DIP Ep 673: USMLE Pharm Crash Course, The Drugs That Matter (Part 4)
» Divine Intervention Podcasts
This episode provides a high-yield pharmacology review specifically tailored for students preparing for the USMLE exams. The host covers cri
Key takeaways
- Digoxin toxicity can present with yellow-green vision changes and is treated with Digibind (digoxin-specific antibody fragments).
- Carbidopa is essential in Parkinson's treatment to prevent the peripheral decarboxylation of levodopa, ensuring more drug reaches the brain.
Main topics
- Digoxin mechanism and toxicity
- Parkinson's disease pharmacotherapy
Notable quotes
Thou shall not give valproic acid to a lady that is pregnant.
Conclusion
The episode serves as an intensive, fact-dense study guide for medical
Transcript preview
Speaker 1 (0:00) All right, welcome. My name is Devine. This is episode 673 of the Devine Intervention Podcasts. And we're going to continue the series on the USMLE Pharm Crash Course, right? The drugs that matter. Basically, the most important drugs that are tested on the USMLE exams. Very high-yield series. If you missed the first three parts, go ahead and check those out. All right, so let's jump right into it. And before we jump into it, if you're studying for a Step 2 or Step 3, I do have a 20-hour Step 2, Step 3 course that begins today. Today, literally the 18th of September. If you're studying for the exams, very comprehensive review, very helpful. I've had tons of people take these courses, getting the 250s, 260s, 270s on their exams even, right? So if you're interested, shoot me an email. It's going to be over Zoom, right? Just click on the link in the... below here or email me through the website divineinterventionpodcast.com and I can give you some more information. You can still sign up. There's still a few spots remaining. All right, so let's jump right into it, right? So what if they give you a question about a patient? You're told that this patient has a history of a very severe heart failure. In fact, that his last measured ejection fraction was 15 % and that he comes to the physician for a follow-up but that he has noticed some issues with reading. He's been noticing like just some issues with his reading and he notices that things seem to have abnormal colors for him. What drug should you be thinking about? Well, I really hope you're saying, Devine, this sounds an awful lot like digoxin toxicity, right? So this person has really bad heart failure. Remember, digoxin is a positive inotrope, right? Although remember, digoxin actually does not improve survival in CHF. It actually... doesn't improve survival, right? But it just makes your heart beat stronger. It's a positive inotrope. And literally the way it works is that it blocks the sodium potassium ATPase pump, right? If you block that pump, remember what does that pump do? It brings three sodiums out of the cell and puts two potassiums into the cell. So if you block that pump, you're going to prevent sodium from coming out of the cell. So there's going to be a buildup of intracellular sodium within your cardiac myocytes. If that happens, then There's this thing called the sodium-calcium exchanger that will stop working, right? The sodium-calcium exchanger is another transporter that we find on cardiac biocytes that basically pumps calcium out of the cell and lets sodium, you know, come into the cell, right? So it lets sodium come down its gradient into the cell because remember, sodium is primarily an extracellular ion. So sodium comes down its gradient into the cell and then calcium gets pumped out. If you increase the amount of intracellular sodium by blocking the sodium potassium ATPase pump, then you're killing that gradient for sodium to rush into the cell for calcium to get pumped out. So guess what? Calcium is going to stay within the lumen of the cardiac myocyte. And that's going to promote inotropy, right? So digoxin is a positive inotrope. That's how it really helps. That's the true mechanism of action. It does increase the intracellular amount of calcium within your cardiac myocytes. right? Now, remember, digoxin can also cause, you know, like yellow-green vision changes, right? And what do you think digoxin will cause to a person's potassium? Well, remember, digoxin can actually cause hyperkalemia because, again, look at its mechanism of action. It inhibits that sodium-potassium ATPase pump, right? Again, that pump takes three sodiums out, puts two potassiums in. If you shut it down, you won't bring in potassium. So, potassium is going to stay on the outside of the cell in the bloodstream. You're going to have hyperkalemia. But One strange thing our friends at the MBMs love to test is that you know that hypokalemia can actually increase your risk of DASH toxicity, right? How exactly does that work? Well, the thing is, remember I just said that digoxin works by inhibiting the sodium potassium ATPase pump, right? The thing is for it to inhibit that pump, it actually binds to a potassium binding site. It actually binds to a potassium binding site. So the thing that's going to happen is that if... you have hypokalemia, there are more binding sites available on the sodium potassium ATPase pump for digoxin to bind. So DIG binds in accumulator and you're going to get in trouble. And how do we fix DIG toxicity? Well, we fix DIG toxicity with a DIG bind, right? You know, basically like anti-DIG FAB fragments, right? Digoxin specific antibody fragments, digoxin specific antibody fragments, right? And remember digoxin can also slow conduction down the AV node. right? It's an avinodal blocking agent. So it can actually cause bradycardia. Just something I want to keep at the back of your mind for exams, right? So if, for example, a person has like AFib and they have WPW or they have like heart block, giving them digoxin may not be the smartest idea in the world, right? Because in those circumstances, giving avinodal blocking agents just going to worsen your condition, right? Now, what if they give you a question about a person, right? You're told that this person is Speaker 1 (4:50) you know, has missed like the last two, you know, this person has a history of Parkinson's disease and they missed the last two doses of their medication, right? And then you're told that, oh, that this person has been having like just severe bradykinesia and all these problems, right? Whenever you see something like this, what drug should you be thinking about, right? Think of levodopa carbidopa, right? Think of L-dopa carbidopa, right? Levodopa carbidopa, right? Remember, these drugs are used to treat Parkinson's, they're... probably the most effective drugs for trading Parkinson's. I mean, typically, you'll start off with a dopamine agonist like, you know, like bromocryptine, cabergoline, right? Or you can use monoamine oxidase B inhibitors like selegiline or asagiline to boost your dopamine levels. Or you can use amantadine, right? It was a drug we used to use for the flu before. But then we noticed that, oh, gee, this then actually increases the release of dopamine within the central nervous system, right? But at the end of the day, all roads are going to lead to levodopa, carbidopa, right? Because again, remember, in Parkinson's, you're... dopamine-producing neurons in your substantia nigra are gone, right? So the thing is, as you use levodopa carbidopa for a long time, you're going to