Electrolytes Flashcards

1
Q

What are some of the s/s of severe hypophosphatemia?

A

effects are primarily related to impairment of cellular engery metabolism
-acute resp failure or failure to wean from vent
-impaired delivery to peripheral tissue
-left shift of oxyhemoglobin cure d/t 2,3-DPG depletion
-extreme muscle weakness
-hemolytic anemia
-impaired leukocyte and plt function

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2
Q

In a pt w/ re-feeding syndrome or who is a concern for re-feeding syndrome, what type of fluids should not be given?

A

IV dextrose containing fluids
-also high carbohydrate TF or TPN
-these lead to increased insulin levels which worsening hypophosphatemia d/t intracellular shifts of phosphate

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3
Q

What is TURP syndrome?

A

excessive absorption of irrigant fluid leanding to hypervolemia, hyponatremia, and low serum osmolality

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4
Q

At what level of hypermagnesemia are deep tendon reflexes lost?

A

10-14mEq/L
-at 5-10mEq/L will see prolonged PR interval and widened QRS
-at 15mEq/L SA/AV node blockade
-at 20mEq/L cardiac arrest

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5
Q

What is the total body water in males?

A

60% body weight

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6
Q

What is the total body water in females?

A

50-55% body weight

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7
Q

What is the total body water in a fetus?

A

90% body weight

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8
Q

What is the total body water in kids?

A

60-65% body weight

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9
Q

What is the total body water in the obese?

A

Up to 10-20% lower compared to similar age and gender

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10
Q

What are the main intracellular cations? Anions?

A

-phosphate and magnesium
-phosphate, sulfate, proteins

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11
Q

What are the main exracellular cations? Anions?

A

-sodium
-chloride, bicarbonate, sulfate, proteins

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12
Q

What determines plasma osmolality?

A

ratio of plasma salutes and water

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13
Q

What is the normal range for plasma osmolality?

A

275-290 mOsm/kg
-mostly driven by Na+ w/ small contributions from glucose and BUN

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14
Q

How do you calculate osmolality?

A

Posm = 2x[Na] + (BUN/2.8) + (gluc/18)

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15
Q

What electrolyte derangement are seen in rhabdomyolysis?

A

due to myocyte breakdown
-hyperkalemia
-hyperphosphatemia
-hypocalcemia

also see:
-hypoalbumenia
-hyperuricemia

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16
Q

What electrolyte derangements are known to worsen digoxin toxicity?

A

-hypokalemia
-hypophosphatemia

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17
Q

What is the average volume made and amount of Na Cl K and HCO3 of the stomach?

A

1-2L
Na 59
K 9.3
Cl 89
HCO¬3 0-1

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18
Q

What is the average volume made and amount of Na Cl K and HCO3 of the duodenum?

A

100-2000mL
Na 105
K 5.6
Cl 99
HCO3 10

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19
Q

What is the average volume made and amount of Na Cl K and HCO3 of the ileum?

A

1-3L
Na 112
K 5
Cl 106
HCO3 15-20

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20
Q

What is the average volume made and amount of Na Cl K and HCO3 of the colon (diarrhea)?

A

500-1700mL
120
90
25
45

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21
Q

What is the average volume made and amount of Na Cl K and HCO3 of the bile?

A

500-1000mL
Na 145
K 5.2
Cl 100
HCO3 50

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22
Q

What is the average volume made and amount of Na Cl K and HCO3 of the pancreas?

A

500-1200mL
Na 142
K 4.6
Cl 77
 HCO3 70

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23
Q

With normal renal function and perfusion what is the principal regulator of serum osmolarity?

A

ADH

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24
Q

When both low plasma osmolarity and low blood volume/pressure are present which effect dominates control of ADH?

A

Low blood volume or pressure will cause an increase of ADH
-this is one of the ways hypovolemic hyponatremia occurs

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25
Q

Why are the elderly more prone to alterations in sodium homeostasis?

A

Aging leads to reduced GFR which limits the ability to excrete a sodium load
-makes them more prone to overexpansion of the extracellular fluid compartment
-they also have impaired thirst mechanism and decreased ability to concentrate urine

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26
Q

What are causes of euvolemic hyponatremia?

A

-hyperlipidemia
-hyperproteinemia

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27
Q

What are causes of dilutional (increased plasma osmolality) hyponatremia?

A

-hyperglycemia
-mannitol

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28
Q

What are causes of hypovolemic hyponatremia?

A

-diuretics
-plasma, GI, or skin fluid losses
-CHF
-hypoproteinemic states (cirrhosis, nephritis syndrome, malnutrition)
-SIADH
-endocrine disorders (hypothyroidism, hypoadrenalism)
-meds (morphine, TCAs, indomethacin)

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29
Q

How much does Na drop for every 100mg/dL rise in glucose?

A

1.3mEq/L

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30
Q

What is the most common cause of hypovolemic hyponatremia?

A

Na losses

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31
Q

What urine studies are diagnostic for SIADH?

A

Uosm > 100 (maximally dilute urine)
UNa > 30 (renal salt wasting)
Serum osm < 280
Euvolemia
(remember this is unregulated free water retention w/o adequate Na reabsorption)

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32
Q

At what Na plasma level do patients typically become symptomatic in hypernatremia?

A

Na > 160

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33
Q

What some causes of hypovolemic hypernatremia?

A

-fever
-hyperventilation
-burns
-hypotonic fluid loss (perspiration, severe diarrhea)
-excessive renal free water loss (hyperglycemia, mannitol)

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34
Q

What fluids should you give to treat hypovolemic hypernatremia?

A

-if hypovolemia is severe enough to cause tissue malperfusion = NS
-if tissue perfusion is adequate = 0.5 NS or D5W

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35
Q

The recovery phase of which renal disorder can be characterized by high-output renal failure leading to severe hypernatremia?

A

acute tubular necrosis

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36
Q

What treatment is both diagnostic and therapeutic for central DI induced hypernatremia?

A

dDAVP (1-desamino-8d-arginine vasopressin)

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37
Q

What is the rate at which hypernatremia should be corrected?

A

no faster 0.5 - 1mEq/L per hour
-if pt is experiencing seizure activity give free water to reduce to level before sz began, or reduce by ~6mmol/L

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38
Q

How do you calculate free water deficit?

A

water deficit = total body water x {1-(serum Na/140)}

39
Q

What is the amount of potassium typically found in the human body?

A

-intracellular = 40 - 50mmol/kg body weight
-only 2% of total body potassium is found extracellular

40
Q

What are the typical extrarenal causes of hypokalemia in a surgical patient?

A

-GI losses (emesis, NGT)
-diarrhea
-burns
-profuse perspiration

41
Q

What are the typical renal causes of hypokalemia in a surgical patient?

A

-diuretic therapy
-tubular disorders (type 1 renal tubular acidosis)
-meds (cisplatin, amphotericin B)

42
Q

What can cause hypokalemia due to an intracellular influx of K+?

A

-metabolic alkalosis
-insulin
-beta2-adrenergic stimulation

43
Q

What are some disorders that can cause hypokalemia?

A

-primary hyperaldosteronism
-renal artery stenosis
-Cushing syndrome

44
Q

How does vomiting lead to hypokalemia when gastric secretions only ave about 10mEq/L of K?

A

-ECV contraction leads to elevated levels of aldosterone
-elevated aldosterone causes enhanced renal Na reabsorption and increased K secretion

45
Q

What is the most serious consequence of hypokalemia?

A

cardiac arrhythmias

46
Q

What are some factors that can exacerbate the potential for arrhythmias in hypokalemia?

A

-metabolic alkalosis
-digoxin
-hypercalcemia

47
Q

What EKG changes are seen in hypokalemia?

A

-flattened T waves
-T wave inversion
-depressed ST segments
-U waves
-prolonged QTc

48
Q

At what level does weakness typically manifest in hypokalemia?

A

K < 2.5

49
Q

What is the total K deficiency when the plasma value drops from 4 to 3?

A

100 - 400mmol^3

50
Q

What can cause hyperkalemia due to an extracellular flux of K+?

A

-severe metabolic acidosis
-insulin deficiency (DM)
-rhabdomyolysis
-succinylcholine (transient) - most commonly seen following paralysis or prolonged bed rest

51
Q

What EKG changes are seen in hyperkalemia?

A

-peaked T-waves
-reduced P-wave amplitude
-QRS widening
-sinusoidal complex
-Vfib

52
Q

What are the approximate total body stores of calcium?

A

1000gm w/ almost 99% in the bones

53
Q

Why does hyperventilation cause hypocalcemia?

A

-acid-base alterations effect the binding of calcium to albumin
-respiratory alkalosis increases the binding affinity of calcium for albumin
-causes reduction in the serum ionized calcium

54
Q

Which patient populations are prone to alternations in calcium homeostasis?

A

-major fluid shifts
-prolonged immobilization
-alterations in GI absorption
-post-op from thyroid or parathyroid cases

55
Q

What is the most frequent cause of hypocalcemia?

A

low serum albumin

56
Q

What are causes of hypocalcemia not due to hypoalbuminemia?

A

-acute pancreatitis
-massive soft tissue infection
-small bowel fistulae
-hypoparathyroidism
-MTP d/t chelation of calcium w/ citrate

57
Q

Approximately how much citrate does each unit of blood contain? How fast can the liver metabolize citrate?

A

-3gm per unit of blood
-metabolizes 3gm every 5 minutes

58
Q

What are the s/s of hypocalcemia?

A

-circumoral numbness or tingling
-numbness or tingling at the finger tips
-tetany
-carpopedal spasm
-seizures
-EKG changes = bradycardia, prolonged QTc

59
Q

What is the most common cause of hypercalcemia?

A

hyperparathyroidism
-primary HPT and malignant causes account for 90% of hypercalcemia

60
Q

What are the s/s of hypercalcemia?

A

-confusion, lethargy, come
-muscle weakness
-anorexia, nausea, vomiting
-constipation
-pancreatitis
-renal stones (in prolonged cases)
-polyuria (d/t induced nephrogenic DI)
-EKG changes (shortened QT)

61
Q

What medication can exacerbate arrhythmias due to hypercalcemia?

A

digitalis

62
Q

When is treatment for hypercalcemia considered urgent?

A

Ca > 15 or EKG changes

63
Q

What is the treatment protocol for hypercalcemia?

A

-large volume hydration w/ NS
-once hydrated –> furosemide
-if severe may need diphosphonates, calcitonin, or mithramycin

64
Q

What is the MOA for diphosphonates and calcitonin in treating severe hypercalcemia?

A

-diphosphonates = inhibits osteoclast resorption and reduces Ca levels by forming Ca-phosphate complexes
-calcitonin = inhibits osteoclast resorption

65
Q

What is the principal intracellular divalent cation?

A

Mg2+

66
Q

Where is 50% of the body’s Mg found?

A

in bone

67
Q

Where does Mg absorption occur?

A

small intestine
-reabsorbed by the renal tubules

68
Q

What are the s/s of hypomagnesemia?

A

similar to hypocalcemia w/ neuromuscular and CNS excitability
-tremor
-tetany
-fasciculations
-Chvostek and Trousseau signs
-impaired parathyroid hormone excretion
-can induce hypocalcemia that is refractory to Ca supplementation

69
Q

What are the s/s of hypermagnesemia?

A

rare to see outside of renal failure or iatrogenic
-flaccid paralysis
-hypotension
-confusion
-EKG changes similar to hyperkalemia

70
Q

What is the treatment for severe hypermagnesemia?

A

-emergently = administration of calcium as calcium gluconate or calcium chloride
-definitive = hydration and diuresis to increase renal excretion, dialysis if there is renal impairment

71
Q

What are common causes of hypophosphatemia?

A

-impaired intestinal absorption
-increased renal excretion
-hyperparathyroidism (d/t increased renal excretion)
-s/p major liver resection d/t rapid phosphate utilization of regenerating hepatocytes
-refeeding syndrome

72
Q

What are some adverse effects of severe hypophosphatemia?

A

-impaired tissue oxygen delivery d/t decreased 2,3-DPG
-muscle weakness
-rhabdomyolysis

73
Q

How is Na transported out of the nephron?

A

ENaC (epithelial sodium channels) = specialized Na-K ATPase
-these are stimulated by aldosterone
-their activation is triggered by hypovolemia, hypotension, and ANP d/t atrial overdistention

74
Q

Which ion channel in the nephron does furosemide act on?

A

inhibits Na reabsorption via Na-K-Cl cotransporter in the loop of Henle

75
Q

Which part of the nephron does furosemide act on?

A

loop of Henle

76
Q

Which channels in the nephron specialize in water reabsorption?

A

aquaporins
-open in response to ADH
-results in movement of water into the medullary interstitium

77
Q

Where in the nephron do you first find aquapornins?

A

collecting ducts

78
Q

What is DI?

A

inadequate or absent effect of ADH leading to closed aquaporins and excessive free water excretion but not Na d/t:
-injury of pituitary (central)
-desensitization of the collecting ducts (nephrogenic), usually d/t toxic effects (ie. lithium)

79
Q

What are the s/s of DI?

A

-very dilute polyuria
-hypernatremia
-hypovolemia

80
Q

What cardiac specific symptoms are seen w/ hypocalcemia?

A

-bradycardia
-CHF
-cardiomyopathy

81
Q

What hematologic specific symptoms are seen w/ hypophosphatemia?

A

-hemolytic anemia
-impaired leukocyte function
-impaired platelet function

82
Q

What are some of the etiologies of hyperkalemia (surgery and trauma specific)?

A

-crush injuries
-reperfusion syndrome
-AKI
-severe metabolic acidosis
-succinylcholine
-hypoaldosteronism

83
Q

What are some of the etiologies of hypermagnesemia (surgery and trauma specific)?

A

rare in the absence of renal failure
-large vol. tissue necrosis (large burns, large crush injuries)
-medication induced (laxative abuse, antacids, lithium)

84
Q

What are some of the etiologies of hyperphosphatemia in critically ill patients?

A

-exogenous = phosphate-based laxatives/enemas or high dose fosphenytoin
-endogenous = rhabdomyolysis or tumor lysis
-extracellular shifts

85
Q

How do the T-waves in hyperkalemia differ from those in hypercalcemia

A

both are peaked
-hyperkalemia = narrow based
-hypercalcemia = broad based

86
Q

What is the goal UOP in a patient being hydrated for hypercalcemia?

A

100-150mL/hr

87
Q

What two electrolyte derrangements can lead to hypocalcemia?

A

-hypomagnesemia
-hyperkalemia

88
Q

What is the fastest rate at which you should correct hypernatremia?

A

0.5mEq/L/hr

89
Q

What are the principal regulators of serum osmolarity?

A

all determined on the kidneys ability to excrete urine, so:
-intact renal function
-appropriate ADH secretion

90
Q

When both low plasm osmolarity and low blood volume/pressure are present what effects dominates the renal response?

A

low blood volume/pressure
-this can lead to hypovolemic hyponatremia

91
Q

For every 100mg/dL rise in glucose by how much does sodium fall?

A

1.3mEq/L

92
Q

How much will the drop of albumin by 1g/dL reduce the baseline anion gap?

A

by 2.5mEq

93
Q

What are typical serum osmolality, urine osmolality, urine sodium, and volume status of SIADH?

A

-serum osm < 280mOsm/kg
-Uosm > 100mOsm/kg
-UNa > 30mEq/L
-euvolemic

94
Q
A