH, ANA) - diagnosis is clinical; abnormal labs suggest alternative diagnosis.

What are the first-line medications for fibromyalgia?

Duloxetine, milnacipran (SNRIs), or pregabalin; tricyclic antidepressants (amitriptyline) also effective; AVOID opioids.

What non-pharmacologic treatments are most effective for fibromyalgia?

Aerobic exercise (most evidence), cognitive behavioral therapy (CBT), sleep hygiene, and patient education.

What is Gout?

An inflammatory arthritis caused by deposition of monosodium urate crystals in joints and soft tissues secondary to hyperuricemia.

What is the classic presentation of acute gout?

Sudden severe monoarticular pain, swelling, erythema, and warmth, most commonly first MTP joint (podagra); often nocturnal onset.

What synovial fluid finding is diagnostic for gout vs pseudogout?

Gout: NEGATIVELY birefringent NEEDLE-shaped monosodium urate crystals (yellow when parallel to polarizer) | Pseudogout: POSITIVELY birefringent RHOMBOID-shaped calcium pyrophosphate crystals (blue when parallel).

What is the treatment for acute gout flare?

NSAIDs (indomethacin), colchicine (within 24 hours), or corticosteroids (oral, IA, or IM); do NOT start or stop urate-lowering therapy during acute flare.

What is the first-line urate-lowering therapy for chronic gout prophylaxis?

Allopurinol (xanthine oxidase inhibitor); target uric acid <6 mg/dL; start low and titrate; bridge with colchicine or NSAID for 3-6 months to prevent flare.

What is Juvenile Idiopathic Arthritis (JIA)?

Chronic inflammatory arthritis lasting >6 weeks in a child <16 years old, after exclusion of other causes.

What are the three main subtypes of JIA?

Oligoarticular (≤4 joints, most common, ANA+, uveitis risk), Polyarticular (≥5 joints, can be RF+ or RF-), Systemic (Still disease - quotidian fevers, salmon-pink rash, hepatosplenomegaly).

What is the classic presentation of systemic JIA (Still disease)?

Daily (quotidian) spiking fevers, evanescent salmon-pink macular rash, arthritis, hepatosplenomegaly, lymphadenopathy, serositis; markedly elevated ferritin and ESR.

What is the most concerning extra-articular complication of oligoarticular JIA?

Anterior uveitis (asymptomatic) - requires regular slit-lamp screening, especially in ANA-positive girls; can cause blindness if untreated.

What is the first-line treatment for JIA?

NSAIDs for symptoms; methotrexate is first-line DMARD; biologics (TNF inhibitors) for severe/refractory disease; intra-articular steroids for oligoarticular disease.

What is Reactive Arthritis?

A sterile inflammatory arthritis occurring 1-4 weeks after a GU (Chlamydia) or GI (Salmonella, Shigella, Yersinia, Campylobacter) infection.

What is the classic triad of reactive arthritis (formerly Reiter syndrome)?

"Can't see, can't pee, can't climb a tree" - Conjunctivitis/uveitis, Urethritis, Arthritis (oligoarticular, lower extremities, asymmetric).

What HLA marker is strongly associated with reactive arthritis?

HLA-B27 (positive in 60-80% of patients); also associated with ankylosing spondylitis, psoriatic arthritis, IBD-associated arthritis.

What are the characteristic skin/mucosal findings in reactive arthritis?

Keratoderma blennorrhagicum (hyperkeratotic palms/soles - resembles psoriasis), circinate balanitis, oral ulcers, nail changes.

What is the treatment for reactive arthritis?

NSAIDs first-line; treat underlying infection if Chlamydia (doxycycline); intra-articular steroids; DMARDs (sulfasalazine, methotrexate) for chronic disease.

What is Rheumatoid Arthritis (RA)?

A chronic systemic autoimmune disease characterized by symmetric inflammatory polyarthritis primarily affecting small joints, with potential for joint destruction and extra-articular manifestations.

What joints does RA classically involve and spare?

Involves: MCPs, PIPs, wrists (symmetric, small joints) | SPARES: DIPs (suggests OA or psoriatic arthritis) and lumbar spine.

What are the most specific and sensitive antibodies for RA?

Anti-CCP (anti-cyclic citrullinated peptide) - most SPECIFIC (>95%); Rheumatoid Factor (RF) - sensitive but less specific (also positive in Sjögren, hepatitis C, others).

What are the characteristic hand deformities in chronic RA?

Ulnar deviation at MCPs, swan-neck (PIP hyperextension, DIP flexion), boutonniere (PIP flexion, DIP hyperextension), Z-thumb deformity.

What is the first-line DMARD for RA and required monitoring?

Methotrexate (weekly, with folic acid); monitor CBC, LFTs, creatinine every 2-3 months; avoid in pregnancy (teratogenic) and severe liver/renal disease.

What is Systemic Lupus Erythematosus (SLE)?

A chronic multisystem autoimmune disease characterized by autoantibody production and immune complex deposition causing inflammation in multiple organ systems.

What is the most sensitive and most specific antibody for SLE?

Most sensitive: ANA (95-99%) - good screening test | Most specific: anti-dsDNA (correlates with disease activity, especially lupus nephritis) and anti-Smith.

What are the classic mucocutaneous features of SLE?

Malar (butterfly) rash sparing nasolabial folds, discoid rash, photosensitivity, oral/nasal ulcers (typically painless), non-scarring alopecia.

What is lupus nephritis and how is it monitored?

Immune complex glomerulonephritis (most common: class IV diffuse proliferative); monitor urinalysis (proteinuria, hematuria, cellular casts), creatinine, anti-dsDNA, complement (C3/C4 decrease in active disease).

What are the first-line treatments for SLE?

Hydroxychloroquine for ALL patients (reduces flares, mortality, organ damage); NSAIDs for arthritis; corticosteroids for flares; immunosuppressants (mycophenolate, cyclophosphamide) for severe organ involvement.

What is Slipped Capital Femoral Epiphysis (SCFE)?

Posteroinferior displacement of the femoral epiphysis through the growth plate (physis) relative to the femoral neck, occurring in adolescents.

What is the classic patient demographic for SCFE?

Obese adolescent boys (10-16 years), more common in African Americans; bilateral in 20-40%; associated with endocrine disorders (hypothyroidism, GH deficiency).

What is the classic presentation of SCFE?

Hip, groin, thigh, OR KNEE pain with limp; patient holds hip in external rotation; obligate external rotation with passive hip flexion.

What is the diagnostic imaging finding in SCFE?

AP and FROG-LEG lateral pelvis X-rays show displacement; Klein line (drawn along superior femoral neck) should intersect epiphysis - in SCFE it does not.

What is the treatment for SCFE?

Surgical urgency - immediate non-weight-bearing and percutaneous in situ pinning with single screw; consider prophylactic pinning of contralateral hip.

What is Ankylosing Spondylitis?

A chronic seronegative inflammatory spondyloarthropathy primarily affecting the sacroiliac joints and axial skeleton, leading to progressive spinal fusion.

What is the classic patient and presentation for ankylosing spondylitis?

Young man (15-30 years), chronic low back pain >3 months, morning stiffness >1 hour, IMPROVED with exercise/worsened by rest, alternating buttock pain.

What HLA marker is associated with ankylosing spondylitis?

HLA-B27 (positive in >90% of patients); however, most HLA-B27+ people do not develop AS.

What are the classic imaging findings in ankylosing spondylitis?

Bilateral symmetric sacroiliitis (earliest), "bamboo spine" (vertebral fusion via syndesmophytes), squaring of vertebral bodies; MRI shows early sacroiliitis before X-ray changes.

What are the extra-articular manifestations of ankylosing spondylitis?

Anterior uveitis (most common, 25-40%), aortic regurgitation, apical pulmonary fibrosis, IBD, cauda equina syndrome, restrictive lung disease.

What is Disc Disease?

Degenerative or herniated changes of the intervertebral disc, often causing radicular pain from nerve root compression.

What is the classic presentation of lumbar disc herniation?

Radicular leg pain (worse than back pain), worsened by sitting/coughing/Valsalva, dermatomal sensory changes, positive straight leg raise test (30-70 degrees).

Which nerve root is most commonly affected by L4-L5 and L5-S1 disc herniations?

L4-L5: compresses L5 root (weak dorsiflexion - foot drop, big toe extension weakness, dorsal foot numbness) | L5-S1: compresses S1 root (weak plantarflexion, diminished ankle reflex, lateral foot numbness).

What are red flag symptoms requiring urgent imaging/intervention in back pain?

Cauda equina syndrome (saddle anesthesia, bowel/bladder dysfunction, bilateral leg weakness), progressive neuro deficit, fever, malignancy history, IV drug use, trauma, age >70.

What is the initial treatment for uncomplicated lumbar disc herniation?

Conservative: NSAIDs, activity modification (stay active, avoid bed rest), physical therapy; 80-90% improve in 6-12 weeks; surgery for cauda equina or persistent severe symptoms.

What is Kyphosis?

Abnormal exaggerated posterior convexity (rounding) of the thoracic spine in the sagittal plane (normal thoracic kyphosis is 20-45 degrees).

What is Scheuermann disease (juvenile kyphosis)?

Rigid thoracic kyphosis in adolescents from anterior wedging ≥5° of three or more consecutive vertebrae; not correctable with extension; treated with bracing or surgery if severe.

What is the most common cause of kyphosis in elderly patients?

Postmenopausal osteoporosis with vertebral compression fractures (Dowager hump); causes loss of height and exaggerated thoracic curvature.

How do you differentiate postural kyphosis from structural kyphosis?

Postural (flexible): correctable with active extension, no vertebral wedging | Structural (rigid): not correctable, vertebral wedging on X-ray (Scheuermann).

What is the treatment for kyphosis?

Postural: physical therapy, posture training | Structural mild-moderate: bracing in growing adolescents | Severe (>75° or progressive): surgical correction; treat underlying osteoporosis.