Renal & Urology — MCQs
On this page
A 57-year-old man with alcoholic liver cirrhosis (Child-Pugh B) presents with increasing abdominal distension and leg oedema. He is treated with therapeutic paracentesis removing 6 litres of ascitic fluid with albumin replacement. Over the next 48 hours, he develops oliguria with urine output 250 mL/24 hours. Blood tests show: sodium 128 mmol/L, potassium 4.2 mmol/L, urea 18.5 mmol/L, creatinine 198 μmol/L (baseline 85 μmol/L), bilirubin 89 μmol/L, albumin 28 g/L. Urinalysis shows sodium <10 mmol/L, no protein, no blood. Renal ultrasound shows normal-sized kidneys with no obstruction. What is the most likely diagnosis?
A 44-year-old woman with CKD stage 4 (eGFR 23 mL/min/1.73m²) secondary to reflux nephropathy attends the pre-dialysis clinic. She asks about different dialysis modalities. Which of the following statements comparing haemodialysis and peritoneal dialysis is most accurate?
A 69-year-old man is admitted following a fall. He has been lying on the floor for approximately 18 hours before being found. On admission, his creatinine is 486 μmol/L (baseline 95 μmol/L), creatine kinase 87,000 U/L, potassium 6.4 mmol/L, phosphate 2.8 mmol/L, corrected calcium 1.98 mmol/L, and urine dipstick shows blood 3+ but no red cells on microscopy. ECG shows tall tented T waves. After initial stabilization of hyperkalaemia, what is the most important principle of fluid resuscitation in this patient?
A 52-year-old woman with no significant past medical history presents with a 3-day history of fever, dysuria, and left loin pain. Temperature is 38.9°C, BP 108/68 mmHg, pulse 110 bpm. Urine dipstick shows leucocytes 3+, nitrites positive, blood 1+, protein 1+. Which organism is most commonly responsible for this clinical presentation?
A 73-year-old man with CKD stage 4 (eGFR 26 mL/min/1.73m²) is admitted with pneumonia. On day 3 of treatment with co-amoxiclav, he becomes confused and develops myoclonic jerks. His renal function has deteriorated with creatinine now 298 μmol/L. EEG shows generalized triphasic waves. Septic screen including blood cultures, lumbar puncture, and CT head are unremarkable. Which of the following is the most likely diagnosis?
A 26-year-old woman presents to the emergency department with a 12-hour history of severe left-sided loin pain radiating to the groin, with nausea and haematuria. CT KUB confirms a 7mm stone at the left vesicoureteric junction with moderate hydronephrosis. Her vital signs show temperature 36.8°C, BP 138/82 mmHg, pulse 94 bpm. Blood tests reveal: WBC 11.2 × 10⁹/L, CRP 8 mg/L, creatinine 92 μmol/L. What is the most appropriate initial management?
A 49-year-old woman with type 2 diabetes and hypertension presents with fatigue. Blood tests show: sodium 138 mmol/L, potassium 4.8 mmol/L, urea 18.2 mmol/L, creatinine 245 μmol/L (baseline 6 months ago was 98 μmol/L), calcium 2.12 mmol/L, phosphate 1.92 mmol/L, albumin 38 g/L, HbA1c 72 mmol/mol. Urine dipstick shows protein 3+, blood negative. Urine ACR is 450 mg/mmol. What is the most likely stage of her chronic kidney disease?
A 64-year-old man with CKD stage 3b (eGFR 37 mL/min/1.73m²) secondary to diabetic nephropathy is started on sodium zirconium cyclosilicate by his nephrologist. His recent blood tests showed potassium 6.2 mmol/L despite dietary modifications. Which of the following best describes the mechanism of action of this medication?
A 58-year-old woman undergoes total abdominal hysterectomy for fibroids. On postoperative day 2, her urine output drops to 20 mL over 6 hours. Examination reveals suprapubic fullness and discomfort. Her vital signs are stable with BP 132/78 mmHg and pulse 88 bpm. A bladder scan shows 650 mL of urine. Blood tests reveal creatinine 165 μmol/L (baseline 78 μmol/L) and urea 9.2 mmol/L. What is the most appropriate immediate management?
A 55-year-old woman undergoes parathyroidectomy for primary hyperparathyroidism. Twenty-four hours post-operatively, she develops perioral paraesthesia and carpopedal spasm. Blood tests show: corrected calcium 1.72 mmol/L, phosphate 1.45 mmol/L, magnesium 0.62 mmol/L, PTH 1.2 pmol/L (low). What is the underlying cause of her hypocalcaemia?
Renal & Urology UK Medical PG Practice Questions and MCQs
Question 21: A 57-year-old man with alcoholic liver cirrhosis (Child-Pugh B) presents with increasing abdominal distension and leg oedema. He is treated with therapeutic paracentesis removing 6 litres of ascitic fluid with albumin replacement. Over the next 48 hours, he develops oliguria with urine output 250 mL/24 hours. Blood tests show: sodium 128 mmol/L, potassium 4.2 mmol/L, urea 18.5 mmol/L, creatinine 198 μmol/L (baseline 85 μmol/L), bilirubin 89 μmol/L, albumin 28 g/L. Urinalysis shows sodium <10 mmol/L, no protein, no blood. Renal ultrasound shows normal-sized kidneys with no obstruction. What is the most likely diagnosis?
- A. Acute tubular necrosis secondary to hypotension during paracentesis
- B. Pre-renal acute kidney injury due to intravascular volume depletion
- C. Spontaneous bacterial peritonitis with sepsis-induced AKI
- D. Contrast-induced nephropathy from recent CT imaging
- E. Hepatorenal syndrome type 1 (Correct Answer)
Explanation: ***Hepatorenal syndrome type 1*** - This diagnosis is characterized by a rapid, progressive rise in **serum creatinine** and **oliguria** in the setting of advanced cirrhosis with ascites, often triggered by events like large-volume paracentesis. - Key supporting features include a **normal renal ultrasound**, extremely low **urinary sodium (<10 mmol/L)**, and failure to improve despite **albumin replacement**, all consistent with intense renal vasoconstriction. *Acute tubular necrosis secondary to hypotension during paracentesis* - In **acute tubular necrosis (ATN)**, urinalysis typically shows granular 'muddy brown' casts and a higher **urinary sodium (>20-40 mmol/L)** due to tubular damage and inability to reabsorb sodium. - The very low urinary sodium in this patient strongly suggests preserved tubular function and intense **renal vasoconstriction**, which is not typical of ATN. *Pre-renal acute kidney injury due to intravascular volume depletion* - While pre-renal AKI also presents with low urinary sodium, it must resolve or significantly improve after adequate **volume expansion** with intravenous fluids or albumin. - This patient received **therapeutic albumin** during the paracentesis yet still progressed to oliguric renal failure, pointing toward the more severe and refractory pathophysiology of **HRS**. *Spontaneous bacterial peritonitis with sepsis-induced AKI* - **Spontaneous bacterial peritonitis (SBP)** is a common precipitant of AKI in cirrhosis, but this patient is not described as having fever, abdominal pain, or an elevated ascitic fluid **neutrophil count**. - While sepsis-induced AKI can lead to renal dysfunction, the clinical timeline specifically follows a **large-volume paracentesis** without other clear signs of infection. *Contrast-induced nephropathy from recent CT imaging* - There is no clinical history provided indicating the patient received **intravenous contrast** for diagnostic imaging prior to the renal deterioration. - **Contrast-induced nephropathy** typically presents with a transient rise in creatinine 48–72 hours post-exposure but is less likely than HRS type 1 in a decompensated cirrhotic patient following a significant physiological stressor like large-volume paracentesis.
Question 22: A 44-year-old woman with CKD stage 4 (eGFR 23 mL/min/1.73m²) secondary to reflux nephropathy attends the pre-dialysis clinic. She asks about different dialysis modalities. Which of the following statements comparing haemodialysis and peritoneal dialysis is most accurate?
- A. Peritoneal dialysis provides superior clearance of middle molecules compared to conventional haemodialysis (Correct Answer)
- B. Peritoneal dialysis has a higher risk of bacteraemia compared to haemodialysis
- C. Peritoneal dialysis provides more stable cardiovascular haemodynamics but has worse long-term patient survival
- D. Haemodialysis is associated with better preservation of residual renal function than peritoneal dialysis
- E. Haemodialysis requires less dietary restriction than peritoneal dialysis
Explanation: ***Peritoneal dialysis provides superior clearance of middle molecules compared to conventional haemodialysis***- **Peritoneal dialysis (PD)** provides continuous solute exchange, which allows for more efficient removal of larger **middle molecules** (e.g., beta-2 microglobulin) compared to the intermittent nature of **conventional haemodialysis (HD)**.- This enhanced clearance of molecules in PD may help in reducing the long-term risk of **dialysis-related amyloidosis** and other complications.*Peritoneal dialysis has a higher risk of bacteraemia compared to haemodialysis*- **Peritoneal dialysis** is primarily associated with an increased risk of **peritonitis**, an infection of the peritoneal cavity, rather than systemic **bacteraemia**.- **Haemodialysis** carries a significantly higher risk of **bacteraemia** and sepsis due to direct vascular access through **central venous catheters** or arteriovenous fistulas.*Peritoneal dialysis provides more stable cardiovascular haemodynamics but has worse long-term patient survival*- While PD does offer better **haemodynamic stability** due to continuous, gentler fluid removal, most studies show **equivalent long-term survival** rates between the two modalities.- Some evidence even suggests a **survival advantage** for PD during the first few years of treatment, particularly in younger patients without significant comorbidities.*Haemodialysis is associated with better preservation of residual renal function than peritoneal dialysis*- **Peritoneal dialysis** is actually superior for the **preservation of residual renal function (RRF)**, which is a major predictor of patient survival and quality of life.- The rapid fluid shifts and intermittent **hypotensive episodes** common in HD often cause a more precipitous decline in native kidney function.*Haemodialysis requires less dietary restriction than peritoneal dialysis*- **Peritoneal dialysis** patients generally require **fewer dietary restrictions**, especially regarding **potassium** and fluid intake, because the dialysis process is occurring 24/7.- In contrast, HD patients must adhere to stricter diets to prevent the accumulation of toxins and fluid during the **interdialytic intervals**.
Question 23: A 69-year-old man is admitted following a fall. He has been lying on the floor for approximately 18 hours before being found. On admission, his creatinine is 486 μmol/L (baseline 95 μmol/L), creatine kinase 87,000 U/L, potassium 6.4 mmol/L, phosphate 2.8 mmol/L, corrected calcium 1.98 mmol/L, and urine dipstick shows blood 3+ but no red cells on microscopy. ECG shows tall tented T waves. After initial stabilization of hyperkalaemia, what is the most important principle of fluid resuscitation in this patient?
- A. Administer 0.9% saline with calcium gluconate to prevent worsening hypocalcaemia
- B. Use aggressive fluid resuscitation aiming for urine output >300 mL/hour to prevent renal failure
- C. Commence isotonic saline resuscitation while monitoring for hypercalcaemia during recovery phase (Correct Answer)
- D. Restrict fluids to 1 L per 24 hours to avoid fluid overload given acute kidney injury
- E. Administer hypertonic saline to correct concurrent hyponatraemia and improve renal perfusion
Explanation: ***Commence isotonic saline resuscitation while monitoring for hypercalcaemia during recovery phase***- This patient presents with **rhabdomyolysis-induced acute kidney injury** (AKI) following prolonged immobilization, evidenced by a massive **Creatine Kinase (CK)** elevation and **myoglobinuria** (positive dipstick for blood with no RBCs).- While initial **hypocalcaemia** occurs due to calcium deposition in damaged muscle, monitoring for **rebound hypercalcaemia** during the recovery phase is essential as calcium is released back into the circulation.*Administer 0.9% saline with calcium gluconate to prevent worsening hypocalcaemia*- Calcium replacement should be avoided in rhabdomyolysis unless the patient is **symptomatic** or has life-threatening hyperkalaemia with ECG changes, as it can worsen **extravascular calcification**.- Calcium levels typically rise spontaneously during the recovery phase, making early aggressive supplementation potentially harmful.*Use aggressive fluid resuscitation aiming for urine output >300 mL/hour to prevent renal failure*- While aggressive hydration is the cornerstone of treatment, the target urine output recommended by clinical guidelines is generally **200-300 mL/hour**; aiming consistently higher than 300 mL/hour may increase the risk of **fluid overload** and respiratory complications.- The priority is high-volume **isotonic saline** to flush myoglobin casts from the renal tubules while balancing volume status.*Restrict fluids to 1 L per 24 hours to avoid fluid overload given acute kidney injury*- Fluid restriction is contraindicated in the early management of rhabdomyolysis as it exacerbates **myoglobin-induced tubular toxicity** and worsens AKI.- Aggressive volume expansion is necessary to neutralize the effects of **hypovolaemia** caused by fluid sequestration in damaged muscle tissue.*Administer hypertonic saline to correct concurrent hyponatraemia and improve renal perfusion*- There is no clinical indication for **hypertonic saline** in this scenario, as it could cause rapid osmotic shifts and does not address the underlying pathology of myoglobinuria.- Standard **isotonic crystalloids** (0.9% Saline) are the preferred fluid for expanding extracellular volume and maintaining renal perfusion in patients with crush injuries.
Question 24: A 52-year-old woman with no significant past medical history presents with a 3-day history of fever, dysuria, and left loin pain. Temperature is 38.9°C, BP 108/68 mmHg, pulse 110 bpm. Urine dipstick shows leucocytes 3+, nitrites positive, blood 1+, protein 1+. Which organism is most commonly responsible for this clinical presentation?
- A. Staphylococcus saprophyticus
- B. Klebsiella pneumoniae
- C. Escherichia coli (Correct Answer)
- D. Proteus mirabilis
- E. Enterococcus faecalis
Explanation: ***Escherichia coli***- **Escherichia coli** is the most common cause of community-acquired **acute pyelonephritis**, responsible for approximately 75% to 95% of cases.- It possesses specialized **P fimbriae** that allow the bacterium to adhere to uroepithelial cells and ascend from the bladder to the **renal parenchyma**.*Staphylococcus saprophyticus*- This organism is a common cause of **uncomplicated cystitis** specifically in young, sexually active females.- It is less frequently associated with ascending **upper urinary tract infections** like pyelonephritis and typically presents within a younger age demographic.*Klebsiella pneumoniae*- While a significant cause of UTIs, it tracks behind E. coli, accounting for roughly 5-10% of cases, often in patients with **comorbidities** like diabetes.- It is a **nitrite-positive** Gram-negative rod but is statistically less likely to be the causative agent in a patient with no significant past medical history.*Proteus mirabilis*- This pathogen is most strongly associated with **urease production**, which leads to an alkaline urine pH and the formation of **struvite (staghorn) calculi**.- Although it causes pyelonephritis, it accounts for only a small percentage of community-acquired cases compared to E. coli.*Enterococcus faecalis*- This is a **Gram-positive coccus** often associated with healthcare-related UTIs, urinary tract instrumentation, or **structural abnormalities**.- Unlike the Gram-negative organisms listed, Enterococcus does not produce nitrites, making it inconsistent with the **nitrite-positive** urine dipstick found in this patient.
Question 25: A 73-year-old man with CKD stage 4 (eGFR 26 mL/min/1.73m²) is admitted with pneumonia. On day 3 of treatment with co-amoxiclav, he becomes confused and develops myoclonic jerks. His renal function has deteriorated with creatinine now 298 μmol/L. EEG shows generalized triphasic waves. Septic screen including blood cultures, lumbar puncture, and CT head are unremarkable. Which of the following is the most likely diagnosis?
- A. Uraemic encephalopathy secondary to acute-on-chronic kidney disease
- B. Antibiotic-induced encephalopathy from beta-lactam accumulation (Correct Answer)
- C. Cerebral abscess with negative neuroimaging
- D. New-onset status epilepticus of unknown cause
- E. Hyponatraemic encephalopathy
Explanation: ***Antibiotic-induced encephalopathy from beta-lactam accumulation***- The patient's **CKD stage 4** significantly impairs renal excretion, leading to the accumulation of renally cleared drugs like **co-amoxiclav** (a beta-lactam antibiotic). This accumulation can cause **neurotoxicity**, manifesting as confusion and **myoclonic jerks**.- The development of symptoms on day 3 of antibiotic treatment, coupled with characteristic **generalized triphasic waves on EEG** and deteriorating renal function, strongly points to **beta-lactam-induced encephalopathy**. *Uraemic encephalopathy secondary to acute-on-chronic kidney disease*- While **uraemic encephalopathy** can present with confusion and **triphasic waves**, a creatinine of **298 μmol/L** is generally not severe enough to trigger such profound symptoms, especially in a patient with chronic kidney disease who has some metabolic adaptation.- The specific onset of symptoms shortly after initiating **co-amoxiclav** makes a drug-induced cause more likely than a purely metabolic one. *Cerebral abscess with negative neuroimaging*- A **CT head** was unremarkable, effectively ruling out a **cerebral abscess** as the cause of the patient's neurological symptoms. Cerebral abscesses are focal lesions that would typically be visible on imaging.- The patient's symptoms (generalized confusion, myoclonic jerks, diffuse EEG changes) are more consistent with a **diffuse metabolic or toxic encephalopathy** rather than a focal structural lesion. *New-onset status epilepticus of unknown cause*- While the patient experiences myoclonic jerks, the overall clinical picture of confusion and **generalized triphasic waves on EEG** is more indicative of an **encephalopathy** rather than primary **status epilepticus**.- Status epilepticus implies continuous or rapidly recurring seizures. Given the context of **CKD** and a new antibiotic, a toxic/metabolic etiology is far more probable than a primary neurological event. *Hyponatraemic encephalopathy*- This condition typically arises from significant **hyponatraemia** (often Na < 125 mEq/L), leading to cerebral edema and neurological symptoms. No information suggests hyponatraemia in this clinical scenario.- While metabolic encephalopathies can share similar EEG findings, the clear association with a renally cleared drug in a patient with **CKD** makes **drug accumulation** the most specific and likely cause.
Question 26: A 26-year-old woman presents to the emergency department with a 12-hour history of severe left-sided loin pain radiating to the groin, with nausea and haematuria. CT KUB confirms a 7mm stone at the left vesicoureteric junction with moderate hydronephrosis. Her vital signs show temperature 36.8°C, BP 138/82 mmHg, pulse 94 bpm. Blood tests reveal: WBC 11.2 × 10⁹/L, CRP 8 mg/L, creatinine 92 μmol/L. What is the most appropriate initial management?
- A. Emergency ureteroscopy and stone extraction
- B. Percutaneous nephrostomy insertion
- C. Analgesia and trial of conservative management with medical expulsive therapy (Correct Answer)
- D. Immediate extracorporeal shock wave lithotripsy (ESWL)
- E. Emergency nephrostomy followed by elective ureteroscopy
Explanation: ***Analgesia and trial of conservative management with medical expulsive therapy***- The patient is clinically stable with no signs of **sepsis**, **acute kidney injury**, or intractable pain, making conservative management appropriate even for a **7mm distal ureteric stone**.- **Medical expulsive therapy (MET)** using alpha-blockers like **tamsulosin** can increase the likelihood of spontaneous passage for stones located at the **vesicoureteric junction (VUJ)**.*Emergency ureteroscopy and stone extraction*- This is an **invasive procedure** reserved for patients with failed conservative management, persistent pain, or complications like infection.- It is not indicated as the **initial step** in a hemodynamically stable patient without evidence of renal compromise.*Percutaneous nephrostomy insertion*- This is a method of **surgical decompression** used specifically for an **infected obstructed system** or high-grade obstruction with sepsis.- This patient is **afebrile** with a normal **WBC and CRP**, indicating such an urgent intervention is not currently required.*Immediate extracorporeal shock wave lithotripsy (ESWL)**- **ESWL** is generally less effective for stones located in the **distal ureter** due to the difficulty of targeting and the surrounding pelvic bone structures.- It is not typically performed as an **emergency procedure** in the acute phase of renal colic.*Emergency nephrostomy followed by elective ureteroscopy*- This approach is indicated for **septic obstruction** or **bilateral obstruction**, neither of which is present in this case.- Routine **hydronephrosis** in the setting of a single ureteric stone with normal creatinine does not warrant bypass of the obstruction.
Question 27: A 49-year-old woman with type 2 diabetes and hypertension presents with fatigue. Blood tests show: sodium 138 mmol/L, potassium 4.8 mmol/L, urea 18.2 mmol/L, creatinine 245 μmol/L (baseline 6 months ago was 98 μmol/L), calcium 2.12 mmol/L, phosphate 1.92 mmol/L, albumin 38 g/L, HbA1c 72 mmol/mol. Urine dipstick shows protein 3+, blood negative. Urine ACR is 450 mg/mmol. What is the most likely stage of her chronic kidney disease?
- A. CKD stage 2 (eGFR 60-89 mL/min/1.73m²)
- B. CKD stage 3a (eGFR 45-59 mL/min/1.73m²)
- C. CKD stage 3b (eGFR 30-44 mL/min/1.73m²) (Correct Answer)
- D. CKD stage 4 (eGFR 15-29 mL/min/1.73m²)
- E. CKD stage 5 (eGFR <15 mL/min/1.73m²)
Explanation: ***CKD stage 3b (eGFR 30-44 mL/min/1.73m²)*** - **Chronic kidney disease (CKD) stage 3b** is characterized by a moderate to severe reduction in kidney function, with an eGFR between **30 and 44 mL/min/1.73m²**. The patient's **creatinine of 245 μmol/L** along with other significant abnormalities indicates a GFR in this severely impaired range. - The notable rise in **creatinine from baseline** (98 to 245 μmol/L), elevated **urea** (18.2 mmol/L), high **phosphate** (1.92 mmol/L), and severe **proteinuria** (ACR 450 mg/mmol, protein 3+) are all consistent with significant renal compromise typical of Stage 3b CKD. *CKD stage 2 (eGFR 60-89 mL/min/1.73m²)* - This stage represents mild GFR reduction, and a **creatinine of 245 μmol/L** is far too high for this category, corresponding instead to significantly impaired function. - The patient's marked **proteinuria (ACR 450 mg/mmol)** and elevated **phosphate** indicate more advanced kidney disease than Stage 2. *CKD stage 3a (eGFR 45-59 mL/min/1.73m²)* - An eGFR in this range would typically be associated with a considerably lower **creatinine** than **245 μmol/L** for a 49-year-old woman. - The presence of symptoms like **fatigue** and significant electrolyte imbalances such as elevated **phosphate** are more typical of later CKD stages. *CKD stage 4 (eGFR 15-29 mL/min/1.73m²)* - This stage denotes severe kidney dysfunction, and while the patient's **creatinine of 245 μmol/L** is high, it is still considered to align with **CKD stage 3b** based on the provided correct option. - Although the patient's symptoms are severe, the eGFR does not yet place her in the **severely impaired (Stage 4)** category if Stage 3b is the most fitting description. *CKD stage 5 (eGFR <15 mL/min/1.73m²)* - This stage signifies **end-stage renal disease (ESRD)**, requiring immediate renal replacement therapy. An eGFR below **15 mL/min/1.73m²** would generally correspond to much higher **creatinine** levels, typically exceeding 400 μmol/L. - The patient's current laboratory values, while indicative of severe CKD, do not yet meet the criteria for **kidney failure** defined by Stage 5.
Question 28: A 64-year-old man with CKD stage 3b (eGFR 37 mL/min/1.73m²) secondary to diabetic nephropathy is started on sodium zirconium cyclosilicate by his nephrologist. His recent blood tests showed potassium 6.2 mmol/L despite dietary modifications. Which of the following best describes the mechanism of action of this medication?
- A. Enhances renal potassium excretion by blocking sodium reabsorption in the collecting duct
- B. Binds potassium in the gastrointestinal tract in exchange for sodium and hydrogen ions (Correct Answer)
- C. Inhibits aldosterone receptors in the distal nephron reducing sodium reabsorption
- D. Stimulates insulin release which drives potassium into cells
- E. Activates beta-2 adrenergic receptors promoting intracellular potassium shift
Explanation: ***Binds potassium in the gastrointestinal tract in exchange for sodium and hydrogen ions***- **Sodium zirconium cyclosilicate** (SZC) is a highly selective, inorganic **cation exchanger** that captures **potassium ions** throughout the entire **gastrointestinal tract**.- It exchanges **potassium** for **hydrogen and sodium ions**, leading to increased fecal excretion of potassium and a rapid reduction in serum potassium levels, suitable for **chronic hyperkalemia**.*Enhances renal potassium excretion by blocking sodium reabsorption in the collecting duct*- This mechanism describes the action of **potassium-wasting diuretics** (e.g., loop or thiazide diuretics), which increase urinary potassium excretion.- **Sodium zirconium cyclosilicate** acts exclusively within the **gastrointestinal lumen** and does not directly enhance **renal potassium excretion**.*Inhibits aldosterone receptors in the distal nephron reducing sodium reabsorption*- This describes the mechanism of **mineralocorticoid receptor antagonists** (MRAs) like **spironolactone** or **eplerenone**.- MRAs are known to cause or worsen **hyperkalemia** by reducing potassium secretion in the collecting duct, which is contrary to the goal of treating hyperkalemia.*Stimulates insulin release which drives potassium into cells*- This describes the mechanism of **insulin-glucose therapy**, an intervention used for **acute hyperkalemia** to rapidly shift potassium from the extracellular fluid into cells.- **Sodium zirconium cyclosilicate** does not influence **insulin release** or cause an intracellular potassium shift; its action is to remove potassium from the body via the gut.*Activates beta-2 adrenergic receptors promoting intracellular potassium shift*- This is the mechanism of **beta-2 agonists** (e.g., albuterol), which are also used for **acute management of hyperkalemia** to temporarily shift potassium into cells.- Beta-2 agonists do not remove potassium from the body, unlike SZC which binds potassium for **fecal excretion** in chronic settings.
Question 29: A 58-year-old woman undergoes total abdominal hysterectomy for fibroids. On postoperative day 2, her urine output drops to 20 mL over 6 hours. Examination reveals suprapubic fullness and discomfort. Her vital signs are stable with BP 132/78 mmHg and pulse 88 bpm. A bladder scan shows 650 mL of urine. Blood tests reveal creatinine 165 μmol/L (baseline 78 μmol/L) and urea 9.2 mmol/L. What is the most appropriate immediate management?
- A. Administer intravenous furosemide 40 mg
- B. Insert a urethral catheter (Correct Answer)
- C. Urgent renal ultrasound
- D. Commence intravenous fluid resuscitation with 0.9% saline
- E. Arrange urgent CT abdomen and pelvis with contrast
Explanation: ***Insert a urethral catheter*** - This patient presents with postoperative **acute urinary retention**, evidenced by **oliguria**, **suprapubic fullness**, and a **bladder scan** showing **650 mL** of urine, leading to **post-renal acute kidney injury (AKI)**. - Immediate **urethral catheterization** is the most appropriate management to relieve the **obstruction**, decompress the bladder, and prevent further renal damage. *Administer intravenous furosemide 40 mg* - Administering a **diuretic** like furosemide is contraindicated as it would increase urine production against an already **obstructed outflow tract**, potentially worsening bladder distention and pain. - This intervention fails to address the underlying cause of the patient's **oliguria**, which is mechanical obstruction, not insufficient urine production. *Urgent renal ultrasound* - While a **renal ultrasound** could confirm **hydronephrosis**, the diagnosis of **bladder retention** and its obstructive nature is already clear from the clinical examination and **bladder scan**. - Pursuing further diagnostic imaging at this stage would delay the essential therapeutic intervention of **bladder decompression**, which is the immediate priority. *Commence intravenous fluid resuscitation with 0.9% saline* - **Fluid resuscitation** is indicated for **pre-renal AKI** due to hypovolemia, but this patient's vital signs are stable and the bladder scan confirms adequate urine production. - Providing additional fluids when there is an **outflow obstruction** would exacerbate bladder distention and discomfort without improving urine output or resolving the AKI. *Arrange urgent CT abdomen and pelvis with contrast* - An urgent **CT with contrast** should generally be avoided in patients with a rapidly rising **creatinine** due to the significant risk of **contrast-induced nephropathy**. - This advanced imaging is not immediately necessary as the clinical picture and bladder scan sufficiently identify the **acute urinary obstruction**, requiring immediate catheterization.
Question 30: A 55-year-old woman undergoes parathyroidectomy for primary hyperparathyroidism. Twenty-four hours post-operatively, she develops perioral paraesthesia and carpopedal spasm. Blood tests show: corrected calcium 1.72 mmol/L, phosphate 1.45 mmol/L, magnesium 0.62 mmol/L, PTH 1.2 pmol/L (low). What is the underlying cause of her hypocalcaemia?
- A. Hypoparathyroidism due to inadvertent parathyroid gland removal
- B. Hungry bone syndrome (Correct Answer)
- C. Hypomagnesaemia-induced parathyroid hormone resistance
- D. Vitamin D deficiency
- E. Acute pancreatitis
Explanation: ***Hungry bone syndrome***- Characterized by rapid **skeletal uptake** of calcium, phosphate, and magnesium following **parathyroidectomy** for chronic hyperparathyroidism.- The crucial diagnostic feature in this patient is the combination of **hypocalcaemia** and **low-normal phosphate**, distinguishing it from hypoparathyroidism which typically presents with hyperphosphataemia.*Hypoparathyroidism due to inadvertent parathyroid gland removal*- Removal of glands causes a lack of PTH, leading to **hypocalcaemia** but characteristically results in **high serum phosphate** due to lost renal phosphate excretion.- While the PTH is low in this case, the **low phosphate** levels point specifically toward bone remineralization rather than simple gland loss.*Hypomagnesaemia-induced parathyroid hormone resistance*- Low magnesium levels can cause **functional hypoparathyroidism** by inhibiting the secretion and peripheral action of PTH.- Though magnesium is low (0.62 mmol/L), the immediate **post-operative context** and low phosphate levels are more specific for the rapid mineral flux seen in **hungry bone syndrome**.*Vitamin D deficiency*- While it can contribute to post-operative hypocalcaemia, it usually presents with a **compensatory rise in PTH** (secondary hyperparathyroidism).- The acute onset of **carpopedal spasms** immediately following surgery is more characteristic of the metabolic shift associated with bone hunger.*Acute pancreatitis*- Can cause hypocalcaemia due to **saponification** of calcium in the retroperitoneum, but this patient's history is specific to neck surgery.- The labs do not match the typical presentation of pancreatitis, and there is no mention of the mandatory **epigastric pain** or elevated amylase/lipase.
Practice by Chapter
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free