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imed3003 > Metabolic Bone Disease > Flashcards

Metabolic Bone Disease Flashcards

1
Q

What kind of conditions arise from imbalances in osteoclast and osteoblast activity?

A

Too much osteoclast too little osteoblast = Osteoporosis

Opposite = stone bone (osteopetrosis) and sclerosteosis (caused by mutation in sclerostin gene)

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2
Q

What part of the bone declines most rapidly with age?

A

Trabecular bone

cortical bone does thin too

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3
Q

What is osteoporosis?

A

Skeletal disorder characterised by compromised bone strength predisposing to increased risk of fracture.

Reduced skeletal mass and progressive discontinuity in bone microarchitecture leading to structural failure and fracture

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4
Q

What does bone strength refer to in relation to bone metabolism and pathology?

A

Bone density + bone quality

Quality = architecture, turnover, damage, etc

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5
Q

How common is osteoporosis?

A

Most common metabolic bone disease with over 1.2 million sufferers in Australia (5% of WAians)

1 in 2 women and 1 in 3 men over 60 years and costs 2.75 billion dollars a year

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6
Q

When is a fracture considered osteoporotic-related?

A

If it results from a fall from standing height or less

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7
Q

What are the most common sites of osteoporotic fractures?

A

Hip

Vertebrae

Wrist

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8
Q

What is the rate of survival 5 years after hip or vertebral fracture?

A

80% of men and women of similar age without fracture

Hip fracture mortality is higher in men than women.

Death not directly attributed to the fracture but other chronic diseases associated that lead to the fracture.

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9
Q

When is the risk of death greatest following a fracture of the hip or vertebrae?

A

It is greatest immediately after the fracture

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10
Q

What percentage of fracture survivors have some degree of permanent disability?

A

7%

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11
Q

What are the factors that determine risk for osteoporosis?

A

Peak bone mass

Rate of bone loss

Imbalance resorption and formation

Calcium metabolism

Hormonal status

Age related changes

Physical activity

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12
Q

What are the types of osteoporosis?

A

Type I: Post menopausal, trabecular, forearm, and spinal fractures

Type II: Age related, cortical and trabecular, hip fractures

Secondary: Caused by endocrine diseases, drugs, glucocorticoids, malabsorption, and rheumatological diseases

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13
Q

What are the clinical features of osteoporosis?

A

Could be asymptomatic but presents with complications like pain, microfractures, deformities

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14
Q

What happens to bone and bone marrow morphology in osteoporosis?

A

Trabeular and cortical thinning

Bone width doesn’t change

Bone marrow loses cellularity with replacement of fat cells in it

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15
Q

How is a clinical diagnosis made for osteoporosis?

A

Serum biochemistry:

Alkaline phosphatase (ALP, bone formation marker)

Carboxy terminal telopeptide of type-1 collagen (CTX, Bone resorption marker)

Serum calcium and serum phosphate

X-ray: not a very good method because it has low sensitivity

X-ray would show decreased bone density, cortical thinning, and fractures

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16
Q

When is a DEXA score said to be Normal, osteopenic, osteoporotic, and severely osteoporotic?

A

Normal >= -1

Osteopenia -1 to -2.5

Osteoporosis

17
Q

What does T score represent?

A

Number of SD a patient is above or below the mean BMD of a young adult

18
Q

How is osteoporosis treated?

A

Bisphosphonates

Denosumab (anti-RANKL)

PTH/PTHrH (despite stimulating production of osteoclasts in daily intermittent doses it stimulates osteoblasts to work)

Calcium + VitD (at older ages it isn’t very useful usually given in combination with other stuff)

Anti-resorptives

19
Q

How do bisphosphonates work?

A

Binds bone surface and bones uptake that and induces apoptosis of osteoclasts.

20
Q

How does Denosumab work?

A

Works like OPG to block osteoclast formation by preventing RANKL from binding osteoclast RANK receptor.

21
Q

What is the problem with use of antiresorptives?

A

It is often administered late where patients are already osteopenic/osteoporotic

Poor compliance

Undesirable effects such as atypical subtrochanteric femoral fractures and osteonecrosis of the jaw

22
Q

What are the downsides of using anabolics?

A

Expensive

Usually administered late after patients are severely osteoporotic

Require daily injection and peak levels of circulating PTH to control levels within 3 hours

Osteosarcoma risk seen in rats

23
Q

What is osteomalacia?

A

aka Ricketts, is defective mineralisation of organic matrix, excess osteoid, deficiency of minerals

24
Q

What does osteomalacia do to bone?

A

Lack of mineralisation affects both quality and quanitity of bone. Reduced stiffness and strength make them susceptible to compressive forces with deformities of weight-bearing bones and pathological fractures

25
Q

What is the cause of osteomalacia/ricketts?

A

VitD deficiency (dietary or sunlight lack/malabsorption)

VitD resistance (phosphate wasting, end organ insensitivity and renal tubular acidosis)

Hypophosphataemia (Renal tubular disorders, antacids)

Drugs (Phenytoin, aluminium, heavy metals)

Neoplasia (Oncogenic osteomalacia)

26
Q

What are the clinical features of osteomalacia?

A

May be asymptomatic

Bone is soft / fragile (fractures)

Bone pain / tenderness

Proximal muscle weakness

Radiology shows generalised osteopenia (multiple bilateral and symmetrical cortical lucencies)

Alterations in the serum concentrations of calcium, phosphorous, vitamin D. (tend to show low to normal serum calcium, low phosphate and high ALP)

27
Q

What are histological features of osteomalacia?

A

Osteoid is increased in amount of surfaces of bone trabeculae

28
Q

What happens in growing bones if a child suffers from osteomalacia?

A

Defective growth

Deformity

Metaphyses near growth plates

Fracture

29
Q

What is the cause of primary hyperparathyroidism?

A

Primary from a parathyroid adenoma (80%)

Parathyroid hyperplasia (15 - 20%)

30
Q

What is the cause of secondary hyperparathyroidism?

A

Chronic hypocalcaemia

Lack of negative feedback

Hypersecretion of PTH

31
Q

What is the result of hyperparathyroidism?

A

Excessive PTH stimulates osteoclastic resorption which results in marked hypercalcaemia

Mobilisation of Ca2+/PO4(2-)

Diffuse osteopenia

Cysts

Marrow fibrosis ‘osteitis fibrosa cystica’

Brown tumours in large localised areas of resorption such as the jaw, the skull, and in long bones

32
Q

What are the clinical symptoms of hyperparathyroidism?

A

Asymptomatic (biochemical abnormality detected incidentally)

Signs and symptoms of hypercalcaemia: Abdominal cramps, constipation, muscle fatigue, peptic ulceration, renal calculi

Bone related disease

33
Q

How is hyperparathyroidism diagnosed?

A

Pathology/radiology of primary/secondary bone changes (Bone changes is essentially identical)

Dissecting / tunnelling bone resorption

Thinning cortical and trabecular bone

Irregular new bone formation

X-rays: Diffuse osteopenia and/or circumscribed lucencies subperiosteal

Microscopic examination shows increased osteoclast number and activity (characteristic tunnelling or dissecting pattern

Mesenchymal cells proliferate in the marrow space and fibrous tissue replaces lost bone

34
Q

How many phases does paget’s disease have?

A

3 phases:

Osteolytic (lots of osteoclasts present and active)

Mixed (lytic and blastic)

Osteoblastic

35
Q

What is the result of paget’s disease?

A

Results in thick, soft, porous bone, prone to compression and deformity

36
Q

What causes paget’s disease?

A

Idiopathic disorder

Relatively common

Late adult life

Virus (Paramyxovirus inclusions?)

Genetic (p62/sequestosome)

May involve:

1 bone or multiple bones

Most commonly pelvis and skull but virtually any bone can be affected

37
Q

What are the clinical symptoms of paget’s disease?

A

Greatly variable, depend upon sites and extent of disease

Can be asymptomatic

Can have complications or no complications

Pain, swelling, deformity, enlargement of bones

Also associated with high output congestive heart failure due to shunting of blood through skin (bone is hypervascular and hot)

38
Q

How is paget’s disease diagnosed?

A

Often asymptomatic

X-ray

Elevated serum ALP and urinary hydroxyproline

Radiology:

Early: radiolucency

Late: Increased bone density, increased microfractures, loss of distinction between cortex and medulla, may have sharp demarcation between normal and affected bone, may extend into soft tissue if florid disease

39
Q

What kind of historlogical features indicate paget’s disease is the likely diagnosis?

A

Chaotic turnover (Extensive resorption and appositional new bone)

Increases in both Osteoclastic and osteoblastic activity with supportive radiologic findings

Disorganized and purposeless changes

Acute: Primarily woven bone; focal mosaic pattern of lamellar bone, resembles jigsaw puzzle with prominent irregular cement lines, osteoclasts present at surface of bone but don’t tunnel and in osteolytic phase osteoclasts may have up to 100 nuclei

Chronic: Thick trabeculae and thicker bones; fine fibrosis of marrow.

imed3003 (48 decks)

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