Potassium Homeostasis — MCQs
A CKD patient develops serum K+ 7.2 mEq/L without ECG changes. Best initial management?
The body fluid compartments of a patient were measured, showing the following ion concentrations: - Sodium (Na): $10 \mathrm{mEq} / \mathrm{L}$ - Potassium (K): $140 \mathrm{mEq} / \mathrm{L}$ - Chloride (Cl): $15 \mathrm{mEq} / \mathrm{L}$ Based on these values, which fluid compartment is being described?
Which of the following is the primary mechanism that drives sodium reabsorption in the proximal tubule?
A patient has hyperaldosteronism. Which lab finding is expected?
All are examples of negative feedback except
Result of liquorice ingestion
Tetany in muscle occurs in spite of normal serum Ca2+ level. Which ion is responsible?
In Bartter's syndrome there is a defect in
On insulin administration, what change is expected in the extracellular fluid (ECF)?
In renal failure, what is the primary cause of metabolic acidosis?
Potassium Homeostasis Indian Medical PG Practice Questions and MCQs
Question 1: A CKD patient develops serum K+ 7.2 mEq/L without ECG changes. Best initial management?
- A. Emergency dialysis
- B. Sodium polystyrene
- C. Insulin with glucose
- D. Calcium gluconate (Correct Answer)
Explanation: **Calcium gluconate** - **Calcium gluconate** is the best initial management for severe hyperkalemia, particularly when the potassium level is very high (above 6.5 mEq/L) even without ECG changes [1]. It acts quickly to directly stabilize the cardiac membrane by **antagonizing the effects of potassium on myocardial excitability**, thereby preventing life-threatening arrhythmias [1]. - It provides immediate cardioprotection, buying time for other therapies to shift potassium into cells or remove it from the body. *Emergency dialysis* - While **dialysis** is the most effective way to remove potassium from the body, it is typically reserved for cases of severe, refractory hyperkalemia, or when other therapies have failed [3]. - It is not the *initial* management for immediate cardiac stabilization, especially if no ECG changes are present and calcium can be administered more rapidly. *Sodium polystyrene* - **Sodium polystyrene sulfonate (Kayexalate)** is a potassium-binding resin that works in the gastrointestinal tract to exchange sodium for potassium, thus removing potassium from the body. - Its onset of action is slow (hours to days), making it inappropriate for acute, severe hyperkalemia requiring immediate intervention. *Insulin with glucose* - **Insulin with glucose** therapy promotes the intracellular shift of potassium, temporarily lowering serum potassium levels [2]. - While effective, its onset of action is typically 15-30 minutes, and it functions as a temporary measure to redistribute potassium, not to acutely stabilize the cardiac membrane, which is the primary concern when potassium is severely elevated.
Question 2: The body fluid compartments of a patient were measured, showing the following ion concentrations: - Sodium (Na): $10 \mathrm{mEq} / \mathrm{L}$ - Potassium (K): $140 \mathrm{mEq} / \mathrm{L}$ - Chloride (Cl): $15 \mathrm{mEq} / \mathrm{L}$ Based on these values, which fluid compartment is being described?
- A. Plasma
- B. ICF (Correct Answer)
- C. Interstitial fluid
- D. ECF
Explanation: ***ICF*** - The measured ion concentrations, especially **high potassium (140 mEq/L)** and **low sodium (10 mEq/L)**, are characteristic of the **intracellular fluid (ICF)**, where potassium is the primary cation and sodium is kept low by the Na+/K+-ATPase pump. - **Chloride levels (15 mEq/L)** are also significantly lower in the ICF compared to extracellular fluids. *Plasma* - Plasma typically has **high sodium (around 140 mEq/L)** and **low potassium (around 4 mEq/L)**, which contradicts the given measurements. - Chloride levels in plasma are usually much higher, around **100-105 mEq/L**. *Interstitial fluid* - Interstitial fluid has an electrolyte composition very similar to plasma, with **high sodium** and **low potassium**, differing mainly in protein content. - This composition is not consistent with the given measurements. *ECF* - The ECF (extracellular fluid), which includes both plasma and interstitial fluid, is characterized by **high sodium** and **low potassium**. - The given ion concentrations, particularly the very **high potassium** and **low sodium**, are directly opposite to the typical ECF profile.
Question 3: Which of the following is the primary mechanism that drives sodium reabsorption in the proximal tubule?
- A. Sodium reabsorption through cotransport with amino acids at the luminal membrane.
- B. Sodium reabsorption through cotransport with glucose at the luminal membrane.
- C. Sodium reabsorption through countertransport with hydrogen ions at the luminal membrane.
- D. Active sodium transport via the Na+-K+-ATPase pump at the basolateral membrane. (Correct Answer)
Explanation: ***Active sodium transport via the Na+-K+-ATPase pump at the basolateral membrane.*** - This pump **actively transports sodium out of the cell** into the interstitial fluid, creating a low intracellular sodium concentration. - The **Na+-K+-ATPase** is the primary driver of sodium reabsorption throughout the nephron, creating the electrochemical gradient for other sodium transporters. *Sodium reabsorption through cotransport with amino acids at the luminal membrane.* - While **sodium-amino acid cotransport** does occur in the proximal tubule, it accounts for only a fraction of total sodium reabsorption. - The primary driving force for this cotransport is the **low intracellular sodium concentration** maintained by the Na+-K+-ATPase. *Sodium reabsorption through cotransport with glucose at the luminal membrane.* - **Sodium-glucose cotransporters (SGLTs)** are crucial for glucose reabsorption in the proximal tubule, moving glucose into the cell along with sodium. - However, glucose cotransport represents a specific mechanism for glucose handling, not the overarching mechanism for sodium reabsorption. *Sodium reabsorption through countertransport with hydrogen ions at the luminal membrane.* - The **Na+-H+ exchanger (NHE3)** is significant for exchanging sodium for hydrogen ions at the luminal membrane in the proximal tubule. - This mechanism is important for **acid-base balance** and some sodium reabsorption, but it is secondary to the Na+-K+-ATPase in driving the overall sodium gradient.
Question 4: A patient has hyperaldosteronism. Which lab finding is expected?
- A. Metabolic acidosis
- B. Hyperkalemia
- C. Hypokalemia (Correct Answer)
- D. Hyponatremia
Explanation: ***Hypokalemia*** - **Aldosterone** increases the excretion of **potassium** in the kidneys, leading to decreased serum potassium levels [1]. - This effect is mediated by aldosterone's action on the principal cells of the collecting duct, promoting potassium secretion into the urine [1]. *Metabolic acidosis* - **Hyperaldosteronism** typically causes **metabolic alkalosis** due to increased hydrogen ion excretion by the kidneys [1]. - Aldosterone promotes the reabsorption of sodium and water, and the excretion of potassium and hydrogen ions, leading to alkalosis [2]. *Hyperkalemia* - **Aldosterone's primary role** is to promote **potassium excretion** in the kidneys [1]. - Therefore, **excessive aldosterone** production would lead to **hypokalemia**, not hyperkalemia. *Hyponatremia* - **Aldosterone** promotes **sodium reabsorption** in the kidneys, which usually leads to normal or even slightly elevated serum sodium levels [1]. - **Hyponatremia** would be an unexpected finding in hyperaldosteronism [3].
Question 5: All are examples of negative feedback except
- A. Regulation of blood CO2 level
- B. Regulation of pituitary hormones
- C. Regulation of blood pressure
- D. Coagulation of the blood (Correct Answer)
Explanation: ***Coagulation of the blood*** - **Blood coagulation** is a classic example of **positive feedback**, where the initial clotting process amplifies itself until bleeding stops - Platelets aggregate and release factors that promote further platelet aggregation and activation of the clotting cascade, thereby **accelerating the response** rather than diminishing it - This is the exception among the options, as it represents positive feedback while all others are negative feedback *Regulation of blood CO2 level* - The regulation of **blood CO2 levels** is a vital example of **negative feedback**, where an increase in CO2 stimulates breathing to expel excess CO2 - This mechanism works to return the blood CO2 concentration to its homeostatic set point, thus **counteracting the initial stimulus** - Central and peripheral chemoreceptors detect elevated CO2 and trigger increased ventilation *Regulation of pituitary hormones* - The regulation of **pituitary hormones** involves **negative feedback loops**, where high levels of target gland hormones inhibit the release of stimulating hormones from the pituitary and hypothalamus - For example, high thyroid hormone levels inhibit TSH release from the pituitary and TRH from the hypothalamus - This effectively **reduces the initial stimulus** and maintains hormonal balance *Regulation of blood pressure* - The regulation of **blood pressure** is primarily controlled by **negative feedback mechanisms** involving baroreceptors, which detect changes in pressure - If blood pressure rises, baroreceptors in the carotid sinus and aortic arch signal the medulla to reduce heart rate and dilate blood vessels - This response **lowers the pressure back to the set point**, maintaining cardiovascular homeostasis
Question 6: Result of liquorice ingestion
- A. Hyperkalemic alkalosis
- B. Hypokalemic acidosis
- C. Hypernatremic acidosis
- D. Hypokalemic alkalosis (Correct Answer)
Explanation: ***Hypokalemic alkalosis*** - **Licorice** contains **glycyrrhizic acid**, which inhibits **11β-hydroxysteroid dehydrogenase** in the kidneys, preventing the conversion of cortisol to inactive cortisone. - This leads to increased cortisol acting on **mineralocorticoid receptors**, mimicking **aldosterone excess**, resulting in **sodium reabsorption**, **potassium excretion** (hypokalemia), and **hydrogen ion excretion** (metabolic alkalosis). *Hyperkalemic alkalosis* - This option is incorrect because licorice ingestion leads to **hypokalemia** due to increased potassium excretion, not hyperkalemia. - While it does cause alkalosis, the associated potassium imbalance is the opposite of this choice. *Hypokalemic acidosis* - This option is incorrect because licorice ingestion causes a **metabolic alkalosis** due to increased hydrogen ion excretion, not acidosis. - Although it correctly identifies hypokalemia, the acid-base disturbance is wrong. *Hypernatremic acidosis* - This option is incorrect as licorice ingestion initially causes **sodium and water retention** (which can lead to hypernatremia in severe cases, but is not the primary driver of the acid-base), but primarily leads to **metabolic alkalosis**, not acidosis. - The combination of hypernatremia and acidosis is not characteristic of licorice toxicity.
Question 7: Tetany in muscle occurs in spite of normal serum Ca2+ level. Which ion is responsible?
- A. Mg2+
- B. K+
- C. Na+
- D. Ionized Ca2+ (Correct Answer)
Explanation: ***Ionized Ca2+*** - While total serum calcium might be normal, **tetany** is specifically caused by a decrease in the concentration of **ionized (free) calcium** in the extracellular fluid. - Ionized calcium is the physiologically active form of calcium responsible for neuromuscular excitability. *Mg2+* - **Hypomagnesemia** can exacerbate hypocalcemia and contribute to tetany, but it is not the primary ion directly responsible for tetany when **total serum calcium is normal**. - A deficiency in Mg2+ can impair the release of **parathyroid hormone** and reduce target organ responsiveness to PTH. *K+* - Abnormalities in **potassium levels** (hypokalemia or hyperkalemia) primarily affect cardiac and muscular excitability, leading to arrhythmias or muscle weakness/paralysis. - While electrolyte imbalances are interconnected, changes in potassium are not the direct cause of tetany due to calcium's role. *Na+* - **Sodium ions** are crucial for nerve impulse transmission and muscle contraction by establishing the resting membrane potential and initiating action potentials. - However, direct changes in sodium concentration do not typically cause tetany; rather, they can lead to neurological symptoms like seizures (hyponatremia) or altered mental status (hypernatremia).
Question 8: In Bartter's syndrome there is a defect in
- A. Descending limb of LOH
- B. Thick ascending limb of LOH (Correct Answer)
- C. DCT
- D. PCT
Explanation: ***Thick ascending limb of LOH*** - **Bartter's syndrome** is characterized by a genetic defect affecting the **Na-K-2Cl cotransporter (NKCC2)** located in the thick ascending limb of the loop of Henle. - This defect impairs the reabsorption of sodium, potassium, and chloride ions, leading to significant **electrolyte imbalances** such as hypokalemia, metabolic alkalosis, and hyperreninemia. *Descending limb of LOH* - The descending limb is primarily permeable to **water** due to aquaporin channels, and impermeable to solutes. - Defects in this segment are not typically associated with the electrolyte derangements seen in Bartter's syndrome. *DCT* - The **distal convoluted tubule (DCT)** is where fine-tuning of sodium and calcium reabsorption occurs, primarily through the Na-Cl cotransporter (NCC) and active calcium transport. - Defects in the DCT are characteristic of **Gitelman's syndrome**, which has similar but generally milder symptoms compared to Bartter's syndrome. *PCT* - The **proximal convoluted tubule (PCT)** is responsible for the bulk reabsorption of filtered substances, including glucose, amino acids, bicarbonate, and about 65-70% of filtered sodium. - While defects here can lead to various syndromes (e.g., Fanconi syndrome), they do not directly cause the specific electrolyte abnormalities seen in Bartter's syndrome.
Question 9: On insulin administration, what change is expected in the extracellular fluid (ECF)?
- A. Hypoglycemia (Correct Answer)
- B. Hyperkalemia
- C. Hyponatremia
- D. Hypocalcemia
Explanation: **Hypoglycemia (Correct Answer)** - Insulin promotes the uptake of **glucose** from the ECF into cells, primarily muscle and adipose tissue - This action leads to a decrease in ECF **glucose concentration**, resulting in **hypoglycemia** if insulin levels are excessive or glucose intake is insufficient - This is the primary and most significant change in ECF composition after insulin administration *Hyperkalemia (Incorrect)* - Insulin actually stimulates the cellular uptake of **potassium**, moving it from the ECF into the intracellular fluid - Therefore, insulin administration typically causes **hypokalemia**, not hyperkalemia - This effect is sometimes used therapeutically to treat hyperkalemia by driving potassium into cells *Hyponatremia (Incorrect)* - Insulin primarily affects **glucose** and **potassium** metabolism and does not directly cause changes in sodium concentration in the ECF - **Hyponatremia** would be more associated with altered water balance or disorders of kidney function, not direct insulin effects - Sodium homeostasis is regulated by the renin-angiotensin-aldosterone system and ADH *Hypocalcemia (Incorrect)* - Insulin has no direct effect on **calcium** levels or its regulation in the ECF - **Calcium homeostasis** is primarily regulated by parathyroid hormone (PTH), vitamin D, and calcitonin, independent of insulin action - Changes in calcium concentration are not expected with insulin administration
Question 10: In renal failure, what is the primary cause of metabolic acidosis?
- A. Use of diuretics
- B. Loss of HCO3-
- C. Increased H+ production
- D. Decreased excretion of acids (Correct Answer)
Explanation: ***Decreased excretion of acids*** - In **renal failure**, the kidneys lose their ability to effectively excrete metabolic acid byproducts, leading to their accumulation in the body. - This accumulation of acids, such as **sulfates**, **phosphates**, and **urea**, consumes bicarbonate buffers, resulting in metabolic acidosis. *Increased H+ production* - While overproduction of **H+ ions** can cause acidosis, like in **ketoacidosis** or **lactic acidosis**, it's not the primary underlying mechanism in most cases of renal failure. - The problem in renal failure is primarily one of **impaired elimination**, not excessive generation, of acids. *Loss of HCO3-* - Loss of **bicarbonate (HCO3-)** can occur in conditions like severe diarrhea or renal tubular acidosis, but it's not the primary cause of metabolic acidosis in general renal failure. - In renal failure, decreased **ammoniagenesis** and impaired reabsorption of bicarbonate can contribute, but the main driver is reduced acid excretion. *Use of diuretics* - The use of **diuretics** (especially loop or thiazide diuretics) typically causes **metabolic alkalosis** due to increased potassium and hydrogen ion excretion, rather than acidosis. - Some diuretics, like **carbonic anhydrase inhibitors**, can cause a mild metabolic acidosis, but this is less common and not the primary cause of renal failure-associated acidosis.
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free