Chemical Pathology/ Abnormal Electrolytes Flashcards

1
Q

What is hyperkalemia?

A

Serum potassium concentration >5 mEq/L

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2
Q

What factors place chronic kidney disease patients at risk for hyperkalemia?

A

They have reduced potassium excretion by the kidneys, are prone to metabolic acidosis, and are more likely to be on medications (RAS antagonists) that have hyperkalemia as a possible side effect.

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3
Q

What type of renal tubular acidosis causes hyperkalemia?

A

Type IV

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4
Q

In general, what are the causes of hyperkalemia?

A
  1. Decreased potassium excretion: renal failure, renal hypoperfusion (heart failure, volume depletion), aldosterone deficiency or insensitivity, medications (ACEIs, potassium-sparing diuretics, NSAIDs)
  2. Excessive release of intracellular potassium (acidosis, trauma, tumors, hemolysis, infection)
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5
Q

Hyperkalemia needs to be treated emergently when what factors are present?

A
  • Electrocardiogram changes (peaked T wave, loss of P wave, widened QRS)
  • rapid rise in potassium
  • potassium >6 mEq/L
  • renal failure
  • moderate to severe acidosis
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6
Q

What medications are used to meet the following goals when treating emergent hyperkalemia?

–> Myocardial stabilization and prevention of fatal arrhythmia

A

Intravenous (IV) calcium gluconate or calcium chloride (does not lower potassium)

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7
Q

What medications are used to meet the following goals when treating emergent hyperkalemia?

–> Cellular uptake of potassium

A
  • IV insulin (glucose is added to prevent hypoglycemia)
  • IV sodium bicarbonate
  • nebulized beta-adrenergic (such as albuterol)
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8
Q

What medications are used to meet the following goals when treating emergent hyperkalemia?

—>Elimination of potassium

A

Furosemide or dialysis depending on the patient’s renal function

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9
Q

What is the medical treatment of nonemergent hyperkalemia?

A

Sodium polystyrene sulfonate (PO or PR)

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10
Q

What is hypokalemia?

A

Serum potassium concentration <3.5 mEq/L

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11
Q

In a stable patient, oral potassium chloride powder (diluted in liquid) may be used to treat most cases of hypokalemia . What is the approximate treatment dose for the following potassium level?

–>Less than 3.0 mEq/L

A

20 mEq PO every 2 hours for four doses

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12
Q

In a stable patient, oral potassium chloride powder (diluted in liquid) may be used to treat most cases of hypokalemia . What is the approximate treatment dose for the following potassium level?

—> 3.0 to 3.5 mEq/L

A

20 mEq PO every 2 hours for two doses

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13
Q

What are some common causes of hypokalemia?

A
  • vomiting (bulimia, infection, hyperemesis gravidarum)
  • diarrhea (infection, excessive laxative use)
  • thiazide and loop diuretics
  • hyperaldosteronism
  • type I and II renal tubular acidosis
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14
Q

In the acute setting of hyperglycemia requiring intense insulin therapy, why is it necessary to administer potassium along with insulin?

A

Insulin promotes potassium uptake into the cells and decreases serum potassium.

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15
Q

Why does vomiting cause hypokalemia even though gastric fluid has little potassium?

A

Loss of hydrogen ions (acidic gastric fluid) → metabolic alkalosis → alkalosis causes potassium shift into cells

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16
Q

What are the symptoms of hypokalemia?

A
  • weakness
  • fatigue
  • muscle cramps
  • constipation
  • arrhythmias (severe cases)
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17
Q

What is hypernatremia?

A

Serum sodium concentration >145 mEq/L. Total sodium may actually be normal or less than normal depending on the patient’s volume status.

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18
Q

What is the difference between hypovolemia (aka volume depletion) and dehydration?

A
  • Hypovolemia refers to the loss of extracellular fluid volume (water plus sodium and other solutes) with resulting decreased tissue perfusion.
  • Dehydration is a kind of hypovolemia but involves a disproportionately greater loss of free water to sodium, causing hypernatremia
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19
Q

What are the common causes of hypervolemic hypernatremia?

A
  • Hyperaldosteronism (eg, idiopathic adrenal hyperplasia, Conn syndrome)
  • Excess sodium administration by physicians (eg, hypertonic intravenous fluid, parenteral nutrition, bicarbonate administered as NaHCO 3 ) or caregivers (eg, errors preparing infant formula)
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20
Q

What is diabetes insipidus (DI) and how does it cause hypernatremia?

A
  • Normally when the body senses dehydration, ADH (antidiuretic hormone) is released.
  • The kidneys then concentrate the urine in order to retain more water.
  • In DI, there is either no production of ADH (central ADH) or there is ADH insensitivity (nephrogenic DI).
  • Inappropriately dilute urine is produced causing an elevation of serum sodium.
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21
Q

What is the major complication of treating hypernatremia too rapidly, especially if the patient has chronic hypernatremia?

A

Cerebral edema

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22
Q

What is hyponatremia?

A

Serum sodium concentration <135. Total sodium may actually be normal or higher than normal depending on the patient’s volume status.

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23
Q

What is the mechanism of hyponatremia in patients with diabetic ketoacidosis (or hyperglycemia nonketotic coma)?

A

Even though glucose is not an electrolyte, it acts as a solute. So in a hyperglycemic state, serum osmolality is high. This draws fluid out of the intracellular compartment into the extracellular fluid. Serum sodium is diluted.

24
Q

Describe the mechanism behind hypervolemic hypoosmolar hyponatremia.

A

In an edematous state (ie, CHF) there is a misperceived volume status. Total body water is increased, but effective circulatory volume is low. In response, the renin-angiotensin-aldosterone system activates (increases sodium and water retention) and ADH is released (increases water retention). Their net effect causes hyponatremia and further exacerbates volume overload.

25
Q

What is the most common iatrogenic cause of hypovolemic hypoosmolar hyponatremia, especially in the elderly?

A

Thiazide diuretics

26
Q

What is the major complication of treating hyponatremia too rapidly, especially if the patient has chronic hyponatremia?

A

Central pontine myelinolysis

27
Q

When a patient develops the syndrome of inappropriate antidiuretic hormone (SIADH), do the following increase or decrease?

–> Serum sodium

A

Decreases

28
Q

When a patient develops the syndrome of inappropriate antidiuretic hormone (SIADH), do the following increase or decrease?

–> Serum osmolality

A

Decreases

29
Q

When a patient develops the syndrome of inappropriate antidiuretic hormone (SIADH), do the following increase or decrease?

–> Urine osmolality

A

Increases

30
Q

What is pseudohyponatremia?

A

Elevated triglycerides or proteins → a decreased proportion of the serum is composed of water (and the sodium in it) → if the lab measures sodium concentration in whole serum (vs. serum water), sodium appears to be too low

31
Q

What is the normal range for serum calcium concentration?

A

9-10.5 mg/dL

32
Q

Lab values for calcium may be falsely low in patients with hypoalbuminemia (lab measures protein-bound calcium, not ionized [free] calcium). What is the formula for corrected total calcium in the setting of hypoalbuminemia?

A

Corrected total calcium (mg/dL) = total calcium (mg/dL) + 0.8 × (4-serum albumin [g/dL])

33
Q

Does hypocalcemia occur with low or high magnesium levels?

A

Low

34
Q

Does hypocalcemia occur with low or high phosphorus levels?

A

High

35
Q

What is the most common symptom of hypocalcemia?

A

Neuromuscular instability (nerve and muscle twitching, muscle cramping, tingling)

36
Q

What is Chvostek sign?

A

It is a sign of tetany seen in hypocalcemia. Tapping the facial nerve where it emerges just anterior to the ear causes spasm of the ipsilateral facial muscles.

37
Q

What is the ECG hallmark of hypocalcemia?

A

Prolonged QTc interval

38
Q

What are the two most common causes of hypercalcemia ?

A
  1. Hyperparathyroidism
  2. Malignancy
39
Q

What are the symptoms of hypercalemia?

A

Multisystem symptoms including “stones, bones, moans abdominal groans, and psychic overtones”: kidney stones, bone pain and osteoporosis, muscle weakness and fatigue, abdominal discomfort, mental dysfunction

40
Q

In metabolic acidosis/alkalosis and respiratory acidosis/alkalosis, are hydrogen, bicarbonate, and carbon dioxide level high or low?

A
41
Q

Of the above(shown in the attached table) acid-base disturbances, for which is hyperventilation the compensatory mechanism?

A

Metabolic acidosis

42
Q

Of the above(in the attached table) acid-base disturbances, for which is hypoventilation the compensatory mechanism?

A

Metabolic alkalosis

43
Q

How is anion gap calculated? g

A

Difference between measured cations and measured anions: [Na] − [Cl] − [HCO 3] = anion gap

44
Q

What is the typical acid-base disturbance(s) in Diabetic ketoacidosis?

A

Increased anion gap metabolic acidosis

45
Q

What is the typical acid-base disturbance(s) in Opiate overdose?

A

Respiratory acidosis

46
Q

What is the typical acid-base disturbance(s) in Chronic renal failure?

A

Increased anion gap metabolic acidosis

47
Q

What is the typical acid-base disturbance(s) in Vomiting?

A

Metabolic alkalosis

48
Q

What is the typical acid-base disturbance(s) in Salicylate intoxication?

A

Respiratory alkalosis and increased anion gap metabolic acidosis

49
Q

What is the typical acid-base disturbance(s) in Lactic acidosis?

A

Increased anion gap metabolic acidosis

50
Q

What is the typical acid-base disturbance(s) in Pulmonary embolism?

A

Respiratory alkalosis

51
Q

What is the typical acid-base disturbance(s) in Chronic renal failure?

A

Increased anion gap metabolic acidosis

52
Q

What is the typical acid-base disturbance(s) in Neuromuscular disorder (ALS, multiple sclerosis, Guillain-Barré)?

A

Respiratory acidosis

53
Q

What is the typical acid-base disturbance(s) in Prolonged diarrhea?

A

Normal anion gap metabolic acidosis

54
Q

What is the typical acid-base disturbance(s) in Methanol, formaldehyde, or ethylene glycol intoxication?

A

Increased anion gap metabolic acidosis

55
Q

What is the typical acid-base disturbance(s) in Renal tubular acidosis?

A

Normal anion gap metabolic acidosis