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Block 7 Week 5 > Walby: Bones > Flashcards

Walby: Bones Flashcards

1
Q

unmineralized bone is called

A

osteoid

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2
Q

lie in a lacuna within the matrix; involved in exchange of nutrients (Ca++ and phosphorous) and waste with blood via canaliculi.

A

osteocytes

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3
Q

This forms 90% of the organic component of bone

A

type I collagen

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4
Q

Compare and contrast the 2 types of collagen deposition

A

woven bone:
fetal skeleton or in adult pathologic states (fractures), grows rapidly, pattern is weaker

lamellar bone:
seen in adults, replaces woven bone at growth plates, deposited slowly, more stable and stronger than woven bone

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5
Q

Most common disease of the growth plate; impaired maturation of cartilage leading to disorganized chondrocytes; results in dwarfism

A

achondroplasia

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6
Q

In achondroplasia, there is a mutation in (blank)

A

fibroblast growth factor receptor 3 (FGFR3)

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7
Q

Compare heterozygous achondroplasia to homozygous achondroplasia

A

heterozygous: shortened extremities, normal trunks, enlarged heads, normal life span
homozygous: comprised respiratory capacity leads to death in infancy - growth hormone not helpful

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8
Q

What is the problem in osteogenesis imperfecta, or brittle bone disease? What happens?

A

abnormality in type I collagen formation leads to too little bone; results in multiple fractures

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9
Q

In osteogenesis imperfecta, autosomal (blank) cases have increased survival

A

dominant

**type I and type 4

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10
Q

What are some features associated with osteogenesis imperfecta?

A 
lax joints
blue sclera in eye (thinned collagen)
deafness
thin skin
small/discolored teeth
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11
Q

Osteoporosis most commonly occurs in these two populations

A

postmenopausal women

senile

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12
Q

In osteoporosis, what is the problem?

A

decreased bone mass/density leads to increased fragility - increased likelihood of vertebral and wrist fractures

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13
Q

Is there a sensitive or specific test for osteoporosis? What do we use?

A

no; use DEXA scans to measure bone density

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14
Q

In osteoporosis, what can complicate femoral neck, pelvis, and spine fractures?

A

pulmonary embolism and pneumonia because the pt is immobile

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15
Q

Compare kyphosis and lordosis

A

kyphosis: curvature of thoracic region
lordosis: curvature of lumbar region

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16
Q

Which is more effective for preventing bone loss, weight training or bicycling?

A

weight training

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17
Q

How to treat osteoporosis?

A 
hormone replacement like bisphosphonates and calcitonin
vitamin replacement (Vit D)
exercise/activity
stop smoking, drinking
don't use corticosteroids
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18
Q

This is the most potent activator of osteoclasts

A

IL-1

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19
Q

What is the problem in Paget’s disease?

A

osteoclast dysfunction

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20
Q

What are the three phases of Paget’s disease?

A
  1. osteoclast/osteolytic stage –> leads to bone loss, hypervascularity
  2. mixed osteoclast/osteoblast stages, which end with predominance of osteoblast activity
  3. ends with a burnt-out osteosclerotic stage
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21
Q

What is the characteristic histologic feature in Paget’s disease?

A

mosaic pattern of bone (woven bone which is weak and prone to fracture), makes bone look like a jigsaw puzzle

**abnormal bone architecture

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22
Q

What is thought to cause Paget’s disease?

A

paramyxovirus-like particles that have been found in osteoclasts

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23
Q

Are most cases of Paget’s disease polyostotic or monostotic?

A

polyostotic

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24
Q

Many cases of Paget’s disease are (blank) and found incidentally on X-rays

A

asymptomatic

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25
Q

Symptoms of Paget’s disease?

A

usu asymptomatic
pain is the most common problem (pain in affected bone)
leonine facies (bone overgrowth in craniofacial area)

**in severe polyostotic disease, increased blood flow can cause functional arterio-venous shunt leading to high-output cardiac failure

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26
Q

These can be seen on plain films in the late stages of Paget’s disease

A

cotton wool spots

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27
Q

Increased incidence of these two tumors in Paget’s disease?

A

giant cell tumor

sarcomas

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28
Q

Treatment of Paget’s disease

A

anti-resorptive agents
bisphosphonates
calcitonin

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29
Q

Bones are abnormally brittle and fracture despite excess deposits and increased density
Rare, inherited, autosomal dominant and recessive states
Can cause Osteosclerosis (bone in bone appearance on radiology)

A

osteopetrosis

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30
Q

Defective mineralization (with an increase in non-mineralized osteoid

A

Vit-D deficiency

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31
Q

Deranged bone growth in children due to Vit D deficiency; overgrowth of epiphyseal cartilage

A

Rickets

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32
Q

Disease of adults due to under-mineralization of bone during remodeling process; bone is weak and prone to microfractures, most likely in vertebral bodies and femoral necks

A

osteomalacia

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33
Q

What are 3 ways that Vit D can aid in Ca+ resorption?

A
  1. stimulates intestinal absorption of Ca and P
  2. works with PTH in mobilizing Ca++ from bone
  3. stimulates PTH-dependent reabsorption of Ca in distal renal tubules
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34
Q

Required for normal mineralization of epiphyseal cartilage and osteoid matrix; maintains supersaturated levels of Ca and P in plasma

A

Vit D

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35
Q

Main problem with Vit D deficiency?

A

hypocalcemia, so you start breaking down more bone or you just get improper mineralization

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36
Q

Symptoms of Rickets

A

frontal bossing of head
pidgeon breast
lumbar lordosis and bowing of legs

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37
Q

What is the problem with hyperparathyroidism?

A

Too much PTH, which stimulates osteoblasts to release mediators which causes osteoclasts to absorb more bone

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38
Q

What is one notable feature of hyperparathyroidism?

A

microfractures of bone form a brown tumor when multinucleated macrophages infiltrate and cause reactive fibrous tissue formation

**osteitis fibrosa cystica

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39
Q

Why can renal insufficiency/failure lead to osteomalacia or problems with the bone?

A

renal failure results in phosphate retention;
when phosphate is high, Ca+ will be low which leads to secondary hyperparathyroidism (release of PTH to try and up Ca++)

**importantly, in the kidneys, Vit D is converted to its active form, so if your kidneys are not working properly, you will have less Vit D production

low vit D and Ca contributes to the osteomalacia

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40
Q

What is one problem when treating renal osteodystrophy?

A

aluminum deposition in the bone due to dialysis and aluminum containing oral meds which bind to phosphate (interfere w calcium hydroxyapatite)

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41
Q

If the overlying tissue is intact in a fracture, it is considered (blank);
If the fracture site communicates with the skin surface and the skin breaks, it is (blank)

A

simple; compound

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42
Q

If the bone is splintered, this is a (blank) fracture; if ends of the bone at fracture site are not aligned, it is a (blank) fracture; if the fracture develops slowly due to increased repetitive loads causing a break, it’s a (blank) fracture

A

comminuted; displaced; stress

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43
Q

T/F: Cartilage is often formed as a part of the early healing of fractures. If the fracture is not immobilized well enough, it may stay as cartilage.

A

True

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44
Q

All instances of avascular necrosis result from (blank). AVN most commonly occurs in the (blank)

A

ischemia; hip

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45
Q

Most common causes of avascular necrosis?

A

idiopathic

steroid administration

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46
Q

2 types of avascular necrosis

A

subchondral infarcts

medullary infarcts

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47
Q

This type of infarct causes chronic pain, which initially is only present during activity, but progressively becomes more persistent. Cartilage may collapse and predispose to severe osteoarthritis, which eventual joint replacement necessary

A

subchondral infarcts

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48
Q

This type of infarct is clinically silent; seen in Gaucher’s disease, dysbarism (pressure changes), hemoglobinopathies; they usually remain stable over time and do not lead to collapse

A

medullary infarcts

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49
Q

T/F: Usually in subchondral infarcts, the cartilage overlying the bone is OK because it gets nutrients from the synovial fluid, not from the underlying medullary area

A

True

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50
Q

What are most cases of osteomyelitis caused by?

A

bacteria which reaches the bone by hematogenous spread or spread from an adjacent infection

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51
Q

Most common bacteria causing osteomyelitis? Most common bacteria causing osteomyelitis in neonates? In sickle cell patients? In trauma?

A

Staph aureus;
E. Coli and group B strep;
Salmonella;
mixed bacterial infections

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52
Q

What are three complications with osteomyelitis that tend to occur commonly in children?

A 
bone abscess
periosteal lift (infected fluid elevates the periosteum)
extension into the joint (infection extending into joint cavity)
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53
Q

Common location for osteomyelitis in children? In adults?

A

metaphysis;

anywhere

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54
Q

What happens to the residual necrotic bone, or sequestrum, in osteomyelitis?

A

it may be resorbed by osteoclasts, or larger areas of necrosis may be surrounded by a rim of reactive new bone, or involucrum

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55
Q

well-defined rim of sclerotic bone surrounds a residual abscess

A

Brodie’s abscess

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56
Q

What can be helpful in localizing osteomyelitic lesions?

A

radionuclide scans

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57
Q

What is the most common method of spread for tuberculous osteomyelitis? What bones are usually involved?

A

hematogenous; favors long bones and vertebrae

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58
Q

In cases of tuberculoid osteomyelitis, the bacillus (TB) needs oxygen, infection usually starts at (blank), then spreads into bone

A

synovium

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59
Q

In tuberculoid osteomyelitis, extension of infection to adjacent soft tissues is common in spinal lesions. Give an example.

A

Cold abscess of psoas muscle

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60
Q

Most common malignant tumor of bone

A

osteogenic sarcoma

61
Q

4 bone forming tumors

A

osteomas
osteoid osteoma
osteoblastoma
osteogenic sarcoma

62
Q

These bone tumors are round to oval - they project from the subperiosteal or endosteal surfaces of the cortex; they are BENIGN but may impinge upon the brain, eye, or oral cavity; they DO NOT undergo malignant transformation

A

osteomas

63
Q

Are osteomas benign or malignant?

A

benign!!!!

**but they can impinge upon the brain, eye, oral cavity, etc

64
Q

Multiple osteomas may be associated with (blank)

A

Gardner’s syndrome (familial polyposis)

65
Q

What’s the difference b/w an osteoid osteoma and an osteoblastoma?

A

they differ in size, location, and symptoms:

osteoid osteoma: less than 2cm
osteoblastoma: greater than 2cm

osteoid osteoma: peripheral skeleton
osteoblastoma: spine

osteoid osteoma: relieved by aspirin
osteoblastoma: not relieved by aspirin

66
Q

If osteoid osteomas and osteoblastomas are not completely excised, what will happen?

A

they will recur if not completely excised

67
Q

This type of bone tumor is less than 2cm; occurs in peripheral skeleton, femur or tibia; it is painful, usually at night due to the production of PGE2; relieved by ASPIRIN

A

osteoid osteoma

68
Q

This type of bone tumor is >2cm; involves spine more frequently; pain is usually a dull ache and is NOT relieved by aspirin

A

osteoblastoma

69
Q

Most common malignant tumor of bone; malignant mesenchymal cells which form bone matrix

A

osteogenic sarcoma (osteosarcoma)

70
Q

How does a primary osteosarcoma differ from a secondary osteosarcoma?

A

primary: arises de novo
secondary: arises in conjunction with Paget’s disease or radiation

71
Q

How old are patients who get osteosarcomas?

A

most are <20yo

72
Q

Where do most osteosarcomas occur?

A

most occur in metaphysis of long bones (60% in the knee)

73
Q

Osteosarcomas are aggressive lesions. Where are they likely to metastasize?

A

to the lung

74
Q

3 types of cartilaginous tumors?

A
  1. osteochondroma (osteocartilaginous exostoses)
  2. enchondroma
  3. chondrosarcoma
75
Q

Most common BENIGN tumors of the bones; tumor composed of mature bone with a cartilaginous cap (cauliflower look)

A

osteochondroma (osteocartilaginous exostosis)

76
Q

Most osteochondromas arise from (blank)

A

metaphysis near growth plate of long bones (leg, pelvis, shoulder blade)

77
Q

pedunculated on a stalk often taking the shape of a cauliflower

A

osteochondroma (osteocartilaginous exostosis)

78
Q

BENIGN lesions formed by mature hyaline cartilage; most occur in short tubular bones of hands and feet

A

enchondroma

79
Q

In this disease, you get multiple enchondromas, usu on one side of the body

A

Ollier’s disease

80
Q

In this disease, you get multiple encondromas associated w hemangiomas of soft tissue

A

Maffucci’s syndrome

81
Q

(blank) develop in 1/3 of patients with multiple encondromas

A

chondrosarcomas

82
Q

Where are enchondromas most likely to occur?

A

in small bones of hands and feet

83
Q

2nd most common matrix forming tumor of bone; often associated with pre-existing enchondroma

A

chondrosarcoma

84
Q

Where do chondrosarcomas begin?

A

in the medullary space, expand and spread to the surface

85
Q

Where do chondrosarcomas occur?

A

in the central skeleton (pelvis, shoulder, ribs)

**clear cell variant in epiphyses of long bones

86
Q

Neoplastic mononuclear cells; abundant reactive osteoclast-like multinucleated cells

A

giant cell tumor of bone

87
Q

Where do giant cell tumors usually occur?

A

epiphyses of long bones

88
Q

What do giant cell tumors look like on radiology?

A

soap bubbles

89
Q

2nd most common childhood malignancy of bone; translocation at t(11;22); affects femur, tibia, and pelvis; pain and inflammation; sheets of small cells with uniform nuclei - small blue cell tumors

A

Ewing’s sarcoma

90
Q

Neoplasm of plasma cells with clock-face chromatin; produces monoclonal IgG spike

A

multiple myeloma

91
Q

Benign, tumor-like condition with possible fractures

Normal trabecular bone is replaced by proliferating fibrous tissue and disorderly islands of deformed bone

A

Fibrous dysplasia

92
Q

What is the difference b/w the mono-ostotic and poly-ostotic forms of fibrous dysplasia?

A

mono-ostotic: starts during adolescence, stops when bone growth stops, seen in ribs, JAW, femur, tibia

polyostotic: can cause problems in adulthood, craniofacial involvement common

93
Q

Unilateral bone lesions, with café-au-lait spots on same side
Precocious puberty
Also associated with hyperthyroidism, Cushing’s disease

A

Polyostotic fibrous dysplasia with endocrine abnormalities

94
Q

Most common disorder of joints

A

osteoarthritis

95
Q

Is osteoarthritis really inflammation? What is happening?

A

no; degeneration of articular cartilage

96
Q

Primary vs secondary osteoarthritis?

A

primary: arises w/o predisposing factors
secondary: arises in joint that has been previously deformed

97
Q

2 most important factors in osteoarthritis?

A
  1. aging

2. mechanical wear and tear

98
Q

Where is osteoarthritis most likely to occur?

A

in weight-bearing joints

99
Q

subchondral bone becomes thickened, and gives appearance of ivory

A

eburnation

100
Q

In osteoarthritis, osteophytes form at the distal IP joints (DIP). These are called (blank)

A

Heberden’s nodes

101
Q

2 clinical signs to be aware of in osteoarthritis

A

subchondral bone cysts

osteophytes

102
Q

Systemic chronic inflammatory disease affecting many organ systems (joints, skin, blood vessels, muscles, lungs)

A

rheumatoid arthritis

103
Q

Does rheumatoid arthritis affect males or females more? When does it usu occur?

A

F>M; onset in 4-5th decade

104
Q

How does the joint involvement in RA differ from osteoarthritis?

A

in osteoarthritis - DIP

in RA - PIP and MP

105
Q

Symptoms of RA?

A

morning stiffness, which gets better w application of heat and movement

joint swelling, redness, warmth

106
Q

What type of RA is this:

Proliferation and hypertrophy of synovial lining cells
+/- villous projections
Infiltration of lymphocytes, macrophages, plasma cells (in synovium)(may also have some neutrophils in the synovial fluid )
+/- lymphoid follicles
Neovascularization

A

non-suppurative proliferative synovitis

107
Q

In RA, (blank) can form along extensor surfaces of the forearm and other points of pressure

A

subcutaneous nodules

108
Q

What are the most likely organisms to cause infectious arthritis?

A

staph
strep
H. influenzae
gram-negative rods

**salmonella in sickle cell patients

109
Q

Predisposing factors for infectious arthritis?

A

immunodeficiency
joint trauma
IV drug use

110
Q

This spirochete can cause damage to joints, esp large joints of the knee, shoulder, elbow. Early disease resembles RA but can have extensive erosion of large joint cartilage

A

Borrelia burgdorferi

111
Q

Commonly called “wear and tear” joint degeneration; characterized by the breakdown of the joint’s cartilage

A

osteoarthritis

112
Q

Characterized by inflammation of the lining of the joints; often leads to join damage, resulting in chronic pain, loss of function and disability

A

RA

113
Q

Uric acid accumulates in tissues as monosodium urate crystals (needle-shaped and birefingent)

A

gout

114
Q

What kind of arthritis does gout cause? Like where does it occur?

A

acute arthritis in the 1st metatarsal

115
Q

What causes primary gout?

Secondary gout?

A

primary is caused by overproduction of uric acid for unknown reasons;

secondary is due to any large increase in urate production (like treatment for lymphoma or leukemia), decreased excretion of uric acid (like chronic renal insufficiency), or Lesch-Nyhan Syndrome (over production/under excretion of uric acid w lack of HGPRT)

116
Q

How do urate crystals ultimately lead to arthritis?

A

they activate complement, generate c3a and c5a, draw in neutrophils and macrophages to the joint and synovium

117
Q

Which body part is usu affected first in gout?

A

big toe

118
Q

If you see sharp birefringent crystals in the synovial fluid, think…

A

gout

119
Q

Deposition of Calcium pyrophosphate crystals
Derived from nucleosides in chondrocytes
Commonly found in knees after trauma/surgery
May be associated with other systemic diseases, such as hemochromatosis

A

pseudogout

120
Q

What do the pyrophosphate crystals look like in pseudogout?

A

coffin-lid shaped

121
Q

This occurs if muscle is deprived of normal innervation, which leads to progressive atrophy and muscle weakness; presents as floppy baby syndrome in infants

A

neurogenic atrophy

122
Q

What kind of atrophy can be seen in cases of neurogenic atrophy?

A

small groups of atrophy

**peripheral nerves supply groups of muscle fibers (motor unit), so damage to the nerve leads to atrophy of the whole motor unit

123
Q

This is the most common type of muscle atrophy

A

type II (fast-twitch) atrophy

124
Q

What can cause type II (fast-twitch) muscle fiber atrophy?

A

disuse
long-term glucocorticoid use
hypercortisol state

125
Q

Antibodies to the acetylcholine receptor (AChR) (~90%)
Antibodies either injure the receptor, or inhibit binding of the neurotransmitter acetylcholine
Titer of antibody does NOT correlate with severity of symptoms

A

Myasthenia Gravis

126
Q

Symptoms of myasthenia gravis?

A

ptosis and diplopia (double vision)
weak facial and neck muscles
respiratory involvement w potential respiratory failure

127
Q

What is one option for the treatment of myasthenia gravis?

A

anti-AChE agents

**inhibit AChE so that ACh cannot be degraded

128
Q

X-linked defect; ABSENCE of dystrophin; causes muscle weakness, especially in proximal muscles

A

Duchenne muscular dystrophy

129
Q

What would you see histologically in DMD?

A

increased CT in muscle

variation in muscle fiber size, some hypertrophy, some atrophy

130
Q

X-linked defect; ABNORMAL dystrophin; similar to DMD in presentation and morphology, but less severe

A

Becker Muscular dystrophy

131
Q

Most common soft tissue sarcoma in kids

A

rhabdomyosarcoma

132
Q

Most common variant of rhabdomyosarcoma

A

embryonal - occurs in head, neck, GU tract, retroperitoneum

133
Q

What do rhabdomycosarcomas look like morphologically?

A

primitive small round blue cells

134
Q

In the GU tract, rhabdomyosarcomas look like gelatinous, grape-like structures and are called (blank)

A

sarcoma botryoides

135
Q

What can cause soft tissue tumors?

A

radiation therapy
trauma
exposure to organic chemicals
AIDS

136
Q

The most common soft tissue tumor; usu benign, slow growing, painless

A

lipoma

137
Q

A variant of lipoma that may present w local pain on the volar surface of the forearm

A

angiolipoma

138
Q

This type of soft tissue infection tends to appear in the 5th and 6th decade of life; usu in deep tissues of proximal extremities; lower extremities and abdomen are common sites

A

liposarcoma

139
Q

Most common in upper extremities and trunk

History of trauma (10 - 15%)
Rapid growth

NOT a true neoplasm, is an over-reaction of fibroblasts
May be confused with sarcoma due to cellularity

A

nodular fasciitis

140
Q

A group of fibroblastic proliferations
Grow in infiltrative fashion
Recur after excision

NOT true neoplasms

Two well-known Superficial Types:
Dupuytren’s contracture (palmar)
Peyronie’s Disease (penile)

A

fibromatosis

141
Q

Give an example of a deep fibromatosis

A

Desmoid tumor

142
Q

This is a superficial fibromatosis that occurs on the hand

A

Dupuytren’s contracture

143
Q

This type of soft tissue neoplasm favors deep tissue of the thigh, knee, and trunk; mets usu to lungs; comprised of fibroblasts and arises from fibrous tissues of the bone

A

fibrosarcoma

144
Q

Who gets fibrosarcomas?

A

males ages 30-40

145
Q

T/F: If infants get fibrosarcomas, they usu are congenital and so they present in the first two years of life

A

True

146
Q

What type of pattern is seen in fibrosarcoma?

A

storiform/herringbone pattern

147
Q

This is a malignant tumor; occurs in the 5th to 7th decade of life; occurs in lower limbs and retroperitoneal areas; most common type of post-irradiation tumor**

A

malignant fibrous histiocytoma or pleomorphic sarcoma

148
Q

Accounts for 10% of all soft tissue sarcomas; arises from mesenchymal cells around joint cavities; most develop in the vicinity of large joints of lower extremities, esp knee

A

synovial sarcoma

149
Q

What is unique histologically about synovial sarcomas?

A

contain mast cells

Block 7 Week 5 (8 decks)

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