L10: Calcium Metabolism and Disorders of Calcium Balance Flashcards

1
Q

What are the 3 main organ systems involved in calcium homeostasis?

A
  1. GIT
  2. Kidneys
  3. Bones
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2
Q

Calcium can be absorbed from the GIT, but it requires something for this to occur - what is it?

A

activated vitamin D (calcitriol)

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3
Q

What is the main calcium reservoir in the body? How is calcium exist in this reservoir?

A

reservoir: bone

- exists as hydroxyapatite

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4
Q

What is bone resorption?

A

bone broken down - Ca2+ released into blood

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5
Q

What type of Ca2+ can be filtered by the glomeruli in the kidneys?

A

ionized (free) calcium

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6
Q

Where in the kidney nephron is Ca2+ reabsorbed the most? Which area of reabsorption has an effect on calcium regulation + dysregulation?

A

70% Ca2+ reabsorbed passively in proximal tubule

15% Ca2+ reabsorbed actively in distal nephron – hasa an effect on regulation

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7
Q

Most of Ca2+ is ionized (free/unbound), but there is some Ca2+ which is bound to something to circulate in the blood. What is it bound to?

A

Albumin

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8
Q

What are the 2 main hormonal mediators of calcium balance?

A
  1. Parathyroid Hormone

2. Calcitriol (Vitamin D)

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9
Q

What cells are PTH secreted from?

A

chief cells of parathyroid hormone

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10
Q

What is the net effect of PTH?

A
  • increase calcium

- decrease phosphate

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11
Q

Describe the effect of PTH in response to hypocalcaemia in the GIT

A
  • promotes calcitriol formation (in kidney)
  • via upregulation of 1-alpha-hydroxylase enzyme
  • calcitriol increases GIT absorption of Ca2+
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12
Q

Describe the effect of PTH in response to hypocalcaemia in the BONES

A
  • increase in osteoclast number + activity

- increases bone resorption

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13
Q

Describe the effect of PTH in response to hypocalcaemia in the KIDNEY

A
  • increase in calcium reabsorption in distal nephron
  • also promotes increase in 1-alpha-hydroxylase enzyme
  • increases renal excretion of phosphate
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14
Q

How does PTH lead to a decrease in phosphate?

A

it increases renal excretion of phosphate

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15
Q

What is the function of 1-alpha hydroxylase enzyme?

A

promotes formation of calcitriol in kidney

– increases GIT absorption of Ca2+

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16
Q

What is the net effect of calcitriol?

A
  • increase Ca2+

- increase phosphate

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17
Q

Describe the effect of CALCITRIOL in response to hypocalcaemia in the GIT

A
  • increase absorption of Ca2+

- via increasing expression of TRPV6 channels

18
Q

Describe the effect of CALCITRIOL in response to hypocalcaemia in the BONES

A
  • increases pyrophosphate levels (mineralization inhibitor)

- increase bone calcium release

19
Q

Describe the effect of CALCITRIOL in response to hypocalcaemia in the KIDNEY

A
  • increases expression of TRPV5 channels + Calbindin-D28k

- increases reabsorption of calcium in distal convoluted tubule + CD

20
Q

What is bone mineralization?

A

the formation + growth of bone (structure)

21
Q

What is the catch phrase for the clinical manifestations of hypercalcaemia?

A

“Stones, bones, groans and pyschiatric overtones”

22
Q

What are the clinical manifestations of hypercalcaemia?

A
  • kidney stones
  • bone pain + weakness
  • abdominal pain + constipation
  • depression, confusion, lethargy
  • shorted QT interval on ECG
  • dehydration
23
Q

What is a common finding of hypercalcaemia on an ECG?

A

shortened QT interval

24
Q

List the 5 main causes of hypercalcaemia

A
  1. PTH Excess
  2. Vitamin D Excess
  3. Increased Bone Resorption
  4. Increased Ca2+ Intake
  5. Thiazides
25
Q

How can thiazides lead to hypercalcaemia?

A

increase Ca2+ reabsorption in the distal nephron

26
Q

In an outpatient, what is the most common cause of hypercalcaemia?

A

Primary Hyperparathryoidism

  • fault in parathyroid glands
  • too much PTH produced
27
Q

In an inpatient, what is the most common cause of hypercalcaemia?

A

malignancy + immobility

28
Q

How can immobility cause hypercalcaemia?

A

immobility leads to decrease in bone mass - bone resorption occurs

29
Q

To diagnose hypercalcaemia, if the PTH level is normal or elevated, what will the diagnosis be?

A

primary hyperparathyroidism

30
Q

To diagnose hypercalcaemia, if the PTH level is low and the PTHrP is elevated, what will the diagnosis be?

A

malignancy

31
Q

List the 5 possible treatment options for hypercalcaemia

A
  1. 0.9% Saline
  2. Frusemide
  3. Bisphosphonates
  4. Calcitonin
  5. Steroids
32
Q

Why may 0.9% saline be given to treat hypercalcaemia?

A
  • hypercalcaemia causes dehydration

- this is used for aggressive rehydration

33
Q

What is the MOA of frusemide? Why is it used to treat hypercalcaemia?

A
  • loop diuretic

- inhibits calcium reabsorption in distal tubule

34
Q

What is the MOA of bisphosphonates? What is it used to treat?

A
  • treatment for hypercalcaemia

- inhibits osteoclast bone resorption

35
Q

What is the management/treatment of primary hyperparathyroidism?

A

Parathyroidectomy

36
Q

What are the clinical manifestations of hypocalcaemia?

A
  • agitation
  • hyperreflexia
  • convulsions
  • hypertension
  • long QT interval
  • Trousseau’s Sign*
  • Chvostek’s Sign*
37
Q

What is Trousseau’s Sign? What is it indicative of?

A
  • upon inflation of BP cuff, get characteristic flexion at wrist and at MCP joint
  • get extension of IP joints

sign of hypocalcaemia

38
Q

What is Chvostek’s Sign? What is it indicative of?

A
  • it is the twitching of the facial muscles in response to tapping over the area of the facial nerve
  • sign of hypocalcaemia
39
Q

List the 4 main causes of hypocalcaemia

A
  1. Hypoparathyroidism
  2. Vitamin D Deficiency
  3. Bone Uptake
  4. Dietary Deficiency of Calcium
40
Q

List the 4 possible treatment options for hypocalcaemia

A
  1. Oral Calcium (calcium carbonate)
  2. IV Calcium (for severe symptoms)
  3. Vitamin D (calcitriol)
  4. Magnesium
41
Q

Why is magnesium given to treat hypocalcaemia?

A
  • magnesium is required for the production and release of parathyroid hormone
  • PTH will increase plasma calcium