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Skin MS: Week 6 > Pathology of Bone > Flashcards

Pathology of Bone Flashcards

1
Q

Non-neoplastic Bone Disease

A

Fractures of healthy bone

Osteoporosis (especially post-menopausal and senile types) - and associated fractures

Osteomalacia

Osteomyelitis

Avascular (aseptic) bone necrosis/infraction

Paget’s disease of bone

Congenital bone disorders

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2
Q

If see osteopenia (generalized decrease in bone mineralization) - Diff dx

A

Osteoporosis, osteomalacia, malignancy, rare hereditary disorders

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3
Q

Neoplasms involving bone

A

metastatic tumors to skeleton

hemic malignancyes (myeloma/plasmacytoma or lymphoma, acute leukemia)

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4
Q

Primary bone tumor/tumor-like lesions

A

Benign and malignant

Relatively uncommon (more common in children)

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5
Q

Misc. tumor-like diseases which can involve bone

A
  • Histiocytosis X (Langerhan’s histiocytosis)
  • Mast cell disease
  • Hyperparathyroidism (osteitis fibrosa cystica)
  • Others: bone cysts, fibrous dysplasia
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6
Q

Pathological fracture

A

•fracture through diseased bone—usually refers to fracture through tumorous or tumor-like bone

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7
Q

Periosteum pathologically

A

painful when irritated (trauma, injury), also lays down bone –> thickening of bone

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8
Q

Serum alkaline phosphatase

A

Marker for osteoblastic disease, also liver disease w/ bile obstruction (in kids, worry about osteoblastic bone disease - adults, more likely liver defect)

If no other liver lab markers elevated, older person w/ elevated SAP – Paget’s

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9
Q

Osteoporosis - ____ faster than _____

A

Osteoclasts (resorption) faster than osteoblasts (bone building)

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10
Q

Biggest danger to kids w/ trauma near epiphyseal plateor osteomyelitis

A

Disrupt epiphyseal cartilage (blood vessel invasion) –> stop growth

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11
Q

Decreased serum Ca (free) –>

A

increased parathyroid hormone –> increase bone resorption –> increase serum calcium

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12
Q

Vit D sources

A

diet and skin synthesis

*** Issues w/ no sun and malabsorption

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13
Q

Vit D processing

A

Skin synthesis, liver metabolism, kidney/PTH –> Vitamin D (OH)2 - active in skeleton

Renal Disease –> Major skeletal consequences

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14
Q

Kidney + PTH –>

A

increased production of Vit D(OH)2, tubular resorption of Ca++, tubular excretion of phosphate

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15
Q

Required for normal mineralization of bone osteoid

A

Vit D(OH)2

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16
Q

For healthy bone, need

A

Ca, P (diet)

Vit D (diet, skin synthesis)

gut (absorbing Ca, P, Vit D)

kidney (makes Vit D (OH)2, resorbs/excretes Ca, P)

parathyroids (master gland for Ca, bone metabolism)

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17
Q

High serum ca

A

Needs to be explained (hyperparathyroidism or cancer?)

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18
Q

Steps of Bone healing

A

Blood clot in fracture site, ingrowth of fibrous tissue, neovascularization

Near fracture –> knows needs to become cartilaginous - then osteocartilaginous - then bone again

Cartilage callus –> woven bone callus –> remodeling into good bone

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19
Q

Complications of fractures through healthy bone

A

Mal-alignment

Non-union/mal-union/pseudoarthrosis

Osteomyelitis (compound fractures)

Growth disturbance (epiphyseal plate injury in children)

Arthritis (if fractures affects articular surface)

Fat embolism syndrome (w/in days of fx)

Immobilization complications (thrombophlebitis/thromboembolism, osteoporosis of immobilized bone)

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20
Q

Type of osteopenia d/t bone atrophy caused by imbalance of bone remoding process

A

Osteoporosis

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21
Q

Osteoporosis: clinical manifestations

A

no clinical manifestations until fracture - often trivial injury fractures

Vertebral fractures most common - compression usually acute/painful but wedge fracture usually painless

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22
Q

Types/Associations of Osteoporosis

A
  • POSTMENOPAUSAL/SENILE types
  • Due to excess corticosteroids (endogenous or exogenous)
  • Hyperparathyroidism (slow leech)
  • Hyperthyroidism (measure TSH)
  • Poor nutrition/malabsorption
  • Immobilization
  • Hypogonadism
  • Multiple other disease associations
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23
Q

Ability of kidneys to ___________ becomes impaired with age

A

hydroxylate Vit D(OH)1 to Vit D(OH)2

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24
Q

Age/menopause /w osteoporosis

A
  • Diminished PTH secretion by parathyroid glands in response to hypocalcemic stimulus (post-menopausal patients)
  • Increased osteoclastic activity upost-menopausal women
  • Decreased ability of osteoblasts to make matrix
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25
Q

•Common osteoporosis = diagnosis of _______

Remember the often more treatable / reversible causes of ________

Decreased bone mineralization (osteopenia) ___________ osteoporosis

A

•Common osteoporosis = diagnosis of exclusion

Remember the often more treatable / reversible causes of secondary osteoporosis

Decreased bone mineralization (osteopenia) does not automatically = osteoporosis

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26
Q

Biggest complication of kyphosis

A

Shrinking thoracic cavity - difficult clearing of lung - pneumonia/infection

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27
Q

Major historical risk factors for osteoporosis in women

A
  • Postmenopausal (within 20 years after menopause)
  • White or Asian
  • Premature menopause
  • Positive family history
  • Short stature and small bones
  • Leanness
  • Low calcium intake
  • Inactivity
  • Nulliparity
  • Gastric or small-bowel resection
  • Long-term glucocorticoid therapy
  • Long-term use of anticonvulsants
  • Hyperparathyroidism
  • Thyrotoxicosis
  • Smoking
  • Heavy alcohol use
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28
Q

Most common fractures in osteoporosis (appendicular)

A

Proximal femur (intertrochanteric or intracapsular), proximal humerus, distal radius (colles’)

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29
Q

Preventrion osteoporosis

A

umaximize peak bone mass (teens/young adults)

uencourage weight-bearing exercise and Ca supplementation

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30
Q

Labs osteoporosis

A

•to exclude secondary causes of osteoporosis/osteopenia

  • serum Ca, P, alkaline phosphatase, 250H–Vit D, TSH, sometimes PTH (renal insufficiency or malabsorption)
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31
Q

Testing osteoporosis

A

Bone desnitometry

uoffer to all women >= 65 yrs and to any woman <65 yrs if risk factors or unexplained fractures present

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32
Q

Most anti-osteoporosis meds ______

A

inhibit bone resorption

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33
Q

Osteoporosis: Biochemical serum markers of bone formation and resorption:

A

currently NOT sufficiently standardized or studied to provide meaningful diagnostic or therapeutic guidance for individual patients

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34
Q

Primary hyperparathyroidism

A

•Hypercalcemia due to primary hyperplasia or NEOPLASTIC enlargement of parathyroid glands

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35
Q

Bony clinical presentation of primary hyperparathyroidism

A
  • Spectrum of bony changes due to variable degrees of osteoclastic bone resorption—ranging from subtle subperiosteal cortical erosions to diffuse osteoporosis to tumor-like skeletal change (osteitis fibrosa cystica/”Brown tumor”)
  • Favors resorption of cortical bone over trabecular bone

Measure PTH levels

***Used to find these cases w/ renal failure

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36
Q

Primary hyperparathyroidism pathology

A

•: osteoclastic bone resorption/peritrabecular fibrosis = osteitis fibrosa

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37
Q

Primary hyperparathyroidism complications

A

Fractures

Constitutional symptoms; metabolic impairment of kidneys; muscle weakness; neuropsychiatric syndromes (all direct effects of ­ Ca++)

Renal stone disease

•NOTE: Secondary hyperparathyroidism (renal disease) may also produce gross skeletal change.

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38
Q

Prognosis - primary hyperparathyroidism

A

Good - remove adenoma, reversible

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39
Q

Screening hyperparathyroidism

A

asymptomatic and detected on biochemical screening studies

primary type — ­Ca and ¯P

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40
Q

Hypercalcemia major causes (from labs)

A

90% of all cases due to malignancy and hyperparathyroidism

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41
Q

Decreased bone mineralization w/ excess osteoid

A

Osteomalacia

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42
Q

Osteomalacia - d/t

A

interference w/ calcium, phosphate, or vitamin D metabolism (need to know what’s causing that interference)

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43
Q

Osteomalacia: Radiologically appears ________

A

osteopenic (like osteoporosis)

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44
Q

Osteomalacia: May present w/ ____________

A

diffuse skeletal pain (without fracture) - vs osteoporosis (sxs w/ fracture)

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45
Q

Osteomalacia associations

A

Environmental: classic childhood rickets

–Poor diet; ¯ sun exposure in northern latitudes

Intestinal malabsorption—commonest cause of Vit D deficiency in USA (celiac?)

Liver or renal disease (impaired hydroxylation of Vit D)

Rare congenital/inborn errors of metabolism

–Deficient Vit D hydroxylation

–Renal tubular phosphate leak

–End organ resistance to Vit D (OH)2

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46
Q

Osteomalacia biochemical profile

A
  • ­serum alkaline phosphatase (>90%)
  • Low serum Ca or P (50%)
  • Decreased urinary Ca excretion (33%)
  • ­PTH (40%) - not as high as in hyper PTism
  • Decreased 1, 25 dihydroxyvitamin D3 (50%)
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47
Q

Classic rachitic picture (children)

A

Widened/distorted growth plates

Bowed legs due to softened bone

Fractures

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48
Q

Renal osteodystrophy/osteomalacia:

A

Due to progressive destruction of second hydroxylation step of Vit D

Most commonly a combination of 2° hyper-parathyroidism as well as abnormal mineralization (mixed uremic osteodystrophy)

Can produce “renal rickets” in children

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49
Q

Infection of bone

A

osteomyelitis

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50
Q

Primary vs secondary mode of acquisition

A
  • “Primary” mode of acquisition: hematogenous spread to bone from often occult source elsewhere (more common in kids)
  • “Secondary” mode of acquisition: spread to bone from adjacent contiguous infection (joint infection/other soft tissue infection) - commonly diabetic ulcers w/ MRSA
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51
Q

Direct infection mode

A

e.g., compound fractures allowing direct injection of common bacteria onto raw fracture surfaces; orthopedic procedures ± prosthetic devices

52
Q

Hematogenous subtype pyogenic/suppurative type osteomyelitis

A

Commonest in children/young adults

Favors long bones: usually begins in metaphyseal region

Half the cases have no obvious “seeding” source of

infection elsewhere in the body

Adults tend to have vertebral infection

Dx: blood or direct bone culture (children may be culture negative)

53
Q

Common pathogens osteomyelitis

A

Staphylococcus aureus (95% of cases without predisposing morbidity)

Streptococcus

Hemophilus influenzae (now uncommon)

Gram-negative bacilli

NOTE: Patients with sickle-cell anemia tend to get salmonella osteomyelitis (worry w/ food posisoning)

54
Q

Sxs osteomyelitis (common bacterial type)

A

Bone pain, erythema, swelling — fever/chills variable

Early infection (<10 days) often not detectable by routine x-ray

–bone scans/MRI scans better at early detection

55
Q

Pathology Osteomyelitis

A

Most infections begin in metaphyseal marrow space

Possibilities:

– Resolution of infection while still a small nidus

– Walled-off chronic infection (Brodie’s abscess)

– Advanced infection: Subperiosteal and intramedullary spread, Death of bone (sequestrum), Periosteal new bone formation

56
Q

Suppruative osteomyelitis longterm/chronic complications

A

Suppurative arthritis (adjacent joints)

Sinus tracks to skin

Growth disturbance (children)

Deformity

Amyloidosis (secondary seen in longterm inflammation)

57
Q

Commonest causes of direct extension/injection osteomyelitis in adults

A

–Compound fractures

–Contamination during orthopedic surgical procedures

–Extension from adjacent joint/soft tissue infection; diabetic vascular disease

–Causative bugs, Rx, and complications similar to hematogenous type

58
Q

Treatment suppurative osteomyelitis

A

Need early/timely dx and tx to avoid chronic

Aggressive (usually I.V.) antibiotic therapy

± Surgical drainage/debridement

Occasionally amputation for chronic cases

59
Q

Tuberculous Osteomyelitis (spread, location in body, severity, incidence)

A
  • Usually 2° to hematogenous spread from lungs
  • Prefers spine (Pott’s disease) and long bones
  • Highly destructive osteomyelitis with tendency to involve neighboring joints
  • Relatively rare form of osteomyelitis in U.S.A. except in Third World immigrants and immunosuppressed patients
60
Q

Fungal osteomyelitis common causes and spread

A

•Blastomycosis (more here) and coccidioidomycosis (Southwest):

Commonest causes of fungal osteomyelitis in non-immunosuppressed patients

Almost always 2° to hematogenous spread from lungs; original pulmonary infection may have gone undiagnosed or be asymptomatic

Bacterial much more common

61
Q

Syphilitic osteomyelitis

A

VERY RARE

Risk currently towards fetus

62
Q

best way to diagnose osteomyelitis at early stage

A

MRI

63
Q

Bone infarcts due to ________ of ____________ causations

Most common identifiable causes

A

•Bone infarcts due to ischemia of varying/often poorly understood causations

Commonest identifiable causes are fractures, corticosteroid Rx, and alcoholism

64
Q

Avascular Bone necrosis/infarction most commonly affects:

A

femoral head:

Can be 2° to subcapital fractures of femoral neck

Causes necrosis of bone with slippage of articular cartilage

65
Q

Legg-Calve-Perthes disease

A

osteonecrosis of femoral head (? due to trauma), especially ages 4-8 (boys 5:1)

66
Q

Avascular bone necrosis/infarction associations

A

Fractures, Legg-Calve-Perthers, Corticosteroid therapy, Alcoholism, Gaucher’s ds, SLE, Sickle Cell anemia, Caisson’s ds

67
Q

Caisson’s disease

A

The bends

Nitrogen comes out too fast - bones are kind of least of the worries

68
Q

Subchondral infarcts

A

typically cause pain w/ activity

69
Q

Medullary infarcts

A

usually clinically silent unless large (e.g., hemoglobinopathy, Caisson’s disease)

70
Q

Multiple infacts

A

especially with chronic corticosteroid Rx

71
Q

Complications of avascular bone necrosis/infarction

A

2° degenerative joint disease

Bone growth deformities (childhood)

Pathologic fracture

72
Q

Paget’s disease of bone (pearls)

(Osteitis deformans)

A

Elderly

Anglosaxon ancestry (strong family hx)

Elevated serum alkaline phosphatase

Deformed bone

73
Q

Paget’s - which bones and how many

A

May involve multiple bones (polyostotic─most patients) or localized to a single bone (monostotic)

Prefers larger bones (skull, pelvis, tibia, femur, spine)

74
Q

Paget’s - focal acceleration of bone resoprtion followed by haphazard new bone formation

3 phases

A

Lytic - inc. osteoclasts w/ bone resorption, inc vascularity

Mixed - inc. osteoclasts w/ inc osteoblasts, inc vascularity

Sclerotic - most characteristic radiologically (osteoblastic phase)

75
Q

Paget’s clinical/imaging featurse

A
  • Most patients asymptomatic
  • Widening / bowing of long bones
  • Distorted / widened pelvic bones
  • General weakening of affected bone causing increased fractures
76
Q

Paget’s sxs

A
  • principally pain (due to fractures, compression of cranial or spinal nerve roots by foraminal encroachment, or secondary degenerative joint disease due to subchondral bone deformity).
  • Sometimes skin overlying an affected bone is warm during lytic / vascular phase (high output CHF possible in polyostotic disease).
77
Q

Radionuclide bone scan - Pagets

A

Sensitive for early phase ds

78
Q

Paget’s Widening of Bone

A

•Widening of bone favors Paget’s disease over other pathology HALLMARK

X-ray features usually typical to experienced radiologist; occasionally may mimic malignant bone disease (need Bx)

79
Q

Paget’s Lab

A

serum alkaline phosphatase typical for active disease

–Suspect Paget’s biochemically if: Older patient, Isolated ­ alkaline phosphatase level, Normal serum calcium, No hepatobiliary disease

80
Q

Complication w pagets

A

bone sarcoma, severe polyostotic ds

81
Q
A
82
Q

Cause of Pagets

A

Current theory:

–Due to a latent viral infection of osteoclasts in a genetically susceptible person

83
Q

Congenital bone disorders

A
  • Localized absence or duplication of a bone(s)
  • Malformation of craniopsinal axis (spina bifida, meningomyelocele, meningoencephalocele)
  • Achondroplasia
  • Osteogenesis imperfecta
  • Osteopetrosis
  • Bone disease associated with mucopolysaccharidosis
84
Q

Osteogenesis imperfecta

A

•Congenital disorders of type 1 collagen

Either qualitatively abnormal or quantitatively too little

Result: insufficient / inadequate collagen for normal osteoid production –> risk of fractures

85
Q

Osteogenesis imperfecta (variants)

A

Variable degrees of osteopenia/osteoporosis

Variable tendencies for fracture depending on genetic subtype

–Spectrum from type II variant, fatal in utero to type 1 variant with fracture tendency that lessens post-puberty

86
Q

Tumors/Tumor-like lesions involving brain (Sxs)

A

•Whether primary or secondary (metastatic) type, symptoms often are nonspecific:

Pain and/or swelling

Pathologic fracture

87
Q

Tumors of bone (Xray Features)

A

•valuable for predicting:

Along with age—likelihood of primary vs metastatic lesion

Ability to subtype primary bone tumors by location and x-ray character

Usually accurate in separating benign from malignant lesions

88
Q

Bone tumors classified as:

A

osteolytic (demineralizing effect) - (i.e. myeloma)

osteoblastic (increased bone density relative to normal bone) (i.e. metastatic prostate cancer)

mixed osteolytic/osteoblastic features

89
Q

Most common sources of metastatic tumor to skeleton

A

lung, breast, prostate

Almost every known malignancy is capable of metastasizing to bone

Larger bones usually perfered (but can be any)

90
Q

_____________________ are the most common malignancies involving bone

A

Metastatic tumors to skeleton

91
Q

Classical myeloma clinical presentation

A

Multifocal osteolytic lesions with bone pain

Often associated hypercalcemia

Fractures common

92
Q

Plastocytoma of bone

A

•localized tumor of plasma cells—eventually tends to evolve towards classic myeloma

93
Q

Hemic malginancies affecting bone

A

Classic myeloma

plasmacytoma of bone

lymphoma

leukemia

94
Q

Lymphoma

A

Most non-Hodgkin’s lymphomas involve bone at some time during their course

May cause sufficient focal tumefaction to compromise bone strength ® pathological fracture

Rarely can see 1° lymphoma of bone

95
Q

Leukemia

A

By definition, always affects bone marrow

Clinically can produce diffuse/multifocal bone or joint pain (especially ALL in children)

May produce skeletal changes 2° to expanded marrow spaces

Occasionally can produce localized tumefaction of bone

96
Q

Osteoblastic hallmark for

A

prostate cancers in males

97
Q

Osteolytic hallmark for

A

myeloma

98
Q

Primary bone tumors mostly arise in _______ (location) and ________ (population)

A

Metaphyses of long bone

Kids

99
Q

Most common primary benign tumors

A

–Osteochondroma

–Giant cell tumor

–Chondroma

–Osteoid osteoma

–Fibroma (metaphyseal fibrous defect)**

100
Q

Most common malignant primary tumors

A

Osteogenic sarcoma (osteosarcoma) - BAD, most common in kids

Chondrosarcoma - most common in adults

Lymphoma

Ewing’s sarcoma - one of most aggressive

Chordoma - bottom or top of spine

**Again, children

101
Q

Osteosarcoma vs chondrosarcoma

A
  • Osteosarcoma is the commonest primary malignant tumor of children/young adults
  • Chondrosarcoma is the commonest primary malignant tumor of middle-aged/older adults
102
Q

Benign vs malignant preference for location w/ primary bone tumors

A
  • Most benign cartilage tumors (chondromas) tend to involve the small bones (hands and feet)
  • Most malignant cartilage tumors (chondrosarcomas) tend to involve the larger bones (long bones, pelvis, ribs, spine)
103
Q

Sarcomas tend to spread via ______

A

hematogenous route (rather than lymph nodes like carcinoma), ie. go to lungs

104
Q

Tx primary bone tumor cancers

A

Aggressive

surgery, chemo, and/or radiation

105
Q

Giant Cell Tumors

A

Primary bone tumor

  • “intermediate” between benign and malignant states
  • 50% recur following simple curettage

can be locally aggressive

•Some can metastasize to lungs

106
Q

Metaphyseal fibrous defect

A
  • Fibroma, fibrous cortical defect
  • Commonest bone lesion
  • Regarded as a non-neoplastic developmental defect
  • Can be found in one-third of children
  • Often regress spontaneously
  • Occasionally are large enough to compromise bone strength/cause pathological fracture
107
Q

Conditions taht may simulate primary/metastaic bone tumors

A
  • Osteomyelitis
  • Paget’s disease
  • Hyperparathyroidism
  • Fibrous dysplasia
  • Exuberant callus (healing fracture site)
  • Avulsion fractures
  • Assorted benign cysts
  • Histiocytosis X
  • Bone infarcts
  • Mast cell disease
  • Giant cell reparative granuloma
108
Q

tx osteosarcoma

A

Pre-op tx and amputation

109
Q

Most common primary malignant bone tumor of adolescents/young adults

A

Osteogenic sarcoma

110
Q

Osteosarcoma sxs

A

pain, pathologic fracture

111
Q

Osteosarcoma favors _________ (location)

A

•metaphyseal regions of large long bones (esp. knee)

112
Q

Variants osteosarcoma

A

common high-grade / aggressive types (grade 3-4)

–40% mortality rate

ulow-grade types

–curable by adequate surgical excision alone

113
Q

Tx failurs of osteosarcoma associated w/

A

local recurrence and pulmonary/other metastases

114
Q

Osteosarcoma may be secondary to

A

Paget’s, prior irradiation, old bone infarcts (link to retinoblastoma gene mutations?)

115
Q

______ bone osteosarcoma more curable

A

jaw

116
Q

Commonest primary bone tumor of middle-aged/older adults

A

swelling, pain

117
Q

Chondrosarcoma sxs

A

swelling, pain

118
Q

chondrosarcoma prefers _______ bones

A

larger long bones, central skeleton

especially pelvis, rare in small bones

119
Q

Chondrosarcoma may grow to _________ before dx

A

very large size (especially pelvis)

usually typical xray features (hallmark)

120
Q

Multiple variants chondrosarcoma

A

Most common are low-grade tumors with slow growth and delayed risk of metastasis

Xray features to differentiate

121
Q

Chondrosarcoma tx

A

adequate surgical excision (can be very late metastasis)

122
Q

Most aggressive/lethal of all primary bone tumors

A

Ewing’s sarcoma

123
Q

Ewing’s sarcoma usually affects ________ and prefers _______ bone

A
  • Usually affects a younger age group than osteogenic sarcoma (esp. peripubertal ages)
  • Prefers diaphysis of long bones & flat bones of pelvis
124
Q

Diff Dx Ewing’s Sarcoma

A

•Some patients: The x-ray features with fever & leukocytosis may mimic osteomyelitis

125
Q

Histology EWing’s sarcoma

A

Composed of small, morphologically undifferentiated tumor cells now known to be primitive neuroectodermal neoplasm (PNET)

–Usually t(11;22)

–Resembling leukemia, lymphoma, neuroblastoma, Wilm’s tumor, small cell Ca

126
Q
A

Skin MS: Week 6 (12 decks)

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