During a routine medical checkup, Shelby, a 26-year-old physio...

Question

During a routine medical checkup, Shelby, a 26-year-old physiotherapy student, is surprised to hear that her blood pressure is 180/110. She also has a rumbling systolic and diastolic abdominal bruit (murmur) that is loudest at the mid-epigastric area. Her physician suspects renal artery stenosis (narrowing). She orders an abdominal ultrasound and renal artery arteriography, which confirm that Shelby has a small right kidney and the distal part of her right renal artery is narrowed by more than 70%. Her physician prescribes diuretics and calcium channel blockers as temporary measures, and refers Shelby to a cardiovascular surgeon. Explain the connection between Shelby's renal artery stenosis and her hypertension. Why is her right kidney smaller than her left? What would you expect Shelby's blood levels of K⁺, Na⁺, aldosterone, angiotensin II, and renin to be?

Accepted Answer

Hi, everyone. Let's look at our next question. John, a 45 year old man visits his doctor complaining of persistent high blood pressure. He has a family history of hypertension and his blood pressure has been difficult to control. Despite being on medication, the doctor suspects that John's hypertension might be due to an abnormality in the renin angiotensin aldosterone system or RAAS pathway. Which of the following will be a medication of choice for John's treatment. A beta blockers, B, calcium channel blockers, C diuretics or D angiotensin converting enzyme or ace inhibitors. Well, all of these are drugs used to treat high blood pressure. But if we were trying to uh remember on a test, which it would be, we do have a clue in the name here. We see that this ras pathway includes Andrew tens and choice D drugs would be angiotensin converting enzyme inhibitors. So if we had no idea, D would be a good guess, but let's be a little more thorough and discuss why those ace inhibitors would be a good choice, which means looking at this ras pathway and reminding ourselves of what that is. So the R is Rennin. So when rein is produced from the kidneys, that's an enzyme that helps in the production of angiotensinogen protein. So, an increase in renin leads to production of angiotensinogen that gets converted into angiotensin one, which is converted into angiotensin too. And the enzyme that catalyzes this conversion is angiotensin converting enzyme. Logical name. So, as you can see, since our drug is an ace inhibitor, that will cause a blocking of this final step, you prevent the production of angiotensin too. So how does that help lower blood pressure? Well, Andrew 10 2 is a baso constrictor. So it causes the blood vessels to constrict which then increases blood pressure. So by blocking angiotensin two, you prevent that effect and by causing an increase in aldosterone that causes the kidneys to hold on to more water. So you have an increase in blood volume and therefore an increase in blood pressure. So, since angiotensin two acts in these two different ways to increase blood pressure, inhibiting that conversion of angiotensin one to angiotensin two interrupts that cycle. And specifically, in this case, if John's doctor thinks he has a defect somewhere in this pathway, then blocking that final step is most likely to have a beneficial effect on his high blood pressure. So that's why choice D is our correct answer. We'll just briefly just touch on the other three drugs to see why they're not the best choice because none of them are involved in affecting this ras pathway choice. A beta blockers block the effect of epinephrine, excuse me, epinephrine, which increases the contract ability of the muscles and therefore increases the blood pressure. So beta blockers prevent that but not part of this rass pathway choice. B, calcium channel blockers decrease contract ability by preventing that calcium from coming into the cell. And of course, as we said, with the beta blockers decrease in contract ability causes a decrease in the blood pressure by decreasing the stroke volume of the heart and therefore the cardiac output. But again, not the ras pathways to know what we're looking for. And finally, to see diuretics cause the body, the kidneys to produce more urine and therefore the body to lose more water. So that reduces blood volume and therefore blood pressure, but again, not involved in this ras pathway. So not the drug of choice. So the medication of choice for John's treatment, when his doctor suspects that his hypertension is due to a defect in the ras pathway is choice D angiotensin converting enzyme or ace inhibitors. See you in the next video.

Key Concepts

Renal Artery Stenosis and Hypertension

Kidney Size and Ischemic Atrophy

Renin-Angiotensin-Aldosterone System (RAAS) and Electrolyte Changes

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