Ca, Pi, and Mg Balance Flashcards
(39 cards)
What are the symptoms of Hypocalcemia?
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.
What are the signs of hypercalcemia?
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
Long QT arrhythmias are due to?
Short QT arrhythmias are due to?
(plasma Ca levels)
Hypocalcemia
Hypercalcemia
How does intracellular Ca binding to membrane proteins affect Na channels? (this happens in hypocalcemia)
• The channel gets fooled into thinking that it is depolarized, hence the threshold is reduced and causes spontaneous firing
Explain why hypocalcemia results in relaxed smooth muscle and active skeletal muscles.
- 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
During hypercalcemia Ca salts may precipitate in soft tissues, leading to their calcification and the development of kidney stones.
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What are the percentages of Ca reabsortion in which segments of the tubule?
- 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
Explain Ca reabsorption in the PT and the LOH. How are these affected by Na reabsorption?
- passive and paracellular.
* Ca reabsorption is proportional to Na reabsorption in the PT and LOH
Explain Ca reabsorption in the DT. How are these affected by Na reabsorption?
• 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
How do DT diuretics affect Ca reabsorption in the renal tubule?
- 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.
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?
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+].
How does Acid-Base affect plasma Ca levels binding to Albumin?
- Acidic ph decreases binding of Ca to albumin
* alkaline pH increases binding of Ca2+ to albumin.
How does Acid-Base affect plasma Ca levels in acute and chronic?
- 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).
How does acid-base affect Ca reabsorption?
- alkalosis increases reabsorption
- acidosis increases Ca excretion.
- chronic metabolic acidosis results in bone demineralization by osteoclasts and osteoblasts.
What is the main symptom of hypophosphatemia?
• 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
How does acid and alkaline affect plasma and intracellular Pi levels? Is there a difference between respiratory and metabolic alkalosis?
• 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.
Why does Alkalosis cause cellular influx of Pi?
• In intracellular alkalosis, phosphofructokinase activity increases. PFK uses Pi, thereby creating a concentration gradient for Pi entry.
How is Pi absorbed in the intestines and excreted in the renal tubules? What segment of the nephron is the site of Pi regulation?
- 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
What are the two most important regulators of Ca and Pi homeostasis?
- parathyroid hormone (PTH), secreted by the chief cells of the parathyroid gland
- calcitriol, the active form of vitamin D3
How do the Chief cells detect low Ca levels?
- 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.
What are the effects of PTH?
- 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)
What does 1-alpha-hydroxylase do?
• converts an inactive form of vitamin D3 (25‐OH‐vitamin D3) to its active form, calcitriol (1,25‐(OH)2‐vitamin D3).
Where is 1-alpha-hydroxylase found? (What cells have this enzyme?) Where does its product calcitriol have effect?
- 1-alpha-hydroxylase resides in the proximal tubule.
* calcitriol stimulates the gut to absorb Ca (and Pi)
How does plasma Pi affect renal regulation of Pi? How does PTH affect renal regulation of Pi?
- 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
