Examkin

Question

Difficulty: MediumMedical History Evaluation

A 71-year-old woman is evaluated in the emergency department for dizziness, decreased urine output, and profound fatigue over the past three days. Her medical history is significant for hypertension, heart failure with reduced ejection fraction, type 2 diabetes mellitus, and osteoarthritis. Two weeks ago, she began taking over-the-counter naproxen for worsening knee pain. Her chronic home medications include lisinopril, furosemide, metoprolol succinate, and sitagliptin. Vital signs show a blood pressure of 98/60 mm Hg and a heart rate of 88/min. Laboratory studies reveal a blood urea nitrogen (BUN) of 56 mg/dL and a serum creatinine of 2.9 mg/dL. A basic metabolic panel one month ago showed a BUN of 18 mg/dL and a serum creatinine of 1.1 mg/dL. During the evaluation of this patient's medical history, which of the following reported medications should be identified as synergistically contributing to her acute kidney injury? (Select all that apply)

  1. NaproxenAnswer
  2. LisinoprilAnswer
  3. FurosemideAnswer
  4. D
    Metoprolol succinate
  5. E
    Sitagliptin

Answer

The medications synergistically contributing to the acute kidney injury are naproxen, lisinopril, and furosemide.
The correct combination of medications involves three distinct mechanisms that synergistically reduce glomerular filtration rate (GFR). Furosemide induces a state of hypovolemia, reducing overall renal perfusion. In a hypovolemic state, the kidneys rely on prostaglandins to dilate the afferent arteriole and angiotensin II to constrict the efferent arteriole to maintain GFR. Naproxen (an NSAID) blocks prostaglandin synthesis, leading to uninhibited afferent vasoconstriction. Concurrently, lisinopril (an ACE inhibitor) blocks angiotensin II production, leading to efferent vasodilation. This combined loss of afferent dilation and efferent constriction, along with volume depletion, leads to a precipitous drop in glomerular hydrostatic pressure and subsequent acute kidney injury.

Step-by-Step Solution

1
Identify the primary clinical problem from the presentation.
The patient has developed acute kidney injury (AKI), evidenced by a significant rise in blood urea nitrogen and serum creatinine.
Establishing the primary diagnosis is required before determining the etiology.
2
Evaluate the patient's medication history for potential nephrotoxic or hemodynamically active agents.
The patient is taking naproxen, lisinopril, and furosemide.
A thorough medical history evaluation must identify drugs that can compromise renal function.
3
Analyze the synergistic mechanisms of the identified medications.
Furosemide causes volume depletion, naproxen causes afferent arteriolar vasoconstriction, and lisinopril causes efferent arteriolar vasodilation. Together, they severely compromise glomerular filtration pressure.
Understanding the combined pharmacokinetic and pharmacodynamic effects confirms the etiology of the AKI.

Key Concept

The synergistic effect of diuretics, NSAIDs, and ACE inhibitors or ARBs (often referred to as the 'triple whammy') can severely compromise renal hemodynamics and precipitate acute kidney injury.
Rate this question

Topics

Medical History Evaluation

More questions from this topic