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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
Q

Factors that increase Mg absorption

9 listed

A
  • Dietary restriction
  • PTH
  • Glucagon
  • Calcitonin
  • Vasopressin
  • Aldosterone
  • Amiloride
  • Metabolic alkalosis
  • EGF
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26
Q

Factors that decrease Mg absorption

8 listed

A
  • Hypermagnesemia
  • metabolic acidosis
  • Phosphate depletion
  • Loop diuretics and thiazides
  • Aminoglycosides and amphotericin
  • Chemotherapy (cisplatin)
  • Immunosuppressants
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27
Q

Dietary restriction of Mg result on Mg absorption

A

Increase

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28
Q

PTH result on Mg absorption

A

Increase

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29
Q

Glucagon result on Mg absorption

A

Increase

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30
Q

Calcitonin result on Mg absorption

A

increase

31
Q

Vasopressin result on Mg absorption

A

Increase

32
Q

Aldosterone result on Mg absorption

A

increase

33
Q

Amiloride result on Mg absorption

A

Increase

34
Q

Metabolic alkalosis result on Mg absorption

A

Increase

35
Q

EGF result on Mg absorption

A

Increase

36
Q

Hypermagnesemia result on Mg absorption

A

decrease

37
Q

Metabolic acidosis result on Mg absorption

A

Decrease

38
Q

Phosphate depletion result on Mg absorption

A

decrease

39
Q

Loop diuretics and thiazides result on Mg absorption

A

decrease

40
Q

Aminoglycosides result on Mg absorption

A

decrease

41
Q
A
42
Q

Loop diuretics result on Mg absorption

A

decrease

43
Q

Thiazides result on Mg absorption

A

decrease

44
Q

Amphotericin result on Mg absorption

A

decrease

45
Q

Chemotherapy (cisplatin) result on Mg absorption

A

decrease

46
Q

Cisplatin result on Mg absorption

A

Decrease

47
Q

Immunosuppressants result on Mg absorption

A

decrease

48
Q

Clinical disorders of magnesium

A
  • Hypermagnesemia
  • Hypomagnesemia
49
Q

Hypermagnesemia etiology

A
  • increased intake such as by antacids (milk of magnesia), enemas, IV therapy with magnesium sulfate (pre-eclampsia)
  • decreased renal filtration
50
Q

Hypomagnesemia etiology

A
  • Reduced intake
  • Redistribution
  • Reduced absorption (proton pump inhibitors)
  • Renal magnesium wasting (drug-induced losses, hormone-induced magnesuria, ion or nutrient-induced tubular losses)
51
Q

Common causes of hypomagnesemia

A
  • if on diuretics blame diuretics
  • If on Proton pump inhibitors blame PPIs
  • not on diuretics or PPI then look for alcohol
52
Q

Common causes of hypermagnesemia

A
  • 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
Q

Milk-Alkali Syndrome

A
  • 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
Q

Hypermagnesia 5-7 mg/dL

A
  • Nausea
  • vomiting
  • Lethargy
  • diminished reflexes
55
Q
A
56
Q

Hypermagnesia 7-12 mg/dL

A
  • Somnolence
  • hypocalcemia
  • absent reflexes
  • bradycardia
  • ECG changes (wide QRS, 1st-degree AVB)
57
Q

Hypermagnesia > 12 mg/dL

A
  • muscle paralysis
  • respiratory muscle paralysis
  • complete heart block
  • cardiac arrest
58
Q

Manifestations of hypomagnesemia

A
  • 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
Q

Tx of hypermagnesemia: normal or near normal renal function (eGFR>45)

A
  • Normal/near normal renal function (eGFR>45) (stop Mg and give furosemide)
60
Q

Tx of hypermagnesemia: moderate renal function (eGFR: 15-45)

A

Stop Mg and give furosemide and IV fluids

61
Q

Tx of hypermagnesemia: Severe renal impairment GFR: <15

A

may require dialysis

62
Q

Tx of Mg associated arrhythmias

A

Give IV 100-200mg elemental calcium

63
Q

Question 1

A
64
Q

Question 2

A
65
Q

Question 3

A
66
Q

Question 4

A
67
Q

Question 6

A
68
Q

Question 7

A
69
Q

Question 8

A
70
Q

Carters vs Gitelman’s

A
71
Q

Question 9

A
72
Q

Question 10

A
73
Q

Question 11

A
74
Q

Question 12

A

CVPR (93 decks)

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