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Physiology Renal Quiz 2 > Ca, Pi, and Mg Balance > Flashcards

Ca, Pi, and Mg Balance Flashcards

1
Q

What are the symptoms of Hypocalcemia?

A 
Bronchospasm
Blood pressure drop
Psychosis and seizures
Parasthesia, cramps, tetany, and Trouseau’s Sign
Long QT arrhythmias
Fractures and Ricket’s
Dry skin and nails.
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2
Q

What are the signs of hypercalcemia?

A 
Blood pressure increase
Lethargy, Depression, short term memory decrease, coma
Conjunctivitis red eye
GFR decrease
Kidney stones
Distal Renal Tubule Acidosis
Short QT arrhythmias
Parasthesia and Muscle weakness
Nausea, vomiting, ulcers, constipation
Anemia, bone fractures
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3
Q

Long QT arrhythmias are due to?
Short QT arrhythmias are due to?
(plasma Ca levels)

A

Hypocalcemia

Hypercalcemia

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4
Q

How does intracellular Ca binding to membrane proteins affect Na channels? (this happens in hypocalcemia)

A

• The channel gets fooled into thinking that it is depolarized, hence the threshold is reduced and causes spontaneous firing

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5
Q

Explain why hypocalcemia results in relaxed smooth muscle and active skeletal muscles.

A
  • Skeletal muscles are innervated and nerves become hypersensitive and is inversely proportional to plasma Ca (intracellular Ca binds to Na channels and fools them into thinking they are depolarized.
  • Smooth muscles are not innervated (as much) and their activity is proportionately dependent on plasma Ca concentration and Ca influx into cells
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6
Q

During hypercalcemia Ca salts may precipitate in soft tissues, leading to their calcification and the development of kidney stones.

A

Blank

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7
Q

What are the percentages of Ca reabsortion in which segments of the tubule?

A
  • 95 to 99% total
  • 70% in the proximal tubule
  • 20% in the thick ascending loop
  • the rest in the PT
  • small amount in the CD
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8
Q

Explain Ca reabsorption in the PT and the LOH. How are these affected by Na reabsorption?

A
  • passive and paracellular.

* Ca reabsorption is proportional to Na reabsorption in the PT and LOH

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9
Q

Explain Ca reabsorption in the DT. How are these affected by Na reabsorption?

A

• active transcellular route (regulated)
• enter the cell through a luminal Ca-channel
• pumped out basolateral side by a Ca2+-ATPase and a Na+/Ca2+ exchanger
• Ca absorption is inversely proportional to Na absorption (if Na absorption goes down, Ca absorption goes up)
o Na inhibits the basolateral Na/Ca exchanger

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10
Q

How do DT diuretics affect Ca reabsorption in the renal tubule?

A
  • DT diuretics such as Thiazadine are “Ca sparing” diuretics.
  • Decrease Na reabsorption in the DT and therefore increase Ca reabsorption in the DT
  • Also since Na reabsorption in the DT is inhibited, it causes Na reabsorption in the PT and LOH to increase, which is proportional to Ca reabsorption in those segments

• Combined synergistic increase of Ca reabsorption by DT diuretics
o K sparing diuretics, that inhibit Na reabsorption in the collecting duct, have a similar, but a much more modest effect, because only small amounts of Ca are reabsorbed in this segment and they are also less potent diuretics.

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11
Q

The DT (and intestines) have to shuttle Ca through their cells to get Ca into the blood. How is intracellular Ca levels maintained to an level that does not negatively affect the cell?

A

Calbindin

  • intracellular free [Ca2+] needs to be kept low
  • DT and intestines express a Ca2+-binding protein, calbindin.
  • Binding of Ca2+ to calbindin maintains a high total intracellular [Ca] thereby allowing a high rate of intracellular diffusion, while maintaining normal ionized [Ca2+].
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12
Q

How does Acid-Base affect plasma Ca levels binding to Albumin?

A
  • Acidic ph decreases binding of Ca to albumin

* alkaline pH increases binding of Ca2+ to albumin.

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13
Q

How does Acid-Base affect plasma Ca levels in acute and chronic?

A
  • alkaline pH increases binding of Ca2+ to albumin.
  • In a chronic setting, no effect on plasma [Ca2+] because PTH maintains [Ca2+] constant.
  • In Acute setting, such as acute hyperventilation, plasma [Ca2+] drop (hypocalcemia).
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14
Q

How does acid-base affect Ca reabsorption?

A
  • alkalosis increases reabsorption
  • acidosis increases Ca excretion.
  • chronic metabolic acidosis results in bone demineralization by osteoclasts and osteoblasts.
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15
Q

What is the main symptom of hypophosphatemia?

A 
•	Symptoms related to reduced ATP levels.
Decreased respiratory ventilation
Decreased Cardiac Output
Distal RTA
Musle weakness
Osteomalacia and Rickets
Hymolysis, decreased leukocyte function and platelet function.
Confusion, stupor, seizures, coma
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16
Q

How does acid and alkaline affect plasma and intracellular Pi levels? Is there a difference between respiratory and metabolic alkalosis?

A

• Alkalosis results in a shift of Pi from extracellular fluid into cells.
o Respiratory alkalosis, which has a larger effect on intracellular pH, results in a greater reduction of plasma Pi than metabolic alkalosis.

17
Q

Why does Alkalosis cause cellular influx of Pi?

A

• In intracellular alkalosis, phosphofructokinase activity increases. PFK uses Pi, thereby creating a concentration gradient for Pi entry.

18
Q

How is Pi absorbed in the intestines and excreted in the renal tubules? What segment of the nephron is the site of Pi regulation?

A
  • 2/3rd of dietary Pi is reabsorbed from the intestine
  • 85% of filtered Pi is reabsorbed in the PT in cotransport with Na.
  • The proximal tubule is also the main site of regulation of Pi excretion because downstream nephron segments reabsorb only a small fraction of the filtered Pi
19
Q

What are the two most important regulators of Ca and Pi homeostasis?

A
  • parathyroid hormone (PTH), secreted by the chief cells of the parathyroid gland
  • calcitriol, the active form of vitamin D3
20
Q

How do the Chief cells detect low Ca levels?

A
  • Low Ca causes PTH release
  • Chief cells express a Ca-sensing receptor (CaSR; a typical G-protein-coupled receptor). CaSR is a negative regulator of PTH release.
  • PTH secretion is under tonic inhibition by the Ca-bound CaSR, and hypocalcemia relieves the chief cells from this inhibition.
21
Q

What are the effects of PTH?

A
  • induces Ca and Pi release from bone (short term and ongoing)
  • stimulates Ca reabsorption in the distal tubule (long term)
  • inhibits Pi reabsorption in the proximal tubule (long term)
  • activates 1-alpha-hydroxylase which converts inactive Vit D3 to active Vit D3 which then increases Ca and Pi absorption in the intestines (long term)
22
Q

What does 1-alpha-hydroxylase do?

A

• converts an inactive form of vitamin D3 (25‐OH‐vitamin D3) to its active form, calcitriol (1,25‐(OH)2‐vitamin D3).

23
Q

Where is 1-alpha-hydroxylase found? (What cells have this enzyme?) Where does its product calcitriol have effect?

A
  • 1-alpha-hydroxylase resides in the proximal tubule.

* calcitriol stimulates the gut to absorb Ca (and Pi)

24
Q

How does plasma Pi affect renal regulation of Pi? How does PTH affect renal regulation of Pi?

A
  • Pi reabsorption in the PT is near Tm
  • increase in plasma [Pi] is spilled in the urine [minute-to-minute regulation of Pi]
  • PTH increases Pi loss by decreasing the number of Na/Pi-cotransporters (This lowers Tm)
  • Hyperphosphatemia lowers Tm and encourages Pi loss
  • Hypophosphatemia increases the Tm and encourages Pi reabsorption
25
Q

What is are phosphatonins? What does FGF23 do?

A
  • hormones collectively known as phosphatonins affect Pi regulation
  • The most important is FGF23, produced by bone, a potent inhibitor of Pi reabsorption.
26
Q

What does Mg do? (This will be broken down into steps)

A

• a co-factor for hundreds of enzymes including the Na/K-ATPase.
• Mg reduces K channels permiability.
• Mg depletion thus increases K loss in the cortical CD.
o Mg deficiency is often associated with K depletion.
• Mg decreases Ca channel permeability
o Mg deficiency results in elevated intracellular [Ca2+].
• Mg is a required coactivator of the Ca-sensing receptor on Parathyroid and bone
• Mg exhibits a similar profile to Ca regarding protein-bound and complexed forms.
• Bone does not contribute to plasma Mg

27
Q

How does Mg affect K regulation?

A

Mg replete plasma increases K reabsorption
• Mg depletion thus increases K loss in the cortical CD.
o Mg deficiency is often associated with K depletion.

28
Q

How does Mg affect intracellular Ca stores?

A

• Mg decreases Ca channel permeability

o Mg deficiency results in elevated intracellular [Ca2+].

29
Q

How does Mg affect the Ca-sensing Parathyroid?

A

• Mg is a required coactivator of the Ca-sensing receptor on Parathyroid and bone

30
Q

Where are the reabsorption sites and percentages of reabsorption of Mg in the renal tubules?

A
  • PT 15% paracellular and unregulated
  • LOH 75% paracellular and unregulated
  • DT 1 to 10% transcellular and regulated
31
Q

What regulates Mg reabsorption vs secretion?

A
  • Mg excretion is regulated primarily by the plasma concentration of Mg
  • Hormonal regulation does not play a role
32
Q

Why are the KD susceptible to KD Stones and Nephrocalcinosis (stones in the interstitium)?

A
  • Ca and Pi concentrations are at near precipitating levels in the ECF.
  • The solubility of Ca salts is influenced by pH.
  • The significant concentration of urine and changes in urine pH affect the possibility of Ca precipitates in the urine (i.e. kidney stones) or in the interstitium (nephrocalcinosis).
33
Q

What are the sites of reabsorption and regulation are different for the Pi, Mg, and Ca?

A

o Pi is regulated at the PT
o Mg is regulated at the early DT
o Ca is regulated at the late DT (aka the connecting tubule)

34
Q

Where are CaSRs expressed in the renal tubules?

A
  • on the basolateral side of the TALH, where Ca and Mg are reabsorbed without water.
  • on the luminal side of CD cells in both principal cells and α-type intercalated cells
35
Q

How does the CaSR on the TALH protect against nephrocalcinosis?

A

• An increase in local interstitial [Ca] activates CaSR, and initiates a signaling cascade that results in decreased Ca and Mg reabsorption, thereby protecting against nephrocalcinosis.

36
Q

How do the CaSR in the principle cells and α-intercalated cells CD protect against KD stones?

A
  • In principal cells, CaSR reduces ADH-dependent water reabsorption, thereby preventing concentration of the tubular fluid.
  • In α-intercalated cells, CaSR stimulates H+ secretion, thereby inhibiting the formation of salts (CaPO4, Mg/NH4PO4) that tend to precipitate at alkaline pH.
37
Q

Unlike most other nutrients, citrate is incompletely reabsorbed in the proximal tubule, thus the urine normally contains moderate amounts of citrate. How does citrate affect Ca and Mg precipitation?

A

Citrate is a natural Ca-and Mg-chelator, and thereby increases the solubility of these ions in the urine.

38
Q

What is Barter’s type I and type 5 and how does it affect Ca and Mg balance?

A

Type I is missing LOH Na/2Cl/K channel. K is wasted. Lumin becomes positive and increases Ca and Mg reabsorption.
Type 5, the basolateral CaSR overactive. The CaSR inhibits the Na/2Cl/K channel. The result is more reabsorption of Ca and Mg.
Both can cause calcification of the KD interstitium.

39
Q

Describe regulation of H2O and H+ transport by Ca in the CD. (Hint Principle cells and Alpha-Intercalated cells)

A

Luminal CD has CaSR on principle and alpha-intercalated cells.
On the Principle cells, CaSR inhibits luminal H2O and causes dilute urine.
On the alpha cells, CaSR stimulates H ATPase and acidifies urine.
Both prevent KD stones.

Physiology Renal Quiz 2 (4 decks)

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