Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MSK Week 6 > 2.6.4. PATH LAB - Bone Pathology I (Part 2 of 3) > Flashcards

2.6.4. PATH LAB - Bone Pathology I (Part 2 of 3) Flashcards

1
Q

Type of Fracture: Simple

A

Simple - overlying skin is intact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Type of Fracture: Compound

A

Compound - bone breaks the skin surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Type of Fracture: Comminuted

A

Comminuted - bone is fragmented

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Type of Fracture: Displaced

A

Displaced - ends of the bone at the fracture site are not aligned

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Type of Fracture: Stress

A

Stress - slowly developing facture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Type of Fracture: Greenstick

A

Greenstick - extending only partially through the bone (common in infants)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Type of Fracture: Pathologic

A

Pathologic - bone weakened by an underlying disease process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens immediately after fracture?

A

Immediately after fracture, rupture of blood vessels results in a hematoma, which fills the fracture gap

Clot forms (fibrin mesh)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

After a fracture, degranulated platelets and migrating inflammatory cells release what?

A

Degranulated platelets and migrating inflammatory cells release PDGF, TGF-β, FGF and other factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Callus formation following a fracture

A

At the end of one week, a soft tissue callus is formed

After ~2 weeks, the soft tissue callus is transformed into a bony callus.

As the callus matures and is subjected to weight-bearing forces, the portions that are not physically stressed are resorbed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When is a fracture technically healed?

A

The healing process is complete with restoration of the medullary cavity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is osteonecrosis?

A

AKA Avascular Necrosis

Infarction of bone and marrow can occur in the medullary cavity or involve both the medulla and cortex

The cortex is not usually affected because of its collateral blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do most cases of osteonecrosis stem from?

A

Most cases stem from fractures or corticosteroid administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Presentation of the infarcts of osteonecrosis:

A

Typically, subchondral infarcts cause pain that initially only occurs with activity, but then becomes constant

Medullary infarcts are usually small and clinically silent except when they occur in the setting of Gaucher’s disease, dysbarism (the “bends”), or sickle cell anemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is/causes osteomyelitis?

A

Osteomyelitis is inflammation of bone and marrow, virtually always secondary to infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes Pyogenic Osteomyelitis? Who is usually the culprit?

A

Almost always caused by bacterial infections, 80-90% are caused by S. aureus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What specific abscess is associated with osteomyelitis?

A

Brodie abscess is a small intraosseous abscess that frequently involves the cortex and is walled off by reactive bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Sclerosing osteomyelitis of Garre?

A

Sclerosing osteomyelitis of Garre typically develops in the jaw and is associated with extensive new bone formation that obscures much of the underlying osseous structure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clinical course of osteomyelitis?

A

Sometimes manifests as an acute systemic illness with malaise, fever, chills, leukocytosis, and marked-to-intense throbbing pain over the affected region.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is mycobacterial osteomyelitis and how does it present?

A

Mycobacterial osteomyelitis tends to be more destructive and resistant to control than pyogenic osteomyelitis.

Present with localized pain, low-grade fevers, chills, and weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Though syphilis can affect bone, bone involvement remains infrequent because the disease is usually diagnosed and treated before this complication develops.

What about congenital syphillis and what is its characteristic finding?

A

In congenital syphilis, bone lesions appear around the 5th month of gestation and are fully developed at birth.

Characteristic finding is “syphilitic saber shin”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Morphology of syphillitic bone?

A

Syphilitic bone infection is characterized by edematous granulation tissue containing numerous plasma cells and necrotic bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

When possible, bone tumors are classified how?

A

When possible, bone tumors are classified according to the normal cell or matrix they produce.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are, in general, Osteoid Osteoma and Osteoblastomas?

A

Benign bone-producing tumors that have identical histologic features but differ in size, sites of origin, and symptoms.

Malignant transformation is rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How big are osteoid osteomas, and where do they normally present?

A

Osteoid osteomas are less than 2cm in diameter and usually occur in young men in their teens and 20s.

Usually occur in cortex of bones in the appendicular skeleton (~50% in femur/tibia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the clinical presentation of osteoid osteoma? How is it usually treated?

A

Have severe nocturnal pain that is relieved by aspirin

Usually treated by radiofrequency ablation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How big is osteoblastoma, where does it normally occur?

A

Osteoblastomas are larger than 2cm in diameter and usually involve the posterior spine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

True/False: Osteoblastoma is manageable with pain meds like Aspirin

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is an osteosarcoma?

A

Malignant tumor in which the cancerous cells produce osteoid matrix or mineralized bone.

Most common primary malignant tumor of bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Any bone can be involved, but tumors usually arise typically where?

A

Any bone can be involved, but tumors usually arise in the metaphyseal region of the long bones of the extremities, and ~50% occur in the distal femur or proximal tibia (knee joint)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Pathology of osteocarcoma and what do we see in radiology?

A

The tumor frequently breaks through the cortex and lifts the periosteum, resulting in reactive periosteal bone formation. The triangular shadow between the cortex and the raised ends of periosteum, known radiographically as Codman’s triangle, is indicative of an aggressive tumor - and is characteristic - but not diagnostic - of osteosarcoma; also has “sunburst” appearance on XRAY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

In osteo sarcoma, ~70% have acquired genetic abnormalities, including mutations to the following:

A

RB - negative regulator of the cell cycle

TP53 - gene product promotes DNA repair and apoptosis

INK4a - encodes two tumor suppressors (p16 and p14)

MDM2 and CDK4 - cell cycle regulators that inhibit p53 and RB function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is achondroblastic osteosarcoma

A

When malignant cartilage is abundant, the tumor is called chondroblastic osteosarcoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What accounts for the majority of primary bone tumors?

A

Cartilage tumors account for the majority of primary bone tumors (both benign and malignant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What cartilage types tend to be related to cartilage-forming tumors?

A

Characterized by the formation of hyaline or myxoid cartilage; fibrocartilage and elastic cartilage are rare components.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is Osteochondroma (aka exostosis)?

A

Benign cartilage-capped tumor that is attached to the underlying skeleton by a bony stalk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Where is Osteochondroma (aka exostosis)?

A

Only develop in bones of endochondral origin and arise from the metaphysis near the growth plate of long tubular bones

38
Q

Genetic causes of Osteochondroma (aka exostosis)?

A

Hereditary exostoses are associated with germline loss-of-function mutations in either EXT1 or EXT2 gene. These genes encode enzymes that synthesize heparan sulfate glycosaminoglycans.

39
Q

Morphology of Osteochondroma (aka exostosis)?

A

1-20 cm in size.

The cap is composed of benign hyaline cartilage and is covered peripherally by perichondrium

40
Q

Clinical treatment/progression of Osteochondroma (aka exostosis)?

A

Usually stop growing at the time of growth plate closure.
Symptomatic tumors are cured by excision.
Osteochondromas rarely progress to chondrosarcoma, but it is possible.

41
Q

What are chondromas?

A

Benign Tumors of hyaline cartilage

42
Q

most common of intraosseous cartilage tumor

A

Enchondromas

43
Q

Morphology of Enchondromas

A

smaller than 3 cm, gray-blue, translucent; well-circumscribed nodules containing cytomorphologically benign chondrocytes; periphery my undergo enchondral ossification and center can calcify and infarct

44
Q

Diseases related to enchondromas?

A

Maffucci syndrome and Ollier disease are NON HEREDITARY disorders characterized by multiple enchondromas

45
Q

Where do we see Juxtacortical chondromas?

A

Juxtacortical chondromas: arise on the surface of bones

46
Q

Genetic causes of chondromas?

A

Heterozygous mutations in the IDH1 and IDH2 genes of chondrocytes

both cause the encoded proteins to acquire new enzymatic activity leading to the synthesis of 2-hydroxyglutarate (oncometabolite= interferes with regulation of DNA methylation); may diffuse into nearby cells and lead to epigenetic changes

47
Q

What do we worry about with patients that have Maffucci?

A

patients with Maffucci are at risk of developing other malignancies (e.g. ovarian carcinomas and brain gliomas)

48
Q

What is a chondrosarcoma?

A

Chondrosarcoma- malignant tumors that produce cartilage

49
Q

Genetic causes of chondrosarcomas?

A

Multiple chondrosarcoma: mutations in EXT genes

chondrosarcomatosis-related & sporadochondrosarcomas: IDH1 & 2 mutations

Sporadic: silencing of CDKN2A common

50
Q

Morphology of chondrosarcoma?

A

Conventional: large bulky tumors made up of nodules of glistening gray-white, translucent cartilage; matrix is often gelatinous or myxoid

spotty calcifications present
central necrosis that creates cystic spaces

spreads to surrounding muscle or fat

51
Q

Histology of chondrosarcoma

A

histologically: cartilage infiltrates the marrow space and surrounds pre-existing bony trabeculae

52
Q

What is a dedifferentiated chondrosarcoma?

A

low grade chondrosarcoma with a 2nd, high-grade component that does not produce cartilage

53
Q

What is a clear cell chondrosarcoma?

A

sheets of large, malignant chondrocytes with abundant clear cytoplasm, numerous osteoclast-type giant cells, and intralesional reactive bone formation (confused with osteosarcoma)

54
Q

What is a mesenchymal chondrosarcoma?

A

islands of well-differentiated hyaline cartilage surrounded by sheets of small round cells; mimics Ewing Sarcoma

55
Q

How do chondrosarcomas present?

Also compare Grade 1 to Grade 3.

A

Present as painful, progressively enlarging masses

Grade 1 rarely metastasize; 70% Grade 3 spread hematogenously, especially to lungs

56
Q

What are Ewing Sarcoma Family Tumors?

A

Ewing Sarcoma Family Tumors: malignant bone tumors characterized by primitive round cells without obvious differentiation

57
Q

Genetic cause of Ewing Sarcoma?

A

t(11;22)(q24;q12): generating in-frame fusion of the EWS gene on chromosome 22 to the FLI1 gene

58
Q

Where does Ewing Sarcoma arise?

A

arises in medullary cavity: usually invades cortex, periosteum, and soft tissue

59
Q

Morphology clinically of Ewing sarcoma?

A

soft, tan-white tumor frequently containing areas of hemorrhage and necrosis

60
Q

Histology of Ewing Sarcoma?

A

sheets of uniform small, round cells that are slightly larger and more cohesive than lymphocytes; scant cytoplasm, may appear clear because of abundant cytoplasm
dense cellularity, but relatively few mitotic figures

61
Q

Radiology of Ewing Sarcoma?

A

Plain radiographs show destructive lytic tumor with permeative margins that extends into the surrounding soft tissues; characteristic periosteal reaction produces layers of reactive bone deposited in an onion-skin fashion

62
Q

Treatment for Ewing Sarcoma?

A

Aggressive malignancies; treat with chemotherapy

Chemotherapy-induced necrosis is an important prognostic finding

63
Q

What causes Giant Cell Tumors?

A

neoplastic cells express high levels of RANKL (promotes proliferation of osteoclast precursors and diff. into mature osteoclasts via RANK expressed by these cells) → localized but highly destructive resorption of bone matrix by reactive osteoclasts

64
Q

Where do Giant Cell tumors arise?

A

Arise in epiphysis (may extend into metaphysis); knee (distal femur/proximal tibia) common, but can happen in any bone

65
Q

What is wrong with remodeling in Giant Cell Tumors?

A

feedback btwn osteoblasts and osteoclasts that regulates this process during normal bone remodeling is absent

66
Q

Clinical morphology of Giant Cell Tumors

A

destroy overlying cortex → bulging soft tissue mass delineated by thin shell of reactive bone (red-brown masses freq. undergo cystic degeneration)

67
Q

Histology for Giant Cell Tumors?

A

histology dominated by multinucleated osteoclast-type giant cells, gives rise to synonym “osteoclastoma” and sheets of uniform, oval mononuclear cells (both cell types have ovoid nuclei with prominent nucleoli)

68
Q

Do Giant cells synthesize bone or cartilage?

A

Nope

69
Q

Radiology of giant cell

A

“Soap bubble” on x-ray

70
Q

What can Giant Cell Tumors look like on exam? How can we treat it?

A

location near joints can cause arthritis-like symptoms and pathologic fractures

treated with curettage (removal with scraping or scooping using a curette)

denosumab: RANKL inhibitor

71
Q

Genetic cause of Aneurysmal bone cyst

A

rearrangements of chromosome 17p13 resulting in fusion of USP6 to the promoters of genes that are highly expressed in osteoblasts (overexpression of USP6)

72
Q

What is biochemically wrong about aneurysmal bone cysts?

A

overexpression of USP6, encodes an ubiquitin specific protease that regulates the activity of transcription factor NFkappaB

73
Q

Morphology of aneurysmal bone cyst

A

multiloculated blood-filled cystic spaces, separated by tan-white septa (composed of plump uniform fibroblasts. multinucleated osteoclast-like giant cells, and reactive woven bone)

74
Q

Morphology of aneurysmal bone cyst

A

multiloculated blood-filled cystic spaces, separated by tan-white septa (composed of plump uniform fibroblasts. multinucleated osteoclast-like giant cells, and reactive woven bone)

bone lined by osteoblasts; deposition follows the contours of the fibrous septa

75
Q

Treatment for aneurysmal bone cysts

A

treatment=surgery

76
Q

What are our two metaphyseal fibrous defects?

A

Fibrous Cortical Defect

Nonossifying Fibroma

77
Q

How big are fibrous cortical defects?

A

about 0.5cm in diamter

78
Q

How big are nonossifying fibromas?

A

5-6cm

79
Q

Morphology typical of both metaphyseal fibrous defects

A

gray-yellow brown cellular lesions containing fibroblasts and macrophages

fibroblasts arranged storiform (pin-wheel) pattern

macrophages may take the form of clustered cells with foamy cytoplasm or multinucleated giant cells

hemosiderin commonly present

80
Q

Clinical presentation of metaphyseal fibrous defects?

A

asymptomatic, are detected incidentally

81
Q

Genetic mutation for fibrous dysplasia and what is fibrous dysplasia?

A

somatic gain-of-function mutation during development in GNAS1

produce constituently active Gs-protein, promoting cellular proliferation

This is just a benign tumor

82
Q

Morphologies of fibrous dysplasias on radiology

A

Radiologically: ground glass appearance with well-defined margination

well-circumscribed, intramedullary and vary greatly in size

large; expand and distort bone

83
Q

What type of macrophages are seen with fibrous dysplasias?

A

foamy macrophages

84
Q

Visual of fibrous dyslasia

A

tan-white, gritty and composed of curvilinear trabeculae (look like Chinese characters)

85
Q

Monostotic?

A

One bone

86
Q

Polyostotic?

A

Multiple bones

87
Q

What is Mazabraud syndrome?

A

usually polyostotic fib. dys. and soft tissue myxomas

88
Q

What is McCune-Albright Syndrome?

A

polyostotic disease, associated with cafe-au-lait spots and endocrine abnormalities (precocious puberty → earlier than normal)

89
Q

Where do most cancers that metastasize to skeleton come from?

A

prostate, breast, kidney, and lung

90
Q

What do tumor cells do when they reach native bone cells?

A

secrete substances like prostaglandins, cytokines, and PTHrP that upregulate RANKL on osteoblasts and stromal cells → stimulating osteoclast activity

91
Q

What matrix bound factors are released that stimulate tumor growth?

A

Tumor growth also supported by release of matrix-bound growth factors (TGF-beta, IGF-1, and FGF) as bone is resorbed

MSK Week 6 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions