Potassium balance and regulation US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Potassium balance and regulation. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Potassium balance and regulation US Medical PG Question 1: A 17-year-old male presents to your office complaining of polyuria, polydipsia, and unintentional weight loss of 12 pounds over the past 3 months. On physical examination, the patient is tachypneic with labored breathing. Which of the following electrolyte abnormalities would you most likely observe in this patient?
- A. Hypophosphatemia
- B. Hypermagnesemia
- C. Hyperkalemia
- D. Hyponatremia (Correct Answer)
- E. Hyperphosphatemia
Potassium balance and regulation Explanation: ***Hyponatremia***
- This patient's symptoms of polyuria, polydipsia, and weight loss, along with **tachypnea and labored breathing**, are highly suggestive of **diabetic ketoacidosis (DKA)**.
- **Hyponatremia** is the **most consistently observed** electrolyte abnormality in DKA, present in nearly all cases at initial presentation.
- This is typically **pseudohyponatremia** caused by the osmotic effect of severe hyperglycemia—glucose pulls water into the extracellular space, diluting the measured sodium concentration.
- The **corrected sodium** can be calculated using: Corrected Na = Measured Na + 0.016 × (Glucose - 100), which typically reveals a more normal sodium level.
- True hyponatremia from sodium loss via **osmotic diuresis** can also occur but is usually masked by the dilutional effect.
*Hyperkalemia*
- While serum potassium may appear normal or even elevated initially due to **transcellular shifts** (acidosis causes potassium to move from intracellular to extracellular space in exchange for hydrogen ions), this is not the most consistently observed abnormality.
- **Total body potassium is always depleted** in DKA due to osmotic diuresis and vomiting.
- Many patients present with normal or even low potassium levels despite acidosis.
- Potassium levels require careful monitoring during treatment as insulin therapy drives potassium back into cells, potentially causing life-threatening hypokalemia.
*Hypophosphatemia*
- While **phosphate levels** can fluctuate in DKA due to osmotic diuresis, initial presentation often involves normal or even elevated phosphate levels due to cellular shifts.
- Significant **hypophosphatemia** is more typically observed during treatment as insulin drives phosphate back into the cells, similar to potassium.
*Hypermagnesemia*
- **Hypermagnesemia** is uncommon in DKA and is usually associated with impaired renal excretion or excessive magnesium intake.
- The symptoms described do not point towards magnesium imbalance.
*Hyperphosphatemia*
- Although cellular shifts can initially raise serum phosphate, sustained **hyperphosphatemia** is not a characteristic or common electrolyte abnormality seen in the acute presentation of DKA.
- More typically, total body phosphate is depleted due to **osmotic diuresis**.
Potassium balance and regulation US Medical PG Question 2: A medical student is studying human physiology. She learns that there is a membrane potential across cell membranes in excitable cells. The differential distribution of anions and cations both inside and outside the cells significantly contributes to the genesis of the membrane potential. Which of the following distributions of anions and cations best explains the above phenomenon?
- A. High concentration of K+ outside the cell and low concentration of K+ inside the cell
- B. High concentration of Na+ outside the cell and high concentration of K+ inside the cell (Correct Answer)
- C. High concentration of Ca2+ outside the cell and high concentration of Cl- inside the cell
- D. Low concentration of K+ outside the cell and high concentration of Ca2+ inside the cell
- E. Low concentration of Cl- outside the cell and high concentration of Cl- inside the cell
Potassium balance and regulation Explanation: ***High concentration of Na+ outside the cell and high concentration of K+ inside the cell***
- This distribution is maintained by the **Na+/K+ ATPase pump**, which actively transports **3 Na+ ions out of the cell** and **2 K+ ions into the cell**, against their concentration gradients.
- This differential concentration of **sodium** and **potassium** ions is critical for establishing the negative **resting membrane potential** as K+ channels allow K+ to leak out, making the inside more negative.
*High concentration of K+ outside the cell and low concentration of K+ inside the cell*
- This statement is incorrect as the normal physiological state is characterized by a **high concentration of K+ inside the cell** and a low concentration outside.
- An increase in extracellular K+ concentration (hyperkalemia) would **depolarize** the cell, affecting excitability.
*High concentration of Ca2+ outside the cell and high concentration of Cl- inside the cell*
- While Ca2+ is indeed in higher concentration outside the cell, Cl- is typically in **higher concentration outside the cell** compared to inside, which contributes to the membrane potential through its electrochemical gradient.
- An elevated intracellular Cl- concentration would make the cell more negative if Cl- channels were open but is not the primary determinant.
*Low concentration of K+ outside the cell and high concentration of Ca2+ inside the cell*
- The first part is correct—low K+ outside is normal—but a **high concentration of Ca2+ inside the cell** is generally an indicator of cellular pathology or specific physiological events like muscle contraction or neurotransmitter release, not a steady-state condition contributing to resting potential.
- Normal intracellular Ca2+ is kept very low due to active pumps.
*Low concentration of Cl- outside the cell and high concentration of Cl- inside the cell*
- This statement is incorrect as **chloride ions** are typically in a **higher concentration outside the cell** than inside.
- The influx of Cl- into the cell, when channels are open, usually hyperpolarizes the membrane, contributing to inhibition, but its gradient is opposite to what is described.
Potassium balance and regulation US Medical PG Question 3: A new drug has been shown to block epithelial sodium channels in the cortical collecting duct. Which of the following is most likely to be decreased upon drug administration?
- A. Urea reabsorption in the collecting tubules
- B. Hydrogen ion secretion in the collecting tubules
- C. Potassium secretion in the collecting tubules (Correct Answer)
- D. Sodium secretion in the collecting tubules
- E. Sodium chloride reabsorption in the distal tubule
Potassium balance and regulation Explanation: ***Potassium secretion in the collecting tubules***
- Blocking **epithelial sodium channels (ENaC)** in the cortical collecting duct reduces sodium reabsorption, which in turn diminishes the electrochemical gradient driving **potassium secretion** into the lumen.
- This is because sodium reabsorption creates a more negative luminal charge, attracting potassium ions to move from the cell into the tubule.
- This is the mechanism of **potassium-sparing diuretics** like amiloride and triamterene.
*Urea reabsorption in the collecting tubules*
- Urea **reabsorption** primarily occurs in the **medullary collecting duct** via urea transporters (UT-A1, UT-A3) and is influenced by the inner medullary osmolarity and ADH.
- Blocking ENaC would primarily affect sodium flux and potassium secretion, with minimal direct impact on urea reabsorption in the collecting duct.
*Hydrogen ion secretion in the collecting tubules*
- **Hydrogen ion (H+) secretion** occurs in the collecting tubules via intercalated cells (α-intercalated cells), which is important for acid-base balance.
- While blocking ENaC can indirectly reduce H+ secretion (by decreasing the lumen-negative potential), the primary and most significant effect is on **potassium secretion**, making this a less likely answer.
*Sodium secretion in the collecting tubules*
- The primary function of ENaC is to **reabsorb sodium** from the tubular lumen back into the blood, not to secrete it.
- Sodium is not normally secreted in the collecting tubules; blocking ENaC would decrease sodium **reabsorption**, not affect sodium secretion.
*Sodium chloride reabsorption in the distal tubule*
- **Sodium chloride reabsorption** in the distal convoluted tubule is mainly mediated by the **thiazide-sensitive Na-Cl co-transporter (NCC)**.
- ENaC are predominantly located in the cortical collecting duct (downstream from the DCT), so blocking them would not directly impact NaCl reabsorption in the distal tubule.
Potassium balance and regulation US Medical PG Question 4: What is the primary mechanism for maintaining acid-base balance during prolonged vomiting?
- A. Increased chloride reabsorption
- B. Increased potassium excretion
- C. Increased bicarbonate excretion (Correct Answer)
- D. Decreased hydrogen secretion
Potassium balance and regulation Explanation: ***Increased bicarbonate excretion***
- Prolonged vomiting leads to the loss of **gastric acid (HCl)**, causing **metabolic alkalosis**. The kidneys compensate by increasing the excretion of **bicarbonate (HCO3-)** to restore acid-base balance.
- This renal compensation is the primary mechanism to eliminate the excess alkali from the body.
*Increased chloride reabsorption*
- In **metabolic alkalosis** due to vomiting, the body tends to reabsorb less chloride, not more, in an attempt to excrete bicarbonate.
- **Chloride depletion** can actually hinder bicarbonate excretion by promoting sodium reabsorption with bicarbonate.
*Increased potassium excretion*
- **Hypokalemia** can occur with prolonged vomiting due to increased aldosterone activity and direct renal loss associated with metabolic alkalosis.
- However, increased potassium excretion itself is not the primary mechanism for correcting the acid-base disorder; rather, it is a consequence or a contributing factor to the imbalance.
*Decreased hydrogen secretion*
- In response to alkalosis, the kidneys would typically decrease, not increase, **hydrogen ion (H+) secretion** in an effort to retain H+ and normalize pH.
- Decreased H+ secretion is a compensatory mechanism, but the direct excretion of bicarbonate is more crucial for correcting the metabolic alkalosis.
Potassium balance and regulation US Medical PG Question 5: A 63-year-old woman presents to your outpatient clinic complaining of headaches, blurred vision, and fatigue. She has a blood pressure of 171/91 mm Hg and heart rate of 84/min. Physical examination is unremarkable. Her lab results include K+ of 3.1mEq/L and a serum pH of 7.51. Of the following, which is the most likely diagnosis for this patient?
- A. Pheochromocytoma
- B. Renal artery stenosis
- C. Cushing’s syndrome
- D. Primary hyperaldosteronism (Conn’s syndrome) (Correct Answer)
- E. Addison’s disease
Potassium balance and regulation Explanation: ***Primary hyperaldosteronism (Conn’s syndrome)***
- The combination of **hypertension**, **hypokalemia (K+ 3.1 mEq/L)**, and **metabolic alkalosis (pH 7.51)** is highly characteristic of primary hyperaldosteronism.
- Excess aldosterone leads to increased sodium reabsorption and potassium/hydrogen ion excretion, causing these electrolyte imbalances.
*Pheochromocytoma*
- This condition involves episodic **hypertension**, palpitations, sweating, and anxiety due to catecholamine excess.
- While hypertension is present, the absence of paroxysmal symptoms and the specific electrolyte abnormalities (hypokalemia, alkalosis) make it less likely.
*Renal artery stenosis*
- This can cause **secondary hypertension** and occasionally hypokalemia, but it typically presents with **renal bruits**, and the metabolic alkalosis is not a direct or prominent feature.
- The elevated renin-angiotensin-aldosterone axis would lead to secondary hyperaldosteronism, but primary hyperaldosteronism is suggested by the overall clinical picture.
*Cushing’s syndrome*
- Cushing's syndrome is characterized by **central obesity**, striae, moon facies, and **hyperglycemia**, among other symptoms.
- While hypertension and hypokalemia can occur in severe cases, the predominant clinical features are not aligned with this patient's presentation.
*Addison’s disease*
- This condition is characterized by **adrenal insufficiency**, leading to hypoglycemia, **hyponatremia**, **hyperkalemia**, and **hypotension**.
- The patient's hypertension and hypokalemia directly contradict the typical presentation of Addison’s disease.
Potassium balance and regulation US Medical PG Question 6: A 57-year-old male is found to have an elevated prostate specific antigen (PSA) level on screening labwork. PSA may be elevated in prostate cancer, benign prostatic hypertrophy (BPH), or prostatitis. Which of the following best describes the physiologic function of PSA?
- A. Regulation of transcription factors and phosphorylation of proteins
- B. Maintains corpus luteum
- C. Response to peritoneal irritation
- D. Sperm production
- E. Liquefaction of semen (Correct Answer)
Potassium balance and regulation Explanation: ***Liquefaction of semen***
- Prostate-specific antigen (PSA) is a **serine protease** produced by the epithelial cells of the prostate gland.
- Its primary physiological role is to **liquefy the seminal coagulum** formed after ejaculation, allowing sperm to become motile and navigate the female reproductive tract.
*Regulation of transcription factors and phosphorylation of proteins*
- This function is characteristic of **kinases** and **phosphatases**, which are involved in intracellular signaling pathways.
- While essential for cellular function, it does not describe the specific role of PSA.
*Maintains corpus luteum*
- The maintenance of the corpus luteum is primarily the role of **luteinizing hormone (LH)** and, in pregnancy, **human chorionic gonadotropin (hCG)**.
- These hormones are involved in the female reproductive cycle, unrelated to PSA.
*Response to peritoneal irritation*
- Peritoneal irritation triggers an inflammatory response involving various immune cells and mediators, but not specifically PSA.
- PSA itself is not directly involved in the systemic or local response to peritoneal inflammation.
*Sperm production*
- **Sperm production (spermatogenesis)** occurs in the seminiferous tubules of the testes under the influence of hormones like FSH and testosterone.
- While semen is the vehicle for sperm, PSA's role is in the post-ejaculatory processing of semen, not in the initial production of sperm.
Potassium balance and regulation US Medical PG Question 7: A 32-year-old woman is admitted to the emergency department for 36 hours of intense left-sided back pain that extends into her left groin. She reports that the pain started a day after a charitable 5 km (3.1 mi) marathon. The past medical history is relevant for multiple complaints of eye dryness and dry mouth. Physical examination is unremarkable, except for intense left-sided costovertebral pain. The results from laboratory tests are shown.
Laboratory test Result
Serum Na+ 137
Serum Cl- 110
Serum K+ 3.0
Serum creatinine (SCr) 0.82
Arterial blood gas Result
pH 7.28
pO2 98 mm Hg
pCO2 28.5 mm Hg
SaO2% 98%
HCO3- 15 mm Hg
Which of the following explains this patient’s condition?
- A. Carbonic acid accumulation
- B. Decreased bicarbonate renal absorption
- C. Decreased renal excretion of hydrogen ions (H+) (Correct Answer)
- D. Decreased synthesis of ammonia (NH3)
- E. Decreased excretion of nonvolatile acids
Potassium balance and regulation Explanation: ***Decreased renal excretion of hydrogen ions (H+)***
- The patient presents with **metabolic acidosis** (pH 7.28, HCO3- 15 mEq/L) with **respiratory compensation** (pCO2 28.5 mm Hg). The anion gap is **normal** (Na+ - (Cl- + HCO3-) = 137 - (110 + 15) = **12 mEq/L**), indicating a **non-anion gap metabolic acidosis**.
- The history of **dry eyes and dry mouth** strongly suggests **Sjögren syndrome**, which is commonly associated with **Type 1 (distal) renal tubular acidosis**.
- In **Type 1 RTA**, the distal tubule alpha-intercalated cells cannot adequately secrete H+ ions, leading to metabolic acidosis with **inability to acidify urine** (urine pH > 5.5). Associated findings include **hypokalemia** (K+ 3.0), **nephrolithiasis** (calcium phosphate stones due to alkaline urine), and hypercalciuria.
- The left-sided flank pain radiating to the groin is consistent with **nephrolithiasis**, a common complication of Type 1 RTA.
*Carbonic acid accumulation*
- **Carbonic acid accumulation** indicates **respiratory acidosis** with elevated pCO2, which is not present here.
- The patient has a **low pCO2 (28.5 mm Hg)**, representing appropriate **respiratory compensation** for the primary metabolic acidosis.
*Decreased bicarbonate renal absorption*
- **Decreased bicarbonate renal absorption** characterizes **Type 2 (proximal) RTA**.
- While Type 2 RTA also causes non-anion gap metabolic acidosis, it is **not typically associated with Sjögren syndrome** and would present with different features (glycosuria, aminoaciduria, phosphaturia as part of Fanconi syndrome).
- Type 2 RTA can acidify urine to pH < 5.5 when serum HCO3- is low, unlike Type 1 RTA.
*Decreased synthesis of ammonia (NH3)*
- **Decreased ammonia synthesis** is characteristic of **Type 4 RTA** or severe chronic kidney disease.
- Type 4 RTA presents with **hyperkalemia** (due to hypoaldosteronism), not the hypokalemia seen in this patient.
- The normal serum creatinine (0.82 mg/dL) rules out significant renal failure.
*Decreased excretion of nonvolatile acids*
- **Decreased excretion of nonvolatile acids** would cause **elevated anion gap metabolic acidosis** (e.g., lactic acidosis, ketoacidosis, or advanced renal failure with accumulation of organic acids).
- This patient has a **normal anion gap (12 mEq/L)** and **normal renal function** (creatinine 0.82 mg/dL), making this mechanism unlikely.
- The clinical context of Sjögren syndrome with dry eyes/mouth points specifically to distal RTA.
Potassium balance and regulation US Medical PG Question 8: A 54-year-old man presents with 3 days of non-bloody and non-bilious emesis every time he eats or drinks. He has become progressively weaker and the emesis has not improved. He denies diarrhea, fever, or chills and thinks his symptoms may be related to a recent event that involved sampling many different foods. His temperature is 97.5°F (36.4°C), blood pressure is 133/82 mmHg, pulse is 105/min, respirations are 15/min, and oxygen saturation is 98% on room air. Physical exam is notable for a weak appearing man with dry mucous membranes. His abdomen is nontender. Which of the following laboratory changes would most likely be seen in this patient?
- A. Metabolic alkalosis and hyperkalemia
- B. Non-anion gap metabolic acidosis and hypokalemia
- C. Respiratory acidosis and hyperkalemia
- D. Metabolic alkalosis and hypokalemia (Correct Answer)
- E. Anion gap metabolic acidosis and hypokalemia
Potassium balance and regulation Explanation: ***Metabolic alkalosis and hypokalemia***
- Persistent **vomiting** leads to the loss of **gastric acid** (HCl) and **potassium**, resulting in **metabolic alkalosis** and **hypokalemia**. The loss of HCl directly removes acid from the body, and the subsequent renal compensation to conserve volume often exacerbates potassium loss.
- The patient's presentation with **dry mucous membranes**, increased heart rate (pulse 105/min), and persistent non-bloody, non-bilious emesis suggests significant volume depletion and electrolyte imbalances consistent with prolonged vomiting.
*Metabolic alkalosis and hyperkalemia*
- While metabolic alkalosis is expected due to gastric acid loss from vomiting, **hyperkalemia** is unlikely. Vomiting typically causes **hypokalemia** due to direct potassium loss and renal compensation mechanisms.
- The body attempts to compensate for volume depletion, leading to increased activity of the **renin-angiotensin-aldosterone system**, which promotes potassium excretion in the urine.
*Non-anion gap metabolic acidosis and hypokalemia*
- **Metabolic acidosis** is characterized by a decrease in blood pH and bicarbonate; however, profuse vomiting of gastric contents primarily leads to **alkalosis** due to the loss of hydrogen ions.
- **Non-anion gap metabolic acidosis** is usually seen in conditions involving bicarbonate loss from the kidneys or gut (e.g., diarrhea, renal tubular acidosis), not vomiting.
*Respiratory acidosis and hyperkalemia*
- **Respiratory acidosis** results from hypoventilation, leading to an increase in blood CO2, which is not suggested by the patient's normal respiratory rate and oxygen saturation.
- Profuse vomiting causes a loss of gastric acid and can lead to compensatory **hypoventilation** to retain CO2 (acid), but this is a secondary response to metabolic alkalosis, and primary respiratory acidosis is not the underlying issue.
*Anion gap metabolic acidosis and hypokalemia*
- **Anion gap metabolic acidosis** typically occurs with the accumulation of unmeasured acids (e.g., lactic acidosis, ketoacidosis, renal failure, poisoning), which is not indicated by the patient's symptoms.
- While **hypokalemia** is consistent with vomiting, the primary acid-base disturbance from prolonged emesis is metabolic alkalosis, not acidosis.
Potassium balance and regulation US Medical PG Question 9: Renal clearance of substance Y is experimentally studied. At a constant glomerular filtration rate, it is found that the amount of substance Y excreted is greater than the amount filtered. This holds true across all physiologic values on the titration curve. Substance Y is most similar to which of the following?
- A. Para-amino hippuric acid (Correct Answer)
- B. Albumin
- C. Bicarbonate
- D. Magnesium
- E. Glucose
Potassium balance and regulation Explanation: ***Para-amino hippuric acid***
- If the amount of a substance excreted is **greater than the amount filtered**, it indicates that the substance undergoes both **glomerular filtration** and **tubular secretion**.
- **Para-amino hippuric acid (PAH)** is a classic example of a substance that is extensively filtered and actively secreted by the renal tubules, making its clearance rate very high and a good estimate of **renal plasma flow**.
*Albumin*
- **Albumin** is a large protein that is normally **not filtered** by the glomerulus due to its size and negative charge.
- Its presence in the urine, indicating a greater amount excreted than filtered (which is normally zero), would suggest **glomerular damage**, but it does not undergo active tubular secretion.
*Bicarbonate*
- **Bicarbonate** is freely filtered at the glomerulus and is primarily **reabsorbed** in the renal tubules, particularly in the proximal tubule.
- Therefore, the amount of bicarbonate excreted is typically **much less than** the amount filtered, not greater.
*Magnesium*
- **Magnesium** is filtered by the glomeruli and undergoes complex regulation involving both **reabsorption and secretion** in various parts of the renal tubule, though reabsorption predominates.
- While magnesium balance is maintained by the kidneys, its excretion does not typically exceed filtration to the extent described for substances primarily handled by secretion.
*Glucose*
- **Glucose** is freely filtered at the glomerulus and is almost **completely reabsorbed** in the proximal tubule under normal physiological conditions.
- The amount of glucose excreted is typically zero, and only exceeds filtration when the **tubular reabsorptive capacity is saturated**, as in uncontrolled diabetes, but it is reabsorbed, not secreted.
Potassium balance and regulation US Medical PG Question 10: A 30-year-old man presents to his physician for a follow-up appointment for a blood pressure of 140/90 mm Hg during his last visit. He was advised to record his blood pressure at home with an automated device twice every day. He recorded a wide range of blood pressure values in the past week, ranging from 110/70 mm Hg to 135/84 mm Hg. The medical history is unremarkable and he takes no medications. He occasionally drinks alcohol after work, but denies smoking and illicit drug use. Which of the following factors is responsible for maintaining a near-normal renal blood flow over a wide range of systemic blood pressures?
- A. Glomerular filtration
- B. Afferent arteriole (Correct Answer)
- C. Aldosterone
- D. Sympathetic nervous system
- E. Efferent arteriole
Potassium balance and regulation Explanation: ***Afferent arteriole***
- The **afferent arteriole** is the **primary site** of **renal autoregulation**, which maintains constant renal blood flow over a wide range of systemic blood pressures (80-180 mm Hg).
- Two key mechanisms operate here: (1) **Myogenic mechanism** - smooth muscle in the afferent arteriole constricts in response to increased stretch from elevated blood pressure, and dilates when pressure decreases; (2) **Tubuloglomerular feedback** - involves juxtaglomerular apparatus sensing changes in distal tubule NaCl delivery and adjusting afferent arteriolar tone.
- The afferent arteriole is the **initial and dominant** site where resistance changes occur to buffer pressure fluctuations before they affect glomerular capillaries.
*Glomerular filtration*
- **Glomerular filtration** is the process by which blood is filtered in the glomerulus, forming an ultrafiltrate.
- This is the **outcome** that autoregulation protects, not the mechanism itself.
- Autoregulation maintains stable GFR despite blood pressure changes.
*Aldosterone*
- **Aldosterone** is a mineralocorticoid hormone that regulates **sodium and water reabsorption** in the distal tubule and collecting duct.
- It acts over hours to days and regulates **volume status** and **chronic blood pressure control**, not acute autoregulation.
- Does not directly regulate renal blood flow in response to acute systemic blood pressure changes.
*Sympathetic nervous system*
- The **sympathetic nervous system** releases **norepinephrine**, causing **vasoconstriction** of both afferent and efferent arterioles.
- This is an **extrinsic** control mechanism that overrides autoregulation during severe stress, hemorrhage, or extreme hypotension.
- Within the **normal autoregulatory range** (80-180 mm Hg), intrinsic mechanisms (myogenic and tubuloglomerular feedback) predominate, not sympathetic control.
*Efferent arteriole*
- The **efferent arteriole** does contribute to GFR regulation, primarily through **angiotensin II-mediated constriction** which helps maintain GFR when renal perfusion pressure drops.
- However, the **primary autoregulatory adjustments** to maintain constant renal blood flow occur at the **afferent arteriole** level through the myogenic mechanism.
- The efferent arteriole plays a more significant role in maintaining GFR during hypotension rather than buffering blood flow changes across the full autoregulatory range.
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