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Electrolyte Imbalance Flashcards

1
Q

What timeline defines acute VS chronic hyponatremia?

A

Acute: <48 hours

Chronic: >48 hours OR duration unknown

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2
Q

Normal serum osmolality value

A

275-299 mOsm/kg

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3
Q

Renal causes for hypovolemic, hypotonic hyponatremia

A
  1. Diuretics
  2. Addison’s disease [aldosterone deficiency]
  3. Acute/chronic renal failure with high urinary output
  4. Recovery phase of ATN
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4
Q

Extrarenal causes for hypovolemic, hypotonic hyponatremia

A
  1. Diarrhea
  2. Vomiting
  3. Dermal fluid loss (sweating/burns)
  4. Bleeding/hemorrhage
  5. 3rd space fluid loss (peritonitis, ascites, heart failure)
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5
Q

Renal causes of euvolemic hypotonic hyponatremia

A
  1. SIADH
  2. Medications (SSRIs, opiates, barbiturates)
  3. Acute/chronic renal failure
  4. Adrenal insufficiency [mineralcorticioids, glucocorticoids, DHEA]
  5. Exercise-associated
  6. Severe hypothyroidism
  • 4) impaired renal free water excretion
  • *5) Effect of ADH & electrolyte loss in sweating
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6
Q

Extrarenal causes of euvolemic hypotonic hyponatremia

A
  1. Decreased salt intake “tea & bread diet” –> seen in elderly
  2. Water intoxication [chronic beer drinker, hypotonic saline solution 0.45% NaCl]
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7
Q

How would water intoxication affect sodium & EC volume status? What are the causes?

A

Euvolemic hypotonic, hyponatremia

CAUSES:

  • Excessive infusion of hypotonic (0.45% NaCl) or sodium-free isotonic IV fluids
  • Primary polydypsia
  • Beer potomania
  • Reset osmostat syndrome
  • Beer has a lot of calories, but no protein, thus you don’t have nitrates to form urea (which comes from protein breakdown)
  • *Chronic beer intake reduces urea, meaning there is no ability to concentrate the urine because there isn’t a gradient in the tubules to use
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8
Q

Renal causes of hypervolemic, hypotonic hyponatremia

A
  1. Acute/chronic renal failure with low urine output
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9
Q

Extrarenal causes of hypervolemic, hypotonic hyponatremia

A
  1. CHF
  2. Cirrhosis
  3. Severe hypoproteinemia (nephrotic syndrome)
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10
Q

Causes of hypertonic hyponatremia

A
  1. Hyperglycemia
  2. IV mannitol
  3. IV radiocontrast use
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11
Q

Definition of isotonic hyponatremia

A

Low serum Na+ levels, normal serum osmolality

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12
Q

Causes of isotonic hyponatremia

A

TURP syndrome
Pseudohyponatremia [hyperlipidemia or multiple myeloma]

  • Absorption of irrigant by the open prostatic blood vessels (not using saline)
  • *Very rare: <1%
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13
Q

Definition, causes & clinical symptoms of pseudohyponatremia

A

Asymptomatic laboratory artifact falsely indicating hyponatremia when sodium hasn’t been reduced or diluted

CAUSES:

  1. Hyperlipidemia
  2. Multiple myeloma (high protein)

CLINICAL FEATURES:

  • Pancreatitis
  • DKA
  • Obstructive jaundice
  • CRAB criteria of myeloma
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14
Q

What is the correlation to regarding the severity in a severely symptomatic hyponatremic patient?

A

Correlates with the extent of brain edema & occurs <48 hours

<120 mEq/L:

  • confusion/coma
  • seizures
  • ataxia
  • respiratory failure
  • headache/vomiting/nausea
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15
Q

In regards to hypovolemic, hyponatremia: extra renal & renal causes would produce what quantitative urine output? (ie: anuria, oliguria, polyuria)

A

Extrarenal: Oliguria [diarrhea, vomiting, hemorrhage]

Renal: Polyuria [Adrenal insufficiency, recovery phase in ATN]

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16
Q

Lab findings suggesting hypovolemia

A
  • Increased BUN/creatinine ratio
  • Increased hematocrit
  • Increased uric acid
  • Urinary sodium: <30 mEq/L
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17
Q

What lab tests would you order (outside of serum studies) in a patient with hypovolemia, hyponatremia

A

TSH [patient has myxedema]

Cortisol/ACTH [adrenal insufficiency]

MDMA [urine drug screening]

BNP [CHF]

Urine chloride

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18
Q

Rapid correction of acute or chronic hyponatremia would cause osmotic demyelination syndrome?

A

Chronic!

Maximum correction rate limit in high risk patients is 8mEq/L in 24 hours

Minimum correction rate in high risk patients is 4-6 mEq/L in 24 hours

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19
Q

Should we treat acute/severely symptomatic hyponatremia patients rapidly or slowly?

A

Rapid!

  • Want to prevent neurologic symptoms & brain herniation due to the hyponatremia
  • 4-6 mEq/L within the first 6 hours of therapy
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20
Q

How to determine if a patient with hyponatremia is euvolemic or hypovolemic

A

Give isotonic saline infusion (0.9% NaCl)

  • If serum sodium increases: Hypovolemic
  • If serum sodium decreases: SIADH [euvolemic]
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21
Q

How to treat euvolemic hyponatremia

A

Fluid restriction: Only 500-1000 mL/day allowed

Pharmacological intervention if there is high urine osmolality (>500 mOsm/kg)

Use urea or vaptans

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22
Q

How to treat hypervolemic hyponatremia

A

Fluid restriction with or without loops diuretics

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23
Q

Managing sodium overcorrection

A

**Overcorrection not necessary in patient who initially started with >120 mEq/L

  • *In patient who started with <120 mEq/L:
  • Replace free water loss with 5% dextrose in water
  • Desmopressin
  • Glucocorticoid therapy (dexamethasone)
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24
Q

Correcting hyponatremia too rapidly causes two complications:

A

from low to HIGH, your pons will DIE (ODS)

from high to LOW, your brain will BLOW (cerebral edema)

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25
Q

Severe hypokalemia definition

A

serum potassium level < 2.5 mEq/L

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26
Q

GI causes of hypokalemia

A

Vomiting
Diarrhea
Laxatives

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27
Q

Renal causes of hypokalemia

A

Rental tubular acidosis (type 1 & 2)
Cushing syndrome
Renin-secreting tumors
Fanconi Syndrome

Diuretics (thiazides, loops, osmotic)
Beta 2 agonists (albuterol/terbutaline)
Glucocorticoids
Licorice (aldosterone like)
Hyperaldosteronism/cortisolism
Hypomagnesmia
28
Q

Causes of hypokalemia, forcing potassium into the cell (intracellular shift)

A

Alkalosis
Insulin
Hypo-osmolality

29
Q

Explain how alkalosis leads to hypokalemia

A
  • Decreased extracellular H+
  • Causes stimulation of Na/H+ anti porter
  • Increases H+ out of the cell & Na+ in
  • Increased Na+ in cell stimulates Na/K+ ATPase
  • More K+ gets placed into cells
  • Hypokalemia occurs

-Decreased extracellular K+ inhibits Na/K+ ATPase
-Decreased extracellular Na+, inhibits Na/H+ antiporter
-Decreases extracellular H+
=ALKALOSIS

30
Q

Explain how hypomagnesemia causes hypokalemia

A
  • Mg is a cofactor for Na/K+ ATPase, thus low levels will disrupt it in the proximal portion of the distal convoluted tubule
  • Causes increases luminal Na+, thus increasing Na+ reabsorption & K+ secretion by principal cells distally
  • Apical ROMK channels in principal cells are normally inhibited by Mg++, but low levels of magnesium allows uninhibited K+ secretion
31
Q

Symptoms of hypokalemia

A

Cardiac arrhythmias (can cause v.fib!)
Muscle weakness/paralysis
Decreased deep tendon reflexes
Constipation

32
Q

EKG of hypokalemia

A

“No POT, no TEA”

T-wave flattening,
ST depression
Presence of U waves (severe hypokalemia)

33
Q

Treatment of hypokalemia

A

IV KCl

*Administer slowly to prevent cardiac arrhythmias! 10 mEq/hr peripheral line or 40 mEq/hr central line

34
Q

Explain how acidosis causes hyperkalemia

A
  • Increased extracellular H+ inhibits the Na/H+ anti porter
  • Decreases intracellular Na+, thus inhibiting the Na/K ATPase
  • Increases extracellular K+ causing hyperkalemia

-Increased extracellular K+ activates Na/K+ ATPase
-Increased extracellular Na+ activates Na/H+ antiporter
-Increased H+ extracellular
=ACIDOSIS

35
Q

Cause of pseudohyperkalemia

A

Release of potassium from RBC lysis

Examples:

  • Blood drawn form the side of IV infusion or central line without previous flushing
  • Prolonged tourniquet use
  • Fist clenching during blood withdrawal
  • Delayed sample analysis
36
Q

Causes of hyperkalemia

A

DO LABSS:

Digoxin
HyperOSMOLARITY
Lysis of cells
Acidosis
Succinylcholine
Sugar (high)
37
Q

What level of potassium is considered severely elevated?

38
Q

Routine labs for hyperkalemia

A

BMP (basic metabolic panel)

CBC (hemolytic anemia present)

Liver chemistry (hemolysis or tumor lysis syndrome)

Blood gas (metabolic acidosis)

39
Q

Aside from routine labs for hyperkalemia, what specific investigation would you do? (labs wise, what would you want to measure)

A

Creatine kinase (Increased in rhabdomyolysis)

LDH (increased in hemolysis)

RAAS

Cortisol (decreased in adrenal insufficiency)

40
Q

EKG changes in hyperkalemia

A

Peaking t waves
QRS widening
Flattening p wave (absent >8 mEq/L)

41
Q

Treatment of hyperkalemia

A

Acute, not chronic treatment:

Calcium gluconate 
Short acting insulin w/ glucose
Dialysis/diuretics
Bicarbonate (treat acidosis)
Beta agonists
42
Q

Definition of hypercalcemia

A

total serum calcium > 10.5 mg/dL (>2.62 mmol/L)

ionized (free) calcium >5.25 mg/dL (>1.31 mol/L)

43
Q

Reasons for PTH mediated hypercalcemia

A

Primary hyperthyroidism: Adenoma (sporadic or MEN syndrome)

Secondary hyperthyroidism: Renal insufficiency or vitamins D deficiency

44
Q

Reasons for non-PTH mediated hypercalcemia

A

Malignancy (SSC of lung)

Osteolytic metastases (multiple myeloma)

Sarcoidosis (activates hydroxylase activity, increasing calcitriol)

Thiazide diuretics

Pagets disease

Hyperthyroidism (Increased thyroid hormone increases osteoclast activity)

45
Q

Hypercalcemic crisis definition

A

Total calcium: > 14 mg/dL (3.5 mmol/L)

Free calcium: > 10 mg/dL (2.5 mmol/L)

46
Q

Equation for corrected calcium (mg/dL)

A

=measured total Ca + [0.8 x (4-albumin concentration in g/dL)]

47
Q

EKG changes in hypercalcemia

A 
QT interval shortening
J waves (in severe)
48
Q

Treatment of severe hypercalcemia

A

IMMEDIATE THERAPY:
IV hydration with isotonic saline
Calcitonin

CAUSE-BASED THERAPY:
Biphosphonates (malignancy)
Loop diuretics (Renal insufficiency, CHF)
Dialysis (>18 mg/dL; 4.5 mmol/L –> renal failure)

49
Q

Definition of severe hypocalcemia

A

Total serum: <7.5 mg/dL (<1.9 mmol/L)

Total free: <3.6 mg/dL (<0.9 mmol/L)

50
Q

What percent of total serum calcium is bound to albumin?

A

40% & is inactive

51
Q

How does PTH respond to pH changes?

A

Increased pH = Increased PTH

Decreased pH = decreased PTH

*Because ie) Decreased H+ means less are binding to proteins, so Ca+ binds to those proteins, thus decreasing ionized calcium levels and increasing PTH

52
Q

What effect does PTH have on serum calcium and phosphate?

A

Increase calcium, decrease phosphate

53
Q

What effect does calcitriol (D3) have on serum calcium and phosphate?

A

Increase calcium & phosphate

54
Q

What effect does calcitonin have on serum calcium and phosphate?

A

Decrease calcium & phosphate

55
Q

What effect does magnesium have on PTH

A

Mild hypomagnesium: Increase PTH

Severe hypomagnesium: Decreased PTH

56
Q

Top 2 causes of hypocalcemia

A

Hypoparathyroidism & vitamin D deficiency

OTHERS:
Loop diuretics
Biphosphonates 
Osteoblastic metastasis 
RTA type 1
Blood transfusions (citrate in blood products chelates serum calcium)
57
Q

What ion does DiGeorge syndrome effect

A

Calcium (because no parathyroid)

58
Q

Causes of secondary hyperparathyroidism

A

Vitamin D deficiency

CKD

Hyperphosphatemia (decreased excretion or increased tissue breakdown)

Acute necrotizing pancreatitis (calcium soap)

59
Q

Cause of pseudohypocalcemia

A

Gadolinium contrast

Hypoalbuminemia

60
Q

Chvostek sign

A

Twitching of facial muscle after tapping on facial nerve (below & in front of ear)

*Due to hypocalcemia

61
Q

Trousseau sign

A

Carpopedal spasm several minutes after inflation of blood pressure cuff at pressures above systolic

*Due to hypocalcemia

62
Q

Labs to order in case of hypocalcemia

A

PTH
Amylase (pancreatitis)
Calcidiol

63
Q

Lab findings in vitamin D deficiency

A

Low calcium, phosphate

High PTH

64
Q

EKG changes in hypocalcemia

A

Prolonged QT interval

65
Q

Treatment of hypocalcemia

A

Calcium gluconate (IV if severe, oral if moderate/chronic)

66
Q

What medication combined with IV calcium can cause life threatening arrhythmias

A

Digoxin/Digitoxin

*cardiac glycosides

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