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Z YEAR 2 BRS ENDO > Calcium Dysregulation > Flashcards

Calcium Dysregulation Flashcards

1
Q

What increases calcium?

A
  1. Vitamin D

2. PTH secreted by parathyroid glands

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2
Q

How do you get vitamin D?

A

Synthesised in skin or intake via diet

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3
Q

What decreases calcium?

A

Calcitonin

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4
Q

What is calcitonin secretion by?

A

thyroid parafollicular cells

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5
Q

What is a good indicator of body vitamin D?

A

Serum 25-OH vitamin D

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6
Q

What is another name for 1,25(OH)2 vitamin D?

A

Calcitrol

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7
Q

What makes Vitamin D3?

A
  1. UVB on skin or diet Vit D2
  2. 7-dehydrocholesterol
  3. Pre vitamin D3
  4. Vitamin D3
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8
Q

What forms Vitamin D3 into 25(OH) cholecalciferol?

A

25 hydroxylase in the liver

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9
Q

What turns 25(OH) cholecalciferol into 1.25(OH)2 cholecalciferol?

A

1 alpha hydroxylase in the kidney

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10
Q

What is the active form of vitamin D?

A
  • Calcitriol

- Once. calicotriol made negative feedback to 1 alpha hydroxlase

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11
Q

What are the effects of calcitriol?

A
  1. Increased osteoblast activity
  2. Increase Ca2+ absorption from gut + in kidney
  3. Increase PO4 3- absorption from gut + in kidney
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12
Q

What does PTH do?

A
  1. Increase Ca2+ reabsorption from bone
  2. Increase Ca2+ absorption in gut
  3. Increase PO4 3- absorption gut
  4. Increase Ca2+ absorption in kidney
  5. Increase PO4 3- excretion in kidney
  6. Increase 1 alpha hydroxylase action in kidney so more calcitrol synthesised
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13
Q

What happens in hypocalcaemia?

A

Sensitises excitable tissues; muscle cramps, tetany, tingling

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14
Q

What are the symptoms in hypocalcaemia?

A
  1. Paraesthesia (hands, mouth, feet , lips)
  2. Convulsions
  3. Arrhythmias
  4. Tetany
  5. Chvosteks’ sign – facial paresthesia
  6. Trousseau’s sign – carpopedal spasm
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15
Q

What are causes of hypocalcaemia?

A
  1. Low PTH levels: hypoparathyroidism

2. Low vitamin D levels

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16
Q

Why might you have low PTH levels?

A
  1. Surgical – neck surgery
  2. Auto-immune (every endocrine gland)
  3. Magnesium deficiency
  4. Congenital (agenesis, rare)
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17
Q

What are reasons for low Vitamin D levels?

A

Deficiency – diet, UV light, malabsorption, impaired production (renal failure)

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18
Q

What are the renal effects of hypercalcaemia?

A

Nephrocalcinosis – kidney stones, renal colic

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19
Q

What are the GI effects of hypercalcaemia?

A
  1. Anorexia
  2. nausea
  3. dyspepsia
  4. constipation
  5. pancreatitis
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20
Q

What are CNS effects of hypercalcaemia?

A
  1. Reduced neuronal excitability – atonal muscle
  2. Fatigue
  3. depression
  4. impaired concentration
  5. Altered mentation
  6. coma (usually >3mmol/L)
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21
Q

What are the causes of hypercalcaemia?

A
  1. Primary hyperparathyroidism
  2. Malignancy
  3. Vitamin D excess (rare)
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22
Q

What primary hyperparathyroidism would cause hypercalcaemia?

A
  1. Too much PTH
  2. Due to a parathyroid gland adenoma
  3. No negative feedback - high PTH, but high calcium
23
Q

What malignancy would cause hypercalcaemia?

A
  1. Bony metastases produce local factors to activate osteoclasts (release calcium)
  2. Certain cancers (eg squamous cell carcinomas) secrete PTH-related peptide that acts at PTH receptors
24
Q

What happens in parathyroid adenoma?

A
  1. Produce too much PTH
  2. Calcium increases, but no negative feedback to PTH due to autonomous PTH secretion from parathyroid adenoma (primary hyperparathryoidism)
25
Q

What is the relationship between PTH and calcium?

A
  1. When Low Ca2+ feedback to parathyroid glands so high PTH

2. When High Ca2+ feedback to parathyroid glands low PTH

26
Q

What is the biochemistry of primary hyperparathyroidism?

A
  1. High calcium
  2. Low phosphate – increased renal phosphate excretion (inhibition of Na+/PO43- transporter in kidney)
  3. High PTH (not suppressed by hypercalcaemia)
27
Q

What is the treatment of primary hyperparathyroidism?

A

Parathyroidectomy

Untreated hyperparathyroidism has risks of

28
Q

What does untreated hyperparathyroidism have a risk of?

A
  1. Osteoporosis
  2. Renal calculi (stones)
  3. Psychological impact of hypercalcaemia – mental function, mood
29
Q

What is secondary hyperparathyroidism?

A

normal physiological response to hypocalcaemia

30
Q

What are the causes of secondary hyperparathyroidism?

A

vitamin D deficiency

31
Q

What are the common cause of vitamin D deficiency?

A

diet, reduced sunlight

32
Q

What are the less common causes of vitamin D deficiency?

A

renal failure – can’t make calcitriol in renal failure

33
Q

What is the biochemistry in secondary hyperparathyroidism?

A
  1. Calcium will be low or low/normal
  2. PTH will be high (hyperparathyroidism) secondary to the low calcium
    - diff from primary hyperparathyroidism where calcium is high
34
Q

How do you treat secondary hyperparathyroidism with people with normal renal function? What are the two forms?

A
  1. Give 25 hydroxy vitamin D
  2. Patient converts this to 1,25 dihydroxy vitamin D via 1a hydroxylase
  3. Ergocalciferol 25 hydroxy vitamin D2
  4. Cholecalciferol 25 hydroxy vitamin D3
35
Q

How do you treat secondary hyperparathyroidism with people with not normal renal function?

A
  1. inadequate 1a hydroxylation, so can’t activate 25 hydroxy vitamin D preparations
  2. Give Alfacalcidol - 1a hydroxycholecalciferol
36
Q

What is the general treatment of secondary hyperparathyroidism?

A

Vitamin D replacement

37
Q

When does tertiary hyperparathyroidism happen?

A

Rare, chronic renal failure

38
Q

What happens in tertiary hyperparathyroidism?

A
  • Occurs in chronic renal failure
    1. Can’t make calcitriol
    2. PTH increases (hyperparathyroidism)
    3. Parathyroid glands enlarge (hyperplasia)
    4. Autonomous PTH secretion causes hypercalcaemia
39
Q

What is the treatment for tertiary hyperparathyroidism?

A

parathyroidectomy

40
Q

What do you look at for patients with hypercalaemia?

A

PTH

41
Q

What is the diagnosis if patient with hypercalcaemia has raised PTH?

A
  • Hyperparathyroidism

- PTH should fall normal

42
Q

How do you diagnose vitamin D deficiency?

A
  1. Calcium will be low or low/normal

2. PTH will be high (hyperparathyroidism) secondary to the low calcium

43
Q

How is vitamin D measured?

A
  • as 25 (OH) vitamin D

- Calcitriol (1,25 dihydroxy vitamin D) is very difficult to measure

44
Q

What are the main regulators of calcium. and phosphate?

A

Homeostasis actions on kidney bone and gut

45
Q

What happens if parafollicular cells are removed?

A

There is no negative effect if parafollicular cells (make calcitonin) are removed e.g. thyroidectomy

46
Q

What is the overall effect of PTH?

A
  1. Increase activity of 1 alpha hydroxylase so more calciferol made so more Ca2+ and PO43- absorbed in gut to increase plasma Ca2+
  2. Acts on osteoclasts in bone to increase plasma Ca2+
  3. Increase Ca2+ reabsorption and PO43- excretion in kidney
47
Q

How is phosphate secreted in kidney?

A
  1. By Na+/PO43- co-transporter and PTH inhibits this channel and stops phosphate from being absorbed and also by FGF23
  2. If low PTH sometimes high phosphate
48
Q

What is FGF23?

A
  1. Inhibits Na+ and PO43- transporter
  2. Inhibits calcitrol so less phosphate reabsorption form gut as well
  3. Secreted by bones
49
Q

What happens in hyperparathyroidism e.g. with adenoma?

A
  1. Parathyroid adenoma producing too much PTH
  2. Calcium increases, but no negative feedback to PTH due to autonomous PTH secretion from parathyroid adenoma
  3. Primary hyperparathyroidism
50
Q

What happens in tertiary hyperparathyroidism?

A
  1. Chronic renal failure and chronic vitamin D deficiency so low calcium
  2. PTH increases a lot
  3. Overtime this PTH all 4 glands v busy and calcium goes up
51
Q

What are the levels like in hypercalcaemia?

A
  • High calcium (hypercalcaemia)

- Low/suppressed PTH

52
Q

What is hypercalcaemia due to sometimes?

A

malignancy

53
Q

What is the diagnosis if patient with hypercalcaemia has raised PTH?

A

hyperparathyroidism

Z YEAR 2 BRS ENDO (13 decks)

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