Practice Connection: Hypertension Question Explained

Hi, this is Dr. Mike Natter here with BoardVitals I'm here to talk a little bit about some questions from the BoardVitals question bank from the internal medicine questions. Let's jump in. A 55-year-old male with hypertension is started on olmesartan for hypertension. He has no other medical problems. A basic metabolic profile and electrolyte panel are checked 1 month later. Which of the following findings is common? A: Hypernatremia B: Hyperkalemia C: Hypoglycemia Or D: Hyperphosphatemia. So this questions is really getting to the heart of the understanding of first of all what the drug is, and understanding the raas system. First looking at the suffix of this medication we see that it's a sartan and sartans are usually ARBs and their in the family of ACEs and ARBs. Both of these drugs are going to interrupt the RAAS system. The RAAS system is active in states when our body believes that it needs more volume in the tank Such as times as hypertension. Similarly, folks who have hypertension secondly to heart failure may also see that effect. So our kidneys are spinning out rennin Rennin is going to go to the liver and the liver is then going to take Angiotensin and convert it to Angiotensin 1 angiotensin 1 is then going to make and enzyme called ACE. ACE will then take Angiotensin 1 to Angiotensin 2. Angiotensin 2 in exchange is going to do a handful of things. One of which is it's going to back down to where the kidney is and go a little bit above and go to the adrenal cortex The first thing in the adrenal cortex is where aldosterone is going to be secreted from. and the setting up of Angiotensin 2 is where aldosterone will be secreted. Aldosterone in normal physiological circumstances is going to go into the nephron It's going to being in sodium and water will follow sodium and then dump potassium. When we bring in sodium and water follows we have now refilled our tank. Our preload is going to go up Our blood pressure is going to go up as well. Now we disrupt that with an ACE or an ARB the reverse will be true. So instead of dumping potassium we will actually be retaining it. So the answer to this question should be Hyperkalemia or a high potassium. Once again this has been Dr. Mike Natter with BoardVitals and that is the question.

One Reply to “Practice Connection: Hypertension Question Explained”

  1. I knew the answer was Hyperkalemia after reading the question provided. It makes sense. Ace inhibitor and A2RB medications can not only supposed to decrease blood pressure but it can increase serum potassium levels. Those meds would not be appropriate to patients with Renal failure and Chronic renal failure.

Leave a Reply

Your email address will not be published. Required fields are marked *