DIP Episode 180 - Hematology For The Surgery Shelf Exam

Okay, welcome. My name is Divine. I'm a resident. This is episode 180 of the Divine intervention podcast. And in this podcast, it's essentially going to be a special topic sort of podcast. I'm going to I'm tightly in this podcast, hematology for surgery. This to be honest, I mean, yes, this is useful for the surgery show because I don't know for whatever reason, like blood related problems make up like 5 to 10% of what's tested on the surgery shelf. But this podcast will also just be ideal literally for any other shelf exam. I would say probably most importantly, like things like like a pizza shelf or an internal medicine shelf. This is just going to be a very good, high-yield quick drive-by of of hematology as necessary to the surgery shelf exam. So let's just jump right into it, right? So the big thing you want to keep at the back of your mind when you're learning about hematology at the anemias, right? And obviously, you know that the anemias you want to be able to break them down as either being like macrositic, macrositic, or neurocytic, right? And the boundaries you want to remember is the number between 80 to 100, right? So anything less than 80, that's a my if the person has an mcv less than 80, that's a macrositic anemia. If the person has an mcv greater than 100, that's a normal that's a macrositic anemia, okay? And then you may occasionally see an mbim exams refer to the term megaloblastic anemia.

Megaloblastic anemia just means that a person has anemia because they have like some problem that has to do with abrandi and synthesis, right? So classically that's from like a B12 or a full-it deficiency. But I think when we'll maybe go after this podcast is just pick out certain high-yield diseases and just sort of talk through them. So I'm just going to jump right into it, right? So what if they give you a question about a patient and they tell you that this patient has like, you know, this patient has been having like fatigue, this literally has like chronic fatigue, shortness of breath. And then they show you like labs. And in those labs you notice that this person has, you know, hemoglobin of 8, right? And their mcv is like 88, okay? And their mchc is elevated. So their main coposcola hemoglobin concentration is elevated. What disease are you thinking about? Well, I hope you're thinking about a hereditary cytocytes, right? So what are the key things you want to keep at the back of your mind with hereditary cytocytes? Well, you want to remember that hereditary cytocytes is inherited in an arosomodominant fashion, right? And it's associated with mutations in the spectrum and anchoring proteins, right? And remember that classically in the question, they will tell you that multiple family members seem to have some kind of blood problem going on, right? When basically this is more of like a strategy for just test-taking.

Whenever you see multiple family members having like a particular problem, you're likely dealing with a genetic disease, right? So when you're picking out answers, pick an answer that has like genetic undertones instead of just picking any like fly by night answer, right? So hereditary cytocytes, again, mutation, or the somodominant inheritance, mutations in inspection and anchoring proteins. And basically, they can show you like a picture on the test, right? And you have like red blood cells that lack central power. It's like the entire like surface area of the red blood cell is covered over by like, you know, whatever color red blood cells normally have, right? So that's hereditary cytocytes for you. And remember that the way you make the diagnosis, right? So you can do something called an osmotic fragility test, right? Because the thing is because those, you have mutations in those inspection and anchoring proteins, then a red blood cell is not able to appropriately maintain its membrane integrity, right? So when you put that red blood cell in hypotonic solution relative to other like normal red blood cells, it will explode very quickly, right? So you can do the osmotic fragility test. But one other thing your friends at the MBME are beginning to, you know, kind of go after with hereditary cytocytes is this test known as the Eocene 5 malaymide test. That's another test that can be used to make the diagnosis of hereditary cytocytes.

And you absolutely want to remember that that HS can be, you have that you have, you have, you have, you have an elevated main copole scola hemoglobin concentration on MBME exams. Now, what do they, and the way you treat it? I mean, because the thing is those parasites actually work pretty well. But the thing that sort of takes them out of circulation is the lever, I mean, not the lever, like your splenic macrophages. So the thing is if you had some mice who are dealing with those splenic macrophages, then the problem, their problems will essentially disappear, right? So in general, the best long-term treatment for hereditary cytocytes is actually to go ahead and get a splenectomy. Because if you get a splenectomy, well, buy by splenic macrophages and then you'll stop having breakdown of those people's aryblot cells. Now, what if they give you a question about a child, right? And let's say this child recently took, you know, like some, let's say he's like the child of missionaries, he's going to like a foreign country. So he takes like primary quenformal ear prophylaxis. And then they tell you that this child suddenly has like central cyanosis, right? Like you say that this child has like peri-oral cyanosis. What are you thinking about? Well, I hope you're thinking about methemoglobinemia, right? In methemoglobinemia, the thing that happens is you get exposed to some kind of patholoxidizing agent. So you can be like primary quen or you can be like a sulfonamide, right?

Or you can be like a nitrate kind of medication. And then those things will convert your Fe2 plus ions in hemoglobin to Fe3 plus. Remember, Fe2 plus is the ferrous form. Fe3 plus is the ferric form. And the thing is, Fe3 plus has no ability to bind oxygen. But Fe2 plus has the ability to bind oxygen. So, if hemo-globin that contains iron in the Fe3 plus from the ferric form is known as methemoglobin, right? So if you have methemoglobinemia, then you, of course, not be able to bind oxygen. And if you're not able to bind oxygen, then you can run into problems with hypoxia, right? So that's why the skin is hypoxic. So how would you treat the skin? Right? Obviously, you go ahead and give a methylene blue, right? Methylene blue will essentially help you convert the Fe3 plus back to Fe2 plus so that you can promote oxygen, oxygen, courage in the body and take away the presence of hypoxia. Now, one other high-heal thing you want to keep at the back of your mind is methemoglobin is not all bad, right? So the thing is, if for example, a person has like cyanide poisoning on an exam, the thing you would want to do is to actually give them like emol nitrate, right?

So you give them a powerful oxidizing agent that convert the Fe2 plus to Fe3 plus because the thing is cyanide has a very strong affinity for methemoglobin and then give those people a thiosol fit and then those like theiform, like there's a thiosyanide like intermediate that can then be safely peed or pooped out from the body, right? So that's how you treat cyanide poisoning. You actually induce a methemoglobinemia, although remember that you can also treat cyanide poisoning with hydroxyl cobalamin. So basically like a derivative of vitamin B12 can also be used to treat methemoglobinemia, right? And then what if they give you a question about like 16-year old African-American kid and this kid comes in with like severe pain in like one of his extremities or something, right? And then they show you like hemoglobin and his hemoglobin is like seven, right? And they tell you that he has had multiple episodes where it's hard to come into the hospital because of like severe pain in his extremities. And then they tell you that the spleen is not possible on physical exam. Well, what are you thinking about under those circumstances? Well, I hope you're thinking about sickle cell disease, okay? I hope you're thinking about sickle cell disease, right? So remember sickle cell disease is inherited in an autosomal recessive fashion, right? So these people have like some mutation where the array blood cells under like conditions of hypovolemia on the conditions of hypoxia, right?

As you must sickle shape, right? As you may sickle shape. And because it's inherited in an autosomal recessive fashion, remember that those people need to have two bad genes to have the disease, right? Versus a person that has sickle cell trait where they're like hemoglobin AS, right? Those people tend to have very mild hemolosis and they don't tend to have like pretty significant, they don't tend to have a significant problems. And one population you want to keep in mind for NVME exams with regards to sickle cell disease are African Americans and people of African ancestry. Those are the people that classically get sickle cell disease on NVME exams. Now, how do you treat sickle cell? I mean, obviously if a person comes out of the pain crisis, you're going to give them opioids, right? But some other things you want to keep at the back of your mind with sickle cell disease is that these people, right? In general, the daily medications they're supposed to take, right? They're supposed to take hydroxyurea, right? Hydroxyurea is an inhibitor of riboninthroethyl reductase, but it also increases the production of hemoglobin F, right? So by giving hydroxyurea, it decreases the number of hemolytic episodes that they have. That's one, two. People with sickle cell disease, especially when they're like really tiny, right?

Like they're like newborns, at least in their like their first couple of years of life, they do need regular penicillin prophylaxis because believe it or not, they can give you a surgery shelf exam question where they describe a patient, you know, he's sure of sickle cell, super high fever. And then they tell you that, oh, the person, you know, seems to have like a white count of like, like 30,000 and the person's like super septic. You want to think about pneumococcal sepsis. Strapiumo is the most common cause, very high yield. Strapiumo is the most common cause of sepsis in a patient with sickle cell disease. So under those circumstances, right, those people need to get daily penicillin prophylaxis because that would decrease the risk of having pneumococcal sepsis. And then because those people have a hemolytic anemia, they also need daily folate supplementation. One classic mb-mine question may be, believe it or not, to give you a question about a patient that has any kind of hemolytic anemia. And then you notice that their mcv is actually above 100. Well, the cause of that macrostilic anemia in that patient is a folate deficiency, right? Whenever you have a mac, like a hemolytic anemia, you need consistent folate replication so that those people don't, you know, develop like a megaloblastic anemia with that.

And then, if they give you a question about a person that has a history of sickle cell disease or a person that has a history of like sickle cell trait, and then they tell you that they have like painless hematuria, I would really hope on that those circumstances that you're thinking about a condition known as a renau-popularynecropsis, okay? renau-popularynecropsis, that's a classic presentation in a person that has a history of sickle cell disease or sickle cell trait. So, I think that's what I'm going to say about sickle cell, although maybe the last thing I should mention is if they give you a question about osteomyelitis and a sickle cell patient, then you certainly want to be thinking about a salmonella, right? Salmonella is the most common cause of osteomyelitis in a patient with sickle cell disease. And then, what if they give you a question about a patient that, you know, they tell you that again, this person, you know, maybe was recently studied treatment for TB, and the new patient has been having like fatigue, and this patient has been having, um, what else? This patient, you know, they may give you like some labs, I don't know, whatever, they may give you some labs, and you notice that the person's hemoglobin is like super low, and this person's MCV is like 68, right? What are you thinking about? Well, I would really hope you're thinking about Cedar Oblastic Anemia, right? Cedar Oblastic Anemia, because remember, if a person is being treated for TB, right?

There's the TB regimen, lathe and TB at TFTB, always includes some kind of isoniasis, right? So if you're taking isoniasis, remember that isoniasis is very good at depleting your B cell population. So if you depleting your B cell population, sorry, not your B cell, whoops, sorry about that, that will deplute your B6, you're vitamin B6 population. If you depleting your vitamin B6 population, right, then you will have decreased the activity of amylo-levelinic acid synthetase, alas, which is the real limiting enzyme in hym synthesis, and if alas is not working, right, then you will not be able to synthesize him, and then you can get a Cedar Oblastic Anemia, and classically, right? You'll see like these ophilic stippling, or NV Me exams, and a person that has Cedar Oblastic Anemia, and then also remember that B6 deficiency can also cause seizures, because if you remember the enzyme glutamate decryboxylase, glutamate decryboxylase is the enzyme that converts glutamate to GABA. It uses vitamin B6 as a co-factor, so if B6 is not available, glutamate decryboxylase doesn't work out so well. So you have increased glutamate, and you have decreased levels of GABA, and those high levels of glutamate will cause seizures, because glutamate is an excitatory neurotransmitter, and the decreased levels of GABA will also not help you, because you have decreased levels of an inhibitory neurotransmitter. That's something that's very high you to know, for example.

But one other thing I also want to mention is, you should also know some other things that could potentially cause Cedar Oblastic Anemia. Cedar Oblastic Anemia is not only caused by B6 deficiency, so paradoxical phosphide deficiency. Cedar Oblastic Anemia can also be a component of certain myelodisplastic syndromes, right? So myelodisplastic syndromes, the classic presentation will just be a person that, you know, they may have like a dry tap on a bone marrow aspiration, and then they may tell you in the NBM question that the person has hyposegmented neutrophils, right? So you're probably used to like, oh, hyper-segmented neutrophils, hyper-segmented neutrophils are classically associated with like B12 or fully deficiency, right? But hyposegmented neutrophils tend to be associated with myelodisplastic syndromes, but one other thing you may find in myelodisplastic syndromes are ringed Cedar Oblast, right? So you can see ringed Cedar Oblast in a person that has a myelodisplastic syndrome. And then, what if they give you a question about a patient, you know, comes in for surgery, you know, he's placed on an anticoagulant, and then they give you two sets of labs, right? And you notice that the person's first lab, you know, had like a pleatle count of, I don't know, like 400,000, and then they show you like, oh, like six days later, the person's pleatle count is like 50,000, right? That's bad, right? Obviously you should begin to think that this person likely has hit, right?

So like, heprinine used the thrombocytopenia. So hit, remember, right? It arises when a person is exposed to like a heprinine product, right? So like either like regular heprin, like on fractionated heprin or like lumolecular with heprin, right? So this person's got hit, and you want to obviously remember the pathophysiology, right? It arises when you have an antibody, right, formed against the pleatle factor four. And in that thing, like activates pleatle, right? So because you activate pleatle, you're depleting your pleatle population, so you have a thrombocytopenia, but because you're also activating pleatle, you're also forming clots, right? So the thing is, you may actually, this is something that for whatever reason, people don't seem to get, but hit, believe it or not, is actually an example of a hyper-quaglubal disorder, right? So obviously, if a person has hit, your first step in management is to stop the heprin, right? This is just a general principle for the purposes of the USMLA exams. If a person is having side effects of a drug, your first step in management is always to stop the drug, okay? You stop the drug, and but you need to remember that those people were placed on the heprin in the first place because they were hyper-quaglubal. And then I also just said that a person that has hit is also hyper-quaglubal, right?

So after you've stopped the heprin product, your next step in management will be to resume a direct thrombin inhibitor, a factor of two inhibitor, right? So you want to give a drug like a gattro band, right? Or you want to give a drug like Gabi Gattro, or you want to give a drug like bivaliridin, okay? Those are drugs that inhibit factor two, okay? They are the drugs of choice for the treatment of heprin-induced thrombocytopenia. They will try to trick you to like, oh switch the person's heprin to lumulecular with heprin. Don't do that, you'll get the question wrong. Or you may try to get you to pick like a factor 10 in hebron, like a pixaban or river oxaban. Those I will just say in general are not appropriate choices on an NBM exam for heprin-induced thrombocytopenia. And then one thing I also think I want to mention that, you know, occasionally my pop-up on tests is what if a person has like, wafrin toxicity, right? And, you know, they're like bleeding, their iron is like super high. What is your next best step in management in reversing that wafrin toxicity? Well, I would really hope that you're thinking about administering something known as 4 F PCC, okay? Like the four factor, pro thrombin complex concentrate, okay? The four factor, pro thrombin complex concentrate is the drug of choice these days for reversing wafrin toxicity. They may try to trick you on the exam and put, what is that old drug called? FFP.

FFP is no longer the agent of choice for reversing wafrin toxicity. Wafrin toxicity is now reversed with the four factor, pro thrombin complex concentrate. If you've ever had any exposure to the US healthcare system and you've ever heard someone refer to the drug case centre, case centre is the four factor, pro thrombin complex concentrate. And then what did they give you a question about a patient that gets like a prosthetic valve, right? And then they ask for like the best long term management of this patient. If a person gets a, you want to remember that if a person gets a valve replacement, you can get one of two options, right? You can get a bioprostetic valve, like a porcine valve, those tend to last for like five to ten years or you can get a mechanical valve, right? Those tend to last theoretically forever, right? Not forever, but you know, not for more than ten years basically, right? The key thing you want to remember, like the surgical application of this, because the thing is the surgery shelf is they'll talk about like medical problems that have some kind of surgical association or some potential surgical complication, right? So the thing is if a person gets a mechanical valve, they do need to be an anti-qualglation for life, okay? And the kind of anti-qualglation you want to go with on the NBM exam is, is a, is wafrin, okay? Wafrin is the drug of choice for anti-qualglation in a person that has a mechanical valve.

That's a very high yield thing to keep at the back of your mind for exams. And again, because I really want to keep this podcast under 30 minutes because I have something I need to run to in like eight minutes, I'm just going to reel through a lot of other like weird high yield things that I miss you on a test. So what if they give you a question about a patient that has like, you know, like a mechanical valve was recently placed? And then the person like three months after the mechanical valve was placed, the person is like, you know, has fatigue, has low hemoglobin, has an elevated LDH, has an indirect hyperbular benemia. What are you thinking about on that little circumstances? Well, I hope you're thinking about like some kind of hemolysis, right? Remember, these mechanical valves, or if a person even has any kind of vascular disease, these people can actually have like himolysis. And if they have himolysis, right, that can cause like, essentially like they can have a hemolytic anemia star presentation, right? So like, because you're like exploding the red blood cells, you may see like she sto sites on a blood smear, they'll have an increased LDH, they'll have an indirect hyperbular benemia. Those are all things that are classically tested on the USML exams. And then, what if you get a question about a patient that has a erotic stenosis and then they tell you that this person has like a microcytica anemia and has hemocort positive stools? What are you thinking about?

Well, I hope you're thinking about Heidi syndrome. It's spelled H-E-Y-D-E, okay? Heidi syndrome, it's like a bleeding diaticist that develops in people that have erotic stenosis. The pathophysiology is kind of poorly understood, but if you read the literature, what people say is that by having erotic stenosis, as when willy-brand factor multimmers at traversing the person's erotic valve, you cleave those vulnerable factor multimmers. And if you cleave a willy-brand factor, then primary hemostasis is not going to happen. And if primary hemostasis does not happen, well, you're kind of in trouble, right? Because those patients would not be able to like form clot, so they have a tendency to have GI bleeds, okay? It's like an anjule dysplasia that arises in the GI tract in a person that has erotic stenosis. That's the classic presentation on the USML exams and also on the surgery shelf. And then, if you're looking in terms of like the pleatlet disorders, right? So let's sort of take them from the bottom, right? So remember that if a person, you know, like primary hemostasis, how does it work? Right? You would have the adhesion phase, where the willy-brand factor joins to GP1-P9. And then, after that happens, you would then have the activation phase where the pleatlet releases ADP. And then that ADP then binds to the ADP receptor. And when the ADP binds to the ADP receptor, right? That's almost like an auto-crain kind of mechanism. You express GP2 B3 A.

And then that GP2 B3 partners up with another GP2 B3 A from another pleatlet under the auspices of fibrenogen. Okay? So the thing is, there are many diseases and disorders that your friends at the MBME, they love to test with, with recompense to these processes, right? So the first disease I'll talk about is one willy-brand disease, right? One willy-brand disease is the deficiency of one willy-brand factor. Well, if you have a deficiency of one willy-brand factor, right? The classic findings on an MBM exam, right, will be a person that, you know, has like very heavy man disease or has like bleeding gums and all that stuff. Or they may tell you that, oh, the person has had like my not trauma and then they have like a life threatening bleed with that. If you see that, think about one willy-brand disease. And the thing is, in general, for purposes of the MBME exam, one willy-brand disease is inherited in an autosomodominant fashion, right? It's inherited in an autosomodominant fashion. And because it's a pleatlet disorder, those people's bleeding times will be increased. But you'll also notice that the PTT would be increased as well. Because remember, one willy-brand factor is a protecting group for factor 8. So when a person has a one willy-brand factor deficiency, aka VWD, they'll also have an elevated PTT because factor 8 now has a decreased half-life in the circulation, right? And the way you treat one willy-brand disease for the most part is to give this more person.

Because that will increase the release of one willy-brand factor from the wibopaladi bodies that you find in endothelial cells. Okay? So that's one willy-brand disease. Next disease I'll talk about is something known as Bernat-Suley syndrome, right? So Bernat-Suley disease is a deficiency of GP1 B9. So again, you have problems with the adhesion step of primary hemostasis. The classic presentation is the me tell you that this person has an abnormal restore-sitting cofactor assay. In fact, let me take a small sidebar here. The restore-sitting cofactor assay is an assay that essentially tells you that a person has problems with the adhesion step of primary hemostasis. So if a person has a wibopaladi disease or a person has Bernat-Suley disease, they will have an abnormal restore-sitting cofactor assay. Okay? But if a person has Bernat-Suley syndrome, again, they will have an inhibited bleeding time, but they will not have an increased BTT because GP1 B9 has nothing to do with... GP1 B9 has nothing to do with factor 8, right? And then the next disease I'll talk about is ITP, right? Emule thrombosatopinic paper. The thing that happens in ITP is that you form autoantibodies against GP2 B3 A. Okay? If you form autoantibodies against GP2 B3, you have problems with the aggregation step of primary hemostasis, right? So again, because it's a pleated disorder, those people will have an elevated bleeding time. That's very high you to know, for example.

And the classic where ITP present you, present in a person that, you know, just has like an isolated thrombosatopinia, right? And then they will tell you that, oh, they've been noticing PTK on their skin, and then they've been also having like these gumplies when they brush their teeth. If you see that, think about ITP. Now please do not confuse ITP with glansman thrombostinia. ITP is when you form autoantibodies against GP2 B3 A. So it's a type 2 hypersensitivity reaction. On the other hand, glansman thrombostinia occurs when you have a deficiency of GP2 B3 A, right? So these people will again also have like an aggregation defect in primary hemostasis, and then they get into trouble. But make sure that you can tell those two things apart. And ITP and glansman thrombostinia, because those do not involve anything with a really brain factor or GP1 B9. Those disorders will be associated with a normal RISTO-C team cofactor acid. And then don't forget your drugs, right? That work on these different pathways like your ADP receptor blockers, right? So things like clopidogrel, prasogrel, tycagreler, right? Those are drugs that tend to shop quite a bit on search-y-shelf exams. And then don't forget your GP2 B3 inhibitors, right? They tend to have like the more exotic names. So things like empty fibatite, things like tyrophibat, right? Things like the MAP. The MAP-A-GES is more of like a monoclonal antibody against GP2 B3. Those are your platelets in Hibitine agents, right?

And then remember aspirin is a cox inhibitor, right? So by inhibiting cox, your platelets essentially will not work because cox is a major enzyme for the production of like a prasoglandins, of prasoglandins. And there is a the estrogen prasoglandins that help with like activating platelets and things like that. So it decreases the synthesis of those things. That's how aspirin works as an antiplacelet agent. And then the next disease I'll talk about is um um anti thrombin 3 deficiency, right? So under thrombin 3 deficiency, the classic presentation is it's actually a hyperquaglable disorder because normally anti thrombin 3's job is to inhibit factor 10 and factor 2, right? So when a person has a deficiency of anti thrombin 3, right? They will be predisposed to forming like multiple plots, right? Because factor 10 and factor 2 are working on a post, that's one. And then one of the way they can present that on an example is they can tell you that a person has like you're giving a person heprin, but the PTT does not appear to increase significantly. Like they will require like more than normal, like super high amounts of heprin to have any kind of positive response with the PTT, right? So when you see that you also want to suspect anti thrombin 3 deficiency. Another thing you can also see that the NV Me can use as a presentation of anti thrombin 3 deficiency is they can describe a patient that has nephrodite syndrome, right?

And then they form like uh like thrombosis of some weird vein, like a renauvein thrombosis. The cause of that is because they essentially spilling anti thrombin 3 in their urine, right? Because their nephrodisi don't work very well, right? So they spilling anti thrombin 3 in their urine and then they get into trouble. And then don't forget um a deficiency of protein, cyan protein, S, right? Those are again also hyperquagulable disorders because remember protein, cyan protein, S, they work to inhibit factor 8 and factor 5. So if those proteins, if you're deficient in those proteins, then you will not be able to neutralize factor 8 and factor 5 and then you get into trouble with hyperquagulability. And then don't forget factor 5 lighting, right? Factor 5 lighting, uh basically when a person has factor 5 they have problems with uh breaking down factor 5, right? They have basically they have factor 5 that is resistant to degradation by protein C, right? So that's why typically if a person if you want to diagnose a factor 5 lighting, you do something called uh activated protein C resistance as a right? So factor 5 lighting is the most common hyperquagulable disorder, right? For the most part is the most common hyperquagulable disorder. And again, it just arises because these people have um a defect in factor 5 that makes it resistant to degradation by protein C, right?

So if they give you a non-specific question about a person just like forming multiple clots, think about factor 5 lighting, although another thing you may want to think about is like antiphosphol polypidantibody syndrome where the person has like multiple you know first trimester pregnancy losses, right? And then they tend because they can thrombose like the utero placental artery and then they can get into trouble. And then um the last thing I think I'll talk about because I really have to run is there's this a disease called a pro thrombin G2 O210 A mutation, right? It's basically a mutation where a person overproduces factor 2, okay? And factor 2, right, is part of secondary hemostasis, right? So obviously if you're overproducing too much factor 2, then these people will have increased production of uh they'll have an increased propensity to form plot. And then I'll just relive three more quick things and then I'll be done. Remember your hemophilia, right? Remember uh hemophilia is a deficiency of factor 8, right? It's in heritatin and um it's in heritatin an x-linked recessive fashion so be in a boy on your exam and the ptt will be elevated but the bleeding time will be normal. Hemophilia B is a deficiency of factor 9. It's also in heritatin an x-linked recessive fashion so be in a boy on your test and the ptt will be elevated but the bleeding time will be normal because remember these are all part of the intrinsic or correlation cascade that's why the ptt goes up.

And then if a person has hemophilia C that's a factor 11 deficiency. The ptt will also be elevated but this does not necessarily have to shop in a boy on your test. It can also shop in a girl because it's in heritatin and orosomo recessive fashion. And again the ptt will be elevated under those circumstances and then um this disease is a hypothyroid genemia that's a disease that's beginning to make its way to the mbm exams. Basically these people it's inherited for the most part in an orosomo recessive fashion and these people essentially have mutations in uh the genes that quote for fibroid gen right so you may think oh these people are gonna bleed a lot no the thing is they actually don't bleed a lot they actually tend to form clots so hypothyroid genemia is actually a hypercloggle bull disorder. The thing that happens is remember what forms fibring? Fibrein is formed by fibrenogen right remember fibrenogen is the zymogen that forms fibring. So if you have a fibrenogen deficiency you're not from fibring and one of the things fibring actually helps with in addition to helping you form clots is that fibrenogen also I mean fibring also helps you break down clots right it also helps you break down clots. So if you have like a fibrenogen deficiency you have less fibring around so you have less of a clots breakdown feature so these people tend to actually be hypercloggle bull and again like I said this disorder is inherited in an orosomo recessive fashion.

So I'm gonna go ahead and pause here um as I do at the end of every podcast I offer to learn for many exams step one step two ck step two cs step three pre clinical medical exams 30th shelf exams if you're a medicine resident that is training exam the ebi-embod exam right and then I tutor like a lot of college like MCATB science courses and then I also do this thing called longitudinal tutoring and also offers this USM Libuster course so if you're interested in any of those things either reach out to me through the website or send me an email at the Vine Intervention Podcasts with an sadeand at gmail.com so have a wonderful rest of your day I'll see you in the next podcast God bless you thank you

The oxidizing agent converts Fe$^{2+}$ (ferrous, oxygen-binding) to Fe$^{3+}$ (ferric, non-oxygen-binding), forming methemoglobin.

Methylene blue, which helps reduce Fe$^{3+}$ back to Fe$^{2+}$.

Osmotic fragility test (or Eosin 5-Malimide test).

Streptococcus pneumoniae.

Stop all heparin products.

Hemophilia A (Factor VIII deficiency) or Hemophilia B (Factor IX deficiency).

Autosomal dominant.

Osmotic fragility test and Eosin 5-Malimide test.

Sodium nitrite (or amyl nitrite).

Thrombophilia/Hypercoagulable state (increased risk of clotting).

It inhibits COX, thereby decreasing the synthesis of potent platelet activators like thromboxane A2.

Salmonella.

Antithrombin III deficiency (or Protein C/S deficiencies).

Autosomal dominant.

Osmotic fragility test and Eosin 5-Malimide test.

Sodium nitrite (or amyl nitrite).

Thrombophilia/Hypercoagulable state (increased risk of clotting).

It inhibits COX, thereby decreasing the synthesis of potent platelet activators like thromboxane A2.

Salmonella.

Antithrombin III deficiency (or Protein C/S deficiencies).