DIP Episode 74 - USMLE Step 3/Medicine ITE/ABIM Board Review Series 1

Okay, welcome. My name is Divine. I am a PGI-1, a transitional year resident. That's ultimately going into radiology. And this will be episode 74 of the Divine Intervention Podcast. This is a new podcast series I'm starting today. And this is a review. It will be a series like many, many podcasts for this. But it will be a series that is targeted primarily towards residents. Okay, this will be a review primarily for the USM list of three exam and the medicine in training exam. Okay, this will very likely also help with the ABIM like medicine board exams. But my primary target with this, these series of reviews I'm starting today are medicine residents that are preparing for the entry in exams and people that are taking the USM list step three. So because this is a relatively new podcast, I will describe my proposed mechanism for going about this material. So basically what I'm going to try to do is for step three, right? You know that there is there's the multiple choice path and there's the CCS part. I'm actually designing these podcasts to help with both. So you'll see what I mean as I go along. But I'm actually trying to attack both things and also again the medicine in training, which is something you'll take every year as a medicine resident. I mean I did a lot of like thinking, a lot of planning, a lot of reflecting actually before sort of coming up with this format. So I sort of mix a lot of sense to me, but I hope it actually works in the end.

But basically the way I'm going to divv this up is I'll give a vignette. This will almost be like a, it will be like a classic presentation of some problem, okay? Where I essentially ask for a diagnosis, right? And then the thing is after I give you the vignettes, the next thing I'll do is I'll give you the diagnosis. And then when I talk about the diagnosis, I'll basically describe everything you pretty much need to know for like your medicine in training exam or your USM list step three. With regards to that diagnosis, I'll talk about like how it's worked up and all that stuff. And I'll also talk about like some of the basic science detail. Again, I'm not going to go into like super super detailed, but believe it or not, there's some basic science on step three. So I'll try to hit those high-yield high points, especially from a college that is classically tested on step three. So I'll talk about those things. And then the next thing I will do is I'll have a section where I talk about like related diseases. So basically I'll essentially describe a few diseases that sort of relate to that primary shift diagnosis that I just gave. Just things where like, oh, maybe you need to know like three or four things about that disease. So that's actually will probably be relatively large. Well, just talk about multiple related diseases. And then as we go along, I'll sort of round up, we're just like talking about like diagnostic tests. You would want to order and why? Okay.

So this is where sort of like the CCS bent comes in. I mean, there will be some cases like some surgery cases where the workup is like call surgery or something like consult surgery. And I will make those no-no when I get to that. So let's try this and please give me some feedback. You can always reach out to me through the email or make a comment. And if there are any changes you want me to make, just let me know. And I'll be more than happy to make them. Some people have suggested putting these podcasts on a podcast app. I have tried Apple podcasts like iTunes like many, many times. And I keep getting error messages. I'll keep trying as much as I can and hopefully we'll go from there. So let's jump right into it. So this is the first series in this USML is the three slasher medicine training exam review. So the first question, right? So let's assume you get a question about a 23 year old male that presents with like a two day history of like fatigue and dyspnea. And then they tell you that physical exam is notable for like congenital pala and tacky cardia. And then I'm telling you that the patient is asking if you think it is safe for him to travel for a missionary trip to an African country giving his symptoms. And then I also tell you that let's say he recently took like a malereo drug cocktail that includes like sulfur, diazinus, prophylaxis ahead of his missionary trip. Right?

So this is a question about a person that young going to an African country took a sulfur drug has like science consistent with anemia, right? Like the congenital pala. So hopefully you're thinking of the oxidizing stress of sulfur, diazin and you're thinking of g6 pd deficiency, right? So again, remember that so this one going into the diagnosis part. So it is a g6 pd deficiency. And classically, right, if a person takes like a sulfur drug or a down time alerials like primacoin, those can induce oxidative stress and that can sort of tip patients over the edge, right? Because remember, if you have a g6 pd deficiency, you cannot regenerate, reduce growth of thion, okay? Also don't forget the association of g6 pd deficiency would like father beings or like a serious infection. These are two scenarios that associated with increased oxidative stress. And the thing is g6 pd deficiency causes more of like an intravascular hemolysis. So it causes like a hemolytic anemia, but your so your haptoglobin levels will actually be low, right? Because remember haptoglobin binds up a free hemoglobin. These people because they also have like an hemolytic anemia, right? They will have like an indirect hyperbiliurabinemia, right? Because the hemolysis will sort of overwhelm your UDP glucoronacyl transferase enzyme, right? So obviously on CBC, these patients will have like a low hemoglobin, they will have like an anemia and then on a peripheral smear, right?

You should see like the classic Heinz bodies. Those are basically red cells that contain an oxidized hemoglobin. And then you will also see like the bite cells, right? The bite cells are raised because you're like reticulated into phyliocystem macrophages, like usually in the spleen literally take a bite out of the red blood cells to remove the Heinz bodies. And please don't forget your classic demographic. If they are telling you an African, one Italian on an exam, they are trying to give you some clues, right? So don't forget the demographic for g6 pd deficiency, right? So like Greeks, Italians, people of Mediterranean descent and like Africans, right? And the thing is if you want to test what g6 pd deficiency, you actually check a g6 pd level, will you do it weeks after the inciting event, right? Because the thing is g6 pd levels may actually be normal under acute circumstances. So again, kind of like if you're thinking of the pathophysiology of the disorder, right? So g6 pd, you need to make any DPH, right? From like that fancy HMP shunt you learn about in Med School. I think that's also known as the pentose phosphate pathway, right? So that basically provides reducing power in the form of like regenerating blue thion that helps you deal with oxidative stress, right? So if we have like more than normal oxidative stress and we have a reduced ability to meet that stress in the setting of like a g6 pd deficiency, right?

You may run into a hemolytic anemia sort of deal, okay? And remember that g6 pd deficiency like many enzyme deficiencies has an autosomal recessive inheritance pattern, okay? And yeah, just one of those big things you want to keep at the back of your mind. So I guess if you want to talk about some related diseases here, don't forget another cause of hemolytic anemia will be a hairiditrius fyrusitis, right? Remember those are classical in people from northern European descent and that's actually a rosomodominant inheritance and it arises from like defects in like spectrum or anchoring, right? So it's like a red blood cell membrane defect. So again, usually they'll give some kind of family history or they may show you like a smear that shows red blood cells with no central power, right? Remember that the MCHCO will actually be high under those circumstances and you can actually make the diagnosis with something called acidified glycerol lysis test. That's actually very high yield to know. Back in the days to do something I believe known as the, um, uh, what was it called? I think it was called like the ham's test but I don't think anyone knows that anymore. I think the thing you want to think about these days is the acidified glycerol lysis test. Okay and, um, in general for hairidigis fyrusitis, right? I want to consider spinectomy as treatment, right?

And again, because this is not an immune mediated hemolytic anemia, just like G6 pd deficiency, your cum test will actually be negative, right? And then don't forget like autoimmune hemolytic anemia, that's like a kind of, if you're going to the immunology route, that's a kind of a type two hypersensitivity reaction, right? Um, this can be like another, again, prominent exam cause of um, a hemolytic anemia with an indirect hyperbular bini. Right? So, classically, what are the rights in a patient that has like a history of like lupus or like a recent like microplasma infection? Remember that one is a sort of like co-daglutinins, right? So like IgM, uh, you can also see then an obese in it like an obi-guy in question where a patient is like taking an alpha methyl dopathol hypertension. Remember alpha methyl dopath just like hydrolyzing an um, myfidepine is one of the safe anti-hypertensives in pregnancy. Uh, for these cases, a direct cum test will be positive, right? And then also don't forget like PNH, so that's a paroxysmone, uh, nocturnal hemoglubinuria, right? So, classically, we'll shop like in a young guy on exams that has like chronic hemolytic anemia and like we're thrombotic phenomena, right? They tell you that he wakes up in the morning and he has like red here, red urine, right? That's why it's called paroxysmone, nocturnal hemoglubinuria. Um, you know, largely arises from like a pig amutation, right?

So you basically have issues with uh, GPI anchors on the surface of your red blood cells, right? So that renders your red blood cells susceptible to complement and medial damage. Um, in general, you want to treat with aculesumab, aculesumab is a super expensive drug, is more, what, it costs more than 400 grand a year and it's basically a monoclonal antibody against C5, okay? So that basically disrupts the formation of the membrane attack complex. And then some tests to think about for this case, I guess, is to, uh, I mean, other CBC obviously because you want to detect the anemia, right? And usually in hemolysis, there'll be a normal siliconemia, right? You want to check a blood smear, right? That can show you like the Heinsbodies, it can show you the bite cells, it can show your spherocyte, if you're dealing with a hereditary spherocyteosis, and clearly you want to get LF Ts, right? You want to detect like any kind of hyperbular minimia, any like AST, ALT changes because I mean, uh, viral hepatitis may also present in a slightly similar fashion. And I mean, you want to like measure Haptoglobin levels, right? Um, to sort of further support your intravascular hemolysis diagnosis and your Haptoglobin will be low in G6 pd deficiency, or any cause of an intravascular hemolysis. And then you may want to also get like viral serologies, again, to sort of check for the hepatitis viruses. And if the patients say, for example, had abdominal pain, right?

You want to get like a red-up or quadrant ultrasound, because actually these many of these simolytic anemias are associated with recurrent ghost stones. So that would be the end of our first case, and I guess I can jump to the second one. So let's assume you're getting signed out from overnight nursing, right? And you tell you about a 35-year-old, uh, Uber driver in the MQ, that has essentially had a urine output of zero over the past like 24 hours, right? And then you tell you that he's creatinine, this morning is like 2.25, but when it was admitted, he's creatinine was like 0.98. And the rest of the question, I guess, I'll let me say that, um, when it was admitted like, let's see like three days ago, he came in with a shortness of breath, and he was confirmed to have like a submassive PE by a CTA, right? So hopefully you already know that this is some kind of AKI, right? So I guess I could re-enough failure. I think I could re-enough failure is the more recent term. I think they've stopped using EKI, but anyway, um, and basically, this arose from contrast nephropathy, right? You got a CTA, right? So contrast nephropathy, right? Very likely will be the intra-inal kind of AKI, right? So essentially like 80 and a cutibular necrosis, right? And really you could have prevented this by just giving a crap ton of fluid, right? So like vigorous fluid replenishment with dioresis, and also like some weird questions, these will probably be more step three than the medicine-intraining.

We could talk about an acetyl-system. No one really uses an acetyl-system in the real world to prevent a contrast nephropathy, but it's a classic thing that's tested on the USML Es. And because this person has an intra-inal kind of AKI, right? If you do like urine studies, you will see like an increased urine sodium, right? So it will be like greater than 40, and the phenol will be greater than 2%, some source is say 3%, but 2% is also a good number, okay? And classically, right? You may also see like the muddy brown casts on urine microscopy. Now, please do not forget, um, 80 N, right? It can also be caused by drugs like NSAI Ds, or you have amino glycosides, right? So like gentamysin, neo-mysin, amicasein, tubramysin, streptomysin. It can also be caused by like, um, anti-biotics, especially like your sephalosporins, right? And also like some chemotherapy education agents can also cause intra-inal AKI, right? So like the platinum analogues like cisplatin, I remember that's the thing that causes like, it's like the post-recharge of chemotherapy and use the, um, nausea and the MSS, right? Then comysin, right? That's used to treat a MRSA infections, and is also now first line for C-DIF. Um, can also cause ATI, right? If the cranic acid remember, if the cranic acid is the only loop diuretic that has no software energy, can also cause ATI, right? And in general, right? If a person has an intra-inal AKI, via B-A-B-N to creatinine ratio will be less than 20.

Now, if you're thinking about related diseases on your exam, right? So like, obviously you want to think about periodal AKI as well, um, that arises more in the setting of like hypovolemia, okay? Although it can actually be caused by NSAI Ds, right? Because remember, NSAI Ds, the inhibit cycloxygeny, so that decreases the synthesis of first-agglandins. If you make less in the way of first-agglandins, you have no dilation of the afrin material, okay? So you will hypo-perfuse the kidneys, okay? So you can get into trouble there. And because these people are basically not profusing the afrin materials in the setting of periodal AKI, the Iranian angiotensin and our dosteroan systems will be revved up, right? So they will try to retain like sodium in the ayurina, right? So the ayurina sodium will be low, it'll be like less than 20. Um, the afina usually will be low as well, already will be like less than 1%, and the ayurina spolarity will be high because again, they are trying to retain volume. Um, generally you will not find any cuss in the Iranian really. The treatment you just give them back, uh, fluids, right? And obviously the BIO and Tukrechanin ratio here will be greater than 20. Now, if you're then talking about like post-trainal AKI on your exam, you'll likely be like in the setting of like nephrolithiasis, um, so like a kidney stone or in the setting of like BPH, right? With like acuda urinary tension.

Uh, basically the values, they don't usually test it for post-trainal AKI because they vary, but the general guideline I'll give you is that early in the disease course for like post-trainal AKI, your urine labs will look very pre-renum, okay? But the thing is as time goes on, your urine lab values will look very intra-renum, okay? Uh, basically you want to do some kind of intervention to relieve the obstruction like placing a fully catheter or breaking up a stone or whatever, okay? And then other related diseases to think about here like a AIN, right? So acuda in the testician of ritis, remember it's a type of like intra-renum AKI and the key finding here is like eosynophilia, so like a ton of eosynophiles in the blood or I guess uh, eosynophiluria, right? So classically it's caused by like your anti-staff lococo penicillins like dicloxacillin, right? So they may easily make this like a mastitis question because these uh, like dicloxacillin is, I'll say like the MBMD drug of choice for the treatment of a mastitis. Um, and the classic presentation triad, right? For AIN is like a person having like fever and having like a rash and having like the eosynophilus business that I've uh talked about already, right? And basically the treatment is you know, stop the offending agent and usually the symptoms will resolve. It doesn't resolve, you can give steroids. Now don't also forget that uh, some crystals may actually cause a renal failure, right?

So if they give you a question about a person that's like thinking of committing suicide or an alcoholic who maybe like drunk antifers because they didn't get access to alcohol, right? Think about um oxalate issues, right? So you can try for mepizok, for mepizok and inhibit alcohol dehydrogenies and help with that. Um, the thing is usually these people already have like a very nice prominent like metabolic acidosis. Um, also don't forget some other high u things associated with hyperoxyluriate, right? So like uh, cruise disease, right? So uh, if a person has cruise disease, they'll actually have increased the absorption of oxalate across that I guess the new terminal helium if you may. And also if you take a crop ton of vitamin C like like call it like hyper vitamin C if you may, uh, that can also cause a hyperoxyluria, right? And then if they give you a question about a person that's like getting chemo for like a lymphoma that develops renal failure, right? I really hope you're thinking about a uric nephropathy from like tumor lysis syndrome on that those are circumstances. And really you could have prevented that by just like vigorous diuresis, uh, you could have administered like a xanthenoxidase inhibitor, right? Like alopeurinolode for buxustat. Remember for pizion is on isothioprinin and xanthenoxidase inhibitor that can get into trouble. And um, also like uric nephropathy you could also maybe have prevented it actually treat it if with like a uricase analogue, right?

So uricase is like an enzyme that converts uric acid to something that's a little more soluble. It's known as alantoine. uricase was originally found in birds but they've made recombinant forms, right? So you see drugs like a raspberry case or piglotticase. Those are uricase analogue that I used to prevent or treat a tumor lysis syndrome, especially a uric nephropathy. Now, um, and remember if a person has tumor lysis syndrome, right? As all those cells are breaking apart, um, the intracellular substance can spill into the circulation like potassium. So these people can get hypercalemia and get arrhythmias, right? So that's a very nice way to get they can link those concepts together on your exam. And then if for example you get a question about like an alcoholic that was like found down and he has renonfili and radiorin or let's assume it's a patient that had like recent seizures or let's assume a patient that recently ran a marathon and they have like radiorin and rising creatine. You really want to think about like ruptomyolisis, um, under those are circumstances, right? So that ruptomyolisis can cause like a like a myoglobin induced anapropathy. Basically for those people your treatment is like very stronger diuresis. Uh, so give them a crap ton of fluid and diuresis them out of the wazoo. And I mean you want to probably, you know, hook up these people to like a monitor, right?

Because again, the hypercalemia that they can get from the myocyte necrosis can get them into arrhythmiaterritory very quickly. Now, for this case, the test you kind of want to think about, right? It's like getting your analysis with like your electrolytes. Um, you want to get a BMP, right? It will help you measure like the BN2 creatine ratio. You want to check for lab anomalies, right? That may sort of indicate the severity of urinofilia, right? And then maybe potentially make you consider that analysis, right? So let's say they have like a severe uremia or metabolic acidosis or hypercalemia, right? And um, I remember, right? If a patient had hypercalemia just to again, sort of integrate concepts here. Remember they will have like a white T-rays on EKG, right? And they will have like picked T-waves, they will have like a sinusoidal waveform. Basically, that's kind of like the progression is like, they have like the picked T-waves, you have like the white QRS, you then begin to have like the sinusoidal waveform on EKG, and then you go to acesteli, right? There is a flat line, which is obviously not a not a great outcome, right? And in general, right, for those people you want to give like calcium gluconeat first to sort of stabilize the myocardium. And then you may want to give like stuff like insulin with D5. Remember insulin with D5 increases the activity of the sodium potassium ATP is pump, so that gets potassium in two cells and relieves the hypercalemia.

You can also give Kx-late, although that's not commonly used much anymore because it can cause a bounding process. That'll be a very nice a step three question. Also, ferozomide, right? Remember, luped diuretics, lupes, lupes, lupes, they lose calcium and potassium in the urine, right? So you can basically use the hypochylemia that arises in the setting of a taking a luped diuretic to also again get rid of some potassium. You can also give the beta, beta 2 agonistabularone that can help and also sodium bicarb as well, because that sodium bicarb will create an alkalosis in the serum that will draw hydrogen ions out of cells and potassium will go in reverse. Okay? And again, you want to maybe also get a CBC to detect like your synofilia if you're thinking about AIN. And then again, you will also want to do like urine studies to again evaluate the kind of ACHI you're dealing with or to look for casts and stuff like that. So I guess you have probably said too much about that key. So let's go on to the next case. It's probably a shorter one, right? So let's assume you have a 23-year-old female. She has a pacifier of like type 1 diabetes and her neighbor finds her down in her apartment, right? And like scoops her up, drives her to the ED, right? And then basically when she gets to the ED, she's like minimally responsive and you start IV fluids on this patient, right? And then they tell you that they draw basic laps and you check some laps, you see like the pH of 6.9.

That's not good if you're pH is 6.9, you're not long for this world. If you don't get treated quickly and then let's say a bicarb is two, remember a normal bicarb is like in the 20s, if your bicarb is two, you're also not long for this world. And you probably want to start that patient on like a bicarb bulls and give them like place them on a bicarb drip, right? And then let's assume the potassium is 6.1 and then their blood glucose is like 1200, right? And then, so obviously this patient is in decay, right? And then you're about to start like therapy for this patient and then the patient begins to like thrash all over the place and tells the nurse, don't stick that needle into me, I don't want you to stick that needle into me, don't give me any bad drugs. And then this will be a classic step three ethics question and they ask like, what's your next best step in management, right? So this is a clear court case of a patient that just lacks capacity to make decisions, right? So notice I did not say competent, right? So competent is a legal term. Capacity is something you can determine as a physician, right? So this patient likes to lack capacity. So basically the right answer here will be to just still treat the patient, okay? The assertion answers you should try to avoid though, right?

So don't pick the answer that says, oh, don't treat the patient or the answer that says go to the court to get an injunction, the patient will be dead by the time you don't get in the court injunction. So you don't want to do that. And obviously, right, don't consult the ethics committee. Consulting the ethics committee is just never a good idea on any MBM exam, it is always the wrong answer. Although in the real world, we consult ethics committees a lot, but on MBM is consulting ethics committees is never the right answer. And basically the key principle we want to remember here is that if there's an emergency and you have a patient that lacks capacity, so like a patient that is like, uptoned or whatever, then go ahead and do what is medically indicated for those patients. In fact, I'll tell you that a common step three scenario is like, they give you a person that lacks capacity, that's what you want to do. Again, always do what is medically indicated. But if a situation is an emergency and the patient has capacity and they tell you like they demonstrate understanding of what you say and everything, then do what's the patient wants. Okay. Now, I guess thinking of this as not necessarily related diseases, but more like related concepts, right? So classic step through situation again is they'll give you a question about a child that's like in an emergency situation. And then they'll tell you that, oh, the parents don't want the indicated treatment.

Basically, you want to override the parents' problems and just do what is medically indicated. Okay. And I guess to sort of tie all this together, I don't forget like the key principles behind in front consent, right? So you want to tell the patient basically what like the intervention or the treatment to administer it entails. You want to, you know, tell them about the benefits, tell them about the risks. And then you also want to tell them if there are any alternatives available. Okay. And again, if it's an emergency situation, you cannot obtain informed consent, just go ahead and do what is medically indicated and you will not go wrong. So that's what I'm going to say about that key is that is more, I guess, of like an ethics scenario that you may see on your exam. Now, the next case I'll go to is for this next case, this is like a surgical case, so I'll just discuss workup at the same time. But I also see like high ill things, this will just be like one lengthy discussion about this case and some associate that high ill things, right? So this is you may get a question about like an old guy has like severe abdominal pain, he's a smoker, has like a pulsatile abdominal mass on exam. And let's say they tell you, they show you an image of like like something sort of like overlying vertebral bodies on imaging, like a lumber vertebral bodies, that's something that maybe you should just look up. It's called like the drip to the other sign.

It's classic for this diagnosis I'm going after. And then they tell you that all this patient is like hemodynamically unstable, has like flank pain or like back pain. I really hope you're thinking about a ruptured or tripooling. Okay. A ruptured tripooling. And I mean, what's the underlying path of physiology for a tripooling, right? Basically, the thing that happens here is that you've essentially like degraded like the last ten and collagen in the media of the abdominal order from like increased like matrix metalloprotonies activity. You see divine? Matrix metalloprotonies, that's super loyal. I promise you it's not loyal, that's all I'm going to say. So basically if you smoke your matrix metalloprotonies activity, so MMP, that's what I was calling from now. Your MMP activity goes up. Okay. So that can degrade the collagen and elastin in the media of persons like abdominal order. And that can cause a tripooling. Okay. Actually, statins actually decrease the activity of MM Ps. So that's potentially why statins may ultimately help a person that has like a family history of tripooling or whatever, but that's something that you probably never see on an exam. But knowing that increased MMP activities observed as the path of physiology of a tripooling is very high, you know, for exams, right? And you may ask yourself like, oh, why would you have back pain? Right? Remember, usually a tripooling like ruptures into like the left-to-retroperitoneum, right?

So sort of remember like your retroperitoneal organs, if you have like retroperitoneal bleed, you have like back pain, right? So like pancreatitis. A lot of your pancreatitis is retroperitoneal. That's why pancreatitis usually presents with like a big gastric pain that reads to the back. And really for tripooling, right? So what are the high your things, the quotation and exam, right? I mean, the most common location usually is like below the renal arteries, right? So you may see the buzzword in for a renaly order on your exam. And it's usually just above the eorticulture bifurcation, right? And before we go into the more acute treatment, I guess I can say that if for example a patient, right, has smoked in the past, right? Has like a pasties show smoking, right? You want to do like a one-time abdominal ultrasound to screen them for tripooling, right? If you check the diameter, right? And it's more than like five and a half centimeters in men, you go ahead and fix. If it's more than five centimeters in women, you also go ahead and fix, right? If it grows by more than half a centimeter in six months or like one centimeter in a year, you also go ahead and fix. If it doesn't mean any of those size cutoffs, but it's symptomatic for any reason, you also go ahead and fix. And in general, right, if you want to do the fix, you can do like open surgery, you can do like an open triply repair, or you can also do like like an endovascular repair, right?

Basically an endovascular repair tends to have like less morbidity, but the outcomes between endovascular repair and open repair of triple laces, basically the the survival outcomes are pretty much the same, okay? And one classic example question you may see is a patient that has like a triple A and the gets fixed and then they die immediately like after surgery or something. Really the most common cause of death in the period period around like a triple A repair is a is a myocardial infarction, okay? I mean, I've seen many patients as an intern that had like some kind of vascular surgery and they like had like from my complications after that vascular surgery. There's one of those weird things you want to keep at the back of your mind. Now, what if you get a question and they say, oh, this person got a triple A repair recently, and then they got like a CTA after surgery and you can still see like some fluid extravacity into like the excluded aneurysm. Well, hopefully you're thinking about something called an endolique, okay? An endolique. An endolique is basically like the whatever thing you put to exclude the aneurysm like it's porous or there's like a defect somewhere where blood can still get into the aneurysm. That's clearly not a good outcome. And actually that is more common with like a endovascular repair of aneurysms.

Now, what if you get a question about a person that has had like a triple repair and then they present with like bloody diarrhea and like severe abdominal pain and like leukocyteosis like immediately after the repair. You really want to think about this chemical lightness on that those are circumstances. Usually you try like conservative therapy but if that's not working out so well or you see like signs of necrosis on imaging, you need to go back to the OR and reset. Those people usually have a pretty bad outcomes. Now, let's assume you get a question like, oh, two years after triple repair, you check like the hemocolf and it's positive on a patient that had that triple repair two years ago and the hemoglobin is like eight, right? The one thing you want to think about and this will be classically something for step three is something known as an eroenteric fistula, okay? An eroenteric fistula. Basically, you formed fistula between the eroenteric and the GI tract and you're basically having like chronic blood loss, right? So they get like an iron deficiency anemia from that. Although remember, right? If you see a guy over 50 or a lady over 50 iron deficiency anemia, you really want to think about a colon cancer, right? Now, how do you work up a triple A in the initial circumstance, right? So let's assume a patient has like a ruptured triple A and they are hemodynamically stable and they ask for the next step in diagnosis or in management, go ahead and do a CTA, okay?

So, actually pay attention here is a very high your diagnostic trick. If a patient has a ruptured triple A, the hemodynamically stable, go ahead and do a CTA. If they are unstable and they have like direct physical exam findings or you examine like the pulsatile mass, just go straight to the or, don't do any other, don't try to get fancy, don't try to do any whatever image, stick them straight straight to the or, okay? Because the mortality is almost like 90% on the other circumstances. Now, if they are unstable, right? Like they are hemodynamically unstable, but you don't have like the direct physical exam findings, like the pulsatile abdominal mass, bloody, bloody, bloody, you can go ahead and do an ultrasound, okay? So, I guess talking about like some relief diseases here, right? So, let's assume you get a question about a patient that has like severe gastric pain and have a history of like strong onset or like chronic steroid use, you hopefully are thinking of like peptic ulcer disease, right? Like a perforated ulcer, it could be like gastric or it could be doodone, remember? If you're gonna be placed on chronic steroids for any reason, right? You need to be also be placed on a PPI, prophylactically, because steroids can cause a peptic ulcer disease and you also need to be placed on a, on a, this was for it, chronicly as well, because steroids in, corticosteroids increase your risk of, of osteoporosis.

Now, what if you get a question about a patient that has like a history of like hypertension and then they have like a tear in chest pain going to the back and like a wide-edmidious thinam or hopefully you're thinking about an aortic dissection, right? Basically, the pathophysis, you have like an intemote here that sort of like dissects through the media. So, you basically create like a trunno false lumen, right? I remember those aortic disactions, there's two types, right? There's like Stanford type A and Stanford type B and the Stanford type, basically if you have any involvement of these any other, that's a type A. For that, you go to surgery, okay? Although usually give a bit of blocker first like perpranolol, right? But if they have just involvement of the dissection, the other only, that's type B, usually try medical management, you don't need to take those people to surgery. Okay. Now, I guess, what if you get a question about an alcoholic, right? Let's make this up. So, alcoholic fat fertile female with like a big gastric thing going to the back, right? Think about acute pancreatitis, right? So, she probably has like gallstone pancreatitis or something. Now, what if you get a question about like a person that has like just severe sodium onset, like left upper quadrant pain, and they tell you that this patient, oh, when you listen to the chest, you hear an irregular irregular, an irregular irregular murmur, right?

Hopefully, you're thinking about those people having a fib and having like acute mesenteric is chemia from that. It's actually very high yield to know for exams that the most common cause again, this is very high yield. The most commonly occluded vessel in the setting of acute mesenteric is chemia is the supermissenteric artery. Now, what if you get a question about like an old patient, has like fever, have like a left lower quadrant pain, like again, old guy, and let's say it has like a history of like pinless bloody bowel movements, hopefully you're thinking about that particularitis, right? For that to me, the diagnosis with a CT with CT of the abdomen with contrast, right? You don't want to do a colonoscopy in the acute setting because you can cause for that trouble, right? And there'll be an attorney that will be very happy to you know decrease your decrease whatever little you're making as a physician. And then don't forget that after the whole episode of the vertebralitis, sort of like killed over, you want to ultimately get some kind of colonoscopy, right? To look for colon cancer. That's classically what you do. That's like a nice clinical pair out there. Now, what if you get a question, I guess that asked for like the biggest risk factor for a triple A? Well, hopefully you know that that is smoking, right? What is the biggest risk factor for eiotic dissection? That's hypertension, right? What's the biggest risk factor for a stroke? That is hypertension as well.

And what is the biggest risk factor for coronary artery disease? Well, I guess the most like the preventive like biggest preventable risk factor for coronary artery disease, that is smoking, okay? That is smoking. So, so again, to sort of summarize here, for step three CCS, you want to, for like the see if you get like a CCS case relating to this, you want to consult surgery as you're putting in your orders. And then don't forget that if a patient has like a triple A, right? Or I mean like the screening guidelines for triple A's, if you have like any smoking history and you're between like 65 and 75, you want to go ahead and get like a one-time screening ultrasound. Again, don't forget your call offs greater than five and a half centimeters if you're a guy greater than five centimeters if you're a lady. And also like I don't see them ever doing this, but if they did this, you'll get it right because you listen to this podcast. If a patient has a first degree relative that has a triple A, you want to go ahead and screen that patient as well. That's just one of those weird things that don't really make his way to like texts, but it's just one of those bizarre things you may want to keep at the back of your mind for exams. So let's, I guess talk about our last case because I don't want this podcast to go for too long. But let's assume you have a 52-year-old male, okay? Presents to the ED, comes in with abdominal pain.

And then your check is temperature and admission is like 95 degrees. So it's kind of hypothermic, right? And then let's say the patient is acting kind of confused and then you do a physical exam and you look like a fluid wave on abdominal exam, you say like spider and geometry, you say like testicular atrophy. I really hope that you're thinking of SBP, right? So like spontaneous bacteria peritonitis for this patient, right? So that's your diagnosis here. Remember SBP is associated with chronic liver disease, right? So classically, you'll be a patient that has a history of chronic liver disease and then they will present like hypothermia, they are white on maybe slightly elevated. Sometimes they can actually be a leukopinic and they'll have like mild mental status abnormalities, right? In fact, there's this test, I know I've read about it somewhere back in there. I think it's called the written trail test, like R-E-I-T-A-N and it's one of those tests that can be used to detect like subtle mental status abnormalities in the setting of a spontaneous bacterial aperitonitis. And in general, for these patients, obviously you want to do a parasympathetic, right? You want to look for bugs or I'll see probably the more classic thing for example is to look for the modern 250 neutrophils, right? You're polymorphineuclear leukocytes in the acidic fluid. And generally, you want to go ahead and give them like a third-generation cephalosporine for treatment, right?

So you can give them like septriaxone or you can give them like septetaxine. And then after this, after they sort of get over the acute episode, you want to sort of place them on like a fluor when you're learning prophylaxis for the foreseebeam future, right? So like o-fluxesin or north-luxesin or something of that feature. So please don't forget, right? I mean, obviously alcoholism is one of the most common causes of cirrhosis in the US, right? And ultimately you can get like porohypertension from that. Now, the thing is remember that porohypertension is not the only thing that can cause the side is, right? So there's many, many things that can cause the side is, right? So for example, if a patient has like ovarian cancer, with like peritonella carcinomatosis, they can also get asides with that. So how do you tell those two things apart? You, if you're sort of fully my trend of thought with this podcast, you're probably arriving at the same thing I'm thinking about, right? So obviously, you would want to know that, oh, if porohypertension is the cause of a side is, there is something known as the serum albumin asides gradient, right? So you basically measure the albumin level in the serum and the albumin level in the asides fluid, okay? And then you subtract both, right? If the number is greater than 1.1, that tells you that porohypertension is the cause of that type of asides, right?

But if something like peritonella carcinomatosis from like ovarian cancer is the cause, right? Or like some kind of lymphatic problem, the SAG gradient, yes, sag gradient, will be less than 1.1. And again, some other just high-yield things remember about like alcoholic liver disease. Remember your ASTL theory should be greater than 2 to 1, right? And one relatively specific finding on MBM is for alcoholic liver disease is an elevation in the gamma glutamil transferase in your GGT level. It's very high yield to know that, right? And then don't forget that alcoholism, right? If you're looking more in the hym under the purview of hematology, right? You may get a macrosidic anemia if you're chronic alcoholic. So here's where you want to be careful. Notice a said macrosidic. I did not see mega-lublastic anemia. Mega-lublastic anemia are a subtype of macrosidic anemia. But the thing is, mega-lublastic anemia is arise from like B12 of like full later deficiency. And classically, if a patient has is like an alcoholic and you have like a macrosidic anemia, you may find 8 cathul sites on a blood smear. That's a classic picture that it can show you on step 3, or you're medicine-intering exam. So that's something you want to look up online. Now don't forget the other, again, key antioxidants of chronic liver disease like testicular atrophy or like spider angiomida or like dinecomastia. And I've actually seen exam questions where they ask about the mechanism behind those findings.

The big thing you want to remember is that the mechanism is from high levels of estrogen. There's like some thought as to why that may be the case. Some people think that, oh, if a patient has chronic liver disease, you have like poor breakdown of like angestine dion. So you have a lot of conversion to estrogen and then that causes all those problems. But just remember that hyperestrogenism is the mechanism behind like the spider angiomida, the testicular atrophy, the gynecomastia that you observe as an antecedents of a chronic liver disease. And then don't forget that if again if a patient has like cirrhosis, then you have like hepatic insect fallopathy, right? And obviously that's as such though high levels of ammonia because your urecycle doesn't work anymore, right? So you want to treat it with like a refaxamine. I believe in the hospital that's a drug known as zyfaxa, right? So you give refaxamine, basically you'll kill the ammonia producing a bacteria in your gut, right? Or you can also give like lactulose, right? This causes like a dire special in the ICU, right? So basically lactulose will help you, it will be converted to lactic acid and then not lactic acid will pair up with the ammonia to be formalmonium and then that is not reabsorbable so you poop it out, okay? And then in some great exam cases you can actually use an amino glycoside like Neomisin to also treat the hepatic insect fallopathy.

Basically like worse like refaxamine, you kill off the gut flora that amicens ammonia. Now don't forget that people that have chronic liver disease, right? You can get like a subgeoviruses that can classically present as like a painless like just large volume hematemesis and an alcoholic, right? And you have like hemodynamic instability, right? In general, your initial treatment you want to like, you know, place large bribes, give them a crap ton of fluid, you also want to like call like your GI folks or whatever, they can do like band-in, you don't want to give them octriotide, right? Octriotide causes a splanchonic visual constriction so that can help with reducing portal pressures. You also want to give like sperm or lactone and it's also very high you to know that you also want to give those patients like a PPI, okay? Because as a subgeoviruses associated with GI bleeds as well, so you want to go ahead and just give those people PPI's, it like very high those PPI's like 80 milligrams IV for example. And then if all these things you're trying like band-in, octriotide, bloody, bloody, bloody, it's not working, go ahead and call your interventional radiologist, they'll basically do a tips procedure whether they will essentially make a conduit that bypasses the liver, they'll basically join the hepatic vein to the portal vein, okay?

Although that also increases your risk of hepatic and cephalopathy because if you're bypassing the liver, well, bye bye urea cycle so your ammonia levels can build up faster. But I guess a subgeoviruses like a very silbally can kill you quicker than hepatic and cephalopathy, okay? But that's a different story. So if a patient alright, let's say they are not having like a varicil bleed, but they have like a lot of varicis, you may want to chronically, so notice this is not an acute treatment, there's a chronic treatment with a propranolone, non-selective beta blocker propranolone so again help with decreasing the portal pressures. Now what I get, what are some related diseases we can talk about here, right? So I mean there are many other things that could cause cirrhosis, right? So don't forget like your alpha and antitripsine deficiency and like panasinara and fissima, I believe that's in heretic in like an orzomo-codominant fashion, right? Thanioclassically present as a patient that has liver disease and then has lung disease, right? So basically fissima in a patient that's like 40 years old, even if they are smoker, think about alpha and antitripsine deficiency and then don't forget hemochromatosis, right? That can also cause so hereditary hemochromatosis, that can also cause cirrhosis, right? And classically, the with-out present is like a HFE gene defect, so they'll basically reabsorb a crap ton of iron, you treat those people phlebotomy, right?

And don't forget that these people, right, they classically have like bruns diabetes on exams, right? So they won't say bruns diabetes on an exam, right? If they do that, everyone will get like a 200 or 300 on step 3 on a holiday, they don't do that, obviously. So the thing that happens is they will have schemed hyperpigmentation, that's the buzz word, you're looking for an exam, and they won't tell you they have diabetes, but they will just show you that the ablolucose is higher than normal than the normal range, and that makes you sort of connect those two ideas in your mind. Schemed hyperpigmentation, diabetes equals hereditary hemochromatosis, right? And those people, right, they can actually get the diabetes, right? Because you're essentially depositing iron in the pancreas, so you have that fancy fainting reaction that you probably remember from your pathoma disease, causing a fibrosis and destruction of the pancreas. That iron can also again deposit in the heart, right? So they can classically get a restrictive cardiomyopathy with that. Notice that hemochromatosis ends in osis, right? I'll say in general, most things that end in osis tend to cause a restrictive disease, either restrictive disease in the heart or restrictive disease in the lungs, right? So for example, like hereditary hemochromatosis, amyloidosis, right? Those things all end in osis and they cause restrictive cardiomyopathy. If you go to the lungs, right?

So like the, what are these things called, so like sarcoidosis, your pneumoconylosis, pulmonary fibrosis, those all end in osis, and they cause a restrictive pattern of a disease, but that's in the lungs. So it's kind of a useful trick to remember, for example. Now, if you see like direct hyperbular minimia, like a patient that has a history of like all sort of collitis, right? So let's just say like the patient like chronic bloodied area, don't forget primaries, chlorosinacolangitis, right? So that's basically where you have like a destruction of your intra and extra-hypatic bowel ducts, right? And remember the classic beats on a string appearance on imaging. Usually that's like an MRCP. Those people may have like p-encapositivity, that's actually another high-o thing to know. And then for those people given also, dial actually doesn't help for the most part. But contrast this with like your 40-something year old female, you know, that has parietas, has like a direct, or I guess you can say, a conjugated hyperbular minimia. For that, you want to think about primary biliric colangitis. Before this, to call it primary biliric cirrhosis, but the name has changed. It's now primary biliric colangitis, right? Remember that unlike PSC that involves both destruction of intra and extra-hypatic bowel ducts. These people just have destruction of intra-hypatic bowel ducts, okay? You treat those with also dial.

Also dial actually improves survival in patients with primary biliric colangitis. And don't forget your classic anti-mydocondral antibodies. And then what if you get a question again, this is all sentient around the liver, right? So what if you say a question about like, you know, young person with like Parkinsonian issues and like ASTALT elevations, and you know like some behavioral problems, think about well-sense disease. Basically, these people have trouble metabolizing copper, right? So, classically on exams, they're seroloplasmic levels, maybe low. And you want to treat with a drug known as triantine. So it's like T-R-I-E-N, T-I-N-E. You can also use penicillamine, right? So remember copper, penicillamine. You may say again, divine. These things look low yield. I promise you, like this is mean like, I mean, I obviously I can't promise anything. But I, I mean, encouraging you to not consider these things as low yield. Just keep in mind that for me to be given these podcasts, I've taken a lot of tests in my past. I promise you these details are not low yield. They actually high yield to know for exams, right? So, classically patients with well-sense disease, right? They can have like copper deposited in their eyes. So they'll have like those fancy shmancy, chisaflisher rings. I can also deposit like in the basal ganglia, right? So they can have like behavioral problems and like Parkinsonian issues.

And then I guess the last thing I may mention with our guest to like related diseases, don't forget like your jahto mutation and your myeloproliferative disorders. The one I'm probably more concerned with here is polycythemia vera, right? Those people have like low levels of epoch. That's actually high yield to know. And remember that classically, polycythemia vera on exams can present as a body, as a body care syndrome where you basically have thrombosis of the hepatic vein. And I guess for this question, right? The asserting tests you want to think about, right? So you want to obviously get like for this case, you want to get like a BMP, you know, like a CBC, you want to get LF Ts, right? Like to check like the ASTLTPTT, you want to check the levels of our bumein. Obviously, there will be low if you have cirrhosis, right? You want to also check like hepatitis serologies, right? You want to check ammonia levels so that you know if you need to initiate like refoxamine or lactulose or Neomysin and stuff like that. So I think that's what I'll say, but that was a pretty comprehensive review of a lot of liver diseases. That's basically what I'll try to do with each case. I'll give you like a classic presentation, give you the diagnosis, talk extensively about that diagnosis in terms of what you mission an exam, like the USML is step three or the medicine in treating exam. I'll talk about like treatment, work upon all that stuff.

And then I'll talk about like related pathologies, right? That again, that you mission your test. I'll just give you like few like three, four, high old things to know about those things. And then I'll just talk about tests you want to order. That's more for the CCS portion of your exam. Let's see, you know what, let me just go through one more case, right? So let's call this case six, right? This one may be a little disjointed, but let's just talk about it. It should be short. But let's assume you get a question about like a patient that has, you know, histro V5, like irregularly regular business on tests. And then we have like sodium onset like leg pain. And then you do a physical exam. The leg is like, you know, explicitly tender. It's pulseless. You're not feeling any pulses. There's like parastegias. There's like parlor. Think about acutely mesquimi, right?

Another patient that classically is pretty supposed to get an acutely mesquimi other than other than a patient on the history of ephysioproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposopropos roposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposopropos roposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposopropos roposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposopro

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oposoproposoproposoproposoproposoproposoproposoproposoproposoproposoproposopropos You can email me through the website or you can use a Divine Intervention Podcasts with an S at Gmail.com So I'll see you in the next podcast.

Have a wonderful week ahead and God bless. Thank you.

Mediterranean descent (Greeks, Italians), Africans, and sometimes Asians.

Heinz bodies (oxidized hemoglobin) and bite cells (due to splenic removal of Heinz bodies).

Increased urine sodium (>40 mEq/L), indicating an intrinsic renal problem.

Fever, rash, and eosinophilia (or eosinophiluria).

Acidified glycerol lysis test.

Usually below the renal arteries or above the aortic bifurcation.

Peaked T waves $\rightarrow$ Wide QRS complex $\rightarrow$ Sinusoidal waveform $\rightarrow$ Flat line (asystole).

Inability to regenerate reduced glutathione, leading to overwhelming oxidative stress.

Severe infection or fava bean ingestion.

PSC involves destruction of both intra- and extrahepatic bile ducts; PBC only affects the intrahepatic bile ducts.

Skin hyperpigmentation (bronze skin), diabetes mellitus, and potential cardiomyopathy/arthritis.

Serum Albumin Ascites Gradient (SAG). A gradient > 1.1 g/dL suggests portal hypertension.

Lactulose (acid-base trapping) or Rifaximin (gut flora reduction).

Allopurinol or Febuxostat (Xanthine oxidase inhibitors).

Inability to regenerate reduced glutathione, leading to overwhelming oxidative stress.

Severe infection or fava bean ingestion.

PSC involves destruction of both intra- and extrahepatic bile ducts; PBC only affects the intrahepatic bile ducts.

Skin hyperpigmentation (bronze skin), diabetes mellitus, and potential cardiomyopathy/arthritis.

Serum Albumin Ascites Gradient (SAG). A gradient > 1.1 g/dL suggests portal hypertension.

Lactulose (acid-base trapping) or Rifaximin (gut flora reduction).

Allopurinol or Febuxostat (Xanthine oxidase inhibitors).