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USMLE Step 1 Question Breakdown: 34 Year Old Woman with Elevated Blood Pressure

A 34-year-old woman with no significant past medical history presents to clinic for a follow up visit after an elevated blood pressure at her last physical examination. In clinic today, her blood pressure is 160/100. Cardiac examination is unremarkable and all pulses are full and equal. There are no signs of peripheral edema. On laboratory evaluation, plasma renin activity is found to be low and serum creatinine levels are normal. The patient receives an abdominal CT, which reveals bilateral enlargement of the adrenal glands.



Which of the following serum lab values are you likely to see in the patient?

Sodium Potassium pH

  1. Normal High Low
  2. High Low Low
  3. Low Low High
  4. Normal Low High
  5. Low High Low

Approach to this USMLE-Style question:

One of the most important test taking strategies for USMLE Step 1 is to begin building a differential as you go through a question stem. If you are not already coming up with a list of possible diagnoses, you will waste valuable time during your exam blocks. So let’s go through this question line by line and see what information we can use to help shape a differential.

To begin, let’s consider the patient demographics:

Young women are generally a healthy cohort, demonstrated here by an unremarkable medical history. As such, she is highly unlikely to get essential hypertension- the most common cause of high blood pressure. When we see there is evidence of an elevated blood pressure, we should immediately begin thinking about the possibility, or probability, of secondary hypertension.

Now let’s move on to the physical exam findings:

The unremarkable cardiac exam with no evidence of edema tells us that this patient is not fluid overloaded. Full and equal pulses bilaterally helps direct us away from a possible vascular diseases such as fibromuscular dysplasia, which can be seen in this patient population.

The laboratory finding of a low plasma renin activity (PRA) is possibly the most important piece of information in this question stem. If we suspect secondary hypertension in this scenario and renin is elevated, the hypertension is likely due to poor renal blood flow (renal artery stenosis secondary to atherosclerosis or fibromuscular dysplasia, for example). In this scenario, serum creatinine would likely be elevated as well. However, we see a decrease in PRA, meaning that there is likely a defect further along in the RAAS pathway causing this secondary hypertension. Our suspicions are confirmed by the presence of bilateral adrenal hyperplasia. The only adrenal hormone in the RAAS pathway is aldosterone, which we know promotes reuptake of sodium and water. This fits well within our framework of secondary hypertension with low PRA. An increase in cortisol secretion (Cushing’s Syndrome) could also cause hypertension and low PRA, however we do not see any other features of excess cortisol exposure in this patient such as central adiposity (buffalo hump, moon facies), facial plethora, or striae.  

Applying our knowledge to the answer options:

Now that we’ve made our diagnosis, we can turn our attention to the electrolyte and pH changes we’ll see with hyperaldosteronism. Aldosterone acts primarily on the Principal cells of the renal collecting tubule, causing a reuptake in sodium and water. The sodium reuptake causes a negative charge to form in the collecting tubule, which is balanced out by the Principal cell secretion of potassium. The alpha-intercalated cells of the collecting tubule will also secrete hydrogen ions as part of this process. The net result of aldosterone is an increase in sodium reabsorption with an increase in potassium and hydrogen excretion (reflected in serum lab values as low potassium, high pH).

We do not see any evidence of volume overload or dehydration on physical exam, which is important to note because serum sodium levels are a reflection of total body water. We also expect that the kidney will compensate for increase sodium reabsorption by increasing water reabsorption as well, limiting an increase in serum sodium concentration. The resulting intravascular volume will increase both renal blood flow and ANP release, both of which help to lower sodium and intravascular volume levels, preventing any significant change in serum sodium. This concept is known as “aldosterone escape” and is integral to understanding why we do not see hypernatremia or volume overload in cases of hyperaldosteronism. Putting these pieces together, we arrive at the correct answer choice of “D”.