DIP Episode 153 - USMLE Step 2CK Rapid Review Series 15 (Surgery)

Welcome. My name is Devine. I am a resident. This is going to be episode 153 of the Divine Intervention Podcast. And in this episode I'll be continuing our rapid review series for the USM Listep 2 CK exam with a focus on general surgery. So let's go ahead and begin. Now what if they give you a question about a patient that has a... They tell you that this patient has been a smoker for a long period of time and then they come into their sense to the ED because they've been having a lot of like... they've been making a ton of urine, they have volume depleted, their blood pressure is low, they've been vomiting, having severe abdominal pain. What are you thinking about? And again long term smoker, what are you thinking about? And usually they will give you like... you know some CBC, like some... they will give you like a CBC, they will give you like a BMP results. What do you think this person has? I hope you're telling that this person likely has a scrimal cell cancer of the lung. So I remember a scrimal cell cancer of the lung in a pyrimenoplastic fashion can produce PT-HRP, right? For a third, who won't release it at peptide? And when it produces PT-HRP that can... that can cause hypercalcemia. And hypercalcemia can cause like the classic, classically describe the stones, bones, groans and psyche overtones. So those people you know they can have like... they can have like diabetes in sepidus, believe it or not. Hypercalcemia induces an effergenic diabetes in sepidus.

It makes the principal cell of the collecting doctor resistant to the effects of... resistent to the effects of... of ADHD. And again you have like abdominal pain, they can have nephrolithiasis and all that stuff. And usually your first step in management under those circumstances is to go ahead and... that was the patient in like a ton of fluid, right? You give them, you put them on an IV normal ceiling. And then you can use other things like you can use like a lube diuretic. Remember lupus-lupus calcium. So you can use a lube diuretic to try to get rid of some of that calcium. And in addition to that one other thing you can also do on an MBM is to give them calcium tonin. Calcium tonin is actually pretty good at... toning down your blood calcium levels are very acutely. So that's a high-yield thing you want to keep at the back of your mind. And then one other thing you should keep in mind with... with hypercalcemia is that it has the ability to... short-tem the QT interval. That's something that's classically tested on the USMLE exams. And then remember for the other lung cancers, right? We have small cell lung cancer. Remember that can certainly cause a lot of endocrine abnormalities. It can cause a uvolymic hyponitrinia, right? Because it produces a... ADHD, right? So like SID, which is a classical syndromic association with small cell lung cancer. And remember that small cell lung cancer can also produce ac TH.

So remember that if a person has like signs of hypercalcysolism and it is not so pressable with high dose dexamethosum, those are the big things you want to keep in mind there. And then remember also if they describe a person that you know has been a smoker for a long period of time. And then this person has like trouble like standing from a chair and they tell you that all the person has like proximal muscle weakness. That is fatigable and sort of like gets better with repetitive nerve stimulation. On the other circumstances, you want to think about Lumberid etymisthenic syndrome. Okay, Lumberid etymisthenic syndrome. Again, classically found in the setting of a small cell lung cancer. You make auto antibodies against the prison. I've taken VOTEG-Gated calcium channel, right? But if you keep using using those muscles, you begin to recruit more calcium to that VOTEG-Gated calcium channel. And those can outcompete the bad antibody and the person symptoms get better. Okay? Remember, for Lumberid etymisthenic syndrome, the symptoms get better with use. And again, remember that small cell lung cancer is considered to be metastatic and diagnosis, right? And on the surgery shelf example, if you get a surgery question and you talk about a patient that... They talk about a patient that has like long cancer, right? And this patient, they tell you that this patient has like a plural effusion. The next step in management is always to tap that plural effusion.

So you do a thoracinthesis. You do the thoracinthesis. If you find my ligament cells, that's the true lung cancer. There's nothing that can be done. There's really no more that can be done for that patient other than to try to drain that fluid. And then you can try to do things like a pyrodesis and all that fun stuff. Unfortunately, lung cancer that's already like in a plural effusion is usually not a good sign. At least both on exams and also in my own personal clinical experience. And then I remember, other high-eoprano-plastic phenomena that can arise with lung cancer, remember polymyocytes, and dermatomyocytes, can certainly arise as per new plastic phenomena in the setting of lung cancer. And then if they describe a person that is smoked for a pretty long period of time, and they tell you that this person has like over the last like four to six weeks, this person has like this sodium onset severe arthritis in the lower extremities and finger clubbing. You want to think about this pyroplastic phenomenon known as a hypertrophic pulmonary rheosodopathy. They really is no treatment other than you treat the cancer and then you can recede. Okay, so I think that's what I'm going to say about lung cancer. Now what if they give you a question about a patient that let's assume they give you a question about a patient, you know that has like a history of like a prostate cancer.

And then they tell you that over the last like three days, this patient has a most sensation below, like I don't know, let's say like below their... Let's see, I think of a suitable level. So let's say, you know, they've lost sensation below their nepotline or something, right? That's a T4 level, right? They've lost sensation below that line. Essentially that patient has like lung cancer. I mean, they have prostate cancer meds, right? To the spinal cord. Remember that to that no, prostate cancer meds on NV Me exams. I mean, obviously this person is obviously presenting signs of a spinal cord compression. As evidenced by the presence of a sensory level, right? So you see that sensory level, you know that there's spinal cord involvement. And whenever you see people say the word sensory level, sensory level just literally means just literally means that, oh, below a certain level, the person has lost like all sensation or has like quadriplegia or whatever, right? So if you have something to keep in mind, that's pathonomonic for a spinal cord lesion. And remember prostate cancer, right? It has the size of the spine via something called the baxin vertebral plexus. That's a thing that tends to pop up on exams. It's like a venus plexus. And remember, right? If a patient has signs of spinal cord compression, acutely the treatment is, you want to go ahead and give them IV dexamethosone, like IV corticosteroids.

And then one other thing you should also consider doing is getting an MRI of the spine, okay? To roll out, I mean, to essentially like see the lesion better. So those are just things you want to keep at the back of your mind. Now, what if you get a question about a patient and they tell you that this patient, let's assume it's a patient with a history of lupus and they present to the family practice office or whatever. Believe it or not. As I know, like me, see, the brain is surgery shell. They don't test stuff like this. Think again, right? They love to test this stuff for sure on exams. The surgery shelf, they just talk about like surgical applications of medical problems or like medical applications of surgical, whichever way it is. But they basically love to test this concept I want to talk about. So the thing is, they describe this person, you know, history of lupus. And then, they tell you that over the last seven days, this patient has been having like really bad nosebleeds, whenever this she brushes her teeth, you know, gives off a lot of blood having like very heavy menstrual bleeding. If you see those kinds of things, what are you thinking about? And then they show you like a platelec count that's like 10,000. What are you thinking about on those circumstances? I would really hope you're thinking about it. It's a lot of people that have a history of lupus and in other circumstances, it can actually just arise in your pathically.

Like people, you know, they have like no history of lupus and in disease, but they just have this like idiopathic, a thrombocytopenia. Remember that the pathophysiology involves a fomine antibodies against GP2 B3 A, right? So those people get a bad, bad, bad thrombocytopenia and then they ultimately get into trouble. For the most part, if they are not bleeding severely and you just notice that, oh, they just have like this thrombocytopenia, you really don't need to do any kind of treatment. But if, for example, you notice that, okay, they have like life-threatening bleed and all that crap, you can do things like give them corticosteroids, corticosteroids work pretty well. You can give IVIG, you can give retoximap. The way I remember that is just remember like, like, sers criteria, like sers, like SIRS. So the S is for steroids, the I is for IVIG, right? The R is for retoximap. In general, that's the order you actually portion in BME exams from like first to third line. And then the S in sers is like the nuclear option. If the patient is not doing really well and you've tried multiple interventions, you know, you're not making much headway. You can consider giving the patient a, you can consider doing a spleenectomy, spleenectomy usually is curative of, of ITP. And remember, right? ITP, yes, it involves making auto-antibodies against GP2 B3. Remember that if you have a deficiency of GP2 B3, that's an example of a glansman thrombostemia, okay? Glansman thrombostemia.

Sometimes you may see it referred to as glansman disease on MBM exams. And because it's a platelet problem, right? Obviously the bleeding time will be low. You may also see a question. I remember a Bernatolise disease, right? Bernatolise disease. Those people have a deficiency of GP1 B9. And then from really brand disease, right? Remember, those are all dominant inheritance. Those people have a deficiency of a, of a really brand factor. And again, these are all platelet problems, right? So the, so the bleeding time will go up. Remember that in ITP, actually the platelet count actually goes down because you have physically destroyed platelets, right? But the amount of mega-caruocytes go up, right? And that should make perfect sense because your mega-caruocytes are precursors to your platelets, right? So if you're having this big, depletelet deficiency, you don't want to try to hopefully fix that. But you're not increasing the number of mega-caruocytes that you have because they are precursors to platelets. And then remember that if a person has a malibrand disease, in addition to the bleeding time going up, one other thing that will also go up is there is the PTT. Because remember, when malibrand factor is a protecting group for factor 8, so when people have malibrand disease where they have that deficiency of a malibrand factor, there is less protection of factor 8, so those people's PTT tends to go up.

So that is one of those higher bleeding disorders that's associated with an increase in bleeding time, but also an increase in PTT. And remember that one way you can differentiate malibrand disease together with a Bernat-Sulee syndrome from glansman disease, for example, is that when malibrand disease and Bernat-Sulee, because they involve like that initial step in primary hemostasis, they will be associated with an abnormal, restocetene co-factor acid. Okay? That is not something you'll find in glansman thrombostinia. And then the way you tell Bernat-Sulee disease from malibrand disease is to look at the PTT. If the bleeding time is elevated, but the PTT is normal, that's Bernat-Sulee. If the bleeding time is elevated, but the PTT is elevated, it's abnormal. That's one of the more vulnerable disease. So those are all high-eal things you want to keep at the back of your mouth. And then, what if they give you a question about a patient? You know, that's like recently gotten like a few hours ago, they got like pneumatic dilution for ecalhesia, or they can even make this a question about a patient that, you know, they came in with like dysphysia, right, and they've been losing weight, so an eGD would biopsy was performed, and then they tell you that, you know, over time, the patient suddenly becomes like, you know, kind of like very sick, starts having like very high fever, is profoundly hypotensive and all that crap, and then they ask for your next best step in management.

I would really hope on that those circumstances, you're thinking about the rupture of the esophagus. Whenever a person has a rupture of the esophagus, one thing your friends at the NV Me absolutely love to test is, they like asking, what is your next best step in diagnosis, right? They would try to give you the answer that involves doing a barium swallow, and resist, begin that answer, I promise you that will be the wrong answer in your exam. When people have an exophageal rupture, because barium can cause a very powerful life threatening immediately as the nitase, you try to avoid doing a barium swallow under those circumstances, so you don't gastro-graphing in them, okay? You use gastro-graphing. The thing is, they know that most people have memorized the term gastro-graphing, so occasionally what they try to do is to again give you another name. For what you know, that's one way your friends at the NV Me can make an exam difficult, right? So the way they do that is that the gastro-graphing, the gastro-graphing, NMR, right? Sometimes it's called water solubil contrast NMR, okay? So that's something you want to keep at the back of your mind for exams. And then, what did they give you a question about a patient that was recently started like on dialysis?

And then they tell you that you know that over the last like two or three weeks, this patient has been having like significant volume overload, has been having shortness of breath, has been having a thotnia, has been having proxysmonectional dysmia, and then they asked like, what's the mechanism behind the patients dysmia? I would hope under those circumstances that you're thinking about high output heart failure, okay? I don't know for whatever reason, the NV Me loves high output heart failure, they tested in many different iterations. So it's one of those weird things that you want to like be like kind of up on with regards to your, with regards to exam. So high output heart failure, right? So why does this person that was recently studied on dialysis? Why does that person have high output heart failure? Well, it makes sense right? Because prior to initiating dialysis, what do you need to establish first, surgically? You need to establish an AV fistula, right? You need to establish an AV fistula. So when you establish that AV fistula, right? Again, you're taking capillaries out of the equation. You're essentially connecting an artery directly to a vein, right? Remember capillaries? Yes, they help you reabsorb, you know, they help you like, you know, exchange nutrients with tissues and all that stuff. But I also think of capillaries as a slowdown mechanism for blood that's going from an arterial to a venial, right?

And that slowdown mechanism is kind of important for the heart, right? You kind of think of it as a time where, you know, as blood is in capillaries, because the exchange of stuff is happening, that's kind of like a time for the heart to take a breather. So if you have direct connections between an arterial and a venial and the go between capillaries gone, then that slowdown mechanism is not there. So the heart does not have time to take a breather. So the heart just keeps working hard, working hard, working hard, working hard. And if that happens, over time that will cause something known as high output heart failure, okay? High output heart failure. It just arises when the heart literally does not get a breather, right? And it's a classic finding in people that are recently initiated on dialysis on NV Me exams. I remember people that have that are initiated on dialysis right there, other things that can happen. Let's say for example, a person has like peritoneal dialysis. Remember that can be a presentation of SBP, right? Spontaneous bacterial peritoneitis on an NV Me exam. So a person, you know, has been on peritoneal dialysis for a while, and then they start complaining of abdominal pain. And then they have like a low grade fever. You really want to think about an, you really want to think about SBP. Your next step in management, in total of those circumstances is to go ahead and, is to go ahead and perform a paracetosis.

And if you find more than 250 neutrophils, your diagnosis is done. You go ahead and start the patient on a third generation cephalosporing, like cephotaxin or cep triaxo to treat the SBP. And then remember, already for a person who is on dialysis and they have like, I mean, if I mean people that go on dialysis, right, tend to be people that have an endstitural disease. Those people, they can develop like a uremia, right? And they can get like a coagulopathy from the uremia. To treat that coagulopathy, right, where they like, bleep bleep bleep bleep bleep, you can actually treat that with a decimal person, okay? You can actually treat that with a decimal person. And remember, other things that can cause high-uport heart failure, right? If a person has a paracetosis disease, right? Those people's bone marrow become hypervascular, that can cause high-uport heart failure. Severe pneumonia, right? It can also cause high-uport heart failure. What else can cause high-uport heart failure? It can be a trauma question on the surgery shelf, where, you know, a person got like a stab wound or something, and then they tell you that you feel a pulse of telmas at the region of the stab wound. That's an IV fistula that can also cause high-uport heart failure. If a person has hemorrhagic, hemorrhagic, hemorrhagic, telangethesia, right? HHT or Oslo Vibramarandu disease, right?

Those people tend to have like telangetages on the skin, they tend to have, they tend to have, telangetages on the skin, a lot of nose bleeds and all that stuff. You want to think of high-uport heart failure as well in those people, because they tend to establish your EV Ms all around the body, okay? So again, those are all high-up things you want to keep at the back of your mind with exams. Now, what if they give you a question about a patient that had like a recent like ERCP for, I don't know, like they did an ERCP with biopsy because the patient came here with like painless jaundice and all that stuff. And then they tell you that this patient is now completely on like severe abdominal pain and the lipase is markedly elevated and all that stuff. What are you thinking about on those circumstances? I would hope you're thinking about acute pancreatitis, right? A acute pancreatitis, remember, the work op is, it's, a acute pancreatitis, one of those things that it's simple to manage in the real world, but the mortality is actually quite high, right? So essentially the way acute pancreatitis is, you make the patient MPL, right? You give them an IV fluids, right? And then you give them like pain medication, preferably opioids. Don't try to feed those patients, that's not a great idea on NBM exams. And remember that people that have pancreatitis, they can also have a hypocalcemia, right? That hypocalcemia can arise from the saponification reaction.

So if they give you a person that, you know, had an episode of acute pancreatitis and then they have like a prolonged acute interval on an EKG, think about the hypocalcemia from a saponification. Remember though, another classic presentation of hypocalcemia NBM exams, especially on the surgery shelf is, or on step 2 CK. Whenever you see me say surgery shelf, also mean step 2 CK. The thing is, they can describe a person, right? You know, that has like a pathway, a anatomy, like the pathway gland, we were sick, and then after that, a section, the patient, you know, starts having like, the patient starts having like seizures, or the patient starts having like a papyrus pathins, and all that stuff. And you want to think about hypocalcemia. I mean, you've literally taken away those people's parathiric glands, right? So they no longer produce parathiric hormones, right? So they can become a cutely hypocalcemic. Obviously, the way you treat those people, especially when a person has a symptomatic hypocalcemia, is to go ahead and perform, to go ahead and give them like an even fusion of calcium gluconite. Calcium gluconite is the rescue agent for symptomatic hypocalcemia, is the rescue agent for symptomatic hyperchylemia, especially when the person has like those picks tea waves on an EKG. And then it's also the rescue agent for magnesium toxicity on NV Me exams.

And then remember that hypocalcemia can also arise when a person has rubbed on myolasis, okay, because that calcium can be sequestered in those necrotic myocytes. So those are all things that can cause hypocalcemia on NV Me's. Another classic one is if a person, you know, a kid is born, and they tell you that this kid has like a ton of murmurs, and this kid has like seizures, and all that crap. Think about hypocalcemia already in the setting of the George Syndrome. Remember in the George Syndrome, the third and fourth-firing jaw pouches do not develop. So since those do not develop, the thymus does not develop. So those people have like a T cell deficiency, so they tend to get like a lot of viral and fungal infections. And then another thing those people tend to develop is hypocalcemia, because they are part of thyroid glands, do not develop. So hypocalcemic seizures in a newborn think about the George Syndrome, and also think about an infant of a diabetic mother. Infants of diabetic mothers can have seizures in the newborn period from two things. It can either be from hypocalcemia, or it can be from hypocalcemia, or describe that in many podcasts in the past. And then, don't forget your transplant rejection. Your friends at the NV Me love to test this from a surgery perspective, transplant rejection. Remember that there's like a cure, there's hyperacute rejection where you're literally beginning to reject the organ in the, in the operating room.

That's mediated primarily by antibodies. And then after that we have acute rejection, right? Acute rejection, that tends to arise in the setting of, you know, like a few days to weeks to up to about a year, actually believe it or not, after the transplant happens. Really for the most part, the thing that causes it is that some of those are the transplanted organ proteins that presented on MEC class 2 to CD4 positive T cells that then ramp up the antibody response and then you ultimately run into a lot of trouble. And then chronic rejection, right, is like years after that, ultimately every transplanted organ will fail. So I guess that's something to, something to keep at the back of your mind. Okay. Now, what if you get a question about a patient that is female, and she has this bulge around the inguinal canal? What kind of hernia you're thinking about? I would really hope you're thinking about, about a femoral hernia, right? I really hope you're thinking about a femoral hernia. And then remember that your friends at the NBME, right? They can give you a question about a patient that has a history of MEN syndrome, especially like MEN1, and then they give you like some labs. And you notice that this patient's potassium is like 2.5. If you see that, what are you thinking about? If you see like really bad hypochylemia, and then you see like chronic diarrhea and a patient that has a history of MEN1 syndrome, what are you thinking about?

I would really hope you're thinking about a vaipoma, right? Remember, people that have MEN1 syndrome, they can get parathyroid problems, so they can get hypercalcemia, they can get pituitary problems, most likely a prolectinoma, and then they can also get pancreatic and urine to drink to tumors, like they can have like a vaipoma, right? Remember, vaipomas can present as WTHA syndrome, right? Where people have like watery diarrhea, and they have like hypochylemia, and they have like echrohedria, right? They can also get gastronoma, right? Like in the setting of the Zolinger-LSN syndrome, where they make a ton of acid, and they tend to get like these like gigenol. Once you see the Boswurjigenol ulcers, you can pretty much stop reading the question and NBM, they are referring to a gastronoma. Remember, these people can also get like glucargonomas, right? So you see a person is like, this person has been normal all his life, and then between the ages of like 40 or 50 something, they develop like this neon-seed diabetes, and then they develop like this rash on your skin, that's the classically described macrolitic migratory erythema that is pathonomonic of a glucargonoma, and then remember that these people can also get insulinomas, right? Again, where they get like weepostriode, right? Like hypochylemia, signs of hypochylemia, and then you give them glucose, their symptoms get relieved. That's weepostriode, that's pathonomonic anembreum exempts one insulinoma.

Remember, those people's levels of insulin will be elevated, right? But in addition, their CPAP type will also be elevated, right? Because that insulin is coming from the, is coming from pancreatic cells of a pancreatic, like it's like endogenously secreted insulin, versus a person that is overdosing on insulin from out from that the bi-former pharmacy where the insulin will be elevated, but their CPAP type levels will be normal. Although in a sulfonial urea, if a person is like, like, factichiously using a sulfonial urea, their insulin and CPAP type will also be elevated, right? Because remember, sulfonial urea is the block that ATP-dependent potassium channel, right? So by doing that, you will see great insulin, right? So sulfonial urea is actually caused elevated levels of insulin, and they also cause elevated like CPAP type levels. But the way you differentiate those from an insulinoma is you do the secretedog screen, and that would sort everything out for you. The secretedog screen will be positive in a person that has that, you know, is overdosing on a sulfonial urea. That's essentially like a blood test for sulfonial urea. The thing is, your friends at the end being realize that every human being has memorized that stuff, with sulfonial urea, right? So they are beginning to test the same concept, but with the Meglidinites, okay?

So don't forget that it is not only a sulfonial urea that block that ATP-dependent potassium channel, there are other things that block that ATP-dependent potassium channel as well, like the Meglidinites. It's just they are more like, they are shorter acting than your sulfonial urea. So they have like a lower risk of hypoglycemia. You know, Meglidinites include drug like Nataglinite and Repaglinite, okay? So they can again, present as we post triad on an MME exam, just something to keep at the back of your mind. And remember that if a person is a diabetic, right? You know, want to be a little wary of prescribing beta blockers for those people, because the thing that can happen is that when you take beta blockers, that can suppress the autonomic response that you get when you become hypoglycemic, and that can be profoundly dangerous. Many people think, oh, my blood sugar on a little, no, not a big deal. But if it or not, people die from hypoglycemia all the time, okay? So it's much better to be hyper-glysemic than it is to be hypoglycemic, right? So again, those are all high-yield things you want to keep at the back of your mind for exams. So I want to try to keep this below 30 minutes. So because again, it's a rapid review series. So I'm going to go ahead and pause here. And like I do at the end of every podcast, I offer one on one tutoring for many exams. Step one, two CK, two CS, step three, preclinical med school exams, third year clerkship shop exams.

And then if you're a new first year med student or a new second year med student or a new third year med school student, there's this then I call longitudinal tutoring that I've sort of talked about in my, in my prior podcast where I tutor you for the exams you take as you're going through those years in med school. But at the same time, I tutor you for the corresponding board exam, the corresponding USML exam that's coming up, the people that I've done this with, they have been wildly successful in the USML exams. And then if you also have a college buddy that needs tutoring for Gen CAM, O-CAM physics, bio-CAM histology and physiology, I'll for one on one tutoring for all those things. And then if you're a medicine resident and you need tutoring for the medicine-entrany exam, or the EBI board exam, I offer tutoring for those. Again, I've worked with some people in the CEO, but you're not a medicine resident. Yes, I'm not a medicine resident, but I have certain life experiences that uniquely position me to tutor people. I mean, the people that I've worked with again for those exams have done really well. So if you want to, if you're wondering what that experience is, you feel free to email me or something, I'd be happy to tell you why I'm experienced in a tutoring exam. And then if you're medicine and applying to residency, so like an ERAS application, I'd offer again one-on-one tutoring and advising for that.

I'm more advising and consulting like personal statements, rec letters, mocking reviews, editing, ERAS applications. And then if you're a college student applying to med school, so like an AMCAZAP, I'll also do a similar thing. So have a wonderful rest of your day. I will see you in the next podcast. God bless you. Thank you.

Watery diarrhea, hypochloremia, and steatorrhea (WASH).

Small cell lung cancer.

Steroids, IVIG, and Rituximab.

Both have prolonged bleeding time; however, abnormal restsestine cofactor assay helps differentiate them from ITP. (Glanzmann = GP2b3 deficiency; B-S = GP Ib9 deficiency).

Acute hypoparathyroidism due to lack of PTH production.

The presence of a sensory level (loss of sensation below a specific dermatome).

Squamous cell carcinoma (or Small Cell Lung Cancer, depending on the context provided in the lecture, but SCLC is emphasized for this syndrome).

Arteriovenous Fistula (AVF) or AVM.

Barium risks severe mediastinitis/pneumomediastinum; use water-soluble contrast agents like Gastrografiling.

Vaptoma (Watery diarrhea, Hypochloremia, Steatorrhea).

George Syndrome.

Hyperacute (antibodies, immediate), Acute (days/weeks), Chronic (years).

Squamous cell carcinoma (or Small Cell Lung Cancer, depending on the context provided in the lecture, but SCLC is emphasized for this syndrome).

Arteriovenous Fistula (AVF) or AVM.

Barium risks severe mediastinitis/pneumomediastinum; use water-soluble contrast agents like Gastrografiling.

Vaptoma (Watery diarrhea, Hypochloremia, Steatorrhea).

George Syndrome.

Hyperacute (antibodies, immediate), Acute (days/weeks), Chronic (years).