Cram The Pance - S1E36 Thrombocytopenia (DIC, TTP, ITP, HUS, HIT)

Episode Date: September 10, 2021

Thrombocytopenia review for your Pance, Panre, and Eor's.►Paypal Donation Link: https://bit.ly/3dxmTql  (Thank you!)--- Support this podcast: https://anchor.fm/scott--shapiro/supportBecome a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

All right, so let's go over thrombocytopinia. So we're going to go over TTP, D-I-C-H-U-S-I-T, and H-I-T. A bunch of letters here. It gets a little bit confusing. I know it could be a little bit intimidating some of these. I try to break it down and make it as easy as I possibly could. Thank you, as always, for the support. The comments, you guys are the best.

I really do appreciate that. And if you haven't checked out the YouTube channel yet, please do its cram the pants on YouTube. A lot of good visuals to go along with the presentations. So let's start off with thrombotic thrombotic thromicinic. TTP, one of the more high-yield topics. So this is a thrombotic micro angiopathy. It's caused by severe deficiency and something known as atom TS-13 protease. So the patho behind this is that atom TS-13 deficiency leads to an increase in something known as Von Willa-Brand factor,

which causes small vessel thrombi. Also causes thrombia. Also causes thromocytopenia, obviously, and microangiopathic hemolytic amoeitic anemia. So a bunch of big terms. Let's focus on what those mean and what's actually going on here. into kind of things that we can understand. So let's break it down. Let's start with Von Willowbrine Factor. It's a glyco protein that's involved in hemostasis. It helps blood clot when it's needed. I like to call them Willie, just makes it a little bit easier. Willey is like sticky paper for platelets. They get stuck to Von Willowbron Factor, Willie, and forms clots. So it's great in moderation. It's great when you need clotting, but not so great if Willie gets out of control and starts this process

all over the body and have a bunch of microthrombi. So that's why we have Adam. That's why we have Adam, 13. Adam keeps Willie in check. So Adam TS13 is a Von Willowbran factor cleaving protease. It basically cuts through the Von Willowbrant factor, keeps it from getting out of control. So without Adam keeping Willie in check, we have TTP and it leads to this uncontrolled platelet rich thrombus formation, among other clinical manifestations we'll talk about. So just remember, Adam keeps Willie in check, but in TTP, Adam's slacking, he's in short supply, and Willie's out of control. He's snatching up all the platelets causing all this micrombia. So that's what you need to remember.

Clinical manifestation. So TTP is one of the ones that has pentat. So the pentat consists of fever, renal failure, hemolytic anemia, thrombocetopinia, and neurologic changes. Most patients are not going to have the entire pentad. It's rare, less than 5%. But they may have one or two of the five. How do you remember the pentad?

I remembered it in school by something known as Fat RN. It's not my own mnemonic, but it was a pretty good one and help me remember what to look out for in the vignette. So fat RN stands for fever, anemia, thrombocytopinia, renal failure, and neurologic changes. Let's go down each one of those and explain. So fever, that's pretty self-explanatory. Anemia. So specifically, microangiopathic hemolytic anemia, also known as MAA, M-A, it's a type of

hemalytic anemia that results from red blood cells passing through those vessels that are just packed with microthrombi, like we talked about before. So the red blood cells pass through all of these. platelets stuck to Willie, all this microthrombi, and these red blood cells are just bumping and banging up against things, and essentially they're torn apart. And it creates something known as schistocytes on the peripheral smear, which we'll go over in a little bit. But it's just these fragmented red blood cells. So you see schistocytes on a smear, you know you're dealing with not just any anemia, but specifically a microangiopathic hemolytic amoeitic anemia. And that's basically, anytime you see

those schistocytes, you know that, or microangiopathic hemalic amoeic anemia, you know those red blood cells have had a bumpy ride through those vessels. It wasn't smooth sailing. Something's going on in the vessels that's tearing them up. Then the other, the T and fat RN, so thrombocidopinia. So you have low platelets. You may see mucutaneous bleeding, patiquiaeura due to the low platelets. And you have low platelets in TTP because instead of your platelets floating around freely in the blood and the serum, Willie snatched them all up. He's holding them hostage. So you wind up with low platelets on labs because all your platelets are stuck to Willie. That's why you have thromocitinia. Renal failure and neurologic changes.

So renal failure, most of the time it's just going to be declining kidney function rather than failure, but know that there can be some renal involvement in TTP, whatever the severity level. And then neurologic changes, headache, confusion, stroke, seizure. So these last two, the renal failure and neurologic symptoms. It's basically from these clots being formed, and they're obstructing floated distal tissue. So whether it's renal tissue, decreasing brain perfusion, which leads to the neurologic symptoms, We have some kind of decrease in perfusion to these organs, which can lead to these problems. So that's fat RN, remember those those manifestations, fever, anemia, thromocytopinia, renal failure, and neurologic changes.

Now diagnosis, diagnosis you're looking for low platelets, thromocitinia, normal coag panel, and schistocytes. So your CBC, you're going to see thromocitonea low platelets. Obviously, you're going to see that in all of these, so that's not a really way to differentiate. but thromocytopinia in tTP generally it's going to be a really severe thrombocytopinia so the platelet count is almost always less than 30,000 so really low platelet count your coag panel your pt, your pttt, it's going to be completely normal because remember we haven't activated our clotting cascade in these patients. They're not using a fibrinogen, none of their clotting factors are being used up. TTP is just a consequence of too much willie attracting too many platelets. So the coag panel is going to be normal, which helps us differentiate from DIC, which we'll go over shortly. Your D-Dimer, of course, is going to be negative two. And then on your smear, like I talked about before, you're going to see schistocytes. Remember, schistocytes means microangiopathic, emolytic anemia. Red blood cells have had a bumpy ride.

They're all torn up and fragmented. So you look for those schistocytes. And then, of course, you can also test for your atom TS-13 level. It's going to be decreased, obviously. This type of testing, though, can take up to a week. It can confirm the diagnosis, but it's never going to guide your treatment. It's something you can do, send out for diagnosis at a later time. But TTP is normally a medical emergency.

It can almost always be fatal if the appropriate treatment isn't initiated promptly. So you can't wait for your AtmTS-13 levels to come back. It doesn't mean they can't throw it in a vignette, but just know in real life that's not something you're going to use to guide your treatment. Now treatment, it's mainly going to be plasma exchange or also known as plasmapheresis. So Plasma Exchange is the mainstay of treatment for TTP. All patients with TTP are going to be treated with Plasma Exchange until their platelet count normalizes. This therapy, before it was around before plasma exchange therapy, the mortality rate for patients with TTP is close to 90%. So this therapy is really crucial in treating these patients.

If you're unfamiliar with plasma exchange, all it is is they take out the bad plasma from the patient with TTP. They replace it with donor plasma. And then what this does is it takes out the bad plasma with all the auto antibodies that are restricting atom. And it replaces it with new plasma that doesn't have these auto antibodies. So next time you donate blood, donate some plasma too, you may save someone's life with TTP. One thing that should be noted, you're exchanging plasma, and that's the mainstay of treatment, but you might be thinking, well, they have severe thrombocytopinia, why don't we do a transfusion and give them some platelets?

Well, you actually never do that in TTP, and the reason is you're feeding the beast essentially. You're giving willy more platelets to hang on to and create some more clots. So giving platelets is a no-no for TTP. You don't feed the beast. Exchange the plasma, fix the problem, but don't help sticky Willie out. And then you also have some adjunct agents, your glucocorticoids, your retuximab. Therefore, they're more severe patients.

They can help decrease the required duration of plasma exchange therapy. But overall, TTP focus on plasma exchange. That's going to be the answer you need. What do you need to know? What do you need to remember? Remember the patho, not enough atom around, willies out of control, causing low platelets, small vessel thrown by. Remember fat RN, fever, anemia, thromocytopinia, renal failure, neurologic symptoms. That's really what's going to be in the vignette.

That's the unique presentation. And then remember your treatment is going to be plasma exchange. It's really all you need to know for TTP. All right. Let's move on to our next one, DIC disseminated intravascular coagulation. It's an acquired syndrome that leads to activation of the coagulation pathway with potential to cause both thrombosis and hemorrhage at the same time. So may say to yourself, it makes no sense.

We have these patients that are developing thrombi, these clots, but then they're also hemorrhaging at the same time. So what happens is due to some underlying pathology, there's this inappropriate trigger or activation of the clotting cascade. So all of a sudden these patients are forming clots all over their body in places that they have absolutely no need for a clot. And then what happens is in doing so, they consume all of their clotting factors. So when they do need a clot, like they get a blood drop or form, they have a laceration. There's no clotting factors left. So they've used up all their clotting factors, so they just bleed and bleed and bleed.

So DIC, some kind of trigger, some trigger, cause these patients to form inappropriate clotting all over the body. And then when they actually need a clot, they need their, you know, their coagulation factors, their clotting factors. There's nothing left. So they just bleed. ETOologies, what you need to know for etiology is these patients are going to be sick, very sick. This isn't going to happen at a patient walking around at the grocery store, playing basketball who develops DIC. Doesn't occur in isolation. There's always going to be an underlying condition leading to it.

It's going to be a patient with sepsis, malignancy, trauma, burns, heat stroke, amphetamine overdose. It doesn't matter the reason. Just knowing the vignette for DIC, if this patient isn't sick, they're not ill, they're not crashing, they're not doing bad, they're not in the ICU. They don't have DIC. That's what you need to focus on. Clinical manifestations, like I just said, the main things to look for is a sick patient who's now bleeding. So remember the vignette, patients can have a history of trauma, sepsis, malignancy, and then they're going to be bleeding. Not just bleeding, but the way they normally describe it in a vignette is a patient.

is oozing. So they're going to say blood oozing from wound sites, catheters, drains, phenopuncture sites, mucosal surfaces. That's the one they love to put in the vignette, oozing from venipuncture IV sites. So sick and bleeding, that's your clinical presentation. And then remember, they're clotting, so they have thrombosis as well. So venous and arterial thrombosis is possible. But in the vignette, really, they're going to focus on that oozing and the sick patient. That's the key. Diagnosis, CBC, thrombocitopenia, like all of these, your platelets, of course, in addition to fibrogenogen are being used up in these clots, so platelets are going to be low.

Your smear, we're going to see schistocytes again. So remember in DIC, it can lead to microangiopathic hemolytic anemia because we have all of that microthrombi throughout the body, shearing up those red blood cells. So those are both the same as TTP, thromocytopinia, scistocytes. The difference is in our coag panel, and that's the key you need to remember for DIC. So PT and PTT was normal in TTP. Now your PT and your PTT are going to be increased. So why?

Well, what is PT and PTT measure? It measures how long it takes to form a clot. It measures your clotting time. What's going on in these patients? They're forming clots all over the place. They have very little clotting factors left. So when you're measuring how long it takes them to form a clot, it's going to take much longer. They barely have the supplies left.

So this patient's going to have an increase. in their PT and their PTT they're going to be increased when you do those labs their fibrinogen is going to be decreased because it's being used up to form the fiber and clot so that'll be low and then your D-dimer is going to be increased so we have these fibrin clots all over the body and D-dimer if you remember it's a fibrin degradation product so it makes sense it would be elevated because we're we're using all of these products to form those clots so D-d-d-d-dimer is going to be increased fibrin is going to be decreased because you're using

it to form those fiber and clots, PT, PTT, your clotting time is going to be increased. Treatment, there's really not much to know here. It's mainly fixing whatever's causing the DIC. So fix the underlying disease. If they're septic, if they have malignancy, burn, trauma, et cetera, fix it if it's possible to fix the DIC. And then supportive. Replace whatever they're low on hemoglobin, give them hemoglobin. If they're low on hemoglobin, give them hemoglobin.

They're low on platelets, unlike TTP, give them platelets. Because here there's no damage in giving them platelets. so there's no autoimmune process that's causing it. So no first line treatment here, just treat the underlying disease and replace whatever they're low on. The way that I used to remember the things that I feel like are important for DIC is instead of DIC, I remember D-DIC. I added on an extra D-D.

The first D-D stands for D-Dimer because remember only D-Dimer is only going to be elevated in DIC. This is in addition to your other COAC factor. So remember D-Dimer is going to be elevated. That's the first D. And that kind of helps you remember. the other stuff going on is elevated to your your PT your PTT the second D stands for dripping because remember they're dripping they're oozing from their venipuncture sites catheters drains etc the I stands for ill because remember this patient is going to be sick

septic trauma malignancy etc they're going to be ill and then the last C stands for clots because remember inappropriate clots or what got the patient into this mess widespread microthrombide clots where they shouldn't be using up all the clotting factors and that is DIC let's move on to HUS hemolytic Euremixen So this is a toxic mediated immune reaction most commonly after a GI infection. It leads to this triad of microangiopathic hemolytic anemia, thrombocytopinia, and acute kidney injury. So this isn't one of those triads that occurs in some patients, some patients may have one of the three, two of the three. This triad is HUS.

You need the presence of all three to make the diagnosis of hemolytic uremic syndrome. So remember again, microangopathic hemolytic amylic anemia. thromocytopinia and acute kidney injury that triad is hus there's a peak incidence in children younger than five it can be seen in adults but bet on the fact bank on the fact that if you get this in a vignette it's going to be a kid it's more common in children and generally that's how they'll give you the most common presentation so look for a kid in hus patho this is an endothelial injury due to exotoxins so these exotoxins are a byproduct of shiga toxin producing ecolon Specifically, the most common one is entrohemorrhagic E. coli.

O.157 H7. This exotoxin release leads to a microvascular thrombosis, which results in the triad. We talked about the microangiopathic hemelitic anemia, thromocytopinia, and the A.k.i, the acute kidney injury, so that triad. So that was a mouthful. Let's actually talk about what's happening here and explain it into something that's a little bit easier to understand. So all that happens here is an infective organism got into the body.

A lot of times, especially in the vignettes, they'll describe it as ingestion of undercooked meat. They'll say a kid was eating a hamburger. So they ingested this infective organism, got into the body somehow. So the organism is releasing exotoxins and it's wreaking havoc on the vascular endothelium, so on the beds of the vessels. It has a predilection for the vascular bed of the kidneys, which is why we often see renal problems in these patients. And the damage to the vascular endothelium leads to microthrombi at the site of damage in the vessels.

If you remember, Virchal's triad and thrombosis, endothelial injury was one of the three components of the triad. And that's what happens in HUS. You have damage from these exotoxins to the vascular endothelium. Now, I mentioned E. coli 0157H7. So is this the only bacteria that can cause HUS? It's not. There's a number of other infective organisms, strepeno, etc. But Shiga toxin producing E. coli will be the cause in about 90% of the cases.

And it's going to be the organism that you get in your vignette. I promise you that. It's the most common cause in the U.S. and Europe. And like I said, it can be fairly certain it's the one they'll give you in the vignette. So remember E. coli. 0157, that's likely going to be the organism causing HUS. Clinical manifestations, you're really looking for two things, GI and renal symptoms. So bloody diarrhea is a big one.

They may also have abdominal pain, vomiting, this prodromal illness that will likely precede the diagnosis of HUS by normally about five to ten days. Diarrhea is the one you'll likely see in the vignette. Not always bloody, but it can be. And then you're looking for some sort of renal manifestation. Hematuria, proteinuria, oliguria, the level of severity can vary, although we have to acute kidney injury requiring dialysis. But just remember in the vignette, they're going to mention some sort of renal manifestation. And then diagnosis, CBC, of course, thrombocytopinia, low platelets. Coag panel is going to be normal.

Remember, the only one that's going to have an abnormal coag panel is DIC. So, quag panel, PT, PTT, normal, D-Dimer, negative, smear, schistocytes, of course. And then serum creatin. This one is pretty unique. So they're going to mention that the serum creatinine is elevated. So otherwise, the labs are pretty similar to TTP, but the elevated serum creatinine is really the only thing that's going to be very different. You can see an elevation in creatine in TTP, but generally not as common and normally not as significantly elevated elevated as you'll see in HUS. So if you see elevated creatine on a vignette and you're suspecting thromocytoppenia, you should be thinking HUS. Treatment is pretty simple. It's going to be supportive. It's primarily supportive. And it's because there's no really proven safe or beneficial therapeutic intervention for HUS. So there's IV flu. Diolysis, red blood cell transfusion, you take care of whatever they need at the time.

The one thing that you should know about treatment, and this is important, you want to avoid antibiotics and antimotility agents. So they have any coli infection. Why aren't you going to use antibiotics? Use antibiotics for every other type of E. coli, UTI, et cetera. But the reason is if you give these patient antibiotics, the antibiotics disrupt the bacterial membrane of the coli organisms, and it actually causes it to dump more out, more exotoxins out because you've disrupted that, that bacterial membrane. So actually more exotoxins from the antibiotics. So you don't use antibiotics in these

patients. It doesn't help. Many cases, it can make it worse. And the reason we don't use antimotility agents is pretty simple because antimotility agents slow down the GI tract, which leads to E. coli hanging out there longer than we'd like it to. So there's no benefit there. We don't want to expose the gut to these toxins any longer than we have to. Now, I mentioned this before, but I just want to mention it again because it's important for my mnemonic that I'm going to give you. Whenever I had a question at HUS, it always mentioned a little kid who ate a hamburger. Clearly it wasn't cooked well and he ingested E. coli. He or she ingested E. coli. There's a number of other foods, undercooked cheese or

other undercooked foods, cheese, poultry, vegetables. But the question I always got was a kid who ate a hamburger that wasn't cooked well enough, developed diarrhea, et cetera, then went on to develop HUS. So the way that I remember the things that I feel like you need to know for HUS is just like in DIC I added on an extra D and HUS I add on an extra S. So HUSS, HUSS, H. So the first H or the H is going to stand for hamburger. That reminds you that in the vignette, you're likely going to see a little kid eating an undercooked hamburger led to that e-coli infection. The U stands for urinary symptoms.

Remember, you're looking for hematuria, oliguria, something going on with some real urinary manifestation or, you know, urinary symptom. The S stands for, unfortunately, I don't have a better word here, but shitting because remember they're going to have likely bloody diarrhea, some kind of GI problem. So shitting for the first S. And then the second S stands for school age because remember this is likely going to be a kid commonly under five years old. So school age, remember this is going to be seen in children most common. So those are the four components that I feel like you need to know to identify HUS in a vignette. So remember again, HUSS, hamburger, urinary symptoms, shitting and school age. All right, let's move on to immune thromocytopinic purpura.

ITP, used to be called idiopathic thrombocytopinic purpra. This is an acquired autoimmune hematologic disorder and it's characterized by isolated thromocytopinia. It's more commonly seen in females and the patho is that you have these auto-antibodies against the platelet membrane, which leads to splenic secrestation and phagocytosis. So really it's really, it's very simple. body's turning against its own platelets and essentially destroying them. And most of the time we don't know why. That's why it used to be called idiopathic.

But there is two mechanisms or triggers that will commonly lead to ITP. So infections, usually viral. And then systemic conditions that can alter the immune homeostasis are your secondary causes of ITP. So HIV, hepatitis, lupus. Clinical manifestations, a lot of patients with ITP are going to be asymptomatic. But if they do develop symptoms, it's going to be symptoms related to. to the thrombocytopinia. So you're looking for one thing and that's bleeding. So whether it's

in the skin with patechia and purpura or in the mucus membranes with bleeding gums, epistasis, that's what you're looking for in these patients bleeding, bleeding gums, epistasis, like I said, because of the thrombocitopenia. That's really pretty simple. There's not too much going on there as far as the clinical manifestations. Diagnosis, the only thing abnormal here is the platelets. So it's isolated thromocitopinia. Everything else is normal. So see, C thrombocytopinia, low platelets, your coag panel is going to be normal, your D-dimer is going to be negative. And then the interesting thing here, because this is the only one you're really going to see this in, your smear is negative. So your red blood cell morphology is usually going to be normal.

So we saw schistocytes and everything else we've discussed so far. So why don't we see it in an ITP? Well, remember, schistocytes are formed when red blood cells have that turbulent or bumpy right in the vessel. There is something going on in the vessels, those microthrombi, that caused these schistocytes in HUS, TTP, DIC. So thrombi, all of those that we went over already presented with thrombi in the vessels for a number of different reasons. And that's why those conditions led to schistocytes. ITP, we haven't mentioned thrombi.

There is no thrombi in ITP generally. It's only a condition of platelet destruction. And that's the reason we don't see schistocytes. Because remember, ITP doesn't really have a lot of unique qualities. It's generally a diagnosis of exclusion. So remember, schistocytes, that's one of the few unique things about this condition. So treatment, there's two things you need to know for treatment, and that's IVIG and steroids. Depends on severity level.

Also be aware that observation is an option for patients. A lot of times kids, too, we try to just observe if we can, especially if they just have minor bleeding or just a mildly decreased platelet count, normally over 30,000 platelets. But normally you start with glucocorticoids because remember, this is an autoimmune process. and in virtually all autoimmune conditions, steroids are going to be our first line, and ITP is no different. So if the platelet has, sorry, if the patient has severe bleeding,

they're really sick, you also have the option of giving them IVIG in addition to the steroids. Again, this is going to be for your patients with severe bleeding, really low platelet count. You add on IVIG, which is intravenous immunoglobulin. So IVIG is made up of healthy pooled immunoglobulins, IG, from the plasma of blood donors.

So you pump these patients full of health. immunoglobulins and essentially gives their platelets a fighting chance at survival. And again, you usually reserve IVIG for patients with severe bleeding where you need to raise their platelet count fast. It really comes down to how bad is the bleeding and how fast do we need to raise the platelet count because IVIG will raise the platelet count in about one to three days or glucocorticoids take about two to 14 days. So steroids usually first, patients severely bleeding add on IVIG.

And that's really all you need to know for treatment. If the patient is refractory, you do have the option of doing a splenectomy. So what do you need to know? You need to know that you have auto antibodies against platelets. You need to look for a female in the vignette, more common in females. Look for isolated thromocytopinia. Remember normal coag panel, normal smear, no schistocytes. And then treatment, steroids, and IVIG, depending on severity level. And then remember, observe if it's just minor bleeding or a child, a lot of times we'll just do observation. And that's all you need to know for ITP. Let's move on to our last one, heparin-induced

thrombocytopinia. So this is a life-threatening immune-mediated adverse drug reaction, which is caused by the emergence of antibodies that activate platelets from exposure to heparin. So this reaction leads to thrombocytopinia and thrombosis due to the activation and consumption of platelets. So let's explain what's going on here. We have thrombosis because this antibodies activating and churning out platelets. So it's leading in thrombosis. But ultimately, we wind up with thrombocitonea. So low platelet count. because these platelets eventually are going to aggregate and clump together, which forms these clots, and they get used up. And rather than floating around in the serum, they're stuck in those clumps. So you have both thromocytopenia and you have your thrombosis as well. So you have a combination of the two.

Now, what you're looking for in the vignette, and in real life, obviously, is a heparin exposure in the last five to ten days is generally what you're looking for. So they had heparin in the last week or so, and that's the key. And now they're throwing clots all over the place. Their platelets are dropping. So it's easy to figure this went out in a vignette. The one thing that I wanted to mention, because this can sometimes throw you off when you're reading a question, is remember, they're not always going to say this patient took heparin.

They may say this patient took daltoparin. This patient took anoxiparin. You need to be aware of your low molecular weight heparin names. So that's anoxiparin, daltoparin. Those are the most common. The way that I used to remember that is heparin ends in P. A-R-I-N, so does anoxiparin, so does dot-de-parin, they all end in parent. So if you ever see that in a vignette and you're like a noxaparin, I can't remember, is that a heparin?

You see, parin ends, they all end in parent. They all end in those last five letters. So you'll be able to remember that that is a heparin product. And you remember, too, because if they give you an answer choice and they want you to switch to a non-heparin agent and you see anoxi-parin, you won't get, you know, confused. So that's just a little side note there. All right, clinical manifestations, thrombosis and thrombotic sequela. So they're going to be clotting venous and arterial thrombosis. So called it like necrosis, limb gangrene, organ infarction, pulmonary emboli.

That's what you're looking for in the vignette. Now, what about bleeding? All the other conditions we focused on bleeding from the thrombocytopenia. But despite thrombocytopinia being present in HIT, it's actually really rare to see bleeding. So really focus on thrombosis for your vignette, that pulmonary embolism. All of that thrombotic sequelaide, that necrosis, limb gangrene because of the blood, the blood can't get through because of that clot. Diagnosis is going to be a combination of clinical and laboratory finding. So CBC, surprise, another thrombocitopinia, of course.

But this thrombocytopinia, you're looking for this really big sudden drop. So you're looking for normally a 50% drop in platelet count. You're going to see it in the vignette. And they're going to mention this patient had heparin or noxparen, whatever, three, four, four. five, six, seven days ago, and their platelet count was however much, 250,000, and four days into treatment, their platelet count is now 20,000. So that's what you're looking for this really big platelet drop. So thromocytopinia, yes, but look for that specific presentation where they say they were on

Heper and a few days later, they had this significant drop. You also have the option of doing HIT antibody testing. That's something else you can do. And then your PT, your PTT is actually usually going to be normal. So remember, this is a platelet activation problem, not a coagulation cascade problem, and it's usually not going to produce the consumptive coagulopathy we saw in DIC, which had the elevated PT, PTT, and D-Dimer. So really you're looking for thrombocytoppenia, significant 50% drop in your HAT antibody testing. There's also something known, if you want to just shut off your ears right now. It's known as the 4T's probability scale.

Don't memorize it. I just want you to know, like, have heard of it before. It's also known as the Warkenton probability scale. It's this grading system that's based on the severity of the thrombocytopinia, thrombosis, timing of platelet countfall, et cetera. I don't think you should memorize it. I just want you to know if you're out in clinicals and you hear somebody talking about this. You'll remember that it's related to HIT.

You don't need to know for your exam, though, so don't memorize it. And one last heads up about the tools we're using for diagnosis. The HIT antibodies, for instance, they can take a while to come back. And you can't wait in HIT. So you have the patient with the right clinical presentation. You have to act really fast. These patients can die in really quickly. So these diagnostic tests like the HOT antibodies are great to confirm later on and be like, yeah, it was right.

But you never wait for these tests to come back when you're treating a patient with suspected HIT. You just treat them right away. So what is treatment? So treatment obviously is going to involve discontinuation of heparin. But then you need to start them on a non-heparin anticoagulant. They're full of clots. You need to anticoagulate. You don't want them to form any new clots, but you just can't use heparin anymore.

So we need an alternative. And the alternative, you have some choices of non-heparin anticoagulants. It's normally going to be with a direct thromid inhibitor. Our gatraband seems to be the one they always like to talk about. That's one of the more common ones. Bivalroodin is another one. These are your parental agents. You can administer these IV for your patients who need urgent anticoagulant.

anticoagulation and these will normally be your first choice. So there's also oral direct anticoagulants like Apixabin, Riveraxibin. And then once you get these patients started on one of these agents, you can bridge them safely to warfarin. Remember, you can't just start somebody on warfarin right off the bat because warfarin creates this transient prothromic state. So if the intent is to bridge to warfarin, you have to start them on one of these agents first, and then you can bridge them slowly to warfarin once they're past that initial transatlantic state. So, if the intent is to bridge to and prothrombic state. So it seems kind of complicated the treatment, but remember the treatment is really simple. It's just stop heparin, start a non-heparin agent. The agent likely is going to be

our Gatraband. That's like I said, always the one they seem to ask about, but any of those direct thromid inhibitors can be used. So stop heparin, start a non-heparin agent. What do you need to know about HIT? Remember, they're going to have heparin exposure in the last five to ten days. They're going to have thromocitopinia, but not just any thrombocitinia. They're going to have that significant drop, about 50% since starting heparin. And then remember thrombosis. You have an activation plus consumption of platelets. So it's thrombosis like venous thrombinary ambuli or consequence of the thrombi like gangrene

and necrosis, as well as your thrombocytopinia from all the platelets being consumed and aggregated in these clots and no longer in the serum. And then remember your treatment is going to be stop heparin, start non-heparin agent like our Yatraman. All right. So that is thrombocytopinia. Let's do five quick questions. Question one.

What pentad of clinical manifestations can potentially be seen in a patient with thrombotic, thrombocytopinic, purpura? So that pentat is going to be fever, anemia, thrombocytopinia, renal failure, and neurologic symptoms. Remember your fat RN. Question two, 57-year-old man who is in the ICU. Being treated for sepsis begins to develop excessive bleeding from his fully catheter and IV site. Labs are drawn which show increased P.T. Pt.T. increased D-dimer as well as a peripheral smear that displays schistocytes. What diagnosis should be suspected in this patient?

That's going to be disseminated intravascular coagulations. Remember, D-DIC-nemonic. First D-D is his D-dimer is elevated. This is the only thromocytopinia. Remember that has the elevated diodimer as well as the other clotting factors, PT and PTT like we see in this patient. Second D dripping. He's dripping from his folicicic. Ivey, et cetera.

Third, he's ill. He's septic. Remember these patients will always be ill. It doesn't happen in a healthy patient. And then remember the last C, which stands for clotting, which is the underlying process going on in the body. The body's making these unnecessary clots throughout the body. So can't clot where it needs to be, which leads to the bleeding that we see in this patient.

Question three, 47-year-old woman who presents with mucutaneous bleeding, has labs drawn which display isolated thromocytopinia with normal coagulation studies. She's later diagnosed with immune thromocytopinic purpura, and she has started on glucocorticoids. After treatment initiation, her platelet count begins to drop and her bleeding becomes more severe. What additional treatment should be added in this patient? So that's going to be intravenous immunoglobulin IVIG. Remember, in ITP, if we're going to initiate treatment, steroids are usually going to be first. And then if the bleeding is severe and the platelets are low, we add on the IVIG like we need to do in this woman.

Question four, clinical manifestations seen in thrombotic, thromocytic peanut perpra are due to increased numbers. of Von Willowbrant factor, increasing platelet adhesion, and causing small vessel thrombosis. The increased numbers of Von Willowbran factor is due to deficiency in which enzyme. So remember, again, that's going to be your Adam TS-13. Remember, Adam is keeping Willie in check, but there's not enough of him in TTP. Question 5, 66-year-old woman receiving thromopropylaxis with low molecular weight heparin. Six days ago develops post-op shortness of breath. Let me say that one more time.

66-year-old woman are receiving thromoprophylaxis with low molecular weight heparin. Six days post-op developed shortness of breath. It is discovered on CT that she has developed a pulmonary embolism. Labs show a platelet count of only 70,000, which is a significant decrease from her platelet count of 275,000 on admission. What treatment should be initiated in this patient for the likely diagnosis? So in this patient, you want to stop heparin and start a non-heparin agent like our gastroband. So this is clearly HIT. She's on heparin.

We see a big drop in our playlist. She's clotting. Recently started heparin. So we stopped the heparin, start a non-heparin agent. And that is thrombocytopinia. Hope that was helpful. Please let me know in the comments if it is. I really do appreciate everything, all the nice comments.

So thank you so much. And good luck in PA school. Good luck on your pants, your pan or your EORs. And thank you again so much.