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Renal > Calcium and Magnesium Physio and Disorders > Flashcards

Calcium and Magnesium Physio and Disorders Flashcards

1
Q

Where is most calcium in your body?

A

In bone, but most of it (99%) isn’t accessible.

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2
Q

Is calcium more in ECF or ICF?

A

ECF. Calcium is normally kept very very low in the cytosol.

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3
Q

Why is 40% of plasma Ca++ not ultrafilterable?

A

Because it’s bound to proteins.

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4
Q

What percentage of plasma Ca++ is in the free ionized (biologically active) form?

A

50%

40% is protein bound, 10% is in complexes with anions like citrate, lactate, phosphate etc.

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5
Q

What effect does low serum albumin have on Ca++ levels?

A

It reduces total serum Ca++, but the free ionized fraction is relatively unaffected (so it won’t cause hypocalcemia symptoms.

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6
Q

Since labs usually measure total Ca++ (unless you ask for free Ca++), how do you correct that value when albumin is low?

A

Corrected serum Ca++ = serum Ca + 0.8*(4 - albumin)

Normal albumin is 4, so if albumin is normal, corrected value won’t be different.

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7
Q

How does acid-base balance affect free Ca++ levels?

A

Acidemia liberates Ca++ from albumin -> increased free Ca++.
Alkalemia -> more Ca++ bound to albumin -> decreased free Ca++.

(Acidosis can mask total Ca++ depletion)

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8
Q

If you were to link intestinal absorption, bone, and kidney Ca+ handling to one most important regulatory molecule each, what would you pick?

A

GI absorption: Vitamin D.
Bone: PTH
Renal Ca++ handling: CaSR

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9
Q

PTH’s effect on calcium?

Ca++’s effect on PTH?

A

PTH raises plasma Ca++.

High Ca++ suppresses PTH.

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10
Q

2 important locations of calcium sensing receptor (CaSR)?

A

Parathyroids: mediates PTH suppression.

Renal tubules.

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11
Q

What effect does Ca++ binding CaSR in the renal tubules?

A

Ca++ binding CaSR inhibits Ca++ reabsorption in the loop of Henle.

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12
Q

3 activities of PTH on Ca++? (2 target organs)

A

Bone -> Ca++ reabsorption via osteoclasts.

Kidney -> Ca++ reabsorption, Vit D activation

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13
Q

In what form in Vit D stored in the body?

A

25-OH-D, aka. calcidiol

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14
Q

What is the active form of Vit D?

A

1,25-(OH)2-D, aka calcitriol.

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15
Q

2 stimuli for activation of 25-OH-D to 1,25-(OH)2-D?

A

High PTH.

Low phosphate.

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16
Q

4 sites of action of calcitriol (1,25-(OH)2-D)?

A

Intestine -> increase Ca++ absorption.
Parathyroids -> PTH suppression.
Kidney -> increased Ca++ reabsorption.
Bone -> increased bone resorption, potentiates PTH.

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17
Q

Most electrolytes (Na, K, PO4, H+) accumulate in kidney failure, but not so for Ca++. Why?

A

Kidney failure -> impaired activation of calcidiol to calcitriol.
When calcitriol is deficient, intestinal absorption is impaired enough to cause hypocalcemia.

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18
Q

What cation’s reabsorption locations in the nephron does that of Ca++ resemble?

A

Na+

Most reabsorption occurs in the proximal tubule, but fine tuning is done distally.

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19
Q

Most important way Ca++ is reabsorbed in the proximal tubule?

A

Paracellular passive transport via solvent drag and diffusion.

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20
Q

How does volume / total Na+ affect Ca++ reabsorption?

A

Low volume / Na+ -> increased Ca++ reabsorption.

High volume / Na+ -> increased Ca++ excretion (calciuria).

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21
Q

What drives Ca++ reabsorption in the thick ascending limb? What generates this gradient?

A

Positive charge in the lumen generated by the activity of NKCC2 and ROMK.

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22
Q

How is Ca++ reabsorption in the thick ascending limb regulated?

A

High Ca++ binds CaSR -> inhibition of NKCC2 and ROMK (like a loop diuretic) -> reduced Ca++ absorption.

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23
Q

How is Mg++ reabsorption in the think ascending limb regulated?

A

Exactly like Ca++. Mg++ binds CaSR -> inhibition of NKCC2 and ROMK -> loss of + charge in lumen -> reduced Ca++, Mg++, K+, etc. reabsorption.

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24
Q

Normal serum Ca++?

A

8.8 - 10.3 mg/dL

not necessary to memorize for the exam… but good to know…

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25
Q

Of our 3 Ca+ regulating organs (intestine, bone, kidney), which is least likely to be the primary cause of hypercalcemia?

A

Kidney. Kidney failure would cause impaired Ca++ excretion, but impaired Vit D activation would have the greater effect.

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26
Q

Effects of hypercalcemia?

A

Often asymptomatic.
Sometimes vague symptoms like constipation, nausea fatigue.
When more severe: neuro, renal, and cardiac problems.

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27
Q

Cardiac manifestations of hypercalemia?

A

Shortened Q-T interval.

When more extreme -> V fib.

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28
Q

4 renal manifestations of hypercalcemia?

A

Polyuria (nephrogenic diabetes insipidus).
Natriuresis (NKCC2 inhibition).
Nephrolithiasis.
Renal insufficiency (acute or chronic)

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29
Q

2 reasons why hypercalcemia causes polyuria?

A

High Ca++ acts like a loop diuretic via CaSR.

High Ca++ inhibits the insertion of Aquaporin-2 in the collection duct membrane, blocking ADH activity.

30
Q

How can hypercalcemia cause acute renal insufficiency?

A

Diuretic effects of hypercalcemia -> volume contraction.

31
Q

How can hypercalcemia cause chronic renal insufficiency?

A

Nephrocalcinosis. (Ca deposits in renal parenchyma)

32
Q

3 main causes of hypercalcemia?

A

Primary hyperPTH.
Malignancy
Vit D intoxication

33
Q

2 mechanisms by which malignancy can cause hyperPTH?

A

Osteolytic metastases.

Humorally mediated.

34
Q

3 humoral mediators of hypercalcemia of malignancy?

A

PTH-related peptide (PTH-rP).
Lymphotoxin (multiple factors).
Calcitriol.

35
Q

2 ways people can get Vit D levels so high that it causes hypercalcemia?

A 
Iatrogenic (Vit D given for renal failure or hypoPTH).
Granulomatous disease (activated macrophages release calcitriol).
36
Q

Clinically, how are hypercalcemia caused by hyperPTH and hypercalcemia of malignancy easy to distinguish?

A

HyperPTH is often asymptomatic to mild and slowly progressing (years).
People with hypercalcemia of malignancy are very sick, and it develops relatively quickly.

37
Q

How would you definitively distinguish hyperPTH from hypercalcemia of malignancy?

A

Measure PTH.

If PTH is high or inappropriately normal in hypercalcemia, it’s primary hyperPTH.

38
Q

3 goals of teatment of hypercalcemia?

How is each achieved?

A

Enhance renal Ca++ excretion - Give istonic saline +/- loop diuretic (depending on volume status).
Suppress bone resorption - bisphosphonates, calcitonin.
Remove Ca++ from blood - hemodialysis.

39
Q

Most common cause of hypocalcemia?

A

Hypoalbuminemia (but this doesn’t reflect a real deficit in ionized Ca++).

40
Q

2 mechanisms of true hypocalcemia?

A

Impaired mobilization from bone (something wrong with PTH/ Vit D).
Tissue or intravascular complexation of Ca.

(Note that impaired GI absorption / renal loss are absent here. Ostensibly, reabsorption from bone should be able to compensate for those and prevent hypocalemia unless an above problem is present.)

41
Q

What musculoskeletal signs can alert you to danger hypercalcemia?

A

Tetany
(can be elicited with Trousseau’s sign: ischemia causes carpopedal spasm)
(also Chvosktek’s sign: tapping on facial nerve -> spasm)

42
Q

What does hypocalcemia look like on ECG?

A

Prolonged QT interval.

43
Q

Neuro effects of hypocalcemia?

A

Depression, altered mental status.

44
Q

5 causes of hypoPTH?

A 
Hypomagnesemia.
Post-surgical.
Autoimmune.
Infiltrative (e.g. hemochromatosis).
Congenital (eg. DiGeorge's)
45
Q

Why does hypomagnesemia cause hypocalcemia refractory to Ca++ repletion?

A

Mild hypoMg++ stimulates PTH release, but severe hypoMg++ actually impairs PTH release.

46
Q

What’s the mechanism of hypocalcemia in autoimmune polyglandular syndrome type I?

A

Activating autoantibodies to CaSR.

causes a variety of problems, including pernicious anemia and predisposition to mucocutaneuous candidiasis

47
Q

What do you measure to determine if someone is Vit D deficient (in terms of intake /production)?

A

25-OH-D, aka calcidiol

The storage form.

48
Q

Intestinal malabsorption can be cause of Vit D deficiency.

A

That makes sense.

49
Q

3 features of Vit D deficiency other that hypocalemia?

A

Osteomalacia, secondary (appropriate) hyperPTH, hypophosphatemia.

50
Q

4 ways to cause hypocalcemia with complexation?

A

Hyperphosphatemia.
Hungry bone syndrome (recall: reduction in PTH post parathyroidectomy),
Citrated blood products.
Acute pancreatitis.

51
Q

4 things to check first when you see hypocalcemia?

A

Make sure it’s real (check albumin, ionized Ca++).
Serum Mg++.
Serum PO4.
BUN and creatinine.

52
Q

Treatment of acute hypocalcemia?

A

IV Ca++
IV Mg++
Correct alkalosis if present (will free Ca++ from albumin).

Oral calcium and Vit D can be given for chronic hypocalcemia.

53
Q

If a patient has renal disease, how do you give Vit D?

A

Calcitriol, as they won’t be able to activate calcidiol.

54
Q

Does bone Mg buffer serum Mg?

A

Nope.

55
Q

What’s unique about where in the neprhon most Mg++ is reabsorbed?

A

Only 10-15% is absorbed proximally.

60-70% is in loop of Henle.

56
Q

Specific protein involved in Mg diffusion paracellularly?

A

Claudin 16 (encoded by paracellin-1)

57
Q

Again, what does Mg++ absorption in the thick ascending limb depend upon?

A

Positive lumen potential generated by NKCC2 and ROMK.

Recall Mg regulates own absorption via CaSR -> inhibition of NKCC2 and ROMK.

58
Q

Significance of hyperMg?

A

It’s not rare, but rarely significant.

Severe hyperMg is induced in the treatment of eclampsia.

59
Q

What condition predisposes to hyperMg?

A

renal insufficiency

60
Q

If hyperMg is severe, what can happen?

A

Neuromuscular problems: loss of reflexes, paralysis, stupor/coma.
Bradycardia/hypotension.
Hypocalcemia (due to inhibited PTH).
Heart block / cardiac arrest.

61
Q

Treatment for hyperMg?

A

Stop giving Mg.
Saline and loop diuretic.
IV Ca++ (for neuro and cardiac effects).
Dialysis (for pts. with kidney failure)

62
Q

There are lots of reasons for GI and renal loss of Mg.

A

True. Some things like proton pump inhibitors, acute pancreatitis are harder to remember.
But things like loop diuretics, diarrhea, hypercalemia, etc. make a lot of sense.

63
Q

Some drugs cause renal Mg wasting.

A

It’s true. Look out for it.

64
Q

If someone has hypoMg, what other electrolytes might be low?

A

K+ and Ca++

65
Q

HypoMg tends to get less attention, but can it cause dangerous arrhthmias?

A

Yes, including long QT and Torsade de pointes.

66
Q

What do neuromuscular symptoms of hypoMg resemble?

A

HypoCa++… including tetany / Chovstek’s and Trousseau’s signs.

67
Q

If you’re not sure what’s causing hypoMg, what should you assess?

A

Fractional excretion.

I’m not going to memorize this formula… it’s on slide 76 if you need it.

68
Q

Can serum Mg look normal… but there’s still Mg depletion?

A

Sure thing. Seen in diarrhea and alcohol-related hypoMg…. and it might be contributing to hypocalcemia.

69
Q

Treatment of severe hypoMg?

A

IV Mg (but it’s inefficient due to CaSR stimulation)

70
Q

Treatment for mild hypoMg?

A

Oral slowly absorbed substances (MgCl2, Mg-lactate).

Treat underlying disease (eg. amelioride for renal loss)

Renal (40 decks)

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