Health & emergency services

NAPLEX — Cardiovascular and Renal flashcards

10 of 80 cards free to study here · 2 topics · the whole deck is built into Willys

Hypertension (including emergencies and pregnancy), HFrEF guideline classes, anticoagulants, reversal agents and antiplatelets, antiarrhythmic toxicities, lipid agents, antianginals, diuretics, potassium binders and drug choices in CKD — mechanisms, risks and counseling, with no doses.

Learn deck · part of PTCB PTCE / NAPLEX · written against: Top-drug lists and federal pharmacy law as of 2026; PTCE content outline effective 6 January 2026. Updated 2026-10-10.

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  1. A patient with bilateral renal artery stenosis starts lisinopril and the serum creatinine climbs steeply within days. What is the mechanism?
    Glomerular filtration in bilateral renal artery stenosis depends on angiotensin II constricting the efferent arteriole. An ACE inhibitor or ARB removes that support, so GFR falls and acute kidney injury follows.

    Watch out: a small creatinine rise (up to about 30 percent) after starting RAAS blockade is expected; a larger rise needs evaluation.
    Cardiovascular › Hypertension
  2. Why is aliskiren not combined with an ACE inhibitor or ARB in a patient with diabetes?
    Aliskiren is a direct renin inhibitor, and adding it to an ACE inhibitor or ARB in diabetes is contraindicated in its labeling. Dual RAAS blockade raises the risk of hyperkalemia, hypotension and renal impairment without improving outcomes.

    Watch out: an ACE inhibitor plus an ARB is avoided too; trials such as ONTARGET found more hyperkalemia and kidney injury with no outcome benefit.
    Cardiovascular › Hypertension
  3. A patient runs out of clonidine tablets and stops them abruptly. What reaction should the pharmacist anticipate?
    Rebound hypertension with sympathetic overactivity (agitation, headache, tachycardia), because the central alpha-2 agonist was suppressing sympathetic outflow. Clonidine is tapered rather than stopped, and the risk is higher if a beta blocker is continued alone.
    Cardiovascular › Hypertension
  4. A patient on long-term hydralazine develops joint pain, a rash and a positive antinuclear antibody test. What is the likely cause?
    Drug-induced lupus, which is more likely in slow acetylators. Procainamide and isoniazid are other classic causes, and symptoms usually resolve after the drug is stopped.

    Watch out: drug-induced lupus typically shows anti-histone antibodies and rarely involves the kidneys or central nervous system, unlike systemic lupus.
    Cardiovascular › Hypertension
  5. What does oral minoxidil's boxed warning say about pericardial effusion and angina, and which drugs are normally given with it?
    Minoxidil can cause pericardial effusion, which sometimes progresses to tamponade, and can worsen angina. It is reserved for resistant hypertension and given with a beta blocker (to blunt reflex tachycardia) and a diuretic (to counter marked salt and water retention).

    Watch out: hypertrichosis affects roughly 80 percent of patients and is particularly distressing to women and children.
    Cardiovascular › Hypertension
  6. A patient with a severe sulfonamide allergy needs a loop diuretic. Which agent avoids the sulfonamide structure, and what is its drawback?
    Ethacrynic acid, the only loop diuretic without a sulfonamide group. It carries a higher risk of ototoxicity than the others.

    Watch out: true cross-reactivity between sulfonamide antibiotics and sulfonamide diuretics is uncommon.
    Renal › Diuretics
  7. How do loop and thiazide diuretics differ in their effect on urinary calcium, and when does that matter?
    Loop diuretics increase calcium excretion, which is why they help in hypercalcemia once the patient is volume-replete. Thiazides decrease calcium excretion, which helps patients with calcium kidney stones but can unmask hyperparathyroidism and cause mild hypercalcemia.
    Renal › Diuretics
  8. Why is metolazone added to a loop diuretic in diuretic resistance, and what is the main risk?
    The loop diuretic's effect is blunted when the distal nephron reabsorbs more sodium; metolazone blocks that downstream segment, producing sequential nephron blockade and a brisk diuresis. The combination can cause severe hypokalemia, hyponatremia and volume depletion, so electrolytes are checked closely.
    Renal › Diuretics
  9. Why might torsemide or bumetanide be chosen over oral furosemide in a patient with heart failure?
    Oral furosemide has variable and incomplete absorption, especially with gut edema, while torsemide and bumetanide are absorbed far more completely and predictably. Torsemide also has a longer duration of action.
    Renal › Diuretics
  10. Which diuretic class is the classic cause of drug-induced hyponatremia in older women?
    Thiazide diuretics, which impair urinary dilution in the distal tubule. Hyponatremia can appear within weeks of starting and is more likely with low body weight and high fluid intake.
    Renal › Diuretics

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Review status: Second-reader reviewed, with corrections applied.

Checked against:

  • NABP NAPLEX competency statements (topic outline only; no text copied)
  • Checked against FDA prescribing information and standard pharmacotherapy references (reference only; no text copied)
  • Checked against the AHA/ACC hypertension guidelines (2017 and 2025), the 2022 AHA/ACC/HFSA heart failure guideline, the KDIGO 2024 CKD guideline, ACOG guidance on chronic hypertension in pregnancy, and the FDA notice of andexanet alfa's December 2025 US withdrawal (reference only; no text copied)

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