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Hyperaldosteronism 1

Hyperaldosteronism
physiology

Question

Vignette: A 45-year-old man presents to the clinic with complaints of fatigue, weakness, and recurrent episodes of palpitations. He also has noticed increased frequency of urination, particularly at night. His blood pressure is 145/95 mm Hg. Laboratory tests reveal elevated levels of plasma aldosterone and decreased levels of plasma renin. A small mass is detected in the right adrenal gland on abdominal CT scan. Which of the following mechanisms is most likely responsible for this patient's symptoms?

Choices

A) Decreased sodium reabsorption in the distal tubule

B) Increased angiotensin II production

C) Increased potassium excretion in the distal tubule

D) Decreased aldosterone production

E) Increased ADH secretion

Answer

C) Increased potassium excretion in the distal tubule

Explanation

The patient's symptoms and findings suggest primary hyperaldosteronism (Conn's syndrome), most likely due to an adrenal adenoma (as suggested by the mass in the adrenal gland). Aldosterone promotes sodium reabsorption and potassium excretion in the distal nephron. Thus, increased levels of aldosterone lead to increased sodium reabsorption and potassium excretion. The increased sodium reabsorption causes water retention, leading to hypertension and increased urination (especially at night, known as nocturia). The increased potassium excretion can cause hypokalemia, which can cause muscular weakness and cardiac arrhythmias (palpitations). The decreased renin is due to a negative feedback mechanism, as high levels of aldosterone inhibit renin secretion.

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