Memorizing Pharmacology Podcast: Prefixes, Suffixes, and Side Effects for Pharmacy and Nursing Pharmacology by Body System

Acid Reducer Drug Suffix TIDINE Pharmacology

The first body system we cover is gastrointestinal and famotidine is one of the H2 blockers we use for conditions like GERD.

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GI: -tidine (not -atadine or -ine) “to dine”

Famotidine, (Pepcid), Nizatidine (Axid), Cimetidine (Tagamet) are H-2 receptor antagonists. Ranitidine (Zantac) is off the market.

MOA: The stomach’s parietal cells secrete stomach acid to lower pH. Histamine-2 will binds the receptors and stimulate them to produce acid. By blocking histamine-2 we can reduce the secreted stomach acid.

Indications: Used for GERD and peptic ulcers, conditions of acid secretion disorders such as Zollinger-Ellison syndrome.

Pharmacokinetics: The onset of action is a bit faster than PPIs which include omeprazole (Prilosec) and esomeprazole (Nexium), but not near as fast as an antacid which works right away, but the antacid only works for a few hours.

Side Effects: Renal (kidney) dose adjustment and can raise serum creatinine as it is a potent inhibitor of tubular creatinine secretion, normally a marker of poor kidney function, though the patient has normal kidney function.

Can antagonize testosterone which can lead to sexual dysfunction and gynecomastia (breasts in men). Spironolactone (Aldactone), an aldosterone antagonist, can similarly cause gynecomastia.  

B12 deficiency along with proton pump inhibitors, decreased acid leads to malabsorption.

Drug Interactions: Since ranitidine (Zantac) was pulled from the market patients might see cimetidine as an OTC alternative, but it does have many drug interactions. Can inhibit the enzymes CYP1A2 (theophylline, asthma), CYP 3A4 (verapamil, CCB), CYP 2C19 (citalopram, SSRI), decrease effects of CYP2D6 (carvedilol, 3rd generation beta blocker)

Inhibits enzymes that break the drug down therefore you have more drug which equals toxicity.

GMRINCE

Neuro/Psych

Atypical antipsychotic – aripiprazole (Abilify)

Traditional Antiepileptics – carbamazepine (Tegretol), phenytoin (Dilantin)

Parkinson’s – pramipexole (Mirapex ER)

SSRIs – citalopram (Celexa), escitalopram (Lexapro), fluoxetine (Prozac)

Cardio

Anticoagulant – warfarin (Coumadin)

Antihypertensives – carvedilol (Coreg), a beta blocker, verapamil, a non-dihydropyridine calcium channel blocker

Antiarrhythmic - amiodarone, risk of QTc prolongation

Endocrine

Antidiabetics – metformin (Glucophage), a biguanide or glipizide (Glucotrol XL), a sulfonylurea

Auto Generated Transcript:

Hey, welcome to the Memorizing Pharmacology Podcast. Suffixes and Side Effects by Body System for Technician and Nursing Pharmacology. I'm Tony Guerra, a pharmacist, and I've written a couple of books: 'Memorizing Pharmacology' and 'Memorizing Pharmacology Mnemonics,' among others. What I wanted to do was kind of show you how to use those books to internalize pharmacology and get better at it. In this podcast, we're going to go through some of the stems, which can be in the prefix position at the beginning of the medication, in the middle (which is an infix), or at the end (which is a suffix). I just said 'suffixes and side effects' because it's alliterative - same starting word, same number of syllables, all that stuff. But what I want to do is go through this and show you how to make sense of something like this because often you will see things like this, where you've got mechanism of action, indication, pharmacokinetics, side effects, drug interactions, and it's just overwhelming. 

What we want to do is take our time and start really internalizing some of these things. What are the things that we can do to make things a little bit better for us? Alright, let's start with the first thing. We want to be going by body system, and it's important that you kind of internalize this GM RINSE mnemonic. It's the prime mnemonic for the body systems that I use in the books. GM RINSE stands for Gastrointestinal, Musculoskeletal, Respiratory, Immune, Neuropsyc, Cardio, Endocrine, and then, yeah, we get into Genito-Genital Urinary and stuff like that. 

But just for now, really, a lot of everything goes into these seven pathophysiologic classes. So what we want to do is say, 'Okay, how can I, as I'm working with this sheet, make it much more relevant to me?' The first thing is, in the books, there are a number of these stems, and there's some really bad advice on the internet about what is the stem and what isn't. I assure you everything in the books is correct. So, the stem we're going to talk about today is 'tadine' - T-I-D-I-N-E. It's not 'adidene,' which is like loratadine; that's an H1 antagonist, so that's something for your allergies. And it's not 'een'; about a fifth of all medications end with 'een,' so morphine, paroxetine, and other opioids and antidepressants end with 'een.' So, that's not really helpful. We want something at the end that really distinguishes the drug class. 

One way to think about it is 'tadine' is a lot like 'tedine.' So when you 'to dine,' you are maybe going to have some stomach acid, and that's how you can kind of make it relevant for yourself. Let's look at some of the drugs in the class: Famotidine (brand Pepcid), Nizatidine (brand Axid), Cimetidine (brand Tagamet). These are all H2 receptor antagonists, and then Ranitidine, which was Zantac, is off the market now. So when we look at these, the first thing I always like to look at is the brand name. See if there's anything that jumps out at me. And I see 'peptic' and 'acid' in 'Pepcid.' I see 'ax' and the word 'acid' with just the 'c' changed to an 'x' in 'Axid,' and I see 'antagonist' in 'Tagamet.' So those words kind of remind me of what these drugs are for. 

If I'm looking at the brand name, just so you know, your brain will do that. The first thing when you hear 'acetaminophen,' your brain says 'Tylenol,' and what it's trying to do is make a connection in your brain to connect something it already knows. So we'll go to the mechanism of action, and we'll read something like, 'Okay, the stomach's parietal cells will secrete stomach acid to lower the pH.' And we just remember if we did have a chemistry class, the pH scale is 1-14, and the lower it is, the more acidic something is, the more basic as you kind of go up towards 14. And histamine 2, when we think of antihistamines, we're thinking of allergies and stuff like that, but there's more than one histamine. Histamine 2 binds to those receptors and stimulates them to produce acid. But by blocking that histamine 2, we can now reduce the secreted stomach acid. 

So, what's it for? Indications. Well, it makes sense, right? We want to use our intuition to figure this out. It's for gastroesophageal reflux disease (GERD) and peptic ulcers - anything where acid secretion is an issue. So Zollinger-Ellison syndrome, not the only place Zollinger probably ever got to be in the front of the class, where you've got the 'Z' last name. And so, pharmacokinetics, that might not be a familiar term to you, but we're just really saying, 'Okay, what are the things that are kind of important?' And what's really important is someone wants relief. They've got this stomach acid that's burning, and they want this to work quickly. 

It's going to be a little bit faster than the proton pump inhibitors like omeprazole (which is Prilosec) and esomeprazole (which is Nexium). And I may be throwing words out there like PPIs (proton pump inhibitors), but the thing about pharmacology is you continue to bring in these words from later. And so, what happens is, as you work through it, those words become more and more familiar. But it's not as fast as an antacid, so just after someone eats, that works right away. The antacid, unfortunately, will only last for a few hours. So, this is all about trade-offs. 

Okay, so the proton pump inhibitor might work longer but takes longer to work. The antacid will work right away but you might have to use it three or four times a day. Those are the kind of trade-offs we're looking at. Side effects, again, we're kind of saying, 'Okay, when might I have to change a dosage or something like that?' Again, we remember that someone's very young; maybe their kidneys and their liver aren't as developed, or someone's getting old, and those kidney and liver are really starting to deteriorate. Either way, maybe we have to make a dose adjustment, and in this case, we would do it renally. 

But the kind of strange thing about cimetidine, and I'm talking about cimetidine being the problem child in this issue, is that famotidine, it's really great, we would use that. But why do we even have to deal with cimetidine if something has many fewer drug interactions? And as I 'll talk about in a minute, cimetidine is over the counter, somebody can just grab it and get it. So, the dose adjustment can raise the serum creatinine; it's a potent inhibitor of tubular creatinine secretion. So normally, creatinine is a marker of poor kidney function, though the patient has normal kidney function. So, it's a little bit goofy that way. It can antagonize testosterone, which can lead to sexual dysfunction and gynecomastia, which is breast development in men. Another drug, spironolactone, or Aldactone, is an aldosterone antagonist, and that can similarly cause gynecomastia.

You might say, 'Well, I've never heard of spironolactone. What is that?' And again, I talk about in the book, to learn pharmacology, you have to have already taken pharmacology. And spironolactone comes from the cardio chapter, and that's why you kind of want to have this really quick course you can do in a weekend; you kind of get it, and then you use these terms over and over again. You can have this B12 deficiency, and say, 'Okay, well, that's just another side effect.' Remember how do I remember it? Well, you connect it to something else. So proton pump inhibitors also can cause this B12 deficiency, and it's really when you affect acid through the H2 blockers or through proton pump inhibitors that you can lead to malabsorption because you have that decreased acid. 

Drug interactions again, since ranitidine (brand Zantac) was pulled from the market, patients might see cimetidine, which is brand Tagamet, as an OTC alternative. But it does have so many drug interactions with cimetidine. And now I'm really going to get into the weeds, and depending on where you are with pharmacology and what level you need to know, you may not need to know the CYP enzymes and which they affect. But what I'm going to go through here is just okay, I'm going to go through some of the CYP enzymes, and what you should do is if you don't really know what drugs they affect, just find one that really stands out to you as more familiar as you go through this. So, it can inhibit the enzyme CYP1A2, and that affects theophylline, which is for asthma. CYP3A4, that's verapamil, a calcium channel blocker. And if you're watching the video, you'll notice that I have underlined part of the word, and what I try to do is always underline any drug that has a stem so that if you do see another drug similar to it, you can kind of internalize those stems and where they go. 

CYP2C19, so it's escitalopram, which is an SSRI. I also like to put the drug class, so you know it's a selective serotonin reuptake inhibitor. Yes, that doesn't tell you it's an antidepressant, but again, it's just kind of getting these terms down, using them, getting the pharmacologic terminology as you would with these. And then it'll decrease the effects of 2D6, so in carvedilol, a third-generation beta blocker. Again, it's going to inhibit the enzymes, and if it inhibits enzymes, this is the thing that you've got to wrap your head around. If it inhibits the enzyme that breaks down the drug, do you have more or less? You have more drug because the thing that breaks down the drug is being held back. So, I'll say that again: it inhibits the enzymes that break down the drug; therefore, you have more drug, which equals toxicity. Okay, so it's really important when you're looking at these drug interactions, is it an inducer or is it an inhibitor? In this case, we have an inhibitor with cimetidine. But if we have an inducer, it's actually going to make the enzymes work quite a bit better, and it's going to make things break down even faster. So, inhibitor or inducer, really important to know as we go through drug interactions. 

And this is something that, especially if you have a patient on a lot of medications, you'll find that there is no real order to things. And what I mean by order is, you have all the medications, and what we really want is not to put them alphabetically but to put them by this drug class. Again, the GM RINSE mnemonic is Gastrointestinal, Musculoskeletal, Respiratory, Immune, Neuro, Cardio, Endocrine. And if you put all of the medications for a patient in that order, then you'll find it's a lot easier to catch duplicates, it's a lot easier to catch mistakes, and it just makes it a lot easier altogether. So, Neuropsych, for example, there's interactions with that. And what I've done here is just to continue getting our familiarity as we kind of listen to the podcast over the episodes, is to just say, 'Okay, what I'm going to do is I'll just put the drug class.' It's an atypical antipsychotic. So it's not really one of the ones that we had traditionally used; it's got an atypical mechanism. And aripiprazole or Abilify also has one of these stems, and it's the 'piprazole' stem. That's a little bit goofy because normally you don't see a stem within a stem. The 'prezole' stem is the one that you would expect for proton pump inhibitors. So, again, I don't have to memorize all this right away. What we're trying to do is just familiarize ourselves with it. 

Traditional anti-epileptics versus newer anti-epileptics. And the reason I know this is because in the books, the order is intentional. So we're going to put all the traditional anti-epileptics together: carbamazepine (in this case, which is Tegretol), phenytoin (which is Dilantin), and then, you know, valproic acid would have been the other one. But by kind of putting those together, you know, we can kind of look at that. And then we look at the stem, so the 'pen' for carbamazepine and then the 'toin' for phenytoin. Parkinson's, it can affect pramipexole, which is Mirapex ER. And there's no stem there, which is kind of a bummer. It just seems like there should be, but nothing there to help us out. And then some of the SSRIs: citalopram (which is Celexa), escitalopram (which is Lexapro). And in the book, I go over the difference between the 'S' and something that doesn't have an 'S' that the 'S' is the sinister or left-handed version of a drug. So citalopram has the left and right kind of mirror images chemically, and then escitalopram just has the left hand. 'Sinister,' you know, it's Latin; they would think that somebody that is left-handed is sinister. 

So as someone who is right-handed but left-footed, I take umbrage to that. And then fluoxetine. The 'oxetine' stem, that's one of those ones we have to be a little bit careful with because although fluoxetine and paroxetine are both SSRIs, you've got something like duloxetine, which is not, atomoxetine, which is not. But I don't want to get in the weeds there. But just, again, underlining the stem just to remind ourselves. Fluoxetine, Prozac. 

Cardio, so the anticoagulant warfarin will interact with cimetidine. And that '-parin' ending, so those are warfarin-like anticoagulants. That's brand Coumadin. And then anti-hypertensives. So, something like carvedilol. And what I would do is I would say, 'Okay, let me underline this stem, D-I-L-O-L.' And maybe you'd heard, 'Wait a minute, I heard beta-blockers were O-L-O-L or the L-O-L.' Well, in this case, we're going to have some vasodilation, and we're going to have that also; we'll have that effect on the heart. So we'll lower that heart rate at the same time that we're dealing with this vasodilation to get rid of the vasoconstriction, which would have been a response to that lowered heart rate. So again, I don't want to get in the weeds, but that's a beta-blocker. We want to make sure that, okay, by looking at that kind of combined ending, I recognize it's not only a beta-blocker but maybe I am at the level where I'm like, 'Oh, that's a third-generation beta-blocker.' 

Verapamil. So the '-pamil' ending, '-pamil.' That one again tells us it is a non-dihydropyridine calcium channel blocker. It's going to be one that also serves as an antiarrhythmic; it's going to affect the heart. And then talking about the antiarrhythmic, amiodarone. This would have a bit of risk of QTc prolongation. So again, really a concern if we have a patient on both medications with cimetidine. And then, you know, kind of sticking with that, kind of organizing everything into the GM RINSE way, we want to have endocrine. So we'll look at some of the anti-diabetics. And we say, 'Okay, well, what would happen if I now have too much metformin because this drug didn't get broken down because those enzymes got affected? Oh, would I have hyper/hypoglycemia?' All right, well, if I have a drug that is meant to lower blood sugar, and I have more of that drug around, I'm going to have hypoglycemia. 

Okay, and the same thing is true with glipizide, sulfonylurea. But with glipizide, it's really, really more of a concern as we're looking at that hypoglycemia. So again, the goal wasn't to overwhelm you with this, but the goal is to say, 'Okay, well, we have a stem, to dean. We recognize that it's an H2 blocker, and we have famotidine, nizatidine, cimetidine. We can learn three drugs all at once, and we can start learning the language of pharmacology as we go through this. So again, if you want to keep up with me on this podcast, I certainly appreciate it. And do pick up Memorizing Pharmacology and Memorizing Pharmacology Mnemonics. There's an audio version, there's an e-book version, there's a print book version. My wife loves watching things on her Kindle, where I always have things on my run or at the gym or whatever in my ear; I always have an audiobook myself. And I think Audible has a way that you can get it for free when they have that trial or whatever. So again, hopefully, you've enjoyed this first episode of the Memorizing Pharmacology Podcast, 'Suffixes and Side Effects by Body System for Technician and Nursing Pharmacology.

Like to learn more?

Find my book here: https://geni.us/iA22iZ

or here: https://www.audible.com/pd/B01FSR7HLE/?source_code=AUDFPWS0223189MWT-BK-ACX0-059486&ref=acx_bty_BK_ACX0_059486_rh_us

and subscribe to my YouTube Channel TonyPharmD here: https://www.youtube.com/c/tonypharmd