Potassium Flashcards
Homeostatic mechanisms maintain plasma K + concentration between____
3.5 and 5.0 mM
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.
principal cells
alpha-intercalated cells
Hypokalemia, defined as a plasma K +concentration of <____ mM
3.5
Systemic _____ can also cause treatment resistant hypokalemia, due to a combination of reduced cellular uptake of K +and exaggerated renal secretion.
hypomagnesemia
_______ can occasionally result from in vitro cellular uptake of K + after venipuncture, for example, due to profound leukocytosis in acute leukemia.
Spurious hypokalemia or “pseudohypokalemia”
Associated with a tenfold increase in in-hospital mortality
Hypokalemia
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.
B
_____ have a greater effect on plasma K +concentration than loop diuretics, despite their lesser natriuretic effect.
Thiazides
The diuretic effect of thiazides is largely due to inhibition of the _____in DCT cells.
Na+ -Cl – cotransporter NCC
High doses of _____can increase obligatory K + excretion by acting as nonreabsorbable anions in the distal nephron.
penicillin-related antibiotics (nafcillin, dicloxacillin, ticarcillin, oxacillin, and carbenicillin)
Renal tubular toxins that cause renal K+ and Mg2+ wasting → hypokalemia and hypomagnesemia.
Aminoglycosides, amphotericin, foscarnet, cisplatin, ifosfamide.
Liddle’s syndrome is caused by autosomal dominant gain-in-function mutations of _____.
ENaC subunits
Patients with Liddle’s syndrome classically manifest severe hypertension with ______, unresponsive to spironolactone yet sensitive to amiloride.
hypokalemia
Mutations in thiazide-sensitive Na+/Cl– cotransporter of DCT.
Gitelman’s Syndrome
TALH transporter defects (Na+, K+, Cl–).
Bartter’s Syndrome
Hypokalemia is a major risk factor for both____
ventricular and atrial arrhythmias.
Electrocardiographic changes in hypokalemia include ______; these are most marked when serum K +is <2.7 mmol/L.
broad flat T waves, ST depression, and QT prolongation
The paralytic effects of hypokalemia on intestinal smooth muscle may cause _____.
intestinal ileus
____ is the mainstay of therapy in hypokalemia.
Oral replacement with K+ -Cl-
____, oral or IV, may be appropriate in patients with combined hypokalemia and hypophosphatemia.
Potassium phosphate
_____ should be considered in patients with concomitant metabolic acidosis.
Potassium bicarbonate or potassium citrate
The use of intravenous administration should be limited to patients _____
unable to use the enteral route or in the setting of severe complications (e.g., paralysis, arrhythmia).
Intravenous K+-Cl should always be administered in ______, because the dextrose-induced increase in insulin can acutely exacerbate hypokalemia.
saline solutions, rather than dextrose
The peripheral intravenous dose is usually _____of K+-Cl –per liter;
20–40 mmol
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.
10–20 mmol/h
Strategies to minimize K +losses
> 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).
Hyperkalemia is defined as a plasma potassium level of _____
5.5 mM
Drugs that impact on the _____ are also a major cause of hyperkalemia.
renin-angiotensin-aldosterone axis
______ 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.
Pseudohyperkalemia
_____ has surpassed tuberculosis as the most important infectious cause of adrenal insufficiency.
HIV
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.
“solvent drag” effect
____ depolarizes muscle cells, causing an efflux of K+ through acetylcholine receptors (AChRs).
Succinylcholine
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
C
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)
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.
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
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.
What is the primary treatment for pseudohypoaldosteronism type II (PHA-II)?
A. ACE inhibitors
B. Thiazide diuretics
C. Spironolactone
D. Sodium bicarbonate
B
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
B
Cardiac arrhythmias associated with hyperkalemia include ______
sinus bradycardia, sinus arrest, slow idioventricular rhythms, ventricular tachycardia, ventricular fibrillation, and asystole
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.
type I
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).
> 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).
Hyperkalemia from a variety of causes can also present with ascending paralysis, denoted _______ to differentiate it from familial hyperkalemic periodic paralysis (HYPP).
secondary hyperkalemic paralysis
The presentation may include diaphragmatic paralysis and respiratory failure.
Secondary hyperkalemic paralysis
Initial laboratory tests for hyperkalemia should include _____
electrolytes, BUN, creatinine, serum osmolality, Mg2+ and Ca2+ , a complete blood count, and urinary pH, osmolality, creatinine, and electrolytes.
_____ are required for calculation of the transtubular K + gradient (TTKG)
Serum and urine osmolality
TTKG >7–8: Consistent with ______ (appropriate renal K+ excretion).
hyperkalemia
TTKG <3: Consistent with ______ (appropriate renal K+ retention).
hypokalemia
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.
≥6.5
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)
B
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
B
A urine sodium concentration <25 mmol/L indicates insufficient sodium delivery to the distal nephron, limiting potassium secretion.
Hyperkalemia Treatment: In hyperkalemic patients with glucose concentrations of _____ mg/dL, insulin should be administered without glucose, again with close monitoring of glucose concentrations.
≥200–250
The recommended dose of insulin in treatment of hyperkalemia
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);
_____, most commonly albuterol, are effective but underused agents for the acute management of hyperkalemia.
β2 -Agonists
______ 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.
Albuterol and insulin with glucose
β2 -agonists
____ has no role in the acute treatment of hyperkalemia, but may slowly attenuate
hyperkalemia with sustained administration over several hours.
Intravenous bicarbonate
The cation exchange resin _
exchanges Na + for K+ in the gastrointestinal tract
and increases the fecal excretion of K
sodium polystyrene sulfonate (SPS)
The recommended dose of SPS is _ of powder, almost always given in a premade suspension with 33% sorbitol.
15-30g
_typically of the colon or ileum, is a rare but usually fatal complication of SPS
Intestinal necrosis
Notably a major side effect of novel intestinal potassium binders
Hypomagnesemia
Therapy with _______ may be beneficial in hypovolemic patients with oliguria and decreased distal delivery of Na+ , with the associated reductions in renal K + excretion.
intravenous saline
_______ 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.
Loop and thiazide diuretics
______ is the most effective and reliable method to reduce plasma K +concentration
Hemodialysis
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
C
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
B
