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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

15

What does Paget's disease lead to?

Disorganised bone: bigger, less compact, more vascular and mores susceptible to deformity and fracture

16

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

20

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

23

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

24

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

29

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)

30

Describe types 1-4 of OI.

-Type I: Milder form-when child starts to walk and can present in adults
-Type II: Lethal by age 1
-Type III: Progressive deforming with severe bone dysplasia and poor growth
-Type IV : Similar to type 1 but more severe