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notes to flashcards year 2 - LCRS1 > endocrine and metabolic bone disorders > Flashcards

endocrine and metabolic bone disorders Flashcards

1
Q

what is the composition of bone?

A
  • 65%: inorganic minerals (Ca hydroxyapatite)

- 35%: organic components (type 1 collagen)

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2
Q

what do osteoblasts do?

A
  • build up bone (synthesise, mineralise and calcify osteoid)

- express receptors for PTH and calcitrol

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3
Q

what do osteoclasts do?

A

break down/resorb bone

lysosomal enzymes

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4
Q

What do osteocytes do?

A

make type 1 collagen and other EC matrix components

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5
Q

describe osteoclast differentiation

A
  • RANKL expressed on osteoblast membrane
  • RANK-R binds RANKL
  • this stimulates osteoclast formation and activity
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6
Q

what is osteoprotegerin?

A
  • acts as a competitive inhibitor for RANKL

- inhibits

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7
Q

describe the first and second hydroxylation steps

A
  • calcidiol is made in liver (1st)

- calcitriol is made in kidneys (2nd)

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8
Q

what does PTH/calcitrol cause?

A
  • causes bone to release Ca and phosphates
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9
Q

what does PTH do?

A

causes kidneys to inc. calcitrol synthesis and dec. excretion of Ca

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10
Q

what does calcitriol do?

A

inc absorption of dietary Ca

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11
Q

what does high EC calcium/ low EC calcium cause?

A

High EC Ca - Ca blocks Na influx so LESS membrane excitability
Low EC Ca - enables greater influx of Na so more membrane excitability

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12
Q

what are the symptoms of hypocalcaemia?

A

too much excitability (PCAT):

  • parathesia
  • convulsions
  • arrhythmias
  • tetany
    signs: Chovstek’s sign, Trousseau’s sign
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13
Q

what is Chovstek’s sign?

A

tap facial nerve below zymgomatic arch, face twitch

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14
Q

what is Trousseau’s sign?

A
  • inflate BP cuff for minutes

- induces carpopedal spasm

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15
Q

what are the causes of hypocalcaemia?

A
  • Vit D def (low calcitriol)
  • renal failure (impaired 1 alpha-hydroxylase activity so low calcitriol)
  • low PTH levels
  • PTH resistance (pseudohypoparathyroisism)
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16
Q

what are the symptoms of hypercalcaemia?

A

stones, abdo maons and psychic groans (slows down)
Stones: renal stones
Abdo moans: GI effects
Psychic groans: CNS effects

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17
Q

what are the causes of hypercalcaemia?

A
  • primary hyperparathyroidism (benign adenoma of parathyroid, PTH high, Ca high)
  • malignancy (tumours ofen secrete PTH-RP, PTH low, PTH-RP high, Ca high)
  • Paget’s disease (condition w/ high bone turn over)
  • Vit D toxicosis
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18
Q

what is the active form of Vit D?

A

calcitriol

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19
Q

what are the effects of calcitriol?

A
  • intestinal absorption of Ca, Mg, PO4
  • regulates osteoblast differentiation
  • renal effects (inc. Ca reabsorption, dec. PO4 reabsorption)
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20
Q

what happens when there is a Vit D def?

A
  • softening of bone
  • bone deformities
  • bone pain
  • severe proximal myopathy
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21
Q

what is Vit D def called in children and adults?

A

children - rickets

adults - osteomalacia

22
Q

what s Vit D3 and Vit D2 called?

A

Vit D3 - cholecalciferol

Vit D2 - ergocalciferol

23
Q

what are the causes of Vit D def?

A
  • block in UVB light catalysation
  • malsabsorption or bad diet
  • liver disease (no 1st hydroxylation)
  • renal disease (no 2nd hydroxylation)
  • receptor defects
24
Q

what is primary hyperparathyroidism?

A

autonomous PTH production due to adenoma

produces a hypercalcaemia

25
Q

what is secondary hyperparathyroidism?

A

no calcitriol so lower Ca so more PTH production to try and normalise serum Ca
not hypercalcaemia

26
Q

what is needed in a diagnosis of Vit D def?

A

Low - calctriol, Ca, PO4
High - PTH
Radiological findings: widened osteoid seams (bone lesions showing excessive osetoclastic bone resorption)

27
Q

what is the treatment of Vit D def?

A
  • normal renal function: give synthetic Vit D (kidney hydroxylates futehr)
  • impaired renal function (give ready hydroxylated Vit D)
28
Q

how does low renal function lead to extra-skeletal deposition?

A
  • low renal function can lead to dec. calcitriol and PO4 excretion
  • leads to higher serum phosphate that binds Ca in blood
  • leads to extra-skeletal deposition
29
Q

what can Vit D toxicosis lead to?

A
  • hypercalcaemia and hypercalciuria due to inc, intestinal absorption of Ca
30
Q

what can Vit D toxicosis occur because of?

A
  • excessive treatment of Vit D def

- granulomatous disease (macrophaes in granuloma produce 1 alpha-hydroxylase which overproduces Vit D)

31
Q

what is osteoporosis?

A
  • condition of reduced bone mass and a distortion of bone microarchitecture which predisposes to fracture after minimal trauma
32
Q

what is the definition of osteoporosis?

A

BMD < 2.5 SDs or more

33
Q

what is BMD measured by?

A

DEXA

34
Q

what are the risk factors for osteoporosis?

A
  • post-menopausal oestrogen def
  • age related def in bone homeostasis
  • hypogonadism in young people
  • endocrine conditions (Cushing’s, hyperthyroisism, primary hyperparathyroidism)
  • iatrogenic
35
Q

what are the different drug classes for the treatment of osteoporosis?

A
  • oestrogen receptor modulators (oestrogen HRT, SERMS)
  • bisphosphonates
  • denosumab
  • teriparatide
36
Q

what is the effect of oestrogen HRT?

A
  • oestrogen has anti-absorptive effects on skeleton
  • women with intact uterus need progestogens to prevent endometrial hyperplasia
  • used limited, concerns with breast cancer
37
Q

what are SERMs?

A

selective oestrogen receptor modulators

  • tissue selective ER antagonists e.g. Tamoxifen
  • tissue selective ER agonists e.g. Raloxifene
38
Q

how does Tamoxifen work?

A

antagonises ERs in breast but has oestrogenic activity in bone

39
Q

how does Raloxifene work?

A

oestrogenic activity in bone and anti-oestrogenic activity on breast and uterus

40
Q

what is the MoA of bisphosphonates?

A
  • bind to hydroxyapatite crystals and are absorbed by osteoclasts (impair ability to resorb bone)
  • dec. osteoclast development/ recruitment and promotes osteoclast apoptosis
41
Q

what are the uses of bisphosphonates?

A
  • first line for osteoporosis

- also used for malignancy, Paget’s and severe hypercalcaemic emergencies

42
Q

what are the pharmacokinetics of bisphosphonates?

A
  • orally active, porrly absorbed (eat on empty stomach)

- remains at site of action for YEARS so mainly used in elderly

43
Q

what are the side effects of bisphosphonates?

A
  • oesophagitis
  • flu like symptoms
  • osteonecrosis of jaw
  • atypical fractures
44
Q

what is denosumab and what does it do?

A
  • human monocloncal antibody
  • binds to RANKL and so inhibits osetoclast activation and bone resorption
  • taken bi-yearly
  • 2nd line drug for osteoporosis
45
Q

what is teriparatide?

A
  • recombinant PTH fragments
  • inc. bone formation and bone resorption
  • formation outweighs resoprtion
  • 3rd line treatment
  • expensive
46
Q

what happens in Paget’s disease?

A
  • accelerated, localised and disorganised bone remodellung
  • excessive bone resorption followed by compensatory inc in bone formation
  • leads to formation of woven bone
  • bone fragility
  • bone hypertrophy and deformity
47
Q

what are the features of Paget’s disease of bone?

A
  • genetic
  • possible viral origin
  • affects men and women equally
  • disease not apparent under 50yo
  • most pt asymptomatic
48
Q

what is Paget’s characterised by?

A
  • abnormal, large and numerous osteoclasts
49
Q

which bones are most commonly affected in Paget’s?

A
  • skull
  • thoracolumbar spine
  • pelvis
  • femur
  • tibia
50
Q

what are the clinical features of Paget’s?

A
  • arthritis
  • fractures
  • pain
  • bone deformity
  • inc. vascularity (warm to touch)
  • deafness
  • radiculopathy (due to nerve compression)
51
Q

what could be used to diagnose Paget’s?

A
  • Ca normal
  • ALP inc (due to over activity of bones secreting ALP)
  • plain X-rays show lytic lesions (early), thickened, enlarged and deformed bones (later)
52
Q

how do you treat Paget’s?

A
  • bisphosphonates

- analgesia

notes to flashcards year 2 - LCRS1 (58 decks)

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