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Charis & Ellie vs MSK part 2 > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

what is osteoporosis?

A

a quantitative defect = reduced bone mineral density and increased porosity
it results in fragility and increased fracture risk (little/no trauma)

bone mineral density less than 2.5 SD below the mean peak value of young adults of the same race and sex

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2
Q

what is osteopenia?

A

one mineral density between 1-2.5 SD below mean peak value

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3
Q

when does physiologyic loss of bone density begin?

A

starts around 30 - slowdown of osteoblastic activity

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4
Q

menopause effect of bone density

A

loss of protective effects of oestrogen - increase in osteoclastic bone resorption - loss of bone mineral density

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5
Q

types of primary osteoporosis

A

post-menopausal osteoporosis

osteoporosis of old age

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6
Q

what is post menopausal osteoporosis?

A

exacerbated loss of bone in the post-menopausal period

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7
Q

what are the risk factors for post-menopausal osteoporosis?

A 
early menopause
environmental factors - white caucasian 
smoking 
alcohol abuse 
lack of exercise 
poor diet
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8
Q

what is the presentation of post-menopausal osteoporosis?

A

Colles fracture and vertebral insufficiency

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9
Q

what is osteoporosis of old age?

A

greater decline in bone density than expected

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10
Q

what are the risk factors for osteoporosis of old age?

A

greater decline in bone density than expected

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11
Q

what are the risk factors for osteoporosis of old age?

A 
early menopause 
environmental factors -white Caucasian 
smoking 
alcohol abuse 
lack of exercise 
poor diet 
chronic disease
inactivity 
reduced sunlight exposure Vitamin D
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12
Q

causes of secondary osteoporosis

A 
corticosteroid use 
alcohol abuse 
malnutrition 
chronic disease - CKD, malignancy, RA
endocrine disorders - Cushing's, hyperthyroidism, hyperparathyroidism
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13
Q

how is osteoporosis diagnosed?

A

DEXA - measure of bone mineral density
compare DEXA with standard peak values for race, sex and age
Serum Ca and P are normal

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14
Q

How is bone mineral density increased?

A

no treatment to increase bone mineral density

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15
Q

what is the aim of osteoporosis treatment?

A

slow any further deterioration and decrease risk of subsequent fracture

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16
Q

what are the pharmacological treatments which help prevent fragility in osteoporosis?

A

Calcium and vitamin D supplements
Bisphosphonates: reduce osteoclastic resorption
o alendronate - oral
o risedronate - oral
o etidronate – oral
o oral bisphosphonates have greatest evidence for efficacy, cost-effectiveness, and low side effect profile
o zoledronic acid – 1/year IV, more expensive than oral forms
Desunomab: monoclonal antibody which reduces osteoclast activity
Strontium: increase osteoblast replication & reduce resorption

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17
Q

how to reduce risk of osteoporosis - build up bone mineral density?

A

exercise
good diet
healthy levels of sunlight
healthy lifestyle

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18
Q

prevention of osteoporosis after menopause?

A

HRT not 1st line
can be considered if side effects with other medications occur
risks:
o breast cancer
o endometrial cancer
o DVT
raloxifene (oestrogen receptor modulator) can also be considered – risk of DVT

19
Q

what is osteomalacia?

A

a qualitative defect = inadequate amounts of calcium and phosphorus - deficient mineralization of osteoid - abnormal softening of bone

20
Q

what is ricketts

A

osteomalacia in children

21
Q

what are the principal causes of osteomalacia?

A 
insufficient Ca absorption from intestine - lack of dietary Calcium 
deficiency of Vitamin D action 
resistance to the action of vitamin D 
phosphate deficiency (increased renal losses)
22
Q

what are specific causes of osteomalacia?

A 
malnutrition (Ca & Vit D)
malabsorption (low Vit D absorption)
lack of sunlight exposure (no activation of Vit D)
hyophosphateamia 
o re-feeding syndrome
o alcohol abuse
 - impairs phosphate absorption
 - malabsorption
 - renal tubular acidosis
long term anticonvulsant use
chronic kidney disease: 
o reduced phosphate resorption
o failure of Vitamin D activation 
inherited renal disorders
o X-linked hypophosphataemia
o vitamin D resistant rickets
23
Q

what are the symptoms of osteomalacia?

A

Bone pain: pelvis, spine, femur
Deformities from soft bones (rickets)
Pathological fractures
Hypocalcaemia: paraesthesia, muscle cramps, irritability, fatigue, seizure, brittle nails
Radiographs: pseudofractures – Looser’s zones (pubic rami, proximal femur, ulna, ribs)

24
Q

how is osteomalacia diagnosed?

A

Abnormal serum bone biochemistry
low Calcium
low serum Phosphate
high serum Alkaline Phosphatase

25
Q

how is osteomalacia treated?

A

vitamin D therapy
calcium supplementation
phosphate supplementation

26
Q

What is hyperparathyroidism?

A 
overactivity of the parathyroid glands 
high PTH (parathyroidism)
27
Q

what are the causes of primary hyperparathyroidism?

A

benign adenoma
hyperplasia
malignant neoplasia (rarely)

28
Q

what are the signs/ symptoms caused by overproduction of PTH leading to hypercalcaemia?

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

what are the blood results indicative of hyperparathyroidism?

A

high serum PTH
high calcium
normal/ low phosphate

30
Q

what is secondary hyperparathyroidism?

A

physiological overproduction of PTH secondary to hypopcalcaemia
vitamin D deficiency
CKD

31
Q

what is tertiary hyperparathyroidism?

A

chronic secondary hyperparathyroidism (usually chronic kidney disease)
adenoma which continues to produce PTH despite biochemical correction

32
Q

what are the symptoms of hyperparathyroism?

A

fragility fractures
lytic lesions in bone = brown tumours/ osteitis fibrosa cystica
need skeletal stabilization

33
Q

what is the treatment of hyperparathyroidism?

A

removal of the adenomatous gland (if applicable)
treat underlying cause e.g. vitamin D supplementation
very high calcium levels: emergency
- IV fluids
- bisphosphates
- calcitonin

34
Q

why does renal dystrophy cause bone changes?

A

chronic kidney disease causes typical bone changes because there is
reduced phosphate excretion
inactivation of vitamin D

35
Q

what are the changes that renal dystrophy can cause?

A

secondary hyperparathyroidism (subsequent)
osteomalacia
sclerosis of bone
calcification of soft tissues

36
Q

What is Paget’s disease?

A

a chronic disorder which results in thickened, brittle and mis-shapen bones
typically 1 or a few bones

37
Q

who gets Paget’s disease?

A

4% of > 55yrs

10% of > 80s

38
Q

what causes Paget’s disease?

A

viral infection - paramyxoviruses

genetic defects

39
Q

what is the pathophysiology of Paget’s disease?

A 
increased osteoclast activity (maybe exaggerated response to vit D)
increased bone turnover 
osteoblasts become more active to correct excessive bone resorption 
new bone fails to remodel sufficiently 
resulting bone 
 - increased thickness and bone density 
 - brittle 
 - fractures easily
40
Q

what are the bones commonly affected by Paget’s disease?

A 
pelvis 
femur 
skull 
tibia 
ear ossicles (deafness)
41
Q

what are the symptoms of Paget’s disease?

A

can be asymptomatic - incidental Xray finding
Arthritis - if close to joint
pathologic fractures
deformity
pain
high output cardiac failure (increased blood flow through pagetic bone)

42
Q

How is Paget’s disease diagnosed?

A 
Serum Alkaline Phosphatase is raised
Calcium & Phosphorus normal 
Radiograph: 
 - affected bone enlarged
 - thickened cortices
 - coarse, thickened trabeculae
 - mixed areas of lysis & sclerosis
Bone scans: marked increased uptake in affected bones
43
Q

how is Paget’s disease treated?

A

Bisphosphates - inhibit osteoclasts
calcitonin - if extensive lytic disease
joint replacement may be necessary
pathological femoral fractures - stabilized with long intramedullary nails/ plates

Charis & Ellie vs MSK part 2 (61 decks)

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