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Musculoskeletal System > Pathology- Bones and Soft Tissue > Flashcards

Pathology- Bones and Soft Tissue Flashcards

1
Q

What is deficient in the mother to cause cretinism?

A

iodine

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2
Q

What are the bone growth problems in cretinism?

A

linear growth impared, fontanel closure of skull fails, failure of ossification of chondrocytes

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3
Q

What type of mucopolysaccharidosis is Morquio syndrome?

A

type IV

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4
Q

What is deposited in the developing bones in Morquio syndrome?

A

glucosaminoglycans (GAGs)

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5
Q

What is the tell-tale sign of Morquio syndrome?

A

dental defects

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6
Q

What are some other Sx of Morquio syndrome?

A

dental defects, mental retardation, corneal opacities, dearing defects, cardiac valve disturbances

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7
Q

What causes achondroplasia?

A

Arrest of growth plate by a defect in FGFR3 signalling

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8
Q

What is the inheritance of achondroplasia?

A

Autosomal dominant

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9
Q

Are achondroplasia patients mentally retarded?

A

No. Just short.

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10
Q

What is deficient in osteogenesis imperfecta?

A

Type I collagen

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11
Q

Where is type I collagen prevalent?

A

Bones, joints, eyes, ears, skin and teeth

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12
Q

What is the inheritance of osteogenesis imperfecta?

A

autosomal dominant

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13
Q

Scenario: You’re on the set of the new movie “Die Hard 8- I’m a Geriatric about to Die.” After passing the elderly Bruce Willis, you bump into the new girl working on the set. After a casual conversation about tentacle porn, you notice something strange as you creepily stare at her. Having taken MSK and reflecting back on inherited diseases, you remember a tell-tale sign of osteogenesis imperfecta. What did you notice on the girl’s face that clued you into this diagnosis?

A

Blue sclera of the eyes

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14
Q

What causes the blue sclera of the eyes?

A

Type I collagen is missing and you can see the veins in the eyeball

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15
Q

What is defective in Osteopetrosis?

A

Osteoclasts (usually in # or fxn)

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16
Q

What are the morphologies of the bones in osteopetrosis?

A

stone-like, but they are abnormally brittle and fracture easily, like chalk

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17
Q

What type of inheritance is the malignant form of osteopetrosis?

A

autosomal recessive

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18
Q

What type of inheritance is the benign form of osteopetrosis?

A

autosomal dominant

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19
Q

What are the most common forms of osteoporosis?

A

senile and post menopausal

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20
Q

When is peak bone mass achieved during your life?

A

young adulthood

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21
Q

What % of bone loss occurs per year?

A

0.7%/year (this is normal)

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22
Q

What are the main physiological causes of bone loss?

A

osteoblats don’t replicate or regulate as well

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23
Q

Why does decreased physical activity increase the rat eof bone loss?

A

weight loading increases bone formation

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24
Q

What important vitamin is seen in increased or decreased bone mass?

A

Vitamin D

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25
Q

When adolescent girls don’t drink their milk and are deficient in Ca intake, what can happen?

A

Bone mass is shunted and this increases susceptibility to osteoporosis

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26
Q

Women may lose what % of cortical bone mass?

A

35%

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27
Q

Women may lose what % of trabecular bone mass?

A

50%

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28
Q

What % of women suffer osteoporotic fractures?

A

1 out of 2 women

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29
Q

Decreased estrogen causes which cytokines to increase?

A

IL-6 and IL-1

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30
Q

What are the roles of IL-6 and IL-1?

A

Stimulates osteoclasts, which eat bone.

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31
Q

Tx with which type of drug increases osteoporosis by increasing bone resorption and decreasing bone formation?

A

Glucocorticoids

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32
Q

What drug can reverse the osteoporotic symptoms of glucocorticoid treatment?

A

biphosphonates

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33
Q

It’s hard to Dx osteoporosis because you really only see it when 30-40% of bone is lost. However, which type of Dx can you use for it?

A

Specialized radiographs which measure bone density

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34
Q

What are the Tx’s for osteoporosis?

A

exercise, appropriate Ca and Vit D diet, estrogen replacement, PTH and biphosphonates.

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35
Q

What causes Paget disease?

A

haphazard bone resorption and synthesis cuz of osteoclast dysfxn

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36
Q

What are the 3 stages of Paget?

A
  1. Osteolytic stage
  2. mixed osteoclastic-osteoblastic stage
  3. osteoblastic stage ending into quiescent osteosclerotic stage
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37
Q

Though Paget increases bone mass, why is it problematic?

A

the framework is disordered and architecturally unsound

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38
Q

What age does Paget occur?

A

Mid adulthood

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39
Q

What is the viral cause of Paget?

A

paramyxovirus infection –> IL-6 produced –> osteoclasts go crazy

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40
Q

What is the physiological cause of Paget?

A

osteoclasts are hypersensitive to vit D and RANKL

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41
Q

What are the clinical features of Paget?

A

most are mild and found incidentally on X ray, enlarged bone, increased serum alk phos, pain possible, bowing of legs, “chalkstick fracturs

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42
Q

~80% of cases of Paget occur in what bones?

A

axial skeleton or proximal femur

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43
Q

What types of tumors occur in 0.7-0.9% of pagets disease?

A

osteosarcomas

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44
Q

What vitamin is deficient in rickets and osteomalacia?

A

D

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45
Q

What happens when vitamin D is deficient?

A

there is ineffective mineralization of the bone, and an increase in nonmineralized osteoid

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46
Q

Who does rickets affect?

A

kids

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47
Q

Who does osteomalacia affect?

A

adults

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48
Q

What makes osteomalacia different than rickets?

A

it represents defective mineralization of bone that has completed its normal development

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49
Q

What is the role of PTH on bone?

A

stimulates osteoclasts to increase bone resorption and Ca++ metabolism

50
Q

What factor mediates PTH’s affect on osteoclasts?

A

RANKL

51
Q

What is the role of PTH on the kidney?

A

Increase Ca++ reabsorption in the renal tubule and synthesize vitamin D

52
Q

What is the role of vitamin D?

A

increase Ca++ reabsorption by the gut and to increase Ca++ metabolization from the bone.

53
Q

Overall, what molecule does PTH increase in the blood?

A

Ca++

54
Q

What are the 4 skeletal changes in renal osteodystrophy?

A

increase osteoclast activity, osteomalacia, osteosclerosis, growth retardation

55
Q

What is osteomyelitis?

A

inflammation of bone and marrow

56
Q

What causes osteomyelitis?

A

bacteria, typically pyogenic and mycobacteria

57
Q

What are the 3 routes that pyogenic osteomyelitis can reach the bone?

A

blood, neighboring tissue and trauma

58
Q

Which pyogenic bacteria is most common in osteomyelitis?

A

staph aureus

59
Q

Which pyogenic bacteria is most common in osteomyelitis in patients with sickle cell anemia?

A

Salmonella

60
Q

Case scenario: a patient has been given treatment for TB for the past few days but complains of pain in the upper extremities and vertebrae. You take a sample and find granulomatous inflammation with caseous necrosis of the bone. What type of bacteria is likely to be at fault?

A

mycobacteria (tuberculosis osteomyelitis)

61
Q

What is it called when there is a TB infection in the vertebrae?

A

Pott disease

62
Q

What are the 5 primary site for metastatic bone tumors?

A

prostate, breast, lung, kidney and GI

63
Q

What is an osteoma?

A

benign lesion in the bone that are not invasive

64
Q

Where are osteomas common?

A

head and neck

65
Q

Where do osteoid osteomas frequently occur?

A

femur and tibia (<2cm in dimension)

66
Q

Do osteoid osteomas affect men or women more?

A

men

67
Q

Where do osteoblastomas occur?

A

spine

68
Q

What is the most common Sx and Tx for osteoid osteomas?

A

local pain, Tx with ASA

69
Q

How do you Tx a osteoblastoma?

A

CUT IT OUT YEAAAAAAAAAAAAAA

70
Q

What is the size of osteoblasomas vs osteoid osteomas?

A

osteoblastomas can grow larger than 2 cm

71
Q

What are osteosarcomas?

A

malignant tumor of the bone

72
Q

What are conventional osteosarcomas?

A

~75% of cases, occur most often during 2nd decade of life, occur around knee, males more affected, etiology is unknown

73
Q

What are osteochondromas?

A

benign bone tumors that are fairly common

74
Q

What type of tissue accumulates in osteochondromas?

A

hyaline cartilage

75
Q

What is Ollier disease?

A

multipel chondromas, especially in the hands and feet

76
Q

What is Maffuci syndrome?

A

multiple chondromas associated with benign vascular tumors of soft tissue

77
Q

What are chondrosarcomas?

A

malignant tumors that typically occur in older patients

78
Q

Where are common sites of chondrosarcomas?

A

shoulder, pelvis, proximal femur and ribs

79
Q

What are giant cell tumors?

A

rare, agreessive bone tumors that occur between ages 20-40 almost entirely in the epiphysis

80
Q

What are the 2 members of the Ewing sarcomas family of tumors?

A
  1. EWS of bone (Ewing sarcoma of bone)

2. Primitive neuroectodermal tumor (PNET)

81
Q

What % of bone tumors are of the Ewing sarcoma family?

A

6-10%, second most common form of bone tumor in children (following osteosarcoma)

82
Q

What gene is translocated in Ewing sarcomas?

A

t11;22 or q24;q12

83
Q

Where do Ewing sarcomas occur?

A

metadiaphysis (femur) or flat bones of pelvis

84
Q

What is the most common disease of the joints?

A

osteoarthritis

85
Q

What happens in osteoarthritis?

A

degeneration of the articular cartilage

86
Q

What is primary osteoarthrits?

A

arises without any caustive agent

87
Q

What is secondary osteoarthritis?

A

changes developing in previously injured joint

88
Q

Is osteoarthritis an inflammatory diesease?

A

NO. inflammation may occur secondarily and aid in progression of the disease

89
Q

Aging, mechanical and genetic factors can cause what cells to lose the capacity to maintain articular cartilage?

A

chondrocytes

90
Q

The risk of osteoarthritis is linked directly to what factor?

A

bone density

91
Q

What are characteristic changes in osteoarthritis?

A

weakening and breakdown of type II collagen. TNF, IL-1 and NO are possible mediators

92
Q

Where does osteoarthritis common affect?

A

hips, knees, lower lumbar and cervical vertebrae

93
Q

Is rheumatoid arthritis an inflammatory disorder?

A

YES. a chronic systemic one, at that.

94
Q

Which HLA antigen is increased in rheumatoid arthritis?

A

HLA-DRB1

95
Q

What tissues are affected with rheumatoid arthritis?

A

skin, blood vessel, heart, lungs, muscles. mainly the joints.

96
Q

What happens at the joints in rheumatoid arthritis?

A

articular cartilage is destroyed and there is ankylosis of the joints (bent, crooked, stiff)

97
Q

When does juvenile rheumatoid arthritis occur?

A

<16 y/o

98
Q

How is juvenile rheumatoid arthritis different than adult?

A

more large joints affected, systemic disease more common, rheumatoid factor absent, ANA sero + is common, oligoarthritis more common

99
Q

What causes gout?

A

an icnreease in tissue uric acid

100
Q

What are the Sx of gout?

A

recurrent episodes of gout because of crystalline aggregates of urate crystals.

101
Q

What can cause gout?

A

Overproduction of uric acid with decreased renal excretion or vice versa

102
Q

How can the urate crystals in gout activate immune responses?

A

activate C3a and C5a which accumulates neutrophils and macrophages in joints, macrophages release cytokines, proinflammatory mediators released (IL-1, TNF, IL-6 and IL-8)

103
Q

What is pseudo-gout?

A

when there is deposition of calcium pyrophosphate crystals in the tissues (CPPD)

104
Q

What is hereditary CPPD?

A

associated with osteoarthritis, mutation in ANKH affecting the pyrophosphate channels

105
Q

What is secondary CPPD assocaited with?

A

previous joint damage, hemochomatosis, mypomagnesemia, hypothyroidism and diabeeeeetus

106
Q

What is the etiology of CPPD/ pseudo-gout?

A

UNKNOWN

107
Q

Where are soft tissue tumors/lesions derived from?

A

mesenchymal cells

108
Q

Are most soft tissue tumors benign or malignant?

A

benign (1:100)

109
Q

What are some causes of soft tissue tumors?

A

Burns, chemicals, kaposi sarcomas with herpes virus 8.

110
Q

What genetic mutations can cause soft tissue tumors?

A

NF1 mutations, P53 mutations (Li Fraumerie), Osler-Weber-Rendu syndrome (hereditary telangectasia)

111
Q

What are the clinical features of herediary telangectasia?

A

autosomal dominant, dilated capillaires/veins, present from birth, widely distributed

112
Q

What are lipomas?

A

benign subcutaneous tissues of fat. most common soft tissue tumor of adulthood

113
Q

What are the clinical features of lipomas?

A

soft, mobile, painless and cured by excision

114
Q

What are liposarcomas?

A

fat tumors of the deep soft tissue of the peroximal extremities and retroperitoneum, one of the most comm on sarcomas of adulthood.

115
Q

What are the 3 types of liposarcomas?

A

well differentated (indolent), myxoid type (intermediate malignant behavior), and pleomorphic (aggressive and readily metastasize)

116
Q

What are rhabdomyosarcomas?

A

skeletal muscle tumors, most common soft tissue sarcomas in children to adolescence.

117
Q

Where do rhabdomyosarcomas commonly occur?

A

head, neck or GI tract

118
Q

What are some clinical features of rhabdomyosarcomas?

A

genetic mutations can cause dysregulation of muscle differentiation, aggressive. Tx with surgery + chemo and radiation

119
Q

What is the most common subtype of rhabdomyosarcomas?

A

embryonal

120
Q

What are the clinical presentation of embryonal rhabdomyosarcomas?

A

typical in nasal cavity, orbit, middle ear, prostate, vagina, bile ducts or paratesticular. this type has the worst prognosis.

121
Q

What are leiomyomas?

A

Benign tumors of smooth muscle that typically arise in the uterus

122
Q

What are leiomyosarcomas?

A

smooth muscle tumors that affect adult women, occur in skin and soft tissues of extremties and retroperitoneum

Musculoskeletal System (8 decks)

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