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Pathology Pt. 5 > Musculoskeletal 2 > Flashcards

Musculoskeletal 2 Flashcards

1
Q

Are osteoclasts multinucleated giant cells that are in the same family as macrophages?

A

Yeah

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2
Q

What is the genetic defect that causes osteogenesis imperfecta?

A

Mutated a1 or a2 chains for type 1 collagen

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3
Q

What are the clinical features of osteogenesis imperfecta (12)?

A
  1. Babies can be stillborn
  2. Multiple fractures at birth
  3. Osteopenia at birth
  4. Blue sclera
  5. Hearing loss
  6. Short stature
  7. Muscle hypotonia
  8. Abnormal dentitions
  9. Lax skin and ligaments
  10. Broad forehead w/ triangular face
  11. Scoliosis (progressive)
  12. Sweating
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4
Q

Do patients with osteogenesis imperfecta have normal intelligence?

A

Yeah

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5
Q

What is the usual pattern of inheritance for osteogenesis imperfecta?

A

Autosomal dominant

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6
Q

Describe the four types of osteogenesis imperfecta.

A

Type I, normal lifespan, bones fracture easily, blue sclera, hearing loss.
Type II, usually fatal in utero, or die shortly after birth from respiratory failure.
Type III, progressive deforming variant, rarely inherited as an autosomal recessive.
Type IV, somewhat similar to type I, more variable phenotype, NORMAL white sclera.

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7
Q

Achondroplasia is a congenital disorder of the ______ ______ and is the most common form of _______ (1/30,000).

A

congenital disorder of the growth plate and most common form of dwarfism.

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8
Q

What is the genetic mutation responsible for achondroplasia? Describe the protein product a little.

A

Point mutation in the fibroblast growth factor receptor 3 (FGFR3). It has kinase activity. The mutation ACTIVATES the receptor –> suppression of chondrocyte proliferation and growth plate expansion.

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9
Q

Name the disease: marked, disproportionate shortening of the proximal extremities, bowing of the legs, a lordotic (sway-backed) posture, disorganized growth plates, normal secondary ossification centers, and short and thick bones.

A

Achondroplasia

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10
Q

Does achondroplasia affect intramembranous ossification, or endochondral ossification? What is the significance of this?

A

Endochondral ossification - affects long bones and not the head.

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11
Q

What are the clinical features of achondroplasia (4)?

A
  1. Large-appearing head - compared with the bones formed from facial cartilage.
  2. Spine is of normal length, limbs are short.
  3. Normal intelligence and life span.
  4. Kyphoscoliosis with complications.
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12
Q

What are the treatments for achondroplasia?

A

GH, skeletal elongation (controversial)

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13
Q

Scurvy (vit. C deficiency, rickets and osteomalacia (vit. D deficiency), osteoporosis, and Paget disease (loss of osteoclast function) are all examples of _______ diseases of bone development.

A

acquired

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14
Q

Osteoporosis is characterized by increased _______ of the skeleton resulting from reduced ______ _____.

A

increased porosity, reduced bone mass

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15
Q

Is osteoporosis associated with an increase in bone fragility and susceptibility to fractures?

A

Yeah

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16
Q

Can osteoporosis be localized or affect the entire skeleton?

A

Yeah

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17
Q

What are the most common forms of osteoporosis?

A

Senile and postmenopausal osteoporosis.

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18
Q

In the case of osteoporosis, the spicules in bone are replaced by ____.

A

fat

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19
Q

At what ages does bone mass reach its peak?

A

25-35 years old

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20
Q

What populations are more prone to osteoporosis?

A

Asians and white folks more than black folks

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21
Q

Is the risk of a 70-year old woman having a hip fracture 7 times higher than that of a 50 year old?

A

Yeah

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22
Q

What is the most common fracture amongst people with osteoporosis?

A

In the neck and intertrochanteric region of the femur (hip fractures)

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23
Q

Females with osteoporosis experience vertebral fractures by a ratio of _____ to men.

A

8:1

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24
Q

The pathogenesis of osteoporosis is reflective of an imbalance of bone ________ by osteoblasts and bone ________ by osteoclasts, as well as osteoblast and stromal cell regulation of ______ _______.

A

imbalance of bone formation by osteoblasts and bone resorption by osteoclasts, as well as osteoblast and stromal cell regulation of osteoclast activation.

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25
Q

What causes secondary osteoporosis?

A

A variety of endocrine and genetic factors

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26
Q

Describe the two types of primary osteoporosis.

A

Type 1: increased osteoclast activity, usually seen in postmenopausal women.
Type 2: aka senile; decreased osteoblast activity, seen in elderly folk of both genders.

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27
Q

Describe how osteoclasts are activated.

A

RANK ligands on the surface of osteoblast and stromal cells bind to RANK receptors (activator for nuclear factor-kB) on osteoclast precursors + macrophage colony stimulating factor (M-CSF) –> precursor differentiation into an osteoclast.

If osteoclast activation isn’t needed, osteoblast/stromal cells make osteoprotegerin (OPG), which binds to RANK ligand so it can’t bind to RANK on precursor cells to activate them.

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28
Q

How does a decline in estrogen lead to bone loss?

A

No estrogen –> more cytokine production (IL-1, IL-2, IL-6, TNF) –> increased RANK-RANKL activity and decreased OPG –> too much osteoclast activation/differentiation.

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29
Q

Name two exogenous substances that can cause secondary osteoporosis.

A
  1. Glucocorticoid therapy

2. Therapies against breast, prostate, etc. cancers

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30
Q

What is the most easily absorbed form of calcium?

A

Calcium citrate - that’s why Trader Joe’s makes Dynamo Calcium orange juice and why proton pump inhibitors can interfere with calcium absorption.

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31
Q

Can cigarette smoking cause/worsen osteoporosis?

A

Yeah

32
Q

Postmenopausal osteoporosis is usually recognizable within ____ years after the onset of menopause.

A

10

33
Q

Senile osteoporosis usually becomes symptomatic after ____ years of age, but in the early stages it is asymptomatic.

A

70

34
Q

What is usually the first sign of osteoporosis?

A

Vertebral fracture, hip fracture, or a slow-healing fracture.

35
Q

Can early diagnosis of osteoporosis be made using screening methods such as bone density scans, ultrasound, and other radiographic techniques?

A

Yeah

36
Q

How does osteoporosis affect the spine?

A

Vertebral compression fractures –> kyphosis (DOWAGER’S HUMP).

37
Q

What is up with serum calcium and phosphorus levels in a patient with osteoporosis?

A

They are normal

38
Q

Can anti-osteoporosis agents cure the disease? Do they stimulate bone formation?

A

They don’t cure, only slow progression. They don’t stimulate bone formation.

39
Q

Name a specific compound that inhibits osteoclast-mediated bone resorption. How does it work?

A

Biphosphonates (Fosamax, alendronate sodium) - inhibits osteoclasts-mediated bone resorption.

40
Q

Is Fosamax the same thing as calcium?

A

Nope, people should take calcium supplements, too!

41
Q

True or false: dietary calcium supplementation in elderly patients reduces the risk of osteoporotic fractures by half.

A

Tru dat

42
Q

What is osteonecrosis?

A

Death of bone/marrow without infection.

43
Q

Aseptic (avascular) necrosis is caused by ischemia and most often involves the _______ of growing bones. Name four causes of bone ischemia.

A

Often involves the metaphysis of growing bones.

Causes:

  1. Vascular compression or disruption (after a fracture).
  2. Steroid use.
  3. Thromboembolotic disease like sickle cell anemia.
  4. Primary vascular disease like vasculitis.
44
Q

Do scaphoid fractures heal easily?

A

No

45
Q

Describe the morphological changes seen in osteonecrosis.

A
  1. Empty lacunae are interspersed with areas of fat necrosis and insoluble calcium soaps.
  2. Cortex usually unaffected because of collateral blood supply.
  3. Osteoclasts can resorb necrotic bony trabeculae, any remaining dead fragments act as scaffolds for new bone formation (creeping substitution).
46
Q

What are the clinical features of osteonecrosis (2)?

A
  1. Subchondral: pain during activity, progressive. Collapse –> severe osteoarthritis.
  2. Medullary: usually clinically silent for large bones.
47
Q

Roughly ______ joint replacements are performed each year to treat the consequence of osteonecrosis.

A

50,000

48
Q

Are primary bone tumors more common than metastasis to bone from other sites?

A

Nope

49
Q

True or false: primary bone tumors exhibit great morphologic diversity and clinical behaviors — from benign to aggressively malignant.

A

True

50
Q

Bone tumors in the elderly are _____ (more or less) likely to be malignant.

A

more

51
Q

How are osteoid osteomas and osteoblastomas treated?

A

Surgical excision

52
Q

At what ages and where do osteoid osteomas and osteoblastomas occur? Which ones are usually larger?

A

Teenage years or in the 20s. Osteoid osteomas usually occur in the proximal femur and tibia and are less than 2cm by definition. Osteoblastomas arise most often in the vertebral column and are larger.

53
Q

Describe the differences between the clinical features of an osteoid osteoma and an osteoblastoma.

A

Osteoid osteomas cause localized pain due to prostaglandin production and it can be relieved with aspirin.

Osteoblastomas cause diffuse (not localized) pain and aspirin does NOT help.

54
Q

What morphological changes are seen in osteoid osteomas and osteoblastomas (5)?

A
  1. Round or oval mass.
  2. Central area is RADIOLUCENT.
  3. Rim of sclerotic bone, more noticeable in osteoid osteomas.
  4. Interlacing trabeculae of woven bone surrounded by osteoblasts.
  5. Loose intervening stroma, vascular CT with variable numbers of giant cells.
55
Q

The most common primary malignant bone tumor, characterized by the formation of bone tissue by tumor cells is a…?

A

osteosarcoma

56
Q

Osteosarcomas represent ___% of all bone cancers and are most common in people between the ages of ____ and ____, with a male:female ratio of ____.

A

20%

common between ages of 10-20

male:female is 2:1

57
Q

What genetic mutations are often found in osteosarcoma cells?

A

2/3 have mutated RB gene, many also have mutated p53

58
Q

Most osteosarcomas develop at sites of greatest bone _____.

A

growth

59
Q

Individuals with hereditary retinoblastomas have a _____x increased risk of developing osteosarcoma.

A

1,000x increased risk

60
Q

What are the clinical features of osteosarcoma (3)?

A
  1. Painful enlarging mass.
  2. Pathologic fracture (can be 1st symptom).
  3. Serum alkaline phosphatase is increased in 50% of patients.
61
Q

What morphological changes are seen in an osteosarcoma (2)?

A
  1. Large, destructive, mixed lytic and blastic mass with indistinct infiltrating margins seen on radiographs.
  2. Tumors break through the cortex and lift the periosteum –> CODMAN TRIANGLE seen on x-ray.
62
Q

How do osteosarcomas metastasize?

A

Hematogenously

63
Q

At the time of diagnosis of osteosarcomas, ___% to ___% have demonstrable pulmonary metastasis.

A

10-20%

64
Q

Chemo and limb-sparing surgery for osteosarcoma give a 5-year disease-free rate of ___ to ___%.

A

60-80%

65
Q

In which bones do osteosarcomas occur most frequently?

A
  1. Distal femur/tibial plateau (50%).
  2. Proximal femur and pelvis (15%).
  3. Proximal humerus (10%).
  4. Jaw, nose (8%).
66
Q

Does everyone with hyperuricemia have gout?

A

No (only 15% do), but all peeps with gout have hyperuricemia.

67
Q

What is the difference between primary and secondary gout? What makes up the majority of cases?

A

Primary gout is hyperuricemia without the presence of other disease (1/3 of cases).

Secondary is hyperuricemia in association with another illness.

68
Q

Describe the epidemiological features of gout (4).

A
  1. Mostly men (only 5% of cases in women).
  2. Rare in young folks.
  3. Peak incidence is in the 5th decade.
  4. Positive correlations exist between the prevalence of hyperuricemia and mean weight, protein intake, alcohol consumption, and other social variables.
69
Q

What is the main characteristic of gout?

A

Increased serum uric acid and monosodium urate crystal deposition in joints and kidneys.

70
Q

Uric acid results from ______ catabolism and is eliminated in the _____.

A

purine catabolism, eliminated in the urine

71
Q

Describe four cellular changes that can cause gout.

A

1, Overproduction of purines

  1. Increased catabolism of nucleic acids due to greater cell turnover
  2. Decreased salvage of free purine bases
  3. Decreased urinary uric acid excretion
72
Q

What are the three morphological classifications of gout?

A
  1. Acute arthritis
  2. Chronic tophaceous arthritis
  3. Gouty nephropathy
73
Q

Describe the morphological changes seen in acute arthritic gout (4).

A
  1. Dense neutrophilic infiltrate in the joint and joint (synovial) fluid.
  2. Long, slender NEEDLE-SHAPED monosodium urate crystals in the cytoplasm of neutrophils and in clusters in the synovium.
  3. Synovium is edematous, congested, and contains monocyte infiltrate.
  4. Attack remits after the crystals abate and re-solubilize.
74
Q

Describe the morphological changes seen in chronic tophaceous arthritic gout (5).

A
  1. Happens after repetitive precipitation of urate crystals.
  2. Urates heavily encrust the articular surfaces and form visible deposits in the synovium.
  3. Synovium becomes hyperplastic, fibrotic, and thickened by inflammatory cells –> erodes underlying bone.
  4. Fibrous or bony ankylosis and loss of joint function in severe cases.
  5. Tophi (hallmark): large aggregations of urate cystals surrounded by intense inflammatory rxn of lymphocytes, macrophages, and giant cells trying to eat the crystals.
75
Q

Describe the morphological changes seen in gouty nephropathy (2).

A
  1. Multiple renal complications associated with urate deposition, medullary tophi, intratubular precipitations, or free uric acid crystals and renal calculi (kidney stone).
  2. Secondary complications such a pyelonephritis can occur, especially when there is urinary obstruction.
76
Q

The clinical features of gout can be divided into four states. Describe each.

A
  1. Acute gouty arthritis: pain in usually one joint (often the MP joint of big toe - PODAGRA).
  2. Intercritical period: asymtomatic interval between attacks (can be a long time, 10 years).
  3. Tophaceous gout: appears in UNTREATED patients in the form of tophi in cartilage, synovial membranes, tendons, and soft tissues.
  4. Renal failure: responsible for 10% of deaths in people with gout.
77
Q

Urate stones make up ___% of all renal calculi in the US and affect up to ___% of gout patients.

A

10% of all renal calculi (stone) in the US and affect up to 25% of gout patients.

Pathology Pt. 5 (7 decks)

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