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PT4023 CA1 > L8 Calcium & Bone > Flashcards

L8 Calcium & Bone Flashcards

1
Q

Generic name for vitamin D

A

Calciferol

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2
Q

Generic name for vitamin D3

A

Cholecalciferol

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3
Q

Generic name for vitamin D2

A

Ergocalciferol

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4
Q

Generic name for 25-hydroxyvitamin D

A

Calcifediol

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5
Q

Generic name for 1,25(OH)₂D

A

Calcitriol

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6
Q

Clinical indications of Cholecalciferol and Ergocalciferol

A
  • Vitamin D deficiency
  • Vitamin D malabsorption
  • Hypoparathyroidism
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7
Q

Clinical indications of Calcitriol

A
  • Secondary hyperparathyroidism of CKD
  • Hypoparathyroidism
  • Hypophosphatemic rickets with decreased calcitriol levels
  • Acute hypocalcaemia
  • Pseudovitamin D-deficient rickets
  • Hereditary vitamin D-resistant rickets
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8
Q

Do children or adults have higher 1,25(OH)₂D levels?

A

children

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9
Q

Main function of vitamin D metabolites

A

The regulation of calcium and phosphate homeostasis, which occurs in conjunction with PTH

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10
Q

Principle target tissues for regulation of calcium and phosphate homeostasis

A

Gut, kidney and bone

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11
Q

Major pathologic complication of vitamin D deficiency

A

Rickets (in children with open epiphyses) or osteomalacia (in adults), due to deficiency of the calcium and phosphate required for bone mineralisation

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12
Q

Which is the most biologically active vitamin D metabolite?

A

1,25(OH)₂D

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13
Q

Best-known cause of abnormal bone mineralisation

A

Vitamin D deficiency

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14
Q

Vitamin D permits osteoblasts to…

A

produce a bone matrix that can be mineralised and then allows them to mineralise that matrix normally

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15
Q

Many hypophosphatemic conditions result from excess circulating __. What is the result of this?

A

FGF23
Can both decrease 1-hydroxylase activity and renal phosphate reabsorption

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16
Q

What causes osteomalacia and rickets?

A

abnormal mineralisation of bone and cartilage

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17
Q

What is osteomalacia?

A

A bone defect occurring after the epiphyseal plates have closed (i.e. in adults)

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18
Q

Rickets occurs in __ bone.

A

growing

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19
Q

What occurs as a result of abnormal mineralisation in patients with rickets?

A

an enormous profusion of disorganised, non-mineralised, degenerating cartilage appears in the zone of provisional calcification, leading to widening of the epiphyseal plate with flaring or cupping and irregularity of the epiphyseal-metaphyseal junctions

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20
Q

What is the clinical term for obvious beaded swellings along the costochondrial junctions in patients with rickets?

A

Rachitic rosary

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21
Q

Why is defective mineralisation more difficult to observe in adults?

A

because once bone growth has ceased (closure of epiphyseal plates), the clinical evidence for defective mineralisation becomes more subtle

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22
Q

Causes of osteomalacia

A
  • Disorders of the vitamin D endocrine system (most significant cause)
  • Disorders of phosphate homeostasis
  • Calcium deficiency
  • Primary disorders of bone matrix
  • Inhibitors of mineralisation
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23
Q

Treatment for vitamin D deficiency

A

Alfacalcidol, Dihydrotachysterol
- promote active transport of calcium & phosphate in GIT (increased reabsorption) & renal tubule (decreased excretion)

24
Q

A single dose of vitamin D has biological effects for how long?

A

up to 6 months

25
Q

What is the best understood target tissue response of 1,25(OH)₂D?

A

intestinal calcium transport

26
Q

Calcium transport through the intestinal epithelium

A
  1. Entrance of calcium into cell from lumen across brush border membrane down a steep electrochemical gradient
  2. Passage through the cytosol
  3. Removal of calcium from cell against a steep electrochemical gradient at basolateral membrane
27
Q

1,25(OH)₂D induces a change in the binding of calmodulin to __.

A

brush border myosin 1
(calmodulin-myosin 1 complex may provide a mechanism for removing calcium from the brush border)

28
Q

Which calcium channel in the brush border membrane is induced by 1,25(OH)₂D? And what is the channel’s role?

A

TRPV6
- likely the major mechanism by which calcium enters the intestinal epithelial cell

29
Q

What is required for calcium transport through the cytosol?

A

a vitamin D-inducible protein called calbindin (exists in either a 28kDa or 9kDa form)

30
Q

Which pump removes calcium from the cell at the basolateral membrane?

A

Ca2+-ATPase (PMCA1b)

31
Q

How is phosphate absorption from the intestine regulated?

A

via NaPi-IIb, whose levels are increased by 1,25(OH)₂D

32
Q

Key feature of the defence against hypercalcemia

A

suppression of PTH secretion
- reduces bone resorption, renal production of 1,25(OH)₂D and intestinal calcium absorption
- increases urinary calcium losses

33
Q

What is the only route of net calcium elimination in hypercalcemia?

A

kidney

34
Q

What causes increased renal calcium excretion in hypercalcemia?

A

a combination of increased filtered load of calcium and PTH suppression

35
Q

Nausea and vomiting in hypercalcemia may predispose to…

A

dehydration and renal azotaemia

36
Q

What compromises calcium clearance, perpetuating the viscous cycle of hypercalcemia?

A

renal insufficiency

37
Q

Only alternative to the renal route for calcium elimination from ECF in a hypercalcemic state?

A

deposition of calcium phosphate and other salts in bone and soft tissues

38
Q

Disorders causing hypercalcemia

A
  • Primary hyperparathyroidism (common)
  • Malignancy-associated hypercalcemia
  • Sarcoidosis and other granulomatous disorders
  • Endocrinopathies e.g. thyrotoxicosis, adrenal insufficiency
  • Thiazide diuretics
  • Hypervitaminosis D and A
  • Milk-alkali syndrome
  • Miscellaneous conditions e.g.s immobilisation, acute renal failure
39
Q

Mnemonic for primary hyperparathryoidism signs and symptoms

A

‘Stones, bones, abdominal groans, and psychic moans’

40
Q

Ophthalmic condition associated with hypercalcemia

A

band keratopathy

41
Q

Temporary hypercalcemia treatment

A
  • Physiological saline (correct volume depletion and increase renal calcium excretion)
  • Bisphosphonates e.g. Pamidronate, Zoledronic acid (inhibit bone resorption)
  • Calcitonin (maintains calcium levels by suppressing PTH)
  • Corticosteroids i.e. Prednisolone (reduce intestinal calcium absorption)
  • Dialysis (in renal failure)
42
Q

Long-term treatment for hypercalcemia

A
  • Sodium cellulose phosphate (Calcisorb - binds calcium in gut) - for patients who over-absorb dietary calcium
  • Inorganic phosphate (sodium acid phosphate)
43
Q

Causes of hypocalcemia

A
  • Hypoparathyroidism
  • Resistance to PTH action
  • Failure to produce 1,25(OH)₂D normally
  • Resistance to 1,25(OH)₂D action
  • Acute complexation or deposition of calcium
44
Q

What are many of the complications of hypocalcemia treatment a result of?

A

the deposition of calcium in soft tissue

45
Q

What ophthalmic condition is common in chronic hypocalcemia?

A

subcapsular cataract

46
Q

Dermatological effects of hypocalcemia

A

dry and flaky skin, brittle nails

47
Q

Treatment for hypocalcemia patients with tetany

A

intravenous calcium: calcium gluconate/calcium glucoheptate, with constant electrocardiographic monitoring

48
Q

IV calcium can mimic and synergise with __ to have serious cardiac effects

A

digitalis

49
Q

Treatment for acute hypocalcemia

A

oral calcium and a rapidly-acting preparation of vitamin D (e.g. calcitriol)

50
Q

Chronic hypocalcemia treatment

A
  • calcium carbonate/calcium citrate
  • in patients with vitamin D deficiency: combined calcium with cholecalciferol
  • in patients with hypoparathyroidism: Alfacalcidol or calcitriol
51
Q

What is osteoporosis?

A

A condition of low bone mass and microarchitectural disruption that results in fractures with minimal trauma

52
Q

Primary vs. secondary osteoporosis

A

Primary: reduced bone mass & fractures in postmenopausal women, or in older men & women due to age-related factors
Secondary: bone loss resulting from specific clinical disorders

53
Q

Two types of endocrine treatment for osteoporosis

A
  1. Anabolic
    - PTH-specific
    - bone gain
  2. Anti-resorptive
    - maintain bone
54
Q

Example of PTH-specific osteoporosis medication

A

Teriparatide

55
Q

What drugs are considered anti-resorptive endocrine treatment?

A
  • Bisphosphonates e.g. Alendronate (inhibits bone resorption)
  • Calcitonin (suppresses PTH), Salcatonin (inhibits bone resorption)
  • SERM e.g. Raloxifene (acts as an agonist at bone oestrogen receptors)
  • HRT
  • Vitamin D e.g. Ergocalciferol (D2)
56
Q

How do SERMs work?

A

They act as agonists at bone & CVS oestrogen receptors, and as antagonists at oestrogen receptors in mammary tissue & uterus

57
Q

How do excessive levels of glucocorticoids cause osteoporosis?

A

Physiologic levels of GCs: osteoblast differentiation
Excessive levels of GCs lead to decreased osteoblast differentiation and increased osteoclast action. GC therapy is associated with an appreciable risk of bone loss.

PT4023 CA1 (8 decks)

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