Calcium Flashcards

1
Q

Threat to calcium homeostasis?

  • gut
  • kidney
  • skeleton
A
  • steatorrhoea
  • renal failure
  • bony metastases
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2
Q

Threat to calcium homeostasis?

- Parathyroid

A

adenoma

damage due to thyroid surgery

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3
Q

Key actions of PTH?

  • hypercalcaemic
  • hypophophatemic
A
  • renal tubular reabsorption
  • bone reabsorption
  • GI tract absorption (incr renal generation of active vit D which then acts on the gut)
  • via reduced tubular reabsorption
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4
Q

Which form of vitamin D is measured

A

fdsfds

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5
Q

What is vitamin D called in the kidney?

A

Calcitriol (active form of bit D)

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6
Q

When is calcitriol used therapeutically?

A

In patients with renal failure (generally not used as a supplement because wuite expensive)

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7
Q

What is the active form of bit D?

A

1,35 - Vit D

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8
Q

What is main action of active vit D?

A

Incr gut (and kidney) calcium reabsorption

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9
Q

Why do we not measure the ionised form of calcium normally when that is the form that is physiologically active?

A

Hard to measure

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10
Q

How much of total serum calcium is ionised? Why can measuring total calcium cause problems? How do you overcome it?

A

45%
Disturbances in albumin (normally 10% of total calcium is bound to albumin) can > misinterpretation
Measure albumin

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11
Q

Threat to calcium homeostasis

- abnormal vit D metabolism?

A

Intake
Synthesis
Metabolism to 1,25 - dihydroxyvitamin D

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12
Q

What is the calculation for adjusted calcium?

A

Total calcium + 0.02 (40-albumin)

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13
Q

Mem aid for hypercalcaemia?

A

Bones (fractures), stones (kidney stones), abdominal groans and moans (psych)

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14
Q

Most common causes of hypercalcaemia

A

Malignancy

Primary hyperparathyroidism

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15
Q

Why is PTH important for hypercalcaemia interpretation? Meaning of each?

A

If PTH is suppressed, that is a normal response. Causes of hypercalcaemia

  • Malignancy
  • Vit D excess
  • Sarcoidosis (cells produce vit D)

If PTH is raised (or inappropriate)
- primary or tertiary hyperparathyroidism (+ calcium receptor defects e.g. familial hypocalcuric hypercalcaemia)

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16
Q

Hyperparathyroidism

  • primary
  • secondary
  • tertiary
A
  • primary parathyroid disorder(adenoma, hyperplasia)
    calcium is high

normal response to chronic hypocalcaemia (CRF, malabsorptions)
Calcium is low

Prolonged secondary state. PTH secretion becomes autonomous
Calcium is high (AFTER a kidney transplant)

17
Q

Markers of bones formation? What’s responsible for it?

A

Alp phos
bone elk phis
collagen peptides
(osteoblasts)

18
Q

Markers of bone resorption? Responsible for it?

A

Collage peptides
Pyridinolines (x links)
Urine hydroxyproline (not used that much)