Sodium handling along the nephron US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Sodium handling along the nephron. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Sodium handling along the nephron US Medical PG Question 1: A 21-year-old male presents to the emergency department with generalized weakness and fatigue. His past medical history is significant for hypertension refractory to several medications but is otherwise unremarkable. He is afebrile, his pulse is 82/min, respirations are 18/min, and blood pressure is 153/94 mmHg. Labs are as follows:
Sodium: 142 mEq/L
Potassium: 2.7 mEq/L
Bicarbonate: 36 mEq/L
Serum pH: 7.5
pCO2: 50 mmHg
Aldosterone: Decreased
Based on clinical suspicion, a genetic screen is performed, confirming an underlying syndrome due to an autosomal dominant gain of function mutation. Which of the following medications can be given to treat the most likely cause of this patient's symptoms?
- A. Thiazide diuretics
- B. Amiloride (Correct Answer)
- C. Mannitol
- D. Acetazolamide
- E. Loop diuretics
Sodium handling along the nephron Explanation: ***Amiloride***
- The patient's presentation with **hypertension**, **hypokalemia**, **metabolic alkalosis**, and **decreased aldosterone** despite these findings is characteristic of **Liddle's Syndrome**.
- **Amiloride** is a potassium-sparing diuretic that directly blocks the **epithelial sodium channel (ENaC)** in the collecting duct, which is overactive in Liddle's Syndrome due to a gain-of-function mutation.
*Thiazide diuretics*
- While commonly used for hypertension, **thiazide diuretics** work by inhibiting the Na+/Cl- cotransporter in the distal convoluted tubule and would likely worsen the **hypokalemia** in Liddle's Syndrome.
- They do not address the primary pathophysiology of **ENaC overactivity** in the collecting duct.
*Mannitol*
- **Mannitol** is an osmotic diuretic primarily used to reduce intracranial pressure or treat cerebral edema.
- It acts in the renal tubule to inhibit water reabsorption and is not indicated for the management of **hypertension** or **electrolyte disturbances** seen in Liddle's Syndrome.
*Acetazolamide*
- **Acetazolamide** is a carbonic anhydrase inhibitor that acts primarily in the proximal tubule to block bicarbonate reabsorption.
- It is used for conditions like glaucoma, altitude sickness, and metabolic alkalosis, but it is not effective for the **sodium retention** and **potassium wasting** characteristic of Liddle's Syndrome.
*Loop diuretics*
- **Loop diuretics** like furosemide work by inhibiting the Na+/K+/2Cl- cotransporter in the thick ascending limb of the loop of Henle.
- Similar to thiazides, they would exacerbate the **hypokalemia** in a patient with Liddle's Syndrome and do not target the underlying cause of **ENaC overactivity**.
Sodium handling along the nephron US Medical PG Question 2: A 54-year-old woman comes to the physician for a follow-up examination after presenting with elevated blood pressure readings during her last two visits. After her last visit 2 months ago, she tried controlling her hypertension with weight loss before starting medical therapy, but she has since been unable to lose any weight. Her pulse is 76/min, and blood pressure is 154/90 mm Hg on the right arm and 155/93 mm Hg on the left arm. She agrees to start treatment with a thiazide diuretic. In response to this treatment, which of the following is most likely to decrease?
- A. Serum uric acid levels
- B. Urinary calcium excretion (Correct Answer)
- C. Serum glucose levels
- D. Urinary potassium excretion
- E. Urinary sodium excretion
Sodium handling along the nephron Explanation: ***Urinary calcium excretion***
- Thiazide diuretics work by inhibiting the **Na-Cl cotransporter** in the **distal convoluted tubule**, which leads to decreased sodium reabsorption and subsequently increased calcium reabsorption.
- This property makes thiazides useful in treating conditions like **hypercalciuria** and preventing **calcium-containing kidney stones**.
*Serum uric acid levels*
- Thiazide diuretics are known to **increase serum uric acid levels** by inhibiting its secretion in the proximal tubule.
- This can precipitate or worsen **gout attacks**, a known side effect of these medications.
*Serum glucose levels*
- Thiazide diuretics can cause **increased serum glucose levels** by impairing insulin secretion and promoting insulin resistance.
- This effect is more pronounced at higher doses and in patients with pre-existing metabolic risk factors.
*Urinary potassium excretion*
- Thiazide diuretics **increase urinary potassium excretion**, often leading to **hypokalemia**.
- This occurs because decreased sodium reabsorption in the distal convoluted tubule leads to increased sodium delivery to the collecting duct, stimulating an exchange for potassium.
*Urinary sodium excretion*
- The primary mechanism of action of thiazide diuretics is to inhibit sodium reabsorption in the distal convoluted tubule, which directly leads to an **increase in urinary sodium excretion**.
- This increased sodium excretion is what drives their diuretic and antihypertensive effects.
Sodium handling along the nephron US Medical PG Question 3: A 42-year-old man is brought to the emergency room because of confusion. His wife says he has been urinating more frequently than usual for the past 3 days. He has not had fever or dysuria. He has bipolar disorder, for which he takes lithium. His pulse is 105/min, and respirations are 14/min. He is lethargic and oriented only to person. Physical examination shows dry mucous membranes and increased capillary refill time. Laboratory studies show a serum sodium concentration of 158 mEq/L and an antidiuretic hormone (ADH) concentration of 8 pg/mL (N = 1–5). Which of the following is the most likely site of dysfunction in this patient?
- A. Hypothalamic supraoptic nucleus
- B. Descending loop of Henle
- C. Juxtaglomerular apparatus
- D. Collecting duct (Correct Answer)
- E. Posterior pituitary gland
Sodium handling along the nephron Explanation: ***Collecting duct***
- The patient presents with **hypernatremia** (Na 158 mEq/L), **polyuria**, and **dehydration** (dry mucous membranes, increased capillary refill time, confusion), indicative of **nephrogenic diabetes insipidus**.
- His ADH level is **elevated** (8 pg/mL), suggesting that the kidneys are not responding to ADH; the **collecting ducts** are the primary site where ADH exerts its effect via aquaporin-2 channels to reabsorb water.
- **Lithium**, which this patient is taking for bipolar disorder, is a well-known cause of nephrogenic diabetes insipidus by interfering with ADH action at the collecting duct level.
*Hypothalamic supraoptic nucleus*
- This nucleus is responsible for synthesizing **ADH**. Dysfunction here would lead to **decreased ADH production** (central diabetes insipidus), but the patient's ADH level is elevated.
- A lack of ADH from this area would not explain the kidney's unresponsiveness to the high ADH levels observed.
*Descending loop of Henle*
- The descending loop of Henle is permeable to water but not directly responsible for ADH-mediated water reabsorption that is impaired in diabetes insipidus.
- Its primary role is to concentrate the filtrate as it descends into the hypertonic medulla.
*Juxtaglomerular apparatus*
- The juxtaglomerular apparatus regulates **blood pressure** and **glomerular filtration rate** through the **renin-angiotensin-aldosterone system**.
- While important for kidney function, it's not directly involved in the ADH-mediated water reabsorption whose impairment leads to nephrogenic diabetes insipidus.
*Posterior pituitary gland*
- This gland stores and releases ADH, which is synthesized in the hypothalamus.
- If the posterior pituitary were dysfunctional, it would lead to **decreased ADH release** (central diabetes insipidus), contradicting the patient's **elevated ADH level**.
Sodium handling along the nephron US Medical PG Question 4: On cardiology service rounds, your team sees a patient admitted with an acute congestive heart failure exacerbation. In congestive heart failure, decreased cardiac function leads to decreased renal perfusion, which eventually leads to excess volume retention. To test your knowledge of physiology, your attending asks you which segment of the nephron is responsible for the majority of water absorption. Which of the following is a correct pairing of the segment of the nephron that reabsorbs the majority of all filtered water with the means by which that segment absorbs water?
- A. Distal convoluted tubule via passive diffusion following ion reabsorption
- B. Distal convoluted tubule via aquaporin channels
- C. Thick ascending loop of Henle via passive diffusion following ion reabsorption
- D. Proximal convoluted tubule via passive diffusion following ion reabsorption (Correct Answer)
- E. Collecting duct via aquaporin channels
Sodium handling along the nephron Explanation: ***Proximal convoluted tubule via passive diffusion following ion reabsorption***
- The **proximal convoluted tubule (PCT)** is responsible for reabsorbing approximately **65-70% of filtered water**, making it the primary site of water reabsorption in the nephron.
- This water reabsorption primarily occurs **passively**, following the active reabsorption of solutes (especially **sodium ions**), which creates an osmotic gradient.
*Distal convoluted tubule via passive diffusion following ion reabsorption*
- The **distal convoluted tubule (DCT)** reabsorbs a much smaller percentage of filtered water (around 5-10%) and its water reabsorption is largely **regulated by ADH**, not primarily simple passive diffusion following bulk ion reabsorption.
- While some passive water movement occurs, it is not the main mechanism or location for the majority of water reabsorption.
*Distal convoluted tubule via aquaporin channels*
- While aquaporin channels do play a role in water reabsorption in the DCT, particularly under the influence of **ADH**, the DCT is not the segment responsible for the **majority of all filtered water absorption**.
- The bulk of water reabsorption occurs earlier in the nephron, independently of ADH for the most part.
*Thick ascending loop of Henle via passive diffusion following ion reabsorption*
- The **thick ascending loop of Henle** is primarily involved in reabsorbing ions like Na+, K+, and Cl- but is largely **impermeable to water**.
- Its impermeability to water is crucial for creating the **osmotic gradient** in the renal medulla, which is necessary for later water reabsorption.
*Collecting duct via aquaporin channels*
- The **collecting duct** is critically important for **regulated water reabsorption** via **aquaporin-2 channels** under the influence of **ADH**, allowing for fine-tuning of urine concentration.
- However, it reabsorbs only a variable portion (typically 5-19%) of the remaining filtered water, not the **majority of all filtered water**.
Sodium handling along the nephron US Medical PG Question 5: Which mechanism primarily regulates sodium reabsorption in the collecting duct?
- A. Glomerulotubular balance
- B. Atrial natriuretic peptide
- C. Antidiuretic hormone
- D. Aldosterone (Correct Answer)
Sodium handling along the nephron Explanation: ***Aldosterone***
- **Aldosterone** is the primary hormone that stimulates **sodium reabsorption** and **potassium secretion** in the principal cells of the collecting duct.
- It acts by increasing the synthesis and activity of **ENaC channels** on the apical membrane and **Na+/K+-ATPase pumps** on the basolateral membrane.
*Glomerulotubular balance*
- **Glomerulotubular balance** refers to the mechanism by which the **proximal tubule** reabsorbs a constant fraction of the filtered load, regardless of changes in glomerular filtration rate (GFR).
- This mechanism maintains a relatively constant delivery of fluid and solutes to downstream segments but does not primarily regulate sodium in the collecting duct.
*Atrial natriuretic peptide*
- **Atrial natriuretic peptide (ANP)** primarily **inhibits sodium reabsorption** in the collecting duct, leading to **natriuresis** and **diuresis**, which is the opposite of sodium reabsorption.
- ANP is released in response to atrial stretch, indicating increased blood volume.
*Antidiuretic hormone*
- **Antidiuretic hormone (ADH)** primarily regulates **water reabsorption** in the collecting duct by increasing the insertion of **aquaporin-2 channels** into the apical membrane, making the collecting duct permeable to water.
- While ADH can indirectly affect sodium concentration by influencing water movement, it does not directly regulate sodium transport to the same extent as aldosterone.
Sodium handling along the nephron US Medical PG Question 6: A 17-year-old boy is brought to the physician by his father because of a 7-month history of fatigue, recurrent leg cramps, and increased urinary frequency. His pulse is 94/min and blood pressure is 118/85 mm Hg. Physical examination shows dry mucous membranes. Laboratory studies show:
Serum
Na+ 130 mEq/L
K+ 2.8 mEq/L
Cl- 92 mEq/L
Mg2+ 1.1 mEq/L
Ca2+ 10.6 mg/dL
Albumin 5.2 g/dL
Urine
Ca2+ 70 mg/24 h
Cl- 375 mEq/24h (N = 110–250)
Arterial blood gas analysis on room air shows a pH of 7.55 and an HCO3- concentration of 45 mEq/L. Impaired function of which of the following structures is the most likely cause of this patient's condition?
- A. Ascending loop of Henle
- B. Collecting duct
- C. Distal convoluted tubule (Correct Answer)
- D. Descending loop of Henle
- E. Proximal convoluted tubule
Sodium handling along the nephron Explanation: ***Distal convoluted tubule***
- The patient presents with **hypokalemia**, **metabolic alkalosis**, **hypomagnesemia**, and **hypocalciuria** (24-hour urine Ca2+ 70 mg, normal up to 250 mg), which are characteristic findings of **Gitelman syndrome**.
- **Gitelman syndrome** is caused by a loss-of-function mutation in the **thiazide-sensitive Na-Cl cotransporter (NCC)**, located in the **distal convoluted tubule**, leading to impaired reabsorption of Na+ and Cl- at this segment.
*Ascending loop of Henle*
- Impaired function of the **Na-K-2Cl cotransporter (NKCC2)** in the **thick ascending limb of the loop of Henle** causes **Bartter syndrome**.
- Bartter syndrome typically presents with **hypercalciuria**, in contrast to the hypocalciuria seen in this patient.
*Collecting duct*
- Dysfunction of the **collecting duct** can lead to various conditions, such as **renal tubular acidosis** or **diabetes insipidus**, depending on which channels or receptors are affected.
- However, the specific combination of **hypokalemia**, **metabolic alkalosis**, **hypomagnesemia**, and **hypocalciuria** points away from primary collecting duct dysfunction.
*Descending loop of Henle*
- The **descending loop of Henle** is primarily permeable to **water** and has a limited role in electrolyte reabsorption.
- Impairment here would primarily affect **urine concentration** and dilution but would not account for the specific electrolyte imbalances observed.
*Proximal convoluted tubule*
- The **proximal convoluted tubule** is responsible for reabsorbing a large fraction of filtered electrolytes, glucose, and amino acids.
- Dysfunction here (e.g., **Fanconi syndrome**) would typically present with **generalized aminoaciduria**, **glycosuria**, **phosphaturia**, and **proximal renal tubular acidosis**, which are not seen in this patient.
Sodium handling along the nephron US Medical PG Question 7: A 78-year-old male with history of coronary artery disease, status post coronary stent placement currently on aspirin and clopidogrel was found down in his bathroom by his wife. His GCS score was 3 and an accurate physical exam is limited. A stat non-contrast CT scan of his brain demonstrated a large right parietal intracranial hemorrhage with surrounding edema. He was promptly transferred to the intensive care unit (ICU) for monitoring. Over the next day, his mental status continues to worsen but repeat CT scan shows no new bleeding. In addition, the patient’s urinary output has been >200 cc/hr over the last several hours and increasing. His temperature is 99.0 deg F (37.2 deg C), blood pressure is 125/72 mmHg, pulse is 87/min, and respirations are 13/min. Which of the following values would most likely correspond to the patient’s urine specific gravity, urine osmolality, plasma osmolality, and serum sodium?
- A. Low, High, High, High
- B. Low, Low, High, High (Correct Answer)
- C. High, High, Low, Low
- D. Low, Low, High, Low
- E. High, Low, Low, High
Sodium handling along the nephron Explanation: ***Low, Low, High, High***
- This patient's presentation, particularly the **large intracranial hemorrhage**, worsening mental status despite no new bleeding, and especially the **high urinary output (>200 cc/hr)**, is classic for **diabetes insipidus (DI)**, often neurogenic DI, due to damage to the posterior pituitary or hypothalamus.
- In DI, there is a deficiency of **ADH (vasopressin)**, leading to the kidneys' inability to reabsorb water. This results in the excretion of large volumes of **dilute urine** (low urine specific gravity, low urine osmolality) and concentration of the plasma (high plasma osmolality and hypernatremia, which means high serum sodium).
*Low, High, High, High*
- This pattern would indicate concentrated urine alongside concentrated plasma and high sodium, which contradicts the presence of **polyuria** and the underlying pathology of **diabetes insipidus (DI)**.
- High urine osmolality and specific gravity would suggest intact ADH function and water reabsorption in the kidneys, which is not what occurs in DI.
*High, High, Low, Low*
- This profile describes a state of **concentrated urine** but **dilute plasma** and **hyponatremia**, which is characteristic of the **Syndrome of Inappropriate Antidiuretic Hormone (SIADH)**.
- SIADH is the opposite of diabetes insipidus, involving excessive ADH leading to water retention, not excessive water excretion.
*Low, Low, High, Low*
- While **low urine specific gravity** and **low urine osmolality** are consistent with diabetes insipidus, a **low serum sodium** (hyponatremia) is not.
- In diabetes insipidus, the loss of free water typically leads to **hypernatremia** as the body becomes dehydrated.
*High, Low, Low, High*
- This combination is inconsistent with any common clinical scenario. A **high urine specific gravity** with a **low urine osmolality** is contradictory, as specific gravity is a measure of urine concentration, which correlates with osmolality.
- Furthermore, a **low plasma osmolality** with a **high serum sodium** is physiologically improbable.
Sodium handling along the nephron US Medical PG Question 8: A 3-year-old boy is brought to the emergency department with a history of unintentional ingestion of seawater while swimming in the sea. The amount of seawater ingested is not known. There is no history of vomiting. On physical examination, the boy appears confused and is asking for more water to drink. His serum sodium is 152 mmol/L (152 mEq/L). Which of the following changes in volumes and osmolality of body fluids are most likely to be present in this boy?
- A. Decreased ECF volume, unaltered ICF volume, unaltered body osmolality
- B. Increased ECF volume, decreased ICF volume, increased body osmolality (Correct Answer)
- C. Increased ECF volume, unaltered ICF volume, unaltered body osmolality
- D. Increased ECF volume, increased ICF volume, decreased body osmolality
- E. Decreased ECF volume, decreased ICF volume, increased body osmolality
Sodium handling along the nephron Explanation: ***Increased ECF volume, decreased ICF volume, increased body osmolality***
- Ingesting **seawater**, which is **hypertonic** (higher sodium concentration than plasma), leads to an increase in total body osmolality because the ingested sodium is absorbed into the extracellular fluid (ECF). This causes water to shift from the intracellular fluid (ICF) to the ECF to equilibrate osmolality, leading to a **decreased ICF volume** and an **increased ECF volume**, consistent with the patient's **serum sodium of 152 mmol/L**.
- The patient's confusion and excessive thirst ("asking for more water") are classic symptoms of **hypernatremia** and **dehydration** at the cellular level, as cells shrink due to water loss.
*Decreased ECF volume, unaltered ICF volume, unaltered body osmolality*
- This option does not align with the ingestion of **hypertonic seawater**, which would inevitably increase ECF volume and body osmolality due to the absorption of excess sodium.
- An **unaltered ICF volume** and body osmolality would imply no significant osmotic shift or change in solute concentration, which contradicts the clinical picture of hypernatremia.
*Increased ECF volume, unaltered ICF volume, unaltered body osmolality*
- While ECF volume would increase due to fluid shift, the ingested **hypertonic** seawater would significantly **increase body osmolality**, not leave it unaltered.
- An **unaltered ICF volume** is unlikely as the osmotic gradient created by hypernatremia would draw water out of cells.
*Increased ECF volume, increased ICF volume, decreased body osmolality*
- Both **increased ECF and ICF volumes** are inconsistent with the hypernatremia caused by seawater ingestion; hypernatremia typically causes fluid to shift *out* of cells, thereby decreasing ICF volume.
- A **decreased body osmolality** would be seen in cases of hyponatremia (excessive water intake or solute loss), which is the opposite of this clinical scenario.
*Decreased ECF volume, decreased ICF volume, increased body osmolality*
- While ICF volume would decrease and body osmolality would increase, the ECF volume is more likely to **increase** initially due to the ingested volume of seawater and the subsequent osmotic shift of water from the ICF.
- A **decreased ECF volume** would typically occur only with massive dehydration or severe fluid loss, not with the ingestion of a significant amount of fluid, even if hypertonic.
Sodium handling along the nephron US Medical PG Question 9: A 58-year-old Caucasian woman visits her primary care physician for an annual check-up. She has a history of type 2 diabetes mellitus and stage 3A chronic kidney disease. Her estimated glomerular filtration rate has not changed since her last visit. Today, her parathyroid levels are moderately elevated. She lives at home with her husband and 2 children and works as a bank clerk. Her vitals are normal, and her physical examination is unremarkable. Which of the following explains this new finding?
- A. Uremia
- B. Acidemia
- C. Hyperuricemia
- D. Hypercalcemia
- E. Phosphate retention (Correct Answer)
Sodium handling along the nephron Explanation: ***Phosphate retention***
- **Chronic kidney disease** often leads to **phosphate retention** because the damaged kidneys cannot effectively excrete phosphate.
- This elevated phosphate stimulates the parathyroid glands to secrete more **parathyroid hormone (PTH)** as a compensatory mechanism, leading to secondary hyperparathyroidism.
*Uremia*
- While uremia (accumulation of nitrogenous waste products) is a feature of chronic kidney disease, it is not the **direct cause** of elevated parathyroid levels.
- Uremia primarily causes symptoms like fatigue, nausea, and altered mental status, but it doesn't independently trigger PTH release in the same direct manner as phosphate retention or hypocalcemia.
*Acidemia*
- **Metabolic acidosis** is common in chronic kidney disease, but it generally **inhibits** PTH secretion, not stimulates it.
- While it can worsen bone disease, acidemia itself does not explain the primary elevation of parathyroid hormone.
*Hyperuricemia*
- **Hyperuricemia** (elevated uric acid levels) is often associated with chronic kidney disease due to decreased renal excretion of uric acid.
- However, hyperuricemia does not directly cause or explain elevated parathyroid hormone levels.
*Hypercalcemia*
- **Hypercalcemia** would typically **suppress** parathyroid hormone secretion, not elevate it.
- In chronic kidney disease, **hypocalcemia** (due to impaired vitamin D activation and phosphate retention) is more common and would stimulate PTH.
Sodium handling along the nephron US Medical PG Question 10: A 38-year-old woman presents to the physician’s clinic with a 6-month history of generalized weakness that usually worsens as the day progresses. She also complains of the drooping of her eyelids and double vision that is worse in the evening. Physical examination reveals bilateral ptosis after a sustained upward gaze and loss of eye convergence which improves upon placing ice packs over the eyes and after the administration of edrophonium. Which of the following is an intrinsic property of the muscle group affected in this patient?
- A. A small mass per motor unit
- B. High ATPase activity (Correct Answer)
- C. High myoglobin content
- D. High density of mitochondria
- E. Increased amount of ATP generated per molecule of glucose
Sodium handling along the nephron Explanation: ***High ATPase activity***
- This patient presents with **myasthenia gravis (MG)**, an autoimmune disorder affecting the neuromuscular junction through antibodies against acetylcholine receptors.
- **Extraocular muscles** and other muscles affected early in MG contain a high proportion of **fast-twitch (Type II) muscle fibers**, which are characterized by **high ATPase activity**.
- **Type II fibers** with high ATPase activity generate rapid, powerful contractions but are **more susceptible to neuromuscular junction dysfunction** due to their higher firing rates and greater dependence on efficient neuromuscular transmission.
- This intrinsic property (high ATPase activity) is why these muscles are preferentially affected in myasthenia gravis.
*A small mass per motor unit*
- While extraocular muscles do have **small motor units** (allowing for precise eye movements), this describes the **innervation pattern** rather than an intrinsic biochemical property of the muscle fibers themselves.
- The question specifically asks about an intrinsic property of the muscle group, referring to the metabolic and contractile characteristics of the muscle fibers.
*High myoglobin content*
- **High myoglobin content** is characteristic of **Type I (slow-twitch) oxidative fibers**, which rely on sustained oxygen delivery for prolonged, fatigue-resistant contractions.
- Muscles preferentially affected in MG have a higher proportion of **Type II fibers**, which have lower myoglobin content compared to Type I fibers.
*High density of mitochondria*
- **High mitochondrial density** is characteristic of **Type I (slow-twitch) oxidative fibers** that depend on aerobic metabolism for sustained energy production.
- While extraocular muscles do have oxidative capacity, the **Type II fibers** preferentially affected in MG have relatively lower mitochondrial density compared to Type I fibers and rely more on glycolytic metabolism for rapid energy needs.
*Increased amount of ATP generated per molecule of glucose*
- **Aerobic respiration** in Type I fibers generates approximately 32 ATP molecules per glucose through oxidative phosphorylation.
- **Type II fibers** rely more heavily on **anaerobic glycolysis**, which produces only 2 ATP per glucose molecule, making them less efficient in ATP generation per glucose.
- The muscles affected in MG have higher proportions of Type II fibers with lower ATP efficiency per glucose molecule.
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