DIP Episode 508 - The Clutch Sickle Cell Disease Podcast (for Step 1-3) Part 2

Welcome, my name is Divine, this is Episode 508 of the Divine Intervention Podcasts. Today's podcast will be wrapping up the series on sickle cell disease. I really hope that you found Episode 507 to be helpful. Honestly, that episode is super, super high yield. So many integrations you can make. And believe it or not, there are so many things our friends at the MVM is love to test with sickle cell disease. I mean, we'll just kind of blow it off. And then it's one of these topics that fit very beautifully into multi-systems processes and disorders. Because many people kind of struggle like, the fine, what in the world are these multi-systems processes and disorders? The thing is the end of making about, you know, about 5 to 10% of the exam, where it's just like some topic, but this topic is like a virus. It just kind of spreads into every discipline. So there are many ways they can go after it. You saw like literally last time we said so many things about hematology, oncology, social sciences, I kid you not. So if you missed out on Episode 507, I'd go ahead and check that out if I were you. But today again, let's go ahead and finish this up. And again, I'm going to give some background, but then I'll try to make some integrations as we go. And then we'll wrap this up. I want to make this as short as sweet as possible. So we talked about the management of sickle cell disease. We started out really started last time saying that I drug see arrays are cornerstone of therapy.

Because we said that I drug see arrays is going to raise your levels of hemoglobin F. And hemoglobin F, we said that whenever you have hemoglobin, you know, have a ton of F in them, right? Offer to gamma 2, that the inhibits that polymerization of those hemoglobin SS. Because remember is the polymerization of those hemoglobin SS that causes those red cells to assume a sickle shape. Right? And we talked about many high yield things about improving survival, blah, blah, blah, blah, blah. Right? We said that things that are in-per-survival, I think is like a drug see-your-rear. And we also talked about getting those antibiotics also in-per-survival. Okay. Now we know that sickle cell disease has some pretty nasty complications, right? So, like for example, people can have strokes. Again, remember I say that those sickle cells, the big problem is that, you know, when, again, what forms a sickling is the oxygenation of those hemoglobin SS. When they're in hypoxic environments, they polymerize, they cause the red cell to sickle. And then that's going to, again, I say that those things have a bunch of problems. Number one, they don't flow as well, right? So because of that slow flow, they're basically causing bloodstasis. That bloodstasis can make you hyper-quaglable. And then another thing I also mentioned is that, hey, these sickle cells, they love to, the control that they assume, some very favorable for the vascular anatomy.

So, they include blood vessels, and that can cause lots of problems, right? So, these, believe it or not, put a half sickle cell disease can get strokes, right? They can get P Es, they can get fat embolism, right? Because they can infarct their bones. They can have a acute chest syndrome, right? They can have like, ulcers on their extremities that don't heal. Because again, they have ischemia of those vessels that are feeding the skin or whatnot. Whenever you see these mastiffines, I just mentioned, right? So, I'm going to say that again, like a stroke or a fat embolism or PE or a acute chest syndrome, right? Or you see like these extremity ulcers that don't seem to be healing. I was strongly encourage you to consider an exchange, transfusion, an exchange, transfusion, right? An exchange, transfusion is, I mean, look at the name, exchange, transfusion. Basically, you hook the patient up to a machine, you remove their blood, but you're transfusing matched normal donor blood, right? And you do this basically so that you can very quickly lower the presence of hemoglobin S-burden. You can actually get your hemoglobin S-burden low pretty quickly, right? Although you can already see that if you're a person getting frequent transfusions that can cause a problem, right?

So, again, if a person has several infarctions or embolized, like, especially fat embolism, they have acute chest syndrome, they have like extremity ulcers that are not healing, then you're next step on the exams to consider an exchange transfusion. Now, I said a PE. Remember, could you do exchange transfusion in the setting of a PE? Absolutely, but remember, you're supposed to treat the PE first and foremost. Do that first before you start thinking about exchange transfusions and things like that. Just FYI, I imagine that most of these people respond to just usual PE therapy. So, they almost will never, I can promise you test exchange transfusions for managing P Es in sickle cell patients. Sickle cell patient has a PE, one of them the way you manage your regular PE, right? But again, several infarctions, right? So, like strokes, strokes, strokes, strokes, you should manage with exchange transfusion, fat embolism, acute chest syndrome, right? Extremity ulcers that don't heal, you really should consider, you really should consider an exchange transfusion that also circumstances. And remember, again, if a person is getting these constant transfusions, they're pretty much getting like a big iron loading to their bloodstream. So, it's actually pretty important to keep in mind that if a person is getting frequent transfusions, frequent transfusions, right?

Because iron overload believe it or not, that iron overload believe it or not can increase morbidity and mortality in people that have sickle cell disease. In fact, if a person is getting recurring transfusions in general, it's not going to do well for your body, right? You're just getting all these transfusions, transfusions, transfusions, right? So, in sickle cell disease patient, those recurring transfusions, right, can cause iron overload. Right? Now, why is iron overload so bad? Well, there's this nasty thing called a fentine reaction where iron is going to make all these friar articles. You can damage your heart, you can cause like restrictive heart disease. You can damage many parts of your body, right? Those friar articles, they are very normally, right? So, remember, people that have, that are getting these transfusions to prevent this iron overload, you generally want to make sure that they are an iron-kilator therapy, right? So, something like deferoxamine or deferoxamine or deferoxamine. Okay, now what's another thing you want to keep at the back of your mind, you know, present the hasicle cell disease? So, what if they give you a question about a person that has a cacillus cell disease? I noticed that the person's hemoglobin, I mean, sorry, the person's creatinine, they tell you that all three months ago when they came for a checkup, their creatinine was like 1.2. And then now their creatinine is like 1.8, 1.9, right?

So, you see their creatinine is kind of heading in the wrong direction, right? And you then even tell you that you would do some urine studies and they notice quite a bit of protein in the urine. So, they will ask you on your exams, what's going to be the next step in management? The next step in management is going to be to use an ACE inhibitor. Okay, it's going to be to use an ACE inhibitor. Again, this is something that many resources do not talk about, but it's very, very high yield to know for you exams, right? People that have cacillus cell disease that have hypertension, ACE inhibitors are the drugs of choice in those people, right? People that have cacillus cell disease and they're beginning to have a renal dysfunction, ACE inhibitors are the drugs of choice in those people, right? So, again, what are the two high yield indications to know for your exams? Forgetting ACE inhibitors in cacillus cell disease patients. Number one, if they have hypertension, ACE inhibitors are the drug of choice. Obviously, you can use ARBS if you're kind of worried about that dry cough from the increase of brain declining. And the second indication is if you have cacillus cell disease, it's torching your kidneys and you begin to leak protein in your urine, you absolutely should be on an ACE inhibitor, okay? And even if you're looking for protein in your urine, even if you don't have hypertension, it doesn't matter. You absolutely should be on an ACE inhibitor, right?

Because, again, those cacillus cells, they can begin to damage the vessels in your kidneys, they can damage your glomeruli and whatnot, and that can cause you to start leaking out a lot of protein, right? And, again, all those occlusions of your renal arteries, of your renal glomeruli, those things can raise the pressures within those glomeruli, right? And over time, because the pressure is the hydrostatic pressure, because you have all these occlusions, your GFR is going to rise transiently, right? But because your kidney is always working on such high pressures, it's going to damage your kidneys over time. That's actually something known as hyperfiltration injury, hyperfiltration injury, right? So, how do ACE inhibitors help here? Well, ACE inhibitors, they cause a dilation of your efferent arterial, when you dilute the efferent arterial, you're going to be lowering the hydrostatic pressures within those glomeruli local pillars. When you do that, that's going to reduce that intra-glomerular hypertension, right? And that can reduce your risk or, you know, can reduce that burden of hyperfiltration injury, of hyperfiltration injury, right? And then I've also mentioned for people that have sickle cell disease, I've said that these people should pretty more take daily foliage, right? Because if you think about it, these people, they turn over their rib blood cells all the time, right? And no more red cell is supposed to live for about four months, 120 days, right?

But for these folks, you know, because their rib blood cells just get turned over all the time, all the time, all the time. They use of their fully quick. I remember we don't have years of fully, like we have years of B12, we only have like months of fully. So, if you're using of your, if you're having all these red cell turn, like all the cell cell turn over, pretty quickly, right? Pumming out all these reticulosites and stuff, you're going to get used up your fully very quick. So, this will should take a fully, pretty, pretty, pretty seriously, right? They should take it seriously, they should take it pretty much every day, right? So, our friends at the NBM is they can write up a question about a person that has sickle cell disease. And they tell you that, hmm, this person's humus system is elevated. Their methamalonic acid is normal. That's a fully deficiency, true and true, right? Remember, B12 and fully both raise your humus system levels. If you have a B12 deficiency or a fully deficiency, your humus system is going to go up, right? But B12 is the only thing that raises your levels of methamalonic acid. Because again, the enzyme that metabolizes methamalono-coe to succino-coe, which we call methamalono-coe mutates, it uses B12 as a cofactor. So, if you don't have an of B12, methamalono-coe mutates is not going to work. So, you're not going to be able to convert methamalono-coe to succino-coe. For those that are taking step one, listen to those podcasts.

Remember, succino-coe is one of those intermediates in the crep cycle. That's something you probably want to keep at the back of your mind for your example, right? Because having high humus system levels is not very good, right? Many people always wonder, man, why is humus system so bad? The reason is bad is that it's very reactive. It's a very reactive molecule. You don't want a reactive molecule kind of floating around in your bloodstream, right? Because I believe it has all these soft hydro groups. Those groups are super reactive. It's almost like oxygen-ferradicals in a sense. It's like oxygen-ferradical light. So, it's very dangerous. It can really cause a lot of damage. It can damage blood vessels, right? You can start getting these thrombotic episodes and all these things, right? It can be a risk factor for stroke in these folks, right? Fully deficiencies actually is not a good thing. Okay. And then remember, people that have sickle cell disease, it's also recommended that they get regular eye exams, right? Regular eye exams, regular eye exams, because again, they can have your skin damage to their right now, right? And again, don't forget, right? This is kind of like basic sickle cell disease 101. Make sure these people get vaccines against these and Catholician organisms, right? Like the pneumococcal vaccine, the strep pneumo vaccine, the hemofluos influenza vaccine, the niacermin and gyros vaccine, right?

The hemofluos influenza, especially the type B vaccine, right? That's the big one, you know? They should get that vaccine, right? And also, you should also try to encourage this pool to get the influenza vaccines every year. I mean, everyone should get the influenza vaccine every year. Well, for sure, for sure, put a half sickle cell disease, yeah, they should certainly get the influenza vaccine, right? You just want to try to do everything to crush the risk of getting infected, right? To reduce the risk of getting infected, right? And then obviously, if a person has an acute pain crisis, you're going to bring them into the hospital. You know, we try to use things that are like not opioids to start, but it doesn't always work out that way, right? If you really, really hurt, you just want to go ahead and put them on opioids, right? You want to go ahead and put them on opioids. You want to go ahead and put them on opioids, okay? You want to go ahead and put them on opioids. Just remember that please do not use a peridine in people that have sickle cell disease. We're going to say that again, do not use a peridine as your opioid in people that have sickle cell disease. That is a terrible idea, right? A peridine in people that have sickle cell disease, right? Preparity has this association with seizures, and I mean, we don't give it credit for it, right? So don't give it to a person that has sickle cell disease, right? It's not a very smart, not a very smart idea.

Now, one other thing I also want to say about money-winner of sickle cell disease is that people that have sickle cell disease sometimes need supplemental oxygen, right? Especially when there are oxygen saturation in healing room air is like less than 92%. Those people should certainly get a supplemental oxygen. If you're looking at this from a P little EO2 perspective, so natural partial oxygen pressure, basically if it's 70 millimetres or mercury or less, those people also deserve supplemental oxygen, right? Now, some of you may wonder, like, man, can't we cure sickle cell disease? Yeah, we certainly can, honestly. We really can, we really can, honestly. We really can cure sickle cell disease with a bone marrow transplant, right? A loginic bone marrow transplant can cure sickle cell disease. Although to be honest with you, we tend to do this in young people, right? So please, don't pick this as an answer choice in a person that's like in their 20s or higher. No, that's no smart. Most people that get bone marrow transplants as a purative measure for sickle cell disease is probably going to be less than 16 years old on your exams. Although to be honest with you, I really have a feeling that in the next few years that's going to change, right? We're really getting good with a lot of these gene therapies. So I kind of have this feeling that, again, this is just a prediction, wild prediction, don't take my word for anything.

And please, by the way, none of this podcast is for medical decision making is purely for educational purposes. That's it. Okay? If you ever want to make a decision concerning your health, consult your physician. All right. I think that's kind of important to get out there, right? But basically these bone marrow transplants, I can almost predict that before the end of this decade, praying trusting God, that sickle cell disease will be something that will be a thin of a bust, something that's pretty, pretty curable. I mean, it affects a ton of people. I mean, I'm an African person, at least by birth. And a ton of people I know have sickle cell. So it's just one of these nasty things that, you know, I really hope that we can find the cure and is, you know, made in a way that's accessible to a large number of people. Anyone that has it should hopefully be able to get it, right? But you can right now cure sickle cell disease, right? So you can do these allogenic, you know, bone marrow transplants. But again, it's going to be done mostly in the young, right? People on the age of 16 for the most part of you, kind of like the best candidates for this stuff. But again, remember, you can reject the graph to just so many things that can pop up, even though suppression, blah, blah, blah, blah. So it's kind of a trade off between the kind of the risks and risks and benefits, right?

And then, remember, people that have sickle cell disease, again, how will, I think maybe let's kind of hit some high-yield things, and then we'll kind of go through and be done here. I feel like there's a few high-yielding hits that I can kind of mention here. So what if they give you a question about a patient at a hospital cell disease? And they tell you that, man, that this person says for the past like one week, I mean, having this weird pain in their hips or in their shoulders or whatever, like in one hip, so not both hips, right? Like in one hip or in one shoulder, even having this pain, you know, when you see this, I want you to think of the evasculine increases of whatever bone, right? So if it's the shoulder, evasculine increases of your humors, if it's the hip, evasculine increases of the femur. Many people are used to evasculine increases of the femur, when our friends at the MDE means believe they're nuts, can give you evasculine increases of the humors of the hemorrhoid head. Just going to give that a back of your mind, right? So remember, again, these are the symptoms of the hemorrhoid. And then, you know, the hemorrhoid is a very important factor. You know, the hemorrhoid is a very important factor. You know, the hemorrhoid is a very important factor. You know, the hemorrhoid is a very important factor. You know, the hemorrhoid is a very important factor. You know, the hemorrhoid is a very important factor. You know, the hemorrhoid is a very important factor.

You know, the hemorrhoid is a very important factor. You know, the hemorrhoid is a very important factor. You know, the hemorrhoid is a very important factor. You know, over the last two hours, they can move the arm. And, you know, they're, they can move the right arm. And they tell you that, ooh, the right lower face is kind of paralyzed. Again, think about like an MC stroke, a left MC stroke, right? Because again, I said that sickle cell disease makes you hyperquaglable, right? Although believe it or not, people that have sickle cell disease, they can also have hemorrhoid strokes. They can have hemorrhoid strokes. In fact, let me kind of give you like a nice epidemiologic tidbit that you should know for your exams. People that, so strokes are of two major kinds, right? They say, is this chemical stroke, these hemorrhoid strokes? Right? The most common kind of stroke associated with sickle cell disease in kids is, is this chemical stroke, right? You tend to have this chemical stroke. But the most common kind of stroke, as well as sickle cell disease, in people that are adults, is actually hemorrhoid stroke. It's kind of a high-yield thing to keep at the back of your mind, for example. Right? The USML is these days, they pride themselves in making sure that you know that you understand epidemiology. So, as I see many of my podcasts, many of my review courses, I keep saying most common cause of this biggest risk factor for that. So, strokes are common in sickle cell disease.

In kids, the most common kind of stroke is going to be an endschemic stroke. Right? And then the most common kind of stroke in adult riskle cell disease is going to be a hemorrhagic stroke. It's going to be a hemorrhagic stroke. Obviously, in these situations, we want to get like a non-conhead CT and then manage as necessary. And then, what if they give you a question about a sickle cell patient? The kind of person has like, you know, high-fever's, certificate rate of pro-corporate pain, and they show you their ASD, L Ts kind of elevated. If you see something like this, don't you think of all this is tightest, right? I can remember, sickle cell disease is a kind of hemorrhagic anemia. So, they keep crushing their red cells. As you crush those red cells, well, something's going to happen from that. You're going to make a ton of indirect bilirubin. I wonder, what is the thing that a body is used to, a body is used to, a script bilirubin. Bial, right? So, a pretty much going to supersetre your bowel with all that indirect bilirubin or direct bilirubin even. And that's going to cause you to have these bilirubin gold stones, right? Those things, lodging the cystic duct, infection bills are behind that bone. You have colicis tightest, right? So, remember, a colicis tightest actually a fairly common complication of sickle cell disease, right? And then, what if they give you a question about a person that has sickle cell disease?

And they say that, you know, for the past three days, they've had this asymmetric swelling of their hands and their feet, or both, or one or the other. If you see that, I want you to think of ductilitis, right? You'll think of ductilitis. Dictilitis is very common in sickle cell disease, especially in people under each five, right? Most times, it's going to be a young person, it's going to be getting ductilitis on the exams, right? And I guess, we're talking about bone pain. Let's also, if you see bone pain and fever in a sickle cell disease patient, that's also my lightest, right? What's the most common cause of osteomyelitis in sickle cell patients? It's going to be salmonella. Salmonella is the most common cause of osteomyelitis in sickle cell patients. Some resources are beginning to see things that are different. Don't go with that on your exams. Go with salmonella, like you do not. Salmonella on the USML is the most common cause of osteomyelitis in sickle cell patients. And remember, if you suspect those two myelitis, you kind of want to get an MRI, right? That's kind of like a smart thing to do. And then, many times, you're going to get, like, a bone culture, so that you can help you guide your anti-baric therapy. Now remember, what if they give you a question about a patient that has sickle cell disease? Right? And they'll tell you that over the last few weeks, they've developed like a dima, right?

So like their body is swelling, they have joglevino's distension, blah, blah, blah, blah. If you think of all these things, right? And the material that you may not hear crackles in the lungs, you want to think about heart failure. Remember, poor memory hypertension is actually quite common in sickle cell disease. And if you don't think about this, but I'm going to say this again, poor memory hypertension is very common in sickle cell disease. I'm going to say that again, poor memory hypertension is very common in sickle cell disease. Because again, that slow-flowing blood, those, that sickle blood, that's including all these small vessels, it can make it hard for blood to flow properly in your poor memory vessels. Over time, you can develop poor memory hypertension. When you develop poor memory hypertension, the right heart is going to fail, right? So people that have sickle cell disease believe it or not, they can develop heart failure. And again, I lambasted on this in the previous podcast, but again, why is it that people that have sickle cell disease are very susceptible to infection? Because they have a functional isplenium, right? Before the age of five, even a minute and a minute and a half, most people that have sickle cell disease, they're splitting pretty much, pretty much gone. Okay, now what if they give you a question about a person? That's a history of sickle cell disease. And the person is coming to the office, you know, because he has my two problems.

He's saying that he's not able to get it up with his wife, he's not to a guy, he's not able to have like a full erection or whatever. And then they ask like, what's the mechanism behind this? Well, I hope you're picking the answer that says occlusion of microvascular, occlusion of microvascular. Remember, if you see a rectal dysfunction, a person that has sickle cell disease, what's the cause? It's prior pizde, right? The thing is, again, those sickle cells really you can't build on sickle cell disease to polyfluous blood and these sickle cells, including blood flow. That's it. That's the honest truth, right? So they can give you a prior pizde in sickle cell disease, believe it or not. But another arena where they can kind of present this business is a rectal dysfunction, right? Because every, probably, let me not say every one kid, but many on kid decks that kid are to the USML Es. People have memorized prior pizde, but sickle cell disease, right? So how will our friends at the MBM is to know the newer exams, kind of advance that concept a bit? They can just give you a rectal dysfunction, right? They can give you a rectal dysfunction, right? So remember, people that have sickle cell disease, if they have prolonged prior pizde, or they keep having repeated bouts of prior pizde, that can certainly be associated with them having a rectal dysfunction. That's a pretty, pretty high up to know for your exams. Okay, now let me ask you this.

What is the most common cause of death in sickle cell disease? What is the most common cause of death in sickle cell disease? It's a Q-chest syndrome. It's a Q-chest syndrome. It's a Q-chest syndrome. Okay? It's a Q-chest syndrome. And many times when a sickle cell patient has a Q-chest syndrome, you're going to see like this diffuse infiltrate, right? So it's going to be like more interstitially nature. You're going to see a lot of interstitial infiltrates in the lungs, right? And again, remember for that, we're going to do an exchange transfusion. Even though the person is going to die, right? You want to make sure you treat a Q-chest syndrome. You may not necessarily die, but you may have like a severely impaired life, right? So it's one of these things that you take seriously and you treat it, right? And believe it or not, a Q-chest syndrome tends to have a very solid association with with these causes of interstitial pneumonia, right? Like chlamydia, microplasma. Those bugs can be very like important triggers of a Q-chest syndrome on the exams, right? On the exams, right? And again, remember, what if they give you a question about a sickle cell patient? And they tell you that this person, you know, for the past two hours, they'll be having severe chest pain, they have fever, they have dysmia, right? And you see multi organ failure, their political count is going down. If you see this, I want you to think of fat emblysm syndrome. You're like divine, that's weird.

I'm sure many of you are seeing divine. All I know about fat emblysm syndrome is, you're in trauma, you break a bone, and then you have P-T-H-I prepared on the skin, you have a Q-Moses, you have low platelets, right? You can get a PE blah, blah, blah, blah. Yes, that's a classic way to test fat emblysm syndrome. But again, don't forget our friends at the MDM's. Again, they're just getting smart about testing these concepts. Fat emblysm syndrome can be found in sickle cell disease. You're going to see this chest pain, you're going to see fever, you're going to see hypoxia, you're going to see low platelets, keep that in mind, you're going to see low platelets, you're going to see a multi organ failure. You know, sometimes they may be kind of throwing that P-T-K-I prepared, but again, they don't always put that, right? And the thing is, they can even make fat emblysm syndrome as a complication of a Q-Chest syndrome. Make it as a complication of a Q-Chest syndrome, okay? They may make it as a complication of a Q-Chest syndrome, right? Just going to keep that at the back of your mind, okay? Just think of it as being like neck and neck, very close. Pretty similar presentation, honestly, the treatment is the same, right? The treatment is still exchange transfusions. Okay, so I think I'm going to go ahead and stop here. Again, this podcast, I promise you, super high-yield, pay attention to this stuff, right?

You're going to get a lot of questions right on your test as a result of episode 507 and 508, right? So I do offer our review courses for step one, I have a 25-hour class coming up in March, and I have a bunch of classes coming up this month in the month of February. That's for step two, step three, I have a 20-hour, step two, step three course, coming up like the last week in February. And then I have courses for step one, all the way to step three, the two and a half hour MBME test against strategy scores, the four-hour bio-stats class, and the five-hour social sciences and ethics class. Again, many people have taken these classes and they've done extremely well on the exam. And these classes are not lectures, they're not. Most of these classes, right, all of them over Zoom, but most of these classes are clinical scenarios, exam style questions, where over, you know, I use these presentations because that's just more realistic to your exam. I also want to be giving you lectures, right? You can get that from any resource. No, what's the unique selling point? You're going to see these presentations, you're going to learn the concepts, you know me, where path of physiology matters, I explain it, and I love to make integrations. So by the end, you've built up like a series of very good skills. You've not just learned the content, you've learned it at a deep level. You've also built up critical thinking and analysis skills.

And then you also end up learning the deferring presentations for many of these diseases. And then also have a 50-hour class coming up in the month of June. I feel interested in that. That's just for step two and step three. Obviously, anything for step two is also for complex level two and three. And then also for one or one tutoring for all the USML Es, and pretty much every medical school exam. And then I have this podcast on Apple Google and Spotify. I have a You Tube channel you can check out. And then I have another website called, Divine Intervention Lifelesses.com. On that website, every week I post two podcasts. We actually have 200 and I think 49 podcasts. I post two podcasts and using a Bible verse or Bible verses address a life lesson. Many people have found those weeks extremely helpful. I usually post them on Fridays and on Sundays. So check out Divine Intervention Lifelesses.com. It's actually an Apple podcast associated with it called the Divine Intervention Life Lessons Podcasting. If you need any help with your errors, applications, more interviews and whatnot, I'd also offer those services. So just reach out to me through the website. Shoot me an email. Shoot me an email, Divine Intervention Podcasts with an s at gmail.com. Or just go to the website. There's a contact page. Just type in, putting your correct email. Probably a non-school email. That may be helpful. Shoot me an email under. I'll read it and get back to you. So thank you for listening to me today.

Have a wonderful rest of your day. God bless you and bye for now. Thank you.

Hypoxia (low oxygenation) of hemoglobin S, leading to polymerization.

Stroke, Acute Chest Syndrome (ACS), Fat Embolism Syndrome, or non-healing extremity ulcers.

Salmonella.

Hemorrhagic stroke (Adults) vs. Ischemic stroke (Children).

ACE Inhibitors (Angiotensin-Converting Enzyme Inhibitors).

Propofol.

They dilate the efferent arteriole, reducing intra-glomerular hydrostatic pressure and preventing hyperfiltration injury.

1) Hypertension; 2) Proteinuria/renal dysfunction (even without hypertension).

Salmonella.

Vitamin B12 and Folate.

Hemorrhagic stroke.

Phrenitis/organ damage (iron toxicity); Chelation therapy (e.g., deferoxamine).

They dilate the efferent arteriole, reducing intra-glomerular hydrostatic pressure and preventing hyperfiltration injury.

1) Hypertension; 2) Proteinuria/renal dysfunction (even without hypertension).

Salmonella.

Vitamin B12 and Folate.

Hemorrhagic stroke.

Phrenitis/organ damage (iron toxicity); Chelation therapy (e.g., deferoxamine).