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LCRS Y2: Endocrinology > Endocrine and metabolic bone disorders > Flashcards

Endocrine and metabolic bone disorders Flashcards

1
Q

Differentiate between primary, secondary and tertiary hyperparathyroidism

A 
Primary = PT gland adenoma secreting lots of PTH
Secondary = normal physiological response to low Ca++, start of renal failure
Tertiary = due to chronic low Ca++, PT glands hypertrophy and then become autonomic
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2
Q

What form of vitamin D is found in the diet?

A

Ergocalciferol

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3
Q

What foods contain vitamin D?

A

Oily fish and eggs

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4
Q

Where is vitamin D hydroxylated

A
  1. Liver

2. Kidney

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5
Q

What enzyme is responsible for the second hydroxylation of vitamin D?

A

1-alpha-hydroxylase

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6
Q

Recall the sequential conversions that lead to vitamin D production from sunlight

A

7-dehydrocholesterol + UVB –> cholecalciferol –> 25-OH-D3 (liver) –> calcitriol (kidney)

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7
Q

Describe the serum calcium, phosphate and PTH and the plasma 25-OH-D3 in primary hyperparathyroidism

A

Calcium: high
Phosphate: low
PTH: high
25OHD3: low

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8
Q

Describe the serum calcium, phosphate and PTH and the plasma 25-OH-D3 in secondary hyperparathyroidism

A

Calcium: low
Phosphate: high
PTH: high
25OHD3: low

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9
Q

Describe the serum calcium, phosphate and PTH and the plasma 25-OH-D3 in tertiary hyperparathyroidism

A

Calcium: high
Phosphate: high
PTH: high
25OHD3: low

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10
Q

What conditions are associated with low vit D?

A

Children: Rickets
Adults: osteomalacia

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11
Q

Differentiate between osteomalacia and osteoperosis

A 
Osteomalacia = vit D deficiency in adults
Osteoperosis = low bone mineral density
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12
Q

How are rickets and osteomalacia different?

A 
Rickets = before epiphysial closure therefore growth retardation + skeletal abnormality as well as pain and proximal myopathy
Osteomalacia = after epiphysial closure so no skeletal abnormality but still pain and proximal myopathy
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13
Q

What are the 2 main effects of renal failure that affect calcium level?

A
  1. Low calcitrol –> low Ca++ absorption –> hypocalcaemia

2. Low phosphate excretion –> high serum phosphate –> hypocalcaemia

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14
Q

How does hypocalcaemia effect bone and what disease state can chronic hypocalcaemia lead to?

A

Decreases bone mineral density, can lead to (RARE) osteitis fibrosis cystica

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15
Q

Recall 4 treatments for OFC

A
  1. Low phosphate diet
  2. phosphate-binding drugs
  3. ACTIVE d3 analogue
  4. parathyroidectomy
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16
Q

What drugs are given to replace vitamin D in patients with normal renal function?

A

Ergocalciferol, cholecalciferol (= inactive D3)

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17
Q

What drugs are given to replace vitamin D in patients with renal dysfunction?

A

1-alpha-hydroxycalciferol (alfacalcidol)

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18
Q

What parameter is used to assess osteoperosis and how is this measured?

A

Bone mineral density T-score

Measured using DEXA scan (Dual Energy X-ray Absorptiometry)

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19
Q

Why are post-menopausal women particularly at risk of osteoperosis?

A

Oestrogen deficiency leads to loss of bone matrix

20
Q

Recall 4 possible endocrine causes of osteoperosis, other than menopause

A
  1. Hypogonadism
  2. Cushing’s
  3. Hyperthyroidism
  4. Primary hyperparathyroidism
21
Q

Recall 2 Iatrogenic causes of osteoperosis

A
  1. Prolonged glucocorticoid use

2. heparin use

22
Q

Recall the 5 possible lines of treeatment for osteoperosis

A
  1. Oestrogen
  2. Selective oestrogen receptor modulators
  3. Bisphosphonates
  4. Denosumab
  5. Teriparatide
23
Q

Why is oestrogen used to treat osteoperosis?

A

Reduces bone resorption

24
Q

What is given in conjunction with oestrogen treatment for osteoperosis, and why?

A

Progestogen - to prevent endometrial hyperplasia/ cancer

25
Q

Recall 2 concerns with oestrogen treatment of osteoperosis

A
  1. Increased breast cancer risk

2. Increased risk of thromboembolism

26
Q

What are the 2 types of selective oestrogen receptor moderator drugs? Give an example for each

A
  1. Selective ER antagonist eg tamoxifen

2. Selective ER agonist eg raloxifene

27
Q

Describe the mechanism of action of bisphosphonates in osteoperosis treatment

A
  1. BP avidly binds to hydroxyapatite
  2. Osteoclasts injest hydroxypatite, and BP along with it
  3. BP promote osteoclast apoptosis
  4. Net reduced bone turnover
28
Q

Recall 3 problems with bisphosphonate treatment

A
  1. Not absorbed well in the gut
  2. Often cause oesophagitis
  3. Can cause osteonecrosis of jaw
29
Q

What is denosumab?

A

Human monoclonal Ab

30
Q

What is the mechanism of action of denosumab?

A

Binds RANK ligands –> prevents osteoclast activity

31
Q

What is teriparatide?

A

recombinant PTH fragment

32
Q

How is teriparatide administered?

A

Daily subcut. injection

33
Q

What is Paget’s disease of the bone?

A

Accelerated, localised but disorganised bone remodelling

34
Q

Describe the pathophysiology of paget’s disease of the bone

A

Osteoclastic overactivity –> compensatory increase in dinovosynthesis of bone = structurally disorganised bone with poor tensile strength

35
Q

Recall the clinical features of Paget’s disease of the bone

A 
Obvious:
Arthritis
Fracture
Pain
Deformity
Less obvious:
Increased vasculatory --> warmth
Deafness
Radiculopathy (due to bone involvement)
36
Q

What is the hallmark biochemical finding in Paget’s disease of the bone?

A

Really high alkaline phosphatase

37
Q

Recall the 2 normal treatmnts for Paget’s disease of the bone

A

Bisphosphonates, analgesia

38
Q

Recall the effector functions of PTH

A

Promotes bone resorption to release Ca++
Promotes Ca++ reuptake in kidney
Phosphorylates inactive Vit D in kidney to calcitriol
Decreases renal phosphate resorption

39
Q

Recall the effector functions of Vit D

A

Increases GUT RESORPTION of Ca++
Promotes bone resorption to release Ca++ (by increasing oesteoblast RANK-L production)
Promotes Ca++ re-uptake in kidney

40
Q

Where in the kidney is phosphate resorbed and by what transporter?

A

PCT

Na+ cotransporter

41
Q

Recall 2 inhibitors of phosphate resorption in the kidney

A

PTH

FGF23

42
Q

What function is shared by PTH and FGF23

A

Inhibition of Na+/ PO4— cotransporter to promote phosphaturia

43
Q

Recall an inhibitor of calcitriol

A

FGF23

44
Q

Recall how PTH levels are controlled

A

Ca++ binds parathyroid gland receptors –> negative feedback

45
Q

Recall a cause of Vit D toxicosis

A

Granulomatous disease

46
Q

Recall the Ca++, phosphate, PTH and ALP in Paget’s

A

Ca++ normal
Phosphate normal
PTH normal
ALP really high

LCRS Y2: Endocrinology (18 decks)

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