Commit to an answer before revealing the explanation. Use the section menu to navigate; each question and answer has its own link. Five-option evidence updates ask for the most defensible direction of change; discuss a justified adjacent response.
Save and export your first responses
First choices and optional confidence stay in this browser and are not sent to the website. Opening an explanation first is recorded. Revisiting an unchanged case preserves the first response; revised cases receive a new version. Website visit analytics are separate. On a shared device, export and clear the history when finished.
Sections in this case
Question and answer links
- W1: A 76-year-old man with BPH, on no prostate medicine, urinates every hour, can barely hold it and gets up five times a ni · Answer
- W2: A 68-year-old woman, unwell for two weeks: sodium 138, chloride 114, bicarbonate 16 mEq/L, albumin 4.0 g/dL; urine sodiu · Answer
- Q3: Leonard, 79: confused, three days of overflow dribbling, a tender bladder palpable to the umbilicus, bladder scan about · Answer
- Q4: Leonard at 14:10: potassium 5.6 mEq/L with a normal ECG; chloride 109, bicarbonate 18, anion gap 10; arterial pH 7.33 wi · Answer
- Q5: Leonard at 19:00: urine output 420, 360, 330, 310 and 300 mL in the five hours since the 950-mL residual drained; BP 138 · Answer
- Q6: If, on arrival — confused, with cloudy catheter urine, pyuria and a positive nitrite — you were thinking "urosepsis," an · Answer
- Q7: Day 3: Leonard is alert; creatinine 1.7 mg/dL and falling; output 110 mL/h; drinking well. BP 146/82 lying and 130/76 af · Answer
Session S4 · 2026-10-29 · supplementary · 20 min Anchor: Acute kidney injury — post-renal AKI from urinary retention (benign prostatic hyperplasia, BPH) · Integrates: geriatric prescribing (anticholinergics), catheter-associated bacteriuria, post-obstructive diuresis, the hyperkalemia and normal-anion-gap acidosis of obstruction, bladder and renal imaging One-line hook: An urgent care treated his frequency as an overactive bladder. Now he is confused, and his creatinine has tripled.
Learning Objectives
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q7
- Recognize post-renal AKI from bladder-outlet obstruction — a palpable bladder, overflow dribbling, a rising creatinine — and decompress with a urethral catheter first.
- Name the drugs that tip an enlarged prostate into retention (anticholinergics such as oxybutynin and diphenhydramine, decongestants, opioids) and deprescribe them.
- Explain the hyperkalemia and normal-gap acidosis of obstruction, calculate the anion gap and urine anion gap, and treat both by relieving the obstruction.
- Manage post-obstructive diuresis: what to replace, what to measure and when to stop.
- Separate catheter bacteriuria from infection, and plan the alpha-blocker and voiding trial at discharge (the drug-dosing review is discussed, not tested).
Warm-Up (individual commit before the case)
Answers for this section: W1 · W2
Two readiness questions. Commit to an answer before you open each reveal.
W1Before the bladder pill
A 76-year-old man with BPH, on no prostate medicine, urinates every hour, can barely hold it and gets up five times a night. Before anyone treats this as an overactive bladder, what comes first, and why?
A trial of oxybutynin at the lowest dose, because frequency and urgency come from an overactive bladder muscle that antimuscarinics relax
A post-void residual by bladder scan, because frequent small voids can be overflow from a bladder that never fully empties
A PSA and urine cytology, because new frequency and urgency in an older man should be treated as cancer until proven otherwise
An evening fluid limit and a recheck in three months, because nocturia in BPH usually responds to lifestyle changes alone
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Frequency, urgency and nocturia are storage symptoms an obstructed outlet produces by itself: a bladder that never empties is always nearly full, so it signals often and spills small amounts (overflow). Anticholinergics — oxybutynin, and the diphenhydramine in "PM" sleep aids — relax the bladder muscle and can turn partial retention into complete retention. A bladder scan after he voids settles it in a minute; interpret the residual with symptoms and repeated measurements; no single cutoff defines all clinically important retention. Why not the others: A — the prescribing cascade: a drug for the symptom that worsens its cause. C — cancer screening neither explains nor relieves a full bladder. D — reasonable later, but it leaves a possible retention unmeasured for three months. Course reading: Evidence for this case
W2Which acid, which kidney?
A 68-year-old woman, unwell for two weeks: sodium 138, chloride 114, bicarbonate 16 mEq/L, albumin 4.0 g/dL; urine sodium 30, potassium 25, chloride 75 mEq/L. What are her anion gap and urine anion gap, and where do they point?
Anion gap 24 — a high-gap acidosis from an unmeasured acid such as lactate; check a lactate and draw blood cultures
Anion gap 8, urine anion gap +20 — a normal-gap acidosis in which the kidney is failing to excrete acid
Anion gap 8, urine anion gap −20 — a normal-gap acidosis with bicarbonate lost outside the kidney, as in diarrhea
Anion gap 8, urine anion gap −20 — a normal-gap acidosis in which the kidney cannot make enough ammonium
Show answer and explanation · Link to this question
Correct answer: C
Learning point: The serum gap is 138 − (114 + 16) = 8; the urine gap is (30 + 25) − 75 = −20. In this simplified normal-gap acidosis, a negative urine gap supports ammonium excretion and an extrarenal bicarbonate loss such as diarrhea. It is an indirect clue, not an ammonium measurement; ketonuria, other urinary anions and very low urine sodium can invalidate the shortcut. Why not the others: A miscalculates the serum gap; B reverses the urine-gap sign; D assigns low ammonium to a pattern usually associated with its excretion. Clinical context remains necessary. Course reading: Evidence for this case
Part 1 — Presentation
Answers for this section: Q3
Leonard is a 79-year-old retired grain-elevator manager brought in by his daughter. He has had BPH for ten years; he stopped his tamsulosin 14 months ago after he got lightheaded getting up at night and nearly fell. This month he has urinated every hour and up to five times a night. Two weeks ago he began an over-the-counter diphenhydramine sleep aid, and ten days ago an urgent care diagnosed "overactive bladder" and prescribed oxybutynin. For three days he has dribbled urine constantly while passing little in the toilet, his lower belly has ached, and he has barely eaten. Since yesterday he has been confused, picking at the sheets. No fever, chills, flank pain or burning.
Past history: BPH; atrial fibrillation; hypertension; post-herpetic neuralgia after shingles two years ago; hyperlipidemia. Creatinine 1.2 mg/dL eight months ago (eGFR 62 at steady state). Social: lives with his wife; former smoker; no alcohol.
Vitals: T 36.9 °C · heart rate 96, irregularly irregular · BP 152/88 · respiratory rate 16 · SpO₂ 96 % on room air · weight 72 kg.
Exam: drowsy, oriented to name only. Pupils 5 mm and sluggish; mouth and skin dry and warm. Lungs clear. A tender, firm midline mass rises from the pubis to the umbilicus, dull to percussion. No flank tenderness. Rectal: smooth, symmetrically enlarged, non-tender prostate without nodules. Trousers soaked with urine. No edema.
| Drug | Dose | Route | Frequency | Indication |
|---|---|---|---|---|
| Apixaban | 5 mg | PO | twice daily | Atrial fibrillation |
| Amlodipine | 5 mg | PO | once daily | Hypertension |
| Gabapentin | 300 mg | PO | three times daily | Post-herpetic neuralgia |
| Atorvastatin | 20 mg | PO | nightly | Hyperlipidemia |
| Oxybutynin (new, 10 days) | 5 mg | PO | twice daily | "Overactive bladder" (urgent care) |
| Diphenhydramine (OTC, 2 weeks) | 50 mg | PO | at bedtime | Sleep |
Bedside bladder scan: about 900 mL. First labs (13:40): creatinine 3.6 mg/dL (1.2 eight months ago) — 3.6 ÷ 1.2 = 3.0× the last known baseline, presumed stage 3 AKI if the rise occurred within seven days; intervening CKD is not excluded by an eight-month-old value; eGFR not valid — creatinine is moving; BUN 64 mg/dL; potassium 5.6 mEq/L. ECG: atrial fibrillation at 96, normal QRS, no peaked T waves.
Q3The first move
Leonard, 79: confused, three days of overflow dribbling, a tender bladder palpable to the umbilicus, bladder scan about 900 mL, creatinine 3.6 mg/dL (1.2 eight months ago), potassium 5.6 mEq/L with a normal ECG; oxybutynin for 10 days, diphenhydramine nightly for 2 weeks. What is the first move?
Renal ultrasound and a nephrology consult before any catheter, because a creatinine of 3.6 may be intrinsic kidney disease
Two liters of IV fluid for prerenal AKI from poor intake, then a voiding trial in the morning once he is rehydrated
Start tamsulosin now and rescan the bladder after he tries to void, to avoid catheterizing a confused 79-year-old man
A urethral catheter now, measuring what drains; stop oxybutynin and diphenhydramine; recheck the BMP in a few hours
Show answer and explanation · Link to this question
Correct answer: D
Learning point: Painful high-volume retention needs prompt drainage and withdrawal of aggravating anticholinergics. It strongly suggests a postrenal contribution, which the subsequent ultrasound and improvement support; the bladder scan alone does not prove that obstruction is the only AKI cause. Recheck potassium and kidney function and monitor urine output after drainage. Why not the others: A delays relief for imaging; B delays drainage, although coexisting volume depletion may still need treatment; C relies on a medicine too slow to relieve current severe retention. Calcium is not routinely indicated for this moderate potassium with a normal ECG, but continued surveillance is essential. Course reading: Evidence for this case
Part 2 — Data
Answers for this section: Q4 · Q5 · Q6
The catheter went in at 14:10 and drained 950 mL of cloudy urine — his true post-void residual. The ED physician sent it for analysis and culture, drew blood cultures and wrote: "Confused elder, pyuria — ?urosepsis. Antibiotics if febrile or hypotensive."
| Test (13:40) | Result | Reference range |
|---|---|---|
| Sodium (mEq/L) | 137 | 136–145 |
| Potassium (mEq/L) | 5.6 | 3.5–5.0 |
| Chloride (mEq/L) | 109 | 98–107 |
| Bicarbonate (mEq/L) | 18 | 22–28 |
| Anion gap, Na − (Cl + HCO₃) (mEq/L) | 137 − (109 + 18) = 10; albumin-corrected 10 + 2.5 × (4.0 − 3.8) = 10.5 | 8–12 |
| Albumin (g/dL) | 3.8 | 3.5–5.0 |
| BUN : creatinine | 64 : 3.6 = 18 : 1 | 10–20 : 1 |
| WBC (× 10⁹/L) / hemoglobin (g/dL) | 8.4 / 13.0 | 4.0–11.0 / 13.5–17.5 |
| Arterial pH / pCO₂ (mmHg) | 7.33 / 35 | 7.35–7.45 / 35–45 |
Winter's formula: expected pCO₂ = 1.5 × 18 + 8 = 35 ± 2; his is 35 — appropriate compensation for a normal-gap metabolic acidosis.
| Urine (catheter specimen, 14:10) | Result | Reference |
|---|---|---|
| Appearance / specific gravity | cloudy / 1.010 | clear / 1.005–1.030 |
| pH | 5.5 | 4.5–8.0 |
| Protein / blood | trace / 1+ | negative |
| Leukocyte esterase / nitrite | 2+ / positive | negative |
| Microscopy | WBC 20–30/hpf; RBC 3–5/hpf; many bacteria; no casts | WBC 0–5; RBC 0–2 |
| Urine sodium / potassium / chloride (mEq/L) | 40 / 18 / 38 | varies |
| Urine anion gap, (Na + K) − Cl | (40 + 18) − 38 = +20 | zero or negative |
| Culture | pending | — |
Renal and bladder ultrasound (16:00, after drainage): both kidneys 11 cm with moderate hydronephrosis on both sides and normal cortex; bladder wall thickened and trabeculated — the mark of an outlet narrowed for a long time; prostate about 60 g.
Why did his creatinine rise at all? Both kidneys drain into one bladder, so a blocked outlet backs pressure up both ureters at once and leaves no healthy kidney to compensate — the physiology of the stone in CBL-11's only kidney.
Q4The potassium and the acid
Leonard at 14:10: potassium 5.6 mEq/L with a normal ECG; chloride 109, bicarbonate 18, anion gap 10; arterial pH 7.33 with pCO₂ 35; urine anion gap +20; the catheter now draining. What explains the potassium and the acid, and what treats them?
Back-pressure has injured the collecting ducts, which cannot secrete potassium or acid (type-4-like); drainage treats both
Lactic acidosis from urosepsis has shifted potassium out of cells; draw a lactate, start broad antibiotics and a bicarbonate drip
Bicarbonate lost from the gut after days of poor intake; give oral sodium bicarbonate, and IV calcium gluconate for the potassium
A hemolyzed sample plus a respiratory acidosis from the sleep aid; repeat the potassium and hold every sedating drug overnight
Show answer and explanation · Link to this question
Correct answer: A
Learning point: Obstruction can impair distal potassium and acid excretion, producing a type-4-like hyperkalemic normal-gap acidosis. The positive urine gap supports this interpretation in context, but does not directly prove low ammonium, particularly in changing kidney function. Drain the obstruction and reassess the biochemical response. Why not the others: B is less supported by the clinical picture, but a normal anion gap alone does not exclude elevated lactate; C has no history of gastrointestinal bicarbonate loss and gives unnecessary calcium; D contradicts the appropriately compensated blood gas. Worsening potassium needs escalation regardless of the initial normal ECG. Course reading: Evidence for this case
Q5Three hundred milliliters an hour
Leonard at 19:00: urine output 420, 360, 330, 310 and 300 mL in the five hours since the 950-mL residual drained; BP 138/78, heart rate 88; still drowsy and only sipping; sodium 138, potassium 4.9 mEq/L, creatinine 3.1 mg/dL. What is the plan for tonight?
Replace each hour's output milliliter for milliliter with 0.9 % saline, so that a drowsy man cannot fall behind overnight
Provide individualized partial fluid replacement while he cannot drink, with close volume, urine-output and electrolyte reassessment
Furosemide 20 mg IV to keep the diuresis brisk and wash out the remaining potassium while both kidneys are still draining
No IV fluid and no labs until morning: this is the kidney unloading retained salt and water, and it will stop on its own
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Sustained output above 200 mL/h after relief of obstruction calls for monitoring for volume and electrolyte losses. Because he cannot drink reliably, give individualized replacement guided by examination, sodium and losses; a partial replacement fraction is a starting approach, not a universal formula. Fluid composition and frequency of labs must follow the trajectory. Why not the others: A automatically replaces every milliliter without assessing needs; C augments an existing diuresis; D ignores his inability to replace losses. If hypotension or hypovolemia develops, resuscitation takes priority over any fixed fraction. Course reading: Evidence for this case
Day 3 — the culture comes back
By the next morning Leonard asked for his hearing aids and the sports page: the confusion had cleared, and the ache in his lower belly had gone with the urine. His output fell to 150–200 mL/h on day 2 and 110 mL/h on day 3, when he was drinking well and the IV replacement stopped. Day 2: potassium 3.9, magnesium 1.6 mg/dL (replaced by mouth), bicarbonate 21, creatinine 2.2. Day 3: creatinine 1.7.
On day 3 the laboratory calls: the catheter urine grew more than 100,000 CFU/mL of Klebsiella pneumoniae. Blood cultures: no growth at 48 hours. His highest temperature has been 37.3 °C, his white count 8.4 → 7.9 × 10⁹/L, his blood pressure steady; no antibiotic has been given.
Q6Evidence update
Concordance-style practice — no expert panel stands behind the key. "Unchanged" means the finding does not move the hypothesis.
If, on arrival — confused, with cloudy catheter urine, pyuria and a positive nitrite — you were thinking "urosepsis," and you then learn that the catheter urine grew more than 100,000 CFU/mL of Klebsiella after 48 hours without fever, with a normal white count, negative blood cultures, and confusion and belly ache that cleared once the bladder was drained and the anticholinergics stopped, this hypothesis becomes:
Much less likely
Less likely
Unchanged
More likely
Much more likely
Show answer and explanation · Link to this question
Correct answer: A
Learning point: A positive culture sounds like confirmation; that is the trap. Bacteriuria is common with impaired emptying, and without localizing symptoms or systemic signs that is asymptomatic bacteriuria, which IDSA 2019 advises not to treat; the pyuria travels with it. Urosepsis needs a body responding to infection — for 48 hours there was none — and the confusion and belly ache had a better explanation that resolved without antibiotics. New fever, flank pain or rigors require prompt reassessment for symptomatic infection. A planned endourologic procedure expected to cause mucosal trauma is a separate indication for culture-directed peri-procedural treatment. Why not the others: B is acceptable if the student explains that infection is less likely but continued reassessment is needed. C fails to update after an alternative explanation resolves without antibiotics; D and E confuse a positive culture with a clinical infectious syndrome. Course reading: Evidence for this case
Part 3 — Course and Decisions
Answers for this section: Q7
Before discharge: BP 146/82 lying, then 134/78 at 1 minute and 130/76 at 3 minutes standing, without symptoms.
Q7The prostate, the catheter and the pills
Day 3: Leonard is alert; creatinine 1.7 mg/dL and falling; output 110 mL/h; drinking well. BP 146/82 lying and 130/76 after 3 minutes standing, without symptoms. He stopped tamsulosin last year after lightheaded nights; his prostate is about 60 g. Which discharge plan is right?
Remove the catheter today and avoid alpha-blockers, since tamsulosin made him dizzy; restart oxybutynin at half dose for urgency
Start doxazosin 4 mg tonight because it treats his blood pressure too, and remove the catheter tomorrow morning before he leaves
Tamsulosin 0.4 mg after the same daily meal with fall precautions; catheter for a planned trial after at least 3 days; urology review
Start finasteride alone, which shrinks the prostate within a week; keep the catheter until urology sees him; treat the Klebsiella
Show answer and explanation · Link to this question
Correct answer: C
Learning point: Restarting at 0.4 mg approximately 30 minutes after the same meal follows the tamsulosin label. Prior dizziness still matters even if today’s drop misses the orthostatic threshold: discuss falls, reassess standing symptoms and other BP medicines. AUA advises at least three days of alpha-blocker treatment before a trial without catheter; the enlarged gland and renal complication warrant urology review for additional medical or procedural treatment. Why not the others: A restarts a contributor to retention; B starts doxazosin at an unsafe initial dose and schedules an early trial; D expects finasteride to act within a week and treats asymptomatic bacteriuria without a procedural indication. Course reading: Evidence for this case
Resolution and Teaching Points
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q7
Leonard went home on day 4 with the catheter on a leg bag, tamsulosin 0.4 mg after the same evening meal with early standing-BP/symptom follow-up and an avoid-unless-reviewed list: oxybutynin, diphenhydramine and the "PM" sleep aids that contain it, and decongestants such as pseudoephedrine. His creatinine was 1.6 mg/dL. Gabapentin — cut to 100 mg at bedtime on admission, because it accumulates as filtration falls — went back to 300 mg at bedtime, for his primary clinician to re-titrate against the label. During AKI, the team reviewed anticoagulation, renal function and bleeding risk daily. At discharge, apixaban was 5 mg twice daily: the label lowers the dose only when two of three are present — age 80 or older, weight 60 kg or less, creatinine 1.5 mg/dL or more — and he had one (AF anticoagulation review — FDA label row).
A week later he voided 280 mL with a residual of 90 mL; the catheter stayed out and urology added finasteride. At six weeks his creatinine was 1.4 mg/dL on two checks three weeks apart. Now that it is steady, the eGFR means something: CKD-EPI 2021 gives 51 mL/min/1.73 m², and Cockcroft–Gault, the estimate specified by some drug labels, gives a clearance of about 44 mL/min at 72 kg. He is not labeled CKD until the three-month creatinine and urine albumin-to-creatinine ratio are back. His BP was 138/80 lying and 128/76 standing.
Clinical Pearl — A palpable bladder is a diagnosis A painful distended bladder with AKI demands prompt retention assessment and drainage when confirmed, followed by output, electrolyte and imaging assessment; mixed AKI causes can coexist.
Clinical Pearl — Overflow wears the costume of an overactive bladder In an older man with BPH, frequency, urgency and dribbling get a bladder scan before any antimuscarinic.
Clinical Pearl — Obstruction acidifies like type 4 High potassium, a normal-gap acidosis and a positive urine anion gap come from an injured collecting duct. Drainage is the treatment.
Clinical Pearl — Post-obstructive diuresis is mostly the kidney doing its job Use clinical status, urine losses and serial sodium, potassium and magnesium to individualize fluid replacement, especially while oral intake is unreliable. Avoid an automatic fluid type or fraction.
Clinical Pearl — A catheter bladder grows bacteria Treat symptoms and systemic signs, not cultures.
Pitfall — Treating the culture Antibiotics for catheter bacteriuria in an afebrile, improving man buy resistance, C. difficile and drug reactions, and treat nothing.
Pitfall — Dosing to the admission numbers A rising creatinine overstates filtration and a falling one understates it: dose renally cleared drugs to the trend, not the admission value, and once it is steady dose apixaban by its label criteria, not by age or eGFR alone.
Concept Links
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q7
Assigned reading: the explanations in this case and the question-linked course evidence guide. The objective map distinguishes tested decisions from concepts taught in explanations.
Concepts: aki-01, aki-07, aki-17, aki-18, lytes-13, lytes-14, lytes-23, lytes-24, structural-04, structural-06, structural-08, structural-18, structural-25.