To Clot or Not To Clot – Anticoagulants!
We’re back to help you understand those difficult anticoagulants, and how you can assess and take care of your patients who need anticoagulants! Don’t miss out!
Cornell Note-Taking System Instructions:
- Record: During the lecture, use the note-taking column to record the lecture using telegraphic sentences.
- Questions: As soon after class as possible, formulate questions based onthe notes in the right-hand column. Writing questions helps to clarifymeanings, reveal relationships, establish continuity, and strengthenmemory. Also, the writing of questions sets up a perfect stage for exam-studying later.
- Recite: Cover the note-taking column with a sheet of paper. Then, looking at the questions or cue-words in the question and cue column only, say aloud, in your own words, the answers to the questions, facts, or ideas indicated by the cue-words.
- Reflect: Reflect on the material by asking yourself questions, for example: “What’s the significance of these facts? What principle are they based on? How can I apply them? How do they fit in with what I already know? What’s beyond them?
- Review: Spend at least ten minutes every week reviewing all your previous notes. If you do, you’ll retain a great deal for current use, as well as, for the exam.
For more information, visit www.nursing.com/cornell
Oh, so yeah, we’re going to talk about anticoagulants and what I want to do like, so for those of you who don’t know me, I’m Nicole Weaver. I’m the curriculum director here at NRSNG. I’ve been a nurse for 10 years, an educator for five. Um, and pharmacology was something I actually really enjoyed in school. I wasn’t good at it, but I enjoyed it. Um, and I enjoyed, uh, just understanding how things happen in the body. And once I really started making some connections between pathol and, and physiology and pharmacology, it really started to help me. So literally when I was in nursing school, I had a huge poster board, like regular sized poster board, but a poster board with the clotting cascade on it, um, and the different drugs and where they affected the clotting cascade. And I literally had that thing up in my apartment, um, when I was in nursing school because that’s how I learned it.
And so what I’ve done, what we’ve done for you guys is we’ve actually put that on this cheat sheet. So I’m going to paste that link one more time. For those of you who have just come in because I’m going to kind of use this cheat sheet as I go cause it’s really helpful. So like I said, one of the best things you can do when it comes to these types of drugs that effect a physiologic process in the body is to make sure you understand that process, right? Cause you don’t understand what’s actually happening in the body. It’s really hard to understand what the drugs are affecting. So we’re going to talk through the clotting cascade. I’m going to kind of draw it out. It’s a little bit complex. So I’m gonna do my best to simplify it as I draw it out. Um, and then we’ll talk about the different drugs and then you guys can ask me whatever questions that you have. But my number one pop quiz here, guys, what’s the number one side effect of anti-coagulants?
Bleeding. Exactly. So just like with any medication, whatever we’re trying to accomplish with that medication, we can always push it too far, right? So if we’re trying to stop clots and stop them from clotting, then of course they could possibly bleed or bleed out or have really significant bleeding issues. So always keep that in mind. So clotting cascade, there’s two major pathways when we’re talking about clotting. And the first question is where does the clots happen? Like where the majority of the clots happen inside where vascular, yeah, inside the blood vessels. So when we start talking about intrinsic and Extrinsic, that’s what we’re talking about is the blood vessels. So remember intrinsic anytime you hear that word inside extrinsic, outside. Um, so then it depends obviously in context of what you’re talking about, right? So in this case, for the clotting cascade, the intrinsic pathway happens inside the vessels and the extrinsic pathway happens outside the vessels or out in the tissues of, you may actually see people call this the tissue pathway also, which is, that’s why. So in terms of happens in the vessels, extrinsic happens in the tissues. There’s one other thing that’s happening in our body all the time. And that is happening in the liver and something is being synthesized in the liver. What is being synthesized or created in the liver
all the time. Our liver is at work making these things. What are they? That’s what you might’ve seen that. So carry great gas. So what we’re making is clotting factors. And what is heavily involved in the creation of clotting factors is vitamin K, k. So in the liver, vitaminK is helping our liver create all of these clotting factors. So what happens now is these clotting factors are going to go in the vessels and you’re going to go into tissues and they’re actually going to start, um, being involved in these clotting pathways, the intensity and the extrinsic pathways. Now, I’ll be really honest with you guys. The specific numbers of the clotting factors involved intensive and extrinsic, the chances of you, number one, the chances of you needing to know that as a staff nurse later, very slim, unless you’re dealing with a patient with a clotting disorder, like a hemophilia, um, or something that affects, you know, factor five Leiden.
So understanding that part, but really, ultimately you need to know what happens after that. So our clotting factors, our intrinsic pathway, we’re gonna see activation of um, nine, 11 and 12 and 11 and 12. And our extrinsic pathway, we’re gonna see activation of setting. So on the cheat sheet, what you’ll see is it says, um, so it says nine, 11 and 12. Here for intrinsic and for extrinsic it says factor seven goes to vectors seven a, that just means it activates and we try to get closer. So focus, so seven to seven a just means activated setting, right? The little age just means active. Okay. So we activate nine 11 and 12 intrinsic and we activate seven extrinsic. And both of those things are actually going to come together in what’s known as the common pathway. So basically we have initiation of vessel damage that causes clotting cascade here, or initiation of tissue damage that causes a clotting cascade here.
And then they both come together and do the same thing from then on. So really it’s just a matter of where it’s, where was the damage starting? Did the damage start in the vessels or did the damage start my tissues? So they come together and they actually activate Dr 10 so we end up with 10 a 10 activated, right? So 10 a and beyond is where all the magic happens. The other thing though that I want you to be aware of is there’s another little pathway happening over here on the intrinsic side and that is what happens when I end up with damage inside my vessels. What else? What other cells do I start see, start to see, get involved. Some inside of blood vessel start to get damage, got some kind of cells in there that come in and start to do stuff. What are they [inaudible]
we’re talking about clotting. What styles in my, in my blood are involved in clotting. There we go. Platelets. Y’All got it. So this intrinsic vessel damage process also activates my platelets and those platelets will then start to aggregate. Platelet aggregation is a fancy word for clumping, right? It’s not a clot yet. It’s just clumping together. So you start from this vessel damage, you’re going to see this activation are common pathway, but you’re also gonna see your platelets start to clump together. Okay, so this is happening over here by itself. While all of this is happening. So two things to know that are just in our body all the time. There’s two little hormones. One are proteins, one is called Prothrombin, and one is called fibrinogen. Now these two proteins are just in our bloodstream. They’re in there, they’re hanging out, they’re already there, all right? As soon as 10 a gets activated, it starts this whole process. Okay? So 10 egg, it’s activated and it turns prothrombin into thrombin. So that’s the first little activation that happens from 10 a 10 a turns prothrombin into thrombin. Once we see thrombin, that goes to that fibrinogen and converts it, and we end up with fibrin.
So now we’ve activated Fibrin, we’ve got platelets aggregating over here. The fibrin and that platelet clump are going to come together and they’re going to create a clot. So I’ve got platelets clump together with fiber and all meshed up in it, and it creates a clock. Platelet clumping by itself, not a clot. Fiber and activation by itself, not a clot. You have to have both platelet aggregation and fiber and activation to get a clot. Does that make sense? Awesome. If at any point anything I say doesn’t make sense, you all, please let me know or ask questions. Okay? Don’t hesitate. So this is our clotting cascade. And I know it seems a little complicated. Like I said, the chances that you really needed to know these exact numbers and they come into play. When you look at a bleeding disorders like hemophilia a, he must only be a factor five Leiden and things like that that affect the clotting factors. But what you really just need to know is we either have vessel damage that starts the process or tissue damage that starts the process. Either way, we activate 10 a, which turns pro-family into thrombin, which turns fibrinogen into fibrin.
And this, uh, [inaudible]
platelet activation happened as well. We got aggregation. So platelet aggregation plus fibrin equals clots. So what happens when you’re looking at this process? If you look at this cheat sheet, you can see the numbers that are on here and the numbers correspond to the categories of medications down here. Okay. So if we can stop really any part of this process, we can prevent clots from happening. Now, one thing I want you to know is anticoagulants. Anytime you see a coagulant, you’re talking about the coagulation process that AMT is like the process. So an anticoagulant is against the clotting process. Okay? So we don’t create new clocks. However, what happens to clocks that are already there? What happens? Do, do my anticoagulants affect clots that are already there
directly? Nope. Nope. So what happens is we prevent new clots and the body will work to break down the clot itself. But the drug itself doesn’t break down the clot. There is one drug I’m here number six to place that we’ll talk about. That is actually not an anticoagulant. It’s a thrombolytic and lytic or licensed means to destroy or to break up. So if thrombo thrombus clot thrombolytic actually will destroy existing clubs. So that’s a debate difference. I want to make sure that, you know, between an anticoagulant and a, um, thrombolytic. Okay. So if someone says, uh, they want to give a medication to break up clots that happened in the body, what should they give Heparin? Aspirin. Those are not your options, right? Cause those are not thrombolytics. It needs to be a thrombolytic. Okay. So here’s what we’re looking at here. And I’m like, Oh man, I think I used all my colors.
I don’t have any extra colors. So remember, we have to have platelet aggregation and fibrin activation to get a quad so we can block really any part of this process and start to be able to prevent clot formation, right? I will tell you though, fibrin can grab onto any little bit of platelets and make the clock right. So, uh, blocking the platelet process is effective, but it’s not nearly as effective as blocking this process in terms of intensity of anticoagulation, right? When we give somebody a platelet aggregate or an anti-platelet, we’re going to see potential for bleeding. We’re going to see potential for bruising, um, or not. Gonna see the, uh, you know, they get cut and they bleed for 10 minutes, right? It’s not as extreme. Um, but you’re still gonna see the same risk for bleeding, risk for bruising. Um, and then of course, if we’re talking about aspirin, we’re talking about the gut issues, right? So big things. What are our two most common anti, excuse me, anti-platelet drugs. I mentioned one of them already. So cheated. So the two most common antiplatelet drugs are aspirin. And what’s the other one? Y’All can give me the trade name if that’s what you remember.
I’m going to write the generic name. So aspirin and Clopidogrel, or Plavix, aspirin, Plavix, those are platelet aggregates, aspirin, Plavix, anti-platelet, right? So aspirin and Plavix, or aspirin and clopidogrel. Those are your two most common anti-platelet drugs. Fun fact, they actually will permanently disabled those platelets. So those platelets have to die off. We have to create new ones in order to be able to clot again. And so that’s why a lot of times you’ll see, hey, if you’re taking aspirin and you have to have surgery, you need to stop taking your aspirin like a couple of days before your surgery. Um, because we need your body to be able to restore and replenish those platelets. So aspirin and Plavix, those are two anti-platelet drugs. And so if we stop this process, we can in in large part stop the actual clotting process because again, we have to have both platelet aggregation and fiber and activation.
Okay? So that’s the first category is your anti-platelets. And then we’re going to Kinda just go from the top down on this side, right? So what anticoagulant do we have that can affect this process up here, this vitamin K clotting factor process. What drug do we use up there? [inaudible] or Warfarin. So warfarin and I’m appreciating where that really small, I apologize. So warfarin is our drug up here. That is a vitaminK antagonist. So it’s actually going to prevent vitaminK from working and therefore we cannot synthesize our clotting factors. So this is where I go. So much critical thinking. Guys, what is the antidote for Warfarin?
Vitamin K, right? Vitamin K. Now you guys, I’m going to be really, I’m going to be really like semantics here. When you write k, make sure you write vitamin K so people don’t think you’re talking about potassium. So vitamin K, vitamin K is the antidote for Warfarin because we’re just saying, hey, we’re friends blocking all my vitamin K. I’ll just give more, right? I’m giving some more, I make some clotting factors, I’ll be fine. Okay, so that’s one class. Let’s work our way down. Okay. So let’s say we now get to, um, the Mike, what time do I do?
So let’s get to time of a, actually, we’ll go over here. We’ll go to Heparin. So heparin and Lovenox, or an Oxa parent, which is a low molecular weight Heparin. So really your heparins are indirect thrombin inhibitors. So this thrombin over here, if I’ve got Heparin on board or an oxen Perron, which is low molecular weight Heparin, I’ve got, oops, I can spell you guys promise. So if I’ve got Heparin or an oxy parent on board, and then I get to this thrombin, that thrombin is no longer going to work. So the thrombin is supposed to activate the fibrin. But if I’m inhibiting thrombin, it’s not gonna work. So I’m not going to get here cause I can’t get to this part. Right? So again, we’re just blocking like parts of the process, right? The one thing to know though is that Heparin itself is also a 10 a inhibitor. So you’re getting both in inhibition of factor 10 and inhibition of thrombin. When you’re using Heparin with low molecular weight Heparin, you’re getting just the thrombin. So which one of the two actually requires monitoring Heparin or an Oxford Paren?
Which one do you have to monitor? Like clotting values and clotting times. Heparin. Yeah, because it’s actually doing kind of double duty here, right? It’s called [inaudible]. It’s blocking [inaudible] and thrombin. So it’s going to have a little bit stronger. What other medication that we already mentioned? We also have to have to monitor for right warfarin because again, this is kind of blocking everything, right? This is really blocking a whole pathway. So these are really stronger, um, stronger as not the right word. Um, so I apologize cause that’s really not the right word, but the ones that block a bigger portion of the process really require monitoring. So warfarin requires monitoring. We’ll talk about that in a second. Heparin requires monitoring and oxygen doesn’t. So then we come over here, we also have another class of drugs that are 10 a inhibitors. Um, and those are your oxa bands and your extra bands.
So a Pixel van and Rivaroxaban, which is Eliquis and Xarelto. So I’m just gonna put the little suffix here. So you know, those are yours, the bams. So benefits of these. Number one, they also require less monitoring, which is nice. Um, we will still monitor these patients but they don’t need like the Q six hour p t t’s or anything like that. Um, but the nice thing about these is heparin has one really severe side effect. Who knows what the really, besides the bleeding, who’s not, knows what the really severe possible side effect of Heparin is. Give you guys a sec. Cause the benefit of these is they don’t cause this.
So I’ll give you a hint. I know you guys are probably typing media hint, it’s Heparin induced. There you go. Heparin induced thrombocytopenia. So what does thrombocytopenia means? I have too few platelets. So if I have, if I’m blocking all of these pathways and I have two few platelets, I’m really, really, really at risk for bleeding to death. At this point. I’m having zero clotting happening. Um, and so heparin induced thrombocytopenia is a reason to not give heparin. Um, in fact, a lot of times we’ll call it an allergy, we’ll say they’re allergic to Hepburn because they developed pit hit. So we switched those patients over to the Rivaroxaban and the Apixaban’s because they don’t cause that problem. Um, Heparin is a more effective medication, but because it requires monitoring and because it has side effects, most people who are going to be longterm on one of these more significant anti-coagulants will be on one of these bands.
There’ll be on Xarelto or Eliquis. Um, uh, Pixvana river rocks band because you don’t have to do all the monitoring. You don’t have the high risk for the thrombocytopenia. Um, and you’re still effective. Um, but I will tell you from personal experience, I have seen more complications, head bleeds, hemorrhagic strokes from Zarelto than I have seen from Heparin coumadin combined. So there’s something to be said for the benefits of monitoring. This is my personal opinion, it’s my personal opinion. But my experience, man, in 10 years when Zarelto came out, I started seeing those hemorrhagic strokes a lot. A Lot, a lot. So classes where we’re at, we got anti-platelet aggregates. We’ve got warfarin up here, inhibiting vitaminK , we’ve got heparin and an ox apparent inhibiting thrombin indirectly and Heparin and pivoting [inaudible]. And we’ve got this, the bands inhibiting 10 AA as well. Notice the x a x a done notice that x a x a.
So if you’re like, oh, what does rivaroxaban inhibit? X a 10, I yay. Memory devices. All right, so one more class and then we’ll get to the clot busters. And that is your drugs that actually directly inhibit thrombin. And those are your, um, after bands. So your [inaudible], your van, um, to big a tran, those, those ones. So they’re directly inhibiting from it. They’re not indirectly inhibiting it. They’re directly inhibiting it. So, um, there you go. So amber said, Ban 10 a or 10, a ban or ban thrombin tro. Bam. Right? So the r gastro ban is gonna directly inhibit thrombin, whereas Heparin was indirect. And so when we start looking at testing and monitoring, we’re less concerned about monitoring down here because, um, the time that it takes to get from down here to down here, it doesn’t matter cause I’m inhibiting after that. Um, so let’s look at monitoring super quickly. There’s two, three major, uh, numbers that will closer for you guys.
Oh my gosh, I’m really bad at the like backwards turning thing. Is that okay? Can you all see that? I’m gonna hold that there for just a second so you all can see it again. This is on that cheat sheet. I’ll send the link again here in just a second. Okay. So what are the clotting numbers lab values that we check? There’s two major ones, one third one as well, PT, PTT. And then I see the third one is INR. So PT and INR tend to go together and then PTT. So here’s how I remember this. Warfarin is most often given p o by mouth. And so we check PT and INR goes with it. So sorry guys, I was mean to sound so I forget. So warfarin is po and we check PT or PT and INR. Most of the time you are looking at INR, it’s normalized ratio, it’s easier.
Um, but that’s how I remember that PTI in our go together, Heparin is usually given by injection of some sort, ivy sub Q injection of some sort. And so we check p t t two letters, three letters. That’s how I remember it stuff. Just simple like weird way to remember. But I remember, but let me just show you prothrombin time tells me how long it takes to get from the top to here, but to create a activating port Robyn. Right? So at the time from here to there, whereas a partial thromboplastin time, is it time it takes to get here? Well, Pepin has no impact on this time. It has impact on what happens after that. So you have to wait a little bit longer and check a different time for the Hepburn because it’s a little farther down. Okay. So warfarin, we check PT or PTI and R and Heparin.
We check PTT. Now in terms of specific numbers and targets, INR, I will tell you, international normalized ratio one is a normal clutter 0.5 1.5, somewhere in there. One average is normal clutter, right? That’s what we’re looking for. That’s why we call it the international normalized ratio, right? So one is normal. Um, typically we’re looking for somewhere around two to three for therapeutic anticoagulation. But again, it’s entirely dependent on the doctor. It’s entirely dependent on the patient and what they have going on. So that’s, that’s going to be a decision that’s made within the care planning process for the provider. But typically INR wise, we’re looking for like a two to three, somewhere in there. I’ve literally had a patient with an INR seven before and I was like, wow, this is not okay. Um, PTT, usually around 40 is normal, so we’re usually looking at something like 60, 70, 80 for like therapeutic. So we’re wanting it to be a little bit longer. We want it to take them a little bit longer to clot so they’re not as likely to clot. Right. That’s why we want longer times, but not so long that they never clot and they die. Right? So,
okay. So ambers question is increased leads to thinning, decrease leads to thicker. So I’m going to answer your question. I will increase and decrease first and then we’re going to talk about thick and thin because if they can stand the same, drives me crazy. So an increased clotting time means that they are more anticoagulated or less likely to clot. They’re more likely to bleed because it takes longer, right? So increased clotting times, it takes longer to clot, more likely to bleed, less likely to clot, right? If we have a decrease in those times, then they’re more likely to clot, they’re going to clot faster. And that’s a problem, right? Especially for someone who’s at high risk for class. We don’t want to see that. So the reason I don’t like thick and thin is because literally it has nothing to do with the thickness and the mess of the blood. That is a a, what’s the word? Um, it’s a term that’s used in the lay world of a blood thinner. Um, and so that’s what people think of. But that’s not technically physiologically appropriate. But you’re correct, that increase would be more bleeding and a decrease would be less bleeding. Absolutely. Yes. Absolutely. Yes.
All right. Questions. So let me, let me drop this link one more time for you guys for this cheat sheet cause I want to make sure everyone gets a chance to grab it. If you are not in chat or you can’t see chat, go to the library and search anticoagulant. Um, and you’ll find it. Now I will tell you, um, currently, uh, we don’t have lectures within farm on anticoagulants, but we will, we don’t have them yet and that’s all I can say. But in the hundred 40 mass nomads, the audio lectures, there is an audio click audio on every single one of these drugs. So you have a place where you can go look those up and listen to those audio lectures on heparins in their, um, outta places in there. Oh, that’s the one we forgot to talk about. So Altuve place or TPA is our clot-buster. It literally comes down here into this process and it rips apart all of the fibrin and it breaks up the clot. It’s a fibrinolytic thrombolytic comes in and it rips up that clock and breaks it. Okay outta place Amber’s name of what that drug alto place or tpa is the other term for it. Yeah. Is it written right there at the bottom?
So activate plasminogen which goes in and breaks up all the fibrin. So alteplase is the only major one. At least it’s on this cheat sheet. And there’s a couple others in practice that actually will destroy existing clots. Everything else just prevents further crops. Kerry, that’s actually a fantastic question and I’m just going to admit I can’t explain d dimer. It’s one thing that my brain has not figured out, but it is about, it’s about timing, um, between platelets and thrombin. Like it’s about, it’s about timing. Do me a favor, carry email, contacted NRSNG, um, attention Nicole or extension tutoring and ask the question and I will get you an answer or a solid answer for that. If anybody else has that question, you can answer or email as well. Um, but I don’t wanna s I don’t want to say it wrong. So definitely shoot, shoot us an email and I will get an answer for you.
Sorry I don’t, I don’t, that’s one thing that I have struggled with it actually. We use D dimer to determine if somebody has developed a clot. So it’s not about breakdown because we would use it to see if we think someone has developed a PE, a pulmonary embolism or something like that. But I’ll get you an answer I promise. Sorry, one of the questions. Can I answer for you? I know I can’t know everything I try. Nope, we can’t. And you know what? I say this all the time. There’s nothing scarier than a nurse that won’t admit when she doesn’t know something. So there you go. Always willing to ask questions, look something up. The best part about this is after this, I’m going to know, cause I’m going to figure it out for you. What other questions can I answer if you guys want anticoagulants, again, really the big thing here is understand what happening in the body and where the different drugs fit in. And that’s going to really help you to process again. They all have the same side effects, bleeding, Patikim, die, bruising, easy bruising, longer bleeding. Um, thrombocytopenia with Heparin is the big thing. Knowing what to monitor.
I know we’re over by a minute or so. Does anybody have any other questions? Thanks amber. Okay, I’ll go look at that.
All right. If nobody has any other questions, I’m going to drop the, um, yeah, you guys. So amber did just post the link in the chat about d dimer if you want to go look at that. Um, if you want an explanation from me, email contact to NRS and g and I will get the answer for you and I promise I will have it by the next time I do this tutoring session. So no, no, no, you’re fine. So I’m going to drop this survey in here. You guys, um, please fill out that survey every time. Even if you fill it out three times a day, give us, you know, what you want to see, especially if you have new ideas. If something else comes up, please let us know how we can help and make tutoring better for you guys, like knowing the answers.
Sorry. All right, y’all okay guys? Well, if there’s no more questions then I will let you guys go. Not yet, but so close. So close. The question is whether or not the video recordings are available yet. So close. Almost good. Amber sets had been a great way to engage during summer break. That’s good. I’m glad. Stay engaged. Don’t overdo it. Like enjoy your break, but it’s nice to stay engaged. All right guys. All right. Well, we love you guys. Have a great day. Go out and be your best selves and as always, happy nursing. No, you’re awesome.