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Question and answer links
- W1: Two protocol office readings are 138/92 and 134/90 mmHg. Using the 2025 AHA/ACC office categories, how is this blood pre · Answer
- W2: A man with hypertension and obesity plans to lose 5 kg. Using the guideline estimate of roughly 1 mmHg systolic reductio · Answer
- Q3: Mr. Hollister, 52, has two protocol office readings averaging 144/91 mmHg. He takes pseudoephedrine most mornings and na · Answer
- Q4: Mr. Hollister's home average is 141/88 mmHg, two weeks off pseudoephedrine and naproxen. On single samples his eGFR is 5 · Answer
- Q5: If you were thinking "primary (essential) hypertension — his weight, salt, alcohol, decongestant and probable sleep apne · Answer
- Q6: Eight weeks after the physical, endocrinology adds spironolactone 25 mg daily. His list is now lisinopril 20 mg, amlodip · Answer
- Q7: At week 15 his electronic chart still carries "CKD stage 3a," auto-entered from visit 1. His eGFR has been 66 and 63 sin · Answer
- Q8: At follow-up, obesity, hypertension, impaired glucose regulation and persistent albuminuria remain on his problem list. · Answer
Session S2 · 2026-10-27 · supplementary · 20 min Anchor: Hypertension — a new diagnosis in primary care · Integrates: CKD screening (UACR, eGFR and chronicity), thiazide electrolyte monitoring, the cheap secondary-cause screen (sleep apnea, decongestant, NSAID, unprovoked hypokalemia), lifestyle with expected mmHg One-line hook: The busiest patient you will see this year has a high blood pressure, three lab values that each look minor, and no time. Read each one against the medication list and the calendar, and one of them changes the diagnosis.
Self-study case. Commit to an answer before you open each folded callout.
Learning Objectives
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8
- Stage an office blood pressure from the average of protocol readings, and confirm it with a 7-day home protocol before labelling or treating.
- Choose a first regimen for confirmed stage 2 hypertension by comorbidity (ACE inhibitor or ARB for albuminuria; a thiazide-like diuretic over hydrochlorothiazide), and counsel lifestyle changes with their expected effect in mmHg.
- Run the cheap secondary-cause screen — decongestant, NSAID, sleep apnea, and a potassium read against the medication list — and prepare a patient correctly for an aldosterone–renin ratio (the preparation is discussed, not tested).
- Predict each diuretic's electrolyte signature and schedule the BMP after starting or changing one.
- Apply the CKD definition — more than 3 months, albuminuria measured by ratio rather than dipstick — before "CKD" goes on a problem list.
Warm-Up (individual commit before the case)
Answers for this section: W1 · W2
W1Which stage?
Two protocol office readings are 138/92 and 134/90 mmHg. Using the 2025 AHA/ACC office categories, how is this blood pressure classified?
Elevated blood pressure, because the average systolic is still below 140
Stage 1 hypertension, because the average systolic falls between 130 and 139
Stage 2 hypertension, because the average diastolic is 90 or higher
Not classifiable, because the two averages fall in two different stages
Show answer and explanation · Link to this question
Correct answer: C
Learning point: Average the readings first: 136/91. Stage 1 is a systolic of 130–139 or a diastolic of 80–89; stage 2 is a systolic of 140 or more or a diastolic of 90 or more. When the two numbers land in different categories, the higher category sets the stage, so a diastolic of 91 makes this stage 2. Why not the others: A — "elevated" is 120–129 with a diastolic under 80; B reads only the systolic; D — the "or" in each definition settles every split reading. Course reading: Evidence for this case
W2Estimating a lifestyle benefit
A man with hypertension and obesity plans to lose 5 kg. Using the guideline estimate of roughly 1 mmHg systolic reduction per kilogram lost, what is a reasonable counseling estimate?
About 5 mmHg lower, with individual response checked by home readings
About 15 mmHg lower, allowing his medication to stop in advance
About 25 mmHg lower, regardless of how much weight he maintains
No meaningful change, unless he reaches a normal body mass index
Show answer and explanation · Link to this question
Correct answer: A
Learning point: Five kilograms × roughly 1 mmHg/kg gives an estimated 5-mmHg systolic reduction. This is an average expectation, not a promise or a reason to stop treatment before measuring the response; diet, exercise and sodium reduction can also help, but their effects should not be added as guaranteed independent benefits. Why not the others: B and C overpromise the effect and medication implications; D dismisses a useful improvement short of normal BMI. Course reading: Evidence for this case
Part 1 — Presentation
Answers for this section: Q3
Mr. Grant Hollister, 52, is the finance chief of a regional freight company. His board requires an executive physical, and this is his first in four years. He feels fine. "I'm here because the board makes me," he says, "and because my wife says I snore like a diesel."
He has no diagnosed medical problems. Four years ago his blood pressure was "a little high" and he was told to recheck it; he did not. He works 60-hour weeks, eats lunch at his desk and dinner in restaurants, and has two or three bourbons most evenings. He golfs every weekend, riding in a cart, and takes naproxen before each round "for the back." He takes extended-release pseudoephedrine most mornings for a stuffy nose. His wife reports loud snoring with pauses in his breathing, and he dozes in afternoon meetings. He has never smoked. His father had hypertension and a stroke at 70.
Vitals. Blood pressure by protocol — 5 minutes of seated rest, back supported, feet flat, arm supported at heart level, a large adult cuff for his 39-cm arm, no talking, two readings a minute apart: 146/92 and 142/90 mmHg (mean 144/91) · Pulse 78 · Resp 14 · SpO₂ 97% on room air · T 36.8 °C · Weight 108 kg · Height 178 cm · BMI 34 kg/m² · Neck circumference 44 cm.
Exam. Crowded oropharynx. Heart regular, no murmur. No abdominal bruit. Femoral pulses full and on time with the radial pulse (no clue to coarctation). No edema. No striae, no moon facies. Fasting screening labs were drawn this morning and will post tomorrow.
Medications (all over the counter)
| Drug | Dose | Route | Frequency | Indication |
|---|---|---|---|---|
| Pseudoephedrine, extended-release | 120 mg | PO | most mornings | Nasal congestion |
| Naproxen sodium | 440 mg | PO | before golf, 2–3 days a week | Low-back pain |
Q3The first visit
Mr. Hollister, 52, has two protocol office readings averaging 144/91 mmHg. He takes pseudoephedrine most mornings and naproxen on golf days, snores with witnessed pauses, and his labs are not back. What is the best plan today?
Start a single-pill ACE inhibitor–thiazide combination, since stage 2 calls for immediate dual therapy
Diet and exercise for 3–6 months, then a drug only if his PREVENT risk is 7.5% or more
Order a renal artery duplex, plasma metanephrines and an adrenal CT before any treatment decision
Stop the pseudoephedrine and naproxen, start a 7-day home BP protocol, and review in 2 weeks
Show answer and explanation · Link to this question
Correct answer: D
Learning point: A mean of 144/91 is stage 2 by office criteria, and confirmed stage 2 is treated at once with two drugs — but one visit is not yet a diagnosis. An office pressure of 130–159/80–99 is the band in which white-coat hypertension (15–30% of high office readings) must be excluded with home or ambulatory readings, and two of his medicines raise pressure: pseudoephedrine constricts arterioles, naproxen retains salt and water. Remove them (saline or steroid nasal spray; acetaminophen or topical diclofenac for golf) and measure what is left. Why not the others: A — the right strategy for confirmed stage 2, applied before confirmation with two pressor drugs still on board; B — the PREVENT 7.5% line decides drug-first versus lifestyle-first only in stage 1; C — imaging before the cheap screen (drug history, sleep questions, potassium) is the expensive way round. Course reading: Evidence for this case
Part 2 — Data
Answers for this section: Q4 · Q5
The screening labs (visit 1, fasting)
| Test | Result | Reference range |
|---|---|---|
| Sodium | 141 | 135–145 mEq/L |
| Potassium | Not reported — specimen hemolyzed; recollect | 3.5–5.0 mEq/L |
| Chloride | 102 | 98–107 mEq/L |
| Bicarbonate | 29 | 22–29 mEq/L |
| Anion gap | 10 | 8–12 mEq/L (Na − [Cl + HCO₃]) |
| BUN | 16 | 7–20 mg/dL |
| Creatinine | 1.45 | 0.7–1.3 mg/dL |
| eGFR (CKD-EPI 2021) | 58 | ≥60 mL/min/1.73 m² |
| Glucose (fasting) | 101 | 70–99 mg/dL |
| Hemoglobin A1c | 5.8 | <5.7 % |
| Calcium | 9.5 | 8.5–10.5 mg/dL |
| TSH | 1.9 | 0.4–4.0 mIU/L |
| LDL cholesterol | 134 | <100 mg/dL |
| Urine albumin-to-creatinine ratio (UACR) | 48 | <30 mg/g |
| Urine dipstick | SG 1.022; protein, blood, glucose, leukocyte esterase and nitrite negative | Negative |
| Urine microscopy | 0–2 RBC/hpf, 0–2 WBC/hpf, no casts | 0–3 RBC, 0–5 WBC/hpf |
Two weeks later (visit 2). He stopped the pseudoephedrine and the naproxen after visit 1. His home readings, taken by protocol on a validated upper-arm monitor — two readings a minute apart each morning and evening for 7 days, day 1 discarded:
| Day | Morning (mean of 2) | Evening (mean of 2) |
|---|---|---|
| 2 | 144/90 | 138/86 |
| 3 | 140/88 | 140/88 |
| 4 | 146/92 | 136/86 |
| 5 | 142/90 | 142/88 |
| 6 | 138/86 | 138/86 |
| 7 | 144/90 | 140/88 |
Home average 141/88 mmHg — above the home threshold of 130/80, so this is sustained hypertension, not white-coat. His wife has filled out the STOP-BANG questionnaire with him (Snoring, Tiredness, Observed pauses, high blood Pressure, BMI, Age, Neck size, male Gender), and nearly every answer is yes; a home sleep study is ordered. You discuss achievable lifestyle changes: sustained weight loss, DASH-style eating, sodium below 2.3 g/day with an ideal limit of 1.5 g/day, regular physical activity, and reducing or eliminating alcohol. Expected responses vary; home readings show his response. A repeat BMP is drawn at 09:40, before he leaves.
Q4The first prescription
Mr. Hollister's home average is 141/88 mmHg, two weeks off pseudoephedrine and naproxen. On single samples his eGFR is 58 and his UACR 48 mg/g; the potassium is being redrawn. Which starting regimen fits him best?
Amlodipine 5 mg alone, adding a second drug in four weeks if needed
Lisinopril 10 mg plus losartan 50 mg, for maximal albuminuria lowering
Lisinopril 10 mg and chlorthalidone 12.5 mg, once the potassium is back
Hydrochlorothiazide 25 mg plus metoprolol succinate 50 mg, both inexpensive
Show answer and explanation · Link to this question
Correct answer: C
Learning point: Confirmed stage 2 hypertension supports two first-line agents. An ACE inhibitor is a reasonable choice with albuminuria, which must be repeated to establish CKD; a thiazide-like diuretic can be a partner. Review the pending potassium before starting either drug and repeat renal function and electrolytes within 1–2 weeks of initiation or dose change in this patient. Why not the others: A delays combination treatment; B combines ACE inhibitor and ARB with avoidable harm; D uses a beta-blocker without a compelling indication and omits a reasonable albuminuria-directed choice. Course reading: Evidence for this case
Q5Evidence update
Concordance-style practice: there is no expert panel behind this key, the teaching explanation. "Unchanged" means the finding does not move the hypothesis — not "I'm not sure."
If you were thinking "primary (essential) hypertension — his weight, salt, alcohol, decongestant and probable sleep apnea explain it," and you then learn that the repeat BMP shows potassium 3.3 mEq/L (no hemolysis) and bicarbonate 30 mEq/L, drawn at 09:40 this morning, before either drug was started, this hypothesis becomes:
Much less likely
Less likely
Unchanged
More likely
Much more likely
Show answer and explanation · Link to this question
Correct answer: B
Learning point: Spontaneous hypokalemia with alkalosis raises concern for primary aldosteronism, so uncomplicated primary hypertension is less satisfactory as the only explanation. Diuretic-associated hypokalemia also supports screening; it should not be dismissed or assigned an arbitrary potassium threshold. Correct potassium and review interfering medicines before interpreting the aldosterone–renin ratio. Why not the others: A is also defensible if the learner explains the magnitude of the shift; B is the suggested response, not an expert-panel score. C underweights the unprovoked finding; D and E move in the wrong direction. Course reading: Evidence for this case
Part 3 — Course and Decisions
Answers for this section: Q6 · Q7 · Q8
Neither drug was started. Mr. Hollister denied diarrhea, licorice and anyone else's pills. For a week he took potassium chloride 20 mEq twice daily and amlodipine 5 mg, a calcium-channel blocker used as a temporary bridge after discussing the screening plan with endocrinology; amlodipine can affect renin and the ratio, so it is not an interference-free drug. With his potassium at 4.1, a morning sample was drawn after 5 minutes seated:
| Test | Result | Reference range |
|---|---|---|
| Plasma aldosterone | 21 | 4–31 ng/dL |
| Plasma renin activity | 0.3 | 0.6–4.3 ng/mL/h |
| Aldosterone-to-renin ratio | 70 | Above 20–30 (cutoff is lab-specific) is a positive screen |
An aldosterone inside its reference range is not normal when renin is suppressed — the ratio is the screen, and his is positive. Lisinopril 10 mg was started after the draw and raised to 20 mg two weeks later; chlorthalidone never was. Endocrinology confirmed primary aldosteronism and discussed medical treatment versus a surgical work-up. CT showed no nodule; that alone does not exclude unilateral disease. He preferred medical treatment, so they did not pursue adrenal vein sampling.
Q6The next-visit check
Eight weeks after the physical, endocrinology adds spironolactone 25 mg daily. His list is now lisinopril 20 mg, amlodipine 5 mg, spironolactone 25 mg, and the potassium chloride 20 mEq twice daily he has taken since the potassium was 3.3. Today his potassium is 4.4 mEq/L and creatinine 1.34 mg/dL. What is your instruction?
Stop the potassium chloride; recheck potassium and creatinine in about a week
Continue all four drugs and recheck the BMP at his three-month visit
Stop the lisinopril, because the spironolactone now protects against his albuminuria
Hold the spironolactone until his potassium has fallen below 4.0 mEq/L
Show answer and explanation · Link to this question
Correct answer: A
Learning point: Spironolactone blocks the aldosterone receptor in the collecting duct, so the kidney stops spending potassium. Its signature is the mirror image of the thiazide's (potassium rises instead of falling), and stacked on an ACE inhibitor, which lowers aldosterone, plus a potassium supplement, it sets up hyperkalemia. The supplement stops the day the MRA starts; potassium and creatinine are checked within about a week, then monthly at first. Why not the others: B — three months is too long to discover a potassium of 6; C — abandons the drug protecting his albuminuria, and an ACE inhibitor plus an MRA is a monitored combination, not a forbidden one; D — 4.4 is normal, and the MRA is the targeted treatment for his disease. Course reading: Evidence for this case
Fourteen and fifteen weeks after the physical — on lisinopril 20 mg, amlodipine 5 mg and spironolactone 25 mg, with no NSAID since visit 1:
| Test | Visit 1 (week 0) | Week 2 | Weeks 14–15 | Reference range |
|---|---|---|---|---|
| Creatinine | 1.45 (on naproxen) | 1.30 | 1.36 | 0.7–1.3 mg/dL |
| eGFR (CKD-EPI 2021) | 58 | 66 | 63 | ≥60 mL/min/1.73 m² |
| UACR | 48 | — | 36 (week 14); 41 on a first-morning repeat (week 15) | <30 mg/g |
| Urine dipstick protein | Negative | — | Negative | Negative |
| Potassium | Hemolyzed | 3.3 | 4.6 (KCl stopped) | 3.5–5.0 mEq/L |
Q7The label on the problem list
At week 15 his electronic chart still carries "CKD stage 3a," auto-entered from visit 1. His eGFR has been 66 and 63 since he stopped naproxen; his UACR was 48 at week 0, then 36 and 41 at weeks 14 and 15, and every dipstick has been negative for protein. Which label is correct?
CKD G3a A2, as recorded from the first visit's eGFR of 58
No CKD, because his eGFR has been above 60 since the naproxen stopped
No CKD, because every urine dipstick has been negative for protein
CKD G2 A2, because his albuminuria has lasted more than 3 months
Show answer and explanation · Link to this question
Correct answer: D
Learning point: CKD is an abnormality of kidney structure or function lasting more than 3 months — a GFR below 60 or a marker of damage such as albuminuria of 30 mg/g or more . His only eGFR under 60 was a single value drawn on naproxen and never repeated, so G3a was never established. His UACR has stayed at 30 mg/g or above on samples more than 3 months apart: CKD by albuminuria with a preserved eGFR — G2 A2, yellow on the KDIGO heat map (moderately increased risk), cause hypertension with primary aldosteronism. Why not the others: A — a stage from one NSAID-affected value with no chronicity; B — forgets that albuminuria alone defines CKD; C — a negative dipstick can miss A2 albuminuria; use the quantitative ratio. Course reading: Evidence for this case
Q8The shared heart–kidney–metabolic risk
At follow-up, obesity, hypertension, impaired glucose regulation and persistent albuminuria remain on his problem list. What does the cardiovascular–kidney–metabolic (CKM) framework add to his care?
It replaces kidney staging with a single cardiac diagnosis
It postpones cardiovascular prevention until heart failure develops
It links these risks so the prevention plan addresses them together
It makes albuminuria irrelevant when creatinine is near normal
Show answer and explanation · Link to this question
Correct answer: C
Learning point: CKM describes interacting metabolic, cardiovascular and kidney risks. Blood pressure, adiposity, glycemia, albuminuria and kidney function should inform one prevention plan, with lifestyle treatment and indicated medicines selected for the individual. CKM framing complements CKD staging and cardiovascular risk assessment; it does not replace either. Why not the others: A removes useful kidney information; B delays prevention; D ignores a marker of kidney and cardiovascular risk. Course reading: Evidence for this case
Resolution and Teaching Points
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8
At week 15 his home average is 126/78 mmHg on three drugs. The sleep study showed moderate obstructive sleep apnea, and he now uses CPAP most nights. He is 5 kg lighter, cooks three dinners a week, and has one bourbon instead of three. Saline spray replaced the pseudoephedrine; acetaminophen replaced the naproxen. His next-visit checklist: the home log, potassium and creatinine monthly for the first months on the ACE inhibitor and MRA, UACR and eGFR at least yearly, CPAP use, weight, and a repeat A1c. Primary care and endocrinology share his care, with nephrology referral if the cause, albuminuria, filtration trend, electrolyte problems or estimated kidney-failure risk warrant it. His board now asks whether the other executives should have their potassium checked.
Clinical Pearl — Confirm before you label An office pressure of 130–159/80–99 earns a 7-day home protocol before it earns a diagnosis: morning and evening, two readings a minute apart, day 1 discarded, the rest averaged; 130/80 or more at home is hypertension. Once stage 2 is confirmed, start two first-line drugs together.
Clinical Pearl — Read the potassium against the drug list Spontaneous or diuretic-associated hypokalemia in hypertension supports primary-aldosteronism screening; a thiazide does not exclude it. The 2025 Endocrine Society guideline suggests screening all people with hypertension.
Clinical Pearl — Prepare the patient before the ratio Correct potassium and obtain morning seated sampling without preceding sodium restriction. Use a specialist-directed medication plan: when safe and necessary, MRAs and other diuretics are withdrawn for four weeks; no-withdrawal strategies also exist. ACE inhibitors, ARBs, beta-blockers and amlodipine can affect interpretation.
Clinical Pearl — Albuminuria picks the first drug; chronicity picks the label Albuminuria makes an ACE inhibitor or ARB a reasonable first-line choice while persistence is assessed. "CKD" waits for the same abnormality after more than 3 months, and the dipstick is never the test for A2.
Clinical Pearl — Every diuretic has a signature Thiazide: low sodium, low potassium, low magnesium, high calcium, high uric acid. Loop: low potassium, magnesium and calcium, with alkalosis. MRA or other potassium-sparing drug: high potassium. Acetazolamide: non-gap acidosis. Check a BMP 1–2 weeks after starting or changing any of them, sooner alongside an ACE inhibitor or ARB.
Pitfall — Treating one number as a diagnosis One office visit, one eGFR, one UACR. Each was a reason to measure again, not a label. The eGFR of 58 was drawn on naproxen, and it vanished.
Pitfall — Replacing the potassium and moving on A low potassium in a hypertensive patient is a question about the kidney and the adrenal, not only a prescription for potassium chloride. And when an MRA starts, the potassium chloride stops.
Concept Links
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8
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: ckd-01, ckd-02, ckd-03, ckd-11, ckd-26, htn-cardiorenal-01, htn-cardiorenal-02, htn-cardiorenal-03, htn-cardiorenal-05, htn-cardiorenal-06, htn-cardiorenal-07, htn-cardiorenal-11, htn-cardiorenal-14, htn-cardiorenal-27, lytes-27.