DIP Episode 323 - Immunocompromised Patients, Transplant Patients, and the USMLEs

Okay, welcome. My name is Devine. This is episode 323 of the Divine Intervention Podcasts. And in this podcast, I'll be talking about immunocompromised individuals, transplant patients and the NVME exams. So this is a podcast where it's going to, it's going to be organized, but it's going to kind of be like a treatment of just people that are immunocompromised and different variations of things. It's almost kind of like a nebulot stop, but I'll try to pare it down and keep a, keep a fluff to a minimum. But basically, I want to emphasize many of the higher points that the NVM Es care about in people that are immunocompromised in people that are post-transplant or you know getting a transplant of some sort. And just emphasize certain scenarios. This is one of those things that are best learned by way of scenarios. So hopefully by the end of this lesson, you should feel a lot better about that this material. And for those of you that listen to this podcast, I mean many of you know I'm a Christian. Many people have given sent me lots and lots of emails now. Oh, Devine, we really like your life lessons. So if you're looking for like Bible-based teaching, very short podcast of like 10 minutes or less on just life lessons. I actually started a new website recently. It's called Divine Intervention Life Lessons. So every now and then I will still talk about some life lessons with these podcasts like the regular Divine Intervention Podcasts.

But I will be making weekly just regular life lesson podcasts on the Divine Intervention Life Lessons Podcasts. It's actually an Apple podcast as well. And I'll encourage you to just go to Divine Intervention Life Lessons.com and you'll get more information on that. And then for those that are studying for step two, CK of step three, I have a test again strategy scores that starts tomorrow between 12 and 4 30 pm Pacific Standard Time. So that's like 5 to 7 30 Eastern time. And then I have the 20 hour comprehensive course studying on Tuesday from 11 PM to 4 PM Pacific Standard Time. So that's pretty much from 2 PM to 7 PM Eastern Standard Time. So if interest teacher should be an email through the website and I'll give you some more information. Okay so let's start off talking about email compromise folks first. And again I'll look at it from many different angles. The theme is on the USMEL exams they are not very oh we're going to talk about this specific thing. No the MBM is about being able to make integrations. So I will try really hard to make integrations with this topic. Some people like when integrations are made, some people don't like it. It's kind of unsettling to people in some respects. What the problem is if you're not able to make integrations then any question that is tested on the USMEL is that goes beyond just basic knowledge. You very likely struggle with those kinds of questions. So it's very important to be able to see from many different modalities.

That's why you may see that a lecture that I may call an immunology lecture. Maybe a lecture that I didn't talk about a lot of hematology, a lot of homonology, a lot of cardiology. That's ultimately the best way to learn and be able to apply information. Because again even in the real world when you see patients as a resident, as a physician they are not going to present us cookie-quarter cases. There are some people that practice cookie-quarter medicine. And again for the most part that's helpful. That's not a problem. You know patients are coming with guardian variety pneumonia and you treat them at no problem. But then maybe some patients are coming with pneumonia but then pneumonia is a manifestation of something else. That's why you see if a person is not properly trained or not able to think in multiple dimensions. You then see them be mis-huge things in patient care. So again I'll encourage you have that mindset that I'll be a multi-modal thinker as I take care of patients. But let me get off that soapbox. Let's jump right into it. So the first thing about immunocompromises in general as a person gets older, right? They get more immunocompromised, right? So a person's immune system gets just weaker in general as they get older. I mean obviously there are things you can do to mitigate that by being healthy, by not having chronic disease.

Because again if you notice during this COVID pandemic, the people that got in trouble quite significantly were people that were really old and had lots of medical comorbidities. Also being malnourished makes you immunocompromised. Many people don't think about it. But infection is a common complication of having an eating disorder like an oraxia nervosa for example. Because again if you are malnourished remember your immune system is literally built on proteins as a macromolecule. So if you are malnourished in that circumstance or a child has quashochor. So they can give you an immediate question about a child with quashochor getting recurrent infections. Well those kids will get a lot of recurrent bacterial infections because they are not consuming protein. Literally you cannot meet antibodies if you don't have adequate amounts of protein in your body. So those kids tend to get recurrent infections with encapsulated organisms, right? Obviously for person has HIV, right? That's more of a matter of cell medicated immunity, right? So they have a T cell problem. And because they have a T cell problem they get a lot of viral infections, a lot of fungal infections, a lot of infections with immunociscus urevesi. In fact I'll talk about bok patterns in a bit. I'll talk about bok patterns in a bit, right? Or if a person has amalignancy, right? Like having CLL for example.

The thing is if you see like a CVD like presentation in a person over the age of 60 on in-beaming exams, they likely have CLL. Usually those people they will have a crazy high white count. But because it's a lymphocytic leukemia, right? It will not be myloids cells that are predominant. A bit lymphoid cells. You notice they have white count is 100,000 80% of it is lymphocytes. And you see them get a recurrent infection. Well the thing is those lymphocytes that are proliferating, they are not really making antibodies. Of the making antibodies, those antibodies are trash. So they don't work. So those people have a risk of recurrent infections. Or if a person has no spleen, remember there are many reasons why people can have no spleen. A common cause on amalignancy is sickle cell disease, right? For a person has sickle cell disease, they have functionally spleen by the age of five because they have auto-infarcted their spleen. Or let's say a person has gotten a spleenctomy for some kind of disorder. Let's say they've gotten it for hereditary sporesitis. Remember, spleenctomy is the treatment of choice in hereditary sporesitis. Or spleenctomy is a third line treatment for immunothermal cytopenia, in patients that have lupus for example, right? So when people have no spleen, they're pretty supposed to get infections. And typically again, those infections tend to be from encapsulated organisms. The most common cause of infection, there's actually very high autonone.

The most common cause of infection and sepsis and people that have no spleen is strepnumococcus sepsis, the most common cause of sepsis and people that have no spleen, right? Or if people have some kind of immunodeficiency disease, so let's say they have like Brotanziga maglubulinemia, where they're B cells don't mature or they have like hyper-IGM syndrome, where they have a claswichin defect, where they can go from IgM to IgG or IgA. And those things are gonna put those people at high risk of high-finding infection, especially again infection with bacterial organisms. Also, if a person is diabetic, diabetes is an immunocompromised state. Many times, as you've seen me in the Australian many podcasts, people that have diabetes tend to get the shortened of the stick with infections. So, you can see normal people getting pylon arthritis, but then you see people that have diabetes getting complications like emphysemitose pylon arthritis, where you have like gas bubbles in the wall of your kidneys, or you see them having a perinepharic abscess where they have a fluid collection in the walls of the kidneys, or you see them getting like colisestitis, but then they get about complication like gangrenos colisestitis on embeem exams, where again you're seeing like gas bubbles in the walls. Of the person's gallbladder, these things tend to have very high morbidity and mortality, right?

Or you see people that have phonies, gangrenos, many times people that have phonies, gangrenos, does basically necrotizing fasciitis of the perineum. Again, that's classically found in people that have diabetes on embeem exams, or think of people that have milk or mycosis, so they'll give you a sinus infection and a person that is in DKA or a person that is in HHS or a person that has poly-control diabetes. Again, those things all arise in people that have diabetes on embeem exams, or you see a person that has recurring candida vaginal infections. Again, that's pretty classic in people that have diabetes. Diabetes is an immunocompromised state. And also this is one of the reasons why people that are pregnant tend to have a lot of infections. Remember pregnancy is an immunocompromised state, because remember, an immune system is not very tolerant of things that are foreign. The thing is when a baby comes from a woman, right? That baby that is green in the woman is almost like a foreign organism. So the body does not necessarily, like basically your immune system develops, again, I'm not going to go deep into immunology here, but the immune system actually develops a kind of tolerance to the baby, so the baby is not destroyed. This is why many times when a person gets pregnant, many inflammatory and rheumatologic disorders tend to calm down. Like for example, it's been well studied in the literature.

Many people that have rheumatoid arthritis tend to have very few flares of rheumatoid arthritis when they get pregnant. But after the baby is delivered, the rheumatoid arthritis comes back in a big, big, big, big way. This is almost like a rule with many rheumatologic diseases, because they is pervasive immune tolerance during pregnancy. That's why many times people that have rheumatologic disease, that disease again, comes down during pregnancy. And then if a person is on chronic cortical stereotherapy, again, I'm just basically giving you many different vignettes that you can use to craft or frame an immunocompromised question on your exam. If you know these different scenarios, then nothing will sound out of the blue to you on the exam. Again, especially on these newer USML exams, because you see people that take these exams and they say, wow, I felt like I was guessing for like most of the questions. Again, it's the same general classic concepts they are testing. They're just finding unusual ways to test these things. So again, that's why you need to be able to think in multiple dimensions. So if a person is on chronic cortical stereotherapy, let's say they have really bad asthma. Again, that can predispose those people to recurrent infections. If a person just got chemotherapy for some kind of malignancy, right? Again, that can predispose these people to getting infections. Or if a person has been on a TNF inhibitor, right?

Like a Dalimimab, a tanner set, which is a decoy TNF receptor, those things that are not predisposed to a person having infections, right? If a person is a post transplant recipient, people that have got in transplants, right, they tend to have, again, they're taking big time immunosuppression. Those things can cause lots of problems in people. And one thing I want to go ahead and say, maybe the next maybe major head in I want to go into is just talking about different patterns of infection, different patterns of infection. Patterns of infection are very helpful for mbim exams because the thing is, for those of you that have listened to my immunodeficiency diseases podcast, that's episode 173, which is a higher podcast by the way to listen to for any of the USM exams. One thing that helps with many of these immunodeficiency disease questions is almost like the mbim is one of their best kept secrets, is just understanding patterns of infection. If you understand patterns of infection, then many times you may not even necessarily need to know the exact immunodeficiency disease that these people are suffering from. You may not need to know the exact diagnosis that, oh, they have scared, or they have this. No, many times you can know what is going on just by the kinds of infections you're getting, right? So the thing is, there are four classic patterns of infection I want to deal with here, but the mbim lost to after.

The first one is if a person has a problem with cell meditated immunity, if a person has a problem cell meditated immunity, remember, cell meditated immunity basically refers to your T cells. So usually these people tend to, the pattern of infection, you'll see pervasively throughout the question is, you'll have problems with viruses, right? They'll have problems with fungi, they'll have problems with parasites, they'll have problems with TB, they'll have problems with your moscis, your vetsy. Those are the classic things you'll find in people that have issues with cell meditated immunity, right? So again, what are some classic diagnosis that go along with cell meditated immunity problems, right? Well, HIV, right? It's an immunodeficiency disease of cell meditated immunity, right? Your T cells basically get destroyed, right? If a person has, if a person is taking big-time chemotherapy, many times that ends up causing a lot of problems with cell meditated immunity, or if you see a new born or a person that is a few weeks old with all these diverse infections, think about scared, right? Severe combined immunodeficiency, that's a cell meditated immunity problem. Another one is if you see a child with seizures or with fish like cranial facial abnormalities or like a VSD or tetralogy of a low, or you notice that they have cleft, cleft, cleft palate, if you see those things, I hope you're thinking about the George syndrome.

Remember, in the George syndrome, your third and fourth pharyngeal pouches don't form. If they don't form, I'm going to form a thymus, so your T cells are not going to mature. That's going to cause a cell meditated immune defect, right? So again, viruses, fungi, parasites, TB, you must see this is your vetsi. That's a classic construct on ambient exams that goes with a cell meditated immunity problem. Now, the next big pattern is humoral immunity, right? So this is B cells. They use many different names for this. B cell meditated immunity. So B cells, right? B cells, or they may call it antibody meditated immunity, or they may call this humoral immunity. The big thing I want you to think about here are bacterial infections, especially in capsuleated organisms. So things like those shane organisms we learn about, strep pneumo, hemofluos influenza, my serb and ingitis, some onelatifi, or B strep, remember strepigalactia, right? Those are all in capsuleated organisms. That's a classic construct for people that have humoral immunity problems, right? So, also people that order some classic diagnosis that go with humoral immunity problems on ambient exams will think about CLL, right? Again, remember CLL is a senior citizen's disease. It's going to be in people over the age of 60 on ambient exams.

If people have multiple myeloma, they'll give your person like, oh, they're creatinine is high, they have like high calcium, they have anemia, they'll have like been in some bone, they can have like low back pain or pain in the a femur or whatever, right? Again, those people are losing all these antibodies. Those plasma cells are useless, right? That's an immunodeficiency state, recurring bacterial infections. If your person has an euphoric syndrome, all the person that have an euphoric syndrome keep getting all these infections, or they're getting it because again, they're pain-out proteins in the urine. Again, these people can peel the antibodies. So again, they have that risk of infections because they literally have an acquired humoral immunity problem. If a person has like many trees disease, right? Remember, many trees disease, they're literally pooping out protein. If you lose in all that protein, again, you're losing either antibodies or you're losing feed stock for antibody production. Again, that's going to make you immunocompromised, right? Or if you say a person that has like a immunoglobulin deficiency, like Ig deficiency, although remember, those people tend to have like an aphylaxis, right? With blood transfusions, right? For patients with scoloidric syndrome, again, these are all for the most part humoral immunity problems. Now, the third major class disease pattern I want to talk about are problems of neutral fields, are problems of neutral fields, right?

So for example, if a person has a recurrence, I will say like probably like the big thing I want to think about with a neutral field problem. And this is very high you to know. And many resources don't talk about this is again, issues with catalysts producing organisms, right? The thing is catalysts is an extremely important enzyme to a neutral field. So if a neutral field is a messed up for any reason, that's going to predispose you to getting recurrent infections, classically an embankment exams, recurrent abscesses with catalysts positive organisms. Usually it's going to be staphoreus, costaphoreus is catalysts positive. But also don't forget these people tend to get recurrence seriousia infections, recurrent noncardial infections, recurrent aspergillus infections. In fact, this is one of those reasons why people that have fibral intropenia tend to get like lead stage aspergillus infections because their neutrophils are not working, right? So who are the classic people that tend to get mutual field problems here? Well, again, the big one, especially in boys on exams, right? CGD, chronic general numeral disease. Again, if you want more specifics on CGD, listen to episode 173, which is my immunodeficiency diseases podcast, just like 150 podcasts ago, basically. Or people that have a complement protein deficiency, especially like a C3 deficiency, or C5 deficiency, those things again make your neutrophils not function as well.

The thing many people don't realize is that there is a very big interaction between your complement system and neutrophil function. Whenever your complement system is not working well, your neutrophils are going to have a hard time, right? So people that have issues with compliments, like people that have paroxysmonectrinal hemoglobinary, PNH, right? Those people, right, they tend to have a lot of neutrophil problems. Again, so again, catalys positive organisms, that's the classic signature, you're looking for an MDMA exam. And then the fourth last pattern I'll talk about are people that have no skin, people that have no skin. Again, the big thing you want to keep in mind are encapsulated organisms. It kind of looks the same as people that have humanoid immunity problems, right? So, again, strep pneumo, right? Again, that's the most common cause of infection and sepsis in these folks. Hemophilus influenza type B, like seramine GDD, this, San Monella, right? One thing I think I want to mention here that many people don't think about is if you have no spleen, you're going to have a hard time with, like, infections that affect red blood cells. Because again, remember, red blood cells are almost like disinfected or cleared by your spleen. So if you have no spleen, the infections that hide in red blood cells, they're going to cause your lots and lots and lots of problems, right? So for example, malaria, malaria is really bad in people that have no spleen.

Babesia, my crudy, remember Babesia is carried by the exodistect, right? Babesia, my crudy can cause problems in people that have no spleen. So if they give you, like, again, very bad hemolytic anemia in a person that lives in New England and is a splinic, think about Babesia potentially as the cause of that infection, right? Again, just very high you to know these classic patterns. I'll tell you that you can almost always get about 50% of Indian questions on immunocompromised people or in your own immunodeficiency disorders. If you just know the classic signatures of infection, again, I broke them up into cell-meditated immunity, humanoid immunity problems, neutrophil problems, remember we said that, not your problems and complement problems, you can kind of lump them together. And then the fourth signature where people that have no spleen, right? The reason I put that fourth group of people that have no spleen is that, again, it is the classic hiccups, lytheropenisms, the getting infections with, but in addition to that, they also tend to get infections with red blood cell infecting organisms, like Babesia, my crudy, or my leery, very important to keep that in mind. Now the next major topic I think I want to hit on with regards to people that are immunocompromised. It's just people that have fibrointropenia. Fibrointropenia is a pretty classic thing that is tested on NV Me exams. So what is the big thing on fibrointropenia?

Basically, these people's absolute utrophil count will be really low, right? It will be really, really low. And really, the way you calculate the person's absolute neutrophil count is just take their webloxel count and multiply it by the percent of neutrophil. So let's say the webloxel count is a thousand and your neutrophils make up 60 percent and your absolute neutrophil count is going to be 60 percent of a thousand, which is 600. So when you see a person that has fever and a really low webloxel count, they likely have fibrointropenia on an NV Me exam. And again, we know many of the causes of fibrointropenia, classically on NV Me exams, is going to be in a person that may be taken a drug that really brought down the neutrophil count. Remember, these drugs that cause a granulose cytosis, things like clasapine that is used to treat psychosis, things like carbonizapine that is used to treat trigeminal neurologia, things like your anti-theraid medications, like PTO, methemazole. Those things can really bring down a person's neutrophil count, right? Of a person has feltis syndrome. For a person who has feltis syndrome, remember, in feltis syndrome, that's the combination of rheumatoid arthritis with your neutropenia, right? And spino-megaly. Those people, if they have that low level of neutrophil, that can predispose them to having fibrointropenia.

And also, if you think of people that are on chemotherapy, these are people that can get fibrointropenia, people that are taking radiation, for some kind of malignancy. Again, those people tend to have a fibrointropenia. In fact, fibrointropenia is the most common complication of people getting chemotherapy. For a person who is basically being treated for cancer, or for some kind of malignancy, the most common life-threatening complication is fibrointropenia. The most common complication is very high-yield, is fibrointropenia. Now, the thing, what are some key things you want to keep in mind with fibrointropenia? Again, I've talked about the causes. Well, some other things you can keep in mind is, if you give your question about a person that has fibrointropenia, I noticed that the aryctrile quadrant is really tender. I want you to think about necrotizing enterocolitis. People that have fibrointropenia, they are pretty spoolsed, very commonly on NBM exams, directly walk quadrant, necrotizing enterocolitis. That's something that sometimes is called a typhlytis. On NBM exams, it's basically like an inflammation of the seacum. But it's really, really bad, really, really life-threatening, has very poor outcomes in general.

And then, another key thing I want you to keep in mind is, if you're in general, if a person is neutropenic, or if a person is taking chemotherapy, and you want to prevent them potentially from developing fibrointropenia, one thing that's very helpful on NBM exams for these people is to consider giving them a GCSF analog or a GMCSF analog, so something like Phil Grassem or Sagramostem. Many times, that's really good profile access against people developing fibrointropenia in the first place. Now, if a person comes in with fibrointropenia, what are you supposed to do for those people? The first thing you're supposed to do for those people is to get blood cultures. Blood, blood, blood cultures. They may give you many different kinds of cultures on your exam, because typically, you're supposed to get many different kinds of cultures in these people. You're supposed to get blood cultures, you're supposed to get a number of puncture, you get CSF cultures, you're supposed to get urine cultures. But if you have to pick one test on the NBM exam for these people, get blood cultures. Blood cultures are the things that you classically do in people that have fibrointropenia on NBM exams. Again, this is very high you to know for tests. And then after you get those blood cultures, what are you supposed to do treatment wise for these people? What is like the first thing you want to do treatment wise for these people?

The high you'll think to give these people on NBM exams is an anti-sudo mono. This is very important, is an anti-sudo mono, anti-biotic. It's an anti-sudo mono, anti-biotic. Because many times, these anti-sudo mono, anti-biotics, they are very good at covering lots and lots and lots of bugs. So you want to give people things, these people things like paparacillin, plus tizobacter. Remember, that's a combination that can treat pseudomonas, or you can give them sephepym. Sephepym is a fourth generation cephalosporing that covers pseudomonas, or you can put them on septazidine. Remember, septazidine is a third generation cephalosporing that covers pseudomonas. So you can put them on a carbapenem, like meropenem, or emipenem, or gorypenem. These are carbapenem, they are very good birth spectrum antibiotics. They tend to cover pseudomonas as well, right? So that's like the first line therapy for febrile intraopenia on NBM exams. But if you notice that for some reason, you've put them on this anti-sodomonal antibiotic. And you'll notice that, well, these people don't seem to get in better, three days, four days, five days later. And they ask you for your next step on an NBM exam. Go ahead and pick the answer that is an anti-fongal. Many times when you see people that have been placed on birth, so this is a construct. Again, NBM exam is an exam of scenarios.

If you notice that people that have febrile intraopenia on an NBM exam have more gotten better, three, four, five days after they were studied on birth spectrum antibiotic therapy. And they ask you for your next step in management. Go ahead and put these people on some kind of anti-fongal therapy, right? You can put them on an amphoteric NB if you want. Or you can put them on something that covers candidate, right? So like an a kino-candin, right? So drugs like cuspophongin or micapongin or anidolophongin. Or you can put them on a drug that covers aspergillus. Many times you want to put these people on aspergillus covering medications, right? So things like voreconazone or bosaconazone, right? Again, you can also use amphoteric NB on NBM exams. Again, this is a very high-yield construct to know for tests. And one thing I also want to say is sometimes your friends at the NBM give unusual presentations of neutropenia in people that are getting sulfonamide therapy. So remember, for person who's getting tri-methodromythoxysol, those things can cause boomerar suppression. Or for person who's taking methyltrixid, remember, methyltrixid kind of works like a sulfonamide. Although it it works more like in the second step in that folic synthesis pathway on dihydrofolid reductis. For person who's taking toxoplasmosis therapy with pyramethamine and sulfodizing, those people, right? Very high-yield to know. Those people can develop febrionotropenia.

And many times the way you rescue those people's bone marrow is by giving them lucovory. Remember, lucovory is a full lening, not full lening acid analog that can be used, that can be used in these folks on NBM exams. Now, one other thing I think I want to also talk about here, since I'm kind of parked on this febrionotropenia is let me spend some time talking about transplant patients. Again, I'm just going to try to hit on the high points that are like the most important to know for purposes of the USMLA exams. Because again, these are things that people tend to confuse. And this is something that can potentially be like an extremely expensive topic that people can get wrong on exams. So the first thing I want you to keep in mind is that getting a transplant increases your risk of cancer, right? Because again, if you even think about it, many people have heard of the drug nivolumab. Nivolumab is an anti-cancer drug because it literally supersists opioid immune system to go and kill the cancer. So the thing is whenever you're immunocompromised, you have a high risk of malignancy. In fact, malignancy is one of the most common complications. I'm not saying the most common, but they are one of the most common complications that are rising in people that are post-transplant, right? Especially like lymphomas. Like many times, people that get a transplant and they are placed on immunosuppressive therapy.

I think I heard a statistic a few years ago that they have like almost like a 44 increase risk of lymphoma. And many times, these people, especially non-hot skin lymphoma, and many times, these people also have a high risk of like just skin cancers, especially female cell cancer of the skin. This is one that is particularly common in kidney transplant recipients on NV Me exams. So again, it's just something you want to keep in mind. Something you want to keep in mind, right? And then obviously I won't be talking about this if I'm talking about immunocompromised people, but people that are post-transplant, they tend to get lots and lots and lots of infections. They tend to get lots and lots and lots of infections. In fact, many times when people are getting transplanted, before they get transplant, I'm going to screen them for all this bad stuff, right? What I mean by bad stuff? You usually want to screen them for like herpes, want to screen them for like CMV, want to screen them for mono, want to screen them for HIV, right? Want to screen them for HB, want to screen them for HB, want to screen them for CIFILIS, right? Want to screen them for TB? Many times people that get transplants, they get screened pretty extensively for infectious diseases. You want to screen them for other emergency infections like toxoplasmosis, right? There are some times before people get certain transplants, they get certain vaccines, right? They get certain vaccines.

They make sure that their vaccines are up to date so that again, they develop some kind of immunity against these infections in the first place. In fact, many times people that are getting transplants, they are placed on just prophylactic antibiotic therapy so that they don't get into trouble, right? In fact, many of these screenings for infections don't just happen right before you get the transplant. They also happen after you get the transplant. After you get the transplant, many times you're going to still like screened for like CMV or for mono, right? Many people tend to get those those screens. So again, it's just very important to give these things a mind for exams. And one thing I will say is if a person gets a transplant and they're asking you, or which of the following interventions can be implemented to reduce the risk of opportunistic infection? I want you to think of picking an answer that says to get back trip, right? So that's TMPSMX or pick the answer that says to get gun-cycle over. It's very important to know this. The thing is CMV and the Mosisis Jervetsi, they love to cause infections, right? Obviously Mosisis Jervetsi is going to cause a pulmonary infection. CMV usually tends to cause a GI infection, so if you want to profile out against these things, you want to put people on a appropriate therapy.

So many times people that get transplants for usually about like at least three months up to a year, they are placed on like trimethybrimsofomethoxesol, they are placed on a gun-cycle over there for CMV prophylaxis. The TMPSMX obviously is going to be for, it's going to be against the Mosisis Jervetsi. In fact, sometimes people that have, people that are getting surgeon transplants, visually like heart transplants, they tend to go on like toxoplasmosis prophylaxis. They tend to go on toxoplasmosis prophylaxis, but again, remember people that are getting these prophylaxis that involve sulfonomytherope, usually want to put those people on folenic acid at the same time, so that they don't get profound bone marrow suppression. Again, you don't want these people getting profound bone marrow suppression. Again, it's very high yield to know these things, again, some of these things may look like just weird stuff, but they are very important to know. And many times when people get infections after getting a transplant, or naming exams, is usually going to be within the first year after the transplant. Many times to be honest, it's going to be within the first month after the transplant. So most times, if you see people get these region infections, it's going to be within the first month. Many times, if people make it past a year, two years after they've gotten a transplant, they tend to do pretty well for the most part, tend to do pretty well for the most part.

But usually within that first one year period, that's like the major zone, especially one first month. But like after that first, like the biggest major zone is the first four weeks after transplant. But really, if you go beyond that one month, right, all these again, CMV infections as pergillus infections, you know, CCS, your VETC, EBV, BAT, CMV, BAT-TB. And again, you usually give you hints in the question, now we're guiding in one direction versus the other. These are things that again can happen after a transplant, right? These are things that can happen after a transplant. Again, very important to give these things in mind, for example. And then another thing I want to talk about, like, maybe this will be the last thing I'll talk about, because this podcast is kind of getting a little long, is it can give you questions on people that have like HIV, right? And their starting CD4 count is very, very low. And then you start treating them for, you start treating them like anti-reduviral therapy, or you start treating them for some opportunistic infection. And then you notice that they have like almost like this paradoxical worsening of that infection. If you see something like that, I really want you to think about immunoconstitution syndrome. Immunoconstitution syndrome is something that they love to test on USML exams. It's somebody love to test on USML exams.

So if you see a person that was immunocompromised before, and then now they're becoming immunocompetent, and then you notice that they have like a paradoxical worsening of like an opportunistic infection or something like that, or some kind of successfully treated infection, I really want you to think about immunoconstitution syndrome. I really want you to think about immunoconstitution syndrome. So again, the thing is, that's why it's important to not just memorize associations, but understand the construct. This is the construct. Previously immunocompromised, now becoming immunocompetent. Because again, the NBM is they know that most people have memorized the HIV association with immunoconstitution syndrome. So the thing is you can get all the kinds of people that can get immunoconstitution syndrome. So if for example a person has, is an organ transplant patient, and they've been on immunosuppressive therapy for a long time. And then let's see, for some reason, you are beginning to decrease the immunosuppression. That can cause immunoconstitution syndrome because the immune system is coming back online. Or you see a woman that is postpartum. Again, remember I just explained at the beginning about how pregnancy is an immunocompromised state, and then the woman becomes postpartum, and then the immune system comes back with a bang that can cause a immunoconstitution syndrome.

Or a person again that has been on prolonged clinical sterotherapy, or on prolonged ten-f and inhibitor therapy. Again, if those therapies are tapered or stopped, those people can get immunoconstitution syndrome on NBM exams. So again, very, very, very important to keep these things in mind for tests. Again, they can give you a person again that was just studied on anti-race reviral therapy. So typically, how do we treat immunoconstitution syndrome? For the most part, we're pressing as HIV, and they have immunoconstitution syndrome. And you know, their symptoms are not severe. Again, many times on USML exams, big pictures, the thing that ultimately matters. If you notice that this will do not have severe symptoms, you just have like a mouth fever, just mouth systemic symptoms. In general, for those people, just go ahead and continue the anti-race reviral therapy. It's not going to be a big problem. But if you notice that their symptoms are very severe, right? You see a person who are like, wow, this person is circling the drain about to die kind of deal. You may need to go ahead and stop that anti-race reviral therapy in those people, right? And many times, if you see evidence of an infection, treat that on the line infection, right? Treat that on the line infection. In some cases, if their symptoms are really severe, you can actually put these people on steroids. So again, kind of like calm down that immunocsystem. You can put them on steroids. You can give them NSAI Ds.

Remember, NSAI Ds, many people think of NSAI Ds as just being relievers. But NSAI Ds are also anti-inflammatory medications, right? So those can help in those circumstances. And then one thing that came to mind that I want to just go ahead and share, if I wrap up the spot castes, if a person is getting a transplant, you need to make sure, like before they get a transplant, on in-beaming exams, there are certain vaccines you're supposed to get before you get a transplant. So what are those vaccines? You want to think of the D-TAP vaccine? The D-TAP vaccine should be given to everybody before they get a transplant, right? The pneumococcal vaccine, you should get it before you get a transplant. The influenza vaccine, you should get it before you get a transplant. And then vaccination against HEPA and HEPB, you should get it before a transplant. Again, this is very, very, very, this is very, very important to know for exams, right? So the way I remember this is I remember this as your A, your B, your D, right? And then intellectual property, IP, does remember that. So your A is HEPA, you get the HEPA vaccine, your B is HEPB, you get the HEPB vaccine, your D is the D-TAP vaccine. And then IP, intellectual property, the I is the influenza vaccine, and then the P is the pneumococcal vaccine. In general, before you get a transplant, you need to get these prophylactic vaccines so that you don't get in trouble with the transplant. So thank you for listening to this podcast.

As I do at the end of every podcast, I can offer review courses for the USML exams, especially step 2, see key step 3. I offer an MME in e-testic and strategy scores. And I have my videos on my You Tube channel. It's called the Divine Intervention USML podcast and videos. So if you sign up for that, that's where you see all my videos, all my shelf review videos and stuff. But if you want the slides that go along with these videos, then go to the website divineinterventionpodcasts.com under the specific episodes. And then also have these podcasts on Apple podcasts, on Google podcasts, and on Spotify. So if you want the most recent 150 podcasts, go to those podcast apps and just subscribe to the podcast and you'll get them. The thing is, you may wonder, okay, divine, how about the podcasts that are older than the most recent 150? Well, those older podcasts on the website, divineinterventionpodcast.com. I have just really, it's either I'm pretty sure it's a Word Press rule, but I'm not able to put more than the most recent 150 podcasts on any of these podcasts apps. So if you want everything from episode one, all the way to episode 323, which is this episode. Go ahead and go to the website and you'll see those podcasts. You can listen to them from the website. You can literally download them from the website. And again, if you subscribe to my website, divineinterventionpodcasts, with an S at the end.com, then you'll usually get an email notification whenever I make a new podcast.

So thank you for listening to this podcast. Again, the quick life lesson I want to share which is something I kind of shared already in the life lessons podcast that I made on my divine intervention life lessons podcast. You can remember if you go to divineinterventionlifelessens.com, you'll see those. But the quick thing I want to just say is make sure whenever you're doing something in life, make sure you're doing it with the right motivation, right? Ask yourself, where is my motivation coming from? This is particularly important in many of us that I medicine, right? Because the thing is, if you have the right motivation, then you'll be able to stand the test of time when adversity comes. Because the thing is whether you like it or not, you will face adversity. If you have, if you make any kind of decent commitment in life, adversity will come. So make sure you have the right kind of motivation. Because again, if you have the wrong motivation things, when adversity comes, you will completely fall away. But if you have the right kind of motivation, when adversity comes, you'll be able to stand the test of time. So don't draw your motivation from human beings. Don't draw your motivation from the congratulations of men. Because again, just as quickly as men can congratulate you and give you all this praise, it is the same men that can crucify you and assassinate your character. So draw your purpose from things that are not ephemeral.

Draw your motivation from things that are permanent. Draw your motivation from God, from your calling, from your purpose. Like ask yourself, what am I doing on this earth? Let that be the thing that is driving what you're doing. Because if the thing driving your what you're doing is, oh, I want to be praised by men. I want to be rewarded by men. I want people to like my posts on Facebook. I want people to see good things about me. If that's where your motivation is from, I have bad news for you. You are liable to get completely just sidelined by adversity, right? Because adversity will come in different ways. Adversity can come just from just straight up adversity. It can come from intense opposition, right? The thing is whenever something good is being done, whenever a commitment has been made, opposition will come, right? But again, the thing that will keep you going through that opposition, will keep you going through that problem is if you have the right motivation, right? So again, one of one example I like giving is again, you see people they're like, oh, I want to get a two seven-year-on-step one, on step two, see, kill, step three. So that I can show off, I can put it on Facebook, I can put it in my CV, I can brandy shape before program directors and stuff. Don't get me wrong. Is there anything wrong with that? Maybe not, although I have my own thoughts on that, but I'm not going to bring that here. Those are my private personal thoughts.

But the thing is, after the CV study really hard, that strong score comes, right? And then there, you know, people say the break them and give them that wonderful part on the back. After all those things are gone, then what next? You see, those people sometimes, these almost slide into depression, you see? Because have you ever wondered, they're some people that are really successful, but then they are really depressed. Again, there are many things that cause depression. This is just one cause, right? But again, some people have these on met or on fulfilled expectations, right? So again, those should not be your motivations for studying hard to do it on USMEL exams. Your motivations should be that, oh, I'm learning this material so that I can help people. I'm learning this material so that I can turn people's lives around. I'm learning this material so that I can do right by my patients. I'm learning this material. So when a patient presents, I will understand exactly what you're presenting and I'll be able to do the very best for them. If you have the right motivation, then it doesn't matter what happens and attending passes you off or resident yells at you or someone says the wrong things about you, right? At the end of the day, you know why you're going into medicine. You have those motivations. You know why you're studying, right? So when you're studying like it motivates you, right?

Because when you have the right kind of motivation, then it's almost like you're standing on a show foundation, you're standing on the right foot. So it's very, very important. It's very, very important. It's very, very important. Half the right motivation, right? Half the right motivation. Don't draw your motivation from people. Don't draw your happiness from the good things that people say about you. Because again, just as quickly as people can see, good, good things about you, the same people can see bad, bad, bad things about you, right? Bipolarity is not just a psychiatric disorder. It's just something that we find in mankind, right? People today, they can be praising you and then tomorrow they can be tearing you down, right? So it's just very, very important. Half the right kind of motivation. If you're doing something, ask yourself, what is the purpose behind this thing? What is my calling behind this step, right? Like for example, this podcast, I love making this podcast because I want people to learn. I want people to understand. I want people to do well on exams. I want people to use this information to succeed. That is my motivation, right? That is my motivation. So the thing is if you have that kind of motivation because for me, I know that teaching for me is not just something I do or something that I'm good at. Thankfully, I'm really good at teaching, right? But teaching for me is a calling.

Like I feel like that's one of the primary reasons why I'm on this earth. I'm not on this earth because oh, I'm just here to pass the time, hit a certain age, go to some place. No, no, no, no, no, no, no, no, no, no, no, that is nowhere on this earth. That is literally not why I'm on this earth. And I will challenge you people that are listening to this podcast. Ask yourself, why am I here? Everyone on this earth has a purpose on this earth. You have a calling on this earth. You have certain people's lives you're supposed to touch on this earth, right? Ask yourself, what is that motivation? The thing is you begin to live a full life when you know what your motivations are and when you have those right motivations. So, you know, strongly encourage you have that motivation. Don't let your motivation be a mini like something you get on Facebook or how many positive comments you get on on Twitter or whatever or the praises of men. No, no, I'm telling you, just as quickly as men can praise you, men can also quickly destroy you, right? And even there's a part of the Bible that talks about how you see some people, they bring the streets and stuff so that men can congratulate them. So, men can see how piles they are and how, oh, wow, they're they're so in touch, you know, they're prayer warriors and stuff. No, no, no, no, no, right? The Bible says that your heavenly father that sees what you're doing secret will reward you openly.

The thing is if you have the right motivation and you're doing the right thing, even if you may feel some temporary adversity. In the long run, you'll succeed. In the long run, you'll be rewarded. In the long run, you'll prosper, right? Again, the thing is you cannot tell the results of a game by looking at the scores at halftime. I mean, for those of you that watched the NBA, I'm sure you've watched games where it was like, wow, 70 to 46, right? You're like, oh, gee, man, this team is completely gone. But then you notice that by the end of the game, wow, the people, you see these people, they just mount this great mighty comeback, right? And then they win, right? So again, you should never judge anything until the very end. It's the very end that determines who is the winner, who is the true winner and who is the true loser, right? So again, have the right motivations. So thank you for listening to this podcast. I hope you're blessed by it. I'll see you next time. God bless you. Thank you.

Infections involving viruses, fungi, parasites, and Tuberculosis (TB).

George Syndrome.

Streptococcus pneumoniae (encapsulated organisms).

Neutrophil function defect, such as Chronic Granulomatous Disease (CGD) or complement deficiency.

D TaP, Pneumococcal, Influenza, Hep A, and Hep B vaccines (mnemonic: A, B, D, IP).

Immune reconstitution inflammatory syndrome (IRIS) or Immunoconstitution Syndrome.

Encapsulated bacteria (e.g., S. pneumoniae, H. influenzae).

Recurrent abscesses, catalase-positive organisms, and infections with unusual pathogens like Aspergillus.

Fibrointropenia (or neutropenic sepsis).

D TaP, Pneumococcal, Influenza, Hep A, and Hep B.

Immune tolerance develops toward the fetus (e.g., reduced RA flares).

Catalase-positive organisms.

Encapsulated bacteria (e.g., S. pneumoniae, H. influenzae).

Recurrent abscesses, catalase-positive organisms, and infections with unusual pathogens like Aspergillus.

Fibrointropenia (or neutropenic sepsis).

D TaP, Pneumococcal, Influenza, Hep A, and Hep B.

Immune tolerance develops toward the fetus (e.g., reduced RA flares).

Catalase-positive organisms.