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YR2: Endocrinology > Endocrine Bone Disorders > Flashcards

Endocrine Bone Disorders Flashcards

1
Q

What are the other effects of calcitriol?

A

Increased reabsorption of Ca2+ and decreased phosphate reabsorption in the kidneys (via FGF23)
Stimulates osteoclast formation from precursors
Stimulates osteoblasts to make osteoclast-activating factors (OAFs e.g. RANKL)

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2
Q

What is Paget’s disease?

A

Accelerated, localised but disorganised bone remodelling
Excessive bone resorption followed by a compensatory increase in bone formation
New bone = woven bone

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3
Q

What is Paget’s disease characterised by histologically?

A

Abnormal, large osteoclasts excessive in number

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4
Q

State 8 clinical features of Paget’s disease and the most commonly affected bones

A 
Increased vascularity (warmth over affected bone) 
Increased incidence of fracture  
Arthritis
Bone pain
Bone frailty
Bone hypertrophy + deformity
Deafness (cochlear involvement)
Radiculopathy (due to nerve compression)
Skull, thoracolumbar spine, pelvis, femur + tibia most commonly affected
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5
Q

Describe how you would diagnose Paget’s disease.

A

Plasma calcium = NORMAL
Plasma ALP = HIGH
Plain X-ray: Lytic lesions (early), thickened, enlarged, deformed bones (later)
Radionuclide bone scan demonstrates extent of skeletal involvement

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6
Q

What are the 2 components of bone in which 95% of the body’s calcium is stored?

A

Inorganic mineral component (65%):
Stored as calcium hydroxyapatite crystals between collagen fibrils
Organic (osteoid) component (35%):
Type 1 Collagen fibres (95%)

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7
Q

What is the normal plasma calcium range?

A

2.2-2.6 mmol/L

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8
Q

State 2 hormones that increase plasma calcium concentration.

A

Calcitriol

PTH

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9
Q

State a hormone that decreases plasma calcium concentration.

A

Calcitonin

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10
Q

What are the 2 direct effects of calcitriol?

A

Increased calcium absorption from the small intestine

Increased mobilisation of calcium in bone

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11
Q

What do osteocytes produce?

A

Type 1 collagen + other extracellular matrix components

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12
Q

Define osteoporosis. What is the consequence of osteoporosis? How is it diagnosed?

A

Bone mineral density (BMD) >,2.5 SD below the average for young healthy adults (T-score of -2.5 or lower)
Loss of bony trabeculae, reduced bone mass, weaker bone, predisposed to fracture after minimal trauma
Diagnosed via DEXA scan

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13
Q

State 5 predisposing conditions for osteoporosis.

A 
Post-menopausal oestrogen deficiency  
Age-related deficiency of bone homeostasis  
Hypogonadism in young men + women 
Endocrine conditions (e.g. Cushing’s syndrome, hyperthyroidism, primary hyperparathyroidism) 
Iatrogenic (e.g. prolonged use of glucocorticoids, heparin)
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14
Q

What are the benefits of oestrogen replacement to prevent osteoporosis in post-menopausal women?

A

Anti-resorptive effect in bone, hence, prevents bone loss

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15
Q

What are the cautions and risks of oestrogen replacement?

A

Women with an intact uterus need additional progestogen to prevent endometrial hyperplasia + reduce the risk of endometrial carcinoma
Increased risk of breast cancer + venous thromboembolism

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16
Q

What are the 1st, 2nd and 3rd line treatments for osteoporosis?

A

Bisphosphonates
Denusomab
Teriparatide

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17
Q

What are bisphonates analogues of?

A

Pyrophosphate

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18
Q

Give 2 examples of bisphosphonates.

A

Alendronate

Sodium etidronate

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19
Q

Describe how bisphosphonates work.

A

Bind avidly to hydroxyapatite crystals in bone + are ingested by osteoclasts
Impair ability of osteoclasts to resorb bone
Decrease osteoclast progenitor development + recruitment Promote osteoclast apoptosis
Result= reduced bone turnover

20
Q

State 4 uses of bisphosphonates.

A

Osteoporosis
Malignancy: hypercalcaemia- reduces bone pain from metastases
Paget’s disease: reduces bony pain
Severe hypercalcaemic emergency (I.V. saline to rehydrate + then bisphosphonates)

21
Q

Describe the pharmacokinetics of bisphosphonates.

A

Orally active but poorly absorbed
Must be taken on an empty stomach
Accumulates at site of bone mineralisation + remains a part of the bone until it is resorbed (months/ years)

22
Q

State 3 unwanted actions of bisphosphonates.

A

Oesophagitis
Osteonecrosis of the jaw (greatest risk in cancer patients receiving IV bisphosphonates)
Atypical fractures (due to over-suppression of bone remodelling)

23
Q

What is denusomab and how often does it need to be given?

A

Human monoclonal antibody
Binds to RANKL, inhibits osteoclast formation + activity
Inhibits osteoclast-mediated bone resorption
Given subcutaneously every 6-12 months

24
Q

What is teriparatide and how often does it need to be given?

A

Recombinant PTH fragment
Increases bone resorption + formation– but formation exceeds resorption
Daily subcutaneous injections
EXPENSIVE

25
Q

What is the role of osteoblasts?

A

Synthesise osteoid + participate in mineralisation/ calcification of osteoid
= Bone formation

26
Q

What is the role of osteoclasts?

A

Release lysosomal enzymes which break down bone

= Bone resorption

27
Q

Describe osteoclast differentiation

A

RANKL expressed on osteoblast surface

RANKL binds to RANK-R to stimulate osteoclast formation + activity

28
Q

What are the 2 types of bone in the body?

How are they formed?

A

Cortical (hard) bone
Trabecular (Spongy) bone
Formed in a lamellar pattern: collagen fibrils laid down in alternating orientations, mechanically strong

29
Q

What are the characteristics of woven bone?

A

Disorganised collagen fibrils

Mechanically weaker

30
Q

Describe how rickets effects children

A

Affects cartilage of epiphyseal growth plates + bone
Skeletal abnormalities + pain
Growth retardation
Increased fracture risk

31
Q

Describe how Osteomalacia effects adults

A

After epiphyseal closure, affects bone
Skeletal pain
Increased fracture risk
Proximal myopathy

32
Q

What causes primary hyperparathyroidism? Describe PTH and Ca2+ levels

A

Adenoma
High PTH (no negative feedback)
High Ca2+

33
Q

What causes secondary hyperparathyroidism? Describe PTH and Ca2+ levels

A 
Low plasma Ca2+, e.g. renal failure, Vitamin D deficiency
High PTH (appropriate physiological response)
Low/ normal Ca2+
34
Q

What causes tertiary hyperparathyroidism? Describe PTH and Ca2+ levels

A

Chronic low plasma Ca2+ e.g. CKD- can’t 1-alpha hydroxyls, can’t make calcitriol, causes secondary hyperparathyroidism, parathyroids increase in size + become autonomous
High PTH
High Ca2+

35
Q

Describe the epidemiology of Paget’s disease

A 
Often +ve FH
Some evidence of viral origin
M + F equally affected
Usually >50s
Most patients are asymptomatic
36
Q

What are the treatment options for Paget’s disease?

A

Bisphosphonates (reduce bony pain + disease activity)

Simple analgesia

37
Q

What receptors do osteoblasts express? Why?

A

PTH + Calcitriol receptors

To regulate balance between bone formation + resorption

38
Q

What does Vitamin D deficiency result in for both children and adults?

A

Inadequate minerilastion of newly formed bone matrix (osteoid)

39
Q

Describe 2 observed effects resulting from vitamin D deficiency

A

Looser zones: Fractures from inadequately mineralised bone baring the weight of the skeleton
Waddling gait: Caused by proximal myopathy + pain

40
Q

How does the ineffective excretion of phosphate in CKD effect calcium levels?

A

Phosphate binds to calcium, further reducing serum calcium levels

41
Q

What are the consequences of tertiary hyperparathyroidism causing high circulating phosphate levels?

A

Calcification, particularly in blood vessels

42
Q

What is Osteitis fibrosa cystica? What is it caused by?

A

Cysts in the bone
Caused by extremely high PTH driving excess osteoclast bone resorption
=”Brown tumours” (radiolucent bone lesions)

43
Q

Describe treatment for Osteitis fibrosa cystica

A

Low phosphate diet
Phosphate binders to reduce GI phosphate absorption
Calcitriol analogues (as can’t alpha hydroxylase)
Parathyroidectomy in tertiary hyperparathyroidism

44
Q

How is BMD measured? Why?

A

DEXA SCAN
Predicts fracture risk
Calcium content of bone measured- the more mineral, the greater the bone density, the greater the bone mass

45
Q

What is osteomalacia? How is it diagnosed? Why?

A 
Vitamin D deficiency (adults) causing inadequately mineralised bone
Diagnosed via blood test
low 25(OH) vit D
low/low N Ca2+
high PTH (secondary hyperparathyroidism)
46
Q

What is the difference in presentation between osteomalacia and osteoporosis?

A

Malacia: can be painful
Porosis: only painful if you fracture

YR2: Endocrinology (19 decks)

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