Examkin

Question

Difficulty: EasyInterpreting Laboratory Results

A 42-year-old man comes to the clinic for follow-up of poorly controlled hypertension. He is currently taking maximum doses of amlodipine and doxazosin. He occasionally experiences muscle weakness and cramps. His blood pressure is 164/100 mm Hg. Physical examination is otherwise unremarkable.

Laboratory studies show:

TestResultReference Range
Sodium146 mEq/L136-145 mEq/L
Potassium2.8 mEq/L3.5-5.0 mEq/L
Chloride103 mEq/L98-106 mEq/L
Bicarbonate31 mEq/L22-28 mEq/L
Blood urea nitrogen14 mg/dL8-20 mg/dL
Creatinine0.8 mg/dL0.7-1.3 mg/dL

Based on the interpretation of these laboratory results, which of the following hormone profiles is most likely in this patient?

  1. Elevated plasma aldosterone concentration and suppressed plasma renin activityAnswer
  2. B
    Elevated plasma aldosterone concentration and elevated plasma renin activity
  3. C
    Suppressed plasma aldosterone concentration and suppressed plasma renin activity
  4. D
    Suppressed plasma aldosterone concentration and elevated plasma renin activity
  5. E
    Normal plasma aldosterone concentration and normal plasma renin activity

Answer

Elevated plasma aldosterone concentration and suppressed plasma renin activity
The correct answer accurately describes the pathophysiology of primary hyperaldosteronism (Conn syndrome). This condition presents classically with hypertension, hypokalemia, and metabolic alkalosis. The autonomous, unregulated secretion of aldosterone from the adrenal gland causes renal sodium retention (leading to volume expansion and hypertension) and simultaneous excretion of potassium and hydrogen ions (leading to hypokalemia and metabolic alkalosis). The resulting volume expansion suppresses the release of renin via the negative feedback mechanism, resulting in a low or suppressed plasma renin activity.

Step-by-Step Solution

1
Interpret the clinical and laboratory abnormalities.
The patient has resistant hypertension, severe hypokalemia, and metabolic alkalosis.
This specific triad of findings strongly points to a state of mineralocorticoid excess.
2
Determine the underlying pathophysiology and its effect on the renin-angiotensin-aldosterone system.
Autonomous aldosterone production causes sodium and water retention, leading to intravascular volume expansion.
Primary hyperaldosteronism (Conn syndrome) is a common cause of secondary hypertension presenting with these exact metabolic derangements.
3
Correlate the pathophysiology with the expected laboratory hormone profile.
The profile will show high aldosterone and low renin.
The autonomously elevated plasma aldosterone concentration drives volume expansion, which is sensed by the juxtaglomerular apparatus, downregulating renin production via negative feedback and leading to suppressed plasma renin activity.

Key Concept

Patients with resistant hypertension accompanied by hypokalemia and metabolic alkalosis should be suspected of having primary hyperaldosteronism, characterized by elevated plasma aldosterone and suppressed plasma renin activity.
Rate this question

Topics

Interpreting Laboratory Results

More questions from this topic