UPSC-CMS 2025 Practice Questions

Q: Which of the following can be used for the management of severe hyperkalaemia? I. Intravenous calcitonin II. Intravenous sodium bicarbonate III. Oral sodium polystyrene sulphate IV. Intravenous calcium gluconate

II, III and IV. ***II, III and IV*** - **Intravenous sodium bicarbonate** helps shift potassium into cells, primarily used in cases of metabolic acidosis. - **Oral sodium polystyrene sulfonate** (Kayexalate) is a cation-exchange resin that binds potassium in the gut, facilitating its excretion. - **Intravenous calcium gluconate** does not lower serum potassium but stabilizes the cardiac membrane, protecting against life-threatening arrhythmias. *I and II only* - **Intravenous calcitonin** is used in hypercalcemia to lower calcium levels and is not indicated for the management of hyperkalemia. - While intravenous sodium bicarbonate is used, relying on it alone with calcitonin would be insufficient and inappropriate. *I and IV only* - **Intravenous calcitonin** is not a treatment for hyperkalemia. - Although intravenous calcium gluconate is crucial for cardiac stabilization, it does not address the underlying hyperkalemia directly, making this option incomplete and incorrect. *'I, II and IV* - **Intravenous calcitonin** has no role in the management of hyperkalemia. - While intravenous sodium bicarbonate and calcium gluconate are important, the inclusion of calcitonin makes this option incorrect.

Q: Which one of the following conditions can cause euvolaemic hyponatraemia?

Hypothyroidism. ***Hypothyroidism*** - Severe hypothyroidism can lead to **euvolaemic hyponatraemia** through impaired water excretion [1]. - This occurs due to increased **antidiuretic hormone (ADH)** secretion and decreased renal free water clearance [1]. *Adrenocortical failure* - **Adrenocortical failure** (e.g., Addison's disease) typically causes **hypovolaemic hyponatraemia** due to reduced mineralocorticoid activity, leading to sodium and water loss [1]. - It's also associated with hyperkalemia, which is not characteristic of euvolaemic hyponatremia. *Nephrotic syndrome* - **Nephrotic syndrome** causes **hypervolaemic hyponatraemia** due to significant protein loss, leading to reduced plasma oncotic pressure, fluid shifts to the interstitial space, and secondary hyperaldosteronism [1]. - The primary fluid imbalance is fluid overload with edema [1]. *Burns* - Severe **burns** primarily lead to **hypovolaemic hyponatraemia** or **hypernatraemia** depending on fluid resuscitation and evaporative losses [1]. - The massive fluid shifts and plasma loss usually result in fluid and electrolyte imbalances that are not euvolaemic [1].

Q: Which one of the following conditions is caused by mutations in the gene that encodes the sodium-potassium-2-chloride cotransporter (NKCC2), and presents with sodium wasting, hypokalaemia, hypomagnesaemia and hypercalciuria?

Bartter syndrome. ***Bartter syndrome*** - This syndrome is characterized by **loss-of-function mutations** in the **NKCC2 cotransporter** in the thick ascending limb of the loop of Henle, leading to impaired sodium and chloride reabsorption. - The resulting electrolyte imbalances include **sodium wasting**, **hypokalemia**, **hypomagnesemia**, and **hypercalciuria**. *Fanconi syndrome* - This syndrome involves a generalized defect in the **proximal renal tubules**, leading to impaired reabsorption of multiple substances including glucose, amino acids, phosphate, and bicarbonate. - It does not specifically involve a mutation in the NKCC2 cotransporter or present with the described electrolyte profile. *Gitelman syndrome* - This condition is caused by a mutation in the **thiazide-sensitive Na-Cl cotransporter (NCC)** in the distal convoluted tubule. - While it shares some features like hypokalemia and hypomagnesemia, it is typically associated with **hypocalciuria**, not hypercalciuria, and a different genetic defect. *Alport syndrome* - This is a genetic disorder affecting type IV collagen, primarily impacting the **glomerular basement membrane**, leading to hematuria, proteinuria, and progressive renal failure. - It is not associated with mutations in electrolyte transporters or the specific electrolyte abnormalities listed in the question.

Q: A 52 year old male has uncontrolled diabetes. Which one of the following tests will help in early detection of nephropathy?

Urine albumin. Urine albumin - **Microalbuminuria**, detected by measuring urine albumin, is often the earliest sign of **diabetic nephropathy**, occurring before changes in GFR or serum creatinine [1], [3]. - **Persistent albuminuria** indicates glomerular damage and is a key marker for monitoring disease progression and treatment effectiveness [3]. *Blood urea level* - **Blood urea nitrogen (BUN)** levels rise significantly only when there's a substantial decline in **renal function**, making it an insensitive marker for early damage [2]. - Factors like dehydration or protein intake can also influence BUN, reducing its specificity for early nephropathy [2]. *Ultrasonography* - **Renal ultrasonography** is useful for assessing kidney size, shape, and identifying structural abnormalities like hydronephrosis or stones. - It is not sensitive enough to detect early-stage changes in **renal function** or microvascular damage characteristic of early diabetic nephropathy. *Serum creatinine level* - **Serum creatinine** levels increase only after a significant portion of kidney function (typically >50%) has been lost [2]. - It is a marker of **reduced glomerular filtration rate (GFR)**, but detecting elevated creatinine means the nephropathy is already more advanced than the microalbuminuria stage [1].

Q: Kidney damage and Glomerular Filtration Rate (GFR) value between 15-29 mL / min / 1.73 m^2 are found in which stage of Chronic Kidney Disease?

Stage 4 (severe). ***Stage 4 (severe)*** - **Stage 4 Chronic Kidney Disease (CKD)** is defined by a **Glomerular Filtration Rate (GFR)** in the range of **15-29 mL/min/1.73 m²** [1]. - At this stage, significant kidney damage is present, indicating **severe reduction in kidney function** with increased risk of complications. *Stage 3A (mild to moderate)* - **Stage 3A CKD** is characterized by a **GFR** between **45-59 mL/min/1.73 m²**, which is a milder reduction compared to the GFR given in the question [1]. - This stage represents a **mild to moderate decrease** in kidney function, falling above the severe range. *Stage 2 (mild)* - **Stage 2 CKD** involves a **GFR** between **60-89 mL/min/1.73 m²**, which is a mild reduction in GFR but typically with persistent kidney damage. - This GFR range is significantly higher than the 15-29 mL/min/1.73 m² specified in the question, representing **earlier kidney dysfunction**. *Stage 5 (kidney failure)* - **Stage 5 CKD** is defined by a **GFR** of **less than 15 mL/min/1.73 m²**, indicating **kidney failure** requiring dialysis or kidney transplant [1]. - The given GFR range of 15-29 mL/min/1.73 m² is higher than that of Stage 5, although it is still considered a **very advanced stage of CKD**.

Q: Which one of the following hereditary tubulo-interstitial kidney diseases has an autosomal recessive mode of inheritance?

Nephronophthisis. ***Nephronophthisis*** - This is a group of **autosomal recessive** disorders characterized by tubulointerstitial nephritis, renal cysts, and progression to **end-stage renal disease (ESRD)**, often in childhood or adolescence [1]. - It is the most common genetic cause of ESRD in children, with classic features including **polydipsia, polyuria**, and anemia [1]. *Juvenile hyperuricaemic nephropathy* - This condition is typically inherited in an **autosomal dominant** pattern. - It is characterized by early-onset hyperuricemia, gout, and progressive renal insufficiency due to changes in **urate transport**. *Medullary cystic kidney disease type 1* - Previously known as **medullary cystic kidney disease**, this is now often referred to as **Autosomal Dominant Tubulointerstitial Kidney Disease (ADTKD)**. - It is caused by mutations in the **UMOD gene** (encoding uromodulin) and is inherited in an **autosomal dominant** fashion [1]. *Medullary cystic kidney disease type 2* - Also categorized under **ADTKD**, this form is caused by mutations in the **REN gene** (encoding renin). - Like type 1, it follows an **autosomal dominant** inheritance pattern leading to progressive chronic kidney disease.

Q: Which of the following findings in a patient are suggestive of acute nephritis? I. Hematuria II. Oliguria III. Reduced size of both kidneys IV. Edema Select the correct answer using the code given below :

I, II and IV. ***I, II and IV*** - **Hematuria**, **oliguria**, and **edema** are classic signs of acute nephritis, indicating inflammation and impaired kidney function [1]. - Oliguria results from reduced **glomerular filtration**, while edema is due to fluid retention secondary to kidney dysfunction. *I and II only* - This option is incomplete as **edema** is also a significant finding in acute nephritis due to fluid overload from impaired renal excretion. - While hematuria and oliguria are key, omitting edema overlooks a critical systemic manifestation. *I and III* - **Reduced size of both kidneys** (III) is typically associated with **chronic kidney disease** [1], not the acute inflammation seen in acute nephritis. - Acute nephritis usually presents with **normal or enlarged kidneys** due to inflammation and swelling. *III and IV* - This option incorrectly includes **reduced kidney size**, which is characteristic of chronic, not acute, kidney disease. - While edema (IV) is present in acute nephritis, the presence of hematuria and oliguria is also crucial for diagnosis.

Q: A 35 year old male presents with increased urine output. On evaluation, his urinary output was around 4L/day; urinary osmolality was 200 mosmol/L. Which of the following are various differential diagnosis? I. Psychogenic polydipsia II. Solute diuresis III. Central diabetes insipidus IV. Nephrogenic diabetes insipidus Select the correct answer using the code given below :

I, III and IV. ***I, III and IV*** - **Polyuria** with a **low urine osmolality** (200 mosmol/L, which is less than plasma osmolality) indicates the excretion of a large volume of dilute urine [1]. - This pattern is characteristic of conditions involving water diuresis, specifically **psychogenic polydipsia**, **central diabetes insipidus**, and **nephrogenic diabetes insipidus**, where the body fails to concentrate urine appropriately [2]. *I and IV only* - While **psychogenic polydipsia** and **nephrogenic diabetes insipidus** can cause polyuria with dilute urine, this option incorrectly excludes **central diabetes insipidus**, which presents with very similar urinary findings [2]. - **Central diabetes insipidus** is a primary disorder of ADH secretion, leading to an inability to concentrate urine [1]. *II and IV* - **Solute diuresis** typically results in urine with a relatively normal or slightly elevated osmolality as it's due to the excretion of osmotically active substances, not pure water. The urine osmolality of 200 mosmol/L points away from significant solute diuresis. - This option also omits **central diabetes insipidus** and **psychogenic polydipsia**, which are strong differentials for dilute polyuria. *I and III only* - This option includes **psychogenic polydipsia** and **central diabetes insipidus** but incorrectly excludes **nephrogenic diabetes insipidus**. - **Nephrogenic diabetes insipidus** also results in the inability to respond to ADH, leading to the excretion of dilute urine and polyuria [2].

Q: Autosomal dominant mutations in which one of the following genes may cause focal segmental glomerulosclerosis associated with abnormal genitalia, Wilms tumor and mental retardation?

WT1. ***WT1*** - Mutations in the **WT1 (Wilms tumor 1) gene** are associated with **Denys-Drash syndrome** and **Frasier syndrome**, both of which feature **focal segmental glomerulosclerosis (FSGS)**, abnormal genitalia, and an increased risk of **Wilms tumor**. - **Denys-Drash syndrome** specifically includes **glomerulopathy**, **pseudohermaphroditism** (abnormal genitalia), and **Wilms tumor**, often with some degree of mental retardation. *INF2* - Mutations in the **INF2 gene** are a common cause of **autosomal dominant FSGS**, often without extra-renal manifestations. - While it causes FSGS, it typically does not present with abnormal genitalia, Wilms tumor, or mental retardation. *LMX1B* - Mutations in the **LMX1B gene** are responsible for **Nail-Patella Syndrome**, which is characterized by abnormalities of the nails, patellae, elbows, and iliac horns. - It can cause FSGS, but it is not associated with abnormal genitalia, Wilms tumor, or mental retardation. *APOL1* - **APOL1 gene variants** (G1 and G2 risk alleles) are strongly associated with a higher risk of developing **FSGS** and other kidney diseases, particularly in individuals of African ancestry. - While it is a significant genetic risk factor for FSGS, APOL1 mutations are not linked to abnormal genitalia, Wilms tumor, or mental retardation.

Q: Which one of the following is correct regarding arginine vasopressin antagonist Tolvaptan?

It is an oral drug. ***It is an oral drug*** - **Tolvaptan** is an **orally active selective vasopressin V2-receptor antagonist** used in the treatment of hyponatremia. - Its oral bioavailability makes it convenient for long-term management of conditions like **syndrome of inappropriate antidiuretic hormone (SIADH)**. *It is useful in hypovolemic hyponatremia* - **Tolvaptan** is primarily used to treat **euvolemic** and **hypervolemic hyponatremia** by promoting **free water excretion**, which is not ideal in hypovolemic states where fluid status needs to be increased. - In **hypovolemic hyponatremia**, the primary treatment is **fluid resuscitation** with isotonic saline, not free water excretion. *It antagonises the V1 receptor* - **Tolvaptan** is a **selective V2-receptor antagonist**, meaning it specifically blocks the action of vasopressin at the V2 receptors in the renal collecting ducts. - Blocking **V1 receptors** would primarily affect smooth muscle contraction and platelet aggregation, which is not the therapeutic target for tolvaptan in hyponatremia. *It should be used for at least 1 year* - The duration of **Tolvaptan** treatment is variable and depends on the underlying cause of hyponatremia and the patient's response. - There is no standard recommendation for a minimum usage period of at least one year; treatment is typically continued as long as necessary and tolerated.

Question 1

Which of the following can be used for the management of severe hyperkalaemia?
I. Intravenous calcitonin
II. Intravenous sodium bicarbonate
III. Oral sodium polystyrene sulphate
IV. Intravenous calcium gluconate

Accepted Answer

II, III and IV

Answer

I and II only

Answer

I and IV only

Answer

I, II and IV

Question 2

Which one of the following conditions can cause euvolaemic hyponatraemia?

Accepted Answer

Hypothyroidism

Answer

Adrenocortical failure

Answer

Nephrotic syndrome

Answer

Burns

Question 3

Which one of the following conditions is caused by mutations in the gene that encodes the sodium-potassium-2-chloride cotransporter (NKCC2), and presents with sodium wasting, hypokalaemia, hypomagnesaemia and hypercalciuria?

Accepted Answer

Bartter syndrome

Answer

Fanconi syndrome

Answer

Gitelman syndrome

Answer

Alport syndrome

Question 4

A 52 year old male has uncontrolled diabetes. Which one of the following tests will help in early detection of nephropathy?

Accepted Answer

Urine albumin

Answer

Blood urea level

Answer

Ultrasonography

Answer

Serum creatinine level

Question 5

Kidney damage and Glomerular Filtration Rate (GFR) value between 15-29 mL / min / 1.73 m^2 are found in which stage of Chronic Kidney Disease?

Accepted Answer

Stage 4 (severe)

Answer

Stage 3A (mild to moderate)

Answer

Stage 2 (mild)

Answer

Stage 5 (kidney failure)

Question 6

Which one of the following hereditary tubulo-interstitial kidney diseases has an autosomal recessive mode of inheritance?

Accepted Answer

Nephronophthisis

Answer

Juvenile hyperuricaemic nephropathy

Answer

Medullary cystic kidney disease type 1

Answer

Medullary cystic kidney disease type 2

Question 7

Which of the following findings in a patient are suggestive of acute nephritis?
I. Hematuria
II. Oliguria
III. Reduced size of both kidneys
IV. Edema

Select the correct answer using the code given below :

Accepted Answer

I, II and IV

Answer

I and II only

Answer

I and III

Answer

III and IV

Question 8

A 35 year old male presents with increased urine output. On evaluation, his urinary output was around 4L/day; urinary osmolality was 200 mosmol/L. Which of the following are various differential diagnosis?
I. Psychogenic polydipsia
II. Solute diuresis
III. Central diabetes insipidus
IV. Nephrogenic diabetes insipidus

Select the correct answer using the code given below :

Accepted Answer

I, III and IV

Answer

I and IV only

Answer

II and IV

Answer

I and III only

Question 9

Autosomal dominant mutations in which one of the following genes may cause focal segmental glomerulosclerosis associated with abnormal genitalia, Wilms tumor and mental retardation?

Accepted Answer

WT1

Answer

INF2

Answer

LMX1B

Answer

APOL1

Question 10

Which one of the following is correct regarding arginine vasopressin antagonist Tolvaptan?

Accepted Answer

It is an oral drug

Answer

It is useful in hypovolemic hyponatremia

Answer

It antagonises the V1 receptor

Answer

It should be used for at least 1 year

UPSC-CMS 2025

Internal Medicine

Pathology

Pharmacology