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Systems Path 1 > Musculoskeletal disorders > Flashcards

Musculoskeletal disorders Flashcards

1
Q

What kind of disorder is dysostosis, and what are 4 of its overall/general features?

A

Congenital disorder. Developmental anomaly of bone

Abnormal mesenchymal migration
Defective ossification of fetal cartilage
Sporadic (isolated) or part of a syndrome
Homeobox gene alterations

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2
Q

What are 3 specific features of dysostosis?

A

Aplasia (absent or incomplete development, abnormal function)
Supernumerary digits
Abnormal fusion of bones

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3
Q

What is dysplasia?

A

Mutations interfere with growth or homeostasis (dwarfism)

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4
Q

What are the 2 general kinds of dysplasia?

A

Bone: osteodysplasia
Cartilage: condrodysplasia

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5
Q

What are 3 notable pathologies of dysostosis?

A

Klippel-fiel syndrome
Polydactyly
Syndactyly

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6
Q

What osteological features are noted with Klippel-fiel syndrome?

A

Idiopathic congenital fusion of any 2 cervical vertebrae

Sprengel’s deformity

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7
Q

What kind of mutations are found with osteogenesis imperfecta (AKA brittle bone disease), and what does it cause?

A

Mutations of type I collagen (alpha 1 or alpha 2 chains).

Abnormal collagen -> premature breakdown.

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8
Q

What anatomy is affected by ostegenesis imperfecta?

A

ECM of eyes, joints, inner ear bones, skin, teeth/

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9
Q

What is the range of severity with osteogenesis imperfecta?

A

Type I: normal lifespan

Type II: Lethal in utero

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10
Q

What 2 lethal conditions does type II osteogenesis imperfecta cause?

A

Cerebral hemorrhage, respiratory failure.

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11
Q

Abnormal collagen of sclera is attributed to what condition?

A

Type I O.I.

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12
Q

What secondary conditions are associated with Type I O.I?

A

Fractures, extremity bowing, scoliosis, ligamentous laxity (dislocations), hearing loss, fragility.

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13
Q

What kind of adjusting is specifically contraindicated by O.I.?

A

Extremity adjusting

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14
Q

What radiologic sign is associated with O.I?

A

Zebra stripe sign

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15
Q

What are children with O.I. normally treated with?

A

Bisphosphonates (cyclical).

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16
Q

What is the most common form of dwarfism?

A

Achondroplasia

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17
Q

With achondroplasia there is decreased cartilage synthesis, which leads to what?

A

Decreased growth plate expansion

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18
Q

What mutation is implicated in achondroplasia?

A

Fibroblast growth factor receptor (FGFR3) gene mutation

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19
Q

What specific issue does mutation of the FGFR3 gene cause?

A

Inhibits epiphyseal (growth plate) chondrocytes

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20
Q

What percent of achondroplasia cases are spontaneous?

A

75%

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21
Q

What percent of achondroplasia cases are autosomal dominant?

A

25%

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22
Q

What deformations are noticed with achondroplasia?

A

Short proximal extremities, lower extremity bowing, frontal bossing, midface hypoplasia (low nasal bridge).

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23
Q

What are some spinal features noted in achondroplasia?

A

Hyper lordosis and kyphosis at birth, bullet vertebrae, scoliosis, spinal stenosis (of foramen magnum and or spinal canal).

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24
Q

How can death occur in achondroplasia patients due to it’s effect on the spine?

A

Death: brain stem compression, cardiovascular abnormalities.

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25
Q

What is thanatophoric dwarfism?

A

Extremely small thorax and shortened leg bones. Perinatal respiratory failure.

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26
Q

T/F

Prognosis is generally very good for those with thanatophoric dwarfism

A

False, its fatal.

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27
Q

What condition is associated with trident hand?

A

Achondroplasia

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28
Q

T/F

Osteopetrosis is a singular condition that is rather common

A

False,

A GROUP of RARE genetic disorders.

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29
Q

What is the primary structural issue with osteopetrosis?

A

Decrease in osteoclast-mediated bone resorption.

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30
Q

What is osteopetrosis AKA?

A

Skeletal sclerosis (“stone-like” bone).

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31
Q

What kind of injury occurs more frequently with osteopetrosis?

A

Fractures

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32
Q

Foraminal stenosis can occur with osteopetrosis, which can lead to what kind of nerve issues?

A

Cranial nerve palsies

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33
Q

With osteopetrosis, often the medullary cavity fills which leads to which 4 problems?

A

Leads to deranged hematopoiesis, which then can cause hepatospenomegaly, recurrent infections, anemia.

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34
Q

What is the treatment for osteopetrosis?

A

Stem cell replacement

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35
Q

What are some radiographic findings associated with osteopetrosis?

A

No medulla, erlenmyer flask deformity (forearm bones).

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36
Q

What is the most important form of osteopenia?

A

Osteoporosis

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37
Q

What is happening to bones with osteoporosis?

A

imbalance of osteoblast/clast homeostasis leading to decrease in bone bone mass = increase porosity.

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38
Q

What are the 2 major categories of osteoporosis?

A

Localized (disuse)

Generalized to entire skeleton

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39
Q

With osteoporosis that is generalized to the entire skeleton, what are the two types?

A

Primary: MC type, senile, post-menopausal
Secondary: various causes - neoplasia, hyperparathyroidism, nutrient deficiency, drug exposure (corticosteroids decreasing bone mineralization), alcohol, smoking.

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40
Q

What kind of bone done osteporosis MC affect, and where is it mostly discovered?

A

Spongy (trabecular/cancellous) bone. Thinned cortex.

Vertebral bodies, femoral neck, calcaneus.

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41
Q

T/F

Primary osteoporosis is not age related

A

False. It’s senile - thus age related.

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42
Q

What decreases noticeably with primary (senile) osteoporosis?

A

GF activity, osteoblast activity. 0.5% bone loss/year.

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43
Q

What stays about the same in primary (senile osteoporosis)?

A

Osteoclast activity

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44
Q

In secondary (post-menopausal) osteoporosis, what is the main causal factor of bone loss?

A

Decrease in estrogens.

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45
Q

What percentage of female osteoporosis patients are postmenopausal?

A

50%

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46
Q

What kind of supplementation is important for dealing with osteoporosis or preventing it?

A

Ca++ and vit D supplementation (MC females are deficient).

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47
Q

T/F

Osteoporosis patients are asymptomatic until skeletal fragility is detected?

A

True

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48
Q

What are the MC fractures associated with osteoporosis?

A

Vertebral compression fx (thoracolumbar)

Femoral neck fracture

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49
Q

With vertebral compression fractures (in osteoporosis patients) What are some secondary issues associated?

A

Dowager’s hump, kyphoscoliosis

Pneumonia

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50
Q

What potentially life threatening issue could arise with a femoral neck fracture in osteoporosis patients?

A

Pulmonary emboli

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51
Q

What is a treatment option for secondary (post-menopausal osteoporosis)? What are the risk factors associated with these treatments?

A

Estrogen therapy.

Increase risk of endometrial and breast cancers.
Increase risk for DVT

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52
Q

T/F

X-ray is a sufficient diagnostic tool for osteoporosis.

A

False,

X-rays are not sensitive enough. Requires 30 - 40% decrease in bone mass to detect.

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53
Q

Besides physical activity, Ca and vit D supplementation, what is another beneficial treatment for general osteoporosis?

A

Antiresorptive pharmacologic agents: bisphosphonates.

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54
Q

Paget’s disease is AKA

A

Osteitis deformans

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55
Q

What are the 3 phases of Paget’s disease?

A

Lytic phase
Mixed lytic and blastic phase
Sclerotic phase (exhaustion of cellular activity)

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56
Q

What are 2 primary finding with Paget’s disease?

A

Regional osteoclastic activity

Excessive bone formation (disorganized lamellar bone which leads to enlarged, fragile bones).

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57
Q

What is the diagnosis for Paget’s disease?

A

Increased serum alkaline phosphatase (byproduct of osteoblast activity).

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58
Q

T/F

Paget’s disease is MC shrouded with an array of symptomatology?

A

False,

MC asymptomatic (70-90%). Incidental X-ray finding, relatively benign.

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59
Q

T/F

Paget’s disease is becoming less and less severe?

A

True

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60
Q

What is the MC features of Paget’s disease?

A

Bone pain, neck & back.

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61
Q

What are 3 other features of Paget’s disease?

A

Osseous deformation, Fx, calor (increased vascularity)

Nerve compression: headache, visual/auditory

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62
Q

What percentage of cases of Paget’s disease transition into sarcoma?

A

1%. Poor prognosis

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63
Q

With Paget’s disease what is MC, solitary or multiple lesions?

A

Multiple

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64
Q

80% of cases of Paget’s disease lesions involve which areas?

A

Pelvis, sacrum, skull

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65
Q

What kind of fractures and bony abnormalities are noted with Paget’s disease?

A

Chalkstick fx. Bowing

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66
Q

What is the treatment for Paget’s disease?

A

Bisphosphonates (intended to slow lytic phase)

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67
Q

What kind of cytological finding is associated with Paget’s disease?

A

Mosaic “jigsaw” pattern.

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68
Q

What radiographic sign is associated with Paget’s disease?

A

Ivory verterbra sign.

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69
Q

What generally happens to bone with vitamin D deficiency, and how?

A

Defective mineralization. Hypocalcemia -> PTH -> demineralized bone

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70
Q

What is rickets?

A

Poor growth plate mineralization (children)

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71
Q

What is osteomalacia?

A

Remodeled bone is undermineralized

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72
Q

What does osteomalacia look like in adults?

A

Mild, similar to osteoporosis (fx). Associated with hyperparathyroidism.

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73
Q

What does the parathyroid gland do?

A

Secretes PTH which maintains serum Ca++

74
Q

What is characteristic of primary hyperparathyroidism?

A

autonomous PTH production

75
Q

What is characteristic of secondary hyperparathyroidism?

A

Renal failure (mild…???)

76
Q

What is the most common cause of excessive PTH secretion?

A

80% from adenoma

77
Q

What is the Dx for hyperparathyroidism?

A

Hypercalcemia, parathyroid immunoassay

78
Q

What is the MC non malignant cause of hypercalcemia?

A

Hyperparathyroidsm

79
Q

T/F

> 50% of people with hyperparathyroidism are asymptomatic

A

True

80
Q

What is happening on a cytological level with hyperparathyroidism?

A

Excessive osteoclast activity impacts skeletal homeostasis causing resorption of cortical and trabecular bone.

81
Q

What kind of neoplasm is associated with hyperparathyroidism?

A

“Brown tumor”

82
Q

What 3 radiologic signs are associated with hyperparathyroidism?

A

Rugger jersey spine, salt & pepper skull, sub-periosteal resorption (eating away at the middle phalanges of the fingers).

83
Q

What are some widespread features of hyperparathyroidism?

A

Bone pain, fx, deformation, kidney stones, fatigue, nausea, anorexia, decreased cognition.

84
Q

What is the tx for hyperparathyroidism?

A

Drinking water, lots of physical activity, avoiding diuretics. Reversible with normalized PTH levels.

85
Q

What are the 7 types of fractures?

A 
Complete/incomplete (MC children)
Closed: overlying skin intact
Compound: overlying skin is intact
Compound (open): Skin is ruptured
Comminuted: fragmented, splintered
Displaced: distal segment is malaligned 
Pathological fx: site of disease (brown tumor, bone cyst, tumor)
Stress fx: develops over time (develops over time)
86
Q

Where are stress fractures MC?

A

Legs and feet

87
Q

What events mark the first week of fx repair?

A

Ruptured vessles -> fibrin mesh -> inflamm cells and fibroblasts -> soft tissue callus, noncalcified.

88
Q

What events mark the second week of fx repair?

A

Woven bone -> chondroblasts

89
Q

What events mark the 6-8 week period and beyond of fx repair?

A

Endochondral ossification -> bony callus. Lifelong remodeling.

90
Q

What are 6 reasons for delayed healing?

A 
Nonunion: large callus formation
Comminuted fx
Inadequate immobilization (disrupts callus formation)
Infection (MC occurs with compound fx
Nutritional deficiencies
Advanced age
91
Q

What are the MC causes of AVN (5)?

A

Corticosteroids, embolism (bends, sickle cell), vasculitis, irradiation, idiopathic

92
Q

T/F

AVN is always painful

A

False,

Can be asymptomatic or painful

93
Q

What subchondral areas are especially prone to AVN?

A

Knee, hip, shoulder, wrist, ankle.

94
Q

What is the eventual new bone growth after AVN called?

A

Creeping substitution

95
Q

What is AVN aka?

A

Osteonecrosis

96
Q

What is joint AVN aka?

A

Osteochondritis dissecans

97
Q

What are the 2 major types of AVN?

A

Subchondral or medullary

98
Q

What is osteomyelitis?

A

Bone marrow inflammation (infection). Leukocytes destroy bone.

99
Q

What is the most common form of osteomyelitis?

A

Acute

100
Q

What are the 3 modes of infx with osteomyelitis?

A 
Hematogenous (sepsis) MC
Adjacent infection (from joint or other tissue)
Traumatic implantation (from surgery or compnd fx - iatrogenic).
101
Q

What are the major symptoms of osteomyelitis?

A

Acute fever, malaise, throbbing pain

102
Q

T/F

With osteomyelitis the agent causing the infx is mostly identifiable

A

False,

50% unidentifiable

103
Q

What organism is responsible MC for pyogenic infx in osteomyelitis?

A

Staphylococcus aureus

104
Q

What is the Dx for pyogenic osteomyelitis?

A

Radiography, blood culture, biopsy

105
Q

What is the involucrum?

A

Reactive/woven lamellar bone surrounding infected bone

106
Q

What is the sequestrum?

A

Dead bone at the site of infx.

107
Q

What is the draining sinus?

A

Ruptured periosteum leads to an abcess in the surrounding soft tissue.

108
Q

What is tuberculosis osteomyelitis AKA?

A

Skeletal TB

109
Q

Where and among whom is skeletal TB MC?

A

Developing countries. In USA: immigrants and immunocompromised

110
Q

What are 3 features of TB osteomyelitis?

A

Caseous granulomas.
Bony destruction
Severe deformation

111
Q

How does skeletal TB spread?

A

Hematogenous (MC), lymphatic

112
Q

What is associated with a multifocal spread of TB osteomyelitis?

A

Immunodeficiency

113
Q

What is associated with solitary spread of TB osteomyelitis?

A

Long bones, vertebrae

114
Q

What is a famous condition of solitary spread TB osteomyelitis, and what does it cause?

A

Pott’s disease. Neurologic deficits

115
Q

What is MC secondary mets to bone or primary bone tumors?

A

Secondary mets to bone

116
Q

What are general features of bone tumors?

A

Bone pain, generally increases (MC), pyrexia, cachexia, anemia, pathologic fx, unexplained bony mass (superficial)

117
Q

What are some characteristics of low back pain from cancer?

A 
>50 years old
History of cancer
Unexplained weight loss
Back pain not alleviated with bed rest
Failure to improve/pain duration >1 month.
118
Q

What 3 characteristics of low back pain are indicative of cancer?

A

> 50 years old, Hx of cancer, cachexia

119
Q

T/F

Malignant bone tumors are MC than benign?

A

False,

Benign is MC

120
Q

What are the 2 MC bone tumors?

A

Matrix, and fibrous producing tumors.

121
Q

What are the 2 MC benign bone tumors?

A

Osteochondroma

Fibrous cortical defects

122
Q

What are the three primary bone cancers?

A

Osteosarcoma
Chondrosarcoma
Ewing’s sarcoma

123
Q

When do bone tumors develop and in what manner?

A

Early development (<40 yrs), benign, asymptomatic

124
Q

Where do bone tumors MC develop?

A

Long bones of extremities.

125
Q

What age range and body part do osteosarcomas develop?

A

10-20 years old. Knee

126
Q

What age range and body part do osteomas develop?

A

40-50, facial bones/skull

127
Q

What are the 3 types of bone forming tumors?

A

Osteoma
Osteoid osteomo and osteoblastoma
Osteosarcoma

128
Q

What is an osteoma?

A

Developmental anomaly. Very similar to normal bone

129
Q

What are some features of osteomas?

A

Exophytic, hard, superficial, solitary, slow growing.

130
Q

Where do osteomas MC develop?

A

Head (skull/facial) & neck.

131
Q

T/F

Osteomas are MC found in young adults

A

False

Middle aged (40-50 yrs).

132
Q

What are 3 noted physical problems associated with osteomas

A

Cosmetic
Sinus obstruction
Local mechanical problems

133
Q

T/F

Osteoid osteomas and osteoblastomas are malignant and MC in females?

A

False,

Benign. MC in males

134
Q

What kind of leasion is noted with OO and OB?

A

Round-to-oval lesion. Near cortex, well-circumscribed. Central “nidus”

135
Q

What is a “rim of sclerosis” MC in?

A

OO

136
Q

What kind of pain is associated with OO and OB?

A

Localized nocturnal pain

137
Q

What is larger, OO or OB?

A

OB

138
Q

Where are OO and OB found?

A 
Cortex of long bones (OO)
Vertebral processes (OB)
139
Q

What is different between the pain elicited by OO and OB?

A

OO: pain relieved by aspirin. Well localized

OB: pain unrelieved by aspirin. Mild and poorly localized.

140
Q

What percentage of diagnosed primary bone cancers are osteosarcomas?

A

20%

141
Q

Who is at the greatest risk for osteosarcomas?

A

Adolescent males

142
Q

What are the features of osteosarcomas of older age (>40)

A

Co-morbid bone pathology (Paget’s disease, AVN, irradiation)

143
Q

What locations do osteosarcomas affect?

A

Metaphysis of bones. Hip, knee, shoulder,

144
Q

What kind of lesion is associated with osteosarcomas?

A

Large, mixed lytic and blastic lesions.

145
Q

With bone tumors, what genes are MC mutated?

A

RB or TP53 gene

146
Q

What aspect of the bone is destroyed with osteosarcomas?

A

Periosteum, medulla

147
Q

What 3 radiologic features are associated with osteosarcomas?

A

Spiculations, sunburst, codman triangle

148
Q

What serves as a 1000x increase in risk for osteosarcomas?

A

Retinoblastoma syndrome

149
Q

What is the long-term survival rate for typical (primary) osteosarcoma (affecting 10-20 yr olds)

A

60 - 70%

150
Q

What is the survival rate for secondary osteosarcomas?

A

Usually fatal

151
Q

What 2 treatments are MC for osteosarcomas?

A

Amputation (limb salvage therapy)

Chemotherapy

152
Q

What are the two kinds of cartilage-forming tumors?

A

Hyaline
Myxoid

Can be malignant or benign. MC benign

153
Q

What is osteochondroma AKA?

A

Exostosis

154
Q

What is an osteochondroma?

A

Benign, hyaline cartilage capped outgrowth

155
Q

What are the 2 types of osteochondromas?

A

Solitary (MC): sporadic, adolescents/young adults

Multiple hereditary osteochondromas: Genetic (mutated TSG’s) childhood onset.

156
Q

Where do osteochondromas arise?

A

On metaphysis of long bones (near growth plate). Knee (MC), pelvis, scapula, ribs, hands/feet.

157
Q

T/F

Osteocondromas are rare after skeletal maturity

A

True

158
Q

What are some features of osteochondromas?

A

Cortex merges with host bone (could be painful)
Slow growing
Sessile or pedunculated

159
Q

What are the 2 types of chondromas?

A

Enchondroma: medullary

Juxtacortical chondroma: bone surface

160
Q

What is affected by solitary chodroma lesions?

A

Metaphysis, tubular bones of hands and feet.

161
Q

What is the name of the condition characterized by multiple chondroma lesions?

A

Ollier disease. AKA multiple endochondromas or endochondromatosis

162
Q

T/F

Ollier disease is bilateral

A

False

Unilateral

163
Q

What color are chondroma lesions?

A

Gray-blue translucent (hyaline) nodules

164
Q

T/F

Chrondromas represent 10% of all benign bone tumors?

A

True

165
Q

What sign is indicative of a chondroma?

A

Ring of sclerosis “O ring” sign.

166
Q

What features are noted of the center of chondroma lesions?

A

Possible osteonecrosis (irregular opacification).

167
Q

T/F

Chondromas are MC asymptomatic

A

True

168
Q

Where is the most common place for solitary endochondromas of the hand?

A

Proximal phalanges

169
Q

Who is most at risk for chondrosarcomas?

A

40-60 yr old males

170
Q

What locations are affected by chondrosarcomas?

A

Intramedullary (MC) or juxtacortical: pelvis, shoulder, ribs, prox. femur.

Rare in distal extremities

171
Q

What special lesion is associated with chondrosarcomas?

A

Expansile “glistening mass” - painful. Neoplastic hyaline and myxoid cartilage (may thicken or erode cortex).

172
Q

What is the MC form of chondrosarcomas?

A

Low grade: slow growing, small. 80-90% 5 year survival. Reactive THICKENING of cortex

173
Q

What are the features of high grade chondrosarcomas?

A

Cortical erosion, large, soft tissue mass of cartilaginous tissue. 70% mets (MC lungs) or other bones. Poor prognosis

174
Q

What is the tx for high grade chondrosarcomas

A

Wide excision, chemotherapy

175
Q

What are fibrous cortical defects and nonossifying fibromas?

A

Benign lesions of macrophages and fibroblasts. Thought to be reactions to periosteal injury.

176
Q

T/F

FCD’s and NOF’s are neoplastic

A

False

177
Q

What lesion is larger, FCD of NOF?

A

NOF

178
Q

Where are FCD’s and NOF’s found?

A

Knee: distal femur (MC), proximal tibia

179
Q

T/F

FDC’s and NOF’s are usually not painful

A

True

180
Q

What gives a greater risk for fracture: NOF or FDC?

A

NOF

181
Q

What is the treatment for NOF and FDC?

A

Self resolve within 2-3 years. Differentiate into cortical bone

Systems Path 1 (9 decks)

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