Where does the anion gap calculation come from and why does it always make us think of piles of mud? What's an easy way to categorize causes of metabolic acidosis as you're forming a differential diagnosis? And if acidosis is such a problem, why don't we just give bicarbonate to replace the deficit?

Renal Tubular Acidosis is a difficult topic to understand, and it tends to bring back bad memories of complicated nephron diagrams... But all of the types of RTAs concentrate down into one of two issues: the kidneys mishandling either bicarbonate or hydrogen. In this episode, we break it down into simple concepts so that you can master RTAs once and for all!

Many of the images in this presentation came with permission from "The Fluid, Electrolyte, and Acid-Base Companion" by Sarah Faubel, MD and Joel Topf, MD. Download a FREE copy here.

In part 1 of 6 in our series on Metabolic Alkalosis, we lay the foundation to understand alkalosis and explain how hypokalemia contributes to alkalosis, which will come into play for various underlying causes of this acid-base disorder. The details of kidney physiology may have been something you pushed out of your brain after the exam was done, but our goal is to take away the intimidation and explain the processes in a way that not only makes sense, but sticks for the long term and will allow you to take better care of your patients.

In part 2 of 6 in our series on Metabolic Alkalosis, we go through the pathophysiology of vomiting-induced alkalosis.

In Part 3 of our series on Metabolic Alkalosis, we look at how acute & chronic kidney disease can directly lead to metabolic alkalosis, which is a direct function of GFR and is often iatrogenic.

In Part 4 of our metabolic alkalosis series, we dive deep into kidney physiology and explain how high volume states in the presence of aldosterone result in metabolic alkalosis. The processes we work through in this episode are very prevalent in our patients, and affects many different disease states.

In Part 5 of our metabolic alkalosis series, we focus on low-volume hypochloremic states. What happens when you have a process like diarrhea that dehydrates your body along with depleting chloride? Aldosterone is triggered to try and restore volume, but that sets up the kidneys for some unintended mishandling of hydrogen and bicarbonate.

In this final part of our metabolic alkalosis series, we go through the pathophysiology of diuretic-induced alkalosis, focusing on loop diuretics & thiazide diuretics.

A patient presents with hypercalcemia. The first two etiologies that should come to mind are primary hyperparathyroidism and malignancy. But if those are ruled out, what's next? Calcium alkali syndrome is the third most common cause of hypercalcemia. Formerly known as "milk alkali syndrome," this metabolic disturbance happens when a patient ingests excess calcium and an absorbable alkaline substance (classically calcium-carbonate, aka Tums). In this first of a 2-part series, we dive into the pathophysiology of how calcium alkali syndrome occurs and in which situations the body fails to compensate. Part 2 will cover the fascinating kidney physiology that perpetuates and worsens the metabolic derangements created by the syndrome.

In Part 2 of our series on Calcium Alkali Syndrome, we focus on the domino-effect pathophysiology that can make this syndrome so severe. The kidneys bear the brunt of these mechanisms, which turn the nephron's fine-tuned transporters against itself.