Flashcards in Metabolic Bone Disease Deck (62)
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1
What are the 2 main cells of bone remodelling?
-Osteoblasts
-Osteoclasts
2
What type of cell do osteoblasts develop from?
Mesenchymal progenitor cell
3
What type of cell do osteoclasts develop from?
Myeloid progenitor cell
4
What is the role of osteoclasts?
Bone resorption
5
What is the role of osteoblasts?
Bone formation
6
How do osteoblasts control osteoclasts?
-When stimulated they produce RANKL
-RANKL binds to pre-osteoclasts
-Activation of osteoclasts
7
What produces vitamin D?
UVB
8
Where is vitamin D stored?
Liver, fat and muscle
9
Where is vitamin D activated?
Kidney
10
In what form is vitamin D found in the skin?
7DHC
11
In what form is vitamin D found in the liver?
25(OH)vit D
12
In what form is vitamin D stored in the kidney?
1,25(OH)2 vit D
13
What happens to PTH when extracellular calcium is reduced?
Increases
14
What is Paget's disease?
-Localised disorder of bone turnover
-Increased bone resorption followed by increased bone formation
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What does Paget's disease lead to?
Disorganised bone: bigger, less compact, more vascular and mores susceptible to deformity and fracture
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What is the aetiology of Paget's disease?
-Strong genetic component
-15-30% are familial
-Loci of SQSTMI
-Restricted geographic distribution: those of Anglo-Saxon origins
-Environmental trigger: Possibility of chronic viral infection within Osteoclast
17
How does Paget's disease present?
-Patient>40 years
-Bone pain
-Bony deformity (occasional)
-Excessive heat over Pagetic bone
-Neurological complications (such as nerve deafness)
18
How is Paget's investigated?
X-ray
-Marked expansion of the bone
-Dense and lucid areas
Bone scan
-Most useful definitive test
Isolated elevation of serum alkaline phosphotase
19
What can rarely develop from Paget's?
Osteosarcoma in the affected bone
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How is Paget's disease treated?
-No evidence to treat asymptomatic Paget’s unless in skull or in area requiring surgical intervention.
-Do not treat based on a raised alkaline phosphatase alone
-Intravenous Bisphosphonate therapy-One off zoledronic acid infusion
21
What is the difference between rickets and osteomalacia?
-Rickets occurs in children before the epiphyseal plates fuse
-Osteomalacia occurs in adults after the epiphyseal plates fuse
22
What causes rickets/osteomalacia?
Severe nutritional vitamin D or Calcium deficiency causes insufficient mineralisation and thus Rickets in a growing child and Osteomalacia in the adult when the epiphyseal lines are closed
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What does vitamin D do?
Stimulates the absorption of calcium and phosphate from the gut and calcium and phosphate then become available for bone mineralisation
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What effect doe low vitamin D have on muscle function?
Impaired function
25
How does Rickets present in infants?
-Stunted growth
-Bandy legs (once they start walking)
-Splayed epiphyses
-Large head (due to failure of fontanelles to close)
-Nodules on sides of ribs
-Failure to thrive
-Fragile
26
What are the symptoms of osteomalacia?
-Bone pain
-Muscle weakness
-Increased falls risk
27
What develops in osteomalacia?
Microfractures
28
What is osteogenesis imperfecta?
-Genetic disorder of connective tissue characterised by fragile bones from mild trauma and even acts of daily life
-Other non bone clinical features
-Broad clinical spectrum
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What is the cause of OI?
Defects in type I collagent (There are 8 types of OI in total with 1 to 4 being the most common)
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