L16 - Disorders of calcium metabolism Flashcards

1
Q

summarise the bone remodelling cycle

A
  1. resorption
  2. reversal
  3. formation
  4. quiescence
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2
Q

resorption initiated by….

A

osteoclasts

———————-> secretion of HCl

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3
Q

what occurs during reversal…

A
  • osteoblasts come and lay new bone : osteoid
  • osteoblasts on top of osteoid
  • move up to bone surface
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4
Q

osteoid

A

unmineralised bone

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5
Q

what occurs during formation in the bone making cycle?

A
  • osteoid gets mineralised
  • osteoblasts get trapped in matrix
  • longer process
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6
Q

primary role of 1,25, hydroxy vitamin D

A
  • activate calcium transport in intestine, increase intestinal calcium absorption
  • inhibits kidney from calcium excretion
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7
Q

features of hypercalcaemia

A
  • lethargy and general aches
  • polyuria, polydipsia
  • anorexia, nausea, vomitting
  • dehydration
  • constipation
  • psychosis
  • bradycardia and heart block
  • kidney failure
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8
Q

PTH-dependent hypercalcaemia

A

PTH normal or raised

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9
Q

PTH-independent hypercalcaemia

A

low PTH

  • thyrotoxicosis
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10
Q

what might be witnessed in primary hyperparathyroidism as a result of excessive bone resorption?

A
  • osteoporosis / fractures
  • subperiosteal resorption
  • osteitis fibrosa cystica
  • brown tumour
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11
Q

osteitis fibrosa cystica

A
  • cystic expansions of bone
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12
Q

brown tumour

A
  • due to increased haemosiderin deposition
  • The brown tumor is a bone lesion that arises in settings of excess osteoclast activity
  • such as hyperparathyroidism.
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13
Q

subperiosteal resorption

A
  • increased action of osteoclasts
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14
Q

definition of secondary hyperparathyroidism

A
  • elevated PTH
  • but normal calcium
  • Secondary hyperparathyroidism is a condition in which a disease outside of the parathyroid glands causes all of the parathyroid glands to become enlarged and hyperactive.
  • most common causes : are kidney failure and vitamin D deficiency.
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15
Q

describe tertiary hyperparathyroidism?

A
  • chronic hypocalcaemia
  • parathyroid responds with elevated PTH
  • but if it goes unchecked the gland enlarge and become autonomous
  • secrete PTH in the absence of hypocalcaemia
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16
Q

trousseau’s sign

A
  • inflate BP cuff to 10mmHG about systolic BP
  • leave cuff on to induce local hypoxia
  • observe flexion at wrist, occurs slowly
  • present in 94% of hypocalcaemia cases
17
Q

chvostek’s sign

A
  • tap over the area of facial nerve
  • observe twitching of facial muscles, twitching of lip to spasm of all facial muscles
  • absent in 1/3rd of hypocalcaemia cases
18
Q

How may sepsis lead to hypocalcaemia in patients?

A
  1. increased cytokine production
    a) reduced parathyroid gland activity
    b) reduced renal 1-a-hydroxylation
    c) resistance to 1,25(OH)2D
  2. LEADS TO LOW IONISED Ca2+
19
Q

psuedohypocalcaemia

A
  • contamination of blood sample with EDTA