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
2
Q
Commons sites of fractures due to OP
A
Spine
NOF
Wrist
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
4
Q
Types of vertebral fractures
A
Wedge
Bioconcave
Crush
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
6
Q
Modifibale risk factors for OP
A
Low BMI
Lifestyle: smoking, alcohol intake
Low bone density
7
Q
Drugs increasing the risk of OP
A
Glucocorticoids Epileptics Aromatose inhibitors Dept injections Thiazides
8
Q
Co-existing comorbdiities increasing risk of OP
A
DM RhA SLE Epilepsy HIV 1' hyperparathyoidim
9
Q
Key determinants of peak bone mass and bone loss
A
Genes Skeletal geometry Body weight Sex hormones Diet Exercise Racial factors
10
Q
FRAX
A
Method used to calculate risk of fracture
Similar to Qfracture
11
Q
Radiological measure of bone
A
Dual-energy X-ray absorptiometry (DEXA)
Low dose of radiation
12
Q
T score
A
The diff between mean bone density between the pt and a healthy young woman
13
Q
Normal T score
A
T > 1.0
Low fracture risk
14
Q
Osteopenic T score
A
T < 1.0 to -2.5
Above avg fracture risk
15
Q
OP T score
A
T < -2.5
High fracture risk
16
Q
What creates a very high fracture risk
A
Severe osteoporosis: T < -2.5 plus one or more fractures
17
Q
Z scores
A
The diff between mean bone density between the pt and a healthy aged-matched woman
18
Q
Pathophysiology of OP
A
BMU
Coupling of osteoclastic and osteoblastic activity
Imbalance of this relationship
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
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)
21
Q
Types of drug treatment for OP
A
Anti-resorptive
Anabolic
Both
22
Q
Anti-resorptive drug treatment for OP
A
Bisphosphonates (alendronate, ibandronate, risedronate, zoledronic acid) HRT Calcium and Vitamin D Calcitriol Raloxifene Denosumab
23
Q
Anabolic drug treatment for OP
A
Intermittent PTH – Teriparatide (injected daily)
24
Q
Anti-resorptive anabolic drug treatment for OP
A
Strontium ranelate – withdrawn
25
Duration of drug treatment for OP
Uncertain, 3-5 for bisphosphonate or up to 10 yrs. w/ denosumab
Drug holidays?
Consider se of treatment
Steroids --> early bone los
26
Some s/e of OP drug treatment
ONJ (osteonecrosis of jaw)
Atypical no
AF
GI
27
Issues w/ diagnosing and treating osteoporosis
Men
Finding patients w/ fractures – fracture liaison service
Glucocorticoid-induced bone loss – bisphosphonates, little long-term data
28
Diagnosing OP in men
BMD data only rather than fracture reduction
DEXA based on female reference ranges
Look for secondary causes
29
Osteogenesis Imperfecta
```
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
```
30
Variable in OI
```
Freq of fractures
Stature
Coloured sclera
Laxity of joints and muscles
Bone deformity
Scoliosis
Brittle teeth
Deafness - otosclerosis
Respiratory failure
Collagen abnormalities
```
31
What is treatment of OI directed towards
Preventing or controlling symptoms
Maximising independent mobility
Developing optimal bone mass and muscle strength
32
Recommendations for OI incl
Care of fractures
Extensive surgical and dental procedures
Physical therapy
Can also use wheelchairs and other mobility aids
33
Osteomalacia
'Soft bones’
State of the skeleton arising from impairment of mineralisation
Majority arise from disturbance of Vitamin D and phosphate metabolism
34
Osteoid
Bone protein matrix, made-up of mostly type 1 collagen and needs to mineralise.
35
Forms of vit D
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
36
Metabolism of vit D
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
37
Actions of calcitriol
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
38
Where does Ca absorption occur
Duodenal
39
Where does Phosphate absorption occur
Entire small intestine
40
Associations between vit D deficiency and osteomalacia
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
41
Clinical features of rickets
Growth plate formation is abnormal and becomes wide and irregular
42
Clinical features of osteomalacia
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
43
Ddx for osteomalacia
FM
Chronic fatigue
Depression
44
Radiology for osteomalacia
Bone softening/ deformity: hourglass thorax, bowing of long bones
Increased fractures, biconcave vertebral bodies
Psuedofractures
45
Psuedofractures
```
Lucent band of decreased cortical density
Perpendicular to bone surface
Often multiple
+/- symmetrical
+/- callus formation
```
46
Where are psuedofractres typically found
Femoral neck
Pelvis
Ribs
47
Investigations for osteomalacia
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
48
Bone biochem for osteomalacia
ACa is usually low
Phosphate may be normal or low
ALP may be normal or increased
Urinary calcium excretion is usually low
49
Investigations to exclude other condns mimicking osteomalacia
```
Liver function
Folate
Iron studies
Coeliac
Autoantibodies
Autoimmune serology
```
50
Treatment for osteomalacia
Treat underlying condn
Vitamin D supplements
Ensure adequate dietary Ca
51
Vit D supplements for osteomalacia
Cholecalciferol as a high loading dose (IM) in adults and then lower maintenance dose in adults
52
Hereditary forms of rickets/ osteomalacia
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
Acquired forms of rickets/ osteomalacia
Tumour-induced osteomalacia/ oncogenic Hypophosphataemic osteomalacia
54
Drugs available for the treatment of bone disease
```
HRT
Calcium and vit D
Bisphosphonates
Raloxifene
PTH
Strontium ranelate
Denosumab
```
55
Main haematological causes of bone pain
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
Paget's disease
Focal disease of bone remodelling
57
Predispostion for Paget's
Genetics – 1st degree relatives of an affected person are 7x more likely
Environment – viral infection e.g. paramyxoviral infection, measles, RSV
58
Epidemiology of Paget's
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
Pathophysiology of Paget's
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
What does Paget's increase risk of
Sarcoma
61
MSK features of Paget's
```
Acetabular protrusion
Bone deformity
Bone pain
Fractures
Spinal stenosis
OA in neighbouring joints
```
62
Spinal stenosis
Bony overgrowth and expansion (not leaving enough space around cord)
63
Why are fractures a feature of Paget's
Bowing of bone creates areas of weakness (10-30% - fissure fractures in LL)
64
Clinical features of MSK
MSK
Bone pain
Degenerative joint disease
Deformity – frontal bossing
65
Bone pain in Paget's
Variable in symptoms severity
Long bones, skull, pelvis
Due to periosteum being well innervated
66
Neurological symptoms of Paget's
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
Cardiovascular features of Paget's
```
Increased cardiac output (increased blood flow to bone)
Heart failure
Aortic stenosis
Endocardial calcification
Atherosclerosis
```
68
Metabolic features of Paget's
Hypercalcaemia
Hyperuricaemia
Immobilisation hypercalciuria
Nephrolithiasis
69
Bones typically affected by Paget's
```
Femur
Spine
Skull
Sternum
Pelvis
But can be any bone in. off
```
70
Examination for Paget's
Deformity
Tender – starched periosteum
Warm – good blood supply
71
Ddx for Paget's
```
Vit D deficiency
Hyperparathyroidism
Hyperthyroidism
Renal osteodystrophy
Malignancy – e.g. metastatic disease and myeloma
```
72
Radiographs for Paget's
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
Complications of Paget's
Deformity and joint pain
Fracture
Osteosarcoma
74
Treatment of Paget's
Analgesia
Treat degenerative bone disease
Bisphosphonates – 5mg zoledronate to reduce osteoclast function
Physiotherapy
Surgery – fractures, joint replacement, spinal stenosis
75
Bisphosphonates for bone disease
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
Benign tumours in bone
Osteoid osteoma - severe pain and v small
77
Benign tumors in cartilage
Chondroma
| Osteochondroma (from growth plate)
78
Benign tumours in fibrous tissue
Fibroma
79
Benign tumours in vascular tissue
Haemangioma
80
Primary bone malignancy
Osteosarcoma
81
Primary cartilage malignancy
Chondrosarcoma
82
Primary fibrous tissue malignancy
Fibrosarcoma
83
Primary bone marrow malignancy
Ewing's sarcoma
| Myeloma
84
Primary vascular malignancy
Angiosarcoma
85
Rare bone primaries
Osteosarcoma
Chondrosarcoma
Ewing's tumour
86
Osteosarcoma
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
Chrondrosarcoma
Half as common, usually in 40s
Painful and progressive
May arise from underlying benign lesions
Most commonly affects axial skeleton
88
Ewing's tumour
```
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
Most common bone secondaries
```
Breast
Lung
Prostate
Kidney
Thyroid
```
90
Why do bone secondaries occurs
The tumours can lodge in bone
91
Steps to metastasis - bone secondaries
Endothelial progenitor cells essential to lead to angiogenesis
Have to induce osteoclasts
Osteoblastic response is variable depending on tumour cell
92
Hx for bone malignancies
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
Examination for bone cancers
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
Investigations for bone cancers
```
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
X-rays for bone caners
Shows bone structure
Lysis/ sclerosis
Must include a whole, long bone
96
Isotope bone scan for bone cancers
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
MRI for bone cancers
Essential in spinal disease
“Skip lesions” in long bones
Evaluation of suspected 1’ bone tumours
98
Management of 1' bone tumours
Treat as primary bone tumour until proven otherwise
| If primary bone – d/w supra-regional service for biopsy there
99
Management for metastasis
Pain – analgesia, bisphosphonates, DXT, surgery
Functional loss – related to pain
Skeletal integrity – unlikely to benefit from surgery
100
Achieving skeletal integrity in bone cancer
Intramedullary nails
Joint replacement
Plate/ screw constructs
Cement augmentation
101
Presentation of pathological vertebral fracture
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
Drug therapy for pathological vertebral fractures
```
Bisphosphonates - 1st line
Denosumab - 2nd line
Teriparatide
Raloxifene
Calcitonin
```
103
Presentation of traumatic spinal fractures
Occur with high energy trauma
| Vertebrae can be crushed in healthy adults after a vertical fall from a standing height
104
Aetiology of traumatic spinal fractures
RTA
Diving into a shallow pool
Falls from above standing height
105
Investigation of traumatic spinal fractures
Cervical spine CT scan
Thoracolumbar spine imaging
MRI - ligament and spinal cord damage
X-rays
106
Management of traumatic spinal fractures
Spinal immobilisation devices are left in place
107
Treatment of traumatic spinal fractures
Stable fractures can be mobilized
| Unstable fractures require immobilization, bracing or internal fixation
108
Prognosis of traumatic spinal fractures
Pt w/ spinal cord damage and neurological symptoms have a poor prognosis and often require extensive rehabilitation on a spinal unit
109
Spinal shock
Period of altered distal function with loss of spincteric control and reflexes (inadequate tissue perfusion after injury)
110
Pathological fractures
One that requires minimal force to sustain, as a result of underlying pathology and weakness in the bone
111
Most common locations for pathological fractures
Vertebral Bodies
Neck of Femur
Wrist (Colle’s Fracture)
Humerus/Shoulder
112
Condns predisposing pathological fractures
```
Osteoporosis
Osteomyelitis
Cancer
Osteomalacia
Paget’s Disease
Non-Cancerous Tumours and Cysts
Hyperparathyroidism
Osteogenesis Imperfecta
```
113
Presentation of pathological fractures
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
Prevention of pathological fractures
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
Prognosis of pathological fractures
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
When does Type I osteoporosis develop
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
Common fractures in Type I osteoporosis
Wrist and spine
118
When does Type II osteoporosis develop
After 70 years
| Sometimes referred to as senile osteoporosis
119
Common fractures in Type II osteoporosis
Hip and spine
120
What types of bone does Type II osteoporosis affect
Cortical bone
121
Technetium bone scan
Sensitive to areas of unusual bone re-building activity
| Good for Paget's
122
Where does OP typically occur
Metabolically active bony trabeculae
123
Pagets vs bone malignancy
Both are progressive but pts are generally unwell with malignancies
124
Lab values for OP
Normal Ca
Normal P
Normal ALP
Normal PTH
125
Lab values for osteomalacia
Decreased Ca
Decreased P
Increased ALP
Increased PTH
126
Lab values for Paget's
Normal Ca
Normal P
Increased ALP
Normal PTH
127
Changes in diet to improve bone strength
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
