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Human Disease > Osteo-articular Pathology > Flashcards

Osteo-articular Pathology Flashcards

1
Q

Name developmental osteo-articular disorders (x3)

A
  • Osteogenesis imperfecta
  • achondroplasia
  • osteopetrosis
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2
Q

Name systemic / generalised osteo-articular disorders (x5)

A
  • infections - osteomyelitis
  • osteoporosis
  • rickets / osteomalacia
  • hyperparathyroidism (skeletal effects)
  • Paget’s disease
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3
Q

Name neoplastic osteo-articular disorders (x4)

A
  • bone forming tumours
  • cartilage tumours
  • fibrous tumours
  • tumours of uncertain histogenesis
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4
Q

Name joint osteo-articular diseases (x2)

A
  • osteoarthritis

- rheumatoid arthritis

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5
Q

What is the outer section of bone called?

A

Cortex

- compact bone

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6
Q

What is the inner section of bone called?

A

Medulla

  • cancellous bone
  • spongy
  • trabeculae
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7
Q

What is in the trabeculae?

A

Bone marrow

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8
Q

What does bone marrow do?

A

makes RBC / WBC

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9
Q

What are the functions of bone? (x4)

A
  • support
  • protect organs
  • host and protect bone marrow
  • supplies calcium and phosphate
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10
Q

Describe intramembranous ossification

A
  1. ossification centre in fibrous connective tissue membrane
    - mesenchymal cells differentiate into osteoblasts
  2. Bone matrix (osteoid) is secreted within fibrous mem
    - osteoblasts secrete osteoid
    - osteoid is mineralised / calcified within a few days = bone matrix
    - trapped osteoblasts become osteocytes
  3. Woven bone and periosteum form
    - osteoid laid down between embryonic blood vessels - random network = trabeculae
    - vascularised mesenchyme condenses on external surface of woven bone to become periosteum
  4. bone collar of compact bone forms and red marrow appears
    - trabeculae thicken just deep to periosteum = woven bone collar - later replaced by mature lamellar bone
    - spongy bone remains internally and its vascular tissue becomes red bone marrow
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11
Q

What bones are created by intracmembranous ossification?

A

Flat bones

  • skull (not occipital bone)
  • part of mandible / maxilla
  • part of clavicles
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12
Q

How long does is take for ostoid to become calcified once secreted from osteoblasts?

A

a few days

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13
Q

What bones are created by endochondrial ossification?

A

long bones

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14
Q

How are bone created by endochondrial ossification?

A
  • Mesenchymal cells form hyaline cartilage
  • bone collar forms on sides of long bone
  • Blood vessels enter central ossification centre (cartilage can’t survive if O2 present, so bone forms) from periosteal bud
  • spongy bone formed
  • medullary cavity forms
  • secondary ossification centres form
  • epiphyseal blood vessels enter secondary ossification centres
  • ossification of the epiphyses
  • hyaline cartilage remains on epiphyseal plate and articular cartilage
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15
Q

What is a periosteal bud?

A

Blood vessels from the periosteum which enter the centre of ossification in endochondrial ossification

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16
Q

What is the medullary cavity?

A

aka marrow cavity

- central part of bone where marrow stored

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17
Q

What are the following:

  • diaphysis
  • epiphysis
  • epiphyseal
A

diaphysis
- bone between epiphyseal plates (middle part)
epiphysis
- bone above eiphyseal plates (top / bottom)
epiphyseal
- plate of cartilage

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18
Q

Describe the growth plate in bone

A

aka epiphyseal plate

  • well ordered columns of chondrocytes
  • chondrocytes release matrix (proteoglycans, water, collagen)
  • hypertrophy of chondrocytes are they get closer to zone of bone formation - reduced proteoglycan release, increased alkaline phosphatase - therefore increased calcification
  • then they become calcified
  • then converted to bone
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19
Q

What happens if bone does not calcify in growth plate?

A

bone does not grow

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20
Q

Where does alkaline phosphatase come from and what does it do in bone formation?

A

from chondrocytes in growth plates

causes calcification of hypertrophy chondrocytes to form bone

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21
Q

Name condition associated with short limbs

A

achondroplasia

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22
Q

What are physical symptoms of achondroplasia?

A
  • short limbs
  • trident hands
  • smaller occipital bone / contracted base of skull

Normal - trunk/thorax

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23
Q

What are trident hands?

A
  • fingers all similar length

- fingers splay at 1st joint

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24
Q

What type of bone formation is faulty in achondroplasia?

A

endochondrial ossification

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25
Q

how many births have achondroplasia?

A

1 in 30,000 live births

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26
Q

What % of achondroplasia is

  • hereditary
  • sporadic
A

hereditary = 25%
- autosomal dominant trait

Sporadic = 75%
- new mutations

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27
Q

Name long bones

A

humerus, ulna, radius

femur, fibula, tibia

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28
Q

How is cartilage different in long bones in achondroplasia|

A

epiphyseal plates don’t develop normally

cartiage at end of long bones is enlarged

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29
Q

What happens in achondroplasia endochondrial ossification?

A
  • disrupted columns of chondrocytes
  • chondrocytes fail to hypertrophy
  • defective calcification
  • bone not formed
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30
Q

Which gene is responsible for achondroplasia and what is the type of mutation?
What does this gene do?

A

Fibroblast growth factor receptor 3 (FGFR3)

  • point mutation
  • in achondroplasia, FGFR3 is always active, so chondrocytes aren’t switched on for hypertrophy
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31
Q

What are three conditions caused by faulty FGFR3?

A
  • achondroplasia (dwarfism)
  • craniosynostosis (abnormal scalp/sutures)
  • lethal dwarism (foetus doesn’t grow)
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32
Q

What is osteogenesis imperfecta?

A

aka brittle bones

  • defective connective tissue
  • abnormal synthesis of type 1 collagen
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33
Q

What % of ORGANIC matter of bone is made of collagen?

A

90%

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34
Q

What makes up 90% of organic matter of bone?

A

Collagen

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35
Q

What mutations cause osteogensis imperfecta?

A

point mutations of many genes.

mainly - COL1A1 and COL1A2

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36
Q

how many types of osteogensis imperfecta are there?

A

8

mild - severe

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37
Q

What determines the severity of osteogenesis imperfecta?

A
  • number of point mutations

- type of point mutations (amino acid substitution at point mutation)

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38
Q

What is the pattern of inheritance for osteogensis imperfecta?

A

autosomal dominant or recessive

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39
Q

What is the organic matrix in bone?

A

collagen / osteoid

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40
Q

What is the inorganic matrix in bone?

A

Calcium

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41
Q

What are symptoms of mild osteogenesis imperfecta?

A
  • delicate bones

- early osteoporosis

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42
Q

What are symptoms of severe osteogenesis imperfecta?

A
  • can be lethal perinatally (just before / after birth)
  • foetus can get fractures

Adults

  • abnormal bone structure
  • defective mineralisation
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43
Q

What are bones like in adults with osteogenesis imperfecta?

A

thin cortex = weak, bendy

epiphyseal cartilage is fine, so normal length bones

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44
Q

What other symptoms can be present in osteogenesis imperfecta? (none bone related)

A

blue/grey eyes
- sclera is thin, so choroidal veins below show through

Dentogenesis imperfecta

  • irregular dentine formation (NB enamel = no collagen)
  • blue /grey hue
  • in type III and IV osteogenesis imperfecta?
  • loose joints for slender weak tendons
  • poor muscle tone
  • early loss of hearing in some children (middle ear bones)
  • protrusion of the eyes
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45
Q

What type of osteogenesis imperfecta gets dentogenesis imperfecta?

A

types Ib, III and IV

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46
Q

What is the most common type of osteogenesis imperfecta?

A

type I

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47
Q

What are symptoms of osteogenesis imperfecta type I?

A
  • fragile bones (fracture, slight spinal curvature)
  • loose joints for slender weak tendons
  • poor muscle tone
  • blue-grey sclera in eye (choroidal veins below show through)
  • early loss of hearing in some children (middle ear bones)
  • protrusion of the eyes
  • type 1A = no dentogenesis imperfecta
  • type IB = dentogenesis imperfecta
  • reduced life exp (risk fatal bone fracture)
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48
Q

Why does life exp reduce in osteogenesis imperfecta?

A

risk of fatal bone fracture

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49
Q

Which type 1 osteogenesis imperfecta is associated with dentogenesis imperfecta?

A

Type IB (not type 1A)

NB type III and IV collagen issues are also linked to dentogenesis imperfecta

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50
Q

What is disorder with v dense bone?

A

osteopetrosis

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51
Q

What is osteopetrosis?

A 
osteoclast defect
bone formation > resorption
become become denser
reduced medullary cavity / space for marrow
reduced haemoposesis, inc WBC 
increased risk infection
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52
Q

What is inhertiance pattern of osteopetrosis?

How common is it?

A

inherited

rare

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53
Q

What is haemoposesis?

A

Formation of blood cells in bone marrow

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54
Q

What does xray of osteopetrosis look like?

A

dense, bright white bone

can’t see medulla

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55
Q

with thick bone of osteopetrosis, is there an increase or decrease in risk of fracture?

A

increase

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56
Q

How many men / women get osteoporosis?

A

1 in 3 women (over 50)
1 in 10 men (over 50)
get fractures from osteoporosis

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57
Q

How many hip fractures are caused by osteoporosis each year?

A

70,000

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58
Q

How many wrist fractures are caused by osteoporosis each year?

A

50,000

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59
Q

How many spinal fractures are caused by osteoporosis each year?

A

40,000

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60
Q

What is most common fracture associated with osteoporosis?

A

hip (70,000 / year) - neck of femur fractures

then wrist (50,000) - radius in wrist - Colles fracture
then spine (40,000) - vertebral crush
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61
Q

How much does osteoporosis cost the NHS each year?

A

£1.7billion!

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62
Q

Define osteoporosis

A

reduced bone mass / density

  • thinner cortex
  • increased trabeculae spaces
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63
Q

What is main cause of osteoporosis?

A

post-menopause

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64
Q

What are other causes of osteoporosis?

A 
Disuse
- prolonged bed rest
- paralysis
- weightlessness (space travel)
Diet
- Vit D, vit C, calcium, protein deficiency
- anorexia
Drugs
- heparin
- ethanol (poor diet)
- steroids - reduces bone mass
Endocrine
- adrenal failure 
- testicular / ovarian failure
65
Q

Name of form of protection against osteoporosis?

66
Q

What is a Colles fracture?

A

fracture of radius in wrist, common in osteoporosis

67
Q

What part of hip is likely to fracture?

A

neck of femur

68
Q

How does spine fracture in osteoporosis?

A

vertebral crush

69
Q

How do steroids cause osteoporosis?

A

reduces bone mass

70
Q

What factors affect bone density?

A
  • ethnicity
  • age
  • gender
71
Q

What age is max bone density reached? and until what age is this level maintained?

A

18yrs

to 25yrs

72
Q

What age does bone density deteriorate?

73
Q

What is max bone density? (g/cm2)

A

1 - 1.1g/cm2

74
Q

What is bone density for someone with osteopenia?

A

0.7 - 0.9g/cm2

75
Q

What is bone density of someone with osteoporosis?

76
Q

At what age is the decreasing bone density levels most critical?

A

30-70yrs

- early menopause / fast density losers = increased risk

77
Q

How many times faster can some individuals lose bone density?

A

10x faster

78
Q

What is the adult version of rickets?

A

osteomalacia

79
Q

What is rickets?

A

inadequate bone mineralisation of existing organic bone matrix in growing bones
- lack of vit D

80
Q

What is osteomalacia?

A

inadequate bone mineralisation of existing organic bone matrix in adult bones

81
Q

What is most common cause of rickets / osteomalacia?

A

lack of vit D

82
Q

What is high risk profile for rickets?

A
  • lack of vit D / sunlight / use of sunscreen
  • lack of calcium
  • poor background
83
Q

What are symptoms of rickets?

A

mechanical weakness in long bones in LOWER limbs

bending / deformed lower limb long bones

84
Q

What are causes of rickets / osteomalacia?

A

Intrinsic Vit D

  • lack in diet
  • poor absorption
  • metabolism of vit D
  • lack of sunlight

Kidney disease

  • chronic kidney disease
  • renal tubular disorders

Inborn errors metabolism

  • familial hypophosphataemia
  • hypophosphatasia
85
Q

What bone disease does familial hypophosphataemia and hypophosphatasis cause and why?

A

Rickets / osteomalacia

  • reduced phosphate in body
  • therefore reduced alkaline phosphatase
  • therefore deficient chondrocytes and osteoblasts
  • therefore reduced bone mineralisation
  • causes rickets
86
Q

What happens to the epiphyseal plate in rickets?

A
  • chondrocytes become disorganised / lines lost
  • fibrous proliferation
  • no calcification
87
Q

How is vit D activated in body?

A
  • skin
  • liver (Vit D hydroxlyated)
  • kidney (Vit D hydroxylated again)
88
Q

What does vit D do?

A

promotes calcium absorption from gut and kidney

- therefore increases calcium for bones

89
Q

What happens to bones if lack of vit D?

A 
cartilage forms (osteoid) instead of bone
- bendy, deformed, easily fractured
90
Q

What bones are affected by osteomalacia?

A
  • adults
  • sites with active turnover
  • structural weakness here
91
Q

What type of fractures are common in osteomalacia?

A

Looser’s zones

- micro-fractures at sites with active bone turnover

92
Q

What are micro-fractures at sites with active bone turnover called?

A

Looser’s zones
- seen on xray
eg hip, neck of femur

93
Q

What are other names for hyperparathyroidism?

A

Osteitis fibrosa cystica

von Recklinghausen’s disease

94
Q

What is von Recklinghausen’s disease?

A

hyperparathyroidism

95
Q

What is Osteitis fibrosa cystica?

A

hyperparathyroidism

96
Q

What does parathyroid hormone regulate?

A

Blood calcium and phosphate levels

97
Q

What is primary hyperparathyroidism?

A

Issue with 1-4 parathyroids
eg tumour - adenoma / carcinoma
excess PTH produced

98
Q

What is an adenoma?

A

benign cancer from glandular cells in epithelial tissue

99
Q

What is a carcinoma?

A

cancer from epithelial cells

100
Q

What is secondary hyperparathyroidism?

A

response to hypocalcemia

  • due to vit D deficiency
  • chronic renal disease
101
Q

How is hyperparathyroidism diagnosed?

A

blood test - raised plasma calcium

102
Q

What happens to PTH release if blood calcium high?

103
Q

What happens to PTH release if blood calcium low?

104
Q

Do most patients with hyperparathyroidism have bone disease symptoms?

A

no, only a small number

105
Q

What happens if hyperparathroidism is mistaken for bone disease?

A

issues will continue in other bone areas until hyperparathyroidism is diagnosed and treated

106
Q

What is Paget’s disease?

A

Excessive breakdown and formation of bone
with disorganised remodelling
irregular scalloped edges
multiple reversal lines

Chronic condition
usually localised (one / few bones)
usually asymptomatic
increase of serum alkaline phosphatase

107
Q

What happens to bone in excessive osteoblasts activity in Paget’s disease?

A
  • excessive bone formation
  • increase bone deformity
  • reduced joint movt
108
Q

What happens to bone in excessive osteoclast activity in Paget’s disease?

A
  • excessive resorption
  • risk of fracture
  • pain
109
Q

Is Paget’s disease symmetrical or unsymmetrical?

A

unsymmetrical

- can occur anywhere

110
Q

what is associated with Paget’s disease?

A

parasytic infection

111
Q

What can Paget’s disease lead to? (another disease)

Who is most at risk of this?

A

osteocarcinoma (malignant)

- young people

112
Q

What disease can cause the scalp to enlarge?

A

Paget’s disease

113
Q

What changes in blood serum in Paget’s disease?

A

increase in serum alkaline phosphatase

114
Q

What age is most susceptible to Paget’s disease?

A

middle age

NB younger ppl more likely to progress to osteocarcinoma

115
Q

What happens if bones of the skull are affected by Paget’s disease?

A

middle ear bones = loss of hearing

skull = uneven thickness, extensive sclerosis and enlargement

116
Q

Which bone disease can cause loss of hearing and why?

A

Paget’s disease

- middle ear bones have excessive resorption / formation

117
Q

Is fibrous dysplasia genetic or non-genetic?

A

genetic

- specific mutations

118
Q

What is fibrous dysplasia?

A

intramedullary fibro-osseous lesion

119
Q

Who is affected by fibrous dysplasia?

A 
all ethnic groups
adults and children
men and women
- men = skull and ribs
- women = long bones
120
Q

Which bone disease has wonky eyes and lips?! (forming a > sign!)

A

fibrous dysplasia

121
Q

Name and describe the two forms of fibrous dysplasia

A

Monostotic - only one bone involved

  • skull - 35%
  • femur/tibia - 33%
  • ribs - 20%

Polyostotic - many bones affected

  • femur / pelvis / tibia - >60% of cases
  • one extremity or one side of body
  • earlier onset cf monostotic
  • associated with
    • McCune-Albright syndrome (endocrine abnormalities and skin pigmentation)
    • Mazabraud syndrome (intramuscular myxomas)
122
Q

Which form of fibrous dysplasia has the later onset?

A

monostotic fibrous dysplasia

123
Q

What bone disease is associated with McCune-Albright syndrome?

A

polyostotic fibrous dysplasia

McCune-Albright syndrome (endocrine abnormalities and skin pigmentation)

124
Q

What bone disease is associated with Mazabraud syndrome?

A

polyostotic fibrous dysplasia

Mazabraud syndrome (intramuscular myxomas)

125
Q

What is most common area for surgery for people with fibrous dysplasia?

A

gnathic (jaw) surgery

126
Q

What is a lytic lesion?

Which bone disease is it associated with?

A

radiolucent area on xray of bone, suggesting it’s been destroyed

  • bone expands and looks like ‘ground glass’
  • can be solid or partly cystic

Found in fibrous dysplasia

127
Q

Where does a lytic lesion in bone spread to?

A
  • remains in the bone - expands the bone

- does NOT cause a periostial reaction or enter soft tissue

128
Q

What is a periosteal reaction?

A

Formation of new bone by the periosteum

Usually due to trauma / bone healing

129
Q

What are the symptoms of fibrous dysplasia?

A
  • usually asymptomatic
  • pain
  • risk of fracture
130
Q

What % of tumours are bone tumours?

Incidence rate?

A

1% (ie rare)

1000 new cases per year

131
Q

What % of bone tumours are osteosarcoma?

Incidence rate?

A

15%

150 new cases per year

132
Q

Name a type of bone tumour

A

osteosarcoma

133
Q

What age get osteosarcoma?

A

under 30yrs

Mainly 12-25yrs

134
Q

Is osteosarcoma usually benign or malignant?

A

benign

malignant = rare

135
Q

What is a classic sign of osteosarcoma?

A

periosteal reaction (ie new bone formation)

  • ‘sunburst’ on xray
  • ie perpendicular ossifications from osseous matrix streams from bone
  • can have skip metastases (to other bone / lung)
136
Q

Where does high grade intramedullary osteosarcoma occur most often in the body?

A

> 50% in knees

  • distal femur (32%)
  • proximal tibia (15%)
137
Q

Where does osteosarcoma occur in the bone?

A

> 90% in metaphyseal (contains epiphyseal plate)

138
Q

Where is osteosarcoma unlikely to occur in the body?

A

ribs
vertebrae
peripheral limbs
head and neck

139
Q

What are the three types of osteosarcoma and what % for each?

A

high grade intramedullary osteosarcoma - 80%
periosteal osteosarcoma - 2%
parosteal - 5%

140
Q

What other bone disease is linked to osteosarcoma?

A

osteoporosis

141
Q

What is visible by bone in osteosarcoma?

A

woven bone

cartilage

142
Q

What is high grade intramedullary osteosarcoma?

A

tumour starts in medulla of bone and progresses towards metaphysis at one end

  • v. aggressive
  • both bone destruction (moth eaten) and formation on xrays
  • bone can completely disappear
143
Q

What is the treatment for high grade intramedullary osteosarcoma?

A

Chemotherapy and resection.

144
Q

What is treatment for parosteal osteosarcoma?

A

‘sharp bite’ - remove tumour on the surface of the bone and part of cortex.

  • no chemotherapy
  • no full resection
145
Q

What is parosteal osteosarcoma?

A

bone tumour on surface of the bone

low grade malignancy

146
Q

Where is the new bone formation most easily seen in high grade intramedullary osteosarcoma on xrays?

A

subperiosteal / above cortex

147
Q

What is Codman’s triangle?

A

Visible on xrays in high grade intramedullary osteosarcoma

- area where periosteum is detached from cortex (acute angled triangle)

148
Q

What does high grade intramedullary osteosarcoma look like histologically?

A

osteoblasts

  • disorganised
  • pleomorphic (cells change size/shape)
  • nuclear hyperchromatism

Osteoid / bone
- disorganised

149
Q

What is osteoarthritis?

A

disorder of synovial joints

  • cartilage degeneration / articular cartilage breakdown
  • secondary changes in neighbouring bone

reduced capillaries in joint, therefore reduced cartilage (needs nutrients from external blood vessels), subchondral bone exposed, osteophytes created to replace cartilage

Not a single disease, but a common response to physiologic and metabolic conditions

150
Q

Which part of long bone isn’t vascularised?

151
Q

What are osteophytess?

A

new bone formation at joint to replace lost cartilage

- reduced joint movt

152
Q

Where does osteoarthritis occur?

A

anywhere

- esp knees / femur (hip) / hands / first metatarsophalangeal joint

153
Q

What are the two types of osteoarthritis?

A

Primary osteoarthritis

  • generalised or erosive
  • unknown aetiology

Secondary osteoarthritis
- joints previous damaged (eg gout, rheumatoid arthritis)

154
Q

What are three main symptoms of osteoarthritis?

A
  • pain
  • stiffness in morning (improves throughout day)
  • joint may ‘gel’ with immobility
155
Q

Who is likely to get osteoarthritis?

A

50+yrs

obese

156
Q

What can cause articular cartilage breakdown in the jaw in osteoarthritis? (x4)

A
  • parafunction
  • poor occlusion
  • trauma
  • genetics
157
Q

What are symptoms of articular cartilage breakdown in the jaw in osteoarthritis? (x4)

A
  • crepitation (crackling sound)
  • pain around the ear
  • limited movt
  • bite shifting
158
Q

What happens to the joint space in osteoarthritis?

A

Joint space narrows

  • subchondrial sclerosis
  • subchondrial cyst formation
  • osteophytes
159
Q

What happens when joint space is reduced?

A

reduced movt

Human Disease (10 decks)

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