Pathophysiology Quiz: Potassium Disorders
20 questions · exam conditions
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Potassium DisordersQuestion 1 of 20

A patient taking digoxin for atrial fibrillation develops hypokalemia after several days of diarrhea. This combination significantly increases the risk of digoxin toxicity due to which cellular mechanism?

Hypokalemia reduces the renal clearance of digoxin, leading to accumulation of the drug.
Potassium and digoxin compete for the same binding site on the Na+/K+-ATPase pump; less potassium results in greater digoxin binding and inhibition.
Both hypokalemia and digoxin cause hyperpolarization of the cardiac myocyte, creating a synergistic arrhythmogenic effect.
The diarrheal illness induces hepatic enzymes that convert digoxin into more cardiotoxic metabolites.
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Pathophysiology Quiz

Pathophysiology Quiz: Potassium Disorders

Practice Potassium Disorders in Pathophysiology with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

What this quiz covers

This quiz focuses on Potassium Disorders, giving you a quick way to practice the rules, question types, and explanations that matter most for Pathophysiology.

How to use this quiz

Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

All questions

Question 1

A patient taking digoxin for atrial fibrillation develops hypokalemia after several days of diarrhea. This combination significantly increases the risk of digoxin toxicity due to which cellular mechanism?

  1. Hypokalemia reduces the renal clearance of digoxin, leading to accumulation of the drug.
  2. Potassium and digoxin compete for the same binding site on the Na+/K+-ATPase pump; less potassium results in greater digoxin binding and inhibition. (correct answer)
  3. Both hypokalemia and digoxin cause hyperpolarization of the cardiac myocyte, creating a synergistic arrhythmogenic effect.
  4. The diarrheal illness induces hepatic enzymes that convert digoxin into more cardiotoxic metabolites.
Explanation: The Na+/K+-ATPase pump is the therapeutic target of digoxin. Potassium (K+) and digoxin competitively bind to an extracellular site on this pump. When extracellular K+ is low (hypokalemia), there is less competition for this binding site, allowing more digoxin molecules to bind to and inhibit the pump. This enhanced inhibition leads to increased intracellular calcium and a higher risk of arrhythmias and other signs of toxicity.

Question 2

An asymptomatic patient with a platelet count of 1,100,000/μL has a routine blood test showing a serum potassium of 6.3 mEq/L. A repeat sample drawn and analyzed as whole blood in a point-of-care blood gas analyzer shows a plasma potassium of 4.3 mEq/L. What is the most likely cause of the initial finding?

  1. Release of intracellular potassium from the large number of platelets during in vitro coagulation. (correct answer)
  2. Systemic release of potassium from megakaryocytes in the bone marrow due to high turnover.
  3. The patient has true hyperkalemia, but the blood gas analyzer is known to be inaccurate at high platelet counts.
  4. Renal retention of potassium secondary to a paraneoplastic syndrome associated with thrombocytosis.
Explanation: When you encounter discrepant potassium values in a patient with thrombocytosis, think about the difference between serum and plasma measurements and how cellular components can interfere with laboratory results. The key insight here is understanding what happens during blood processing. In the initial test, blood was collected in a tube without anticoagulant, allowing it to clot naturally to produce serum. During this clotting process, the massive number of platelets (1,100,000/μL - normal is 150,000-400,000/μL) become activated and release their intracellular contents, including potassium. Since platelets contain high concentrations of intracellular potassium, their lysis during clotting artificially elevates the measured serum potassium to 6.3 mEq/L. This phenomenon is called pseudohyperkalemia. The repeat sample used anticoagulated whole blood analyzed immediately, preventing platelet activation and degranulation. The plasma potassium of 4.3 mEq/L reflects the patient's true physiologic state. Option A correctly identifies this mechanism of in vitro potassium release during coagulation. Option B incorrectly suggests systemic release from bone marrow megakaryocytes, but this wouldn't explain the discrepancy between sampling methods. Option C reverses the accuracy - the blood gas analyzer gives the true value, not the serum measurement. Option D proposes true hyperkalemia from renal causes, which doesn't explain why the plasma value is normal. Remember: When you see discrepant electrolyte values with extreme cell counts, always consider pseudoelectrolyte abnormalities caused by cellular lysis during specimen processing. The anticoagulated sample typically reflects the true physiologic state.

Question 3

Immediately following successful surgical revascularization of an acutely ischemic limb, a patient develops a life-threatening cardiac arrhythmia. This is most likely precipitated by a sudden systemic surge of potassium originating from what source?

  1. Washout of potassium from the interstitial fluid and damaged cells of the reperfused ischemic limb. (correct answer)
  2. A reflex surge in aldosterone secretion triggered by surgical stress, causing acute renal potassium retention.
  3. Systemic metabolic alkalosis from lactate metabolism, driving potassium out of cells body-wide.
  4. Release of potassium from activated platelets aggregating at the site of vascular repair.
Explanation: When you encounter questions about reperfusion injury, focus on what happens when blood flow suddenly returns to previously ischemic tissue. The key pathophysiological concept is that ischemic cells accumulate toxic metabolites and lose membrane integrity, creating a "toxic soup" that gets flushed into systemic circulation upon reperfusion. During acute limb ischemia, cells experience hypoxia and switch to anaerobic metabolism. This damages cell membranes and disrupts the sodium-potassium pump, causing potassium to leak from intracellular to extracellular spaces. Additionally, cell death releases large amounts of intracellular potassium. When surgical revascularization suddenly restores blood flow, this accumulated potassium gets rapidly washed into the systemic circulation, potentially causing life-threatening hyperkalemia and cardiac arrhythmias. Option A correctly identifies this washout mechanism from damaged ischemic tissue. Option B is wrong because aldosterone actually promotes potassium excretion, not retention, and wouldn't cause the immediate surge described. Option C misunderstands the metabolic picture—reperfusion typically causes metabolic acidosis (from lactate washout), not alkalosis, and this wouldn't be the primary source of the potassium surge. Option D incorrectly suggests platelets as the source; while platelets do contain some potassium, they're not the major reservoir involved in reperfusion injury. Study tip: Remember that reperfusion injury involves the "3 K's"—potassium (hyperkalemia), kidney damage (from myoglobin), and cardiac complications. The timing is crucial: these effects happen immediately upon restoration of blood flow, not hours later.

Question 4

Immediately following successful surgical revascularization of an acutely ischemic limb, a patient develops a life-threatening cardiac arrhythmia. This is most likely precipitated by a sudden systemic surge of potassium originating from what source?

  1. Washout of potassium from the interstitial fluid and damaged cells of the reperfused ischemic limb. (correct answer)
  2. A reflex surge in aldosterone secretion triggered by surgical stress, causing acute renal potassium retention.
  3. Systemic metabolic alkalosis from lactate metabolism, driving potassium out of cells body-wide.
  4. Release of potassium from activated platelets aggregating at the site of vascular repair.
Explanation: When you encounter questions about reperfusion injury, focus on what happens when blood flow suddenly returns to previously ischemic tissue. The key pathophysiological concept is that ischemic cells accumulate toxic metabolites and lose membrane integrity, creating a "toxic soup" that gets flushed into systemic circulation upon reperfusion. During acute limb ischemia, cells experience hypoxia and switch to anaerobic metabolism. This damages cell membranes and disrupts the sodium-potassium pump, causing potassium to leak from intracellular to extracellular spaces. Additionally, cell death releases large amounts of intracellular potassium. When surgical revascularization suddenly restores blood flow, this accumulated potassium gets rapidly washed into the systemic circulation, potentially causing life-threatening hyperkalemia and cardiac arrhythmias. Option A correctly identifies this washout mechanism from damaged ischemic tissue. Option B is wrong because aldosterone actually promotes potassium excretion, not retention, and wouldn't cause the immediate surge described. Option C misunderstands the metabolic picture—reperfusion typically causes metabolic acidosis (from lactate washout), not alkalosis, and this wouldn't be the primary source of the potassium surge. Option D incorrectly suggests platelets as the source; while platelets do contain some potassium, they're not the major reservoir involved in reperfusion injury. Study tip: Remember that reperfusion injury involves the "3 K's"—potassium (hyperkalemia), kidney damage (from myoglobin), and cardiac complications. The timing is crucial: these effects happen immediately upon restoration of blood flow, not hours later.

Question 5

A patient with Addison's disease (primary adrenal insufficiency) presents with a serum sodium of 130 mEq/L and a potassium of 6.0 mEq/L. The hyperkalemia is most directly caused by a deficiency in which hormone's action on the principal cells of the collecting duct?

  1. Angiotensin II
  2. Cortisol
  3. Antidiuretic hormone (ADH)
  4. Aldosterone (correct answer)
Explanation: In Addison's disease, the adrenal cortex fails to produce adequate mineralocorticoids (aldosterone) and glucocorticoids (cortisol). Aldosterone is the primary hormone responsible for promoting potassium secretion in the principal cells of the collecting duct by upregulating ENaC and ROMK channels. Its deficiency leads to impaired potassium excretion and subsequent hyperkalemia.

Question 6

A patient with chronic kidney disease on hemodialysis misses two consecutive sessions. His serum potassium rises to 7.2 mEq/L. An ECG shows a QRS duration of 0.16 seconds.

The widening of the QRS complex in this patient is primarily due to the effect of severe hyperkalemia on which aspect of cardiac electrophysiology?

  1. Delaying conduction through the AV node, which slows the signal from the atria to the ventricles.
  2. Slowing intraventricular conduction velocity due to persistent inactivation of fast sodium channels. (correct answer)
  3. Shortening the duration of the ventricular action potential, leading to asynchronous repolarization.
  4. Increasing the automaticity of ectopic pacemakers within the His-Purkinje system.
Explanation: The QRS complex represents ventricular depolarization. Severe hyperkalemia causes a significant partial depolarization of the cardiac myocyte resting membrane potential. This sustained depolarization leads to the prolonged inactivation of a large fraction of fast voltage-gated sodium channels, which are responsible for the rapid upstroke (Phase 0) of the action potential. With fewer available sodium channels, the speed of depolarization and conduction through the ventricular myocardium is slowed, resulting in a widened QRS complex.

Question 7

A patient with persistent vomiting develops a serum potassium of 3.0 mEq/L and a serum bicarbonate of 34 mEq/L (metabolic alkalosis). Which mechanism is a major contributor to the hypokalemia in this clinical state?

  1. Suppression of aldosterone by alkalosis, leading to increased renal potassium wasting.
  2. Extracellular H+ ions moving into cells to buffer alkalosis, in exchange for K+ ions moving out of cells.
  3. Direct loss of large quantities of potassium-rich gastric fluid through emesis.
  4. Intracellular shifting of K+ in exchange for H+ moving out of cells to buffer the extracellular alkalosis. (correct answer)
Explanation: In metabolic alkalosis, the extracellular fluid has a deficit of H+ ions. To buffer this change, H+ ions move out of the intracellular fluid into the extracellular fluid. To maintain electroneutrality, this is coupled with the movement of K+ ions from the extracellular fluid into cells via the H+/K+ exchanger. This intracellular shift is a major contributor to the development of hypokalemia in alkalotic states.

Question 8

A patient is admitted with profound weakness. Lab results: Serum K+ 2.2 mEq/L, Serum HCO3- 36 mEq/L, Blood pressure 170/100 mmHg, Urine K+ 60 mmol/day (high).

Which underlying condition provides the most complete pathophysiological explanation for this constellation of findings?

  1. Primary hyperaldosteronism, causing hypertension, renal potassium wasting, and metabolic alkalosis. (correct answer)
  2. Laxative abuse, causing large-volume diarrhea and subsequent volume depletion.
  3. Surreptitious vomiting, leading to volume contraction, metabolic alkalosis, and renal potassium loss.
  4. Gitelman syndrome, a genetic disorder causing renal salt wasting, hypokalemia, and metabolic alkalosis.
Explanation: When you encounter a patient with hypokalemia, metabolic alkalosis, and hypertension, you need to systematically consider the underlying mechanisms that could produce this triad of findings. Primary hyperaldosteronism perfectly explains this constellation. Excess mineralocorticoid activity causes three key effects: (1) sodium retention leading to hypertension, (2) excessive renal potassium wasting (explaining the high urine K+ of 60 mmol/day), and (3) hydrogen ion loss creating metabolic alkalosis. The profound hypokalemia (2.2 mEq/L) and elevated bicarbonate (36 mEq/L) fit this pathophysiology precisely. Option B (laxative abuse) would cause hypokalemia and metabolic alkalosis, but you'd expect hypotension from volume depletion, not hypertension. The high urine potassium also doesn't fit, as the kidneys would conserve potassium in response to GI losses. Option C (surreptitious vomiting) explains the metabolic alkalosis and can cause secondary renal potassium wasting, but again, volume contraction typically produces hypotension, not the hypertension seen here. Option D (Gitelman syndrome) causes hypokalemia and metabolic alkalosis, but this genetic tubulopathy typically presents with normal or low blood pressure due to salt wasting, not hypertension. The key distinguishing feature is hypertension combined with renal potassium wasting. This combination specifically points to mineralocorticoid excess, as other causes of hypokalemia with metabolic alkalosis typically cause hypotension or normal blood pressure. Study tip: Remember the "hyperaldosteronism triad" – hypertension, hypokalemia, and metabolic alkalosis. When you see all three together with high urine potassium, think primary hyperaldosteronism first.

Question 9

An elderly patient with hypertension, type 2 diabetes, and moderate chronic kidney disease is started on lisinopril. This medication increases the risk of hyperkalemia by initiating which of the following physiological cascades?

  1. Blocking the epithelial sodium channel (ENaC), thus preventing the secretion of potassium.
  2. Inhibiting angiotensin-converting enzyme, which reduces angiotensin II levels and subsequently decreases aldosterone secretion. (correct answer)
  3. Causing a systemic metabolic acidosis, which promotes the movement of potassium out of cells.
  4. Directly stimulating potassium reabsorption in the proximal tubule of the nephron.
Explanation: Lisinopril is an ACE inhibitor. It blocks the conversion of angiotensin I to angiotensin II. Angiotensin II is a potent stimulator of aldosterone release from the adrenal glands. By reducing angiotensin II levels, lisinopril causes a decrease in aldosterone secretion. Since aldosterone is crucial for promoting potassium excretion in the distal nephron, its reduction leads to potassium retention and an increased risk of hyperkalemia, especially in patients with pre-existing kidney disease.

Question 10

An elderly patient with hypertension, type 2 diabetes, and moderate chronic kidney disease is started on lisinopril. This medication increases the risk of hyperkalemia by initiating which of the following physiological cascades?

  1. Blocking the epithelial sodium channel (ENaC), thus preventing the secretion of potassium.
  2. Inhibiting angiotensin-converting enzyme, which reduces angiotensin II levels and subsequently decreases aldosterone secretion. (correct answer)
  3. Causing a systemic metabolic acidosis, which promotes the movement of potassium out of cells.
  4. Directly stimulating potassium reabsorption in the proximal tubule of the nephron.
Explanation: Lisinopril is an ACE inhibitor. It blocks the conversion of angiotensin I to angiotensin II. Angiotensin II is a potent stimulator of aldosterone release from the adrenal glands. By reducing angiotensin II levels, lisinopril causes a decrease in aldosterone secretion. Since aldosterone is crucial for promoting potassium excretion in the distal nephron, its reduction leads to potassium retention and an increased risk of hyperkalemia, especially in patients with pre-existing kidney disease.

Question 11

A patient with diabetic ketoacidosis (DKA) has an initial serum potassium of 6.1 mEq/L despite significant total body potassium depletion. Following administration of intravenous insulin and normal saline, the serum potassium falls to 3.2 mEq/L within four hours.

What is the primary pathophysiological mechanism responsible for this rapid and profound decrease in serum potassium?

  1. The correction of metabolic acidosis causes a rapid shift of hydrogen ions out of cells in exchange for potassium ions moving into cells.
  2. The administered intravenous fluids cause a significant dilutional effect, lowering the concentration of potassium in the serum.
  3. Insulin directly stimulates the activity of the Na+/K+-ATPase pump on cell membranes, driving potassium from the extracellular to the intracellular space. (correct answer)
  4. Rehydration improves renal perfusion, leading to a massive and immediate increase in the urinary excretion of potassium.
Explanation: While correction of acidosis and improved renal function contribute to lowering potassium, the most significant and rapid effect comes from insulin. Insulin directly upregulates the Na+/K+-ATPase pump, which actively transports potassium into cells, causing a rapid shift from the extracellular fluid and a subsequent drop in serum levels.

Question 12

A patient with Addison's disease (primary adrenal insufficiency) presents with a serum sodium of 130 mEq/L and a potassium of 6.0 mEq/L. The hyperkalemia is most directly caused by a deficiency in which hormone's action on the principal cells of the collecting duct?

  1. Angiotensin II
  2. Cortisol
  3. Antidiuretic hormone (ADH)
  4. Aldosterone (correct answer)
Explanation: In Addison's disease, the adrenal cortex fails to produce adequate mineralocorticoids (aldosterone) and glucocorticoids (cortisol). Aldosterone is the primary hormone responsible for promoting potassium secretion in the principal cells of the collecting duct by upregulating ENaC and ROMK channels. Its deficiency leads to impaired potassium excretion and subsequent hyperkalemia.

Question 13

A patient with persistent vomiting develops a serum potassium of 3.0 mEq/L and a serum bicarbonate of 34 mEq/L (metabolic alkalosis). Which mechanism is a major contributor to the hypokalemia in this clinical state?

  1. Suppression of aldosterone by alkalosis, leading to increased renal potassium wasting.
  2. Extracellular H+ ions moving into cells to buffer alkalosis, in exchange for K+ ions moving out of cells.
  3. Direct loss of large quantities of potassium-rich gastric fluid through emesis.
  4. Intracellular shifting of K+ in exchange for H+ moving out of cells to buffer the extracellular alkalosis. (correct answer)
Explanation: In metabolic alkalosis, the extracellular fluid has a deficit of H+ ions. To buffer this change, H+ ions move out of the intracellular fluid into the extracellular fluid. To maintain electroneutrality, this is coupled with the movement of K+ ions from the extracellular fluid into cells via the H+/K+ exchanger. This intracellular shift is a major contributor to the development of hypokalemia in alkalotic states.

Question 14

An asymptomatic patient with a platelet count of 1,100,000/μL has a routine blood test showing a serum potassium of 6.3 mEq/L. A repeat sample drawn and analyzed as whole blood in a point-of-care blood gas analyzer shows a plasma potassium of 4.3 mEq/L. What is the most likely cause of the initial finding?

  1. Release of intracellular potassium from the large number of platelets during in vitro coagulation. (correct answer)
  2. Systemic release of potassium from megakaryocytes in the bone marrow due to high turnover.
  3. The patient has true hyperkalemia, but the blood gas analyzer is known to be inaccurate at high platelet counts.
  4. Renal retention of potassium secondary to a paraneoplastic syndrome associated with thrombocytosis.
Explanation: When you encounter discrepant potassium values in a patient with thrombocytosis, think about the difference between serum and plasma measurements and how cellular components can interfere with laboratory results. The key insight here is understanding what happens during blood processing. In the initial test, blood was collected in a tube without anticoagulant, allowing it to clot naturally to produce serum. During this clotting process, the massive number of platelets (1,100,000/μL - normal is 150,000-400,000/μL) become activated and release their intracellular contents, including potassium. Since platelets contain high concentrations of intracellular potassium, their lysis during clotting artificially elevates the measured serum potassium to 6.3 mEq/L. This phenomenon is called pseudohyperkalemia. The repeat sample used anticoagulated whole blood analyzed immediately, preventing platelet activation and degranulation. The plasma potassium of 4.3 mEq/L reflects the patient's true physiologic state. Option A correctly identifies this mechanism of in vitro potassium release during coagulation. Option B incorrectly suggests systemic release from bone marrow megakaryocytes, but this wouldn't explain the discrepancy between sampling methods. Option C reverses the accuracy - the blood gas analyzer gives the true value, not the serum measurement. Option D proposes true hyperkalemia from renal causes, which doesn't explain why the plasma value is normal. Remember: When you see discrepant electrolyte values with extreme cell counts, always consider pseudoelectrolyte abnormalities caused by cellular lysis during specimen processing. The anticoagulated sample typically reflects the true physiologic state.

Question 15

A patient experiences an episode of acute flaccid paralysis after a large carbohydrate meal. Labs during the episode reveal a serum potassium of 2.1 mEq/L. This presentation is classic for hypokalemic periodic paralysis. The paralysis is precipitated by a massive intracellular shift of potassium driven by what physiological trigger?

  1. The release of epinephrine in response to the metabolic stress of the meal.
  2. A sudden loss of potassium through the kidneys stimulated by the glucose load.
  3. An exaggerated muscular response to the post-prandial release of insulin. (correct answer)
  4. A transient defect in acetylcholine receptors induced by high blood glucose.
Explanation: In hypokalemic periodic paralysis, individuals (often with an underlying genetic channelopathy) are exquisitely sensitive to the normal physiological effects of insulin. A large carbohydrate meal leads to a significant insulin surge. Insulin potently stimulates the Na+/K+-ATPase pump in skeletal muscle, causing a massive and rapid shift of potassium from the extracellular fluid into the muscle cells. This acute, severe hypokalemia hyperpolarizes the muscle membrane, causing flaccid paralysis.

Question 16

A genetic disorder characterized by hypokalemia, metabolic alkalosis, and hyperreninemic hyperaldosteronism, which pathophysiologically mimics the chronic use of a loop diuretic due to a defect in the Na-K-2Cl cotransporter, is known as:

  1. Gitelman syndrome
  2. Liddle syndrome
  3. Bartter syndrome (correct answer)
  4. Type 4 Renal Tubular Acidosis
Explanation: Bartter syndrome is a group of inherited disorders caused by mutations in genes encoding proteins of the Na-K-2Cl cotransporter (NKCC2) or other related channels in the thick ascending limb of the loop of Henle. This defect impairs salt reabsorption, leading to volume depletion, activation of the RAAS (hyperreninemic hyperaldosteronism), and downstream effects of potassium and hydrogen wasting, thus mimicking the exact effects of a loop diuretic like furosemide.

Question 17

A patient with diabetic ketoacidosis (DKA) has an initial serum potassium of 6.1 mEq/L despite significant total body potassium depletion. Following administration of intravenous insulin and normal saline, the serum potassium falls to 3.2 mEq/L within four hours.

What is the primary pathophysiological mechanism responsible for this rapid and profound decrease in serum potassium?

  1. The correction of metabolic acidosis causes a rapid shift of hydrogen ions out of cells in exchange for potassium ions moving into cells.
  2. The administered intravenous fluids cause a significant dilutional effect, lowering the concentration of potassium in the serum.
  3. Insulin directly stimulates the activity of the Na+/K+-ATPase pump on cell membranes, driving potassium from the extracellular to the intracellular space. (correct answer)
  4. Rehydration improves renal perfusion, leading to a massive and immediate increase in the urinary excretion of potassium.
Explanation: While correction of acidosis and improved renal function contribute to lowering potassium, the most significant and rapid effect comes from insulin. Insulin directly upregulates the Na+/K+-ATPase pump, which actively transports potassium into cells, causing a rapid shift from the extracellular fluid and a subsequent drop in serum levels.

Question 18

A patient is admitted with profound weakness. Lab results: Serum K+ 2.2 mEq/L, Serum HCO3- 36 mEq/L, Blood pressure 170/100 mmHg, Urine K+ 60 mmol/day (high).

Which underlying condition provides the most complete pathophysiological explanation for this constellation of findings?

  1. Primary hyperaldosteronism, causing hypertension, renal potassium wasting, and metabolic alkalosis. (correct answer)
  2. Laxative abuse, causing large-volume diarrhea and subsequent volume depletion.
  3. Surreptitious vomiting, leading to volume contraction, metabolic alkalosis, and renal potassium loss.
  4. Gitelman syndrome, a genetic disorder causing renal salt wasting, hypokalemia, and metabolic alkalosis.
Explanation: When you encounter a patient with hypokalemia, metabolic alkalosis, and hypertension, you need to systematically consider the underlying mechanisms that could produce this triad of findings. Primary hyperaldosteronism perfectly explains this constellation. Excess mineralocorticoid activity causes three key effects: (1) sodium retention leading to hypertension, (2) excessive renal potassium wasting (explaining the high urine K+ of 60 mmol/day), and (3) hydrogen ion loss creating metabolic alkalosis. The profound hypokalemia (2.2 mEq/L) and elevated bicarbonate (36 mEq/L) fit this pathophysiology precisely. Option B (laxative abuse) would cause hypokalemia and metabolic alkalosis, but you'd expect hypotension from volume depletion, not hypertension. The high urine potassium also doesn't fit, as the kidneys would conserve potassium in response to GI losses. Option C (surreptitious vomiting) explains the metabolic alkalosis and can cause secondary renal potassium wasting, but again, volume contraction typically produces hypotension, not the hypertension seen here. Option D (Gitelman syndrome) causes hypokalemia and metabolic alkalosis, but this genetic tubulopathy typically presents with normal or low blood pressure due to salt wasting, not hypertension. The key distinguishing feature is hypertension combined with renal potassium wasting. This combination specifically points to mineralocorticoid excess, as other causes of hypokalemia with metabolic alkalosis typically cause hypotension or normal blood pressure. Study tip: Remember the "hyperaldosteronism triad" – hypertension, hypokalemia, and metabolic alkalosis. When you see all three together with high urine potassium, think primary hyperaldosteronism first.

Question 19

A patient with chronic kidney disease on hemodialysis misses two consecutive sessions. His serum potassium rises to 7.2 mEq/L. An ECG shows a QRS duration of 0.16 seconds.

The widening of the QRS complex in this patient is primarily due to the effect of severe hyperkalemia on which aspect of cardiac electrophysiology?

  1. Delaying conduction through the AV node, which slows the signal from the atria to the ventricles.
  2. Slowing intraventricular conduction velocity due to persistent inactivation of fast sodium channels. (correct answer)
  3. Shortening the duration of the ventricular action potential, leading to asynchronous repolarization.
  4. Increasing the automaticity of ectopic pacemakers within the His-Purkinje system.
Explanation: The QRS complex represents ventricular depolarization. Severe hyperkalemia causes a significant partial depolarization of the cardiac myocyte resting membrane potential. This sustained depolarization leads to the prolonged inactivation of a large fraction of fast voltage-gated sodium channels, which are responsible for the rapid upstroke (Phase 0) of the action potential. With fewer available sodium channels, the speed of depolarization and conduction through the ventricular myocardium is slowed, resulting in a widened QRS complex.

Question 20

A genetic disorder characterized by hypokalemia, metabolic alkalosis, and hyperreninemic hyperaldosteronism, which pathophysiologically mimics the chronic use of a loop diuretic due to a defect in the Na-K-2Cl cotransporter, is known as:

  1. Gitelman syndrome
  2. Liddle syndrome
  3. Bartter syndrome (correct answer)
  4. Type 4 Renal Tubular Acidosis
Explanation: Bartter syndrome is a group of inherited disorders caused by mutations in genes encoding proteins of the Na-K-2Cl cotransporter (NKCC2) or other related channels in the thick ascending limb of the loop of Henle. This defect impairs salt reabsorption, leading to volume depletion, activation of the RAAS (hyperreninemic hyperaldosteronism), and downstream effects of potassium and hydrogen wasting, thus mimicking the exact effects of a loop diuretic like furosemide.