Potassium

Question 1

Homeostatic mechanisms maintain plasma K + concentration between____

Answer 1

3.5 and 5.0 mM

Question 2

The ___ of the connecting segment (CNT) and cortical CD that play a dominant role in renal K + secretion, whereas alpha-intercalated cells of the outer medullary CD function in renal tubular reabsorption of filtered K + in K+ -deficient states.

Answer 2

principal cells

alpha-intercalated cells

Question 3

Hypokalemia, defined as a plasma K +concentration of <____ mM

Answer 3

3.5

Question 4

Systemic _____ can also cause treatment resistant hypokalemia, due to a combination of reduced cellular uptake of K +and exaggerated renal secretion.

Answer 4

hypomagnesemia

Question 5

_______ can occasionally result from in vitro cellular uptake of K + after venipuncture, for example, due to profound leukocytosis in acute leukemia.

Answer 5

Spurious hypokalemia or “pseudohypokalemia”

Question 6

Associated with a tenfold increase in in-hospital mortality

Answer 6

Hypokalemia

Question 7

Which of the following statements about nonrenal potassium loss is correct?
A. Vomiting causes hypokalemia primarily through direct gastric potassium loss.
B. BK channel upregulation in the colon is a key mechanism in several intestinal disorders.
C. Noninfectious diarrhea does not contribute to significant hypokalemia.
D. Gastric losses from nasogastric suctioning are the main driver of hypokalemia in hospitalized patients.

Answer 7

B

Question 8

_____ have a greater effect on plasma K +concentration than loop diuretics, despite their lesser natriuretic effect.

Answer 8

Thiazides

Question 9

The diuretic effect of thiazides is largely due to inhibition of the _____in DCT cells.

Answer 9

Na+ -Cl – cotransporter NCC

Question 10

High doses of _____can increase obligatory K + excretion by acting as nonreabsorbable anions in the distal nephron.

Answer 10

penicillin-related antibiotics (nafcillin, dicloxacillin, ticarcillin, oxacillin, and carbenicillin)

Question 11

Renal tubular toxins that cause renal K+ and Mg2+ wasting → hypokalemia and hypomagnesemia.

Answer 11

Aminoglycosides, amphotericin, foscarnet, cisplatin, ifosfamide.

Question 12

Liddle’s syndrome is caused by autosomal dominant gain-in-function mutations of _____.

Answer 12

ENaC subunits

Question 13

Patients with Liddle’s syndrome classically manifest severe hypertension with ______, unresponsive to spironolactone yet sensitive to amiloride.

Answer 13

hypokalemia

Question 14

Mutations in thiazide-sensitive Na+/Cl– cotransporter of DCT.

Answer 14

Gitelman’s Syndrome

Question 15

TALH transporter defects (Na+, K+, Cl–).

Answer 15

Bartter’s Syndrome

Question 16

Hypokalemia is a major risk factor for both____

Answer 16

ventricular and atrial arrhythmias.

Question 17

Electrocardiographic changes in hypokalemia include ______; these are most marked when serum K +is <2.7 mmol/L.

Answer 17

broad flat T waves, ST depression, and QT prolongation

Question 18

The paralytic effects of hypokalemia on intestinal smooth muscle may cause _____.

Answer 18

intestinal ileus

Question 19

____ is the mainstay of therapy in hypokalemia.

Answer 19

Oral replacement with K+ -Cl-

Question 20

____, oral or IV, may be appropriate in patients with combined hypokalemia and hypophosphatemia.

Answer 20

Potassium phosphate

Question 21

_____ should be considered in patients with concomitant metabolic acidosis.

Answer 21

Potassium bicarbonate or potassium citrate

Question 22

The use of intravenous administration should be limited to patients _____

Answer 22

unable to use the enteral route or in the setting of severe complications (e.g., paralysis, arrhythmia).

Question 23

Intravenous K+-Cl should always be administered in ______, because the dextrose-induced increase in insulin can acutely exacerbate hypokalemia.

Answer 23

saline solutions, rather than dextrose

Question 24

The peripheral intravenous dose is usually _____of K+-Cl –per liter;

Answer 24

20–40 mmol

Question 25

If hypokalemia is severe (<2.5 mmol/L) and/or critically symptomatic, intravenous K+ -Cl – can be administered through a central vein with cardiac monitoring in an intensive care setting, at rates of _____; higher rates should be reserved for acutely life-threatening complications.

Answer 25

10–20 mmol/h

Question 26

Strategies to minimize K +losses

Answer 26

>Minimizing the dose of non-K+-sparing diuretics >Restricting Na + intake, and using clinically appropriate combinations of non-K+ -sparing and K+ -sparing medications (e.g., loop diuretics with ACE inhibitors).

Question 27

Hyperkalemia is defined as a plasma potassium level of _____

Answer 27

5.5 mM

Question 28

Drugs that impact on the _____ are also a major cause of hyperkalemia.

Answer 28

renin-angiotensin-aldosterone axis

Question 29

______ can occur in the setting of excessive muscle activity during venipuncture (e.g., fist clenching), a marked increase in cellular elements (thrombocytosis, leukocytosis, and/or erythrocytosis) with in vitro efflux of K+ , and acute anxiety during venipuncture with respiratory alkalosis and redistributive hyperkalemia.

Answer 29

Pseudohyperkalemia

Question 30

_____ has surpassed tuberculosis as the most important infectious cause of adrenal insufficiency.

Answer 30

HIV

Question 31

Hyperkalemia due to hypertonic mannitol, hypertonic saline, and intravenous immune globulin is generally attributed to a ______, as water moves out of cells along the osmotic gradient.

Answer 31

“solvent drag” effect

Question 32

____ depolarizes muscle cells, causing an efflux of K+ through acetylcholine receptors (AChRs).

Answer 32

Succinylcholine

Question 33

A patient receives a large dose of lysine intravenously. What is the most likely mechanism leading to hyperkalemia? A. Direct inhibition of potassium channels B. Reduced renal excretion of potassium C. Cation-K+ exchange at the cellular level D. Solvent drag effect

Answer 33

C

Question 36

Which of the following hereditary conditions is characterized by lifelong salt wasting, hypotension, and hyperkalemia? A. Bartter’s syndrome B. Gitelman’s syndrome C. Autosomal recessive pseudohypoaldosteronism type I (PHA-I) D. Pseudohypoaldosteronism type II (PHA-II)

Answer 36

C Autosomal recessive pseudohypoaldosteronism type I (PHA-I) Explanation: Recessive PHA-I is caused by mutations in ENaC subunits, leading to impaired Na+ reabsorption and K+ secretion, resulting in salt wasting, hypotension, and hyperkalemia.

Question 37

Which of the following features differentiates pseudohypoaldosteronism type II (PHA-II) from Gitelman’s syndrome? A. Hyperkalemia in PHA-II, hypokalemia in Gitelman’s syndrome B. Hypertension in Gitelman’s syndrome, hypotension in PHA-II C. Reduced bone density in Gitelman’s syndrome, increased bone density in PHA-II D. Metabolic acidosis in Gitelman’s syndrome, metabolic alkalosis in PHA-II

Answer 37

A Hyperkalemia in PHA-II, hypokalemia in Gitelman’s syndrome Explanation: PHA-II (hereditary hypertension with hyperkalemia) is characterized by hyperkalemia and metabolic acidosis, while Gitelman’s syndrome presents with hypokalemia and metabolic alkalosis.

Question 38

What is the primary treatment for pseudohypoaldosteronism type II (PHA-II)? A. ACE inhibitors B. Thiazide diuretics C. Spironolactone D. Sodium bicarbonate

Answer 38

B

Question 39

Which genetic mutation is responsible for pseudohypoaldosteronism type II (PHA-II)? A. Mutations in SCN4A B. Mutations in WNK1 and WNK4 C. Mutations in SLC12A3 D. Mutations in CYP11B2

Answer 39

B

Question 40

Cardiac arrhythmias associated with hyperkalemia include ______

Answer 40

sinus bradycardia, sinus arrest, slow idioventricular rhythms, ventricular tachycardia, ventricular fibrillation, and asystole

Question 41

Hyperkalemia can also cause a ____ Brugada pattern in the electrocardiogram (ECG), with a pseudo–right bundle branch block and persistent coved ST-segment elevation in at least two precordial leads.

Answer 41

type I

Question 42

Classically, the ECG manifestations in hyperkalemia progress from >tall peaked T waves (5.5–6.5 mM), to a >loss of P waves (6.5–7.5 mM), to a >widened QRS complex (7.0–8.0 mM), and, ultimately, a to a >sine wave pattern (>8.0 mM).

Answer 42

>tall peaked T waves (5.5–6.5 mM), to a >loss of P waves (6.5–7.5 mM), to a >widened QRS complex (7.0–8.0 mM), and, ultimately, a to a >sine wave pattern (>8.0 mM).

Question 43

Hyperkalemia from a variety of causes can also present with ascending paralysis, denoted _______ to differentiate it from familial hyperkalemic periodic paralysis (HYPP).

Answer 43

secondary hyperkalemic paralysis

Question 44

The presentation may include diaphragmatic paralysis and respiratory failure.

Answer 44

Secondary hyperkalemic paralysis

Question 45

Initial laboratory tests for hyperkalemia should include _____

Answer 45

electrolytes, BUN, creatinine, serum osmolality, Mg2+ and Ca2+ , a complete blood count, and urinary pH, osmolality, creatinine, and electrolytes.

Question 46

_____ are required for calculation of the transtubular K + gradient (TTKG)

Answer 46

Serum and urine osmolality

Question 47

TTKG >7–8: Consistent with ______ (appropriate renal K+ excretion).

Answer 47

hyperkalemia

Question 48

TTKG <3: Consistent with ______ (appropriate renal K+ retention).

Answer 48

hypokalemia

Question 49

However, patients with significant hyperkalemia (plasma K + concentration _____ mM) in the absence of ECG changes should also be aggressively managed, given the limitations of ECG changes as a predictor of cardiac toxicity.

Answer 49

≥6.5

Question 50

What is the first priority in the diagnostic approach to hyperkalemia? A. Measure serum aldosterone levels B. Assess the need for emergency treatment C. Obtain a detailed dietary history D. Calculate the transtubular potassium gradient (TTKG)

Answer 50

B

Question 51

A patient with hyperkalemia has a urine sodium concentration <25 mmol/L. What is the most likely cause? A. Tubular resistance to aldosterone B. Reduced distal sodium delivery C. Hypertonicity-induced potassium redistribution D. Primary aldosterone deficiency

Answer 51

B A urine sodium concentration <25 mmol/L indicates insufficient sodium delivery to the distal nephron, limiting potassium secretion.

Question 52

Hyperkalemia Treatment: In hyperkalemic patients with glucose concentrations of _____ mg/dL, insulin should be administered without glucose, again with close monitoring of glucose concentrations.

Answer 52

≥200–250

Question 53

The recommended dose of insulin in treatment of hyperkalemia

Answer 53

The recommended dose is 10 units of intravenous regular insulin followed immediately by 50 mL of 50% dextrose (D50 W, 25 g of glucose total);

Question 54

_____, most commonly albuterol, are effective but underused agents for the acute management of hyperkalemia.

Answer 54

β2 -Agonists

Question 55

______ have an additive effect on plasma K + concentration; however, ~20% of patients with ESRD are resistant to the effect of _____; hence, these drugs should not be used without insulin.

Answer 55

Albuterol and insulin with glucose β2 -agonists

Question 56

____ has no role in the acute treatment of hyperkalemia, but may slowly attenuate hyperkalemia with sustained administration over several hours.

Answer 56

Intravenous bicarbonate

Question 57

The cation exchange resin _ exchanges Na + for K+ in the gastrointestinal tract and increases the fecal excretion of K

Answer 57

sodium polystyrene sulfonate (SPS)

Question 58

The recommended dose of SPS is _ of powder, almost always given in a premade suspension with 33% sorbitol.

Answer 58

15-30g

Question 59

_typically of the colon or ileum, is a rare but usually fatal complication of SPS

Answer 59

Intestinal necrosis

Question 60

Notably a major side effect of novel intestinal potassium binders

Answer 60

Hypomagnesemia

Question 61

Therapy with _______ may be beneficial in hypovolemic patients with oliguria and decreased distal delivery of Na+ , with the associated reductions in renal K + excretion.

Answer 61

intravenous saline

Question 62

_______ can be used to reduce plasma K+ concentration in volume-replete or hypervolemic patients with sufficient renal function for a diuretic response; this may need to be combined with intravenous saline or isotonic bicarbonate to achieve or maintain euvolemia.

Answer 62

Loop and thiazide diuretics

Question 63

______ is the most effective and reliable method to reduce plasma K +concentration

Answer 63

Hemodialysis

Question 64

Which therapy is most effective for rapidly removing potassium in severe or refractory hyperkalemia? A. Sodium polystyrene sulfonate (SPS) B. Loop diuretics with isotonic saline C. Hemodialysis D. Patiromer

Answer 64

C

Question 65

Which of the following potassium binders is associated with hypomagnesemia as a side effect? A. Sodium polystyrene sulfonate (SPS) B. Patiromer C. Sodium zirconium cyclosilicate (ZS-9) D. Loop diuretics

Answer 65

B