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Y3 IWB > PATHOLOGY- Bone Disorders > Flashcards

PATHOLOGY- Bone Disorders Flashcards

1
Q

What is bone?

A

Ridged inflexible mineralised connective tissue

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2
Q

What is bone mineralised by?

A

Calcium and phosphate salts

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3
Q

Why are bones important structurally and metabolically ?

A

Structural
1. Provides physical integrity/ support
2. Protects squishy organs
3. Allows for insertion of muscles and tendons

Metabolic
1. Provides minerals
2. Important in haematopoiesis

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4
Q

What minerals does bone provide

A
  1. Calcium
  2. Phosphorous
  3. Magnesium
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5
Q

What is haematopoiesis?

A

It is the formation, development and maturation of blood cells in adult bone marrow

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6
Q

Where does haematopoiesis occur in adults?

A

Bone marrow

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7
Q

Name the parts that make up bone

A
  1. Non cellular mineralised matrix
  2. Cells that maintain the matrix
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8
Q

What is the non cellular mineralised matrix that makes up bone made up of?

A
  1. Type I collagen- osteoid
  2. Calcium phosphate (calcium hydroxyapatite)
  3. Regulatory protein and growth factors
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9
Q

What is type 1 collagen in bone called?

A

Osteoid (extraceulluar matrix in bone)

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10
Q

List the cells that maintain the matrix in bone

A
  1. Osteoblasts
  2. Osteocytes
  3. Osteoclasts
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11
Q

Why is mineralisation critical?

A

The osteoid would be soft and bendy if it wasn’t mineralised

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12
Q

What do osteoblasts do?

A

They build up the bone

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13
Q

What is the origin of osteoblasts

A

Mesenchymal origin

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14
Q

What is the function of osteoblasts?

A
  1. They secrete osteoid
  2. Needed for mineralisation
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15
Q

What are osteocytes

A

Inactive osteoblasts that are trapped in the bone

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16
Q

What is the origin of osteoclasts

A

Macrophage lineage

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17
Q

What do osteoclasts do?

A

They are involved in bone resorption and remodelling

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18
Q

How can bone be categorised?

A
  1. Maturity type
  2. Location type
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19
Q

Name the different types of bone based on maturity

A
  1. Woven bone (immature bone)
  2. Lamellar bone
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20
Q

Describe woven bone

A

It is immature bone as the osteoid collagen is random
It is remodelled into lamellar bone

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21
Q

What causes the random osteoid formation in woven bones?

A

Rapid bone turnover by osteoblasts

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22
Q

What is woven bone remodelled into?

A

Lamellar bone

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23
Q

Where is woven bone found?

A

Fractures
Fetal developemt

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24
Q

Describe lamellar bone

A

Made up of parallel bands/ sheets of lamellae

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25
Q

Where is lamellar bone found?

A

Makes up the majority of normal healthy adult bone

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26
Q

What are the two different types of lamellar bone?

A

Compact/cortical bone
Cancellous/ trabecular bone

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27
Q

Which type of bone is stronger from woven and lamellar?
WHY?

A

Lamellar bone is much stronger due to regular arrangement of lamellae

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28
Q

Name the different types of bone based on location?

A
  1. Cortical/ compact
  2. Cancellous. trabecular
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29
Q

Describe Cortical bone

A

Forms hard outer shell and regular shape
It is highly organised
Follows the Haversian system

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30
Q

What system does cortical bone follow?

A

The Haversian system

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31
Q

What is the Haversian system

A

Columns of lamellar bone (v compact and dense)

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32
Q

Describe cancellous/ trabecular bone

A

Spongy non structural “filler” bone

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33
Q

What is found in the spaces between cancellous bone?

A

Bone marrow

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34
Q

How are the different bone types organised?

A

Cortical bone surrounds cancellous bone

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35
Q

Why is bone remodelling important?

A
  1. To maintain bone strength as your bones constantly suffer from trauma like micro fractures through the day
  2. To be able to release metabolites
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36
Q

List the stages of the bone remodelling cycle

A
  1. Activation
  2. Resorption
  3. Reversal
  4. Formation
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37
Q

How is bone remodelling activated?

A

By hormones or damage

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38
Q

What happens when bone remodelling is activated by hormones of damage>

A
  1. Osteoblasts are activated
  2. Cytokines are released
  3. Osteoclasts stick to the surface of the bone
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39
Q

What is the next stage after activation in the bone remodelling cycle

A

Resorption

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40
Q

What happens in the Resorption stage of the bone remodelling cycle

A
  1. Mono nuclear osteocytes that are stuck to the surface of bone secrete substances
  2. These substances reabsorb bone
  3. Create pits on the surface
  4. Mono nuclear osteocytes undergo apoptosis or migrate
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41
Q

What is the next stage after Resorption in the bone remodelling cycle

A

Reversal

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42
Q

What happens in the reversal stage of the bone remodelling cycle

A

Monocytes clear debris for bone formation

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43
Q

What is the last stage after reversal in the bone remodelling cycle

A

formation

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44
Q

What happens in the formation stage of the bone remodelling cycle

A
  1. Osteoblasts are recruited
  2. They secrete osteoid matrix and initiate mineralisation
  3. Osteoblasts sit on the new bone
  4. some undergo apoptosis and some are incorporated as osteocytes
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45
Q

What is another name for immature bones?

A

Woven bone

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46
Q

What is another name for mature bones

A

Lamellar bone

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47
Q

Compact and cancellous bone are both what type of bone?

A

Lamellar bone

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48
Q

What is osteoarthritis?

A

Progressive erosion of articular cartridge

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49
Q

Is osteoarthritis just erosion?

A

No it is a complex imbalance of damage and repairs

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50
Q

What happens in osteoarthritis

A

Cartilage is worn away and underlying bone is exposed
This leads to damage and the formation of cysts / osteophytes causing inflammation pain
This ultimately leads to narrowing joint space

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51
Q

What are osteophytes

A

Abnormal growth in bone

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52
Q

How common is osteoarthritis?

A

uptown 80% of over 65s have evidence of having osteoarthritis

but only 1/4 have symptoms

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53
Q

What are some of the symptoms of osteoarthritis

A
  1. Pain/ functional limitation
  2. Morning stiffness
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54
Q

What are some of the signs of osteoarthritis

A
  1. Crepitus (crunchy)
  2. Restricted movements
  3. Bony enlargement
  4. Instability/ muscle wasting
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55
Q

What are the differences between signs and symptoms

A

Signs are something you observe as a
clinical
Symptoms are things patients present with

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56
Q

What is a primary cause for disease?

A

Unknown cause or unknown origin for a disease

no underlying cause for the disease

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57
Q

Give some secondary causes of osteoarthritis

A
  1. Pre existing joint damage
  2. Metabolic disease
  3. Systemic disease
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58
Q

How do you investigate osteoarthritis

A
  1. Blood tests to make sure rheumatoid factor is negative and to look for bone markers
  2. X-ray will show cartilage loss, joint space narrowing and cysts
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59
Q

What would a raised rheumatoid factor suggests?

A

the patient may have rheumatoid arthritis

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60
Q

How do we manage osteoarthritis

A
  1. Physical: weight loss, hydrotherapy
  2. Medications: NSAIDS, steroids
  3. Surgery: joint replacement
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61
Q

What is rheumatoid arthritis?

A

It is an autoimmune disease consisting of persistent inflammation (synovitis) leading to chronic symmetrical

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62
Q

List the 3 factors that strongly influences the progression of rheumatoid arthritis

A
  1. Gender: women at higher risk
  2. Genetic: associated with human leucocyte antigen (HLA)
  3. Environmental: periodontal disease may contribute to it
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63
Q

Who is most affected by rheumatoid arthritis?

A

Younger (30-50)
x3 more women

rarer 1%

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64
Q

What does synovitis

A

Inflammation

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65
Q

What happens in rheumatoid arthritis

A

Citrullination of self antigens leading to loss of normal tolerance as the antigens are no longer recognised as self cells
Auto immune response occurs leading to inflammation leading to damage

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66
Q

What is citrullination?

A

Protein modification from arginine to citrulline

67
Q

What are the differences between rheumatoid arthritis and osteoarthritis?

A

Rheumatoid arthritis is an autoimmune synovitis leading to mass formation and sticking of joins together
Osteoarthritis is just breakdown of cartridge leading to damage to bone

68
Q

What is ankylosis

A

Abnormal stiffening/ immobility in joint due to bony fusion

69
Q

How do we investigate rheumatoid arthritis

A
  1. Blood tests: bony markers present and look for anti citrullinated peptide antibodies. Can also look for rheumatoid factor
  2. X rays show synovitis and joint damage
70
Q

How do we manage rheumatoid arthritis

A

Theres no cure

Can give them anti inflammatories, steroids, anti-TNF, disease modifying anti rheumatic drugs (DMARD)

71
Q

What is Paget’s disease?

A

A disorder of bone turnover/ remodelling

72
Q

What happens in paget’s disease?

A

Increased osteoclastic bone resorption leading to increased new bone formation
Formation happens at a faster rate than resorption but woven bone is made

73
Q

What is the problem with increased formation of woven bone?

A

Woven bone is weaker than lamellar bone

This can leaf to deformity and increased risk of fracture

74
Q

What is the aetiology of paget’s disease

A

Unknown aetiology
Suggested to be a combination of environmental and genetic
Mutation in osteoblast gene

75
Q

How is paget’s disease presented in most people?

A

60-80% asymptomatic
Some present with bone pain/ joint pain or bone deformities

76
Q

If Paget’s disease is mainly asymptotic how is it diagnosed?

A

Usually patients come in for an X-ray and the x ray shows changes

77
Q

Describe how the bone in patients with Paget’s disease may look

A

Cotton wool like appearance (hypercementosis)

78
Q

What are some of of the side effects of having Paget’s disease?

A
  1. Nerve compression leading to deafness
  2. Spinal stenosis
  3. Hydrocephalus
  4. Cardiac failure, myocardial hypertrophy due to increased blood flow
  5. Pathological fractures
  6. Osteosarcoma
79
Q

What is hypercementosis

A

Excessive cementum on the roots of teeth

80
Q

Name the 3 stages of paget’s disease

A
  1. Hot osteolytic phase
  2. Mixed phase
  3. Cold osteosclerotic phase
81
Q

What happens in the hot osteolytic phase of Paget’s disease?

A

Osteoclasts are breaking down bone

82
Q

What happens in the mixed phase of Paget’s disease?

A

Both osteoclasts and osteoblasts are working

83
Q

What happens in the Cold osteosclerotic phase of Paget’s disease?

A

Burn out inactive phase but bone is still weak and woven

84
Q

How do we treat paget’s disease?

A

With bisphosphonates

85
Q

How do biphosphonates work?

A
  1. Inhibit osteoclasts recruitment
  2. Inhibit osteoclast activity
  3. Slow bone loss
86
Q

Other than Paget’s disease what else can biphosphonates treat?

A

Used in osteoporosis

87
Q

What is a serious side effect of using biphosphonates?

A

BRONJ
Bisphosphonate
Related
Osteonecrosis of
Jaw

88
Q

What is osteomyelitis?

A

Inflammation of bone / bone marrow

89
Q

What is osteomyelitis almost always due to?

A

Virtually always secondary to infection

90
Q

How do most people develop osteomyelitis

A
  1. Haematogenous spread (through blood)
  2. Extension from adjacent site
  3. Direct implantation
91
Q

What is the most common cause for children developing osteomyelitis

A

Haematogenous spread

92
Q

What is the most common cause for adults developing osteomyelitis?

A

Fractures
Surgical infections
Diabetic foot

93
Q

Describe the clinical presentation of osteomyelitis

A
  1. Fever
  2. Localised bone pain
  3. Overlying tenderness/ erythema
94
Q

How do you diagnose osteomyelitis

A
  1. MRI / bone scan
  2. Blood cultures
  3. Bone culture and sensitivity test
95
Q

How do we treat osteomyelitis

A

Immobilise
Antibiotics
Can drain or make excision

96
Q

How common is chronic osteomyelitis

A

Occurs in 5-25% of cases

97
Q

What is the cause of osteomyelitis of the jaw and when does it happen?

A

It has a poly microbial cause and is secondary to odontogenic infection

98
Q

Name some different types of osteomyelitis

A
  1. Chronic osteomyelitis
  2. Osteomyelitis of the jaw
  3. Tuberculosis osteomyelitis
99
Q

what is tuberculous osteomyelitis

A

Haematogenous spread from reactivated primary TB focus
Spine involvement = (Pott’s disease - Percival Pott )

100
Q

Define fractures

A

Loss of bone integrity

101
Q

What can fractures be caused by?

A

Mechanical injury and/or diminished bone strength

102
Q

Give examples of different types of fractures

A
  1. Simple
  2. Compound
  3. Comminuted
  4. Displaced
  5. Stress
  6. Greenstick
  7. Pathologic
103
Q

what is a simple fracture

A

skin intact

104
Q

What is a compound fracture?

A

A fracture where bone is exposed

105
Q

what is a comminuted fracture

A

fragmentation

106
Q

what is a displaced fracture

A

misaligned ends

107
Q

What is a stress fracture

A

A slow developing fracture due to repeated repetitive loads

108
Q

What is a greenstick fracture

A

Partial fracture through bone

109
Q

What is a pathologic fracture

A

Weakened bone due to existing disease

110
Q

List the 3 phases of fracture healing

A
  1. Inflammatory phase
  2. Reparative phase
  3. Remodelling phase
111
Q

What is another name for the reparative phase of fracture healing

A

Endochondral

112
Q

What happens in the inflammatory phase of fracture healing

A
  1. Haematoma forms
  2. Macrophages, neutrophils and platelets release cytokines
  3. Fibroblasts and mesenchymal cells go to fracture site
  4. Granulation tissue forms around the fracture ends
  5. Neurovascularisation
  6. Osteoblasts, chondrocytes, fibroblasts proliferate
  7. Fibrosis results in callus formation
113
Q

What are the benefits of a haematoma forming?

A

Stems blood flow from site of injury and is also a source of haemopoietic cells and growth factors

114
Q

What is granulation tissue?

A

Vascular tissue

115
Q

What does the inflammatory phase ultimately lead to the formation of?

116
Q

What happens in the reparative phase of bone healing

A
  1. Primary callus forms quickly
  2. Cartilage provides provisional stabilisation
  3. Endochondral ossification converts soft callus to hard callus
117
Q

Why is the reparative phase also known as the endochondral phase

A

As endochondral ossification converts soft callus into hard callus

118
Q

What is soft callus?

119
Q

What is hard callus

A

Woven bone

120
Q

What happens in the remodelling phase of bone healing

A
  1. Bony callus tissue is resorbed
  2. Osteoblast and osteoclast remodel to bones original cortex structure
121
Q

What is osteonecrosis?

A

Infarction of bone/marrow

122
Q

What is osteonecrosis also known as?

A

Avascular, aseptic or ischaemic necrosis

123
Q

What are most cases of osteonecrosis due to?

A

Alcohol
Steroids
Fractures

124
Q

What is the underlying cause of ALL cases of osteonecrosis?

A

Vascular insufficiency through mechanical injury to blood vessels, thromboembolism, external pressure

125
Q

how do you get osteonecrosis in the head and neck

A

BRONJ/MRONJ
traumatic injury
radiation (osteoradionecrosis)

126
Q

Is osteonecrosis due to infection?

A

NO it is aseptic

127
Q

What do patients with osteonecrosis osteoarthritis display?

A

Joint pain (shoulder or hip)
Can be asymptomatic

128
Q

What will an MRI of osteonecrosis show?

A

Bone marrow oedema / plain x ray

129
Q

How do we manage osteonecrosis

A
  1. Surgical decompression
  2. Grafts
  3. Joint replacement
130
Q

What controls serum calcium in the body

A

Vitamin D
Parathyroid hormone

131
Q

What is released if calcium levels are low?

A

Parathyroid hormone

132
Q

How does the parathyroid hormone help increase low calcium levels

A
  1. Increased osteoclast bone resorption
  2. Increased intestinal calcium absorption
  3. Increased synthesis of 1,25-dihydroxyvitamin D3
  4. Increased renal tubular resorption Ca
  5. Increased renal excretion of PO4
133
Q

How does vitamin D increase calcium levels?

A

Increases intestinal absorption of calcium which increases mineralisation of bone

134
Q

What effect does serum calcium have on vitamin D?

A

When there is low calcium levels, there is Vitamin D induced bone resorption which then increases calcium levels
decreases bone resorption with HIGH serum calcium

135
Q

what happens to calcium in vitamin d defiicnecy and what does this cause

A
  1. Vitamin D deficiency causes low Ca levels
  2. This increases PTH
  3. This increases calcium but lowers PO4

Vit D increases bone resportion with low serum calcium but does opposite with high serum calcium

136
Q

What is another term for rickets

A

Osteomalacia

137
Q

What causes rickets?

A

Defective mineralisation

138
Q

What is rickets

A

Defective mineralisation of epiphyseal plate in children that can lead to weakened (bendy) bones

139
Q

What is osteomalacia?

A

Defective mineralisation of epiphyseal plate in adults that can lead to weak bone formation during remodelling and makes the patient vulnerable to fractures

140
Q

What is the aetiology of rickets/ osteomalacia

A

Anything that interferes with bone mineralisation Eg

  1. Deficient intake or absorption of vitamin D
  2. Defective 1alpha hydroxylation eg renal failure
  3. Primary renal phosphate wasting
  4. Inhibitors or mineralisation
  5. Defective vitamin D receptors
141
Q

What causes vitamin D deficiency?

A
  1. Nutritional (dietary, inadequate exposure to sunlight)
  2. Malabsorption e.g. coeliac disease, IBD
  3. Vitamin D dependent rickets (VDDR) type 1 and 2
142
Q

What happens in vitamin D deficiency?

A
  1. Reduced serum calcium phosphate
  2. Parathyroid hormone secreted causing bone to demineralise
  3. Increased serum calcium
  4. Bone is now poorly mineralised
143
Q

Give some dentinal complications of rickets

A
  1. Familial hypophospataemia
  2. Hypoplasia
  3. Missing teeth
144
Q

Give some signs and symptoms of Familial hypophospataemia

A
  1. Abnormally large pulp chamber
  2. Thin enamel
  3. Dentinal defects/ globular dentin
  4. Dentinal abscesses more common
145
Q

What is hyperparathyroidism?

A

Anything that causes pathological increase of parathyroid hormone

146
Q

What can increased parathyroid hormone lead to ?

A
  1. Increased osteoclast bone resorption
  2. Increased intestinal calcium absorption
  3. Increased synthesis of 1,25- dihydroxyvitamin D3
  4. Increased renal tubular resorption of calcium
  5. Increased renal excretion of PO4
147
Q

Name the 3 types of hyperparathyroidism

A
  1. Primary: Autonomous hyperparathyroidism
  2. Secondary: Compensatory hyper secretion
  3. Tertiary: persistent hyperparathyroidism even when decreased calcium corrected
148
Q

What is primary hyperparathyroidism the most common cause of?

A

Asymptomatic hypercalcemia

149
Q

What is primary hyperparathyroidism caused by?

A
  1. Adenoma
  2. Hyperplasia
  3. Malignancy
150
Q

What symptoms do patients with primary hyperparathyroidism present with?

A
  1. Bone disease/ bone pain (BONE)
  2. Renal stones (STONES)
  3. GI disturbances including constipation, nausea, peptic ulcers (GROANS)
  4. CNS alterations eg depression and seizures(MOANS)
151
Q

What is secondary hyperparathyroidism categorised by?

A

Any condition that causes reduced calcium leading to increased para thyroid hormone

152
Q

What is osteogenesis imperfecta also known as?

A

Brittle bone disease

153
Q

What is osteogenesis imperfecta caused by?

A

Gene mutation affecting the type 1 collagen gene (osteoid)

154
Q

What is osteogenesis imperfecta usually presented with?

A

Increased fractures (can start in utero)

155
Q

List some dentinal manifestations of osteogenesis imperfecta

A

Dentinogeneisis imperfecta type II

156
Q

Name the 2 types of ossification

A
  1. Endochondral
  2. Intramembranous
157
Q

Which type of ossification occurs in the maxilla and mandible?

A

Intramembranous ossification

158
Q

What is Intramembranous ossification

A

Deposition of bone within primitive mesenchymal tissue

159
Q

What is achondroplasia due to?

A

FGFR3 gene mutation

160
Q

What is the purpose of the FGFR 3 gene

A

It inhibits endochondral growth

161
Q

What happens with the FGFR 3 gene undergoes gene mutation?

A

Can impair cartilaginous growth

162
Q

What does FGFR3 stand for

A

Fibroblast growth factor receptor

163
Q

What can patients with achondroplasia present with?

A

Short limbs
Normal skull/ trunk

164
Q

List some craniofacial issues patients with achondroplasia may suffer from

A
  1. Macrocephaly / prominent forehead
  2. Flattened/ depressed nasal bridge
  3. Hypoplasia of midfacial structures
  4. Maxilarry hypoplasia
  5. Relative overgrowth of the mandible
  6. Narrowing of anterior palate, open Bute
  7. Orthodontic intervention

Y3 IWB (31 decks)

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