Bone Conditions and Gout Flashcards
Describe osteosarcoma
Accounts for 20% of primary bone cancers
Malignant, found in males <20 as primary tumour
Less common in older (usually secondary to Paget, bone infarcts, radiation, familial retinoblastoma, Li-Fraumeni)
Where does osteosarcoma commonly occur
Metaphysis of long bones (often knee region)
Characteristics of osteosarcoma
Pleomorphic osteoid-producing cells (malignant osteoblasts); aggressive
Presents as painful enlarging mass or pathologic fractures
Codman triangle/sunburst pattern on x-ray
Tx for osteosarcoma
Primary usually responsive to surgery/chemo, secondary has poor prognosis
Epidemiology for chondrosarcoma
Common in adults >50
Location of chondrosarcoma
Medulla of pelvis, prox femur & humerus
Characteristics of chondrosarcoma
Tumor of malignant chondrocyte
Lytic (> 50%) cases with intralesional calcifications, endosteal erosion, cortex breach
Epidemiology of Ewing’s sarcoma
Common in white males < 15
Location of Ewing’s
Diaphysis of long bones (especially femur), pelvic flat bones
Characteristics of Ewing
Anaplastic small blue cells of neuroectodermal (mesenchymal) origin (resemble lymphocytes)
“Onion skin” periosteal reaction
Dx & Tx of Ewing
Test for fusion protein EWS-FLI1 - t(11;22)
Aggressive w early mets but responsive to chemo
Pathogenesis of OA
Mechanical—wear and tear destroys articular cartilage (degenerative joint disorder) = inflammation w inadequate repair
Chondrocytes mediate degradation and inadequate repair
Pathogenesis of RA
Autoimmune—inflammation induces formation of pannus (proliferative granulation tissue), which erodes articular cartilage and bone.
Predisposing factors to OA
Age, female, obesity, joint trauma
Predisposing factors to RA
Female, HLA-DR4 (4-walled “rheum”), tobacco smoking
⊕ rheumatoid factor (IgM antibody that targets IgG Fc region; in 80%), ACPA (more specific)
Presentation in OA
Pain in weight-bearing joints after use (eg, at the end of the day), improving with rest
Asymmetric joint involvement
Knee cartilage loss begins medially (“bowlegged”)
No systemic symptoms
Presentation in RA
Pain, swelling, and morning stiffness lasting > 1 hour, improving with use
Symmetric joint involvement
Systemic symptoms (fever, fatigue, weight loss)
Extraarticular manifestations are common
What are the extraarticular manifestations to RA
Rheumatoid nodules (fibrinoid necrosis with palisading histiocytes) in subcutaneous tissue and lung (+ pneumoconiosis = Caplan syndrome)
ILD, pleuritis, pericarditis, anemia of chronic disease, Felty syndrome (anemia + splenomegaly), AA amyloidosis, Sjorgen, scleritis, carpal tunnel
Joint findings in OA
Osteophytes (bone spurs), joint space narrowing (asymmetric), subchondral sclerosis and cysts
*Synovial fluid NONinflammatory (WBC <2000/mm3)
Herberden nodes (DIP) and Bouchard nodes (PIP, 1st MCP)
Joint findings in RA
Erosions, juxta-articular osteopenia, soft tissue swelling, subchondral cysts, joint space narrowing (symmetric)
Deformities: cervical subluxation, ulnar finger deviation, swan neck, boutonniere
Involves MCP, PIP, wrist; not DIP or 1st CMC
Tx of OA
Activity mods, acetaminophen, NSAIDs, intraarticular glucocorticoids
Tx of RA
NSAIDs, glucocorticoids, disease-modifying agents (eg, methotrexate, sulfasalazine), biologic agents (eg, TNF-α inhibitors)
Define gout
Acute inflammatory monoarthritis caused by precipitation of monosodium urate crystals in joints
Risk factors for gout
male sex, hypertension, obesity, diabetes, dyslipidemia, alcohol use. Strongest risk factor is hyperuricemia
Causes of hyperuricemia
Underexcretion of uric acid (90% of patients)—largely idiopathic, potentiated by renal failure; can be exacerbated by alcohol and certain medications (eg, thiazide diuretics)
Overproduction of uric acid (10% of patients)—Lesch-Nyhan syndrome, PRPP excess, increased cell turnover (eg, tumor lysis syndrome), von Gierke disease
Dx of gout
Crystals are needle shaped and ⊝ birefringent under polarized light (yellow under parallel light, blue under perpendicular)
Serum uric acid levels may be normal during an acute attack
Symptoms of gout
Asymmetric joint distribution
Joint is swollen, red, painful
Classic manifestation is painful MTP joint of big toe (podagra)
Tophus formation (often on external ear, olecranon bursa, or Achilles tendon)
When does acute attacks in gout occur
after a large meal with foods rich in purines (eg, red meat, seafood), trauma, surgery, dehydration, diuresis, or alcohol consumption (alcohol [beer > spirits] metabolites compete for same excretion sites in kidney as uric acid = decreased excretion & it builds up in blood)
Tx of gout
Acute: NSAIDs (eg, indomethacin), glucocorticoids, colchicine
Chronic (preventative): xanthine oxidase inhibitors (eg, allopurinol, febuxostat)
Define calcium pyrophosphate deposition disease
Deposition of calcium pyrophosphate crystals within the joint space
Occurs in patients > 50 years old; both sexes affected equally
Causes of calcium pyrophosphate deposition disease
Usually idiopathic, sometimes associated with hemochromatosis, hyperparathyroidism, joint trauma
Presentation of CPPD
Pain and swelling with acute inflammation (pseudogout) and/or chronic degeneration (pseudo-osteoarthritis)
Most commonly affected joint is the knee
Dx of CPPD
Chondrocalcinosis (cartilage calcification) on x-ray
Crystals are rhomboid and weakly ⊕ birefringent under polarized light (blue when parallel to light)
The blue P’s of CPPD—blue (when parallel), positive birefringence, calcium pyrophosphate, pseudogout
Prophylaxis of CPPD
Colchicine
