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Year 1 Semester 2 Metabolism, Endocrinology & Haematology > S11) Calcium Metabolism > Flashcards

S11) Calcium Metabolism Flashcards

1
Q

What are the normal serum calcium levels?

A

Normal serum calcium levels are 2.2-2.6mmol/L

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2
Q

How is calcium transported in the blood?

A
  • Free ionized Ca2+
  • Bound to plasma proteins
  • Complexed with citrate
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3
Q

Where is most of the calcium in the body stored?

A

Skeleton – 99% is sequested bone in the form of hydroxyapatite crystals

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4
Q

What are the two primary functions of the skeleton?

A
  • Structural support
  • Maintains serum [Ca2+] (bone resorption & deposition)
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5
Q

Regulation of serum calcium is critically important for the execution of its various functions.

Identify some of these functions

A
  • Regulates heart rhythm
  • Mediates nerve transmission at NMJ
  • Role in intracellular signalling pathways
  • Assists in normal blood clotting
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6
Q

Which three substances are involved in the regulation of calcium levels?

A
  • Parathyroid Hormone
  • Vitamin D
  • Calcitonin
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7
Q

Explain the role of PTH in regulating serum calcium levels

A
  • Stimulates bone resorption and release of Ca2+ into circulation
  • Stimulates Ca2+ reabsorption in kidney and excretion of phosphate
  • Stimulates hydroxylation of 25-hydroxyvitamin D3 to make active Vitamin D (calcitriol)
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8
Q

Explain the role of dietary vitamin D in regulating serum calcium levels

A
  • Increases intestinal absorption of dietary Ca2+ and renal reabsorption of Ca2+
  • Increases bone resorption
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9
Q

Explain the role of calcitonin from the thyroid gland in regulating serum calcium levels

A

Calcitonin counteracts the effects of PTH

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10
Q

In terms of the feedback regulation of serum calcium, outline the body’s response to increases in calcium levels

A
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11
Q

In terms of the feedback regulation of serum calcium, outline the body’s response to decreases in calcium levels

A
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12
Q

Where are the parathyroid glands found?

A
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13
Q

What are the two kinds of cells found in the parathyroid glands?

A
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14
Q

Explain how calcium regulates the synthesis of PTH

A

Synthesis is regulated both at transcriptional and post transcriptional levels:

  • Low serum calcium up-regulates gene transcription (prolongs survival of mRNA)
  • High serum calcium down-regulates gene transcription
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15
Q

Describe the storage and synthesis of PTH

A
  • PTH is continually synthesised but little is stored
  • Chief cells degrade hormone as well as synthesis it
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16
Q

Identify the target organs of PTH and the different physiological effects brought about

A
  • Bone – increase resorption
  • Gut – activates Vitamin D and hence increases transcellular Ca2+ uptake from GI tract
  • Kidney – decreases Ca2+ loss to urine
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17
Q

Where are calcium phosphate crystals found?

A

Calcium phosphate crystals found within collagen fibrils aka. hydroxyapatite crystals

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18
Q

Bone is dynamic.

Describe the processes of bone resorption and bone deposition

A
  • Bone deposition: osteoblasts produce collagen matrix which is mineralised by hydroxyapatite
  • Bone resorption: osteoclasts produce acid, dissolving the micro-environment hydroxyapatite
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19
Q

In 1-2 hrs PTH stimulates osteolysis.

In 4 steps, describe the action of parathyroid hormone on bone

A

⇒ PTH induces osteoblastic cells to synthesise and secrete cytokines

⇒ Cytokines stimulate differentiation and activity in osteoclasts and protect them from apoptosis

⇒ PTH decreases osteoblasts’ activity exposing bony surface to osteoclasts

⇒ Reabsorption of mineralized bone releases of Pi and Ca2+ into extracellular fluid

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20
Q

Describe the effect of PTH on the tubular cells in the kidney in terms of calcium and phosphate reabsorption

A

A – PTH increases Ca2+ reabsorption in ascending limb and DCT

B – Pi is removed from circulation by inhibiting its reabsorption in the ascending limb and DCT (prevents calcium stone formation)

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21
Q

Dietary intake of calcium is typically 1000 mg/d.

Describe how this is usually absorbed?

A
  • Only 30% is absorbed by a paracellular uptake
  • Absorption is significantly increased by Vitamin D via transcellular uptake
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22
Q

How can we obtain Vitamin D?

A

Vitamin D is a lipid soluble vitamin that can be derived from plants or through action of sunlight on cholesterol in the skin

23
Q

Identify and describe the two forms of Vitamin D

A
  • D3 (cholecalciferol) made in skin and from dairy using sunlight
  • D2 (ergocalciferol) made when yeast and fungi are added to margarines as a supplement
24
Q

Identify two shared characteristics of the two forms of Vitamin D

A
  • Both form calcitriol (active form of Vitamin D)
  • Both are equipotent
25
Q

Describe how active Vitamin D takes two hydroxylation reactions to turn cholecalciferol from skin or diet into calcitriol

A
  • In the liver (C-25): 25-hydroxyvitamin D (major circulating hormone)
  • In the kidney (C-1): 1,25(OH)2 / calcitriol
26
Q

How is Vitamin D3 transported?

A

In the circulation vitamin D3 is bound to transcalciferin with only a small fraction in free form

27
Q

Describe the hydroxylation of Vitamin D3 in the kidney

A
  • Pre-vitamin is bound to carrier small enough to be filtered by the glomerulus and enter PCT
  • Conversion to active form occurs by enzyme 1α-hydroxylase
28
Q

What is the t1/2 of the active form of Vitamin D?

29
Q

Explain the control of Vitamin D3 hydroxylation

A
  • Elevated serum calcium prevents C-1 hydroxylation
  • Elevated PTH stimulates C-1 hydroxylation to form calcitriol
30
Q

What is the effect of calcitriol?

A

Calcitriol decreases the urinary loss of calcium by stimulating reabsorption in the kidney

31
Q

Describe the structure of cells in the thyroid gland

32
Q

Calcitonin is the third hormone involved in Ca2+ regulation.

How is it secreted?

A

Calcitonin is secreted by parafollicular cells (C cells) of thyroid gland

33
Q

Which two conditions result from imbalances in calcium regulation?

A
  • Hypocalcaemia
  • Chronic hypercalcaemia
34
Q

Why is EDTA / citrate used during blood donations?

A
  • Calcium has a role in blood clotting
  • EDTA/citrate is used to chelate calcium ions
  • Prevents donated blood from clotting
35
Q

Why are recipients of massive blood transfusions given intravenous calcium?

A
  • Citrate in donated blood binds with calcium in blood thus depleting free calcium ions
  • IV calcium gluconate restores free calcium ion levels
36
Q

Describe the aetiology of hospital setting hypercalcaemia

A
  • Malignant osteolytic bone metastases
  • Multiple myeloma
37
Q

Identify four common cancers that metastasise to bone causing lytic lesions and hypercalcemia

A
  • Breast
  • Lung
  • Kidney
  • Thyroid
38
Q

Prostate cancer is a common cause of bone metastases.

Why does is not lead to hypercalcaemia?

A

Prostate cancer causes osteoblastic metastases that do not cause hypercalcemia

39
Q

What are the common sites for bone metastases?

A
  • Vertebrae
  • Pelvis
  • Proximal parts of the femur
  • Ribs
  • Proximal part of the humerus
  • Skull
40
Q

What is hyperparathyroidism?

A

Hyperparathyroidism is a rare hormone disorder due to the excessive production of parathyroid hormone by the parathyroid glands

41
Q

What are the clinical features of primary hyperparathyroidism?

A
  • One of the parathyroid glands develops an adenoma and secretes excessive amounts of PTH
  • Serum calcium rises and serum phosphate falls
42
Q

What are the clinical features of secondary hyperparathyroidism?

A
  • All parathyroid glands become hyperplastic
  • Seen in patients with Vitamin D deficiency
43
Q

Identify some possible causes of Vitamin D deficiency

A
  • Dietary
  • Environment
  • Chronic renal failure (failure of C-1 hydroxylation)
44
Q

In 5 steps, explain the effects of Vitamin D deficiency on calcium levels

A

⇒ Vitamin D deficiency

⇒ Low calcium absorption

⇒ Low serum calcium levels

⇒ PTH levels rise

⇒ Activated osteoclasts mobilise calcium from bone in an attempt to maintain normal serum calcium

45
Q

Describe the serum biochemistry in the following conditions:

  • Primary Hyperparathyroidism
  • Secondary Hyperparathyroidism
  • Malignant hypercalaemia
46
Q

What are the symptoms of primary hyperparathyroidism?

A
  • Moans – tired, exhausted, depressed
  • Groans – constipation, peptic ulcers, pancreatitis
  • Stones – kidney stones + polyuria due to impaired sodium and water reabsorption
  • Bones – bone and muscle aches
47
Q

What is the role of calcium in neuronal activity?

A

Calcium raises the threshold for nerve membrane depolarisation and therefore the development of an action potential

48
Q

In terms of the role of calcium in neuronal activity, describe the symptoms of hypercalcaemia and hypocalcaemia

A
  • Hypercalcaemia leads to supression of neuronal activity – lethargy, confusion, coma
  • Hypocalcaemia leads to ‘excitable’ nerves – tingling, muscle tetany and even epilepsy
49
Q

What are the symptoms of severe hypercalcaemia (serum calcium > 3.0 mmol/l)?

A

Polyuria leads to dehydration which then exacerbates the hypercalcemia:

  • Lethargy
  • Weakness
  • Confusion
  • Coma
  • Renal failure
50
Q

How is severe hypercalcaemia treated?

A

Rehydration is the mainstay of treatment

51
Q

Where is symptomatic hypocalcaemia seen (serum calcium < 2.10 mmol/l)?

A

Seen mostly in post total-thyroidectomy patients because of inadvertant removal/ischaemia of parathyroid glands

52
Q

Motor homunculus due to tetany of muscles is a feature of symptomatic hypocalcaemia.

Which clinical sign presents?

A

Carpopedal sign

53
Q

Compare and contrast osteoporosis with osteomalacia in terms of:

  • Mineral:matrix
  • Physiological process
  • Consequences
  • Risk factors / causes

Year 1 Semester 2 Metabolism, Endocrinology & Haematology (20 decks)

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