Aldosterone actions on distal tubule US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Aldosterone actions on distal tubule. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Aldosterone actions on distal tubule US Medical PG Question 1: An investigator is studying patients with acute decompensated congestive heart failure. He takes measurements of a hormone released from atrial myocytes, as well as serial measurements of left atrial and left ventricular pressures. The investigator observes a positive correlation between left atrial pressures and the serum level of this hormone. Which of the following is most likely the mechanism of action of this hormone?
- A. Increases potassium excretion at the collecting ducts
- B. Constricts afferent renal arteriole
- C. Decreases sodium reabsorption at the collecting tubules (Correct Answer)
- D. Decreases reabsorption of bicarbonate in the proximal convoluted tubules
- E. Increases free water reabsorption from the distal tubules
Aldosterone actions on distal tubule Explanation: ***Decreases sodium reabsorption at the collecting tubules***
- The hormone described, exhibiting a positive correlation with left atrial pressure and released from atrial myocytes, is **Atrial Natriuretic Peptide (ANP)**.
- ANP promotes **natriuresis** (sodium excretion) and **diuresis** by directly inhibiting sodium reabsorption in the collecting tubules, thereby reducing blood volume and cardiac preload.
*Increases potassium excretion at the collecting ducts*
- While ANP does promote fluid and electrolyte excretion, its primary effect is on sodium and water, not a direct increase in **potassium excretion**. **Aldosterone**, not ANP, primarily increases potassium secretion in the collecting ducts.
- This option describes a mechanism more consistent with **mineralocorticoid activity**, which is counteracted by ANP.
*Constricts afferent renal arteriole*
- ANP generally causes **vasodilation** of the afferent arteriole and constriction of the efferent arteriole, increasing glomerular filtration rate (GFR).
- **Angiotensin II** is a primary constrictor of the afferent and efferent renal arterioles, which is the opposite effect of ANP.
*Decreases reabsorption of bicarbonate in the proximal convoluted tubules*
- This mechanism is primarily involved in **acid-base balance** and is influenced by factors like parathyroid hormone or respiratory/metabolic acidosis/alkalosis.
- ANP's main action is on **sodium and water balance**, not directly on bicarbonate reabsorption.
*Increases free water reabsorption from the distal tubules*
- **Vasopressin (Antidiuretic Hormone, ADH)** is responsible for increasing free water reabsorption in the distal tubules and collecting ducts.
- ANP's action is to *increase* water excretion, working in opposition to ADH to reduce circulating fluid volume.
Aldosterone actions on distal tubule US Medical PG Question 2: A 32-year-old woman comes to the physician because of a 2-month history of fatigue, muscle weakness, paresthesias, headache, and palpitations. Her pulse is 75/min and blood pressure is 152/94 mm Hg. Physical examination shows no abnormalities. Serum studies show:
Sodium 144 mEq/L
Potassium 2.9 mEq/L
Bicarbonate 31 mEq/L
Creatinine 0.7 mg/dL
Further evaluation shows low serum renin activity. Which of the following is the most likely diagnosis?
- A. Aldosteronoma (Correct Answer)
- B. Cushing syndrome
- C. Renal artery stenosis
- D. Pheochromocytoma
- E. Laxative abuse
Aldosterone actions on distal tubule Explanation: ***Aldosteronoma***
- The patient presents with **hypertension**, **hypokalemia**, and **metabolic alkalosis** (elevated bicarbonate), which are classic signs of primary hyperaldosteronism.
- **Low serum renin activity** in conjunction with these findings points directly to an **aldosterone-producing adenoma (aldosteronoma)** as the most likely cause.
*Cushing syndrome*
- While Cushing syndrome can cause **hypertension** and **hypokalemia**, it is primarily characterized by features of **hypercortisolism** such as central obesity, moon facies, striae, and muscle wasting, which are not described here.
- The primary defect in Cushing syndrome relates to cortisol excess, not primary aldosterone overproduction leading to low renin.
*Renal artery stenosis*
- **Renal artery stenosis** causes **secondary hyperaldosteronism**, typically presenting with **hypertension** and **elevated renin activity** due to decreased renal perfusion.
- This contradicts the patient's low serum renin activity, making it an unlikely diagnosis.
*Pheochromocytoma*
- **Pheochromocytoma** presents with paroxysmal or sustained **hypertension**, **palpitations**, **headaches**, and **sweating** due to catecholamine excess.
- It does not typically cause **hypokalemia** or **metabolic alkalosis** as seen in this patient.
*Laxative abuse*
- **Laxative abuse** can cause hypokalemia and metabolic alkalosis, but it is typically associated with **chronic diarrhea** and volume depletion, which are not mentioned.
- It does not directly cause **hypertension** and is not associated with low renin activity in the context of aldosterone excess.
Aldosterone actions on distal tubule US Medical PG Question 3: A 64-year-old African American female comes to the physician's office for a routine check-up. The patient's past medical history is significant for hypertension, diabetes, and osteoarthritis in her right knee. Her medications include metformin, glimepiride, lisinopril, metoprolol, hydrochlorothiazide, and ibuprofen as needed. Her only complaint is an unremitting cough that started about 3 weeks ago and she has noticed some swelling around her mouth. The drug most likely responsible for her recent symptoms causes its primary renal hemodynamic effect on which part of the kidney?
- A. Collecting duct
- B. Distal convoluted tubule
- C. Juxtaglomerular cells
- D. Efferent arteriole (Correct Answer)
- E. Afferent arteriole
Aldosterone actions on distal tubule Explanation: ***Efferent arteriole***
- The patient's symptoms of an **unremitting cough** and **angioedema** (swelling around her mouth) are classic side effects of **ACE inhibitors**, such as **lisinopril**.
- ACE inhibitors primarily exert their renal hemodynamic effects by **dilating the efferent arteriole**, leading to a decrease in intraglomerular pressure and glomerular filtration rate.
*Collecting duct*
- The collecting duct is the primary site of action for **vasopressin (ADH)** and **aldosterone**, regulating water and sodium reabsorption, respectively.
- While other medications like **thiazides** (used by the patient) affect distal tubules and collecting ducts indirectly, their direct impact on the collecting duct is not the cause of angioedema or cough.
*Distal convoluted tubule*
- The distal convoluted tubule is the main site of action for **thiazide diuretics** (e.g., hydrochlorothiazide), which inhibit the Na-Cl cotransporter.
- This tubule segment is not directly involved in the mechanism leading to angioedema or cough caused by ACE inhibitors.
*Juxtaglomerular cells*
- Juxtaglomerular cells are responsible for producing **renin**, which is the initial step in the **renin-angiotensin-aldosterone system (RAAS)**.
- While ACE inhibitors block the conversion of angiotensin I to angiotensin II, they do not directly act on the juxtaglomerular cells themselves to cause their side effects.
*Afferent arteriole*
- The afferent arteriole is primarily regulated by **sympathetic tone** and local factors, and is the main site of action for medications like **NSAIDs** (e.g., ibuprofen, which the patient takes as needed).
- While NSAIDs cause **afferent arteriole constriction** and can impair renal function, they do not cause angioedema or a chronic cough.
Aldosterone actions on distal tubule US Medical PG Question 4: A 6-year-old boy is brought to the physician by his mother for a follow-up examination. He has persistent bedwetting. Over the past year, his parents have attempted various methods to prevent him from wetting his bed, including fluid restriction in the evenings, sticker rewards, and bedwetting alarms, with no improvement. The patient wets his bed 2–3 times a week. He does not have problems going to the bathroom during the day. The physician prescribes an oral medication that successfully controls his symptoms. The most likely effect of this drug on the principal cells of the kidney is increased activity of which of the following?
- A. Phospholipase C
- B. Adenylate cyclase (Correct Answer)
- C. Steroid hormone response element
- D. Guanylate cyclase
- E. Tyrosine kinase
Aldosterone actions on distal tubule Explanation: ***Adenylate cyclase***
- The drug prescribed is likely **desmopressin** (DDAVP), an analog of **antidiuretic hormone** (ADH), used to treat **nocturnal enuresis** by reducing urine production during the night.
- ADH binds to **V2 receptors** on the principal cells of the collecting ducts, activating **adenylate cyclase** to increase **cAMP** production, which then inserts **aquaporin-2 channels** into the apical membrane, leading to increased water reabsorption.
*Phospholipase C*
- **Phospholipase C** is typically activated by signaling pathways involving **Gq proteins**, leading to the production of **inositol triphosphate (IP3)** and **diacylglycerol (DAG)**, which then increase intracellular **calcium** and activate **protein kinase C**.
- While some ADH receptors (V1) activate phospholipase C, the **V2 receptors** in the kidney responsible for water reabsorption primarily act through **adenylate cyclase**.
*Steroid hormone response element*
- **Steroid hormones** (e.g., aldosterone, cortisol) diffuse through the cell membrane and bind to **intracellular receptors**, which then translocate to the nucleus and bind to **steroid hormone response elements** on DNA to directly alter gene transcription.
- This mechanism is associated with a slower, long-term effect on gene expression, rather than the rapid modulation of water reabsorption seen with ADH.
*Guanylate cyclase*
- **Guanylate cyclase** produces **cyclic GMP (cGMP)**, which is involved in various signaling pathways, notably those mediated by **nitric oxide (NO)** and **natriuretic peptides**.
- cGMP signaling is more commonly associated with vasodilation and regulation of blood pressure, and it is not the primary mechanism of action for ADH in water reabsorption in the kidney.
*Tyrosine kinase*
- **Tyrosine kinase receptors** are often involved in growth factor signaling, insulin action, and cytokine responses, where ligand binding leads to receptor dimerization and phosphorylation of tyrosine residues on the receptor and downstream proteins.
- This mechanism is distinct from the G protein-coupled receptor (GPCR) pathway utilized by ADH.
Aldosterone actions on distal tubule US Medical PG Question 5: A 44-year-old male presents to his primary care physician with complaints of fatigue, muscle weakness, cramps, and increased urination over the past several weeks. His past medical history is significant only for hypertension, for which he was started on hydrochlorothiazide (HCTZ) 4 weeks ago. Vital signs at today's visit are as follows: T 37.2, HR 88, BP 129/80, RR 14, and SpO2 99%. Physical examination does not reveal any abnormal findings. Serologic studies are significant for a serum potassium level of 2.1 mEq/L (normal range 3.5-5.0 mEq/L). Lab-work from his last visit showed a basic metabolic panel and complete blood count results to all be within normal limits. Which of the following underlying diseases most likely contributed to the development of this patient's presenting condition?
- A. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
- B. Adrenal insufficiency
- C. Cushing's disease
- D. Hyperaldosteronism (Correct Answer)
- E. Pituitary adenoma
Aldosterone actions on distal tubule Explanation: ***Correct: Hyperaldosteronism***
- This patient presents with **hypokalemia** (2.1 mEq/L), fatigue, muscle weakness, cramps, and increased urination, a constellation of symptoms highly suggestive of **primary hyperaldosteronism**.
- While **hydrochlorothiazide (HCTZ)** can induce hypokalemia, the severity in this case (2.1 mEq/L) strongly suggests an underlying pathology compounded by the diuretic, given that his previous labs were normal. Hyperaldosteronism directly causes **potassium wasting** in the kidneys, and the diuretic exacerbates this effect.
- The normal blood pressure control on HCTZ and the development of severe hypokalemia points to an underlying aldosterone excess being unmasked by the thiazide diuretic.
*Incorrect: Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)*
- SIADH is characterized by **euvolemic hyponatremia** due to excessive ADH secretion, leading to water retention and dilution of sodium.
- It does not typically cause hypokalemia; instead, potassium levels are often normal or slightly reduced due to dilutional effects rather than direct renal wasting.
*Incorrect: Adrenal insufficiency*
- Adrenal insufficiency, such as Addison's disease, typically presents with **hyponatremia**, **hyperkalemia**, fatigue, and hypotension, which is contrary to this patient's presentation of hypokalemia and normal blood pressure.
- It involves a deficiency in mineralocorticoids (like aldosterone) and glucocorticoids, leading to impaired sodium and water retention and reduced potassium excretion.
*Incorrect: Cushing's disease*
- Cushing's disease is characterized by excessive cortisol production, leading to symptoms like **central obesity**, **moon facies**, **buffalo hump**, and **hypertension**. While some patients may develop hypokalemia due to mineralocorticoid effects of very high cortisol, it's not the primary feature and other classic signs are absent in this case.
- The presenting symptoms of severe hypokalemia, muscle weakness, and cramps without other typical Cushingoid features make this diagnosis less likely.
*Incorrect: Pituitary adenoma*
- Pituitary adenomas can cause various endocrine disorders depending on the hormones secreted (e.g., prolactinoma, acromegaly, or ACTH-secreting adenoma causing Cushing's disease).
- A non-functioning pituitary adenoma does not directly cause hypokalemia or the specific constellation of symptoms seen here, and the patient lacks features of specific hormone-secreting adenomas.
Aldosterone actions on distal tubule US Medical PG Question 6: A new drug X is being tested for its effect on renal function. During the experiments, the researchers found that in patients taking substance X, the urinary concentration of sodium decreases while urine potassium concentration increase. Which of the following affects the kidneys in the same way as does substance X?
- A. Aldosterone (Correct Answer)
- B. Furosemide
- C. Spironolactone
- D. Atrial natriuretic peptide
- E. Hydrochlorothiazide
Aldosterone actions on distal tubule Explanation: ***Aldosterone***
- **Aldosterone** acts on the **principal cells** of the **collecting duct** to increase sodium reabsorption and potassium secretion.
- This action leads to a decrease in urinary sodium concentration and an increase in urinary potassium concentration, matching the effects of drug X.
*Furosemide*
- **Furosemide** is a **loop diuretic** that inhibits the **Na-K-2Cl cotransporter** in the **thick ascending limb** of the loop of Henle.
- This inhibition leads to increased excretion of sodium, potassium, and water, resulting in higher urinary sodium concentration.
*Spironolactone*
- **Spironolactone** is an **aldosterone antagonist** that blocks aldosterone's effects on the collecting duct.
- This leads to increased sodium excretion and decreased potassium excretion (potassium-sparing effect), which is the opposite of drug X.
*Atrial natriuretic peptide*
- **Atrial natriuretic peptide (ANP)** is released in response to atrial stretch and causes **natriuresis** (increased sodium excretion) and **diuresis**.
- It works by dilating afferent arterioles and constricting efferent arterioles, increasing GFR, and inhibiting sodium reabsorption, thus increasing urinary sodium concentration.
*Hydrochlorothiazide*
- **Hydrochlorothiazide** is a **thiazide diuretic** that inhibits the **Na-Cl cotransporter** in the **distal convoluted tubule**.
- This leads to increased sodium and chloride excretion but typically causes potassium wasting (hypokalemia), which differs from the increased urinary potassium concentration seen with drug X.
Aldosterone actions on distal tubule US Medical PG Question 7: A 33-year-old male presents to his primary care physician with complaints of headaches and muscle weakness. His physical exam is entirely within normal limits except for a blood pressure of 150/95. Subsequent routine blood lab work showed a sodium level of 146 and potassium level of 3.0. What is the best pharmacological therapy for this patient?
- A. Fludrocortisone
- B. Spironolactone (Correct Answer)
- C. Lisinopril
- D. Hydrochlorothiazide
- E. Propranolol
Aldosterone actions on distal tubule Explanation: ***Spironolactone***
- This patient's symptoms (hypertension, **hypokalemia**, and **hypernatremia**) are classic for **primary hyperaldosteronism**. **Spironolactone** is an **aldosterone antagonist** that blocks the effects of aldosterone, effectively treating both the hypertension and electrolyte abnormalities.
- Aldosterone antagonists directly target the underlying pathology by countering the excessive mineralocorticoid activity, making it the most appropriate pharmacological therapy for primary hyperaldosteronism.
*Fludrocortisone*
- **Fludrocortisone** is a **mineralocorticoid** used to *replace* aldosterone in conditions like Addison's disease where aldosterone production is deficient.
- Administering fludrocortisone in a patient with excessive aldosterone (primary hyperaldosteronism) would worsen their condition by exacerbating hypertension, hypokalemia, and hypernatremia.
*Lisinopril*
- **Lisinopril** is an **ACE inhibitor** that works by blocking the conversion of angiotensin I to angiotensin II, leading to vasodilation and decreased aldosterone secretion.
- While ACE inhibitors can lower blood pressure, they are not the primary treatment for **primary hyperaldosteronism** because the condition involves autonomous aldosterone production **independent of the renin-angiotensin-aldosterone system (RAAS)**.
*Hydrochlorothiazide*
- **Hydrochlorothiazide** is a **thiazide diuretic** that works by increasing the excretion of sodium and water, thereby lowering blood pressure.
- However, thiazide diuretics also increase potassium excretion, which would further worsen the patient's existing **hypokalemia**, making it an inappropriate choice.
*Propranolol*
- **Propranolol** is a **non-selective beta-blocker** that lowers blood pressure by reducing heart rate and cardiac output.
- While useful for hypertension, beta-blockers do not address the underlying electrolyte disturbances characteristic of **primary hyperaldosteronism** and are not a first-line treatment for this specific condition.
Aldosterone actions on distal tubule US Medical PG Question 8: A 61-year-old man with longstanding diabetes and coronary artery disease presents to the ER with chest pain and dyspnea. The echocardiogram reveals moderate-to-severe mitral regurgitation and an ejection fraction of 27%. A chest X-ray shows bibasilar infiltrates. A new drug is added to his medication regimen, and the physician mentions urinary frequency, increased breast tissue development, and erectile dysfunction as possible side effects. What is the mechanism of action of this drug?
- A. Inhibits Na-Cl symporter on the distal convoluted tubule
- B. Inhibits epithelial Na-channels on the cortical collecting duct
- C. Inhibits mineralocorticoid receptor on the cortical collecting duct (Correct Answer)
- D. Inhibits Na-K-2Cl symporter on the ascending loop of Henle
- E. Inhibits beta-adrenergic receptors to decrease SA node automaticity
Aldosterone actions on distal tubule Explanation: ***Inhibits mineralocorticoid receptor on the cortical collecting duct***
- The patient's presentation of **heart failure** (chest pain, dyspnea, low ejection fraction, bibasilar infiltrates, mitral regurgitation) along with the side effects of **urinary frequency**, **gynecomastia**, and **erectile dysfunction** are characteristic of **spironolactone** or **eplerenone**.
- These drugs are **aldosterone antagonists** that work by inhibiting the **mineralocorticoid receptor** in the cortical collecting duct, leading to diuresis and beneficial effects in heart failure.
*Inhibits Na-Cl symporter on the distal convoluted tubule*
- This describes the mechanism of action of **thiazide diuretics**, such as hydrochlorothiazide.
- While thiazides cause urinary frequency, they are not typically associated with gynecomastia or erectile dysfunction.
*Inhibits epithelial Na-channels on the cortical collecting duct*
- This mechanism describes **potassium-sparing diuretics** like amiloride and triamterene (not aldosterone antagonists).
- These drugs primarily prevent sodium reabsorption and potassium secretion, but they do not cause gynecomastia or erectile dysfunction as directly as spironolactone.
*Inhibits Na-K-2Cl symporter on the ascending loop of Henle*
- This is the mechanism of action for **loop diuretics**, such as furosemide or bumetanide.
- Loop diuretics are potent diuretics and cause urinary frequency but are not known to cause gynecomastia or erectile dysfunction.
*Inhibits beta-adrenergic receptors to decrease SA node automaticity*
- This mechanism describes **beta-blockers**, such as metoprolol or carvedilol, which are often used in heart failure management.
- While beta-blockers can cause erectile dysfunction, they do not cause urinary frequency or gynecomastia.
Aldosterone actions on distal tubule US Medical PG Question 9: 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
Aldosterone actions on distal tubule 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.
Aldosterone actions on distal tubule US Medical PG Question 10: Two days after vaginal delivery of a healthy newborn at term, a 32-year-old woman, gravida 2, para 2, is unable to breastfeed. Her labor was complicated by antepartum hemorrhage and she received two units of packed red blood cells. Her pulse is 99/min and blood pressure is 90/55 mm Hg. Further evaluation of this patient is most likely to show which of the following sets of serum findings?
$$$ ACTH %%% Aldosterone %%% Cortisol $$$
- A. ↑ ↓ ↓
- B. ↓ ↑ ↓
- C. ↑ normal ↑
- D. ↓ normal ↑
- E. ↓ normal ↓ (Correct Answer)
Aldosterone actions on distal tubule Explanation: ***↓ normal ↓***
- This scenario describes **Sheehan's syndrome**, caused by **postpartum pituitary necrosis** due to severe hemorrhage and hypotension during delivery.
- Decreased **ACTH** (adrenocorticotropic hormone) leads to secondary **adrenal insufficiency**, causing decreased **cortisol**. **Aldosterone** secretion, primarily regulated by the **renin-angiotensin system**, remains largely normal because only the zona glomerulosa of the adrenal cortex, which produces aldosterone, is regulated directly by the renin-angiotensin-aldosterone system (RAAS), whereas the pituitary regulates the zona fasciculata and zona reticularis.
*↑ ↓ ↓*
- This pattern (high ACTH, low aldosterone, low cortisol) suggests **primary adrenal insufficiency** (Addison's disease), where the adrenal glands themselves are failing, leading to a compensatory increase in ACTH. However, this patient's condition is due to pituitary damage.
- In primary adrenal insufficiency, both **cortisol** and **aldosterone** would be low, and **ACTH** would be elevated due to a lack of negative feedback.
*↓ ↑ ↓*
- This pattern (low ACTH, high aldosterone, low cortisol) is inconsistent with most common adrenal or pituitary pathologies. Low ACTH and low cortisol would suggest secondary adrenal insufficiency, but high aldosterone does not fit.
- **Hyperaldosteronism** with secondary adrenal insufficiency is rare and not indicated by the patient's presentation.
*↑ normal ↑*
- This pattern (high ACTH, normal aldosterone, high cortisol) suggests **Cushing's disease** (pituitary adenoma secreting ACTH), or an ectopic ACTH tumor, or a state of acute stress.
- The patient's **hypotension** and inability to breastfeed point away from Cushing's and towards hypopituitarism.
*↓ normal ↑*
- This pattern (low ACTH, normal aldosterone, high cortisol) could be seen in states of iatrogenic **exogenous corticosteroid use**, leading to suppressed ACTH and endogenous cortisol, or in an adrenal tumor producing cortisol independent of ACTH.
- This is inconsistent with the symptoms of postpartum hemorrhage and inability to lactate, which indicate a **deficit** rather than an excess of pituitary hormones.
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