Ca/Mg/PO4 Balance Flashcards

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1
Q

What are clinical symptoms of hypo/Hypercalcemia?

A

Hypo: Increased Nerve and muscle excitability, tetany, arrhythmia

Hyper: Decreased NM excitability, Cardiacproblems

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2
Q

What is total plasma calcium?

A

9-10.5 md/dL

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3
Q

How does Ca affect pH in blood?

A

Increased free Ca++ in. Blood —> Acidosis

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4
Q

Where is Calcitonin released from, and what is it’s action?

A
  • Released from thyroid gland

- Promotes Bone mineralization

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5
Q

What is Calcitriol, and where is it produced?

A
  • Active form Vitamin D
  • Produced in kidneys
  • Increases Ca++ Reabsorption from GI tract
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6
Q

How do Loop diuretics, Thiazides, and PTH affect CA++ Reabsorption?

A

Loop diuretics -> Decrease

Thiazides and PTH -> Increase

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7
Q

What is the primary and secondary way that Ca++ is absorbed?

A

Primary: Solvent Drag -> Paracellular transport (80%)

Secondary: Active transport —> Transcellular Ca++ ATPase and Na/Ca antiporter(20%)

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8
Q

How does Furosamide affect Calcium?

A
  • Loop diuretic

- Blocks Calcium uptake into cell from lumen

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9
Q

How do Thiazides diuretics increase Ca+ Reabsorption?

A
  • Inhibit Na/Cl symport which is linked to Na/K Pump

- Na/Ca exchanger is activated on basolateral membrane which increases Ca Reabsorption

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10
Q

How does PTH increase Ca in the blood? (4)

A
  • Activates Osteoclasts for bone reabsorption
  • Increases Renal reabsorption
  • stimulates Calcitriol —> GI absorption
  • Decreases plasma phosphate by increasing excretion of phosphates
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11
Q

How does Vitamin D affect Ca/Phosphate levels?

A

creates absorption of Ca and PO4

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12
Q

What are trousseau sign and chvostek sigh?

A

Trouseau -> Muscle spasm of upper extremity

Chvostek -> Facial nerve tapping -> facial muscle spasm ipsilaterally

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13
Q

What is the main cause of hyperparathyroidism?

A

Adenoma

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14
Q

What is nephrolithiasis and nephrocalcinosis

A
  • Death of kidney due to development of calcium oxolate stones
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15
Q

What is common in 90% of patients with renal failure? What is the mechanism of it?

A

Secondary hyperparathyroidsism

Accumulation of phosphate in plasma due to low excretion in kidneys —> Binds CAA decreasing free ionized calcium —> Hypocalcemia

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16
Q

What is indicative of Renal osteodystrophy n a radiograph?

A
  • Osteitis fibrosis cystica: Brown tumor “Giant cells” and substitution of bone with CT
17
Q

What are Phosphate binders an what do they treat?

A

Medications which bind phosphates in the gut so it cannot be absorbed

Treat hyperphosphatemia in chronic renal disease

18
Q

What is a common mistake in hypophosphatemia that can cause further damage?

A

Infusion of glucose,

Glucose —> Insulin -> glycolysis -> Transport of phosphates into cell

19
Q

A patients presents with Fanconi syndrome, except K levels are normal. What is a likely cause?

A

Hypophosphataemia

20
Q

What is normal excretion of phosphate?

A

10%

21
Q

What is the action of phosphatonins?

A

Inhibit Renal phosphate reabsorption

22
Q

What tole does phosphate play in pH balance?

A

Serves an a Buffer in Urine and kidneys

23
Q

How does Mg reabsorption differ from other ions?

A

Primarily reabsorbed in the thick ascending limb

24
Q

What is the most common cause of hypomangnesemia?

A

Diuretics