Potassium Regulation — MCQs
All of the following are true about potassium, except
Hyperkalemia aciduria is seen in
Where does potassium reabsorption primarily occur in the kidney?
A patient has hyperaldosteronism. Which lab finding is expected?
Which of the following is not an effect of efferent arteriole constriction:
In Bartter's syndrome there is a defect in
Which causes raised angiotensin in blood?
Cerebral blood flow is regulated by all of the following except:
Which of the following is not an absolute indication for hemodialysis?
Assertion: RMP depends on proteins and phosphate ions. Reason: Diffusion potential can be calculated using nernst equation. Choose the best statement regarding the assertion and reason.
Potassium Regulation Indian Medical PG Practice Questions and MCQs
Question 1: All of the following are true about potassium, except
- A. Mostly concentrated inside the cells
- B. Leaves the cell in the presence of insulin (Correct Answer)
- C. Plasma concentration increases at time of metabolic acidosis
- D. Ingestion of acetazolamide results in potassium loss
Explanation: ***Leaves the cell in the presence of insulin*** - Insulin promotes the uptake of **potassium into cells**, primarily by stimulating the Na+/K+-ATPase pump. - Therefore, insulin actually causes potassium to enter the cell, not leave it, which helps to **lower extracellular potassium levels**. *Mostly concentrated inside the cells* - **Potassium (K+)** is the primary intracellular cation, with concentrations approximately 30 times higher inside cells than outside. - This high intracellular concentration is crucial for maintaining **resting membrane potential** and cellular functions. *Plasma concentration increases at time of metabolic acidosis* - In **metabolic acidosis**, hydrogen ions (H+) shift into cells in exchange for potassium ions, which move out of cells into the extracellular fluid. - This H+/K+ exchange mechanism leads to an **increase in plasma potassium concentration**. *Ingestion of acetazolamide results in potassium loss* - **Acetazolamide** is a carbonic anhydrase inhibitor that acts on the proximal tubule of the kidney. - It inhibits bicarbonate reabsorption, leading to increased delivery of sodium and water to the collecting duct, which promotes **potassium secretion and loss**.
Question 2: Hyperkalemia aciduria is seen in
- A. Type I Renal Tubular Acidosis
- B. Type IV Renal Tubular Acidosis (Correct Answer)
- C. Sigmoidocolostomy procedure
- D. Type II Renal Tubular Acidosis
Explanation: Type IV Renal Tubular Acidosis - This condition is characterized by **hyperkalemia** and **aciduria**, often due to a deficiency in aldosterone or a renal tubular insensitivity to aldosterone [1]. - The impaired aldosterone action leads to reduced potassium excretion and decreased ammonium production, both contributing to **hyperkalemia** and metabolic acidosis [1]. *Type I Renal Tubular Acidosis* - Type I RTA (distal RTA) is characterized by a defect in acid secretion in the distal tubule, leading to **hypokalemia** and metabolic acidosis with persistently high urine pH [2]. - Patients typically excrete an alkaline urine despite systemic acidosis, contrasting with the aciduria seen with hyperkalemia [2]. *Sigmoidocolostomy procedure* - A sigmoidocolostomy can lead to **hyperchloremic metabolic acidosis** due to the reabsorption of chloride and excretion of bicarbonate by the colonic mucosa. - However, it typically causes **hypokalemia** as potassium is secreted into the colonic lumen from the blood. *Type II Renal Tubular Acidosis* - Type II RTA (proximal RTA) involves a defect in bicarbonate reabsorption in the proximal tubule, resulting in **hypokalemia** and metabolic acidosis. - The kidney's ability to acidify urine is still largely intact in the distal nephron once the bicarbonate buffer system is overwhelmed.
Question 3: Where does potassium reabsorption primarily occur in the kidney?
- A. Primarily in the PCT (Correct Answer)
- B. In the glomerulus
- C. Limited to the descending limb of Henle
- D. In the collecting duct through secretion
Explanation: ***Primarily in the PCT*** - The **proximal convoluted tubule (PCT)** reabsorbs the majority (65-70%) of filtered potassium, making it the **primary site** of potassium reabsorption. - This reabsorption occurs primarily through **paracellular routes** along with water and sodium reabsorption (solvent drag). - The PCT plays a crucial role in maintaining overall **potassium homeostasis** by retrieving most of the filtered load before the filtrate reaches distal segments. *In the glomerulus* - The **glomerulus** is responsible for **filtration** of blood, not reabsorption of substances. - All small solutes, including potassium, are freely filtered across the **glomerular capillaries** into Bowman's capsule. - Filtration is the first step; reabsorption occurs in tubular segments. *In the collecting duct through secretion* - The **collecting duct** is primarily involved in **potassium secretion** into the urine, regulated by aldosterone, to fine-tune potassium balance. - While some reabsorption can occur via intercalated cells, the net effect in the collecting duct is **secretion**, not reabsorption. - This is critical for regulating final urinary K+ excretion. *Limited to the descending limb of Henle* - The **descending limb of the loop of Henle** is primarily permeable to **water** but relatively impermeable to solutes. - **No significant potassium reabsorption** occurs in the descending limb. - Significant K+ reabsorption also occurs in the thick ascending limb (20-25% of filtered load), but the PCT remains the primary site.
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: Which of the following is not an effect of efferent arteriole constriction:
- A. Increased glomerular hydrostatic pressure
- B. Decreased blood flow in peritubular vessels
- C. Decreased GFR (Correct Answer)
- D. Increased oncotic pressure in peritubular vessels
Explanation: ***Decreased GFR*** - **Efferent arteriole constriction** typically *increases* GFR, not decreases it - Constriction raises **glomerular hydrostatic pressure** (PGC) by increasing resistance to outflow, which *enhances* the driving force for filtration - The initial and predominant effect is an **increase in GFR**, making "Decreased GFR" NOT a typical effect - Only with *severe* prolonged constriction might GFR eventually fall due to markedly reduced renal blood flow and extreme protein concentration *Increased glomerular hydrostatic pressure* - This IS an effect of efferent arteriole constriction - Constriction increases resistance to blood leaving the glomerulus, causing blood to "back up" and **raising hydrostatic pressure** in glomerular capillaries - This elevated pressure directly increases the filtration force *Decreased blood flow in peritubular vessels* - This IS an effect of efferent arteriole constriction - Blood exits the glomerulus through the efferent arteriole to reach peritubular capillaries - Constriction restricts this outflow, resulting in **reduced blood flow** to downstream peritubular vessels *Increased oncotic pressure in peritubular vessels* - This IS an effect of efferent arteriole constriction - As filtration increases due to higher glomerular pressure, plasma proteins (which cannot be filtered) become more concentrated in the blood - This concentrated blood flows into peritubular capillaries, resulting in **elevated oncotic pressure** that favors reabsorption
Question 6: 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 7: Which causes raised angiotensin in blood?
- A. Raised cardiac output
- B. Increased sympathetic tone
- C. Increased blood volume
- D. Decreased blood pressure (Correct Answer)
Explanation: ***Decreased blood pressure*** - A decrease in blood pressure is the **primary physiological trigger** that signals the kidneys to release **renin**, initiating the **renin-angiotensin-aldosterone system (RAAS)**. - Renal baroreceptors in the juxtaglomerular apparatus sense decreased renal perfusion pressure and stimulate renin release. - Renin converts **angiotensinogen** to **angiotensin I**, which is then converted to **angiotensin II** (the active form) by **angiotensin-converting enzyme (ACE)**. - This represents the most direct and important mechanism for raising angiotensin levels in response to hemodynamic changes. *Raised cardiac output* - **Increased cardiac output** generally leads to **increased blood pressure**, which would suppress renin release and reduce angiotensin levels. - The body's homeostatic mechanisms aim to lower blood pressure in response to increased cardiac output, not raise angiotensin. - This has the opposite effect on the RAAS system. *Increased sympathetic tone* - While **increased sympathetic tone does stimulate renin release** via β1-adrenergic receptors on juxtaglomerular cells, it is typically a **secondary mechanism** that occurs in response to decreased blood pressure. - Sympathetic stimulation is one of three major stimuli for renin release, but in physiological terms, it usually acts as part of the compensatory response to hypotension rather than as an independent primary cause. - The question asks for the cause of raised angiotensin, and decreased blood pressure is the more direct and primary trigger. *Increased blood volume* - **Increased blood volume** results in **elevated blood pressure**, which would suppress renin release and consequently lower angiotensin levels. - Atrial natriuretic peptide (ANP) is released in response to increased blood volume, which inhibits renin secretion. - This has the opposite effect on angiotensin levels.
Question 8: Cerebral blood flow is regulated by all of the following except:
- A. Calcium ions (Correct Answer)
- B. Blood pressure
- C. Arterial PCO2
- D. Potassium ions
Explanation: ***Calcium ions*** - While **calcium ions (Ca²⁺)** are mechanistically essential for vascular smooth muscle contraction and relaxation, they are **not considered a primary regulatory signal** for cerebral blood flow (CBF) in the same way as the other factors listed. - Ca²⁺ acts as an **intracellular second messenger** that mediates the effects of other regulatory factors (like PCO2, K⁺, and vasoactive substances), rather than being a direct extracellular regulatory signal itself. - The question refers to primary regulatory factors that directly modulate CBF, not the intracellular mechanisms by which vascular smooth muscle responds. *Blood pressure* - **Cerebral autoregulation** maintains relatively constant CBF despite changes in **mean arterial pressure (MAP)** between approximately 60-150 mmHg. - Blood pressure is a **key regulatory factor** - when MAP falls below or exceeds this range, CBF becomes pressure-dependent. - This protective mechanism prevents cerebral ischemia or hyperemia with systemic blood pressure fluctuations. *Arterial PCO2* - **Arterial partial pressure of carbon dioxide (PaCO2)** is one of the **most potent direct regulators** of CBF. - **Hypercapnia** (increased PaCO2) causes cerebral vasodilation and increased CBF (approximately 1-2 mL/100g/min increase per 1 mmHg rise in PaCO2). - **Hypocapnia** (decreased PaCO2) causes vasoconstriction and reduced CBF, utilized therapeutically in managing elevated intracranial pressure. *Potassium ions* - **Increased extracellular K⁺** in the perivascular space causes **direct vasodilation** of cerebral arterioles. - This mechanism is crucial for **neurovascular coupling** (functional hyperemia) - when neurons are active, they release K⁺, which dilates nearby vessels to increase local blood flow. - K⁺-mediated vasodilation helps match cerebral perfusion to metabolic demand during neuronal activity.
Question 9: Which of the following is not an absolute indication for hemodialysis?
- A. GI bleeding (Correct Answer)
- B. Convulsions
- C. Pericarditis
- D. Hyperkalemia of 6.5 mEq/L
Explanation: ***GI bleeding*** - While patients on dialysis may experience gastrointestinal bleeding, it is not a direct indication for initiating or continuing **hemodialysis**. - **GI bleeding** in end-stage renal disease (ESRD) patients can be due to various causes and requires specific management of the bleeding itself, not necessarily an alteration in dialysis prescription. *Convulsions* - **Convulsions** in patients with renal failure, especially due to uremia, are a severe manifestation of **uremic encephalopathy**. - This is an absolute indication for **hemodialysis** as it rapidly removes uremic toxins causing central nervous system dysfunction. *Pericarditis* - **Uremic pericarditis**, characterized by inflammation of the pericardium due to accumulation of uremic toxins, is a serious complication of renal failure. - It is an absolute indication for **hemodialysis** to prevent further cardiac complications like cardiac tamponade. *Hyperkalemia of 6.5 mEq/L* - Severe **hyperkalemia** (typically > 6.0-6.5 mEq/L) is a life-threatening electrolyte imbalance that can cause cardiac arrhythmias. - **Hemodialysis** is highly effective in rapidly removing potassium from the body and is an absolute indication, especially if unresponsive to other medical therapies.
Question 10: Assertion: RMP depends on proteins and phosphate ions. Reason: Diffusion potential can be calculated using nernst equation. Choose the best statement regarding the assertion and reason.
- A. Assertion false, Reason true
- B. Both true, Reason is the explanation of assertion
- C. Assertion true, Reason false
- D. Both true, Reason is not the explanation of assertion (Correct Answer)
Explanation: ***Both true, Reason is not the explanation of assertion*** - The **Assertion is TRUE**: The resting membrane potential (RMP) does depend on intracellular **proteins and phosphate ions**, which are large, non-diffusible anions that remain trapped inside the cell. These molecules contribute significantly to the **net negative charge** of the intracellular compartment and create the **Gibbs-Donnan effect**. At physiological pH, most intracellular proteins are negatively charged, and phosphate ions (HPO₄²⁻, H₂PO₄⁻) are major intracellular anions. While the primary determinants of RMP are the concentration gradients and membrane permeabilities of K⁺, Na⁺, and Cl⁻ ions, the presence of non-diffusible anions (proteins and phosphates) is essential for establishing the baseline negative intracellular environment. - The **Reason is TRUE**: The **Nernst equation** (E = RT/zF × ln[ion]out/[ion]in) is indeed used to calculate the **equilibrium potential** (also called diffusion potential) for a single permeable ion. This equation determines the membrane potential at which the electrical gradient exactly balances the concentration gradient for that specific ion, resulting in no net ion movement. - **However, the Reason does NOT explain the Assertion**: The Nernst equation calculates equilibrium potentials for diffusible ions like K⁺, Na⁺, and Cl⁻. It does NOT explain the contribution of **non-diffusible** anions (proteins and phosphates) to the RMP. The actual RMP, which involves multiple ions with different permeabilities, is calculated using the **Goldman-Hodgkin-Katz (GHK) equation**, not the Nernst equation. The two statements are independently true but address different aspects of membrane potential physiology. *Assertion false, Reason true* - This is **incorrect** because the assertion is actually TRUE. Intracellular proteins and phosphate ions do contribute to the RMP by providing fixed negative charges that influence the distribution of diffusible ions and create the electrochemical environment necessary for RMP establishment. *Both true, Reason is the explanation of assertion* - This is **incorrect** because while both statements are true, the Nernst equation (Reason) does not explain how proteins and phosphate ions contribute to RMP (Assertion). The Nernst equation applies only to permeable ions, whereas proteins and phosphates are impermeant molecules whose role is explained by the Gibbs-Donnan equilibrium and their contribution to fixed negative charges. *Assertion true, Reason false* - This is **incorrect** because the reason is TRUE. The Nernst equation is a fundamental and valid equation in membrane physiology that accurately calculates the equilibrium potential for any permeable ion based on its concentration gradient.
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