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Year 2 > CORTEX biochemistry > Flashcards

CORTEX biochemistry Flashcards

1
Q

What is osteoporosis?

A

Reduced bone mineral density and increased porosity

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2
Q

Osteoporosis can be described as a quantitive defect, what does this mean?

A

The bone is normal but there’s not enough of it

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3
Q

What does osteoporosis increase your risk of?

A

Fractures (i.e fragility fractures)

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4
Q

Define osteopenia and osteoporosis

A

Osteopenia - 1-2.5 SDs below mean

Osteoporosis - >2.5 SDs below mean

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5
Q

When does loss of bone density begin?

A

30 y/o

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6
Q

Describe physiological loss of bone density and mention the relevance of menopause

A

Slowdown of osteoblast activity with age

Increased osteoclastic bone reabsorption post-menopause due to reduced oestrogen

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7
Q

List the two types of primary bone osteoporosis

A

Type 1 post menopausal

Type 2 osteoporosis of old age

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8
Q

What are the risk factors for post menopausal osteoporosis?

A 
Early menopause
White people
Smoking
Alcohol 
Lack of exercise
Poor diet
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9
Q

Which types of fractures tend to occur in post menopausal osteoporosis?

A

Colles fractures

Vertebral insufficiency

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10
Q

What are the risk factors for osteoporosis of old age?

A 
Chronic disease
Inactivity 
Reduced sunlight exposure (low vit D)
Smoking
Alcohol
Poor diet 
White people
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11
Q

Which types of fractures tend to occur in osteoporosis of old age?

A

Femoral neck fractures

Vertebral fractures

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12
Q

List the causes of secondary osteoporosis

A

Corticosteroid use
Alcohol abuse
Malnutrition
Chronic disease (CKD, malignancy, rheumatoid arthritis)
Endocrine disease (cushing’s, hyperthyroidism, hyperparathyroidism)

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13
Q

How is osteoporosis diagnosed?

A

DEXA scanning
Normal serum calcium
Normal serum phosphate

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14
Q

How is osteoporosis managed?

A 
Calcium supplements
Vitamin D supplements 
Biphosphonates 
Monoclonal antibody (desunomab)
Strontium
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15
Q

How is osteoporosis managed?

A

Exercise
Diet
Sunlight exposure

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16
Q

List some biphosphonates

A

Alendronate
Risedronate
Etdronate
IV zoledronic acid (once per year)

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17
Q

How do biphosphonates work?

A

Reduce osteoclast reabsorption

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18
Q

How does desunomab work?

A

Reduces osteoclast activity

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19
Q

How does strontium work?

A

Increases osteoblast replication and reduces absorption

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20
Q

Why is intranasal calcitonin not used to treat osteoporosis?

A

Increased cancer risk with no benefit over other treatments

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21
Q

HRT is recommended as first line treatment of osteoporosis in post menopausal women. T/F

A

False - considered if side effects with other medications

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22
Q

What are the risks of HRT?

A

Breast cancer
Endometrial cancer
DVT

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23
Q

What is raloxifene? What is the risk of it?

A

Oestrogen receptor modulator

DVT

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24
Q

Osteomalacia is a qualitative bone defect, what does this mean?

A

Bone quantity is normal but the quality is sub-par

25
Q

What is osteomalacia?

A

Abnormal soft bones that have not been mineralised due to deficiencies in calcium and phosphorus

26
Q

What is Rickets?

A

Abnormal soft bones that have not been mineralised due to deficiencies in calcium and phosphorus occuring in CHILDREN

27
Q

What are the causes of osteomalacia and ricket’s?

A

Lack of dietary calcium
Deficiency of vitamin D
Resistance to vitamin D
Phosphate deficiency (increased renal loses)

28
Q

What are the specific pathologies which lead to osteomalacia and ricket’s?

A 
Malnutrition 
Malabsorption
Lack of sunlight exposure 
Hydrophosphateamia 
Long term anti-convulsant use 
Chronic kidney disease
29
Q

What are the causes of hydrophosphateamia?

A

Re-feeding syndrome
Alcohol abuse
Malabsorption
Renal tubular acidosis

30
Q

Which inherited renal diseases can be the cause of osteomalacia and rickets?

A

X-linked hydrophosphateamia

Vitamin D resistant ricket’s

31
Q

How does osteomalacia/ricket’s present?

A

Bone pain (pelvis, spine, femur)
Bony deformity
Pathological fractures
Hypocalcaemia

32
Q

Is bony deformity more common in osteomalacia or ricket’s?

A

Ricket’s

33
Q

How does hypocalcaemia present?

A 
Paraesthesia 
Muscle cramps
Irritability 
Fatigue
Seizures
Brittle nails
34
Q

What may be typically seen on a radiograph of someone with osteomalacia or ricket’s?

A

Pseudofractures (looser’s zones) of pubic rami, proximal femur, ulna or ribs

35
Q

How does osteomalacia/ricket’s present biochemically?

A

Low calcium
Low serum phosphate
High serum alk phosphatase

36
Q

How is osteomalacia/ricket’s treated?

A

Vitamin D therapy
Calcium supplements
Phosphate supplements

37
Q

What is hyperparathyroidism?

A

Over activity of parathyroid glands (i.e high parathyroid hormone)

38
Q

What causes primary hyperparathyroidism?

A

Adenoma
Hyperplasia
Neoplasia

39
Q

What is the result of primary hyperparathyroidism?

A

High PTH –> hypercalcaemia

40
Q

How does primary hyperparathyroidism present biochemically?

A

High calcium
High PTH
Phosphate low/normal

41
Q

How does hypercalcaemia present?

A 
Bones (pain)
Stones (renal)
Groans (fatigue, depression)
Myalgia
Nausea
Thirst
Polyuria 
Osteoporosis
42
Q

What is secondary hyperparathyroidism?

A

Overproduction of PTH secondary to hypocalcaemia caused by CKD or vit D deficiency

43
Q

What is tertiary hyperparathyroidism?

A

Patients with chronic secondary hyperparathyroidism develop a parathyroid adenoma producing ectopic PTH

44
Q

What is usually the cause of chronic secondary hyperparathyroidism?

A

CKD

45
Q

What bone problems can hyperparathyroidism cause? How are they treated?

A

Fragility fractures
Brown’s tumours/osteitis fibrosa cystica (lytic bone lesions)
Stabilisation

46
Q

How is hyperparathyroidism treated?

A

Removal of cause (e.g adenoma, cancer, etc)

Treatment of cause (e.g vit D deficiency, etc)

47
Q

How is hypercalcaemia treated?

A

IV fluids
Biphosphonates
Calcitonin

48
Q

What type of bone changes are caused by CKD? Why?

A

Secondary hyperparathyroidism causes osteomalacia, bone sclerosis and soft tissue calcification
Reduced phosphate excretion and inability to activate vit D

49
Q

What is Paget’s disease?

A

Chronic bone disease causing thick, brittle and deformed bones

50
Q

How many bones does paget’s disease affect? Which bones?

A

One or two

Pelvis, femur, skull, tibia

51
Q

Which age groups are typically affected by Paget’s?

A

> 55 (increasing age)

52
Q

Which two factors may increase incidence of Paget’s?

A

Viruses (paramyxoviruses)

Genetic defects

53
Q

Describe the pathogenesis of Paget’s disease

A

Increased osteoclast activity (exaggerated vit D response) –>
Increased bone turnover –>
Osteoblasts become more active in a bid to compensate –>
New bone does not remodel correctly –>
Brittle, easily fractured bone

54
Q

What happens if Paget’s occurs in ear ossicles?

A

Conductive deafness

55
Q

How does Paget’s disease present?

A 
Asymptomatic until picked up on x-ray 
Arthritis 
Pathological fractures
Deformity 
Pain
High output cardiac failure
56
Q

How does Paget’s disease present biochemically?

A

High alk phosphatase
Normal calcium
Normal phosphate

57
Q

How does Paget’s appear on an x-ray?

A

Enlarged bone with thickened cortices
Thickened trabeculae
Mixed lysis and sclerosis

58
Q

How does Paget’s appear on bone scans?

A

Increased uptake in affected bones

59
Q

How is Paget’s treated?

A

Biphosphonates
Calcitonin (extensive lysis)
Joint replacement
Femoral shaft fractures stabilised with IM nails

Year 2 (72 decks)

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