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Step 1 Crush 250! - Hans > MSK 424 - 428 > Flashcards

MSK 424 - 428 Flashcards

1
Q

explain why estrogen is bone protective

A

estrogen blocks apoptosis in bone forming osteoblast and induces apoptosis in bone-resorbing osteoclast

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2
Q

what bone cell secretes acid and collagenases?

A

osteoclast

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3
Q

what cell is multinucleated and is derived from monocyte?

A

osteoclast

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4
Q

what bone path takes place in epiphysis?

A

Giant cell tumor

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5
Q

what bone paths take place in metaphysis?

A

osteosarcoma, osteochondroma

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6
Q

what bone paths take place in diaphysis?

A

Ewing sarcoma, myeloma, osteoid osteoma

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7
Q

which bone path is associated with nighttime pain, central nidus, and pain released by aspirin?

A

osteoid osteoma

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8
Q

3 characteristics of Ewing sarcoma?

A
  1. anaplastic small blue cell malignant tumor
  2. extremely aggressive with early metastases, but responsive to chemotherapy
  3. “onion skin” periosteal reaction in bone
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9
Q

what population is most affected by Ewing sarcoma?

A

boys

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10
Q

what is the 2nd most common primary malignant tumor after multiple myeloma?

A

osteosarcoma (osteogenic sarcoma)

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11
Q

name 5 predisposing factors for osteosarcoma (osteogenic sarcoma)

A
  1. paget dz of bone
  2. bone infarcts
  3. radiation
  4. familial retinoblastoma
  5. Li Fraumeni syndrome (germline p53 mutation)
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12
Q

what is the age distribution who get osteosarcoma?

A

biomodal distribution (10-20 yr old and more than 65)

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13
Q

what other malignancy has also bimodal distribution?

A

hodgkin (young adulthood and more than 55)

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14
Q

on x-ray, how will osteosarcoma look like?

A

codman triangle (from elevation of periosteum) or sunburst pattern on x-ray

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15
Q

what is the most common benign tumor?

A

osteochondroma

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16
Q

does osteochondroma transform to chondrosarcoma?

A

rarely yes

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17
Q

what is the characteristic of osteochondroma?

A

mature bone with cartilagionus (chondroid) cap

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18
Q

what bone tumor is characterized as soap bubble appearance on x-ray with multinucleated giant cells

A

giant cell tumor

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19
Q

what is the most common site of giant cell tumor?

A

epiphyseal end of long bone around knee

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20
Q

in paget dz of bone, hearing loss is due to

A

auditory foramen narrowing

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21
Q

name the 4 stages of paget dz of bone

A
  1. lytic (osteoclast)
  2. mixed (osteoclast + osteoblast)
  3. sclerotic (osteoblast)
  4. quiescent (minimal osteoclast/osteoblast)
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22
Q

explain the pathophysio of the paget dz of bone

A

common, localized disorder of bone remodeling cause by inc in both osteoblastic and osteoclastic activity

23
Q

what bone path is associated with mosaic pattern of woven and lamellar bone?

A

paget dz of bone

24
Q

what is the most common site of osteonecrosis (avascular necrosis) and why?

A

femoral head (due to insufficiency of medial circumflex femoral artery)

25
Q

name 7 causes for osteonecrosis

A

ASEPTIC

  1. alcoholism
  2. sickle cell
  3. storage dz (Guacher)
  4. exogenous steroid
  5. pancreatic
  6. trauma
  7. idiopathic
  8. caisson (the bend)
26
Q

what is another name for idiopathic cause of osteonecrosis?

A

Legg Calve Perthes dz

27
Q

phosphorylation of myosin is done by what enzyme and will this lead to contraction or relaxation?

A

myosin light chain kinase, contraction

28
Q

dephosphorylation of myosin is done by what enzyme and what will this lead to?

A

myosin light chain phosphatase, relaxation

29
Q

inc Ca2+ calmodulin complex activates which enzyme?

A

myosin light chain kinase

30
Q

bones of axial and appendicular skeleton and base of skull are considered as what type of bone formation?

A

endochondral ossification

31
Q

what is membranous ossification?

A

bones of calvarium and facial bones

32
Q

woven bone is formed directly without

A

cartilage

33
Q

cartilaginous model of bone is first made by

A

chondrocytes

34
Q

what is the pathophysio of achondroplasia?

A

(gain of function), constitutive activation of fibroblast growth factor receptor (FGFR3) inhibiting chondrocyte proliferation

35
Q

mode of inheritance of achondroplasia?

A

autosomal dominant with full penetrance (homozygosity is lethal)

36
Q

how is Laron syndrome diff from achondroplasia?

A

small genitalia, dec linear growth, everything small due to defective growth hormone receptor

37
Q

treatment drugs for type 2 (senile) osteoporosis?

A

bisphosphonate, PTH analog (teriparatide), SERMs, calcitonin, denosumab

38
Q

what is denosumab?

A

monoclonal antibody against RANKL

39
Q

what bone path is associated with bone filling marrow space leading to pancytopenia and extramedullary hematopoiesis?

A

osteopetrosis (marble bone dz)

40
Q

what is defective in osteopetrosis?

A

failure of normal bone resorption due to defective osteoclast leading to thickened, dense bones that are prone to fracture

41
Q

what mutation is responsible for osteopetrosis?

A

mutations in carbonic anhydrase II impairing the ability of osteoclast to generate acidic environment necessary for bone resorption

42
Q

what renal path will also have impaired carbonic anhydrase?

A

proximal (type2) urine pH

43
Q

what is the treatment for osteopetrosis?

A

bone marrow transplant is curative as osteoclast is from monocytes

44
Q

what path is associated with “bone-in-bone” appearance on x-ray?

A

osteopetrosis

45
Q

what is the diff btw osteoporosis and osteomalacia in terms of bone mineralization?

A

normal bone mineralization in osteoporosis

abnormal bone minerailization in osteomalacia (rickets)

46
Q

4 causes for primary osteoporosis?

A
  1. long term steroid use
  2. anticonvulsant
  3. anticoagulants
  4. thyroid replacement therapy
47
Q

what symptoms/fractures can you get from osteoporosis?

A
  1. vertebral compression fractures associated with acute back pain, loss of height, kyphosis
  2. fractures of femoral neck
  3. fractures of distal radius (Colles fractures)
48
Q

2 bone paths with normal lab values?

A
  1. osteoporosis

2. osteopetrosis

49
Q

what two bone paths will have the opposite lab values (Ca2+, PO43-, PTH, except for ALP)?

A

osteomalacia/rickets and hypervitaminosis

50
Q

2 causes for hypervitaminosis?

A
  1. oversupplementation

2. granulomatous dz (sarcoidosis)

51
Q

explain how the lab values will be diff btw 1’ hyperparathyroidism vs 2’

A

1’: high PTH –> high Ca2+ –> low PO43-, high ALP

2’: high PO43- –> low Ca2+ –> high PTH, high ALP

52
Q

in 2’ hyperparathyroidism, what causes high PO43- conc?

A

usually due to dec PO43- from ESRD

53
Q

in 2’ hyperparathyroidism, what causes low serum Ca2+?

A

due to low activated vit D due to ESRD

Step 1 Crush 250! - Hans (41 decks)

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