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MSK > Cortex- pathology, biochemistry, histology > Flashcards

Cortex- pathology, biochemistry, histology Flashcards

1
Q

what are the possible causes if benign bone tumours

A

neoplastic, developmental, traumatic, infection or inflammatory

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2
Q

what is the most common benign bone tumour

A

osteochondroma

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3
Q

what does an osteochondroma look like

A

bony outgrowth on the external surface with a cartilaginous gap

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4
Q

what are the symptoms of osteochondroma

A

non usually, can cause local pain

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5
Q

when should osteochondromas receive treatment and what treatment)

A

1% risk of malignant transformation

any lesion growing in size or producing pain may require excisional biopsy

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6
Q

what can cause multiple osteochondromata

A

autosomal dominant hereditary disorder

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7
Q

what is an enchondroma

A

an intermedullary and usually metaphyseal cartilagenous tumour

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8
Q

what causes an enchondroma

A

failure of normal enchondral ossification at the growth plate

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9
Q

what do enchondromas look like

A

usually lucent, can undergo mineralisation with a patchy sclerotic appearance

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10
Q

what is the risk of an enchodroma

A

can weaken the bone resulting in pathological fracture

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11
Q

where so enchondromas commonly occur

A

in the femur, humerus, tibia and small bone of the hands and feet

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12
Q

how do you strengthen a bone with an enchondroma

A

curettage the tumour and fill with bone graft

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13
Q

what is a simple bone cyst (aka unicameral bone cyst)

A

a single cavity benign fluid filled cyst in a bone

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14
Q

what causes a simple bone cyst

A

growth defect from the physis

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15
Q

where do you get simple bone cyst

A

(as growth defect in physis) metaphyseal in long bones (proximal humerus and femur), can also occur in the talus or calcaneus

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16
Q

why is curattage with a bone graft a possible option for a simple bone cyst (+/- stabilisation)

A

as it may weaken bone causing pathological fracture

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17
Q

what is an aneurysmal bone cyst

A

lots of chambers filled with blood or serum

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18
Q

where do you get aneurysmal bone cysts

A

can occur in the metaphyses of long bones, flat bones (ribs, skull) and vertebral bodies

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19
Q

what are the risks with an aneurysmal cyst

A

they are locally aggressive, cause cortical expansion and destruction and usually pain. risk of pathological fracture

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20
Q

what is the treatment for aneurysmal cysts

A

curattage and bone graft/ bone cement

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21
Q

where do you get giant cell tumours

A

metaphyseal and epiphysis regions, can extend to subchondral bone adjacent to the joint

commonly occur around knee, and in the distal radius, other long bones, pelvis and the spine

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22
Q

what is the risk of giant cell tumours

A

can be locally aggressive, destroy cortex, painful, can cause pathological fracture, 5% can metastasise to the lung (still considered benign)

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23
Q

what are the benign bone tumours

A

osteochondroma, enchondroma, simple and aneurysmal bone cyst, giant cell tumour, fibrous dysplasia, osteoid osteoma, brodies abscess

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24
Q

when do giant cell tumours occur

A

after the physis has fused

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25
Q

what is the histology of giant cell tumours

A

multinucleated giant cells

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26
Q

what do giant cell tumours look lie on x ray

A

soap bubble appearance

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27
Q

what is the treatment for a giant cell tumour

A

intalesional excision with use of phenol, bone cement or liquid nitrogen to destroy remaining tumour material (reduce the risk of recurrence)

if very aggressive lesion which has destroyed cortical then may need joint replacement

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28
Q

what are the reg flags of bone cancer

A

constant pain, usually severe and at night, weight loss, fatigue, loss of appetite

(all unexplained skeletal pains should be investigated- at least an x-ray)

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29
Q

what age does bone cancer occur

A

can happen at any age

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30
Q

what do malignant primary bone cancers look like on x rays

A

aggressive and destructive signs: cortical destruction, a periosteal reaction (raised periosteum producing bone), new bone formation (sclerosis as well as lysis from destruction), extension into the surrounding soft tissue envelope

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31
Q

what is the most common form of primary bone tumour

A

osteosarcoma

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32
Q

who usually gets osteosarcoma and where

A

younger age groups (adolescence and early childhood) 60% involving bones around the knee.
also seen in proximal femur, proximal humerous and pelvis

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33
Q

what is the usually method of bone cancer metastasis

A

haematogenous, can also be lymphatic

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34
Q

how many patient have metastasis at diagnosis

A

10%

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35
Q

what is the role of chemo in bone cancer treatment

A

not radiosensitive adjuvant chemotherapy can prolong survival

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36
Q

what is a chondrosarcoma

A

a cartilage producing primary bone tumour

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37
Q

how does a chondrosarcoma compare to an osteosarcoma

A

less common and less aggressive

occurs in older age groups

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38
Q

where do you get chondrosarcoma and what are they like

A

in pelvis or proximal femur

large and slow to metastasise

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39
Q

what chemo does chondrosarcoma respond to

A

none

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40
Q

what are fibrosarcomas and malignant fibrous histiocytoma

A

fibrous malignant primary bone tumours

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41
Q

what are the malignant primary bone cancers

A

osteosarcoma, chondrosarcoma, fibrosarcoma, malignant fibrous histiocytoma, ewing’s sarcoma

(+ lymphoma and myeloma)

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42
Q

who an where do fibrosarcomas and malignant fibrous histiocytomas occur

A

in abnormal bone (bone infarct, fibrous dysplasia, post irradiation, paget’s disease

in adolescent or young adults usually

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43
Q

what is ewings sarcoma

A

malignant tumour of primative cells in the marrow (2nd most prevalent)

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44
Q

what bone cancer has the poorest prognosis

A

ewings sarcoma

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45
Q

who gets ewings sarcoma

A

most cases between ages 10 and 20

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46
Q

what are the symptoms of ewings sarcoma

A

fever, raised inflammatory markers and a warm swelling (may be misdiagnosed as osteomyelitis)

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47
Q

does ewings sarcoma respond to chemo and radio

A

is chemo and radio sensitive

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48
Q

what is the treatment for primary bone tumours

A

usually involves surgery to remove the tumour and surrounding tissue to reduce risk of recurrence

adjuvant therapies and neo-adjuvant therapy prior to surgery

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49
Q

what staging investigations should be done for bone cancer

A

bone scan, CT chest, MRI, biopsy

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50
Q

what is lymphoma

A

cancer of the cells of the lymphatic system/ macrophages

can occur as primary bone tumour

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51
Q

what is hodgkins lymphoma

A

type of lymphoma arising from lymphocytes

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52
Q

where does primary lymphoma of the bone usually affect and what is the treatment

A

the pelvis or the femur

surgical resection

53
Q

what are signs of metastatic lymphoma and what is the treatment

A

lymphadenopathy and splenomegaly

chemotherapy and radiotherapy

54
Q

what is the usual survival for metastatic lymphoma

A

less than 2 years

55
Q

what is a myeloma

A

a malignant B cell proliferation, arises from the marrow

56
Q

how can myeloma present

A

as a solitary lesion (plasmacytoma) or with multiple osteolytic lesions throughout the skeleton (multiple myeloma)

patients may present with pathological fracture

57
Q

what are the symptoms of multiple myeloma

A

patients usually 45-65

weakness, back pain, bone pain, fatigue and weight loss, marrow suppression resulting in anaemia and recurrent infection

58
Q

how do you diagnose myeloma

A

plasma protein electrophoresis, early morning urine collection for bence jones protein assay

59
Q

what are the treatments for plasmacytoma and multiple myeloma

A

plasmacytoma- radiotherapy

multiple myeloma= chemotherapy

60
Q

list 5 primary malignant tumours which commonly metastasise to bone

A 
(all carcinoma except thyroid)
breast
prostate 
lung
renal
thryroid adenocarcinoma
61
Q

describe the bone metastasis of breast and its survival

A

can be blastic (sclerotic) or lytic

survival 24-26 months

62
Q

describe the bone metastasis of prostate cancer, treatment and survival

A

produces sclerotic metastases

radiotherapy and hormone manipulation can reduce fracture risk

survival 45% at one year

63
Q

describe the bone metastasis and survival of lung caner

A

lytic bony metastases

6 months

64
Q

describe the bone metastasis, treatment and survival of renal cell cancer

A

potentially large an very vascular lytic blow out boney metastasis

with a single bony metastasis amenable to resection (nephrectomy) surgery can be curative

multiple bone metastases survival is 12-18 months

65
Q

what bones are commonly involved in metastasis

A

vertebra, pelvis, ribs, skull, humerus and long bones of lower limb

66
Q

if metastasis is suspected, what tests should be done

A

breast/ PR exam

CXR may detect a pulmonary lesion

blood tests: serium calcium (hypercalcaemia), LFTs (liver mets), plasma protein electrophoresis (for myeloma), FBC and U&Es

67
Q

when might joint replacement or skeletal stabilisation be required

A

painful lesions
those that occupy >50% of diameter of bone
those with cortical thinning
those in risk of impeding pathological fractures

68
Q

what are the two forms of sift tissue swelling

A

diffuse (e.g. synovitis or oedema) or local

69
Q

what are the forms of local soft tissues swellings

A

inflammatory (bursitis, rheumatoid nosules), infection (abscess), cystic lesions (ganglion, meniscal cyst, bakers cyst), benign neoplasms and malignant neoplasms

70
Q

what should be included in a local soft tissue swelling history and examination

A

history:
painful? growing or fluctuated in size? solitary or multiple?

exam:
site, size, definition, consistency (cystic, solid, soft, hard), surface (smooth irregular), mobility or fixity, temperature, pulsatility, transilluminable (fluid filled)
pulsatility 
overlying skin changes 
local lymphadenopathy
71
Q

what are features suggestive of a benign soft tissue tumour

A

smaller size, fluctuation in size (malignant tumours don’t regress in size), cystic lesions, well defined lesions, fluid filled lesions and soft/ fatty lesions

72
Q

what are features of a possibly malignant soft tissue neoplasm

A

larger lesions (>5cm), rapid growth in size, a solid lesion, ill defined, irregular surface, associated lymphadenopathy, systemic upset (weight loss, apetite, fatigue)

73
Q

what investigations might be needed for a swelling of unknown nature

A

MRI, ultrasound (to confirm a cystic lesion), biopsy

74
Q

what is the commonest benign soft tissue tumours

A

lipoma

75
Q

what is a lipoma

A

neoplastic proliferation of fat

76
Q

what are malignant soft tissue tumours arising form connective tissues called

A

sacromas

e.g.
angiosarcoma- blood vessels
fibrosarcoma/ malignant fibrous histiocytoma- fibrous tissue
phabdomyosarcoma- skeletal muscle
synovial sarcoma- synovial lining of joints and tendons

77
Q

where do you get ganglion cysts

A

around a synovial joint or synovial tendon sheath

78
Q

what causes ganglion cyst

A

as a result of herniation or out pouching of a weak portion of the joint capsule or tendon sheath

weakness can be developmental (juvenile bakers cysts) or as a result of underlying joint damage/ arthritis with build up of pressure within the joint (adult bakers cyst, mucous cyst)

79
Q

describe what ganglion cysts are like

A

well defined, may be quite firm and readily transilluminate

80
Q

why would a ganglion cyst be excised

A

for local discomfort or cosmesis

81
Q

what is a bursitis

A

an inflamed bursae

82
Q

what is a bursae

A

a small fluid filled sac lined by synovium around a joint which prevents friction between tendons, bones, muscle and skin

83
Q

what are 4 commonly inflamed bursae and why do they occur

A

(repeated pressure or trauma)
pre-patellar bursitis
olecranon bursitis
bunions

84
Q

what are bunions

A

bursitis over the medial 1st metatarsal head in hallux valgus

85
Q

what are two less common causes of bursitis

A

bacterial infections can cause a bursal abscess

gout

86
Q

what happens over time with bursitis

A

the fluid component of the swelling may subside but a thickened bursal sac may be left

87
Q

what is the treatment for sebaceous cysts and implantation dermoids

A

may require excision and or biopsy

88
Q

why can an abscess occur on a limb

A

cellulitis, bursitis, penetrating wound or infected sebaceous cyst

89
Q

what is the treatment for abcesses

A

antibiotics + incision and drainage

90
Q

what is avascular necrosis

A

an ischaemic necrosis of bone predominantly

91
Q

what sites are prone to AVN

A

femoral head, femoral condyles, head of the humerus, the capitellum, proximal pole of the scaphoid, proximal part of the talus

92
Q

what can cause AVN

A

fracture, idiopathic,

alcoholism and corticosteroids can alter fat metabolism- fats gets into circulation- promote coagulation in prone areas/ increase fat content in the marrow (compresses venous outflow)

primary hyperlipidaemia

thrombophilia

sickle cell disease

antiphospholipis deficiency in SLE

the bends

93
Q

what does AVN result in

A

necrosis of a segment of bone resulting in patchy sclerosis

subchondral collapse and irregularity of the articular surface

94
Q

how can AVN affect osteoarthritic joints

A

causes collapse of articular surface and rapid deterioration

95
Q

what is the treatment for AVN

A

if articular surface not collapsed- drilling under fluoroscopy to decompress bone, prevent further necrosis and promote healing

if collapsed- joint replacement (or fusion in wrist foot/ ankle)

96
Q

what is the biochemistry of osteoporosis

A

quantitative defect resulting in reduce bone density and increase porosity = fragility

97
Q

what is osteopenia

A

intermediate stage before osteoporosis

98
Q

when does loss of bone density normally start to occur- why

A

age 30 due to gradual breakdown in osteoblastic activity

99
Q

why do post menopausal females lose more bone mineral density

A

increase in osteoclastic bone reabsorption with the loss of protective effects of oestrogen (post menopausal osteoporosis)

100
Q

what are the risk factors for post menopausal osteoporosis

A

early menopause, familial, environmental, smoking, alcohol abuse, lack of exercise, poor diet

101
Q

what are the two type of osteoporosis

A

post menopausal and old age

102
Q

what are the risk factors for old age osteoporosis

A

same as post menopausal with added:

chronic disease, inactivity, reduced sunlight exposure (vit D)

103
Q

what usually happens in patients with post menopausal osteoporosis

A

colles fractures and vertebral insufficiency

104
Q

what fractures are common in old age osteoporosis

A

femoral neck fractures and vertebral fractures

105
Q

what other that the two types can osteoporosis arise from

A

coticosteroid use, alcohol abuse, malnutrition, chronic disease (CKD, malignancy, RA) and endocrine disorders (cushings, hyperthyroidism, hyperparathyroidism)

106
Q

how is osteoporosis diagnosed

A

DEXA scanning- provides measure of bone mineral density

107
Q

what are the treatments for osteoporosis

A

can only slow progression

  • exercise
  • good diet
  • healthy levels of sunlight exposure
  • calcium and vit D suppliments
  • biophosphates (alendronate, risedronate, etidronate - reduce osteoclast resorption)
  • desunomab (a monoclonal antibody which reduced osteoclast activity)
  • strontium (increased osteoblast replication and reduces resorption)
108
Q

what is the biochemistry of osteomalacia and rickets

A

a qualitative defect of bone with abnormal softening of the bone due to deficient mineralisation of osteoid (immature bone)

109
Q

what is osteomalacia and rickets secondary to

A

inadequate amounts of calcium and phosphorus

110
Q

what are the primary causes of osteomalacia and rickets

A

either insufficient calcium absorption from the intestine due to lack in diet or a deficiency/ resistance to the action of vit D

or a phosphate deficiency caused by renal losses

malnutrition, lack of sunlight (no vit D activation)

hypophosphataemia (refeeding syndrome, alcohol abuse, malabsorption, renal tube acidosis)

long term anticonvulsant use

chronic kidney disease

111
Q

what are the symptoms of osteomalacia and rickets

A

bone pain, deformities, pathological fractures, symptoms of hypocalcaemia (paraesthesiae, muscle cramps, irritability, fatigue, seizures, brittle nails)

also pseudofractures (loosers zones)

112
Q

what are the biochemical markers of osteomalacia

A

low calcium, low serum phosphate and high serum alkaline phosphatase

113
Q

what is the treatment for osteomalcia and rickets

A

vit D therapy, calcium and phosphate supplements

114
Q

what are there high levels of in hyperparathyroidism

A

parathyroid hormone and calcium

115
Q

what can cause primary hyperparathyroidism

A

a benign adenoma, hyperplasia, malignant neoplasia (rarer)

116
Q

what does an overproduction of PTH result in

A

hypercalcaemia- fatigue, depression, bone pain, myalgia, nausea, thirst, polyuria, renal stones, osteoporosis

117
Q

what causes secondary hyperparathyroidism

A

physiological overproduction of PTH secondary to hypocalcaemia usually caused by vit D deficiency or CKD

118
Q

what is tertiary hyperparathyroidism

A

when patients with chronic secondary hyperparathyroidism develop an adenoma which will continue to produce PTH

119
Q

what is pagets disease

A

chronic disease that results in thickened brittle and miss-shapen bones

120
Q

what are cement lines

A

lines surrounding osteon

121
Q

what is freibergs disease

A

osteochondritis of the 2nd metatarsal head

122
Q

what is kohlers disease

A

osteochondritis of the navicular bone

123
Q

what is panners disease

A

osteochondritis of the capitellum of the elbow

124
Q

what is kienbocks disease

A

osteochondritis of the lunate (within the wrist)

125
Q

where do you get chondrosarcomas

A

axial skeleton

126
Q

who gets chondrosarcomas

A

older patients

127
Q

who gets osteosarcomas and where

A

younger patients

long bones, particularly at the metaphysis

128
Q

what can osteosarcomas occur secondary to

A

pagets disease

129
Q

what is pagets disease associated with

A

osteosarcoma in older patients

high cardiac output failure

MSK (71 decks)

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