Electrolyte Disorders B&B

Question 1

What are the classic signs and symptoms of hyperkalemia vs hypokalemia?

Answer 1

1. arrhythmias
2. Muscle weakness/paralysis.
3. hyperkalemia EKG changes -
   peaked T waves, QRS widening
4. hypokalemia EKG changes - flattened T waves, U waves

*these make sense considering K+ needed for cardiac/ skeletal muscle

Question 2

what are 2 mechanisms by which hyperkalemia can occur?

Answer 2

1. most commonly due to decreased K+ excretion in the urine - acute/chronic kidney disease or Type IV RTA (aldosterone resistance)
2. increased K+ release from cells - acidosis, insulin deficiency, beta blockers, digoxin, cell lysis, hyper-osmolarity

Question 3

provide a cause for each of the following mechanisms by which hypokalemia can develop:
a. Increased renal loss.
b. increased GI loss
c. Increased entry into cells.
d. Magnesium levels.

Answer 3

a. Increased renal loss - diuretics, Type I and II RTAs

b. increased GI loss - vomiting, diarrhea

c. Increased entry into cells - hyperinsulin, beta agonists, alkalosis

d. Magnesium levels - hypomagnesium (promotes K+ loss, must be corrected before K+ can be normal)

Question 4

what is the effect of acute hypercalcemia on the kidneys?

Answer 4

down regulation of aquaporin channels —> loss of ability to concentrate urine —> excessive water excretion —> nephrogenic diabetes insipidus (polyuria)

—> decreased GFR —> acute renal failure

Question 5

how can sarcoidosis cause hypercalcemia?

Answer 5

Granulomatous macrophages produce 1-alpha hydroxylase —> hyper-vitaminosis D

too much Vitamin D can cause hypercalcemia

Question 6

How can hypocalcemia cause tetany?

Answer 6

Ca2+ blocks Na+ channels in neurons, so when there is low Ca2+ neurons are hyper-excitable —> spontaneous contractions (tetany = muscle twitches)

on the other hand, hypercalcemia would decrease neuron excitability and cause weakness

Question 7

describe how calcium and phosphate levels change in renal failure

Answer 7

Phosphate levels increase, which precipitates plasma calcium

1,25-OH2 vitamin D also decreases, causing a decrease in calcium absorption from the gut

These both contribute to hypocalcemia, which causes an increase in PTH

Question 8

how do the following cause hypophosphatemia?
a. Primary hyperparathyroidism.
b. Diabetic ketoacidosis.
c. Refeeding syndrome in alcoholics.
d. Fanconi syndrome.

Answer 8

a. Primary hyperparathyroidism - PTH decreases PO4 reabsorption

b. Diabetic ketoacidosis - glucose induced diuresis

c. Refeeding syndrome in alcoholics - low PO4 from poor nutrition

d. Fanconi syndrome - proximal tubule dysfunction causes urinary wasting

Question 9

what is the main acute symptom of hypophosphatemia and how does it typically present?

Answer 9

Weakness due to ATP depletion, often presents as respiratory muscle weakness

Question 10

which two electrolytes are affected by magnesium levels?

Answer 10

magnesium blocks calcium and potassium channels:

hyperMg decreases PTH secretion (—> hypocalcemia), but very low Mg also inhibits PTH release (—> hypocalcemia)

hyperMg blocks ROMK in cortical collection duct (—> hyperkalemia), so there is excess K+ excretion when Mg is low (—> hypokalemia)

Question 11

when might you see hyponatremia with high osmolarity? (2)
When might you see hyponatremia with normal osmolarity? (2)

Answer 11

hyperglycemia or mannitol (osmoles) can cause hyponatremia with a high osmolarity

Hyperlipidemia or hyperproteinemia (multiple myeloma) can cause hyponatremia with a normal osmolarity - pseudohyponatremia, artifact in serum sodium measurement (not true hyponatremia)

Question 12

Is a patient has hyponatremia how can you use urine osmolarity to make a diagnosis?

Answer 12

if urine is diluted, kidneys are responding appropriately/ ADH levels are low (as should be), and problem is outside the kidneys

if urine is not diluted, then kidneys are not responding appropriately/ there is too much ADH OR drug/pathology is interfering with kidney function

Question 13

explain why thiazide diuretics are more likely to cause hyponatremia than loop diuretics

Answer 13

loop diuretics diminish the medullary gradient (block Na+ reabsorption in TAL), making it difficult to reabsorb free water (more powerful diuretic)

thiazide diuretics do not affect medullary gradient (block Na+ reabsorption in distal tubule), so free water can still be reabsorbed - higher likelihood of excess water, setup for hyponatremia

Question 14

Explain how adrenal insufficiency can cause hyponatremia

Answer 14

cortisol normally suppresses ADH release - loss of cortisol means an increase in ADH secretion —> increase in water reabsorption

Also, a loss in aldosterone —> increase in ADH secretion

Question 15

explain how volume status can be normal when there is SIADH (syndrome of inappropriate antidiuretic hormone secretion)

Answer 15

too much ADH is released, causing fluid retention

Body responds by decreasing RAAS:
—> decreased aldosterone increases sodium excretion, worsening hyponatremia
—> decreased aldosterone also decreases water resorption from the kidneys, resulting in normal volume status

*note euvolemia + hypotonic hyponatremia is part of diagnostic criteria for SIADH

Question 16

which of these is not a cause of hypervolemic hyponatremia?
a. Cirrhosis.
b. Primary hypoaldosteronism
c. CHF
d. Renal failure

Answer 16

cause hypervolemic hyponatremia (inability to excrete enough water):
a. Cirrhosis.
c. CHF
d. Renal failure

primary hypoaldosteronism causes hypovolemic hyponatremia (type of primary adrenal insufficiency)

Question 17

what is the main use of Vaptan drugs that block ADH (tolvaptan, lixivaptan, conivaptan)?

Answer 17

block ADH, main use is severe hyponatremia in heart failure (hypervolemic)

Question 18

what is the cause of central Pontine myelinolysis?

Answer 18

aka “osmotic, demyelination syndrome”, associated with overly rapid correction of low sodium

—> loss of corticospinal and corticalbulbar tracts —> quadriplegia

Question 19

which two drugs are known to cause acquired diabetes insipidus?

Answer 19

diabetes insipidus: loss of ADH activity —> hypernatremia, polyuria and polydipsia

1. lithium
2. amphotericin B

Question 20

how can fluid restriction and vasopressin/desmopressin administration be used to diagnose diabetes insipidus?

Answer 20

fluid restriction should cause urine concentration - if urine is still dilute (8 hours), absent/ineffective ADH

administering vasopressin/desmopressin should concentrate urine if kidneys work - if it does, then cause of DI is central, but if not, then it is nephrogenic DI

Question 21

what is the use of desmopressin

Answer 21

desmopressin is ADH (vasopressin) analog without vasopressor effects - can cause water reabsorption without raising blood pressure

can be used to treat central diabetes insipidus

Question 22

which 2 classes of drugs can be used to treat nephrogenic diabetics insipidus?

Answer 22

1. thiazide diuretics: paradoxical antidiuretic effect in DI - increase in proximal Na/H2O reabsorption causes less H2O to be delivered to collecting tubules, triggering ADH release
2. NSAIDS: inhibit renal synthesis of prostaglandins, which are ADH antagonists