Bone Conditions and Gout Flashcards

1
Q

Describe osteosarcoma

A

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)

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2
Q

Where does osteosarcoma commonly occur

A

Metaphysis of long bones (often knee region)

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3
Q

Characteristics of osteosarcoma

A

Pleomorphic osteoid-producing cells (malignant osteoblasts); aggressive
Presents as painful enlarging mass or pathologic fractures
Codman triangle/sunburst pattern on x-ray

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4
Q

Tx for osteosarcoma

A

Primary usually responsive to surgery/chemo, secondary has poor prognosis

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5
Q

Epidemiology for chondrosarcoma

A

Common in adults >50

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6
Q

Location of chondrosarcoma

A

Medulla of pelvis, prox femur & humerus

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7
Q

Characteristics of chondrosarcoma

A

Tumor of malignant chondrocyte
Lytic (> 50%) cases with intralesional calcifications, endosteal erosion, cortex breach

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8
Q

Epidemiology of Ewing’s sarcoma

A

Common in white males < 15

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9
Q

Location of Ewing’s

A

Diaphysis of long bones (especially femur), pelvic flat bones

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10
Q

Characteristics of Ewing

A

Anaplastic small blue cells of neuroectodermal (mesenchymal) origin (resemble lymphocytes)
“Onion skin” periosteal reaction

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11
Q

Dx & Tx of Ewing

A

Test for fusion protein EWS-FLI1 - t(11;22)
Aggressive w early mets but responsive to chemo

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12
Q

Pathogenesis of OA

A

Mechanical—wear and tear destroys articular cartilage (degenerative joint disorder) = inflammation w inadequate repair
Chondrocytes mediate degradation and inadequate repair

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13
Q

Pathogenesis of RA

A

Autoimmune—inflammation induces formation of pannus (proliferative granulation tissue), which erodes articular cartilage and bone.

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14
Q

Predisposing factors to OA

A

Age, female, obesity, joint trauma

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15
Q

Predisposing factors to RA

A

Female, HLA-DR4 (4-walled “rheum”), tobacco smoking
⊕ rheumatoid factor (IgM antibody that targets IgG Fc region; in 80%), ACPA (more specific)

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16
Q

Presentation in OA

A

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

17
Q

Presentation in RA

A

Pain, swelling, and morning stiffness lasting > 1 hour, improving with use
Symmetric joint involvement
Systemic symptoms (fever, fatigue, weight loss)
Extraarticular manifestations are common

18
Q

What are the extraarticular manifestations to RA

A

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

19
Q

Joint findings in OA

A

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)

20
Q

Joint findings in RA

A

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

21
Q

Tx of OA

A

Activity mods, acetaminophen, NSAIDs, intraarticular glucocorticoids

22
Q

Tx of RA

A

NSAIDs, glucocorticoids, disease-modifying agents (eg, methotrexate, sulfasalazine), biologic agents (eg, TNF-α inhibitors)

23
Q

Define gout

A

Acute inflammatory monoarthritis caused by precipitation of monosodium urate crystals in joints

24
Q

Risk factors for gout

A

male sex, hypertension, obesity, diabetes, dyslipidemia, alcohol use. Strongest risk factor is hyperuricemia

25
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
26
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
27
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)
28
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)
29
Tx of gout
Acute: NSAIDs (eg, indomethacin), glucocorticoids, colchicine Chronic (preventative): xanthine oxidase inhibitors (eg, allopurinol, febuxostat)
30
Define calcium pyrophosphate deposition disease
Deposition of calcium pyrophosphate crystals within the joint space Occurs in patients > 50 years old; both sexes affected equally
31
Causes of calcium pyrophosphate deposition disease
Usually idiopathic, sometimes associated with hemochromatosis, hyperparathyroidism, joint trauma
32
Presentation of CPPD
Pain and swelling with acute inflammation (pseudogout) and/or chronic degeneration (pseudo-osteoarthritis) Most commonly affected joint is the knee
33
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
34
Prophylaxis of CPPD
Colchicine