biochem cortex Flashcards

1
Q

what is osteoporosis in general terms?

A

is a quantitative defect of bone characterised by reduced bone mineral density and increased porosity (i.e. the bone is of normal quality, there is just not enough of it). WHO defines osteoporosis as bone mineral density less than 2.5 standard deviations below the mean peak value of young adults of the same race and sex.

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2
Q

what is osteopenia?

A

is an intermediate stage where bone mineral density is between 1 to 2.5 standard deviations below mean peak value.

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3
Q

what does osteoporosis cause?

A

leads to fragility of the bone and increased fracture risk with fractures occurring after little or no trauma.

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4
Q

is loss of bone mineral density a normal physiological phenomenon ?

A

yes - usually occurs around the age of 30 due to a very gradual slow down in osteoblastic activity

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5
Q

who tends to lose more bone density - males or females and why?

A

females due to after the menopause there is an increase in osteoclastic bone resorption with the loss of protective effects of oestrogen.

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6
Q

there is 2 types of primary osteoporosis - describe type 1 and what are the further risk factors predisposing for type 1

A

Known as Post‐Menopausal Osteoporosis with an exacerbated loss of bone in the post‐menopausal period.Further risk factors include smoking, alcohol abuse, lack of exercise and poor diet.

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7
Q

what type of fractures tend to occur in type 1 osteoporosis ?

A

colles fractures (a fracture of the radius in the wrist, with a characteristic backward displacement of the hand.) and vertebral insufficiency fractures.

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8
Q

what is type 2 osteoporosis ? and what are the risk factors which predispose people to it?

A

known as Osteoporosis of old age with a greater decline in bone mineral density than expected.Risk factors are similar with the added risks of chronic disease, inactivity and reduced sunlight exposure (Vitamin D).

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9
Q

what fractures are commonly seen in type 2 osteoporosis ?

A

Femoral neck fractures and vertebral fractures predominate in this group

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10
Q

what can osteoporosis occur secondary to ?

A

conditions including corticosteroid use, alcohol abuse, malnutrition, chronic disease (CKD, malignancy, Rheumatoid arthritis) and endocrine disorders (Cushing’s, Hyperthyroidism, Hyperparathyroidism).

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11
Q

how is osteoporosis diagnosed ?

A

DEXA scanning which measures bone mineral density - values are then compared to standard peak values for race and sex

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12
Q

Are serum calcium and phosphate levels normal in osteoporosis ?

A

Yes the are normal

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13
Q

what is the aim of treatments in osteoporosis ?

A

they cannot increase bone mineral density so the aim of them is to slow down the decrease in bone mineral density.

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14
Q

Describe the first-line treatment of osteoporosis

A
  • Biposphonates - alendronic acid, risedonate sodium, ibrandronic acid, zoledronic acid
  • plus - Calcium and vit D supplementation - ergocalciferol and calcium
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15
Q

If side effects occur with the standard treatments used for osteoporosis what could be used ?

A

HRT could be used but there is an increased risk of cancers and DVT’s. Raloxifene (an oestrogen receptor modulator) could be used as another option but again there is a risk of DVT’s.

Raloxifene or denosumab (HRT)

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16
Q

what is osteomalacia ?

A

It is a defect of bone with abnormal softening of the bone due to deficient mineralization of osteoid (immature bone) secondary to inadequate amounts of calcium and phosphorus.

17
Q

what is ricketts?

A

it is the same as osteomalacia but occurs in young children and subsequently has effects on the growing skeleton

18
Q

what is the underlying causes of osteomalacia and ricketts?

A

insufficient calcium absorption from the intestine because of lack of dietary calciumor a deficiency or resistance to the action of vitamin D or phosphate deficiency caused by increased renal losses.

19
Q

what are some of the causes of osteomalacia and ricketts?

A

malnutrition (Ca & vit D)malabsorption (low vit D absorption)lack of sunlight exposure (no activation vit D)hypophosphateamia (re‐feeding syndrome, alcohol abuse – impairs phosphate absorption, malabsorption, renal tubular acidosis)long term anticonvulsant use and chronic kidney disease (reduced phosphate resorption & failure of activation vitamin D).

20
Q

what are the signs and symptoms of osteomalacia and ricketts?

A

Patients may complain of bone pain, have deformities from soft bones (particularly rickets), sustain pathological fractures easily and have symptoms of hypocalcaemia (paraesthesiae, muscle cramps, irritability, fatigue, seizures, brittle nails).

21
Q

what may radiographs show for patients with ricketts and osteomalacia ?

A

pseudofractures (aka Looser’s zones)

22
Q

what is the difference in bone biochemistry when comparing osteoporosis to ricketts and osteomalcia ?

A

serum bone biochemistry is abnormal with typically a low calcium, low serum phosphate and high serum alkaline phosphatase - for osteomalacia and ricketts wheres its normal for osteoporosis.

23
Q

What is the treatment of osteomalacia and ricketts ?

A

Treatment involves vitamin D therapy (erogcalciferol or colecalciferol) with calcium and phosphate supplementation.

24
Q

what is hyperparathyroidism?

A

it is overactivity of the parathyroid gland with high levels of PTH

25
Q

what can hyperparathyroidism cause ?

A

can result in fragility fractures and can also cause lytic lesions in bone (known as Brown Tumours or osteitis fibrosa cystica) which may need skeletal stabilization.

26
Q

describe renal dystrophy

A

This describes the typical bone changes due to CKD. Reduced phosphate excretion and inactive activation of vitamin D results in secondary hyperparathyroidism with subsequent osteomalacia, sclerosis of bone and calcification of soft tissues.

27
Q

what is pagets disease ?

A

A chronic disorder which results in thickened, brittle and mis‐shapen bones.

28
Q

Describe the pathology of pagets disease

A
  • Increased osteoclast activity (possibly due to an exaggerated response to vitamin D) results in increased bone turnover. Osteoblasts become more active to try to correct excessive bone resorption.
  • The osteoblasts form new bone however the new bone fails to remodel sufficiently and the resulting bone despite its increased thickness and bone density is brittle and can fracture easily.
29
Q

what factors predispose to pagets disease ?

A

Viral infection (paramyxoviruses) and genetic defects

30
Q

what are the commonly affected areas by pagets disease ?

A

Bones commonly affected include the pelvis, femur, skull, tibia and sometimes the ear ossicles (resulting in conductive deafness).

31
Q

what are some of the symptoms of pagets disease ?

A

It can also cause arthritis (if close to the joint), pathologic fractures, deformity, pain and high output cardiac failure (due to increased blood flow through pagetic bone).

32
Q

what are the changes in mineral levels due to pagets disease ?

A

Serum alkaline phosphatase is raised whilst calcium and phosphorus are usually normal.

33
Q

what are the radiological features of pagets disease ?

A

demonstrate that the affected bone is enlarged with thickened cortices and coarse, thickened trabeculae with mixed areas of lysis and sclerosis.

34
Q

What is the treatment of pagets disease ?

A
  • 1st line: bisphosphonate
  • adjunct: calcium and vitamin D supplementation
  • plus: supportive therapies
  • 2nd line: calcitonin
  • adjunct: calcium and vitamin D supplementation
  • plus: supportive therapies