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PATH STORE > MSK Pathology > Flashcards

MSK Pathology Flashcards

1
Q

Achondroplasia is a defect in

A

cartilage = failure of long bone growth

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2
Q

Specific achondroplasia mutation

A

AD, Activating mutation in FGF23 –> FGF23 inhibits chondrocytes

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3
Q

Achondroplasia presentation

A

Short arms and legs (endochondral ossificaiton), normal torso and head (intramembranous ossification is unaffected)

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4
Q

Osteogenesis imperfecta defect

A

AD mutation resulting in defective Type I collagen synthesis

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5
Q

The classic triad of OI- type 3

A

Multiple Fractures in strange places Blue sclera Hearing loss (inner ear bones Fx)

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6
Q

Examples of type 1 collagen

A

tendons, ligaments, the endomysium of myofibrils, interstitial stroma, the organic part of the bone, the dermis, the dentin, and organ capsules.

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7
Q

Labs for Osteopetrosis

A

Pancytopenia

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8
Q

2 Neuro complications of osteopetrosis

A

Vision/hearing impariment due to compression of nerves by foramina

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9
Q

Pathogenesis of osteopetrosis. Mechanism?

A

Lack of osteoclast function

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10
Q

Rickets/Osteomalacia defect

A

Excessive unmineralized osteoid; bad quality bone

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11
Q

MCC of Rickets/OM

A

Vitamin D deficiency

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12
Q

Osteomalacia lab values (Ca, Phos, PTH, Alk Phos)

A

Low Ca and Phos (low vitD) High PTH High Alk Phos (osteoblasts are driven by PTH. They are still working fine)

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13
Q

Osteoporosis is a reduction in

A

Trabecular bone mass (endosteal and periosteal resorption)

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14
Q

3 major Risk factors for osteoporosis

A

weight bearing exercise, menopause, Age

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15
Q

Effect of estrogen on bone development

A

Estrogen inhibits RANK, Loss of estrogen after menopause = more active osteoclasts

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16
Q

2 fracture-related complications of osteoporosis

A

Vertebral compression Fx Hip Fx

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17
Q

besides vertebral fractures which vertebral complications do osteoporosis pts have

A

Kyphosis and decreased height

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18
Q

Osteoporosis labs (Ca, Phos, PTH, alk phos)

A

All normal! Normal labs in the face of bone pain distinguishes this from osteomalacia

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19
Q

Paget disease of bone underlying problem

A

Imbalance b/w osteoblasts and osteoclasts (too much), viral infection, genetics

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20
Q

paget disease progression

A

Overactive osteoclasts –> osteoclasts start burning out –> osteoblasts activate –> lay down poor structure bone

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21
Q

A 58-year-old male patient reported to the dental hospital with a complaint of difficulty in vision.

History revealed that there were swellings in the skull bones, which started 6 years back. All swellings gradually increased in size. X-Ray skull attached. Diagnosis?

A

Pagets

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22
Q

4 classic SSx of paget’s disease of bone

A

Bone Pain Hearing loss/ Vision changes Increasing hat size Coarsening of facial features

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23
Q

Characteristic lab abnormality in paget’s disease

A

Isolated elevated ALk Phos with everything else normal

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24
Q

histology of paget’s

A

mosaic pattern of lamellar bone

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25
Q

2 major complications of paget disease

A

High output heart failure, Osteosarcoma

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26
Q

location of hematogenous osteomyelitis in kids (< 2 years) vs adults

A

Kids = epiphysis, Adults = metaphysis

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27
Q

MCC (most common cause) of osteomyelitis overall

A

S. aureus

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28
Q

MCC of osteomyelitis in diabetic or IV drug user

A

Psudomonas

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29
Q

MCC of osteomyelitis in sickel cell

A

salmonella typhi

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30
Q

Xray appearance of osteomyelitis

A

Lytic bone lesion surrounded by sclerosis (lytic lesion = sequstrum) (sclerosis = involurcrum)

The diagnosis is strongly suggested by the characteristic radiographic findings of a lytic focus of bone destruction surrounded by a zone of sclerosis.

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31
Q

Osteoma association

A

Gardner syndrome (FAP, fibromatosis, osteomas)

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32
Q

Osteoid osteoma is a tumor of

A

Osteoblasts

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33
Q

Gross appearance of osteoid osteoma

A

Tumor of osteoblasts surrounded by a ring of reactive bone

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34
Q

Osteoid osteoma imaging

A

Bony mass with a radiolucent core (osteioid from the osteoblasts)

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35
Q

Classic location of osteoid osteoma

A

Cortex of long bones

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36
Q

The classic presentation of osteoid osteoma

A

Humerus or femur pain that resolves with aspirin

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37
Q

Osteoblastoma location

A

Everything is the same as an ostoid osteoma, but it is located in the vertebra

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38
Q

Osteoblastoma presentation

A

Back pain that does not respond to aspirin (r/o osteoid osteoma)

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39
Q

diagnosis and location of origin

A

Osteochondroma arises from the lateral projection of the epiphyseal plate

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40
Q

Structure of osteochondroma

A

Bone with an overlying cartilage cap

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41
Q

Giant cell tumor location

A

Epiphysis of long bones. ONLY TUMOR IN THE EPIPHYSIS

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42
Q

Giant cell tumor is a proliferation of

A

Stromal cells

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43
Q

Xray of Giant cell tumor

A

“bubble” appearance of the epiphysis

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44
Q

osteosarcoma AKA

A

osteogenic sarcoma

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45
Q

Osteogenic sarcoma is a proliferation of

A

osteoblasts

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46
Q

primary osteosarcoma location

A

METAPHYSIS of long bones (unlike giant cell tumors)

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47
Q

3 major risk factors for sec. osteosarcoma

A

Paget Disease Radiation exposure LiFraumeni Sydnrome Gardner

48
Q

diagnosis?

A

Xray of osteosarcoma

49
Q

Ewing sarcoma is a proliferation of

A

neuroectodermal cells (poorly differentiated)

50
Q

Ewing sarcoma location and population

A

Diaphysis of long bones in kids

51
Q

Ewing sarcoma translocation

A

11:22

52
Q

Xray of Ewing sarcoma

A

Onion skinning

53
Q

mechanism of onion skinning

A

As tumor grows laterally, the periostium will continue forming new layers

54
Q

chondrosarcoma location

A

pelvis or central skeleton

55
Q

Osteoblastic bone metastasis

A

Prostate Cancer

56
Q

Ewing sarcoma histology

A

malignant small blue cells

57
Q

Articular cartilage is composed of

A

Type II collagen (hyaline)

58
Q

The classic pattern of OA involvement

A

ASYMMETRIC involvement of Leg and hip joints + DIPs

59
Q

Classic OA presentation

A

Morning stiffness that worsens with activity and improves with an NSAID

60
Q

3 Xray findings of OA

A

Osteophytes UNILATERAL Joint space narrowing Subchondral sclerosis

61
Q

RA HLA association

A

HLA DR4

62
Q

Histology of RA

A

Pannus formation –> inflammed granulation tissue

63
Q

Pathogenesis of RA, 3 steps

A

autoimmune synovial Inflammation –> pannus formation –> bony ankylosis (cartilage and bone damage)

64
Q

Rheumatoid factor description

A

IgM against IgG

65
Q

Most specific serum marker for RA

A

anti CCP (cyclic citrullinated peptide)

66
Q

A pattern of joint involvement in RA

A

Symmetric involvement of PIPs, Wrists, elbows and knees NO DIP!

67
Q

3 Extraarticular manifestations of RA

A

Rheumatoid Nodules Amyloidosis and synovial cysts

68
Q

Rheumatoid nodule histology

A

Fibrinoid necrosis surrounded by palisading histocytes

69
Q

cell type responsible for swan neck deformity

A

Myofibroblasts w/in the granulation tissue of the pannus and ossification

70
Q

Xray of RA

A

BILATERAL joint space narrowing, and flexion-hyperextension abnormality

71
Q

2 complications of RA

A

Anemia of chronic Dz (elevated hepcidin) Secondary amyloidosis (constant inflammation)

72
Q

Type of pain in all seronegative spondyloarthropathies

A

Similar to RA. Worse in morning, improves with use

73
Q

4 subtypes of seronegative spondyloarthropathies and their pattern of joint involvement (Symmetric vs Asymmetric)

HLA association :

A

PAIR ASAS Psoriatic (Asymmetric) Ankylosing spondylitis (Symmetric) Inflammatory Bowel Dz (Asymmetric) Reactive Arthritis (Symmetric)

HLA B27

74
Q

Psoriatic arthritis x-ray finding

Other findings:

A

Pencil in cup deformity of DIP

Nail deformities

75
Q

Ankylosing spondylitis joints involved

A

Spine and bilateral sacroiliac- may lead to vertebral fusion

76
Q

Ank Spond Extraarticular manifestation

A

Uveitis

77
Q

Reactive Arthritis (Reiter) triad

A

Conjunctivitis Urethritis Arthritis “Cant pee, cant see, cant climb a tree”

78
Q

CLassic reactive arthritis case

A

2 weeks after GI or STD, pt presents with knee or low back pain

79
Q

Joint fluid in reactive arthritis

A

Negative for infection

80
Q

3 MCC septic arthritis

A

Staph Strep Gonorrhea

81
Q

Atypical Triad of gonococcal arthritis

A

Polyarthralgia Tenosynoviits Dermatitis (pustules)

82
Q

Joint fluid difference in Acute Gout vs Septic arthritis

A

Septic = purulent w/ WBCs but no crystals

Gout= WBCs + crystals

83
Q

3 common causes of secondary gout

A

Leukemia/Myeloproliferative Disorders (increased cell turn over) Lesch Nyhan Renal insufficiency

84
Q

Mechanism of Lesch Nyhan causing gout

A

HGPRT deficiency = no salvage pathway of purines = increased Purine metabolism into Uric Acid

85
Q

What is the actual causative agent in Gout

A

Monosodium Urate Crystals

86
Q

Major cellular mediator in gout flares

A

Neutrophils

87
Q

histology/gross of tophi

A

Aggregates of crystals with fibrosis and giant cell reactions Essentially it is chronic granulomatous inflammation around the crystals (i.e. giant cells and fibrosis)

88
Q

where are tophi located

A

soft tissues and joints

89
Q

Gout synovial fluid analysis

A

Needle-shaped crystals with negative birefringence.

The crystals that turn yellow are the ones that are parallel to the light The ones that are blue are perpendicular

90
Q

Crystals in pseudogout

A

Calcium pyrophosphate, rhomboid-shaped, blue

91
Q

Fibromyalgia SSx

A

Widespread (not just proximal) PAIN w/o weakness Sleep problems Concentration problems

92
Q

Polymyalgia rheumatica SSx

A

Proximal muscle pain WITHOUT weakness

93
Q

3 Dermatomyositis SSx

A

Bilateral proximal muscle WEAKNESS, Rash Gottron papules

94
Q

Ab to differentiate dermatomyositis from SLE (both cause malar rash and can have +ANA.

A

anti Jo1

95
Q

Biopsy of dermatomyositis

A

Perimysial inflammation “perimysium is closest to the skin, dermatomyositis involves the skin”: CD 8 T cells.

96
Q

Cell type involved in dermatomyositis

A

CD4T cells

97
Q

Biopsy of polymyositis

A

Endomysial inflammation

98
Q

Cell type in polymyositis

A

CD8 poly = multiple…8 is more than 4…polymyositis has CD8. dermatomyositis has CD4

99
Q

Myasthenia gravis effects on receptor

A

Competitive inhibition of post synaptic Ach receptor –> this is why high ACh can reverse sx

100
Q

Association with MG

A

Thymic hyperplasia/thymoma Thymectomy will improve Non-MSK

101
Q

Lambert Eaton defect

A

AutoAb to presynaptic Ca Channels, preventing Ach release

102
Q

MCC of Lambert Eaton

A

Small cell lung cancer

103
Q

How to differentiate MG from LE on PE

A

MG symptoms worsen with use but improve with ACHEs

LE symptoms improve with use but not ACHEs

104
Q

liposarcoma is a proliferation of which cell

A

Lipoblast

105
Q

most common site for rhabdomyosarcoma

A

Vagina of a young girl

106
Q

Rhabdomyosarcoma is a malignancy of

A

Rhabdomyoblasts

107
Q

Rhabdomyosarcoma immunohistochemical stain

A

Desmin positive

108
Q

Which bones in fibrous dysplasia

A

Flat bones (skull, face, ribs)

109
Q

3 stages of osteitis deformans

A

Lytic - Osteoclasts go crazy Mixed - Osteoclasts start burning out, osteoblasts wake up Sclerotic - osteoblasts go crazy

110
Q

Tumors that metastasize to bone

A

Breast > Prostate > Lung > Thyroid > Kidney > Testicular

111
Q

Tumor in the diaphysis/medulla of a small bone (metatarsal, metacarpal)

A

Chondroma

112
Q

A 25-year-old man presents with lower back pain and a diastolic murmur at the right 2nd intercostal space. Diagnosis?

A

Ankylosing Spondyitis

113
Q

why does alcohol precipitate gout attacks?

A

EtOH competes for the same excretion sites in the kidney as uric acid, leading to a build up of uric acid in the blood

114
Q

Other name- anti-Jo 1 Ab

A

histidyl tRNA synthase

115
Q

A two-month-old male infant was referred to the department of pediatric gastroenterology because of hepatosplenomegaly and thrombocytopenia. Past medical history of the patient revealed that he was hospitalized in the first day of his life in the neonatal unit because of poor feeding and onset of sepsis workup was done. X-ray shows thickened bone and decreased marrow cavities of various bones. Diagnosis?

A

osteopetrosis

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