Osteoporosis Flashcards

1
Q

What are the types of bones

A

Flat bones and long bones

Cortical and trabecular bone

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2
Q

What are osteoclasts

A

largely nucleated cells responsible for bone resorption

Under the influence of RANKL, interleukins, PTH, cytokines etc. which initiate bone resorption

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3
Q

How is mineralised bone formed

A

After osteoclastic resorption and apoptosis, proliferation of osteoblasts occurs

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4
Q

What are osteoblasts

A

single nucleated mesenchymal stem cells involved in bone formation. Function as a group of connected cells called an osteon. Hydroxyapatite is produced.

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5
Q

What are markers of bone resorption

A

urine, hydroxyproline, C telopeptide of type 1 colalgen, N telopeptide of type 1 collagen serum, NTX, CTX

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6
Q

What are markers of bone formation

A

bone specific alkaline phosphatase, osteocalcin, P1CP. P1NP

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7
Q

What is DEXA

A

a bone density scan using densitometry X-ray measures how much mineral is in the area being measured. Results are given as standard deviation, the number of units above or below average

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8
Q

What is osteoporosis

A

Systemic skeletal disorder characterised by low bone mass and microarchitecture deterioration of bone tissue and an increased risk of fracture. Bone mineral density or BMD below 2.5 SD is described as osteoporosis.

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9
Q

Why are women at greater risk of osteoporosis

A

decrease in oestrogen production at menopause, which accelerates bone loss
2% at 50 to 50% at 80

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10
Q

What are the modifiable determinants of low bone structure

A

low body mass (BMI under 18.5), alcohol intake over 14 units per week, smoking, current or frequent use of glucocorticoid, vitamin D and calcium homeostasis

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11
Q

What are the non-modifiable determinants of low bone structure

A

age, gender (women accumulate less peak bone mass and lose more following menopause), ethnicity (Caucasians and Asians are at higher risk), previous fragility fractures, family history of hip fractures

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12
Q

How does diabetes contribute to osteoporosis

A

low bone turnover, reduced anabolic effect if insulin and IGF1. Poor vision, neuropathy increase fracture potential

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13
Q

How does chronic kidney disease contribute to osteoporosis

A

renal osteodystrophy is complex, osteitis fibrosa cystic due to secondary hyperparathyroidism or low bone turnover disease (osteomalacia, adynamic bone disease)

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14
Q

How does inflam rheumatic disease contribute to osteoporosis

A

increased expression of RANKL, interleukins, steroids

GI diseases: inflammation, intestinal malabsorption, bowel surgery and steroid

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15
Q

What is FRAX

A

calculates 10 yr absolute risk of major osteoporotic fractures and hip fracture

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16
Q

What investigations need to be undertaken for osteoporosis

A
Bone profile - corrected CA, PO4, Mg, alkaline phosphatase (marker of bone turnover)
Pth
25 OH vitamin D 
Renal functions and LFTs
Serum electrophoresis
Coeliac screen
TFTs
Gonadotrophins
DEXA
X-rays
MRI
Many elderly are on proton pump inhibitors to reduce the effects of aspirin
17
Q

What do bisphosphonates do

A

prevent vertebral, non-vertebral and hip fractures in men and women
Available as weekly, monthly tablets and year infusion
Treat for a period of 3-5 years unless on steroids, over 75 or previous history
Long term risk of osteonecrosis of the jaw and atypical fractures

18
Q

How to treat younger post menopausal women

A

HRT (Selective oestrogen receptor modulators

Testosterone replacement in some hypogonadal men )

19
Q

What is denosumab

A

Human monoclonal antibody that targets and binds with high affinity and specificity to RANKL, preventing activation of RANKL on the surface of osteoclast precursors an osteoclasts
Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function and survival
In postmenopausal women, it significantly reduces the risk of vertebral, non vertebral and hip fractures

20
Q

What is hypophosphatasia

A

heritable rickets, sub-normal BALP (bone alkaline phosphatase) activity

21
Q

What is homocysteinurea

A

autosomal recessive disorder, cystathionine beta-deficiency, Marfnoid habitus, thromboembolism and osteoporosis

22
Q

What is mucopolysaccharidosis

A

diminished activity of lysosomal enzymes that degrade glycosaminoglycans and accumulation of complex CHO within the bone marrow

23
Q

What is Paget’s disease of the bone

A

Localised disorder of bone remodelling
Disorganised mosaic of new bone formation resulting in less compact, more vascular and bone susceptible to deformity and fracture
Driven by genetic and environmental factors
Rare in people less than 55 years of age
Men are more commonly affected
Presents with bone pain, deformities, fractures or isolated increase in BALP
Bisphosphonates are the mainstay of treatment

24
Q

What is Teriparatie

A

rhPTH(1-34) produced using recombinant DNA technology
Identical to the 34 N-terminal amino acid sequence of endogenous human PTH
Anabolic agent

25
Q

What is the relation between cancer and bone disease

A

Bone metastasis occur in 80% of patients with advanced breast or prostate cancer and 15-30% of thyroid, lung or renal cancer
Metastatic cancer cells flourish within the bone microenvironment
Present as severe pain, pathological fractures or abnormalities in calcium

26
Q

What is the role of vitamin D

A

essential for musculoskeletal health. Promotes calcium absorption from the bowel, enables mineralisation of newly formed osteoid tissue in bone and plays an important role in muscle function.

27
Q

What is the recommended serum 25OHD level

A

> 50nmol/L

28
Q

What is the treatment for vit D deficiency

A

Oral vitamin D3/cholecalciferol

29
Q

Describe vitamin D absorption pathway

A

D3 goes to liver, converted to 25(OH)D3.
25(OH)D3 converted to 1,25(OH)2D3 in kidneys. This is responsible for calcium homeostasis, muscle health, bone health, immunomodulation, blood pressure regulation, cardiovascular health
25(OH)D3 converted to 1,25 (OH)2D3 in prostate gland, breast, colon and lungs. This is for regulation of cell growth