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Flashcards in JOINTS Deck (25)
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1
Q

MONOARTHRITIS

Common 5

A
  1. Septic arthritis—including tuberculosis. Marked juxtaarticular
    osteopenia with loss of definition of subchondral bone plate.
  2. Trauma—evidence of fracture or lipohaemarthrosis.
  3. Osteoarthritis (OA)—marginal osteophytes, subchondral sclerosis
    and/or cysts, joint space narrowing. Commonly involves weightbearing joints.
  4. Calcium pyrophosphate deposition disease (CPPD)—
    chondrocalcinosis is characteristic; most commonly seen in knee,
    wrist, symphysis pubis and intervertebral discs. Arthropathy mimics
    OA but has a characteristic distribution: radiocarpal, patellofemoral,
    C1/2. Large clustered subchondral cysts are common.
  5. Gout—well-defined juxtaarticular erosions + periarticular soft tissue
    mass ± calcification (tophi—highly suggestive). The joint space and
    bone density are relatively preserved. Most commonly involves the
    hallux MTPJ; other sites include intertarsal, ankle and knee.
2
Q

MONOARTHRITIS Less common

A
  1. Neuropathic (Charcot) arthropathy—seven Ds: joint degeneration, destruction, dislocation, deformity, debris (loose bodies), distension (effusion) and increased density (subchondral sclerosis). Due to reduced pain sensation and proprioception, most commonly seen in diabetics. The joint involved suggests the underlying cause:
    (a) Ankle/foot—diabetes, alcoholism, dysraphism, leprosy,
    congenital insensitivity to pain (young patients, multiple
    involved joints), amyloidosis, neurosyphilis.
    (b) Knee—steroid injection, alcoholism, congenital insensitivity to pain, neurosyphilis.
    (c) Hip—alcoholism, steroid injection, neurosyphilis.
    (d) Spine—spinal cord injury, diabetes, syrinx (C-spine), neurosyphilis (L-spine).
    (e) Shoulder/elbow—syrinx.
    (f) Wrist—diabetes, syrinx.
    (g) Small joints of hand/feet—diabetes, leprosy, congenital insensitivity to pain.
  2. Avascular necrosis—e.g. in hip. Can mimic OA but changes
    mainly involve one side of the joint with relative preservation of
    the joint space.
  3. Monoarticular presentation of a usually polyarticular
    arthritis
  4. Viral—typically hips in children, a.k.a. ‘transient synovitis’.
  5. Pigmented villonodular synovitis (PVNS)—well-defined erosions
    + synovial nodules on MRI showing low T2 signal and blooming
    on the gradient echo due to haemosiderin. Most cases occur in
    the knee; less commonly other large joints. A localized form
    limited to Hoffa’s fat pad can also occur.
  6. Synovial osteochondromatosis—multiple intraarticular loose
    bodies + calcification. Can be primary (uniform in size) or
    secondary (different sizes + coexistent OA)
3
Q

THE MAJOR POLYARTHRITIDES
Synovial
2

A
  1. Rheumatoid arthritis*—proximal and symmetric distribution,
    especially MCPJs and carpus; other sites include feet (especially 5th
    MTPJ), knees, ankles, elbows and shoulders. Features include
    synovitis, juxtaarticular osteopenia, joint space narrowing,
    periarticular erosions, subluxation and ankylosis.
  2. Juvenile idiopathic arthritis*—presents in childhood. Common
    joints include hips, knees, ankles, elbows, hands and feet, C-spine.
    Features include soft tissue swelling, juxtaarticular osteopenia,
    periostitis, epiphyseal overgrowth, joint effusions and subluxation
    (e.g. carpus, hip, C1/2). Periarticular erosions, joint space
    narrowing and ankylosis are late features
4
Q

THE MAJOR POLYARTHRITIDES

Entheseal

A
  1. Seronegative spondyloarthropathies—enthesitis + proliferative entheseal erosions with preserved bone density; classically asymmetrical, oligoarticular involvement of peripheral joints.
    (a) Psoriatic arthritis—usually asymmetric and distal (especially distal interphalangeal joints). Can present with dactylitis (‘sausage digit’). Occasionally symmetrical, resembling rheumatoid arthritis. Pencil-in-cup appearance and arthritis mutilans in severe disease. Acroosteolysis and interphalangeal joint ankylosis may be seen and are suggestive.
    (b) Chronic reactive arthritis—usually seen in young adults, following an STI or gut infection. Similar in appearance to psoriatic arthritis but the hands are typically spared. Commonly involves the feet, SIJs and spine. Calcaneal enthesitis (+ erosions) is suggestive. Dactylitis may also be seen.
    (c) Ankylosing spondylitis
    —typically involves SIJs and the spine.
    Other joints include hips, shoulders and knees.
    (d) Enteropathic arthritis—associated with IBD. Distribution is
    similar to ankylosing spondylitis
5
Q

THE MAJOR POLYARTHRITIDES
Degenerative
2

A
  1. Osteoarthritis—e.g. hands; involves interphalangeal joints, thumb
    carpometacarpal and triscaphoid joints. The erosive form causes
    central erosions resulting in a ‘gull-wing’ deformity ± ankylosis.
  2. Neuropathic arthropathy
6
Q

THE MAJOR POLYARTHRITIDES

Depositional

A
  1. Gout.
  2. CPPD.
  3. Haemochromatosis*—resembles CPPD but has a predilection for
    the index and middle finger MCPJs with hook-like osteophytes
7
Q

ARTHRITIS WITH OSTEOPENIA

7

A
  1. Rheumatoid arthritis*—typically polyarticular.
  2. Septic arthritis—typically monoarticular.
  3. SLE*—typically causes symmetric osteopenia and joint subluxation
    (especially MCPJs) without erosions.
  4. Systemic sclerosis—joint contractures, acroosteolysis and
    well-defined soft tissue calcifications (calcinosis).
  5. Reactive arthritis*—juxtaarticular osteopenia in early phase.
  6. Juvenile idiopathic arthritis*.
  7. Haemophilic arthropathy—epiphyseal overgrowth, periarticular
    erosions, diffuse T2 hypointense synovial thickening + blooming on
    gradient echo MRI, due to recurrent haemarthrosis. Males only
8
Q

ARTHRITIS WITH PRESERVATION OF

BONE DENSITY

A
  1. Osteoarthritis.
  2. CPPD.
  3. Gout.
  4. Seronegative spondyloarthropathies.
  5. Neuropathic arthropathy.
9
Q

ARTHRITIS WITH PERIOSTEAL REACTION 4

A
  1. Seronegative spondyloarthropathy—mainly psoriatic arthritis
    (hands) and chronic reactive arthritis (feet). Fluffy appearance,
    represents entheseal bony proliferation.
  2. Septic arthritis—associated bone destruction and/or abscess.
  3. Juvenile idiopathic arthritis*—most often seen around
    metacarpals/metatarsals.
  4. HIV-associated arthritis—similar to chronic reactive arthritis
10
Q

ARTHRITIS WITH PRESERVED OR WIDENED

JOINT SPACE 6

A
  1. Any early arthritis.
  2. Gout.
  3. Acromegaly*—‘spade-like’ terminal phalanges, enlarged
    sesamoids, thickened soft tissues, e.g. heel pad.
  4. SLE*.
  5. PVNS and primary synovial osteochondromatosis.
  6. Multicentric reticulohistiocytosis—symmetric erosive arthritis
    involving PIPJs and DIPJs + acroosteolysis; mimics psoriatic arthritis
    but with nodular soft tissue swelling.
11
Q

ARTHRITIS WITH SOFT TISSUE NODULES

7

A
  1. Rheumatoid arthritis*—subcutaneous rheumatoid nodules;
    typically on extensor surface of the forearm and other pressure
    points; more common in seropositive individuals. Intraarticular T2
    hypointense rice bodies may also be present (also seen in infection
    especially TB).
  2. Gout—tophi: eccentric, lobulated juxtaarticular soft tissue masses,
    typically around extensor tendons ± characteristic foci of
    calcification. Heterogeneous T2 signal on MRI.
  3. PVNS—synovial nodules that bloom on gradient echo sequences ±
    extraarticular extension, e.g. into tendon sheath (giant cell tumour
    of tendon sheath).
  4. Synovial chondromatosis—nonossified variant of
    osteochondromatosis. T2 hyperintense chondroid nodules on MRI.
  5. Sarcoidosis*—periarticular granulomas causing characteristic
    lace-like lytic bone lesions, especially in finger phalanges.
  6. Amyloidosis*—large well-defined erosions + soft tissue swelling.
    On MR: low T1/T2 signal thickening of capsule, ligaments and
    tendons. Can involve wrists, shoulders, hips or knees; usually
    bilateral. History of primary/secondary amyloidosis or dialysis.
  7. Multicentric reticulohistiocytosis—mainly involves hands
12
Q

ARTHRITIS MUTILANS 8

A

Common causes
1. Rheumatoid arthritis.
2. Psoriatic arthritis.
3. Neuropathic arthropathy—diabetes, leprosy or congenital
insensitivity to pain. Leprosy causes distal bone resorption giving a
‘licked candy stick’ appearance.
4. Juvenile idiopathic arthritis
.

Less common causes
5. Chronic reactive arthritis*.
6. Gout—typically hallux MTPJ/IPJ.
7. Mixed connective tissue disease—acroosteolysis and sheet-like 
soft tissue calcification.
8. Multicentric reticulohistiocytosi
13
Q

ACROOSTEOSCLEROSIS

A
  1. Normal variant—most common in middle-aged women.
  2. Psoriatic arthritis—ivory phalanx.
  3. Rheumatoid arthritis*—in association with erosive disease.
  4. Systemic sclerosis—osteosclerosis may precede or coexist with
    osteolysis.
  5. Any cause of sclerotic bone lesion affecting terminal phalanx
14
Q

INTRAARTICULAR LOOSE BODY

4

A
  1. Trauma—osteochondral or avulsion fracture.
  2. Synovial osteochondromatosis—more commonly secondary,
    due to OA with loose chondral bodies of different sizes ±
    calcification. Primary form is rare, due to synovial metaplasia
    with multiple uniform loose bodies (no significant OA unless
    late in disease).
  3. Osteochondritis dissecans—characteristic age (adolescents) and
    location (femoral condyles, capitellum, talar dome).
  4. Neuropathic arthropathy.
15
Q

CALCIFICATION OF ARTICULAR
CARTILAGE (CHONDROCALCINOSIS)
8 (4-4)

A

Common causes

  1. Osteoarthritis.
  2. CPPD.
  3. Hyperparathyroidism*.
  4. Gout.

Rare causes

  1. Haemochromatosis*—similar distribution to CPPD.
  2. Acromegaly*.
  3. Wilson’s disease.
  4. Alkaptonuria*
16
Q

SACROILIITIS

Bilateral symmetric

A
  1. Ankylosing spondylitis*—associated with fine, vertical
    intervertebral syndesmophytes.
  2. Osteoarthritis (mimic)—sclerosis ± marginal bridging osteophytes,
    no erosions.
  3. Enteropathic arthritis—identical to ankylosing spondylitis.
  4. Hyperparathyroidism (mimic)*—subchondral bone resorption,
    joint space widening.
  5. Osteitis condensans ilii (mimic)—sclerosis on iliac side of SIJs.
    Seen in parous women.
  6. Late manifestation of bilateral asymmetric disease
17
Q

SACROILIITIS

Bilateral asymmetric 4

A
  1. Psoriatic arthritis—associated with bulky, asymmetrical
    intervertebral syndesmophytes.
  2. Chronic reactive arthritis*—identical to psoriatic arthritis.
  3. Gout.
  4. Early manifestation of bilateral symmetric disease
18
Q

SACROILIITIS

Unilateral

A
  1. Septic arthritis.

2. Early manifestation of bilateral disease.

19
Q

WIDENING OF THE SYMPHYSIS PUBIS
>10 mm in early childhood, >6 mm in young adults, >3 mm in
older adults.

A

Common causes
1. Pregnancy (3rd trimester)—usually resolves by third month
postpartum.
2. Trauma.
3. Osteitis pubis—especially athletes. Subchondral bone irregularity
and sclerosis.
4. Septic arthritis—with irregular bone destruction.

Less common causes
5. Inflammatory arthritis—rheumatoid arthritis or seronegative
spondyloarthropathy.
6. Hyperparathyroidism*—subperiosteal bone resorption, usually no
sclerosis.
7. Neoplasia—direct invasion by bladder cancer, or lytic metastases.
8. Osteonecrosis—following radiotherapy for pelvic cancer

20
Q

PROTUSIO ACETABULI
Acetabular line projects medial to ilioischial line by >3 mm (men)
or >6 mm (women)

A

Common causes
1. Idiopathic.
2. Trauma—typically unilateral.
3. Rheumatoid arthritis*.
4. Bone softening—e.g. Paget’s disease, osteomalacia, fibrous
dysplasia.
5. Chronic septic arthritis—typically unilateral.

Less common causes

  1. Marfan* and Ehlers-Danlos* syndromes.
  2. Osteogenesis imperfecta.
21
Q

Coxa magna—widened, flattened (toadstool)

femoral head 6

A
  1. Developmental hip dysplasia (DDH)—shallow acetabulum.
  2. Slipped capital femoral epiphysis (SCFE)—medial position of
    femoral head relative to femoral neck.
  3. Perthes’ disease—normal position of femoral head and acetabulum.
  4. Juvenile idiopathic arthritis*.
  5. Previous trauma.
  6. Previous septic arthritis
22
Q

Coxa plana—flattened, sclerotic femoral head

A
  1. Any cause of avascular necrosis—especially Perthes’ disease
23
Q

Coxa valga—femoral angle increased (femoral neck
more vertical)
5

A
  1. Neuromuscular disorders—most commonly cerebral palsy,
    resulting from abductor muscle weakness or adductor spasticity.
  2. Previous femoral neck fracture.
  3. Juvenile idiopathic arthritis*.
  4. Hereditary multiple exostoses.
  5. Skeletal dysplasias—e.g. mucopolysaccharidoses, diastrophic
    dwarfism
24
Q

Coxa vara—femoral angle reduced (femoral neck

more horizontal)

A

Common causes

  1. Developmental hip dysplasia.
  2. Slipped capital femoral epiphysis.
  3. Perthes’ disease.
  4. Previous femoral neck fracture.
  5. Previous septic arthritis.
  6. Bone softening—e.g. osteomalacia, rickets (metaphyseal fraying), Paget’s disease, fibrous dysplasia (characteristic shepherd’s crook deformity).
  7. Idiopathic—coxa vara of childhood.

Less common causes
8. Skeletal dysplasias—e.g. osteogenesis imperfecta, multiple
epiphyseal dysplasia, cleidocranial dysplasia.
9. Proximal focal femoral deficiency—congenital, usually unilateral.
Rudimentary or absent femoral head/neck + variable shortening of
shaft ± pseudarthrosis

25
Q

ENLARGEMENT OF THE DISTAL FEMORAL

INTERCONDYLAR NOTCH 9

A

Common causes
1. Juvenile idiopathic arthritis.
2. Haemophilia—males only; can look identical to juvenile idiopathic arthritis. A dense joint effusion (haemarthrosis), if present, favours haemophilia.
3. Rheumatoid arthritis
.
4. Psoriatic arthritis.
5. Postoperative—notchplasty common as part of anterior cruciate
ligament reconstruction.

Less common causes
6. Septic arthritis—especially indolent (e.g. mycobacterial) infection.
7. Gout.
8. PVNS.
9. Synovial osteochondromatosis.
10. Synovial haemangioma—large feeding vessels on cross-sectional
imaging.