calcium and bone Flashcards

calcium regulation: explain the hormonal regulation of blood calcium ion concentration; list the causes and clinical features of hypercalcaemia and hypocalcaemia

1
Q

diagram of calcium homeostasis: interaction between PTH and vitamin D

A

diagram; PTH to increase serum Ca2+: increases Ca2+ reabsorption from bone, causes kidney to reabsorb Ca2+, regulates production of active vitamine D (calcitriol); inactive vitamin D (calcidiol) is from liver and undergoes 1a hydroxylation under control of PTA, increasing serum Ca2+ by increasing Ca2+ absorption from gut

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2
Q

phosphate absorption regulation

A

Na+/PO43- absorbed via cotransporter from urine in proximal convoluted tubule; PTH from blood inhibits this, as does fibroblast growth factor 23 (FGF23 - from osteocytes); this also inhibits calcitriol synthesis, reducing PO43- reabsorption from gut

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3
Q

where does phosphate reabsorption occur

A

via gut and kidneys

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4
Q

what does increase phosphate reabsorption cause to Na+

A

less Na+ excretion in urine (as co-transported in)

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5
Q

effect on serum PO43- in hyperparathyroidism

A

low as increased urine phosphate excretion (PTH inhibits Na+/PO43- transporters)

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6
Q

regulation of PTH secretion: high [Ca2+] ECF

A

Ca2+ binds to Ca2+ sensin receptor on parathyroid cell -> receptor activation leads to inhibition of PTH secretion

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7
Q

regulation of PTH secretion: low [Ca2+] ECF

A

Ca2+ not bound to Ca2+ sensin receptor -> no inhibition -> PTH secreted -> PTH action in body leads to increased [Ca2+] ECF

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8
Q

role of vitamin D in calcium homeostasis

A

diagram

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9
Q

where is vitamin D obtained from

A

vitamin D obtained from diet (ergocalciferol to inactive vitamin D calcidiol in liver) or sunshine (UVB light); in kidney, 1a-hydroxylase (stimulated by PTH) produces calcitriol (active vitamin D)

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10
Q

effect of cacitriol on PTH, and Ca2+

A

negative feedback on PTH; increases Ca2+ gut absorption, maintenance in bone, renal Ca2+ reabsorption

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11
Q

5 causes of vitamin D deficiency

A

malabsorption or dietary insufficiency, lack of sunlight (block UVB light), liver disease (can’t convert to calcidiol), renal disease (no stimulation of renal 1a-hydroxylase by PTH to convert to calcitriol), receptor defects in gut, bone, kidney and parathryoid gland

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12
Q

2 examples of diseases causing GI malabsorption of vitamin D

A

coeliac, inflammatory bowel

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13
Q

inheritance and prevalence of vitamin D receptor defects, and response to treatment

A

autosomal recessive, rare, resistant to vitamin D treatment

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14
Q

high EC Ca2+ (hypercalcaemia) effect on nerve and skeletal muscle excitability

A

Ca2+ blocks Na+ influx as more competition, so less membrane excitability

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15
Q

low EC Ca2+ (hypocalcaemia) effect on nerve and skeletal muscle excitability

A

enables greater Na+ influx as less competition, so more membrane excitability

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16
Q

4 signs and symptoms of hypocalcaemia (CATs go numb)

A

parasthesia (hands, mouth, feet, lips), convulsions, arrythmias, tetany

17
Q

explain symptoms of hypocalcaemia

A

sensitises excitable tissues, to muscle cramps/tetany, tingling

18
Q

what do Chvostek’s and Trousseau’s signs indicate

A

neuromuscular irritability due to hypocalcaemia

19
Q

describe Chvostek’s sign

A

tap facial nerve just below zygomatic arch -> positive response is twitching of facial muscles

20
Q

describe Trousseau’s sign

A

inflation of BP cuff for several minutes to induce carpopedal spasm

21
Q

4 causes of hypocalcaemia

A

vitamin D deficiency, low PTH levels (hypoparathyroidism), PTH resistance (e.g. pseudohypoparathryoidism), renail failure

22
Q

3 caues of low PTH levels (hypoparathyroidism)

A

surgical (neck injury), auto-immune, Mg2+ deficiency

23
Q

how does renal failure cause hypocalcaemia

A

impaired 1a hydroxylation, decreasing production of 1,25(OH)2D3

24
Q

signs and symptoms of hypercalcaemia

A

reduced neuronal excitability so atonal muscles; “stones” - renal effects, “abdominal moans” - GI effects and “psychic groans” - CNS effects”

25
Q

renal effects of hypercalcaemia

A

polyuria and thirst, nephrocalcinosis, renal colic, chronic renal failure

26
Q

GI effects of hypercalcaemia

A

gut slowed down so: anorexia, nausea, dyspepsia, constipation, pancreatitis

27
Q

CNS effects of hypercalcaemia

A

fatigue, depression, impaired concentration, altered mentation, coma

28
Q

4 causes of hypercalcaemia

A

primary hyperparathyroidism, malignancy (these 2 account for 90% of cases), conditions with high bone turnover, vitamin D excess (rare)

29
Q

how might malignancy cause hypercalcaemia

A

tumours/metastases often secrete a PTH-like peptide; cancer cells in bone cause release of Ca2+

30
Q

conditions with high bone turnover causing hypercalcaemia

A

hyperthyroidism, Paget’s disease of bone (immobilised patient)

31
Q

diagnostic approach to hypercalcaemia: normal axis

A

parathyroid cells detect low Ca2+, so increase PTH which raises Ca2+ - negative feedback to switch PTH off when sufficiently raised

32
Q

diagnostic approach to hypercalcaemia: primary hyperparathyroidism

A

raised Ca2+, low PO43- (PTH inhibits PO43- reabsorption in kidney), raised unsuppressed PTH (autonomous PTH secretion) as no negative feedback

33
Q

diagnostic approach to hypercalcaemia: hypercalcaemia of malignancy

A

raised Ca2+, suppressed PTH (no issue in parathyroid glands, but cancer deposits in bone causing release of Ca2+ from bone)