Hello.
Thank you so much for your question. I am so glad you are enjoying the course.
Electrolyte abnormalities also commonly occur as a complication of diuretic treatment. The normal physiologic response to increased sodium and water loss is the stimulation of homeostatic mechanisms that attempt to more vigorously retain sodium and water. Predominant among these mechanisms is the RAAS. Less commonly—although significantly—vasopressin release is sometimes also stimulated by a marked fall in blood pressure secondary to heart disease or diuretic treatment. One of the effects of the stimulation of these homeostatic mechanisms is altered handling of electrolytes. Increased activity of aldosterone will tend to favour sodium retention and potassium loss in the distal nephron. This leads to one of the more commonly observed consequences of loop diuretic administration: hypokalaemia. Hypokalaemia is less likely to be observed in patients if they are concurrently receiving treatments that tend to counteract the RAAS. More widespread use of angiotensin-converting enzyme inhibitors and spironolactone, in addition to loop diuretics, mean that hypokalaemia now is seen less frequently. The situation in which it is now probably most likely to be encountered is during the emergency stabilization of patients where they are likely to receive large doses of furosemide and might not yet have been started on other agents.
Hypokalaemia can contribute to the development, or worsen the symptoms, of hepatic encephalopathy. Hypokalaemia increases proximal tubule ammoniagenesis. Approximately 50% of proximal tubule ammonia production is returned to the systemic circulation via the renal veins.
Hope that helps.
Scott 🙂
