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MSK (USMLE) > Bone Conditions and Gout > Flashcards

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
Q

Causes of hyperuricemia

A

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
Q

Dx of gout

A

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
Q

Symptoms of gout

A

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
Q

When does acute attacks in gout occur

A

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
Q

Tx of gout

A

Acute: NSAIDs (eg, indomethacin), glucocorticoids, colchicine
Chronic (preventative): xanthine oxidase inhibitors (eg, allopurinol, febuxostat)

30
Q

Define calcium pyrophosphate deposition disease

A

Deposition of calcium pyrophosphate crystals within the joint space
Occurs in patients > 50 years old; both sexes affected equally

31
Q

Causes of calcium pyrophosphate deposition disease

A

Usually idiopathic, sometimes associated with hemochromatosis, hyperparathyroidism, joint trauma

32
Q

Presentation of CPPD

A

Pain and swelling with acute inflammation (pseudogout) and/or chronic degeneration (pseudo-osteoarthritis)
Most commonly affected joint is the knee

33
Q

Dx of CPPD

A

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
Q

Prophylaxis of CPPD

A

Colchicine

MSK (USMLE) (16 decks)

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