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X. MRCS: Pathophysiology > Bone > Flashcards

Bone Flashcards

1
Q

Functions of bone

A

Haematopoiesis
Lipid and mineral storage
Support
Protection

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2
Q

Components of bone

A

Cellular components: Osteoblasts, osteoclasts, osteocytes

Extracellular matrix

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3
Q

Structure of bone

A 
Woven bone (primary bone)
Lamellar bone (secondary bone)
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4
Q

Compact bone

A

Lamellae are organised into osteons

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5
Q

Osteon

A

Concentric circles of lamellae
Surround vertical Haversian canal (transmits neurovascular and lymphatic vessels)
Connected by horizontal Volkann’s canals
Ostecytes are located between lamellae within cavities called lacunae
Lacunae are interconnected by series of tunnels called canaliculi

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6
Q

Spongy bone

A

Interior part, deep to compact bone
Honeycombe appearance. 3D network of columns. Crosslink to form trabeculae.
Strong against multidirectional force
Spaces between trabeculae are filled with bone marrow

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7
Q

Bone marrow

A

Red bone marrow: haematopoietic stem cells

Yellow bone marrow: adipocytes

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8
Q

Periosteum

A

Layer of connective tissue surrounded external surface

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9
Q

Ossification

A

Process of producing new bone:
Endochondrial ossification: hyaline cartilage is replaced by osteoblasts secreting osteoid
Intremembranous ossification: mesenchymal tissue is condensed into bone
Both produces primary bone, replaced by mature secondary bone

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10
Q

Remodelling

A

Mature bone is reabsorbed and new bone formed

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11
Q

Parts of long bones

A

Epiphysis: joint facing bone
(Metaphysis: growth plate)
Diaphysis: shaft

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11
Q

Parts of long bones

A

Epiphysis: joint facing bone
Metaphysis:
(Physis: growth plate)
Diaphysis: shaft

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12
Q

Fracture healing stages

A

Hematoma formation
Fibrocartilaginous callus formation
Bony callus formation
Bone remodeling

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13
Q

Fracture healing: haematoma

A

Days 0-5
Periosteum and vessels in bone bleed
Damaged bond tissue releases: TNFa, ILs and BMPs (bone morphogenetic proteins)
Attracts macrophages: remove damaged tissue and release VEGF (vascular endothelial growth factor)

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14
Q

Fracture healing: Fibrocartilaginous callus formation

A

Days 5-11
VEGF stimulates angiogenesis at site
Fibrin-rich granulation tissue develops in haematoma
Mesenchymal stem cells differentiate (driven by BMPs) to fibroblasts, chondroblasts, osteoblasts
Chondogenesis occurs: laying down collagen
Woven bone layer down by osteoprogentior cells

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15
Q

Fracture healing: Bony callus formation

A

Days 11-28
Cartilaginous callus undergoes endochondrial ossification
Woven bone continues to be laid down
Blood vessels continue to proliferate
Formation of hard calcified immature bone

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16
Q

Fracture healing: bone remodelling

A

Days 18+
Hard callus undergoes repeated remodelling
Centre of callus is replaced by compact bone
Callus edges replaced by lamellar bone

17
Q

Salter Harris Classification

A

I: transverse through physis
II: physis & metaphysis, sparing epiphysis
III: physis & epiphysis, sparing metaphysis
IV: physis, metaphysis, epiphysis
V: compression fracture of physis
(VI-IX additional classifications now also)

18
Q

Bone tumours

A

Primary

Secondary (metastasis)

19
Q

Primary bone tumours: classifications

A 
Bone forming
Cartilage forming
Fibrous tissue
Giant-cell tissues
Marrow tumours
20
Q

Bone forming tumours

A

Benign: osteoma, osteoid osteoma, osteoblastoma
Malignant: osteosarcoma

21
Q

Cartilage forming tumours

A

Benign: chondroma, osteochondroma, chondroblastoma
Malignant: chondrosarcoma

22
Q

Fibrous tissue bone tumours

A

Benign: fibroma, fibrzomatosis
Malignant: fibrosarcoma

23
Q

Giant cell tumours

A

Benign osteoclastoma

Malignant osteoclastoma

24
Q

Marrow tumours

A

Malignant:
Ewing’s tumour
Myeloma

25
Q

Metastatic bone cancer

A

Most common cause of bone cancer
Primaries: renal, thyroid, lung, prostate, breast
Most common site: spine

26
Q

Osteoid osteoma

A

Benign. Arise from osteoblasts
10-20 years. M>F.
Typically small (<2cm), located around metaphysis of long bones
Sx: localised progressive pain, made better with NSAIDs. Localised swelling, tenderness, limp.
XR: small mass, radiolucent nidus with rim of reactive bone
Rx: conservatively. serial imaging 4-6mnths. resolve spontaneously

27
Q

Osteochondroma

A 
Benign. Outgrowth from metaphysis covering with cartilagenous cap. 
10-20 years. M>F. 
Sx: usually asymptomatic
XR: pedunculate bony outgrowth
Rx: conservatively. serial XRs 4-6mnths.
28
Q

Chondroma

A

Benign. Arise from chondroblasts
20-50years.
Commonly affecting long bones of hands, femur or humerus
Sx: usually asymptomatic. Can present as pathological fracture
XR: well circumscribed oval lucency with intact cortex
Rx: depending on size and clinical features.
Small risk of transformation into chrondrosarcoma

29
Q

Giant cell tumour

A

Benign. Arise from multinucleated giant cells and stroll cells
20-30years
Usually affecting epiphysis of long bones
Sx: pain, swelling, limitation of joint movement
XR: eccentric lytic area, “soap bubble” appearance
Rx: surgical resection w. bone grafting/recon

30
Q

Osteosarcoma

A

Malignant. Most common malignant primary bone tumour
Bimodal age: 10-14, >65 (typically with Paget’s disease). RF: Li-Fraumeni syndrome
Most commonly at metaphysis of distal femur or proximal tibia
Sx: localised contact pain. soft tissue mass.
XR: medullary and cortical bone destruction. Significant perisoteal reactions (“Codman’s triangle or “sunburst pattern”)
Tissue biospy required.
Rx: aggressive surgical resection + chemo
Mets: lung and bone

31
Q

Ewing’s sarcoma

A

Malignant. Paeds. M>F.
Arise from poorly differentiated neuroectodermal cells.
Commonly affect diaphysis of long bones
Sx: painful, enlarging mass. tenderness.
XR: lytic lesion with periosteal reactions, layers of reactive bone “onion skin” appearance.
Rx: neoadjuvant chemo + surgical excision

32
Q

Chondrosarcoma

A

Malignant. Tumour of cartilage.
Commonly primary lesions. Can be malignant change from benign chondromas
40-60
Axial skeleton (pelvis, shoulder, ribs)
Sx: painful enlarging mass.
XR: lytic lesions with calcification, cortical remodelling and endosteal scalloping
Rx: wide en-bloc excision

33
Q

Diseases of bone structure

A

Osteogenesis imperfecta
Osteoporosis
Rickets
Osteomalacia

34
Q

Osteogenesis imperfecta

A

Abnormal synthesis of collagen from osteoblasts
Sx: fragile bones, bone deformities, blue sclera
Autosomal dominant

35
Q

Osteoporosis

A

Reduction in bone density, reducing structural integrity. Osteoclast activity outweighing osteoblasts.
Type 1: postmenopausal (decreased oestrogen)
Type 2: senile (>70yrs)
Type 3: secondary (co-existing disease, e.g. CKD)

36
Q

Osteoporosis

A

Reduction in bone density, reducing structural integrity. Osteoclast activity outweighing osteoblasts.
Type 1: postmenopausal (decreased oestrogen)
Type 2: senile (>70yrs)
Type 3: secondary (co-existing disease, e.g. CKD)

37
Q

Rickets

A

Vitamin D or Ca deficiency in children with growing bones

Osteoid mineralised poorly and remains pliable. Epiphyseal growth plates become distorted under weight of body

38
Q

Rickets

A

Vitamin D or Ca deficiency in children with growing bones

Osteoid mineralised poorly and remains pliable. Epiphyseal growth plates become distorted under weight of body

39
Q

Osteomalacia

A

Vitamin D or Ca deficiency in adults with remodelling bones
Osteoid laid down by osteoplasts is poorly mineralised leading to increasingly weak bones and increased susceptibility to fracture

X. MRCS: Pathophysiology (13 decks)

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