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CPR Exam 3 > Lecture 6: Fluid and Electrolyte Disturbance - Ca, Mg, PO > Flashcards

Lecture 6: Fluid and Electrolyte Disturbance - Ca, Mg, PO Flashcards

1
Q

Free Ca2+ is important for what part of tissue excitability/AP’s?

Effect of low and high Ca2+ levels?

A
  • Calcium controls the AP threshold
  • ↓ Ca2+ lowers threshold
  • ↑ Ca2+ raises threshold
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2
Q

What is the effect of hypoalbuminemia on serum Ca2+ levels?

A
  • Decreases TOTAL serum [Ca2+]
  • WITHOUT affecting ionized Ca2+ level

*Ionized Ca2+ is free and unbound!

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3
Q

If serum albumin is abnormal, clinical decisions should be based on which level of Ca2+?

A

IONIZED Ca2+ levels

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4
Q

Which 3 hormones regulate Ca2+ levels?

A
  1. Calcitriol (1,25 OH Vit D3) –> works to ↑Ca2+
  2. PTH –> works to ↑Ca2+
  3. Calcitonin –> ↓Ca2+
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5
Q

3 major sites of regulation for Ca2+?

A

1) Kidney
2) Bone
3) Intestine

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6
Q

What are the main effects of PTH on serum ion levels?

A

↑ plasma [Ca2+] and ↓ plasma [PO43-] —> increased ionized plasma Ca2+

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7
Q

What are the 3 main sites of action for PTH?

A
  • Distal nephron to increase Ca2+ reabsorption
  • Inhibits PO43- reabsorption in proximal tubule
  • Enhances bone release of Ca2+
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8
Q

Secretion of PTH is controlled chiefy by serum [Ca2+] acting where?

A

Calcium-sensing receptors on parathyroid cells

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9
Q

65% of filtered calcium is reabsorbed where?

Predominantly by which type of transport?

A
  • Proximal tubule
  • Predominantly paracellular (passive)
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10
Q

Where in the nephron is the major site of calcium regulation?

A

Distal tubule

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11
Q

How is calcium reabsorbed in the distal tubule, the major site of regulation?

Regulated by which hormone?

A
  • Renal epithelial Ca2+ channel (TRPV5) - along with calnindin
  • Regulated by 1,25 vitamin D3 (calcitriol)
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12
Q

What are major causes of Hypercalcemia?

A
  • Primary hyperparathyroidism
  • Thiazide diuretics
  • Milk-alkali syndrome (i.e., antacids)
  • Malignancy
  • Immobilization syndrome
  • Granulomatous Dz
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13
Q

Hypercalcemia is almost always causes by increased entry of calcium into the ECF due to what 2 factors?

A
  1. Bone resorption
  2. Intestinal absorption
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14
Q

Severe hypercalcemia is often associated with symptoms related to what 2 systems and what are they?

A
  1. GI sx’s = anorexia, N/V, and constipation
  2. Neuro = weakness, fatigue, confusion, stupor, and coma
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15
Q

How does polyuria, nausea and vomiting associated with hypercalcemia contribute to worseing sx’s?

A

Cause marked hypovolemia, resulting in impaired calcium excretion, thereby worsening the hypercalcemia

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16
Q

What are drugs/treatments that can be given for the management of hypercalcemia?

A
  • ECF volume replacement w/ 0.9% saline
  • Furosemide = Ca2+ losing diuretic
  • Calcitonin
  • Glucocorticoids
  • Hemodialysis
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17
Q

For hypercalcemia not responding to saline diuresis, and especially if secondary to malignancy, therapy with what is required?

A

Bisphosphonates

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18
Q

True hypocalcemia is present only when which level is reduced?

A

Ionized calcium

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19
Q

Common causes of hypocalcemia?

A
  • Hypoparathyroidism
  • Acute pancreatitis
  • Chronic kidney disease
  • Rhabdomyolysis = Ca2+ in injured ms.
  • Parathyroidectomy
  • Pseudohypoparathyroidism –> failure to respond to PTH
  • Familial hypocalcemia
  • Vit D deficiency
  • Septic shock
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20
Q

Major cardiovascular signs/sx’s of hypocalcemia?

A
  • Hypotension
  • CHF
  • Dysrhythmias
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21
Q

Major neuromuscular irritability signs/sx’s of hypocalcemia?

A
  • Paresthesias, numbness
  • Muscle twitching and cramping
  • Tetany
  • General fatigability and muscle weakness
  • Seizures
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22
Q

Trousseau’s sign and Chvostek’s sign will be (+) in which settings?

A
  • Hypocalcemia
  • Hypomagnesemia
  • Alkalosis (decreases ionized Ca2+)
23
Q

In an emergency situation in which hypocalcemia is suspected and seizures, tetany, hypotension, or cardiac arrhythmias are present what is the treatment?

A

IV calcium

24
Q

Pts w/ chronic, mild hypocalcemia or hypoparathyroidism can be managed how?

A

Calcium and vitamin D supplements

25
Q

What % of body phosphorous is in the ECF?

A

1%

26
Q

Effect on serum phosphate levels with CHO or glucose infusion?

A

Decreased

27
Q

What are the 4 major regulatory hormones for Phosphate?

Which decrease and which increase levels?

A
  • PTH –> ↓ serum PO43- and ↑ renal excretion
  • FGF-23 –> ↓ serum PO43- and ↑ renal excretion
  • 1,25(OH)D3 —> ↑ PO43- and ↑ intestinal phosphate absorption
  • Insulin —> ↓ serum PO43- and shifts phosphate into cells
28
Q

Where is FGF-23 released from and what is its effect on serum PO43- levels?

A

Promotes PO43- excretion by the kidney = decreased serum levels

29
Q

A major portion of phosphate is reabsorbed in the PCT by which transporter?

What 2 hormones regulate this transpoter?

A

NaPi2 = highly regulated by PTH and FGF-23

30
Q

Why is a fall in GFR highly problematic for phosphate regulation?

A

Kidneys excrete 900 mg/day or about 65% of our intake!

31
Q

What are 2 major causes of decreased renal excretion of phosphorous leading to hyperphosphatemia?

A
  • CKD stages 3-5
  • Acute renal failure/AKI
32
Q

Many of the signs and sx’s of an acute rise in serum phosphate are the result of what?

A

Concomitant hypocalcemia due to deposition of calcium in soft tissues and a resultant fall in ECF ionized Ca2+

33
Q

Severe hyperphosphatemia may result in what tissue manifestations?

A

Tissue ischemia or calciphylaxis (vascular calcification/necrosis)

34
Q

Chronic hyperphosphatemia contributes to what disorder?

A

Renal osteodystrophy

35
Q

How is acute hyperphosphatemia managed clinically?

A

Saline diuresis

36
Q

How is hyperphosphatemia managed in end-stag kidney disease?

A

Reduce dietary intake/intestinal absorption (phosphate binders)

37
Q

What is Renal Osteodystophy?

How does CKD contribute to its development?

A
  • Bone demineralization due to CKD
  • Due to HYPERparathyroidismsecondary toHYPERphosphatemia… kidney unable to excrete phosphate
  • Combined w/ HYPOcalcemia –> kidney unable to activate vit D to calcitriol needed for Ca2+ absorption from diet
38
Q

What are the treatment options for Renal Osteodystrophy associated w/ CKD?

A
  • Ca2+/Vit D supplementation
  • Restriction of dietary phosphate, use of phosphate binders
  • Hemodialysis/renal transplantation
  • Cinacalet (calcium sensitizer drug, lowers PTH)
39
Q

What is often times a cause of death in starving people/anorexics when given a large bolus of food too quickly?

A
  • Re-feeding HYPOphosphatemia
  • Too much phosphate will be taken up into cell as hexokinase phosphorylates glucose
40
Q

What are some of the major causes of Hypophosphatemia?

A
  • re-feeding hypophosphatemia
  • Alcohol-related
  • Diabetes mellitus –> Tx w/ large dose of insulin
  • Urinary loss —> Fanconi syndrome
  • Oncogenic osteomalacia –> tumor making FGF-23
41
Q

Chronic hypophosphatemia causes what in children and adults?

A
  • Rickets in children
  • Osteomalacia in adults
42
Q

What are some of the muscular and CV abnormalities causes by hypophosphatemia?

A
  • Weakness
  • Rhabdomyolysis
  • Impaired diaphragmatic function
  • Respiratory and Heart failure
43
Q

What are 2 hemologic abnormalities caused by hypophosphatemia?

A
  • Hemolysis
  • Platelet dysfunction
44
Q

Hypophosphatemic patients frequently have low levels of what other ions that need to be corrected?

A
  • Hypokalemic
  • Hypomagnesemic
45
Q

What is the function of ionized magnesium found intracellularly?

A

Crucial role as cofactor in many biochemical and physiological processes such as ATPases, reg. of ion channels and translational processes

46
Q

What is the major site of magnesium reabsorption in the nephron?

A

Thick ascending limb

*Hence why loop diuretics cause hypomagnesemia, although thiazides cause more severe hypomagnesemia

47
Q

What is the site of magnesium fine-tuning in the nephron?

Primary driver of cellular Mg2+ influx?

A
  • DCT
  • Electrical potential is primary driver
48
Q

Hypomagnesemia is most often seen in which patients?

A

ICU patients (60%)

49
Q

Hypomagnesemia in ICU patients is primarily caused by what 5 factors?

Which drugs can caused decreased reabsorption?

A
  • Decreased nutrition
  • Diuretics
  • Decreased reabsorption due to PPIs = IMPORTANT!!!
  • Decreased albumin
  • Aminoglycosides
50
Q

How common is hypermagnesemia?

A

Rarely seen, due to efficient elimination by kidneys!

51
Q

Although rare, what are 3 causes of Hypermagnesemia?

A
  • End-stage renal disease
  • Massive intake i.e., Epsom salt
  • Magnesium infusion i.e., in pregnant women w/ pre-ecclampsia/ecclampsia to limit neuromuscular excitability
52
Q

If plasma magnesium is >12 mg/dL what signs/sx’s will occur?

A

Muscle paralysis –> flaccid quadriplegia, apnea and respiratory failure, complete heart block, and cardiac arrest

53
Q

Treatment of hypermagnesemia in pt w/ normal renal function vs. reduced renal function vs. end-stage renal disease?

A
  • Normal = stop administration and wait and/or add loop or thiazide diuretic
  • Reduced funtion = same as above + add saline infusion
  • End-stage = dialysis

CPR Exam 3 (14 decks)

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