Case 14: The Young Hypertensive

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.

Session S5 · 2026-11-03 · in-session · 37 min Anchor: Integrative review — secondary hypertension, hypertension in pregnancy and hypertensive emergency, followed over eight years · Integrates: hypokalemic alkalosis as the secondary-HTN clue, primary aldosteronism screen and its confounders, FMD vs atherosclerotic RAS, pheochromocytoma (warm-up), OCP as a substance cause, pregnancy and the kidney, preeclampsia / HELLP, emergency vs severe HTN without target-organ damage One-line hook: A 26-year-old's "a little high" blood pressure at a work physical — and the same woman will test you again at 8 weeks pregnant, at 34 weeks, and on postpartum day five.

Learning Objectives

Answers for this section: Q1 · Q2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12

1. Confirm hypertension with standardized office technique plus a 7-day home protocol, stage it, and decide drug-first versus lifestyle-first by the 2025 AHA/ACC thresholds.
2. Name the secondary-hypertension red flags in a young woman and run the cheap screen: stop the estrogen pill, correct potassium, draw a morning seated aldosterone–renin ratio (a normal potassium does not cancel it) knowing which drugs confound it, and read a urine chloride in hypokalemic alkalosis.
3. Use the renin result to separate an adrenal source of aldosterone from a renal-artery source; distinguish fibromuscular dysplasia from atherosclerotic renal artery stenosis, image with duplex or CT angiography, start medical therapy with a BMP at 1–2 weeks, and know who is referred for revascularization.
4. Manage chronic hypertension in pregnancy: stop the ACE inhibitor the day pregnancy is known, switch to labetalol or nifedipine, and treat at ≥140/90 (reading a pregnancy creatinine, treating asymptomatic bacteriuria and recognizing physiologic hydronephrosis are discussed, not tested).
5. Recognize preeclampsia with severe features and HELLP, treat severe-range blood pressure within 30–60 minutes, and choose the right clock for severe hypertension: mean arterial pressure down by no more than about 25% in the first hour for a non-pregnant adult's emergency, oral treatment when there is no target-organ damage, and the pregnancy rule — and when it applies.

Warm-Up (individual commit before the case)

Answers for this section: Q1 · Q2 · Q3

Three readiness items. They test prerequisite knowledge only; no reasoning is graded from them.

Part 1 — Presentation

Answers for this section: Q4 · Q5

Visit 1 (age 26). Ms. Lindqvist (fictional) is a 26-year-old woman seen in the occupational-health clinic for a pre-employment physical before starting work as a dental hygienist. No complaints. She feels well, runs three times a week, does not smoke, has two glasses of wine on weekends, and uses no recreational drugs, energy drinks, decongestants or licorice. No headaches, palpitations or sweating spells. No snoring. Periods are regular on a combined oral contraceptive she has taken for six years. No prior pregnancies. Family history: mother with hypertension diagnosed at 55; no early strokes, kidney disease or adrenal disease. Her last recorded BP, at a college health visit at 21, was 118/72.

The nurse's first reading, taken while she was still talking, was 171/104. After five minutes seated with back and arm supported and feet flat, a correctly sized cuff and no conversation, readings two and three were 164/98 and 160/98 (average 162/98), heart rate 76, both arms within 4 mmHg. She went home with a validated upper-arm monitor and the 7-day protocol — two readings each morning and evening — and the twenty-four readings from days 2–7 averaged 154/96.

Vitals (visit 1): BP 162/98 (office average) · HR 76 · T 36.8 °C · RR 14 · SpO₂ 99% · Weight 61 kg · Height 168 cm · BMI 21.6.

Exam: thin, comfortable. No moon facies, striae or proximal weakness. Thyroid normal. Lungs clear; heart regular, no murmur. Abdomen soft, with a faint systolic bruit in the epigastrium, best heard with the breath held. Femoral and pedal pulses full and symmetric; no radial–femoral delay. No edema. Fundi: no hemorrhages, exudates or papilledema.

Pause — commit before the reveal

Part 2 — Data

Answers for this section: Q6 · Q7 · Q8

Labs drawn at visit 1, before any antihypertensive, on no diuretic, no laxative, no vomiting.

BUN:creatinine 17:1. Venous pH on a second sample 7.47 (7.35–7.45) with pCO₂ 46 mmHg. Expected pCO₂ for a bicarbonate of 32 is 40 + 0.7 × (32 − 24) ≈ 46 mmHg, so the compensation is appropriate: a simple metabolic alkalosis.

Urinalysis (first-morning, clean catch): SG 1.015 · pH 6.5 · protein negative · blood negative · glucose negative · leukocyte esterase negative · nitrite negative. Microscopy: 0–2 RBC/hpf, 0–2 WBC/hpf, no casts, no crystals. UACR 12 mg/g (A1, <30).

Spot urine electrolytes (same morning): urine sodium 85 mEq/L · urine potassium 42 mEq/L · urine chloride 48 mEq/L.

ECG: sinus rhythm 74, PR 150 ms, QRS 86 ms, QTc 418 ms, no U waves, no LVH by voltage.

Before any hormone level is back, the routine panel already holds the first clue.

Pause — commit before the reveal

Six weeks later. Off the OCP, on amlodipine 5 mg daily and oral potassium chloride 40 mEq daily, her home average is 142/90 and her potassium is 3.9 mEq/L. The hormone pair, drawn seated at 8 a.m.:

Part 3 — Course and Decisions

Answers for this section: Q9 · Q10 · Q11 · Q12

Imaging. Renal duplex ultrasound: right kidney 11.0 cm, left 10.8 cm (no asymmetry), normal cortical thickness both sides. Right renal artery peak systolic velocity 265 cm/s (above 180–200 suggests stenosis), renal-to-aortic ratio 3.9 (above 3.5 is significant), with a beaded, irregular mid-to-distal segment; left artery normal. CT angiography (urine hCG negative the same morning; creatinine 0.7): multifocal alternating stenoses and small aneurysmal dilations of the mid and distal right main renal artery — the "string of beads" — with maximal narrowing about 70%; no ostial plaque, a smooth aorta, a normal left renal artery, normal adrenal glands.

What happened next. BMP at day 10 on lisinopril 10 mg: creatinine 0.8 mg/dL (a 14% rise — accepted), potassium 4.1 mEq/L; KCl stopped. At six weeks, home average 126/80 on lisinopril 10 mg and amlodipine 5 mg. She met the vascular team, understood that angioplasty might let her stop medication, and chose to defer it while she settled into the new job; she agreed to revisit the decision in a year and to use a progestin-only method. Amlodipine came off at one year; lisinopril was titrated to 20 mg. She never came back for the angioplasty conversation.

Visit 2 (age 29, three years later) — the obstetric clinic. She is eight weeks pregnant by dates — planned, but sooner than expected. Still on lisinopril 20 mg daily. No headache, no visual symptoms, no dysuria. Office BP 138/88 (standardized, average of two), HR 84.

Three findings the student neither over-treats nor under-treats. Her 8-week creatinine of 0.9 mg/dL reads "normal" on the lab slip, but pregnancy raises GFR by 40–50% and usually lowers creatinine, so 0.9 warrants review against baseline and repeat measurement rather than reassurance from the nonpregnant reference interval; her bicarbonate of 21 is pregnancy's normal compensation for a mild respiratory alkalosis, not an acidosis. At the 12-week visit the routine prenatal urine culture grows E. coli >10⁵ CFU/mL, and a repeat specimen grows the same organism; she has no dysuria, frequency, fever or flank pain. This is asymptomatic bacteriuria — bacteria without symptoms — and pregnancy is one of the two situations (the other is before endourologic procedures associated with mucosal trauma) in which it is screened for and treated, because in pregnancy it can progress to pyelonephritis, and pyelonephritis in pregnancy is admitted. She receives cephalexin 500 mg PO every 6 hours for 5 days; fosfomycin 3 g PO as a single dose is the alternative. Nitrofurantoin is avoided near term and when eGFR is below 30; trimethoprim and fluoroquinolones are avoided in pregnancy. At 20 weeks an obstetric ultrasound notes "mild right hydronephrosis." She is asymptomatic, the creatinine is unchanged, and no stone is seen. This is the physiologic dilation of pregnancy — right more than left, present in 80–90% of third-trimester kidneys, gone 4–6 weeks after delivery — so it is documented and left alone: no CT, no stent, no urology referral.

Visit 3 (34 weeks) — labor and delivery triage. Two days of a frontal headache that acetaminophen does not touch, and since this morning a steady ache under the right ribs. No visual scotomata, no seizures, no vaginal bleeding; fetal movements present. On labetalol 200 mg BID and aspirin 81 mg daily (started by her obstetrician at 12 weeks for preeclampsia prophylaxis). BP 168/112; repeated at 15 minutes, 170/110. HR 92. RUQ tender; brisk reflexes without clonus; 1+ pretibial edema; lungs clear; SpO₂ 98%.

Naming it. Preeclampsia is new hypertension ≥140/90 after 20 weeks with either proteinuria ≥0.3 g/g — quantified by a urine protein-to-creatinine ratio (UPCR), not a dipstick — or new organ dysfunction. She has chronic hypertension, so this is preeclampsia superimposed on it, with severe features: BP ≥160/110, headache, right-upper-quadrant pain, platelets under 100,000 and transaminases more than twice normal. Low platelets, high transaminases, and schistocytes with a high LDH are HELLP — hemolysis, elevated liver enzymes, low platelets — a variant of severe preeclampsia. Her UPCR of 0.9 g/g is proteinuria (≥0.3), not nephrotic range (>3.5 g/g); the dipstick 2+ was only a screen.

Course. IV labetalol brought her to 146/94 within 40 minutes; magnesium was started; she delivered a 2,140-g girl by cesarean the next morning after a failed induction. Platelets reached a nadir of 78,000 on postpartum day 1 and then recovered; AST was normal by day 4, and she went home that afternoon on labetalol 200 mg BID and extended-release nifedipine 30 mg daily, with instructions to check her BP twice a day.

Postpartum day 5 — the emergency department. She returns with a pounding headache since the night before, "like at 34 weeks." She has taken every dose of both drugs. BP 184/118; repeated at 15 minutes, 180/116. HR 88. Awake, oriented, speech normal; no visual symptoms, no scotomata, no RUQ pain, no shortness of breath, no chest pain. Neurologic exam normal, no clonus, fundi without papilledema or hemorrhage. Lungs clear. Platelets 168,000/µL, AST 38 U/L, creatinine 0.8 mg/dL, UPCR 0.4 g/g (falling), hemoglobin 10.2 g/dL. Non-contrast head CT, ordered for the headache, is normal.

Pause — commit before the reveal

Resolution and Teaching Points

Answers for this section: Q1 · Q2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12

She received IV labetalol 20 mg and then 40 mg; at 50 minutes her BP was 148/96 and the headache had eased. Magnesium sulfate ran for 24 hours; platelets, transaminases and creatinine repeated at six hours were unchanged; and extended-release nifedipine was increased to 60 mg daily. Her BP was checked every other day for two weeks and weekly to 12 weeks. By six weeks she was on nifedipine alone at 124/80, and her UPCR was 0.1 g/g at 10 weeks. She breastfed; enalapril (the ACE inhibitor preferred while nursing) replaced nifedipine at four months, and she chose a copper IUD — no estrogen again.

At the 12-week postpartum visit the conversation she had deferred at 26 was reopened. The right renal artery FMD was re-imaged, she chose balloon angioplasty, her pressure fell over the following months, and the ACE inhibitor was tapered off. At 34 — eight years after the work physical — her BP is 122/78 on no medication, creatinine 0.8 mg/dL (eGFR 99), UACR 15 mg/g. She is planning a second pregnancy and knows three things before she conceives: her recurrence risk is increased and needs individualized counseling; her obstetrician will restart low-dose aspirin at 12 weeks; and any ACE inhibitor or ARB should be reviewed and changed before a planned pregnancy; an unexpected positive test requires prompt cessation and clinical review. She also knows that a woman who has had preeclampsia carries a lifelong excess of cardiovascular disease and chronic kidney disease, which is why her blood pressure, UACR and creatinine are checked every year.

Clinical Pearl — Hypertension at 26 is a work-up, not a diagnosis Onset before 30 (or after 50), a young woman, hypokalemia, a bruit, resistant hypertension, paroxysms, flash pulmonary edema, asymmetric kidneys: any one is a reason to ask why. The cheap screen is a medication and substance history (OCP, NSAIDs, decongestants, stimulants, licorice, energy drinks), a BMP and a UA with UACR. Screen for primary aldosteronism with an aldosterone–renin ratio when there is resistant hypertension, a low potassium (spontaneous or on a diuretic), an adrenal nodule or early-onset hypertension — and never let a normal potassium cancel it: most people with primary aldosteronism have one.

Clinical Pearl — Hypokalemic alkalosis: let the urine chloride sort it Potassium low, bicarbonate high. Urine chloride under 20: the body is chloride- and volume-depleted (vomiting, a diuretic that has worn off, contraction) — saline and KCl fix it. Urine chloride 20 or above: something is still driving the collecting duct, and saline will not fix it; blood pressure splits the group — high in mineralocorticoid excess, normal or low with a diuretic still in use or Bartter/Gitelman syndrome. Replete magnesium first if it is low, or the potassium will not stay up.

Clinical Pearl — Renin is the fork in the road High aldosterone with suppressed renin supports autonomous adrenal production when assay thresholds, potassium and medication context fit. High renin shifts the differential toward secondary activation but is not specific to renal artery stenosis. A beaded mid-to-distal renal artery in a young adult supports FMD; selected angioplasty may improve or sometimes cure hypertension, with variable success. Atherosclerotic disease has a different risk profile and is generally managed medically, with selective revascularization decisions.

Clinical Pearl — Pregnancy rewrites the reference ranges Pregnancy lowers usual creatinine values, so assess an apparently normal result against the pregnancy context and prior values. eGFR equations are not validated for pregnancy. Confirm concerning changes and involve obstetrics/nephrology. Review ACE inhibitors and ARBs before conception and stop promptly if pregnancy occurs; use pregnancy-appropriate BP treatment.

Clinical Pearl — Two clocks for severe hypertension Non-pregnant adult at ≥180/120: ask about acute target-organ damage. Yes = emergency — IV nicardipine or labetalol, MAP down by no more than about 25% in hour one (aortic dissection and severe preeclampsia have their own targets). No = oral agent and 1–2-week follow-up; IV treatment harms. Pregnant or postpartum at ≥160/110 for 15 minutes: treat within 30–60 minutes to 140–150/90–100 whatever the symptoms; a headache or RUQ pain is a severe feature, and magnesium sulfate follows.

Pitfall — Imaging the adrenal before the biochemistry, or blocking the receptor before the draw Correct potassium and interpret aldosterone with renin, assay units, medication effects and pretest probability. Amlodipine can be practical during evaluation but is not a guarantee of an unconfounded ratio. Repeat a negative or equivocal screen when suspicion remains high; biochemical evaluation precedes adrenal localization.

Pitfall — Applying the adult "asymptomatic severe hypertension" rule to a postpartum woman "Headache only, normal exam, normal CT — oral meds and see her in two weeks" is the correct discharge for a 55-year-old man. For a woman five days after HELLP it is the discharge that precedes a seizure. Context decides the clock.

Concept Links

Answers for this section: Q1 · Q2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12

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: glom-04, htn-cardiorenal-01, htn-cardiorenal-02, htn-cardiorenal-03, htn-cardiorenal-04, htn-cardiorenal-06, htn-cardiorenal-08, htn-cardiorenal-11, htn-cardiorenal-12, htn-cardiorenal-13, htn-cardiorenal-14, htn-cardiorenal-15, htn-cardiorenal-18, lytes-11, lytes-25, structural-16, structural-17.