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CVPR > CVPR Week 8: CVPR Week 8: Renal handling of P > Flashcards

CVPR Week 8: CVPR Week 8: Renal handling of P Flashcards

1
Q

How much Magnesium does the body typically store?

A

24g

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2
Q

Where does the body have magnesium?

A

99% is intracellular

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3
Q

What is the normal magnesium concentration?

A

1.7-2.6 mg/dL

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4
Q

How is magnesium structured in the body

A
  • only 70% of serum magnesium is free
  • the other 30% is complexed to albumin
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5
Q

Describe Mg flux between body compartments

A

Similar to calcium!

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6
Q

Mechanisms of intestinal Mg absorption

A
  • Paracellular
  • Transcellular
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7
Q

Describe renal handling of Mg

A

PCT 10-20%

TALH 70%

DCT 10%

CD 0%

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8
Q

What is the major site of Mg reabsorption in the kidney?

A

TALH

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9
Q

Loop diuretics effects on Mg

A

Inhibit NKCC2 and cause hypomagnesemia

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10
Q

Bartter syndrome and Mg

A

mutations in ROMK, NKCC2, CIC-Kb, Barttin and CaSR

cause

  • metabolic alkalosis
  • hypokalemia
  • normo-hypomagnesemia
  • hypercalciuria
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11
Q

Describe Familial hypomagnesemia

A
  • with hypercalciuria and nephrocalcinosis
  • mutations in Claudin 16 and 19
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12
Q

Describe Mg handling in TALH

A
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13
Q

Main mechanism of Mg handling in the DCT

A

Transcellular route

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14
Q

Describe Mg handling in the DCT

A
  • The process is coupled to potassium and sodium transport
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15
Q

The transcellular route of magnesium transport in the DCT is in part controlled by

A
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16
Q

Mg and loop diuretics

A

Loop diuretics inhibit NKCC2 and cause hypomagnesemia

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17
Q

Bartter syndrome and Mg

A

mutations in ROMK, NKCC2, CIC-Kb, Barttin and CaSR

  • Metabolic alkalosis
  • hypokalemia
  • normo-hypomagnesemia
  • hypercalciuria
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18
Q

Familial hypomagnesemia etiology

A

Mutations in Claudin 16 and 19

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19
Q

Familial hypomagnesemia manifestation

A

hypomagnesemia with hypercalciuria and nephrocalcinosis

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20
Q

Main mechanism for Mg handling in the DCT

A

Transcellular root

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21
Q

Describe Mg handling in the DCT

A
  • Process is coupled to potassium and sodium transport
  • Epidermal growth factor is an important controller of the process
  • Anti-EGF drugs in oncology are associated with hypomagnesemia
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22
Q

Thiazide diuretics and Mg

A

Thiazide diuretics act on the NCC channel and produce hypomagnesemia

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23
Q
A
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24
Q

Anti-EGF drugs and Mg

A

Since EGF is an important controller of the transcellular reabsorption route in the DCT, Anti-EGF drugs used in oncology are associated with hypomagnesemia

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25
Factors that increase Mg absorption 9 listed
* Dietary restriction * PTH * Glucagon * Calcitonin * Vasopressin * Aldosterone * Amiloride * Metabolic alkalosis * EGF
26
Factors that decrease Mg absorption 8 listed
* Hypermagnesemia * metabolic acidosis * Phosphate depletion * Loop diuretics and thiazides * Aminoglycosides and amphotericin * Chemotherapy (cisplatin) * Immunosuppressants
27
Dietary restriction of Mg result on Mg absorption
Increase
28
PTH result on Mg absorption
Increase
29
Glucagon result on Mg absorption
Increase
30
Calcitonin result on Mg absorption
increase
31
Vasopressin result on Mg absorption
Increase
32
Aldosterone result on Mg absorption
increase
33
Amiloride result on Mg absorption
Increase
34
Metabolic alkalosis result on Mg absorption
Increase
35
EGF result on Mg absorption
Increase
36
Hypermagnesemia result on Mg absorption
decrease
37
Metabolic acidosis result on Mg absorption
Decrease
38
Phosphate depletion result on Mg absorption
decrease
39
Loop diuretics and thiazides result on Mg absorption
decrease
40
Aminoglycosides result on Mg absorption
decrease
41
42
Loop diuretics result on Mg absorption
decrease
43
Thiazides result on Mg absorption
decrease
44
Amphotericin result on Mg absorption
decrease
45
Chemotherapy (cisplatin) result on Mg absorption
decrease
46
Cisplatin result on Mg absorption
Decrease
47
Immunosuppressants result on Mg absorption
decrease
48
Clinical disorders of magnesium
* Hypermagnesemia * Hypomagnesemia
49
Hypermagnesemia etiology
* increased intake such as by antacids (milk of magnesia), enemas, IV therapy with magnesium sulfate (pre-eclampsia) * decreased renal filtration
50
Hypomagnesemia etiology
* Reduced intake * Redistribution * Reduced absorption (proton pump inhibitors) * Renal magnesium wasting (drug-induced losses, hormone-induced magnesuria, ion or nutrient-induced tubular losses)
51
Common causes of hypomagnesemia
* if on diuretics blame diuretics * If on Proton pump inhibitors blame PPIs * not on diuretics or PPI then look for alcohol
52
Common causes of hypermagnesemia
* Will have pre-eclampsia and you will be asked to either give or withhold magnesium * If not pregnant will have kidney disease * If they are taking antacids they may have milk-alkali syndrome
53
Milk-Alkali Syndrome
* MAS: consists of hypercalcemia, various degrees of renal failure and metabolic alkalosis due to ingestion of large amounts of calcium and absorbate alkali. * Magnesium may be elevated either because of renal impairment OR because the "alkali" was Milk of Magnesia
54
Hypermagnesia 5-7 mg/dL
* Nausea * vomiting * Lethargy * diminished reflexes
55
56
Hypermagnesia 7-12 mg/dL
* Somnolence * hypocalcemia * absent reflexes * bradycardia * ECG changes (wide QRS, 1st-degree AVB)
57
Hypermagnesia \> 12 mg/dL
* muscle paralysis * respiratory muscle paralysis * complete heart block * cardiac arrest
58
Manifestations of hypomagnesemia
* Neuromuscular hyper-excitability * Cardiovascular manifestations * abnormalities of calcium metabolism * Hypokalemia (in patients with preserved renal function or moderate renal insufficiency one cannot correct hypokalemia without replacing concurrent magnesium deficit (EXAM RELEVANT POINT))
59
Tx of hypermagnesemia: normal or near normal renal function (eGFR\>45)
* Normal/near normal renal function (eGFR\>45) (stop Mg and give furosemide)
60
Tx of hypermagnesemia: moderate renal function (eGFR: 15-45)
Stop Mg and give furosemide and IV fluids
61
Tx of hypermagnesemia: Severe renal impairment GFR: \<15
may require dialysis
62
Tx of Mg associated arrhythmias
Give IV 100-200mg elemental calcium
63
Question 1
64
Question 2
65
Question 3
66
Question 4
67
Question 6
68
Question 7
69
Question 8
70
Carters vs Gitelman's
71
Question 9
72
Question 10
73
Question 11
74
Question 12

CVPR (93 decks)

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