Calcuim and Phosphate metabolism Flashcards

1
Q

What is the distribution of calcium in the body?

A
  • 1st largest pool- ~90% calcium in bone in form of hydroxyapatite crystals.
  • 2nd largest pool : intracellular calcium mitochondria and ER
  • Smallest pool : ECF (interstitial calcium and blood calcium.
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2
Q

What are the two primary calcium channels in the cell membrane and their controls?

A
  • Voltage gated channels: Muscles and nerve cells. These are controlled by electric membrane potential.
  • Ligand Gated channels: When ligand binds to receptor it opens channel. Most cells have this and is controlled by hormones and neurotransmitters.
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3
Q

How is calcium absorbed in the intestine?

A

absorption occurs by either passive diffusion: If there is high calcium content in the lumen. Or active transport when there is low calcium in the lumen. This is regulated by vitamin D.

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4
Q

How is calcium reabsorbed in the kidney?

A

• Ca++ reabsorbed at proximal tubules, then distal tubules then ascending loop of henlee.

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5
Q

What is the calcium distribution in the bone?

A

• soluble portion of bone ( amorphous crystal and soluble calcium) which is between osteoblasts and osteocytes.

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6
Q

What are the cell types in the parathyroid gland?

A

◦ Chief cells create PTH
◦ Oxyphil cells: Fxn’s unknown

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7
Q

How do the Chief cells in the parathyroid gland sense calcium and magnesium levels to initiate the synthesis and release of PTH?

A

• Chief cells have a calcium sensor which, when decrease is detected it will cause release of PTH

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8
Q

What is the overall effect of PTH on calcium and phosphate metabolism?

A

Effect of PTH is to increase calcium and decrease phosphate.

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9
Q

What are the effects of PTH on amorphous bones?

A

◦ Transfer calcium across the osteoblast-osteocyte membrane
◦ No effects of phosphate concentrations in the blood

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10
Q

What are the effects of PTH on stable bones?

A
  • PTH stimulates osteoblasts to secrete receptor activator of nuclear factor kappa b ligand ( RANK or RANK L). RANK L will activate Osteoclast precursor, which will create an active osteoclast.
  • This will also cause inhibition of OPG or osteoprogesterin, which competes to bind with ligand, and will decrease the creation of osteoclasts.
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11
Q

What are the effects of PTH in the kidney?

A
  • PTH will decrease Phosphate reabsorption in the proximal convoluted tubules.
  • Ca++ reabsorption increases in the distal convoluted tubules.
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12
Q

How does PTH regulate the synthesis of the active vitamin D?

A
  • PTH can promote the fxn of 1a - hydroxylase which will produce calcitriol. This will also be the reason 24-hydroxylase is produced which can also be formed because of high serum phosphate. The result is 24-25 (OH)2 D (inactive)
  • 24- hydroxylase inactivates 1,25 (OH)2 D.
  • feedback regulations. ***
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13
Q

How does the active vitamin D regulate calcium and phosphate metabolism?

A

1.) Ca++ absorption in intestine
2.) Ca++ absorption in kidney
3.) Ca++ and phosphate release in bone.
All will result in increase in calcium

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14
Q

What are the primary functions of calcitonin?

A
  • Calcitonin counteracts the fxns of vitamin D and PTH.
  • Inhibits osteoclasts and stimulates osteoblasts- decrease in mvmt of ca++ from labile bone calcium pool to the ECF.
  • Inhibits Ca2+ absorption in the GI,
  • Increases renal excretion of calcium and phosphate.
  • This can lead to hypocalcemia and hyphosphatemia.
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15
Q

How does too much blood transfusion cause hypocalcemia?

A

When given too much blood (i.e transfusion) the blood product will have too much citrate and EDTA which can chelate Ca++ (or make it form a complex that is not absorbable

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16
Q

Why does hypocalcemia cause cells to be more excitable?

A

Sodium channels are unstable, cells more easily excited. Cells depolarize easier.

17
Q

What are the characteristic clinical symptoms during hypocalcemia?

A

◦ Involuntary muscle contraction.
‣ Chvosteks sign: Twitch of facial muscles that occurs when gently tapping an individuals cheek in front of the ear.
‣ Trusseaus sign: Involuntary contraction fo muscles in hand. wrist ( i.e carpopedal spasm) this occurs after the compression of the upper arm with a blood pressure cuff.
◦ Tetany: involuntary muscle contraction
◦ Other: muscle cramps, abd pain, perioral tingling, seizures.

• Can cause arrhythmias ( torsades de pointes ( prolonged ST segment, prolonged QT)

18
Q

How do you treat hypocalcemia?

A

Treatment: Normalize calcium
• give calcium gluconate
• supplement vitamin D

19
Q

What are the common causes of hypercalcemia?

A
  • acidosis
  • Parathyroid overgrowth
  • Malignant Tumors
  • Excess vitamin D
20
Q

How does acidosis cause hypercalcemia?

A

• Acidosis can cause hypercalcemia - this is because there is lots of protons, so the proteins available to bind calcium are decreased, leading to a relative increase in free calcium levels (hence hypercalcemia symptoms) and decreased bound calcium. However, total calcium levels can be normal.

21
Q

What are the characteristic clinical symptoms during hypercalcemia?

A
  • Can cause slower or absent reflexes (classic symptoms)
  • Slow muscle contraction (constipation/ muscle weakness)
  • Confusion, hallucination, stupor
  • Organ Mineralization
  • Kidney/ urinary stones.
  • You will see Osborn wave (and short QT interval)
  • Bradycardia
  • AV block
22
Q

How does hypercalcemia cause kidney stones?

A

Hypercalciuria causes loss of fluid and dehydration. This will lead to formation of calcium oxalate stones.

23
Q

How do you treat hypercalcemia?

A
  • Treatment : Lower Ca2+ levels with medications
  • Increase urinary excretion : Rehydrate ( more ca2+ filtered), Loop diuretics ( inhibit ca2+ resorption) Furosemide?
  • Increase GI excretion ( glucocorticoids) -> decrease calcium absorption.
  • Prevent bone resorption: Bi-phosphates and calcitonin -> inhibits osteoclasts