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MBBS - Year 1 > Clinical skills - Bone pain > Flashcards

Clinical skills - Bone pain Flashcards

1
Q

Osteoporosis

A

A systemic skeletal disease characterised by low bone mass and deterioration of bone tissue, w/ consequent increase in bone fragility and susceptibility to fracture

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2
Q

Commons sites of fractures due to OP

A

Spine
NOF
Wrist

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3
Q

Consequences of hip fractures

A

20% of pts die within a year
50% of survivors are incapacitated
20% require long-term residential care
High risk of future fracture or mortality

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4
Q

Types of vertebral fractures

A

Wedge
Bioconcave
Crush

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5
Q

Non-modifiable risk factors of OP

A

Age (major determinant of hip fracture risk)
Gender
Previos fragility fracture at a characteristic site
Endocrine e.g. early menopause
Parental hx of hip fracture

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6
Q

Modifibale risk factors for OP

A

Low BMI
Lifestyle: smoking, alcohol intake
Low bone density

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7
Q

Drugs increasing the risk of OP

A 
Glucocorticoids 
Epileptics 
Aromatose inhibitors 
Dept injections 
Thiazides
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8
Q

Co-existing comorbdiities increasing risk of OP

A 
DM 
RhA
SLE
Epilepsy 
HIV 
1' hyperparathyoidim
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9
Q

Key determinants of peak bone mass and bone loss

A 
Genes 
Skeletal geometry 
Body weight 
Sex hormones 
Diet 
Exercise 
Racial factors
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10
Q

FRAX

A

Method used to calculate risk of fracture

Similar to Qfracture

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11
Q

Radiological measure of bone

A

Dual-energy X-ray absorptiometry (DEXA)

Low dose of radiation

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12
Q

T score

A

The diff between mean bone density between the pt and a healthy young woman

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13
Q

Normal T score

A

T > 1.0

Low fracture risk

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14
Q

Osteopenic T score

A

T < 1.0 to -2.5

Above avg fracture risk

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15
Q

OP T score

A

T < -2.5

High fracture risk

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16
Q

What creates a very high fracture risk

A

Severe osteoporosis: T < -2.5 plus one or more fractures

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17
Q

Z scores

A

The diff between mean bone density between the pt and a healthy aged-matched woman

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18
Q

Pathophysiology of OP

A

BMU
Coupling of osteoclastic and osteoblastic activity
Imbalance of this relationship

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19
Q

Investigations for OP

A 
FBC 
ESR/CRP 
Serum calcium (albumin)
Alkaline phosphatase 
Liver tests 
Thyroid 
Myeloma screen 
25-hydroxyvitamin D (25OHD)
PTH 
Endocrine: sex hormones/ diabetes/ cortisol 
GI: coeliac disease antibodies 
Markers of bone marrow 
Urine Ca excretion
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20
Q

Strategies for treatment of OP and prevention of fractures

A 
Diet 
Exercise 
Lifestyle 
Treat underlying diseases 
Drug treatment 
Falls intervention (medical, OT, physio)
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21
Q

Types of drug treatment for OP

A

Anti-resorptive
Anabolic
Both

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22
Q

Anti-resorptive drug treatment for OP

A 
Bisphosphonates (alendronate, ibandronate, risedronate, zoledronic acid)
HRT 
Calcium and Vitamin D
Calcitriol 
Raloxifene 
Denosumab
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23
Q

Anabolic drug treatment for OP

A

Intermittent PTH – Teriparatide (injected daily)

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24
Q

Anti-resorptive anabolic drug treatment for OP

A

Strontium ranelate – withdrawn

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25
Q

Duration of drug treatment for OP

A

Uncertain, 3-5 for bisphosphonate or up to 10 yrs. w/ denosumab
Drug holidays?
Consider se of treatment
Steroids –> early bone los

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26
Q

Some s/e of OP drug treatment

A

ONJ (osteonecrosis of jaw)
Atypical no
AF
GI

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27
Q

Issues w/ diagnosing and treating osteoporosis

A

Men
Finding patients w/ fractures – fracture liaison service
Glucocorticoid-induced bone loss – bisphosphonates, little long-term data

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28
Q

Diagnosing OP in men

A

BMD data only rather than fracture reduction
DEXA based on female reference ranges
Look for secondary causes

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29
Q

Osteogenesis Imperfecta

A 
Syndrome of bone fragility due to mutations in type 1 collagen gene
Most cases (85-90%) are caused by a dominant genetic defect 
There are 7 types – type 1 is most common and mildest and type 11 most severe
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30
Q

Variable in OI

A 
Freq of fractures 
Stature 
Coloured sclera 
Laxity of joints and muscles 
Bone deformity 
Scoliosis 
Brittle teeth 
Deafness - otosclerosis 
Respiratory failure 
Collagen abnormalities
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31
Q

What is treatment of OI directed towards

A

Preventing or controlling symptoms
Maximising independent mobility
Developing optimal bone mass and muscle strength

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32
Q

Recommendations for OI incl

A

Care of fractures
Extensive surgical and dental procedures
Physical therapy
Can also use wheelchairs and other mobility aids

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33
Q

Osteomalacia

A

‘Soft bones’
State of the skeleton arising from impairment of mineralisation
Majority arise from disturbance of Vitamin D and phosphate metabolism

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34
Q

Osteoid

A

Bone protein matrix, made-up of mostly type 1 collagen and needs to mineralise.

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35
Q

Forms of vit D

A

D2/ ergocalciferol which is plant derived and consumed in food
D3/ cholecalciferol which is formed from the effect of UV-B sunlight on 7-dehydrocholesterol in skin

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36
Q

Metabolism of vit D

A

Hydoxylated to 25OHD in liver

Hydoxylated to 1,25(OH)2D in liver or can be metabolised in other cells to form 24,25(OH)2D

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37
Q

Actions of calcitriol

A

Facilitates calcium and phosphate absorption from the gut
Triggers osteoblast RANKL –> activates osteoclasts –> releasing calcium into the circulation
Triggers osteoblast production of a number of mediators resulting in laying down bone osteoid
Decreases PTH synthesis and secretion

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38
Q

Where does Ca absorption occur

A

Duodenal

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39
Q

Where does Phosphate absorption occur

A

Entire small intestine

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40
Q

Associations between vit D deficiency and osteomalacia

A

Dark skinned immigrants and their breastfed babies
Elderly and infirm
Partial gastrectomy/ intestinal malabsorption
Chronic liver disease/ chronic renal failure
Anticonvulsant medication
Strict diets e.g. lacto vegetarian
Excessive high factor sunblock
Rare hereditary cases

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41
Q

Clinical features of rickets

A

Growth plate formation is abnormal and becomes wide and irregular

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42
Q

Clinical features of osteomalacia

A

Can exist without symptoms
Bone and muscle pains, however, are common, often non-spp, chronic and widespread
Myalgias and weakness in hip and proximal leg musculature is typical
Bowing of bone

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43
Q

Ddx for osteomalacia

A

FM
Chronic fatigue
Depression

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44
Q

Radiology for osteomalacia

A

Bone softening/ deformity: hourglass thorax, bowing of long bones
Increased fractures, biconcave vertebral bodies
Psuedofractures

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45
Q

Psuedofractures

A 
Lucent band of decreased cortical density 
Perpendicular to bone surface 
Often multiple 
\+/- symmetrical 
\+/- callus formation
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46
Q

Where are psuedofractres typically found

A

Femoral neck
Pelvis
Ribs

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47
Q

Investigations for osteomalacia

A

Bone biochem
25OHD is usually <30 nmol/L (12mg/L) and PTH increased >6.9 pmol/L
Renal function needs testing because low GFR is associated w. phosphate retention
Rarely need bone biopsy

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48
Q

Bone biochem for osteomalacia

A

ACa is usually low
Phosphate may be normal or low
ALP may be normal or increased
Urinary calcium excretion is usually low

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49
Q

Investigations to exclude other condns mimicking osteomalacia

A 
Liver function 
Folate 
Iron studies 
Coeliac 
Autoantibodies 
Autoimmune serology
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50
Q

Treatment for osteomalacia

A

Treat underlying condn
Vitamin D supplements
Ensure adequate dietary Ca

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51
Q

Vit D supplements for osteomalacia

A

Cholecalciferol as a high loading dose (IM) in adults and then lower maintenance dose in adults

52
Q

Hereditary forms of rickets/ osteomalacia

A

Hereditary vit D resistant rickets
Hypophosphataemic vit D resistant rickets/ X-linked hypophosphatemia (XLH)
Autosomal dominant Hypophosphataemic rickets (ADHR)
Pseudo vitamin D deficiency ricket

53
Q

Acquired forms of rickets/ osteomalacia

A

Tumour-induced osteomalacia/ oncogenic Hypophosphataemic osteomalacia

54
Q

Drugs available for the treatment of bone disease

A 
HRT 
Calcium and vit D 
Bisphosphonates
Raloxifene 
PTH 
Strontium ranelate 
Denosumab
55
Q

Main haematological causes of bone pain

A

Infiltration/ destruction of bone by tumour e.g. plasma cell myeloma
Bone infarction e.g. sickle cell disease caused by occlusion of blood vessels
Bleeding into joints e.g. haemophilia
Rapidly proliferating bone marrow e.g. acute leukaemia, G-CSF

56
Q

Paget’s disease

A

Focal disease of bone remodelling

57
Q

Predispostion for Paget’s

A

Genetics – 1st degree relatives of an affected person are 7x more likely
Environment – viral infection e.g. paramyxoviral infection, measles, RSV

58
Q

Epidemiology of Paget’s

A

2nd most common metabolic bone disease
More common in males
Often asymptomatic – unusual after presentation to involve other bones
Mostly seen in pts 40+

59
Q

Pathophysiology of Paget’s

A

Increased osteoblastic and osteoclastic activity
Normal bone is replaced by abnormal haphazard bone – poor bone architecture, expansion of poor-quality bone (weak)
Marrow is replaced w/ fibrous tissue and blood vessels

60
Q

What does Paget’s increase risk of

A

Sarcoma

61
Q

MSK features of Paget’s

A 
Acetabular protrusion 
Bone deformity 
Bone pain 
Fractures 
Spinal stenosis
OA in neighbouring joints
62
Q

Spinal stenosis

A

Bony overgrowth and expansion (not leaving enough space around cord)

63
Q

Why are fractures a feature of Paget’s

A

Bowing of bone creates areas of weakness (10-30% - fissure fractures in LL)

64
Q

Clinical features of MSK

A

MSK
Bone pain
Degenerative joint disease
Deformity – frontal bossing

65
Q

Bone pain in Paget’s

A

Variable in symptoms severity
Long bones, skull, pelvis
Due to periosteum being well innervated

66
Q

Neurological symptoms of Paget’s

A

Related to bony symptoms and compression of neurological structures

Cerebellar dysfunction 
Cranial nerve palsies 
Spina stenosis/ cauda equina 
Deafness - narrowing of canals
Tinnitus 
Para or quadriplegia
67
Q

Cardiovascular features of Paget’s

A 
Increased cardiac output (increased blood flow to bone)
Heart failure 
Aortic stenosis 
Endocardial calcification 
Atherosclerosis
68
Q

Metabolic features of Paget’s

A

Hypercalcaemia
Hyperuricaemia
Immobilisation hypercalciuria
Nephrolithiasis

69
Q

Bones typically affected by Paget’s

A 
Femur 
Spine
Skull 
Sternum 
Pelvis 
But can be any bone in. off
70
Q

Examination for Paget’s

A

Deformity
Tender – starched periosteum
Warm – good blood supply

71
Q

Ddx for Paget’s

A 
Vit D deficiency 
Hyperparathyroidism 
Hyperthyroidism 
Renal osteodystrophy 
Malignancy – e.g. metastatic disease and myeloma
72
Q

Radiographs for Paget’s

A

Bones are typically expanded, show cortical, thickening, coarsened trabeculae and a mixture of lytic and sclerotic areas
Use plain radiographs, CT, MRI, PET CT and isotope bone scans
‘Blade of grass lesion’

73
Q

Complications of Paget’s

A

Deformity and joint pain
Fracture
Osteosarcoma

74
Q

Treatment of Paget’s

A

Analgesia
Treat degenerative bone disease
Bisphosphonates – 5mg zoledronate to reduce osteoclast function
Physiotherapy
Surgery – fractures, joint replacement, spinal stenosis

75
Q

Bisphosphonates for bone disease

A

Poorly absorbed orally
High affinity for bone
Activated by osteoblast acid
Taken up into osteoclast causing apoptosis
One dose is enough to treat for a number of years

76
Q

Benign tumours in bone

A

Osteoid osteoma - severe pain and v small

77
Q

Benign tumors in cartilage

A

Chondroma

Osteochondroma (from growth plate)

78
Q

Benign tumours in fibrous tissue

A

Fibroma

79
Q

Benign tumours in vascular tissue

A

Haemangioma

80
Q

Primary bone malignancy

A

Osteosarcoma

81
Q

Primary cartilage malignancy

A

Chondrosarcoma

82
Q

Primary fibrous tissue malignancy

A

Fibrosarcoma

83
Q

Primary bone marrow malignancy

A

Ewing’s sarcoma

Myeloma

84
Q

Primary vascular malignancy

A

Angiosarcoma

85
Q

Rare bone primaries

A

Osteosarcoma
Chondrosarcoma
Ewing’s tumour

86
Q

Osteosarcoma

A

Most common, usually under 20 yrs.
Affects long bones – growth plate e.g. knee
Radiology – sunburst appearance due to lifting of periosteum and Codman triangle

87
Q

Chrondrosarcoma

A

Half as common, usually in 40s
Painful and progressive
May arise from underlying benign lesions
Most commonly affects axial skeleton

88
Q

Ewing’s tumour

A 
Small round blue cell tumour 
2nd commonest in childhood 
From the medullary (long bones and pelvis) cavity 
Onion on X -ray 
May present w/ metastases
89
Q

Most common bone secondaries

A 
Breast 
Lung 
Prostate 
Kidney 
Thyroid
90
Q

Why do bone secondaries occurs

A

The tumours can lodge in bone

91
Q

Steps to metastasis - bone secondaries

A

Endothelial progenitor cells essential to lead to angiogenesis
Have to induce osteoclasts
Osteoblastic response is variable depending on tumour cell

92
Q

Hx for bone malignancies

A

Bone pain – red flag symptoms
Symptoms from the primary if diagnosed
Functional impairment
Establish co-morbidities and pt expectations and understanding
Look at social circumstances
Previous DXR (radiotherapy) and chemotherapy

93
Q

Examination for bone cancers

A

Consistency w/ history and expected findings
Beware co-existing pathologies
Scarring and skin changes
Neurology and vascularity
May not be any abnormalities – high index of suspicion

94
Q

Investigations for bone cancers

A 
Serum biochem 
Plain X-rays - essential 
Isotope bone scan - highlights areas of metabolic activity 
CT - good for structure 
MRI - defines soft tissue involvement 
Bone biopsy
95
Q

X-rays for bone caners

A

Shows bone structure
Lysis/ sclerosis
Must include a whole, long bone

96
Q

Isotope bone scan for bone cancers

A

No value in assessing structure
Limited use in myeloma
Beware sacral lesions
Darker areas show glucose uptake - could be malignancy or growth plates in a child (symmetrical)

97
Q

MRI for bone cancers

A

Essential in spinal disease
“Skip lesions” in long bones
Evaluation of suspected 1’ bone tumours

98
Q

Management of 1’ bone tumours

A

Treat as primary bone tumour until proven otherwise

If primary bone – d/w supra-regional service for biopsy there

99
Q

Management for metastasis

A

Pain – analgesia, bisphosphonates, DXT, surgery
Functional loss – related to pain
Skeletal integrity – unlikely to benefit from surgery

100
Q

Achieving skeletal integrity in bone cancer

A

Intramedullary nails
Joint replacement
Plate/ screw constructs
Cement augmentation

101
Q

Presentation of pathological vertebral fracture

A

Thoracic or lumbar back pain after a minor fall Frequently multiple vertebrae
Loss of height and kyphotic deformity of the spine
No pain but complaints of shrinking or becoming round-shouldered

102
Q

Drug therapy for pathological vertebral fractures

A 
Bisphosphonates - 1st line
Denosumab - 2nd line 
Teriparatide 
Raloxifene
Calcitonin
103
Q

Presentation of traumatic spinal fractures

A

Occur with high energy trauma

Vertebrae can be crushed in healthy adults after a vertical fall from a standing height

104
Q

Aetiology of traumatic spinal fractures

A

RTA
Diving into a shallow pool
Falls from above standing height

105
Q

Investigation of traumatic spinal fractures

A

Cervical spine CT scan
Thoracolumbar spine imaging
MRI - ligament and spinal cord damage
X-rays

106
Q

Management of traumatic spinal fractures

A

Spinal immobilisation devices are left in place

107
Q

Treatment of traumatic spinal fractures

A

Stable fractures can be mobilized

Unstable fractures require immobilization, bracing or internal fixation

108
Q

Prognosis of traumatic spinal fractures

A

Pt w/ spinal cord damage and neurological symptoms have a poor prognosis and often require extensive rehabilitation on a spinal unit

109
Q

Spinal shock

A

Period of altered distal function with loss of spincteric control and reflexes (inadequate tissue perfusion after injury)

110
Q

Pathological fractures

A

One that requires minimal force to sustain, as a result of underlying pathology and weakness in the bone

111
Q

Most common locations for pathological fractures

A

Vertebral Bodies
Neck of Femur
Wrist (Colle’s Fracture)
Humerus/Shoulder

112
Q

Condns predisposing pathological fractures

A 
Osteoporosis
Osteomyelitis
Cancer
Osteomalacia
Paget’s Disease 
Non-Cancerous Tumours and Cysts
Hyperparathyroidism 
Osteogenesis Imperfecta
113
Q

Presentation of pathological fractures

A

Mild to severe pain near the broken bone.
Bruising, tenderness, and swelling near the broken bone.
Numbness, tingling, or weakness near the broken bone.
Loss of movement.
Several days of pain can precede the fracture

114
Q

Prevention of pathological fractures

A

Exercise on a regular basis to keep muscles strong and improve bone health.
Get enough vitamin D and calcium.
Use prosthetics or assistive devices, such as supportive shoes, a walking stick, or a zimmer-frame.
Avoid high-intensity activities.

115
Q

Prognosis of pathological fractures

A

Cancer - marker of end-stage
Other condns - suggests worsening or current treatment isn’t effective
Risk of delayed-union, malunion or non-union - further issues

116
Q

When does Type I osteoporosis develop

A

Between the ages of 50 and 70 when the protective effects of oestrogen in women begin to fade
Can also occur after gonadal failure in men

117
Q

Common fractures in Type I osteoporosis

A

Wrist and spine

118
Q

When does Type II osteoporosis develop

A

After 70 years

Sometimes referred to as senile osteoporosis

119
Q

Common fractures in Type II osteoporosis

A

Hip and spine

120
Q

What types of bone does Type II osteoporosis affect

A

Cortical bone

121
Q

Technetium bone scan

A

Sensitive to areas of unusual bone re-building activity

Good for Paget’s

122
Q

Where does OP typically occur

A

Metabolically active bony trabeculae

123
Q

Pagets vs bone malignancy

A

Both are progressive but pts are generally unwell with malignancies

124
Q

Lab values for OP

A

Normal Ca
Normal P
Normal ALP
Normal PTH

125
Q

Lab values for osteomalacia

A

Decreased Ca
Decreased P
Increased ALP
Increased PTH

126
Q

Lab values for Paget’s

A

Normal Ca
Normal P
Increased ALP
Normal PTH

127
Q

Changes in diet to improve bone strength

A

High in calcium rich foods such as milk, cheese, yogurt, white bread, oily fish
High in protein rich food such as meat, fish, milk, cheese and yogurt
High in omega-3 rich food such as oily fish
High in vitamin K rich foods such as green leafy vegetables

MBBS - Year 1 (93 decks)

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