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Systems Path 1 > Musculoskeletal disorders Pt. II > Flashcards

Musculoskeletal disorders Pt. II Flashcards

1
Q

What kind of lesions are found with fibrodisplasia?

A

Benign lesion, failure of body differentiation.

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2
Q

How does fibrodysplasia affect bone growth?

A

Arrested development of bone

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3
Q

How does FD affect size and morphology of bone?

A

Well circumscribed,intramedullary, variable size. Possible osseuous deformation.

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4
Q

What are the three categories of FD

A
  1. ) Monostotic: single bone involvement
  2. ) Polyostotic: mutliple bone involvement
  3. ) Polyostotic + cafe au lait spots & endocrinopathy
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5
Q

What is type 3 FD AKA

A

McCune-Albrite syndrome.

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6
Q

What age is Monostotic FD normally seen?

A

Between ages 10-30

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7
Q

Where is Monostotic FD detected?

A

ribs, femur, tibia, jabones, calvaria, humerus. Minimal bony distortion/enlargement

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8
Q

T/F

Monostotic FD is very symptomatic?

A

False, asymptomatic.

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9
Q

What are some features of polyostotic FD

A

No endocrinopathy, late childhood/adolescence

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10
Q

What morphological bone features are noticed with polyostotic FD?

A

Severe deformation, pathologic fx, is common.

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11
Q

Where is Polyostotic FD seen?

A

Femur, calvaria, tibia, humerus, pelvis

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12
Q

How often is craniofacial involvement?

A

50% of all cases.

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13
Q

What radiographic features are indicative of Polyostotic FD?

A

Well defined margins “ground glass” apprearance. “Shepherd’s crook” disorder

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14
Q

What is the treatment for Polyostotic FD?

A

Excision, orthotic hardware.

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15
Q

McCune-Albright syndrome is how much of polyostotic FD cases?

A

3% of all cases of FD.

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16
Q

What are some specific endocrine related issues with MC-albrite syndrome?

A

Precocious puberty prompts evalutation, MC females. Endocrine hperfunction: hyperthyroidism, pituitary adenoma, adrenal hyperplasia.

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17
Q

What are the 3 major aspects of A&P are affected by MC-Albrite syndrome?

A

Skin, skeletal, endocrinopathy.

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18
Q

T/F

MC-Albrite syndrome is generally severe

A

False,

variable severity

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19
Q

What is the disperal of lesions like with MC-Albrite syndrome?

A

Skin and bony lesions are commonly unilateral (femur, tibia)

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20
Q

T/F

Ewing sarcoma and Primitive Neuroectodermal Tumor are variant of the same malignant tumor

A

True

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21
Q

What are some features of Ewing Ssarcoma and PNET?

A

“Small round cell tumors” of bone.

Hemorrhage and necrosis, medulla and cortex.

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22
Q

T/F

Ewing Sarcoma is highly differentiated?

A

False, highly undifferentiated

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23
Q

What percent of primary bone cancers are Ewing’s sarocoma?

A

10%

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24
Q

How common is Ewings sarcoma in pediatric bone CA?

A

2nd MC

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25
Q

Neural differentiation and Homer-Wright rosettes are indicative of what?

A

PNET

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26
Q

What is the MC age for Ewing Sarcoma and PNET, who is at risk?

A

10-20 years MC. Caucasian males most at risk

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27
Q

What morphological features are found with Ewing Sarcoma and PNET

A

Fempainful enlarging mass, loong bone diaphysis. “onion-skinning” or “sunburst” appeerance on the periosteum.

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28
Q

What areas are most affected by Ewing Sarcoma and PNET?

A

Femur (MC) or pelvis

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29
Q

Ewing Sarcoma and PNET stimulate proinflammatory cytokines which mimics what?

A

Infection. Elevating pyrexia, leukocytosis, and ESR

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30
Q

Onion skinning appearance of periosteum is indicative of what condition?

A

Ewing Sarcoma

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31
Q

What is the survival of 70% of Ewing Sarcoma PNET patients?

A

5-year survival

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32
Q

What gives for a worse prognosis for Ewing sarcoma and PNET?

A

Invasion of surrounding tissues

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33
Q

What is the treatment for Ewing Sarcoma and PNET?

A

Excision, chemotherapy

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34
Q

Ginat cell tumor of bone inolves what kind of cells?

A

Multinucleated giant cells (osteoclast-like), neoplastic monocunlear cells.

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35
Q

What age group is most associated with giant-cell tumor of bone?

A

Age 20-40

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36
Q

What kind of lesions are associated with Giant-cell tumor of bone?

A

Large, lytic, solitary, eccentric (off center) lesions

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37
Q

What areas are the lesions found with giant-cell tumor of bone

A

Knee (MC): dist. femur/prox. tibia. Locally invasive, erode cortex
Epiphysis/metapysis

At the ends of bones basically

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38
Q

How can giant-cell tumor of bone be identified

A

Biopsy

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39
Q

Is giant-cell bone tumor of bone painful?

A

Yes, arthritic like pain.

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40
Q

What x-ray features of giant-cell bone tumor?

A

Osteolytic, eccentric, thin shell of reactive bone.

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41
Q

Is it certain whether giant cell bone tumors are malignant or not?

A

No.

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42
Q

How many cases of giant-cell bone tumors metastasize?

A

2% MC lungs

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43
Q

What is the treatment for giant-cell bone tumors?

A

excision, radiation.

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44
Q

What are some radiographic features of giant cell bone tumor?

A

Thin “shell” of cortex

“Soap bubble” appearance

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45
Q

What is secondary mets to bone?

A

Any cancer that spreads to bone

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46
Q

T/F

Secondary metastasis is more common than primary bone cancers

A

True

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47
Q

What are the mechanisms for secondary mets?

A
  1. ) Direct extension (physical contact)
  2. ) Circulation: lymphatic or hematogenous (sarcomas: hematogenous, carcinomas: lymphatics)
  3. ) Intraspinal seeding
48
Q

What does secondary mets do to bone?

A

Lytic, blastic, or mixed (MC)

49
Q

Where is secondary mets found MC?

A

Axial skeleton, prox. femur/humerus because of

red marrow: stasis, nutrient rich (implantation & growth)

50
Q

What are the MC forms of secondary mets?

A

Adults: prostate (blastic), breast (lytic), lung
Children: neuroblastoma, Wilms tumor, osteosarcoma, Ewing sarcoma, rhabdomyosarcoma (malignancy of skeletal myocytes).

51
Q

What are the 5 types of arthridites?

A
  1. ) Degenerative (OA, DJD)
  2. ) Immune-mediated (RA, ankylosing spodylitis)
  3. ) Metabolic (Gout, pseudogout “CPDD”)
  4. ) Infectious
  5. ) Neoplastic
52
Q

T/F

Osteoarthritis is the major source of morbidity in the elderly

53
Q

What is the most common joint disorder?

A

Osteoarthritis

54
Q

What is osteoarthritis often confused with?

A

Rheumatoid arthritis

55
Q

What does OA involve?

A

Degeneration of articular cartilage (collagen). Decreased proteoglycans = matrix breakdown

56
Q

T/F

OA is always inflammatory

A

False, not necessarily inflammatory. Patient symptomotology does not always include pain.

57
Q

What are secondary changes with OA

A

Subchondral changes. Mechanical wear and tear (age). Genetic influence.

58
Q

What is primary OA

A

Insidious, oligoarticular (involves just a few joints). No trauma, adults

59
Q

What is secondary OA

A

Predisposing injury or deformity. Trauma (obesity), deformity, systemic disease

60
Q

What percentage of cases of OA occur in children?

A

5%, usually secondary to another condition.

61
Q

Where does OA occur in the spine and extremeties?

A

Cervical, lumbar, DIP joints, 1st MCP joints, 1st TMT joint.

62
Q

Where do females and males most experience OA?

A

Females: Knees and hands
Males: Hips

63
Q

How can OA degrade a disk?

A

Decreasing proteoglycans which cause dehydration of the disk.

64
Q

What bony changes happen with OA

A

Matrix cracks, softening/degradation (condromalacia), exposure of subchondral bone, sclerosis of bone (eburnation), osteophytosis. Inflammation may develop secondary to degeneration.

65
Q

In advanced cases (all subchondral bone of affected area is exposed) what is seen in the bone?

A

Sunchondral fx -> exposure to synovial fluid -> subchondral cysts.

Possible joint mice: joint locking & pain.

66
Q

What does eburnation mean?

A

“Ivory-like”.

67
Q

What properties provide elasticity and tensile strength to joints?

A

Proteoglycans and type II collagen (healthy condrocytes)

68
Q

What does OA do to chondrocytes?

A

Distrupts functions, which decreases the resiliency of cartilage. Causes degeneration in normal cartilage.

69
Q

What are some risks for OA?

A

Mechanical stress (age 50-60), genetics, increase bone density, increase estrogen. NOT simply wear-and-tear.

70
Q

What are some features of OA?

A

Insidious, deep/achy pain, crepitus, decrease ROM, worse in morning. Generally slowly progressive.

71
Q

What are some nervous system issues implicated in OA?

A

Osteophytes may impinge nerve roots. Radiculopathy (pain, weak, numb) spasm, atrophy.

72
Q

What is the tx for OA?

A

Palliative

Ice, heat, NSAIDs, adjust, joint replacement.

73
Q

What are some radiographic signs of OA?

A

Loss of joint space (dehydration). No ankylosis.

74
Q

What kind of condition is RA?

A

Systemic, chornic autoimmune disease?

75
Q

What cells are implicated in the autoimmunity of RA?

A

CD4+ T cells, cytokines, macrophages.

76
Q

What is destroyed in RA?

A

In joints: increase collagenase and osteoclast activity

77
Q

What are the 2 things that RA patients are tested for?

A

Anti-CCP antibodies (70% of cases) inflamamtion: smoking or infection.

IgM autoantibodies: 80% Rheuamtoid factor (RF), IgG immune complex. MC

78
Q

What are the general features of RA?

A

Weakness, malaise, low-grade fever, cachexia. Insidious, aching, joint stiffness, decrease ROM.

79
Q

T/F

RA affects large joints that are affected symmetrically

A

False,

Symmetric, small joints. Hands, feet, ankles, wrists, elbows, kness (although rare, usually it will be OA with the knee).

80
Q

What are some features of joint harm with RA?

A

MC, MCP & PIP (Bouchard’s). “Fusiform swelling”

Spine: 30% have atlanto-axial instability

81
Q

What are some features of joint destruction with RA?

A

Pannus (granulation tissue), articular destruction/disability. 10-15 years to develop usually. Ulnar deviation, swan-neck deformity. Eventual ankylosis.

82
Q

What are some key differences of RA and OA?

A

RA: autoimmune, inflammatory, ankylosis
OA: degenerative, non inflammatory, NO ankylosis.

83
Q

What is Jevenile rheumatoid arthritis?

A

Autoimmune. Group of multifactorial disorders, MC neg. for RF.

84
Q

What are some diagnostic criteria for JRA?

A

Early onset of pain (<16 years old), lasting up to or longer than 6 weeks.

85
Q

What joints are MC affected by JRA

A

Large joints: knees, hips.

86
Q

T/F

Males are more likely to develop JRA?

A

False,

Girls 2-3x more likely to develop than males.

87
Q

What is the acronym for seronegative spondyloarthropothy categories?

A

P.E.A.R

P: Psoriatic arthritis (psoriasis)
E: Enteropathic arthritis (inflammatory bowel disease)
A: Ankylosing spondylitis
R: Reactive arthritis

88
Q

What are some characteristics of seronegative spondyloarthropathies?

A

Sacroiliitis, spinal ligaments (syndesmophytes)

89
Q

Ankylosing spondylitis is AKA?

A

Marie Strumpell disease

90
Q

What are some features of AS?

A

Sacroiliitis (inflammation), referred gluteal pain.

Syndesmophytes: bamboo spine, decreased lordosis, decreased flexion

91
Q

What are some notable symtoms related to AS?

A

Morning stiffness
Nocturnal LBP (unrelieved when lying down)
Decreased chest expansion: ankylosing of rib joints
Fusion

92
Q

T/F

95% of AS cases are HLA-B27 positive

93
Q

What causes gout?

A

The result of abnormal purine metabolism. Uric acid accumulation, monosodium urate crystals (tophi). Failed crystal phagocytosis

94
Q

What is the presentation of gout like?

A

Acute inflammation, recurrent (destruction, fibrosis)

95
Q

What is primary gout?

A

Hyperuricemia (↑ uric acid production)
•Idiopathic, 90% of cases
•Hypothesized enzyme defects

96
Q

What is secondary gout?

A

Co-morbid disease or drug exposure

•Renal disease, leukemia, multiple myeloma, diuretics

97
Q

Who is at risk for getting gout?

98
Q

Where does gout MC manifest?

A

In hallux (MTP) = podagra

99
Q

What are the 3 types of gout?

A
  1. Asymptomatic hyperuricemia
  2. Acute gouty arthritis: cycles, hours-to-weeks (erythema)
  3. Repeated: “chronic tophaceous arthritis”
    •Fails to resolve between cycles
    •20% die of renal failure (gouty nephropathy)
100
Q

Where are the possible tophi deposition locations with gouty arthritis?

A
  • Toes
  • Fingers
  • Helix of the ear
  • Prepatellar bursa
  • Olecranon
101
Q

What is a late stage problem with gout?

A

Irreversible joint deformity

102
Q

What is Pseudogout AKA?

A

Chondrocalcinosis or CPDD

103
Q

What is pesudogout (CPDD)

A

Altered pyrophosphate metabolism. Pyrophosphate crystal deposition into joints
•Knee, wrist, shoulder, hip, elbow, ankle

104
Q

T/F

Pseudogout (CPDD) is MC inherited

A

False

MC sporadic

105
Q

What is the age of onset for CPDD?

106
Q

What happens with inflammation lasting weeks in CPDD?

A

Destruction of joint 50% of the time.

107
Q

What are the tx for CPDD?

A

NSAIDS, corticosteroids (palliative meds)

108
Q

What is HADD?

A

Hydroxyapatite deposition disease AKA calcific tendonitis

Hydroxyapatite accumulate in tendons, produces “soft tissue opacities”

109
Q

What causes HADD?

A

Idiopathic, possible dystrophic Calcification

110
Q

What symptoms are noted with HADD?

A

Pain, swelling, reduced ROM

111
Q

At what locations does HADD appear?

A

Rotator cuff muscles (MC), elbow, wrist, hip, ankle

112
Q

What is DISH and what is it AKA?

A

Diffuse idiopathic skeletal hyperostosis

AKA Forestier disease

113
Q

What areas does DISH affect?

A
  • Tendinous & ligamentous insertions
  • Anterior longitudinal ligament (ALL)
  • Spine: cervical, thoracic spine (T7-11)
114
Q

What are the two types of infectious arthritis?

A
  1. Suppurative arthritis

2. Lyme arthritis

115
Q

What is suppurative arthritis?

A

Suppurative: pus forming

•Bacteremia → seeds to joints

116
Q

What are the features of suppurative arthritis?

A

Acute inflammation, ↓ ROM, fever, ↑ ESR

117
Q

Where does suppurative arthritis occur?

A

90% monoarticular

•Knee (MC), hip, shoulder, elbow, wrist, S-C joint

Systems Path 1 (9 decks)

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