NCLEX Clotting and Blood Thinners Questions for Nurses
Good morning. I’m live on Facebook already I can see it from the from the Facebook page oh there you go sorry guys, I need to see your chat rooms so I can see your questions or I mean concerns or anything. So I'm trying to fix it so I can see it all on there you go. So Facebook Live. I guess I can see it now. All right, so let me introduce myself. This is Jay Padang I'm from ibis and I'm here to represent Ibis. And absolutely for you, for everybody's information. This is a joint project, you know, between review centers, like English exam review centers, if I'm not mistaken, it's Swoosh, the other one would be Niners. And for NCLEX review centers like aspire and I pass so I would like to recognize everybody especially Connetics college I would say because this is really a good medium for, for knowledge and education, especially making us an NS as an instrument to everyone's journey to NCLEX and be able to be successful and come here in the US that's really my main goal to see you guys here and work as a nurse and not just a nurse, but as a good nurse. Okay, so this is another hour another hour of education. It's free, you know, NCLEX education and I'm going to discuss about clotting cascade and at the same time, the blood thinners like you know, your anti platelets, or anti co AGGS at the same time your tremble effects Okay, so I guess I may start now so can I share my screen because it's from the facilitators and I cannot share it from here I'm sorry alone so I cannot actually see who's in for some reason on oops so it's in Facebook though alone having hard time.
Can I see the live comments? I cannot see the live comments on my end for some reason I don't know. Hello, let me just fix it. Okay. There you go. I guess I can see it now. Hello me so just a little shout out to you guys. Mr. Elvin, by the way MJ Padang from IPASS. Good evening all the viewers from also from my past Miss Maria okay who else Miss Maria is also from our IPASS online academy she is also a passer by NCLEX and probably you're from Connetics as well. So hold on, let me see. Okay, so let's start so I guess I can share my screen now. Are we are we ready sorry guys up for the delay Oh, hello, Mr. Felix from Kenya. How are you doing sir? How can you doing? By the way I'm here in Texas. It's seven o'clock in the morning. It's 707 to be exact. And in the Philippines. My home country is 8pm 8:07pm So for those of you watching in the Philippines hello guys okay.
Miss Linda is also here if I'm not mistaken Are you here also last time, I saw some people from Africa or from other parts of the world last time from Nigeria. Okay. I have some friends from Nigeria as well. Even my workmates are also from Nigeria. And they're really good friends of mine. I love the people there. I haven't been there. But you know, I have some friends. Like I said, I love them. I love their sincerity right. Click percent. Okay, hold on. So to my stream yard, I guess. So I thought it was coming from my end. All right. There you go. Share Screen. There you go. All right already. I guess you can see my screen now. Huh? Okay, so let's, let's start. So like I said, Can you see my screen? Can you say yes. Oh, it's 3:08pm in Kenya. So hello there. Good afternoon. So you can see my screen now, huh? All right. So I'm gonna discuss to you about this is a free lecture again, for those of you who just came in, it's a free lecture about hemostasis. coagulation are also known as coagulation. And at the same time, the blood thinners so how can we counter up with your coagulation? All right, I'm gonna draw something like this. For a start, okay. All right. This is what's this, by the way? Forgive my drawing. So this is like a weighing scale an old way, or an old method of weighing scale, right. So I'm talking about homeostasis here. Right, I'm talking about homeostasis. When you say homeostasis, this is about balance, right? This is about balance. When you say about balance, there should be a medium, right? And medium. Since I told you about what's, what's our discussion today, it's something about coagulation. So I'm going to put here on this corner, or this portion here. We call it a short coagulation. Right? Calculation, or also known as it's more medical, when you say it like hemostasis, right from the word itself. Hemo. That's blood. When you say like stasis, it's not moving. It's not dynamic. It's not circulating. Alright. So and that is because you know, it involves coagulation.
It involves clotting. All right. So on the other hand, And I would write here, your anticoagulation. All right. Remember, the first subject in your anatomy and physiology is always I mean, is homeostasis. It's something about the balance. So there's something like here, this is your medium right here. And what is your medium by the way, between your coagulation and anticoagulation? All right. Again, what's the medium between your coagulation or hemostasis, and your anticoagulation? So there's again, there should be like a balance. If your calculation you also have your anticoagulation. And the medium is what is for you to have a good normal blood flow. All right, I'm gonna write it here. A normal blood flow, no coagulation, or not even bleeding. All right. So, coagulation can happen, either physiologically, normally, or coming from a disease or disorder. All right, coming from a disease or disorder, the blood, normally your blood is viscous, right? It's viscous. When you for example, we can when you draw blood and then put it in a specimen container on a tube. It doesn't have heparin on it, it will coagulate. Because again, normally your blood is viscous. Normally it will coagulate. Right. So there should be something like a mechanism, which is an anticoagulation mechanism in your body to make it like smoothly flowing. That's your anticoagulants in your body, which also happens in a normal situation, or by giving some medications, right. It's also influenced by your anticoagulants, blood thinners in general.
So this is basically your blood thinners that we're going we're going to discuss about most specifically and more importantly, later on. Alright, let's discuss first your coagulation, your hemostasis. Your hemostasis involves two things in order for you to have or to create the clots. Alright, so and what are those things? It involves your primary hemostasis which in which we're going to talk about and as well as your secondary hemostasis. Any questions? Are we good? Okay. And of course, I every lectures that I have, I'm always starting it with the foundation, you cannot understand what is or what are blood thinners, what is anti cleaved that what's the action of your anti platelets, your anticoagulants, your thrombolytics if you don't understand the foundation about hemostasis coagulation at the same time anticoagulation guys passing NCLEX. Passing NCLEX is not just passing NCLEX you know what I mean? You have to be a good nurse, you have to pass your NCLEX in order for you to be to become a good nurse here in the US or Australia or Canada or wherever it's applicable. You have to meet the standards. Alright. So it's challenging, right? It's challenging. What makes it challenging because you need to know what are the basics you need to know what is really you know, what is really NCLEX? And what is really becoming a nurse here in the US. All right, that's why I'm saying foundation is always the key. If you don't understand the foundation, you will not understand also, you know, the disease processes. Okay, so back in our lecture, so normally, I would write it here, I'm sorry. So normally, right here we have primary hemostasis. And as well as your secondary hemostasis. Your primary homeostasis involves your work involves your platelet Okay, your secondary hemostasis involves your coagulation factors, all right, your coagulation factors.
Okay. So, your coagulation factors, I would also include here I would say coagulation factors and that means to say involving your thrombin and as well as your fibrin so I would say here coagulation factors, which involves the to maintain which is your thrombin. The same time your fibrin Okay, so we have three things here, your platelet, your thrombin at the same time, you're fibrin. Your primary, your primary hemostasis involves your platelet. Your secondary hemostasis involves your coagulation factors, your thrombin and your fibrin Guide. ACL thrombin is basically what you're trumping is water soluble, I'm going to make it green. And your fibrin is non water soluble. Okay? It's non water soluble.
So what does it mean? When you say like non water soluble? When the fibrin is made, it's absolutely a mesh, right? When the fibrin is made, it means to say it's already stabilized, the club is already stabilized, it's non soluble. Okay, so there must be something like a mechanism to break down your fibrin because this is very sticky, you know, that makes your club stabilized and cemented in your blood vessel. Alright, so this is your primary and your secondary hemostasis. I'm going to draw that I'm going to emphasize more on that in my drawing. And in the presence of disease or disorder, give me an example of your disorder that causes clot formation, or that causes hemostasis. Come on, guys. I will, I'll have to look at your chat room here. So give me some examples, most common examples, or conditions that causes you to have hemostasis Come on, and make it in red.
Okay, this is a very NCLEX thing. It's a very complex thing. And of course, if it comes out in your NCLEX, definitely, of course, it's always consistent with what you see in the hospitals. By the way, I'm working in a medical surgical telemetry. And I can really see you know, what's really going on in there. It's a very active floor and it's very, very consistent with what's really going on what's really coming out in your NCLEX hemophilia, it's something about breathing DVT. Very good. So I would say like VT your venous thromboembolism, collectively known as your VT, which means that your DVT at the same time, your pulmonary embolism and your pulmonary embolism is actually caused by your deep vein thrombosis. Again, like I said, it's collectively known as your venous thromboembolism. Guys, we're still talking about hemostasis here. All right, when you say like hemostasis, again, Hemo means blood stasis means the blood is not moving. Because you know, it involves coagulation. All right, and that includes your primary and your secondary hemostasis. Give me other conditions, guys, give me other conditions. DVT. And I would say like coronary artery disease in which if you don't take care of it, it will lead into your acute coronary syndrome.
Your acute coronary syndrome comes in two forms your acute myocardial infarction. That's basically your acute myocardial infarction. Sorry. So that comes with two classification, your non STEMI and as well as your ST elevation in which we don't like it, all right, because the damage is more like you know, as compared to your non STEMI. We're not going to talk about mi here or ACS, this is basically your MI. All right. All right. So what else we also have your CVA. Right, your stroke, specifically of your ischemic type. All right, specifically a real ischemic type. Give me some more. You told me about DVT. Give me some more, let's just say your arterial stenosis as well. Arterial your arterial stenosis, or let's just say collectively as your peripheral arterial disease, right, peripheral arterial diseases, or let's just say venous insufficiency. All right. These conditions are just an example of your conditions that causes hemostasis. All right, more importantly, which is always coming out in your lecture DVT or pulmonary embolism, collectively known as your VT, your acute coronary syndrome, your CVA as well as your PA these peripheral arterial diseases and some of the venous insufficiency disorders, all right, which again, causes coagulation or hemostasis. All right, it's either normally because your blood is not going viscous, or it's either influenced by a disease or a disorder. I've mentioned it already. Okay, so there should be a balance right? There should be a balance. In a normal situation.
There's always like an anticoagulation. That's why your blood runs smoothly in your blood vessels. Again, the medium is your normal blood flow. You understand? All right. And another situation which is influenced by medication, we have your blood thinners your blood painters, I would classify it into three according to its, of course, when you give like that dangerous is always like bleeding, right? So it's always like bleeding, right? It's always like bleeding. Again, this is an anticoagulation mechanism. It's influenced by your medic medication or in a normal situation or a normal physiologic response. If you have a coagulation, we have your bleeding, right? So I will categorize it, like I said, according to its bleeding risk, we're going to discuss later on about your anti platelet Alright, so antiplatelet In other words, this involves your primary hemostasis Alright, the risk here is mild, mild risk for bleeding. Right? And the other one is your anticoagulants. Okay, this involves your secondary hemostasis. Alright. And the risk here is moderate risk. Alright, so these are the risks. The mild risk for your antiplatelet my risk for bleeding for anticoagulants, which involves your secondary hemostasis, your coagulation factors, which is moderate risk. And lastly, your five Brenau lithics.
Okay, your fibrinolytic switch also invokes your secondary hemostasis specifically to your fibrin All right, we already discussed about fiber a little bit right? Your fiber is non water soluble. You need to have a stronger anticoagulants, right? Not really anticoagulants, a stronger medication, which is your fiber analytics are also known as your thrombolytics. Okay, so hold on, let me just exit this one. All right, and the risk here for bleeding is severe. So we classify it according to being mild being moderate, and severe risk in your bleeding, or antiplatelet is mild risk for bathing. But again, there's always like a bleeding, right? There's always like a bleeding in terms of risk. anticoagulants moderates risk for bleeding. And finally, your fibrin analytics, the strongest of them all. If it's the strongest if it's the most potent, that means to say that you have higher risk for developing, you know, this severe risk of bleeding in terms of its category. All right, because it involves already your five brain. We're gonna give examples later on. Okay, so let me review your homeostasis here. Your balance between your coagulation at the same time your anticoagulation before anything else I forgot. It's always my norm to say something like a word of wisdom to you guys. You came into this journey, right? I'm going to start it with I would say like three words for you to to carry or 244, you know, take away words. Before we will end this discussion later on. Okay, I'm going to start it first with one word. Listen, guys, I'm not going to end up this, you know, this discussion if I don't have any words of wisdom.
Number one word is inspiration. All right, number one word is inspiration. Just a little pause on our lecture, we've, we've done your balance, or homeostasis or between your calculation and your anticoagulation. I'm just gonna review it in a little moment. Okay, so I will give you the first word, which is inspiration. All right, for what? You always have to be motivated. Whatever inspiration that you have, it will always propel you to success. All right? Whenever you are tired, for example, in your review, during the process, I would recommend like six months, three months is too early. You have to double time. All right, the ideal way, the ideal timeframe is usually six months. Okay? Whenever you get tired, that's a lot. Alright. Whenever you get tired in the middle of your fuel journey, while preparing your NCLEX, you always think about your inspiration. You always think about why did you take this examination? So that will propel you to your success? All right. That's the first word that I'm going to say in the middle or along the way. I'm going to give you the second one. And the third one would be you know, before we end our discussion today, that makes sense inspiration, you always have to have a motivation.
Why did you take this NCLEX like I said, Whenever you get tired, look back. Why did you take this examination? Again, that will bring you to your success later on. Let's go back to your balance here. So between coagulation and your anticoagulation, coagulation means hemostasis. All right, in order for you to have or to meet the balance, which is normal blood flow, your body needs to pour. For example, if I've got Galatian your body needs to produce anticoagulants in a disease or disorder we're in you can also develop coagulation basing on what I discussed like BT E, C, ad CPAP, AB, and some beans insufficiencies because of a certain collapse. In that particular disorder you need to have it's overwhelming, you need to have medications, which you know, balances the situation. And that's what we call as your blood thinners, your blood thinners are classified into three, I would classify it according to its risk for bleeding. Number one is mild risk for bleeding, which is your anti platelet primarily, which involves your primary hemostasis. That's your platelet. All right, and your anticoagulants, which involves your secondary hemostasis. All right, it's moderate, moderate risk for bleeding.
And lastly, your fibrin Analytics, which also involves your secondary hemostasis, which specifically, you know, pertaining to your fibrin and that is high risk for severe risk for bleeding. Okay, so that's how we're going to categorize that later on, I'm going to give you the medication specifically. Alright, because that's the bulk of your topic for today. And that's basically your NCLEX let me bring you to this drawing. All right, let me bring you to this drawing. So to better emphasize what's really going on if we have clapping, alright. So, this is your play if you have some form of like I said in a normal situation even in normal situation your blood is normally or naturally viscous, it will create clotting mechanism right? How much more if you have injury and the your blood vessels this is your blood vessels by the way, all right, this is your blood vessel in the inner portion we call it as your endothelium right your endothelial from the word itself, endo means within alright. So, this is subject for wear and tear. So at anytime you always have, you know, you anticipate injury to that blood vessel and how much more if you have some form of a disorder, okay. So let's just say this is injured, this is injured, alright. So, this is injured or traumatized because, um, for example, like wear and tear without even a presence of your, you know, not even a presence of your disorders because of wear and tear, platelet arrives, right, platelet so what is platelet again? Is it primary Namo stasis or secondary hemostasis? That is basically your platelet.
All right, which is your primary hemostasis. Alright, they will adhere to the area. What's the difference? Difference between your adhesion and aggregation? Guys? What's the difference between your aggregation and as well as adhesion? Can anyone tell me what's the difference between your adhesion and aggregation? This is very important. This is very basic. Okay. watching live from gun as well. All right, burgers disease can for instance, yeah, can also cause some call forms of calculation. All right, what else? All right. What did they tell you? What's the difference between adhesion and aggregation? adhesion is primarily platelet going to the area sticking to the area, the first platelets that will arrive to the area, that's basically your platelet adhesion. All right. If this platelets will invite more platelets to arrive in the area, that's what we call platelet aggregation. All right. So again, platelet addition is the first few platelets that will arrive to the area, okay, and the next field in the next platelets that will go to the area or that will stick to the area, we call them as your platelet aggregation they will aggregate to each other. So one plate to another plate to another platelet. Those are what we call a short platelet aggregation. Anyway, this is your primary hemostasis which involves your platelet okay, so this time on, you know where I'm talking here. So there should be a certain medication to you know, to prevent platelet from coming in, or platelet from adhering or from you know from aggregating.
All right, that's your platelet. Now, the second thing, second thing is your what a second thing or your coagulation cascade. All right, which is again and which involves your coagulation cascade or coagulation factors, sorry. So the green ones, I would make it bigger, but they are absolutely small. All right, this is what we call as your coagulation cascade. All right? When you say like cascade, it's a series of events. Again, this is your secondary hemostasis involving your work, your coagulation, your coordination factors, coagulation factors, I'm gonna draw something like this. Okay? I'm gonna draw something like, let's make it black. Draw something like this. There you go. Okay, your calculation factors, by the way, you calculation factors is made up of three pathways. I'm gonna put it here intrinsic. And this one here is your extrinsic pathway. Alright, so this is intrinsic pathway, an extrinsic pathway. And in the middle, we call it a short common pathway. Alright, right. So I'm discussing to you guys, what is coagulation cascade? Right? Before I'll go to that, let me move on to my drawing here.
And the last one would be one, the last one would be your fibrin, right? The last byproduct will be your fiber in your fiber. And actually, what again, like I said earlier, stabilizes your gluts and it's none water soluble. Let's go back to this to these pathways. The intrinsic pathway, the instant extrinsic pathway and the common pathway. Again, it involves coagulation factors that coagulation factors that involves here are what factors 1211, nine and eight in your intrinsic pathway. In your extrinsic pathway, the involved clotting factors are three and seven, okay three and seven in your common pathway, so, this is one this is second and this is third, they will meet in the common pathway by the way. So this is 10. This is five, this is clotting factors, number two and clotting factors. Number one, when you say clotting factors, number two, it involves your thrombin. What is your thrombin? Again, thrombin is water soluble. And clotting factor number one, it involves your fibrin which is basically what non water soluble. So coming from an intrinsic pathway and extrinsic pathway, it will develop to form a fibrin that issue coagulation cascade. By the way, let's take a look at other measures. Here are other parameters that you need to remember, your let's make it read your factor seven, your factor then your factor to even your factor nine or defendant dependent to your vitamin K. If you don't produce or synthesize your vitamin K, this factor seven 910 and two is not going to happen again without the presence of your vitamin K.
So I'm going to put an arrow on it. Okay. So vitamin K, again, has a role in your clotting mechanism. Okay, Vitamin K has a role in your clotting mechanism. All right, we measure the time in your intrinsic pathway before it goes to your you know, to your common pathway. So we measure here, what do we measure here, we measure your, your partial thromboplastin time, right? Your partial thromboplastin time, the normal time of your partial thromboplastin is about 25 to 35 seconds, okay? And also in your extrinsic pathway, we also measure your PT and as well as your INR. Okay, your PT as well as your own or your INR don't mean forget about your pee. Think about your INR. It's the calculated probe prothrombin time already, okay, your INR is about 0.9 to 1.18. Without any again, without any influences of your medications without any influence of your warfarin, for example. Your Warfarin works here, by the way, your Warfarin works here. Okay. And your heparin also works here. That's why you mentioned your PCP, warfarin, you measure your INR. Okay.
Anyway, back to here, intrinsic extrinsic pathway, just to you know, just to summarize it. We have graphing factors involved here, seven 910 and two is the pendants are your vitamin K, that's your target. And the byproduct is your fibrin. Okay, the byproduct is your fibrin and we don't want vibrant to develop because again, it's not water soluble, it will stabilize your club. So that's your clapping formation. Alright, that's your clapping formation. Let me draw here versus, okay, there should be a normal mechanism, there should be certain things that needs to balance the clapping in order for you to have a good, good, you know, blood flow. That's your medium, right? Basing on what I discussed earlier. So I'm gonna put here something like this are the chemicals involved here. I'm gonna write here. Let's just make it red. All right. Is it really showing? Yeah, I guess so. So this is your it's letter H. That's a heparin molecule. Alright, that's a heparin molecule. Your heparin molecule binds to a specific kind of protein, which is what we call as your anti thrombin. The green one is what we call as your anti thrombin. Alright, the green one is an anti thrombin, which means anti thrombin is anti clotting factors. Number two, alright, so it's against your clotting factors. Number two, later on, when I discussed the medications, I would relate it to my drawing, right? I would relate it to my drawing, there's another chemical here, actually, it's a complex chemical.
All right, it's a complex mechanism we're in you have I'm gonna draw something like this. And it binds to a specific I'm gonna make it black this time. Right. This is what we call as your thrombomodulin. Alright, this is what we call a short thrombomodulin. Complex, right thrombomodulin complex from the word itself. thrombo. It will modulate module in means while it's a protein that modulates your thrombin, specifically your thrombin. Alright, bye some other proteins like your protein C and your protein as well. So there are two proteins involved here protein s and as well as your protein C. So that's why it's called complex, your protein C and your protein S together with your thrombomodulin will actually be activate your thrombin. Alright, will be activated thrombin. And lastly, I'm going to make it green again. And lastly, we have your this is a protein which is a shortcut. I'm just going to make a shortcut alright. So, this is a complex kind of mechanism. I will say that this is your plasmin Alright, your plasmin your plasmin actually is a broken down plasminogen. When you break down your plasminogen you will create your plasmin right? Remember plasminogen when you say like Jen, these are complex, you know these are complex protein. When you break them down, it will form plasmids specifically when you break down your plasminogen coming from your labor, it will create plasmid, okay, and there should be a certain protein or uncertain enzyme, not an enzyme. It's a polypeptide I'm not mistaken. We call it as your tissue plasminogen.
This is not a shortcut anymore. I'm already discussing this one. So we call them a short PPA. Normally your body produces TPA. Your TPA is a tissue plasminogen activator. In other words, it will break down your plasmin manual plasminogen to foreign plasma in your plasma and works with your fibrin so it will fight your fight brain. Again plasmin fights your fight brain. So it's an anti fight brain kind of you know, chemical. It's a fibrinolytic it will break down your fibrin. The byproduct between the two of them is what we call as your D dimer. That's why have you heard about the dimer guys? Have you heard about D dimer? When you say D dimer when your D dimer is elevated? The normal value is 500 or less than 500. If it's more than 500. That means to say you are developing clots, right? Again if your D die is elevated that means to say that your body is producing tissue plasminogen activator to again to break down your plasminogen to form plasma and because your body is producing lots of vibrate that's an indication again that your body is forming clots. The dimer can be increased in the presence of your pulmonary embolism, for instance, that's what I mentioned earlier. All right. So this is the balance guys, if you have clot formation here, if we have gluts formed here, we also have certain mechanisms that will, you know, break down your gluts by again, by producing antithrombin.
Together with your heparin molecule, they will bind together to enhance anticoagulation activity. We also have your protein C protein s, your thrombomodulin is a protein, which we'll also break down your class, specifically your thrombin and reward itself thrombomodulin Can you still follow? Are you still with me guys, it will modulate your thrombin a, I'm gonna deactivate you. And lastly, we also have your tissue plasminogen activator, which will break down your plasminogen to form plasmin. Because plasmin is anti fibrin. They're byproducts when the plasma and fibrin fighting together byproducts is what we call a short D dimer. And some other byproducts, which is collectively known as your fibrin degradation products. I'm not gonna mention anything about that. One of them is your d dimer, which is very sensitive to your blood draws, I mean to your, you know, to your serum, right. So anyway, this is your mechanism. Why did I discuss this? Why did I discuss this? Because this is the target of your pharmacology. This is the target of your antiplatelets the targets of your anticoagulants in terms of its mode of action in the targets of your, your fiber in the Olympics. Right. So did you understand this? Are we good? So let's move on to your medications.
Let's move on to your medications. Guys. Any questions? Thank you, Mr. Oduro. You're coming from where? All right, Mr. Mr. Irvin, she's he's from his from our Niners closer, are you doing again, this is I really love this, you know, this platform of Connetics, this is Connetics College in coordination with other review centers like us, buyer, miners and swash. So guys, I really thank you guys for helping us, you know, at least to become instruments of these people's success. And I'm really happy about it. Right. So anyway, always wants to refresh memory. Yes, this is really refreshing. Right.
You know, our preview is not just review. There are many things back in college that we're not able to reconcile in terms of, did you understand it really well? We're not all right. There are many discussions to college that we're not we're not able to understand because probably lack of time. All right. So. So like I said, for example, in Ibis as much as possible, I will really discuss about the foundation, there are many, you know, discussions in college that were not able to reconcile, and it's very important, so it's not really a review. After all, that's why I call it Academy. Because, you know, as much as possible, everything is there. You know, so, you know, we'll have to give as much as we can. Alright, so let's go back to your medications to your medications. Alright, so we have three classifications of your medications according to risk. All right. So my address, moderate risk and severe risk for bleeding, right? All of the blood thinners causes bleeding antiplatelet causes well antiplatelet causes mild risk for bleeding. All right, so underplayed that's give me an example of your anti platelets. I'm just going to make it green. I would say the examples we have bought, come on, come on, guys. Come on. So what are the what are the examples of your anti platelets? Most commonly what most commonly what?
A very famous medication. Now were discussing about your blood thinners, this is kind of fast, you know, discussion? Aspire RN, very good. Your aspirin, the famous aspirin, it's an antiquated medication at the same time. At the same time, a blood thinner. I mean, it's an adequate at the same time and NSAIDs, right. So let's go back here. I think I forgot something here. In order for you to prevent platelet. We also have some chemicals. Alright. We also have some chemicals which is what we call as your nitric oxide. Forget about this. We're not done yet. We have nitric oxide, it's just too much right. We have nitric oxide the same time, your cyclin your process cyclin your pasta cyclin from the words of pasta prostaglandin it's something about inflammatory response. All right prostor cyclin, your pasta siping your nitric oxide or anti platelets, alright, again, your nitric oxide and your prostor cyclin are anti platelet chemicals that is normally produced in your body. Now let's go back to your aspirin. Your aspirin activates that certain mechanism in order for it to prevent your platelet from coming from adhering at the same time from aggregating that your aspirin. Give me something else guys. heparin is an anticlimax, right. So unpopulated. Those are two different things on the plate, that's your aspirin. The other one would be what the other one would be your clopidogrel alright are copied to grill. Give me something else. The other one would be prasugrel, prasugrel. Okay. And the other one we would be like Calgary lower.
All right. Your aspirin, clopidogrel and your Prasad Grande, your tech regular, I cannot pronounce it really well. I'm still having a hard time in pronouncing it saying it. These are antiquated medication. Your aspirin specifically acts to your to your blood vessel in terms of preventing your prostate cyclin cycle. Okay, or mechanism. Alright, so your process cycling cycle is also found in your inventory response. So in other words, it's an antiquated, you know, kind of Medicare at the same time, it's an anti inflammatory kind of medication. Right. Your Copy the granule. prasugrel is actually the mode of action, let's just write it in red. All right, the mode of action of your aspirin is to stimulate I mean to I mean, preventing your platelet basically, and your Copyblogger passerelle. And you're like Calgary Lord is actually an anti ADP. And ADP is a chemical which is produced by platelets. And ADP, again is a chemical that is produced by platelets.
What happens if you produce this ADP, it will promote platelet aggregation, hey, if I'm the platelet, I'm going to produce ADP. I'm going to produce ADP to invite more platelets to adhere I mean to aggregate to the area. Okay, again, your platelet is able to produce certain chemical sector ADP to invite more platelets right so, that's the work of your capito girl your prasugrel and ticagrelor are aspirin is more on to your process cycle in cycle All right, that's the mode of action specifically Okay. By the way, when you say antiplatelet This is also a common question in your NCLEX paying it will you know it will it will alarm to your mind and say like it will come out in your NCLEX please take note and remember that antiplatelet is the primary you know, reason why you get platelet is to prevent further class. Okay, this is to prevent further clots, specifically of your platelet because again, platelets involve in your hemostasis Alright, so your aspirin or clopidogrel, prasugrel and ticagrelor.
So the nursing responsibility again, this is something to do with your NCLEX. So I already wrote it down. So not to consume time. Please monitor the platelet, what's the normal platelet count, the normal platelet count is 150,000 to 400,000. Okay, let's remember this is an antiplatelet you monitor for the platelet count, okay, if it's less than 50,000 You have to hold the medication informed the physician and then hold the medication in form HCP or if the doctor will order anti platelet without looking at the platelet count please question the order. Did you understand again please question the order if the value of your plate that is less than 50,000. Okay, less than 50,000. Again hold in form the position or question the position if it's you know if he or she is about to order, an anti platelet How about your hemoglobin And our magic number here is not less than seven. If it's less than seven, your patient is high risk for, you know, there must be something going on. All right, your patient is high risk for bleeding at the same time you're giving an anti, you know, anti platelet medication, just putting your patient into high risk for bleeding. Alright, so the magic number there is seven, please do not give the medication. If your hemoglobin is seven, H and H means hemoglobin and hematocrit, your hemoglobin, right? So what's the antidote? This is platelet aspirin. What's the answer to aspirin by the way? So? What's the antidote to aspirin by the way? So anyway, so I'm just going to skip this one.
More importantly, we're going to have an antidotes discussion about your anti Cohen's at the same time your fibrinolytic, I would say, right. So anyway, so this is your platelets. So what did you monitor guys, you monitor for your platelet? At the same time, your hemoglobin? What about your toxicity? All right. What about your toxicity? Aspirin toxicity? This is also a common question, right there aspirin toxicity. Your aspirin toxicity is a very common thing, which is characterized by what's characterized by tinnitus. All right, that's a sign. This is an NCLEX tip. So they usually ask about tinnitus, again, related to your aspirin toxicity, because it's auto toxic. Aspirin is basically auto toxic. All right. So in here, what we do is this is what I'm talking about. So there's after all, there should be the you know, there's an antidote. There's always an antidote for everything, right? So in including, you know, everything, so there's always like a balance. If you remember that I started my lecture about balance, right? So there's always like a balance. So, there should be like an antidote, if you have aspirin toxicity, I would say NCLEX is always asking about activated charcoal. Alright.
Take note that activated charcoal, this is the one that you give if you have aspirin toxicity, you answer that activated charcoal and what else other things other than tinnitus, which is a very common thing is your respiratory alkalosis which clinically you can see your patient that is, you know, hyperventilating. So I would write your hyperventilating hyperventilation, there you go, your patient will hyperventilate, respiratory alkalosis in your blood gases, and as well as tinnitus. Again, if you have aspirin toxicity or they're gonna get activated charcoal, alright, and of course, you have to monitor the bleeding Science Monitor the bleeding science we're going to discuss to you about the bleeding signs, you know, from head to toe, the most common you know bleeding signs that you can see from your patient. Okay, let's move on to your antiguo OGS romantico is in general just like your anti platelets, it will prevent what it will prevent I'm gonna write it here at the side it will prevent which is also a common NCLEX thing. It's an NCLEX that prevent the size of the existing prevent the size of the existing class. At the same time it will also prevent further clouds just like your platelets and they click that sorry, again and they go eggs will prevent the size the existing size of your class of the existing class at the same time prevent further coagulation cascade in that's is your heparin. Your heparin is this is what you're telling me earlier. Alright, so your heparin your heparin is an anticoagulant that is not an antiplatelet. Those are two different things. When you say heparin we have two types of your brain, your unfractionated and your low molecular heparin. Your unfractionated is the IV form, in a form of a drip. That's how you administer it. Your low molecular weight heparin in a form of sub q. That's the route of administration. This is a very, very, you know, a common topic in your NCLEX. In fact, this is the bulk of your blood thinners in terms of you know, what they ask.
All right, what are the examples of your low molecular weight heparin. Okay. So I would say your unfractionated in terms of its mode of action. Before I proceed with the examples. Your unfractionated is actually let me write here. The mode of action is specific to your words specific to you or factor two and factor 10 as well, clotting factors number two and clotting factors number 10. So here they are actually called as your direct acting, direct acting oral anticoagulants direct acting oral or direct acting, let's just say direct acting and they go eggs. Alright, which means to say it will directly add to your clotting factors, for example, clotting factor number two, and clotting factor number 10. I guess we're having a good time here. It's already almost eight. Right? So this is a big topic. By the way, let me just make it like that. Can I extend a little bit? Can we extend a little bit of time? I guess for like, 30 minutes. That'd be fine. Right. So I guess this topic is really good. I will say this topic is really good, right? So this will help you. So your low molecular weight heparin is actually specific to your clotting factors number 10. Okay, specific to your clotting factors number 10. So what are the examples of your low molecular weight heparin, so I'm gonna make it where is my pen? I'm gonna make it green. That's your enoxaparin. Alright, your enoxaparin you're not suffering what else? You're Fulda paradox. All right.
This is a newer version of your enoxaparin paradox. Right? If you notice, if you notice enoxaparin x a, and as well as x here, in Oaxaca, in in your phone, the paradox x means what 10 clotting factors number 10, specific to your clotting factors number 10. All right, that's your enoxaparin and as well as your food in the paradox enoxaparin the problem you're not suffering is that it's high risk for developing your what your heparin induced thrombocytopenia. Alright, so higher risk in developing your heparin induced thrombocytopenia, you will find the paradox is lesser risk of developing hits, I would put an arrow on it. Okay, that's your heparin and fractionated that your IV drip your low molecular weight heparin. So that's specific to your cutting factors number 10. Your fractionated is specific to your not only your time but as well as your clotting factors. Number two, you already understood you know what clotting mechanism is right? In your enoxaparin are the examples of your low molecular sub q and foond. The party knocks Alright, so in saffron is lesser chances of heparin induced thrombocytopenia, your phone The paradox is lesser, I mean, he looks up and is higher chances of hit from the bar enough is lesser chances of your hips. Okay. So let me move on to your nursing care related to your anticodon specifically of your Heparin, of course, you need to check for the signs and symptoms of your reading, check for your platelet as well.
Again, our parameter here is if it's less than 50,000, or let's just say if the platelet is 50% less of the baseline. If your platelet is for example, 300,000 went down to 150,000. So that could be hits heparin induced thrombocytopenia, specifically, for example, your unfractionated and as well as you're not suffering from the paradox, lesser chances of your hips, okay. And of course, your H and H, your hemoglobin count of less than seven you need to inform the doctor and you have to understand that this is to be measured your PTT, your magic number here from the word itself. I mean, from the word itself, your PTT always remember, it looks like letter H. That's why you have to monitor that. Okay? And your PTT is to be measured only for your unfractionated, alright, your unfractionated, you don't measure it in your what? In your sub q. I will put here IV fractionated. So your PTT again, p dT it looks like letter H. So that's how you measure it. And so, your PTT is the magic number here that you need to remember. Please do not exceed more than 70 seconds again, more than 70 seconds. More than 70 seconds is already as I mean higher risk for bleeding. More than 70 seconds. This is already high risk for beat.
I'm gonna highlight this one. Again, if it's more than 70 seconds, that's the magic number. It has to be less than that therapeutic. All right, if it's more than 70 seconds, your patient is high risk for bleeding. Did you understand? What's the antidote for your heparin toxicity? What's the antidote for your heparin toxicity? The antidote for your heparin toxicity is what? Your Protamine sulfate. Alright? This is also a common thing, right? Your heparins I mean, you're praying you're Protamine sulfate. Remember, this is heparin. If you look at the mode of action. Look at the drawing here. So it basically binds to your anti thrombin. So heparin is an anti thrombin. Let me add it here. So heparin is an anti thrombin. I'm gonna make it read. It's an anti thrombin enhancer, right? So it's an anti thrombin enhancer, it enhances your anti thrombin activity, it will bind to your anti thrombin so that it will deactivate your thrombin specifically to your Traumeel going back to your nursing interventions, no please. When you do your subcutaneous and this is also NCLEX. When you do your subcutaneous injection, please do not massage. Right Do not massage or do not rub please, no massage to the side and no rubbing to the side.
And another question which is common to subcutaneous you know, Heparin, low molecular weight heparin, please do not ask for it. All right, just leave it as is and then inject it to your patient. Another thing another question related to this low molecular weight heparin, specifically of your phone, the paradox I'm gonna write here subcutaneous, full the paradox. Phone, the PA Rhinox. Your phone The paradox is withheld for a patient having spinal anesthesia. All right, for a patient having spinal anesthesia, a patient having spinal as the anesthesia. You should hold blood thinners in general and more specifically, your from the bottom knocks within six hours. post op. All right, the magic number there is six hours. So within six hours of your post op status, please no blood thinners, you can only give blood thinners especially if your patients have been spinal anesthesia, an epidural catheter only after six hours and special mention to your phone the paradox again a low molecular weight kind of heparin. Okay, so hold within six hours after surgery, especially if your patient is with spinal anesthesia and epidural catheter is inserted there for pulling the battery. No special mention. I'm always repeating that so you will remember it. Okay. So next up, we have your warfarin, your warfarin. Okay. Your Warfarin is the P O form. Right. This is the P O form of your heparin basically. All right. So P O form of your heparin so your Warframe is the mode of action is this is an anti vitamin K. So anti vitamin K, in other words, it's a vitamin K inhibitor. Alright, it's a vitamin K. I'm having a hard time writing it because it's looking like it's hanging a little bit. inhibitor. There you go. It's an anti vitamin K or an inhibitory to your vitamin K.
That's the work of your warfarin. So what do you need to monitor of course the signs of bleeding. All right, and you also monitor the INR. Okay, the INR. The INR should be what the INR should be not more than three to five seconds. Don't forget, that's the magic finger here. If it's more than three to five seconds, again, if it's more than three to five seconds. Patient is high risk for bleeding. Right? The patient is high risk for bleeding, you might call that medication, H and H again, hemoglobin is not less than seven. That's the magic figure here in your NCLEX. No need for platelet has no need for platelet checking. You don't need that. It's only for your ward. It's only for your heparin because heparin can induce your hyper Amin heparin induced thrombocytopenia, so no need for platelets checking. What's the antidote for your Warframe? What's the antidote for your Warframe? What's the antidote for your Warframe guys? bite them in A write your vitamin K, because they fight each other. Right. So they are, you know, they are protagonists, they are counteracting to each other. So antidote is vitamin K common questions related to your Warfarin related to vitamin K specifically. question Where do you get abundant? You know, Vitamin K, from a green leafy vegetables? Right? From a green leafy vegetables? green leafy vegetables, okay, from green leafy vegetables? Do you need to increase the green leafy vegetables or lowered amounts of green leafy vegetables intake? No, you just have to be consistent. All right, you just have to be consistent. Again, green leafy vegetables, you just have to be consistent in terms of intake, you don't need to lower your intake or increase your intake of your green leafy vegetables. Okay, just have to be consistent. Another thing is that your antibiotics, antibiotics, does that affect your vitamin K? Yes, it affects your vitamin K, it affects your warfarin. Because antibiotics remember antibiotics doesn't only kill the microorganism at the same time, it also kills the microorganisms inside your colon. Alright? The colonic microorganisms, there is actually four can synthesize your vitamin K.
So whenever you give your antibiotics to your patient, again, it will affect your vitamin K, eventually it will affect your Warfarin to get that. So that's your vitamin K, these are the things that you need to remember related to your vitamin K in relation to your warfarin. Okay. So again, for your antidote, Vitamin K, you just have to be consistent to Warfarin hand, that's your Warframe. Let's move on to your other anticoagulants, your other anti co OGs. I'm having a really hard time you know in terms of to maximize my, my lecture in a minimize time. So I would say there are the modal opposite of this antico x is again the same thing. It's a direct acting oral anticoagulants for example, we have your argatroban All right, your argatroban The other thing is your bivalirudin bivalirudin, which is a lot guys. And the other one would be your, your, the big, the bigger trend. These are very common to your NCLEX. Right, I'm gonna write it again. The bigger trend, you go argatroban in your bivalirudin dice, these are your IV form and your the bigger trend is your P O. Okay? So they directly up to your words to your clapping factors. Number two, all right, on the other hand, we have the famous APICs urban we have the famous your rivaroxaban. All right. And lastly your adopt Serban. Wow, this is basically your what? Pharmacology so it's kind of hard, right? But it's doable APICs urban SPO everything is like P O here and your adoptable is also P O okay, this is from the word itself APICs ser Roxa adoxa Clapping factors number 10 clotting factors number 10x Absolutely it's a cofactor which is you know your x a.
So clotting factor 10 Right. So for argatroban by bilirubin and the bigger plan is clotting factors number two pixelmon ribber, oxygen and oxygen or Po. These are alternates for your what alternates for your Warfarin or right. So this is an alternative to your warfarin. And when you say like argatroban by beluga, then when the big Adtran these are alternates to your heparin. For some reason, for example, like your patient is allergic, you know, to your Heparin, you do your argatroban you gave you a regard to ban by bilirubin and you're the bigger trunk as well. Okay, the good thing about your Pixa and the Baratza and doxorubicin alternates to your warfarin, you don't need much of ovulation laboratories. Alright. So warfarin, by the way, is very good in patients with what with ESRD don't forget, and as well as with valvular problems or bipolar disease. Okay, we valvular disease, again with ESRD at the same time with valve disease, let me move on. So again, you're APICs a band in relation to your warfarin. This is not given to a patient having ESRD. And this is not also good for a patient having valvular disease, in other words would be Warfarin instead.
The bad thing about Warfarin because there's so many blood works. On the other hand, when you say like picks up on river oxygen, which has a lower risk of bleeding, right, no need for CO works laboratories, you just have to check for check for BU and creatinine. Because this medication is or can cause kidney problems as well. Alright, so check form it's written here already your BU and creatinine. You also check for your hemoglobin is, you know, the magic number is seven. And it's not combined with heparin. Don't forget, it's not combined with your heparin because it's a very strong medication. Right. So let's go to your thrombolytics. Guys, your thrombolytics if your heparin if your anticorrosion undepleted prevent clots, alright, prevent clots. Okay, your thrombolytics disobey gluts. So it's a clap Buster, it will be sold. Claps, okay, the Sorbs class. So this is a strong kind of medication from politics. The examples of these medications are what? Your alteplase, alright, your alteplase can be given IV in an hour. All right, IV in an hour, or catheter assisted, or catheter assisted, when you say that better assisted, you're going to insert it to your, for example to your groin. And you will give them medication, it can stay there, you know, it can stay there up to 72 hours. So your patient is high risk for bleeding for about three days. But usually the clot will be sold about 24 hours. All right.
So it's either IV or catheter assisted. Kind of jumbo lysis. That's your alteplase guys. This is a very strong medication, please. The nursing intervention here is what no IV, no extra IV, no is no sub, you know, ABGs no arterial blood gas monitoring? Because, again, your patient is high risk for bleeding. All right? It's not given through a central line. Why do you think it's not given to a central line, because a central line it's not compressible? Might as well give it for example, IB might as well give it like peripheral because at any time, it will bleed out, you can compress. If you're gonna give it to a central, for example, IG or subclavian, you cannot compress so you cannot prevent the bleeding. Again, this is an NCLEX step for your thrombolytics. It's given, you know, nap central line peripheral IVs spine. Alright. So avoid contraindications. There's lots of contraindications. For example, if you are if you had surgery, within two weeks surgery within two weeks, we're almost done here. Surgery within two weeks, two weeks time. All right. If you're AB malformation if you have a your tick aneurysm All right. Let's just say aneurysm in many types, aneurysms what else? Your take aneurysm if you are with trauma. If you have trauma for the past three months, and who knows you have some form of you know, bleeding in your brain.
So let's just say head trauma. All right, let's just say head trauma. So if you are if you had CVA ischemic form for the past three months, alright, because who knows you already got your thrombolytics. Again, you are very high risk for bleeding. This is the severe risk kind of category, right? So what else? Your tic aneurysm? And let's just say your tic de section as well. Right, your tic dissection, we're in there staring off your aorta, so you're also high risk for bleeding. These are just some of the Contra indications. Again, you cannot give your tumble latex if you have this contraindications with you guys. Right. Before I move on to the general teachings to your blood thinners generally, generally. Okay. You forgot about my second word. I forgot about my second word. What's my first word inspiration. My second word for today is adversity. I should have relayed it to your you know, the time I said about pharmacology, which is kind of difficult, kind of difficult topic. But these are some of the adversities that we're encountering during our during our preparation. Right? However, you know, adversity always come, it always come down, you know, during the middle of our struggle during the middle of our journey in every journey that we are encountering, right? However, if you have adversities in your life, at the end of the day, we still do our best. We do our best shots.
We do our best in order to surpass these adversities. Okay, so I'm telling you guys, please, even if it's difficult, even if it's challenging, as long as you do your best, we are made by the Almighty to have abilities to overcome these situations. All right. We are not done you know, forget my forgive my word. We're not dumb enough to do not understand these kind of concepts because we learn it in college already. But again, like I said, at the end of the day, we do our best. Okay, we strive hard, we work hard, because we want to get this journey. We want to get the success. That's the second word. I'm gonna give you the last word later on. Alright, so general teachings blood thinners, please avoid egos or egos right. And what is this? This is a mnemonic guys are almost done. So your ad goes is Vitamin E letter E stands for vitamin E, sorry, that's vitamin K. Okay, so letter G A is your gingko biloba, a memory enhancer. We have ginseng. All right, we have garlic in as well. So what's the other one? garlic in your? What else? Ginkgo biloba, ginseng, garlic and as well as your ginger. All right. How can I forget this, the 4g is the fourth This is our herbal medications that causes bleeding. So avoid gingko biloba.
Avoid garlic and as well as avoid ginger. Again, this will put your patient at risk for bleeding. This is in general, if you're taking blood thinners and lastly, we have your Omega three omega three, avoid Omega three as well. I'm also going to put your letter S letter S stands for St. John's wort. St. John's wort is a medication for an herbal medication for depression. So St. John's wort is also putting your patient at risk for bleeding. So please take note of this medication. So avoid a ghost or ego's if you're taking any blood thinners. Alright, of course I mentioned about labs and it's you know, specific, you know, blood thinners and the breeding science. So what are the breeding signs for example, in your neuro, okay, your patient might complain headache, that could be also a sign of bleeding, which is intracranial which is more severe course intracranial hemorrhage, what else your patient might experience nose bleeding epistaxis, your patient might experience gingival bleeding, your patient might experience GI bleeding, upper GI bleed in the form of your coffee ground, you know, vomit vomitus or in a form of your hematemesis a fresh blood and it could be a form of your lower GI bleeding or in your patient will put fresh blood Hamato Petia or your BlackBerry stool. These are the common things these are nursing, really. And the patient might have bruising, guys, bruising is just normal, right?
Again, bruising is normal. You don't panic if your patient is having bruising if your patient is taking blood thinners Did you understand Okay, so again, the most common signs and symptoms of your bleeding that you can see from your patient which is also common, commonly asked in your NCLEX are GI bleed. Okay, but whenever the patient feels having like abdominal pain, it doesn't mean that your patient is already having abdominal bleeding or GI bleeding. Right? Not unless if your patient is vomiting blood or having some coffee ground aspirate upper GI or lower GI having some fresh blood or Hema to Keisha or Blackberry stool, that's a sign of bleeding, you need to report that to your physician. In other words, you need to hold your medication. Alright. And you can also have hematuria you can also have vaginal bleeding. These are the signs of your bleeding that you need to inform your physician again most commonly your GI bleed, right? And please avoid trauma. These are very common You know, NCLEX thinks no contact sports. You have to increase fiber in your diet, increase oral fluid intake, so as to avoid constipation because constipation can cause if you have hemorrhoids there, it can cause bleeding to your hemorrhoids and then you're taking blood thinners, you have to have a well lit horse because we don't want fall from our patients.
We don't want injury. All right. Avoid fall as well. That's also a favorite in your NCLEX soft bristle toothbrush to avoid gingival bleeding. No flossing, please. No flossing. And lastly, I mean, no razors and bruising is also what bruising is also normal. Question mark, because bruising can be normal. Okay, unless if your patient is having active bleeding, and then that's a problem. No razors as well. Okay, no razors as well. Question. This is kind of a critical thinking guys. All right. Because some of the some of the references that we have, we cannot combine blood thinners. QUESTION Can you combine blood thinners or not? Can you combine blood thinners or not? Can you the answer is just yes or no. Yes or no? Can you combine blood thinners yes or no? Guys come on. Can you combine blood thinners? For example, can you combine antiplatelet and as well as your anticoagulant? Oh, okay. Can you Is that okay? If your patient is having for example, like DBT which will lead or can lead to pulmonary embolism. And your patient is also having coronary artery disease which is acute coronary syndrome. The patient is very high risk. Good.
You can you can I was just soliciting your answer guys. It's either yes or no. Okay. You can have for example in in coronary artery disease patient depends upon your doctor's prerogative. But in general, in general, what we do is as much as we can, we don't combine it in a nursing perspective, right. If the patient is taking two medications at the same two blood thinners at the same time, it has to be prescribed by the position. So it still Yes, as long as it's prescribed by the physician, especially if your patient is high risk to develop clots, for example, like having DVT recurrently. The same time, the patient just had a heart attack your acute coronary syndrome, they might get dual therapy of your unreclaimed. That's for example, getting aspirin and getting grupy to grill. Plus the fact that this patient is also developing some form of acute coronary syndrome. Because the patient is smoking, the patient is hypertensive, the patient is diabetic, et cetera, et cetera. High cholesterol. These are very high risk individuals. The doctor might add another Enrico lungs. So now they plated and antico eggs can come together as long as it's prescribed by the physician. All right, combining your heparin sorry, it's, it's a little bit slow me, you know, my laptop. Because I'm using a different app, heparin and a different app for my drawing heparin at the same time, your warfarin, this is what we call as bridging right.
So this is bridging from your work Heparin, which is IV and then became sub q, and then bridging it to become P Oh, by the way, Warfarin is a long term kind of medication. Okay. So you're gonna get it, you know, long term, the problem in your Warfarin is that you know, too many like blood works, make your INR you need to monitor it. Okay, can you give this one together? Yes, it can overlap to each other. Okay. Your Warfarin works after five days, okay. It works after five this? Okay. This is the problem of warfarin, it doesn't work immediately, unlike your rivaroxaban. And like your, your picks have been so big, right? Remember, you're a big Saba and your blocks have been or alternative to your warfarin, it works immediately. And like a warfarin, it works after five days. So before your Warfarin works, please keep your heparin for a period of five days. All right, for a period of five days. By the time you understand what I'm saying here by the time your Warfarin is already working, and how do you know if it's already working? Of course check for your PT and most importantly, your INR if it's already therapy. Take, as long as it's not more than a magic number is 3.5 seconds. Did you get that? Right, Heparin, and Warfarin can go together, right? So they can overlap to each other. Right? In five days time, you're able to see the Warfarin is already working, how do you know, check the INR level? As long as it's not, you know, more than three to five seconds. 3.5 seconds. You're good.
Okay. Lastly, my word of wisdom is, above all, spirituality. So what's the number one thing inspiration? Because we are motivated by our, you know, our, our inspiration, why would we take this examination, secondly, is adversity. Along the way, you will encounter some struggles during your review process, you know, talking about NCLEX. Right, but again, you do your best. Alright. And lastly, is spirituality. For you know what, because everything is absolutely useless, if you don't have a good spirituality, if you don't have a good relationship to the man above all, to the glory and honor to God. And that's our lecture for today. Thank you guys. Any questions? Mr. Joon said it depends upon the VT e score. That's really correct. So I that's a separate discussion in terms of indication or in general, you can give it to like a total ablation patients with vascular problems. We have CVA and many things, for example, like acute coronary syndrome. All right. So thank you, thank you for today. I extended 30 minutes, I did not expect. He was absolutely anticipating that I can extend due to some difficulties as well in, you know, in technicalities, but I was able to do it, we were able to do it. Thank you. Thank you, and hope to see you guys in another in another free lecture. All right, and if you're a student and I pass, I'll see you there. Our next cycle will be will be soon. I guess it's almost, I mean, two weeks from now, I guess. So thank you. Thank you. And thank you for Connetics for giving us an opportunity to again to become an instrument at least to help you guys. You know, achieve your goals right together with other review centers. Thank you and God bless everyone. Inspiration, adversity, spirituality, takeaways. All right. Thank you