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BRS - Endo > Regulation Of Ca+ And PO4 > Flashcards

Regulation Of Ca+ And PO4 Flashcards

1
Q

What is calcium?

A

Most abundant metal in our bodies

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2
Q

How is the body’s calcium requirement met?

A

Diet meets all requirements

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3
Q

What is the recommended calcium intake for an adult?

A

1000 mg/day

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4
Q

Why is calcium important?

A
  • Neuromuscular excitability
  • Muscle contraction
  • Bone strength
  • Intracellular 2nd messenger
  • Intracellular co-enzyme
  • Hormone/neurotransmitter stimulus-secretion coupling
  • Blood coagulation (factor IV)
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5
Q

How is Calcium approximately distributed in the body?

A

Skeleton (99%)
Intracellular (1%)
Extracellular (0.1%)

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6
Q

How is extracellular calcium distributed?

A

Ionised (45%)
Bound (the rest)
→ to plasma proteins (45%)
→ as anions

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7
Q

How is calcium stored in bones + teeth?

A

As calcium hydroxyapatite crystals

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8
Q

What part of total body calcium is biologically active?

A

Extracellular, unbound + ionised calcium

approx 50% of serum calcium

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9
Q

Why is phosphate important?

A

Essential component of:
• High energy compounds e.g. ATP
• 2nd messengers
• Fundamental molecules eg DNA, RNA, phospholipids

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10
Q

Why are phosphates + calcium regulated by the same hormones?

A

Extracellular phosphate is inversely proportional to extracellular calcium

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11
Q

What hormones regulate + increase calcium?

A

Parathyroid Hormone + Vitamin D (mainly act on gut, bone + kidney)

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12
Q

What hormone regulates + decreases calcium?

A

Calcitonin

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13
Q

What are the 2 sources + types of Vitamin D?

A

Diet = vitamin d2 (ergocalciferol)

Sun + skin = vitamin d3 (cholecalciferol)

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14
Q

How is Vitamin D3 synthesized?

A

When UVB meets skin:

7-dehydrocholesterol → pre-vitamin D3 → vitamin d3

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15
Q

How is vitamin D2 + D3 used to synthesize the active form of vitamin D?

A

Vitamin d2 + d3 → 25(OH)cholecalciferol
Enzyme: 25-hydroxylase, in liver
25(OH)cholecalciferol → 1,25(OH)cholecalciferol
Enzyme: 1-alpha hydroxylase, in kidney

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16
Q

Why is serum 25(OH)cholecalciferol useful?

A

Can be measured as a good indicator of vitamin D levels

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17
Q

What is calcitriol?

A

Active form of Vitamin D, 1,25(OH)calciferol

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18
Q

How does Vitamin D regulate its own synthesis?

A

Decreases transcription of 1-alpha hydroxylase

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19
Q

How does calcitriol regulate calcium in the bones?

A

Increases calcium in bloodstream by increasing osteoclasts activity indirectly

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20
Q

How does calcitriol regulate calcium + phosphates in the kidneys?

A

Increases reabsorption of calcium + phosphate

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21
Q

How does calcitriol regulate calcium + phosphates in the gut?

A

Increases reabsorption of calcium + phosphate

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22
Q

What is PTH?

A

parathyroid hormone

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23
Q

Where is PTH produced + secreted?

A

chief cells in the parathyroid glands (embedded behind the thyroid gland)

24
Q

How is PTH secretion regulated?

A

G-protein coupled receptors on chief cells detect changes in circulating calcium concentration

25
Q

What happens to PTH secretion when serum calcium conc. is high?

A

PTH secretion is inhibited

26
Q

What happens to PTH secretion when serum calcium conc. is low?

A

PTH is secreted

27
Q

What is the relationship between PTH secretion and serum calcium?

A

both are inversely proportional

28
Q

How does PTH regulate calcium in bones?

A

Increases calcium in bloodstream by increasing osteoclasts activity indirectly

29
Q

How does PTH regulate calcium + phosphates in the gut?

A

increases absorption from gut

30
Q

How does PTH regulate calcium + phosphates in the kidneys?

A

increases calcium reabsorption from distal tubules + renal collecting ducts, BUT decreases phosphate reabsorption + plasma conc.

31
Q

How does PTH effect Vitamin D synthesis?

A

stimulates conversion of 25-hydroxy vitamin D → 1,25-dihydroxy vitamin D (calcitriol),
up-regulates 1-alpha hydroxylase

32
Q

How does Vitamin D effect PTH synthesis?

A

25(OH) vitamin D inhibits PTH secretion

33
Q

What is the difference between osteoblast and osteoclast?

A 
Osteoblast = BUILD bone
Osteoclast = CONSUME bone
34
Q

Why do PTH and Calcitriol INDIRECTLY increase osteoclast activity?

A

osteoclasts don’t have receptors; osteoblasts do - so hormones bind to osteoblasts + cause osteoclast precursors to form, creating new osteoclasts

35
Q

What is calcitonin?

A

hormone that reduces serum calcium (mechanism still unknown)

36
Q

Where is calcitonin produced + secreted?

A

parafollicular (C) cells of thyroid gland (however, removal of thyroid gland don’t affect serum calcium)

37
Q

How is calcitonin secretion regulated?

A

increase in serum calcium is detected by parafollicular cells + calcitonin release is triggered

38
Q

What does calcitonin regulate calcium?

A

decreases osteoclast activity (by increasing osteoblast activity) + increasing calcium excretion in kidneys

39
Q

What is FGF23?

A

fibroblast growth factor 23, protein that regulates phosphates + vitamin D

40
Q

How does FGF23 regulate phosphate reabsorption in kidneys?

A

decreases the expression of NPT2 (sodium-phosphate co-transporter) in the proximal tubule, decreasing phosphate reabsorption

41
Q

Where is FGF23 secreted from?

A

osteocytes when serum calcium levels are elevated

42
Q

What is hypocalcaemia?

A

low serum calcium levels

43
Q

What are the consequences of hypocalcaemia?

A

enables greater sodium influx → more membrane excitability → sensitises excitable tissues

44
Q

What are some general symptoms of hypocalcaemia?

A 
Paraesthesia (tingling, prickling, pins + needles)
Convulsions
Arrhythmias
Tetany
Muscle Cramps
45
Q

What are two specific signs of hypocalcaemia?

A

Chvostek’s Sign + Trousseau’s sign

46
Q

What is Chvostek’s Sign?

A

Tap facial nerve just below zygomatic arch; Positive response = twitching of facial muscles → Indicates neuromuscular irritability

47
Q

What is Trousseau’s sign?

A

Carpopedal spasm due to inflation of blood pressure cuff for several minutes = neuromuscular irritability

48
Q

What are causes of hypocalcaemia?

A
  • Low PTH levels = Hypoparathyroidism
  • Neck surgery
  • Auto-immune
  • Magnesium deficiency
  • Congenital (agenesis, rare) - Vitamin D deficiency
49
Q

What are causes of Vitamin D deficiency?

A
  • Malabsorption or dietary insufficiency
  • Inadequate sun exposure - - Liver disease
  • Renal disease
  • Vitamin D receptor defects
50
Q

What are consequences of Vitamin D deficiency?

A
  • Lack of bone mineralisation = ‘soft’ bones
  • In children – rickets (bowing of bones)
  • In adults – osteomalacia (fractures, proximal myopathy)
51
Q

What is hypercalcaemia?

A

high serum calcium

52
Q

What are the consequences of hypercalcaemia?

A

Ca2+ BLOCKS Na+ influx, so LESS membrane excitability

53
Q

What are signs + symptoms of hypercalcaemia?

A
  • Atonal muscles
  • Renal effects: Nephrocalcinosis – kidney stones, renal colic
  • GI effects:
    Anorexia, nausea, dyspepsia, constipation, pancreatitis
  • CNS effects:
    Fatigue, depression, impaired concentration, altered mentation, coma
54
Q

What are causes of hypercalcaemia?

A
  • Primary hyperparathyroidism

- Malignancy

55
Q

How does primary hyperparathyroidism cause hypercalcaemia?

A

too much PTH, usually due to a parathyroid gland adenoma, no negative feedback - high PTH, but high calcium

56
Q

How does malignancy cause hypercalcaemia?

A

Bony metastases produce local factors to activate osteoclasts, certain cancers (e.g. squamous cell carcinomas) secrete PTH-related peptide that acts at PTH receptors, vitamin D excess

BRS - Endo (9 decks)

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