Primary Bone Tumors Flashcards

1
Q

What are the s/sx of hyperparathyroidism?

A
  • Bones
  • Stones
  • Abdominal Groans
  • Psychiatric overtones
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2
Q

What is the effect of PTH on ca resorption in the renal tubules?

A

Increases Ca resorption, and increases phosphate secretion

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3
Q

What is the effect of PTH on Vit D?

A

Increased synthesis of active form

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4
Q

What happens to Serum Ca and phosphate levels with PTH excess?

A

Increased

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5
Q

What is the most common cause of excess PTH?

A

Primary hyperparathyroidism

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6
Q

What is the tunneling reabsorption seen in Hyper PTH?

A

Lines on x-ray r/t osteoclast resorption 2/2 PTH

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7
Q

What are the brown tumors seen in hyperparathyroidism?

A

Collection of fibrous tissue, giant cells, and hemosiderin in bones that appear as areas of hypo-lucency on x-ray

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8
Q

What is renal osteodystrophy?

A

Chronic renal failure causes decrease in 1,24 (OH) D3 deficiency and associated secondary increase in PTH

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9
Q

What causes the osteomalacia with dialysis and renal osteodystrophy?

A

Metabolic acidosis, and increased PTH

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10
Q

What are the complications from renal osteodystrophy?

A

Osteitis fibrosa cystica

Osteomalacia

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11
Q

what is the pathophysiology behind Paget’s disease of the bone?

A
  1. Aggressive osteoclast-mediated bone resorption and

2. Imperfect osteoblast mediated bone repair

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12
Q

What is the progression of the pathophysiology of paget’s disease of the bone?

A

First aggressive osteoclast resorption is more prominent, then imperfect osteoblast rapri becomes the larger factor

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13
Q

What is the supposed infectious etiology of Paget’s disease?

A

Paramyxovirus increases expression of RANK receptor

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14
Q

What are the three major stages of Paget’s disease of the bone?

A
  1. Osteolysis
  2. Osteoblastic
  3. Osteosclerosis
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15
Q

Pt complaining of hat size changes = ?

A

Paget’s disease of the bone

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16
Q

What are the histological findings of Paget’s disease of the bone?

A
  • Sclerosis of the bone with wide trabeculae

- Large amounts of osteoid

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17
Q

What happens to the osteoclasts with Paget’s disease of the bone?

A

Increased size

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18
Q

What is the definition of scurvy?

A

Defective osteoid synthesis and collagen support of the blood vessels

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19
Q

What are the characteristic hair findings of scurvy?

A

Corkscrew hairs and petechiae

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20
Q

Where does hydroxylation of proline take place within a cell?

A

rER

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21
Q

What are some major complications of scurvy?

A

Subperiosteal hemorrhages

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22
Q

What, generally, is avascular necrosis?

A

Infarction of bone and marrow 2/2 ischemia

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23
Q

What are the common mechanisms that lead to avascular necrosis? (4)

A
  • Fracture (mechanical vascular interruption)
  • Corticosteroids
  • Idiopathic
  • Sickle cell disease
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24
Q

What are the gross characteristics of AVN?

A

Wedge shaped infarct in the bone, with separation of the subchondral area from the periosteum

25
Q

Why is the femoral head particularly susceptible to avascular necrosis?

A

Hip fracture can shear off blood supply

26
Q

What is the blood vessel that supplies the head of the femur?

A

Branch of the obturator artery

27
Q

What are the two blood vessels that supply the neck of the femoral head?

A

Medial and lateral circumflex arteries

28
Q

What is the first thing to happen when a bone is fractured?

A

Organization of a hematoma into a procallus

29
Q

What happens with a fractures after a procallus has formed?

A

Conversion of the procallus to fibrocartilaginous callus caused by deposition of woven bone

30
Q

What happens with a fracture after a fibrocartilaginous callus has formed

A

Replacement of the mesenchymal cells by osseous callus, with bone remodeling along stress lines

31
Q

What is the order of calluses that occurs with fractures? (3)

A

Procallus
Fibrocartilaginous callus
Osseous callus

32
Q

How much more common are fractures relative to primary bone tumors?

A

3000-4000x

33
Q

What are greenstick fractures?

A

Incomplete fractures with closed skin, with bowing on the opposite side

34
Q

What are stress fractures?

A

Fractures that develop slowly over time following a new repetitive stress

35
Q

What are pathological fractures?

A

Diseased bone–non-traumatic

36
Q

What is a compound fracture?

A

fracture where a part of the bone breaks through the skin

37
Q

What is the enzyme that is defective with Gaucher’s disease?

A

Defect in glucocerebrosidase

38
Q

What is happening in the 0-3 day timeframe of fracture healing?

A

Hemorrhage, inflammatory infiltrate, and granulation tissue

39
Q

What is happening in the 3-7 day timeframe in fracture healing?

A

Chronic inflammation with granulation tissue and osteoclastic activity

40
Q

What is happening in the 7-35 day time frame of fracture healing?

A

Progressive increase in cartilage woven bone and cartilage formation

41
Q

What is happening in the 35+ day time frame of fracture healing?

A

Secondary callus, and replacement of woven bone by lamellar bone

42
Q

What are the five major impediments to fracture healing?

A
  • infection
  • non-union
  • Poor circulation
  • Drugs
43
Q

What is osteomyelitis?

A

Inflammation of the bone and marrow caused by infection

44
Q

What are the bacteria that commonly cause osteomyelitis in sickle cell patients?

A

Salmonella

45
Q

What are the three major routes of spread for osteomyelitis?

A
  • Hematogenous
  • Direct extension
  • Open fracture or surgery
46
Q

What is the most common bacterial cause of osteomyelitis in general?

A

Staph aureus

47
Q

What usually follows initial osteonecrosis with osteomyelitis?

A

Subperiosteal pyogenic abscesses

48
Q

What is the sequestrum with chronic osteomyelitis?

A

Residual necrotic bone

49
Q

What is the involucrum with chronic osteomyelitis?

A

Rim of reactive bone around sequestrum

50
Q

What is a brodie abscess?

A

Walled off abscess in bone by sclerotic bone

51
Q

True or false: viable organisms may persist in brodie abscesses

A

True

52
Q

What are some complications of chronic osteomyelitis?

A

Draining sinuses to the skin, which may serves as a nidus for sepsis or cancer

53
Q

What cancer do patients with chronic osteomyelitis have an increased risk for?

A

Osteosarcoma

54
Q

What usually causes tuberculosis osteomyelitis?

A

Hematogenous spread, but can be direct extension

55
Q

What bones in particular are affected with tuberculous osteomyelitis?

A

Vertebrae and long bones

56
Q

What is Pott’s disease?

A

TB of the vertebral bodies, producing a gibbus deformity (loss of vertebral body encroaches on spinal cord)

57
Q

Why is there a resurgence of tuberculous osteomyelitis in developed countries?

A

Immigration and immunosuppressed people

58
Q

What is the general progression of tuberculous osteomyelitis?

A

Starts in the synovium, then progresses to the epiphysis and through the medullary cavity