Biochemical Disorders of Bone Flashcards

1
Q

What is osteoporosis

A

A quantitative defect of bone, where there is reduced bone density and increased porosity i.e. quality is normal there just isn’t enough of it

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2
Q

WHO definition of osteoporosis

A

bone mineral density <2.5 standard deviations below the mean peak value of young adults of the same race and sex

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3
Q

WHO definition of osteopenia

A

An intermediate stage where bone density between 1 - 2.5 standard deviations below mean peak value.

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4
Q

Around what age does loss of mineral bone density start to occur and how does it happen

A

age 30

gradual decrease in osteoblastic activity

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5
Q

Why do females tend to lose more bone density after the menopause

A

Increase in osteoclastic bone resorption and loss of the protective effects of oestrogen

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6
Q

Types of primary osteoporosis

A
  1. Post-menopausal

2. Osteoporosis of old age with a greater decline in bone density than expected

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7
Q

Risk factors for type 1 osteoporosis

A

smoking
lack of exercise
poor diet
alcohol abuse

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8
Q

Most common fractures in Type 1 osteoporosis

A

Colles #

Vertebral insufficiency #

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9
Q

Risk factors for Type 2 osteoporosis

A

lack of sunlight
chronic disease
inactivity

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10
Q

Most common # in Type 2 osteoporosis

A

femoral neck #

vertebral #

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11
Q

Conditions causing secondary osteoporosis

A
Corticosteroid abuse 
Alcohol abuse 
Malnutrition 
Chronic disease (malignancy, CKD, RA) 
Endocrine disorders (Cushings, hyperthyroidism, hyperparathyroidism)
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12
Q

Dx of osteoporosis

A

DEXA scanning - provides a measure of bone density to allow comparison to mean values

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13
Q

What is the treatment aim for osteoporosis

A

Slowing down further loss of bone density - there are no treatments that can increase bone density!

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14
Q

Pharmacological measures to prevent fragility fractures in osteoporosis

A

Calcium and Vit D supplements - if dietary intake poor

Bisphosphonates (alendronate, risedronate, etidronate)

Desunomab (monoclonal Ab that reduces osteoclast activity)

Strontium (increases osteoblast replication)

Zoledronic acid (once yearly IV bisphosphonate)

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15
Q

Which treatment is not recommended as first line for the prevention of osteoporosis after the menopause?

A

HRT - increased risk of breast and endometrial Ca and increased risk of DVT.

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16
Q

When can HRT be considered for prevention of osteoporosis?

A

If side effects with other medications occurs

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17
Q

Which medication is considered first line for Tx of osteoporosis

A

Oral bisphosphonates

- cheap, effective, low s/e profile

18
Q

What is osteomalacia

A

A qualitative effect of bone where it is abnormally soft due to defective mineralisation due to inadequate calcium and phosphorus

19
Q

What is Rickett’s disease

A

the same as osteomalacia, but in children

20
Q

Causes of Osteomalacia

A
  1. insufficient calcium absorption in the small intestine (either because there isn’t enough in the diet, or resistance to the action of Vitamin D)
    - malnutrition
    - lack of sunlight exposure
  2. phosphate deficiency from increased renal losses
    - re-feeding syndrome
    - alcohol abuse (cause renal tubular acidosis)
    - CKD
    - long term anticonvulsant use
21
Q

Presentation of osteomalacia

A

bone pain
bone deformities
pathological fractures
symptoms of hypocalcaemia (paraesthesia, muscle cramps, irritability, fatigue, seizures, brittle nails)

22
Q

Bone chemistry in osteoporosis

A

Normal calcium and phosphate

23
Q

Bone chemistry in osteomalacia

A

low calcium
low phosphate
high alk phos

24
Q

Tx of osteomalacia

A

Vit D therapy

calcium and phosphate supplements

25
Q

what is hyperparathyroidism

A

Overactivity of the parathyroid gland with high levels of parathyroid hormone

26
Q

Causes of primary hyperparathyroidism

A

Benign adenoma
Parathyroid hyperplasia
Malignant neoplasia (rare)

27
Q

Consequences of raised PTH

A

there will be increased resorption of calcium from bone and raised ca reabsorption from the kidneys - therefore increased serum Ca

28
Q

symptoms of hypercalcaemia

A
fatigue 
depression 
bone pain 
myalgia 
nausea 
thirst 
polyuria 
renal stones
osteoporosis
29
Q

biochemistry in primary hyperparathyroidism

A

raised PTH
raised Ca
low or normal phosphate

30
Q

What is secondary hyperparathyroidism

A

physiological overproduction of PTH in response to a low Ca

31
Q

Causes of secondary hyperparathyroidism

A

Vit D deficiency

CKD

32
Q

What is renal dystrophy

A

typical bone changes due to CKD

- reduced phosphate excretion and inactivation of Vitamin D, resulting in secondary hyperparathyroidism

33
Q

How is phosphate excreted from the body

A

kidneys

34
Q

What is Paget’s disease of bone

A

A chronic disorder resulting in thickened, brittle and mis-shapen bones.

35
Q

Pathophysiology of Paget’s

A

There is increased osteoclastic activity that results in increased bone turnover. Osteoblasts then become more active to try to compensate. The osteoblasts form new bone but it cannot remodel sufficiently. So it is thicker but still brittle.

36
Q

Presentation of Paget’s disease

A

Can be Asymptomatic

Arthritis (if close to the joint)
Pathological fractures
High output cardiac failure - due to increased blood flow through pagetic bone)
Conductive deafness - Pagets can affect the ear ossicles

37
Q

Biochemistry in Paget’s disease

A

Raised Alk Phos
Normal calcium
Normal phosphate

38
Q

Tx of Paget’s

A

Bisphosphonates (inhibit osteoclasts)

Calcitonin - if excessive lytic disease

Joint replacement

39
Q

Only biochemical abnormality in Pagets

A

Raised Alk Phos!!!

40
Q

Examples of bisphosphonates

A

alendronic acid
risendronate
zolendronate

41
Q

most common locations for Paget’s disease

A

predominately affects central bones

  1. pelvis
  2. femur
  3. skull
  4. tibia
  5. ear
42
Q

How are patients advised to take oral bisphosphonates, and why

A

take at least 30 minutes before breakfast with plenty of water + sit upright for 30 minutes following

?bisphosphonates cause a variety of oesophageal problems