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ABSITE Review: What to Study the Night Before the ABSITE (Podcast)
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ABSITE Review: What to Study the Night Before the ABSITE (Podcast)
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>> Behind the knife. The surgery podcast, where we take a behind the scenes intimate look at surgery from leaders in the field. >> All right, well welcome back to another episode of Behind the Knife, and this week we're putting out a special episode. For those of you residents out there, which we have a feeling there's a large part of our listenership that are trying to cram in for the ABSITE. >> And a little disclaimer, this is not a comprehensive ABSITE review. More so, this is the week before the ABSITE.
We wanted to go over some of those more commonly tested, high-yield facts that are the things you kind of cram for the night before the ABSITE. >> And brain dump them for the entire year after that. >> Exactly. And in no better way to get started than the mechanism of action for different antibiotics. These are tested every year, and I can never remember them. So, first off, just to go into the inhibitors of cell wall synthesis. These are penicillins, cephalosporins, carbapenems, monobactams, and vancomycin.
And the next category is the ribosome inhibitors for protein synthesis. Now these are on every year. They always ask you if it's a 50S, if it's a 30S, if it inhibits the 30S or the 50S, the subunit of the ribosome. Unfortunately, there's not a good pneumonic for this. It's hard to remember, so you just kind of have to memorize it. So for the 30S ribosome, that's tetracycline, aminoglycoside, and linezolid. Again, the 30S tetracycline, aminoglycoside, linezolid.
For the 50S, that's erythromycin, clindamycin, and Synercid. Another common class asked is the quinolones, and these are an inhibitor of the DNA helicase. >> I call that a helicase. >> Tomato, tomato. And then for metronidazole or Flagyl, this produces oxygen radicals that break up the DNA.
>> I've seen that one on there a few times. All right. And we just wanted to continue on and do resistance, mechanism of antibiotic resistance. So classically this has been on there since step one. How does penicillin resistance work? It's due to a plasmid for beta lactamase, so it transfers DNA that teaches the bacteria how to avoid the beta lactamases. >> And I believe that's the most common method for acquiring antibiotic resistance is the transfer of plasmids, is that right?
>> That's what Pfizer says, and then for MRSA, the resistance is caused by a mutation of cell wall binding protein. One other question I've seen on there before is adjusting antibiotic levels, specifically like vancomycin or gentamicin for their peaks and troughs. So, Jason, what do you do if your peak level comes back too high? >> So if the peak is too high, you want to decrease the amount of each dose of the antibiotic. >> And if you send off that trough right before you're about to re-dose the medication and the trough comes back too high?
>> So if your trough is too high, you want to keep the dose the same, but you want to decrease the frequency of doses. In other words, increase the time interval between doses of the antibiotic. >> And Jason, there are a few side effects that are commonly tested. How about those third generation cephalosporins? >> Yeah, so I've seen this a couple times, for third generation cephalosporins like ceftriaxone, the common side effect is cholestasis or cholestatic jaundice, sludging in the gallbladder. >> And those dreaded aminoglycosides, and while you're doing this, can you tell us which ribosome it acts on also?
>> Yes, so, of course. The aminoglycosides is on the 30S ribosome. Again, it's irreversible binding, so it's bactericidal. Common side effects, these you really have to watch for, especially in the elderly population, but nephrotoxicity and ototoxicity. So the nephrotoxicity with the aminoglycosides is actually reversible whereas the ototoxicity is permanent and irreversible. >> And what's a common name of an aminoglycoside? I can never remember.
>> So these are, you know, gentamicin, tobramycin. >> And another one that's on there is Flagyl. What is a complication of Flagyl? >> So for Flagyl you need to advise your patients not to drink on Flagyl because there is a disulfiram-type reaction, so they get very sick. But the more concerning side effect is peripheral neuropathy with the long-term use of Flagyl. >> And one thing, for erythromycin, we always talk about it on the ABSITE for being a prokinetic [inaudible].
What receptor does it bind to? >> So, the erythromycin acts on your motilin receptors. >> Now that was a very brief overview for antibiotics, and a little throwback here to earlier in the podcast, and if you haven't listened to these, maybe after the ABSITE you should give a listen to our transplant podcast. Dr. Kirk, the chair of surgery at Duke and a transplant surgeon, actually when we sat down with him in May gave us a review of transplant medications, which is commonly on the ABSITE. So here is Dr. Kirk in a review of transplant medications.
>> One thing, I know every year when it comes to ABSITE time, I refresh myself on the immunosuppressants. Can you just briefly take us through the primary regimens you have patients on because I know it changes quite drastically. >> Right, well almost all patients, greater than 95 percent of patients are on a calcineurin inhibitor regimen, and in the United States, that's almost always tacrolimus. Knowing the mechanisms of tacrolimus, blocking the calcineurin, calmodulin pathway, preventing the nuclear factor of activated T cells from becoming activated, that's always on the test.
So if you see a calcineurin inhibitor or a nuclear factor of activated T-cell check that box. The other adjuvants, most people are on triple immunosuppression, so people are typically on a calcineurin inhibitor and an antimetabolite. The most common one in the United States is mycophenolate mofetil. It is a, it interrupts purine synthesis, so if you've seen purine and mycophenolate mofetil, check that one. And then most people are on some steroids, and the mechanisms that are most important there is it prevents the nuclear translocation of NF-kappa B, and then from there as a myriad actions, both on antigen presentation and T-cell activation.
Knowing those three subgroups, calcineurin inhibitors, antimetabolites, and steroids will get you pretty far along, and if that doesn't work, C is always a great answer. [laughter] >> All right, thank you, Dr. Kirk, for that great review of transplant medications. And now on to, we asked on Twitter what do people review right before the ABSITE, and the most common response was the GI hormones. And you would think we would have these memorized by now considering they've been asked on every exam in med school and surgery residency, but still, most of us have to review these before the ABSITE, because they are commonly asked.
So, Jason, let's just get started. How do you remember the mechanism of action of CK, cholecystokinin? >> And, yeah, and we should give credit where credit is due here. There is actually a great, kind of review of these on the U.S. MLE boot camp website. We'll put a link to that on our website and on our podcast. So CCK is, you know, cholecystokinin, so cholecyst, gallbladder, kinin meaning move, so this is the only hormone that causes gallbladder contraction, cholecystokinin, gallbladder contraction.
And it's also important, you should remember that it's important for lipid digestion, and so, of course, what else is important in addition to bile for lipid digestion. It's the pancreatic enzyme. So CCK acts along with secretin, but CCK is the important stimulator of the secretion of pancreatic enzymes. >> Right, and then so what is, so if CCK tells the pancreas to secrete the enzymes, what does secretin tell the pancreas to do?
>> So secretin tells the pancreas to secrete bicarb. >> And we can never forget the most annoying question to me is they'll say what is the source of the CCK or the enzyme that causes the pancreas to release enzymes? >> So CCK is released from I cells, and those are located in the duodenum and the jejunum. >> And then how about the secretin? I can remember this one. >> So, secretin is easy.
Secretin is secreted from S cells, secretin, S cells, and that's also from the duodenum. >> And, yeah, when acid reaches the duodenum, this increases the secretion of secretin. >> And that makes sense too, if you have an acidic environment in the duodenum, you want to make that more alkaline, it's going to release a hormone, secretin, that's going to stimulate the pancreas to release bicarb.
>> All right. And let's jump over to gastrin, a commonly tested enzyme. Where is the source of gastrin? >> So gastrin is another used one. Gastrin is from G cells, and these are in your stomach antrum. So that makes sense when you think about things like retained antrum syndrome, where you have hypersecretion of gastrin. >> Great. And, what is the syndrome called that you have a hypersecretion of gastrin?
>> So, this is your Zollinger Ellison syndrome, it's the hypersecretion of gastrin. >> And it's the only hormone that promotes gastric functions, acid secretion, and motility. So that one is one of the more straightforward ones. >> So given, one of the GI hormones that I never remember and I always get wrong on all the practices questions and on the outside is GIP. So can you please walk us through and help us remember what GIP does?
>> Yeah, so GIP actually stands for two things. Commonly, we know it as the gastric inhibitory polypeptide, and this is in reference to it reducing gastric acid secretion, but a less commonly known name is the glucose insulinotropic polypeptide. And so, and this is important because there's questions that we'll say if a patient gets an oral dose of glucose or if they get an IV dose of glucose, which one will cause more insulin to be released? Thanks to GIP, an oral dose of glucose will cause increased insulin response.
And it's important to always know that GIP comes from K cells in the duodenum and jejunum. So GIP will inhibit gastric acid secretion, and it will increase insulin secretion that's released from the K cells in the duodenum and jejunum. >> And the last big high yield on is somatostatin, and this one's a pretty easy one. If you can just remember that it comes from D cells in the pancreatic islet cells and GI mucosa. This is, basically shuts everything down and inhibits most of the function, the secretion of almost everything, and it's an antigrowth hormone.
>> Yeah, and so, and I've missed this before, it actually also, you know, we think of things that are trying to counteract acid, it also counteracts bicarb, so it also does not increase the release of bicarb, it stops that also. >> So, it just shuts everything down. >> And that is it for our GI hormones. We're going to talk a little bit more about these when we talk about neuroendocrine tumors of the pancreas. >> Okay, so the next thing that always gets me relates to immunology, and it's those darn interleukins in cytokine.
So, Kevin, if you could just walk us through some of the high-yield, commonly asked interleukins as to what they do, that would be awesome. Yeah, so we're just going to go through IL-1 through 10, and the thing to remember is there's IL-1, and then the rest of them that are important are even numbers. So IL-1, we should all know this, induces fever. Macrophages release it and causes fever. So that's the big things to know for IL-1. The rest of them are going to be even numbered.
IL-2, and this is what our transplant medications work on that Dr. Kirk was referring to, it activates the natural killer in cytotoxic T cells. So IL-2 is kind of asking for help, getting help from the natural killer in cytotoxic T cells. And then your IL-4, this is what tells the B cells to produce antibodies. So it tells the B cells to turn into plasma cells to make antibodies. So IL-4 makes antibodies.
It encourages the production of antibodies. And then Jason, how about IL6, 8, and 10? >> So, IL-6 is the, this is your acute phase reactant, so it increases hepatic acute phase proteins. That's 6. Number 8, IL-8, induces the PMN, chemotaxis, and angiogenesis. So IL-8 attracts neutrophils essentially and promotes angiogenesis. IL-10 is kind of a suppressor.
It down regulates the immune system. >> So it's kind of the somatostatin of the interleukins. >> One could say that, Kevin. >> All right, and now we're going to jump straight into antibodies. So, Jason, which interleukin increases the production of antibodies? >> That would be IL-4. >> Right. So you're going to make, it has B cells turn into plasma cells, and there's just a couple commonly asked questions about antibodies. So what is the most common antibody in that it crosses the placenta to provide protection to newborns?
>> The IgG. So IgG is the most common, crosses placenta, provides protection to newborns. >> And how about the most common one to be found in breast milk and is also in secretions and mucosal linings? >> So that's IgA. So IgA is the one that kind of coats the mucosa and is the first line against things that you ingest. >> And it binds pathogens, prevents adherence and invasion. And then for our type hypersensitivity, and you also see this used with parasite infections, which is that?
>> So it's your IgE. >> It binds the mast cells and causes release of histamines and the rest of it. And then our last one is the largest antibody, it's actually IgM, and primarily responsible for the immune response. It does not cross the placenta. It is the primary antibody in ABO incompatibility, and it causes red blood cell clumping. It's also the most common antibody in the spleen and responsible for the patients that get the overwhelming post-splenectomy infection, the lack of this enzyme allows them to get the OPSI.
And now we're going to jump into the hypersensitivity reactions, and these are pretty straightforward once you have them memorized. So Jason, we kind of referenced this one. You know, your friend that eats the peanuts and is peanut allergic, what's happening in them? >> So this is your, and again, this is just rogue memorization, so that's why we're going through it this week. So this is your type one hypersensitivity reaction. It has to do with IgE binding to mast cells. You get a mass histamine release, which causes bronchoconstriction, rhinorrhea, flushing, hypotension.
It's your anaphylactic-type response. >> That's thanks to IgE, and what do you do for the treatment of that? >> So this is, you know, first and foremost, airway management and then you have your antihistamine, steroids, and epinephrine. >> And then type two, when do you see this happen? >> So type two is an antibody dependent transfusion reaction. Or, I'm sorry, antidependent reaction, and you see this, which is a transfusion reaction. So this is due to IgG and IgM.
So the antibody binds to the cell-bound antigen, and it stimulates macrophages, neutrophils, natural killer cells, and eosinophils, and it also activates your complement system. >> And this is the job of our adaptive immune system, to cause a type two reaction to foreign antigens, so you can kind of remember it that way. It's a good thing most of the time. And then these last two, they're just only testing questions. You see the type three hypersensitivity, Jason, when do you see this?
>> So this is your serum sickness, and then you also see this with lupus and-- yeah, yeah. So you see this with your serum sickness or in lupus, so it's a complex of the antigen and antibody, that deposits in the vessels walls and induces inflammation. >> And you can treat this with steroids, antihistamines, and plasmapheresis. So, yeah, if you see serum sickness on the test, type three hypersensitivity. And then last but not least, our type four hypersensitivity, Jason.
What is the classic question, they're going to have a med student that has to get this done every year. >> Yeah, so they're going to ask about the wheel that is raised when you get your PPD checked, you're tuberculosis test. They're going to ask what type of reaction is it. It's a delayed hypersensitivity reaction. It's T cell mediated through your T cell immune response. It's antibody dependent, and it's a type four hypersensitivity reaction. >> And so the type four, you also remember, this is the chronic rejection in organs, organ transplant, and we actually, there was a question on one of the question banks talking about this with liver transplants.
They don't have much acute rejection, but you'll see the vanishing bile ducts with the chronic rejection. That's a type four hypersensitivity. And so Jason, we're just going to have all the listeners out there, I know they really to quiz themselves here. So we're just going to do a quick rundown, and we're going to go out of order here. So, what do you guys think the function of IL-6 is? >> Am I supposed to answer now? >> Yeah, just give them like a second so they can think of it in their head and then-- >> Got you.
We'll they've had a second. IL-6 increases your acute phase reactants, the hepatic acute phase proteins. >> IL-4. >> It increases B cell antibody production. >> IL-1. >> IL-1 gives you a fever, and it's released by macrophages. >> IL-10. >> The infamous somatostatin of the interleukins. It down regulates the immune system.
>> Yeah, I coined that term. IL-2. >> IL-2 activates your natural killer and cytotoxic T cells. >> And IL-8. >> IL-8 attracts neutrophils, so it increases PMN chemotaxis and angiogenesis. >> Now that the pain of interleukins is done, we're going to jump into another painful, maybe slightly less painful topic, but commonly tested topic, wound healing. So Jason, what are the three main stages of wound healing?
>> So your stages of wound healing, first inflammation, which makes sense. You need to attract all the right players. Two, proliferation. Three, is your maturation and remodeling phase. >> And what is sort of the time course that these are taking place? >> So, inflammation typically happens in your, you know, the first, the first few days, within four to six days the inflammation phase is generally complete. And then there's a little bit of overlap, and then, you know, your proliferation, and all the cells are making all the stuff they need to heal the wound, and this happens anywhere from four days to about three weeks.
And again, a little bit of, or a little bit of overlap, but then the remodeling phase kicks in at about three weeks, and this can continue on for years. >> So, the question that's pretty much guaranteed to be on the test is the order of cell arrival. What is the first cell that recognizes the endothelial damage and will be at the site of injury? >> Yeah, this is a common one, and it's always tempting to say neutrophils, because you know neutrophils get there fast in inflammation, but if you think about an injury, the first cells there are the platelets.
The platelets come in. It's immediate. It's short lived. They release your alpha and dense granules, which have your transferring growth factor, and your platelet derived growth factor, and they start attracting all the right cells there to heal the wound. >> Yeah, I've talked myself out of this one before thinking it was just hemostasis related, but platelets are very important for wound healing. >> Yeah, order of cell arrival, first is platelets.
Next come the neutrophils. So, and this is in the first couple days, first 48 hours, the predominant cells is neutrophils. From then, the macrophages come in, and these are some may say the most important cell for wound healing. >> Yes. >> And this typically happens about three to four days. So they release more factors, more platelet-derived growth factor, TNF alpha, interleukin-1, they attract, you know, the cells that are really going to rebuild the wound, so the fibroblast, and they're also very fundamental in removing debris during this time period.
>> Yep. So I think platelets and neutrophils are there for the inflammation phase primarily, and then you have your macrophages that are coming in, and they're the main player in the proliferation phase. And then we have our fibroblasts and our lymphocytes. What do fibroblasts do, Jason? >> Fibroblasts help create your collagen and all, you know, the structural elements that are going to reheal the wound. >> What vitamin is essential for collagen production? >> Vitamin C.
>> Oh, and then another important thing is what is the most common, the one thing they always ask is which is the most common, or the most important cell for wound contraction? >> That would be the myofibroblasts. >> And when do those come in? >> So that will happen during the proliferation phase, about 10 to 15 days out, and then one thing they talk about frequently is epithelialization, and this occurs most commonly from actually the hair follicles. So the hair follicles are the source of epithelialization, but it also comes from the wound edge and the sweat glands.
But it requires granulation tissue to be there before epithelialization can occur. And then, Jason, we can't forget to talk about type three and type one collagen. >> All right. This always comes up. >> So, collagen deposition by fibroblasts provides the wound strength. So what is the initial collagen that is produced in the first 48 hours? >> So it can get a little tricky depending on how they ask the question. So in the first 48 hours, the most predominant collagen produced or the type of collagen that's getting made the most is the type three.
So type three is the highest produced during that time period, but it's important to remember that type 1 is always the most common and the most predominant. >> So it's going to vary depending on if they're asking you which is the most type being produced or which is the most predominant in the wound. >> And when is the peak strength of a wound? >> So, the peak strength occurs at about eight to 12 weeks. >> Is it as strong as the previously undamaged skin? >> It's never going to be as strong, but it reaches about 80 percent at eight to 12 weeks.
>> And one kind of last point on wound healing, to touch back, how do steroids prevent wound healing? We have those patients that Crohn and ulcerative colitis patients that are getting their surgeries done. So we talked about the most important cell in wound healing is the macrophages. So steroids actually inhibit the macrophages, the neutrophils, and the fibroblasts from getting to the wound. So we can understand how steroids would prevent wound healing, and Jason, how do you prevent this complication, at least theoretically?
>> Well, theoretically, you can give some vitamin A, and this helps with the steroid inhibition of wound healing. >> Okay, our next high-yield topic is going to be related to nutrition. We got a lot of requests for this. Specifically, the mineral in vitamin deficiencies. So, again, this is just memorization, but these can be quick, easy points you can pick up, as long as you just go through these right before the test. So, Kevin, I'm going to name some symptoms, and you're going to tell me what vitamin or mineral deficiency is associated with that.
So, for hyperglycemia, encephalopathy, and neuropathy, what do you think? >> Goes straight to chromium. >> That's right. >> So all diabetic patients. No, I'm just kidding. >> For a cardiomyopathy and just generalized weakness? >> The cardiomyopathy question is selenium. And Jason, just to turn that around on you, what is the chemotherapeutic that can cause a cardiomyopathy?
>> That's doxorubicin. >> Good job. >> And at what dose, what cumulative does that become important? >> Oh, you got me beat there. >> And that occurs due to toxicity secondary to O2 radicals, and it occurs at a cumulative dose of 500 milligrams per meter squared. Believe it or not, that does show up every once in a while on the test. >> And he did just look that up. >> I kind of knew it.
Okay, so let's say they give you somebody with a pancytopenia, and they ask you what mineral deficit. >> Then you want to start thinking about their copper. >> And as we were just talking about, wound healing. So somebody has poor wound healing. And you can see this sometimes with people on TPN. >> Yeah, they can get a zinc deficiency. So make sure you're clicking that little box that says replace trace elements, because that'll get them their zinc.
>> Yep. So let's say they ask you encephalopathy, decreased phagocytosis, but a really important one is weakness and failure to wean off the ventilator. What do they need? >> So, the weakness and encephalopathy and a common question kind of related to this is the kind of prisoner of war patient that eats a high-glucose diet. They're going to be low in their phosphate. >> Yep, definitely. >> So, if you're having a hard time weaning someone off the ventilator, and they're CO2 is just too high, what could this be related to?
>> So that's hugely usually overfeeding, and so they have too high of carbohydrates, so they have more CO2 to get rid of. >> So, what kind of respiratory quotient would you see with that? >> So, typically those respiratory questions are going to be greater than one. >> Yeah. >> Like 1.2 is kind of the answer on the test. What's a fat-dependent-- >> So fat's generally about 0.7. >> Yeah, and kind of the ideal they say is like a respiratory quotient of like 0.85. Okay. Back to vitamins.
>> And I actually have a little mnemonic for remembering that because they'll ask, a lot of times on the test they'll give you a respiratory quotient, and they'll ask you what the predominant thing in their nutrition is, and so typically it's either fat, protein, or carbohydrate, so it goes in that order. Fat 0.7, protein 0.8, and carbohydrate 1.0. And my little stupid mnemonic for memory that is feeding produces CO2. So FPC in that order, 0.7, 0.8, and 1.0. >> Fantastic.
>> That's a free one. You can use that one and tell your friends. Okay. Back to our mineral deficiencies and symptoms, so what's associated with Wernicke's encephalopathy and cardiomyopathy? >> Yeah, that can, this is, you want to think about the alcoholic patient, and they'll have a thiamine deficiency, which is what vitamin, Jason? >> That was one of your B vitamins, your B1. >> B1, so thiamine, B1, Wernicke's encephalopathy, cardiomyopathy, think of the alcoholic patient.
>> Yeah, how about somebody with peripheral neuropathy, glossitis, and sideroblastic anemia, if you even remember what that means. >> Yeah, I have no clue what sideroblastic anemia is, but I do remember glossitis and peripheral neuropathy being a pyridoxine or a B6 deficiency. >> Okay. Going on. So what about a megaloblastic anemia, a neuropathy, and your red, beefy tongue? >> Right. So there's two things this could be, but because you said peripheral neuropathy, I know that this a cobalamin or a B12 deficiency.
>> Now what about if I didn't say peripheral neuropathy and I just said megaloblastic anemia and glossitis. >> Yep. If it's just a megaloblastic anemia and glossitis, it could be folate or B12, so they'll give you the peripheral neuropathy to differentiate normally. >> And what's the, what is that neurologic test where your posterior cord, where you close your eyes and you put your hand and you can't-- the Romberg sign, is that right? >> Oh, yeah, yeah, I think that sounds about right. >> I think I'm thinking back to my step one, step two, med school days.
>> Clearly scored higher. >> Well, that goes without saying. How about the old pellagra, the diarrhea, dermatitis, and dementia? >> This is what I feel like I get on the day of the ABSITE, and so that is generally a niacin deficiency. >> Okay, so real quick then, how about some vitamin deficiencies. So, what do you get with vitamin A deficiency? >> Night blindness. >> Vitamin K.
>> Coagulopathy. >> And that's something we deal with frequently, so everybody should know that one. >> Now is that your PT or your PTT? Oh gosh, oh my gosh, I think that's your PT. >> Yes, is that the intrinsic or extrinsic? >> That is your extrinsic pathway. >> Yep. And does warfarin or heparin influence that? >> Warfarin. >> So, yeah, so remember, that can be on the test.
I use WEPT, warfarin, extrinsic PT. So you can remember, you know, if it acts on the extrinsic or intrinsic system and which it'll affect. >> Excellent, okay, moving on. Vitamin D. >> So, this is the bone problems, you're going to get the rickets, osteomalacia, and osteoporosis, and out here in Seattle, this is a serious problem right about now. >> And last but not least, vitamin E. >> Vitamin E, the test question is you can get a neuropathy.
Maybe it's just me, but I hate the functional endocrine pancreatic tumors. So, Jason, let's just try and help our listeners out as we learn this with them. If you have a patient that is coming in with fasting hypoglycemia symptoms of palpitations, increased heart rate and diaphoresis that is relieved with glucose, and they have a tumor in their pancreas, what are you concerned about? >> So that's the classic Whipple's triad, hypoglycemia, symptoms of hypoglycemia with palpitations, increased heart rate, diaphoresis, relieved with glucose, and you think about a, well you think about Munchausen's syndrome, so you need to check for a C-peptide.
So, the C-peptide should be increased as well if you're thinking about a functional neuroendocrine tumor. So this is the insulinoma. >> And the reason the C-peptide should be high is because this is a normal byproduct of insulin. So, if insulin is being used and produced endogenously, it'll increase the C-peptide. Exactly. So this is actually the most common islet cell tumor of the pancreas. Unfortunately, most of these are benign, about 90 percent of them are benign, and these are evenly, you know, a lot of times they'll ask you the neuroendocrine tumors, it depends on where they're located, raises your suspicion for different things.
The insulinomas are evenly distributed throughout the pancreas. So how do you treat this Kevin? >> So, if they're less than 2 centimeters, you can enucleate them, or if it's greater than two centimeters, you should do a formal resection. >> What about if it's metastatic? >> If it's metastatic, that's when you'll put them on chemotherapy with either 5FU, streptozocin or octreotide. >> Okay. >> And Jason, just quickly, what are the two common neuroendocrine tumors that you see in the head of the pancreas?
>> So, the head of the pancreas, it's somatostatin and gastrinoma. >> Yep. So, you should keep that in the back of your mind here as we keep going through these. >> So, speaking of gastrinoma, what's the gastrinoma triangle? Do you remember that? >> Yeah, since I have Pfizer here, it's the common bile duct, the neck of the pancreas, and the third portion of the duodenum. So, that is one of the questions when they ask you about gastrinoma. They are probably going to ask you where it is located, and that is where you will find it.
And Jason, what syndrome can you find this in? >> So this is in your MEN syndrome, your MEN1, where it's pituitary, pancreas, and parathyroid. >> And what is the gene for MEN1? >> That's the menin gene. >> And what do you want to treat first in a patient that has MEN1? >> For those, you want to first address the parathyroid hormone, or the parathyroid hyperplasia.
>> Okay, and back to gastrinomas now, which are a part of MEN1. These can be 50 percent malignant and 50 percent obviously benign, and sometimes there are multiple of them. And so there are test questions on how you diagnose this. Jason, what is the stimulation test that you can do? >> Well, yeah, before you do that, the first thing you do is just test the serum gastrin, because if you have serum gastrin levels over 1000, that's typically diagnostic.
However, if they're kind of in that gray zone, you can do the secretin stimulation test. Now, interestingly, secretin normally will decrease your gastrin production, but in a gastrinoma, it actually increases, so they get an increasing gastrin over 200 with the administration of secretin. >> And since you brought it up, where is, what is the cell that secretes secretin? >> So, secretin is from the S cells, and those are located in the duodenum.
>> Fantastic. And then what if, what kind of scan can you do to identify if you're, you're-- you do your secretin-stimulation test, and the gastrin elevates with that paradoxically, what, but you can't find it. There's no real good lesion seen on MRI. What do you want to do? >> So, you can do an octreotide scan that can bind to the octreotide or the somatostatin receptors and help you localize it.
>> Great. >> And then this is the same for, is insulinoma less than 2 centimeters you can enucleate and greater than 2 centimeters for more resection. All right. We just have two more tumors left or maybe three. We'll really quickly go through these. So, Jason, you have a patient that comes in. They've got diabetes. They've got that stomatitis, and they have a dermatitis, and they also have this rash going throughout their body.
Their glucose is crazy elevated. What are you concerned about? And they have a mass on their pancreas. >> Yeah, so this is, and I've seen this on the test several times, and they always have the rash, they always have the dermatitis. So that's kind of the giveaway, the diabetes and the dermatitis and the pancreatic mass. This is a glucagonoma, and so you get your diagnosis by doing a fasting glucagon level. Typically, these rarer, I mean these are very rare, and with these rare pancreatic tumors, it kind of makes sense that the rare ones are the more malignant ones.
So mostly these are malignant, and they're located in the distal pancreas. >> Perfect. And now you have a patient coming in, they also have diabetes. They have some gallstones. They have some right upper quadrant pain, steatorrhea, and hypochlorhydria, and a pancreatic mass. What are you concerned about? >> So, again, these are very rare. This is the other one that's common in the head of the pancreas.
This is your somatostatin tumor. Diabetes, gallstones, steatorrhea, hypochlorhydria, and a mass at the head of the pancreas. >> What is the, so somatostatinomas are in the head of the pancreas. What is the other one commonly found in the head of the pancreas? >> Well, aside from adenocarcinoma, but for your neuroendocrine tumors, it would be a gastrinoma. >> Right. And last one, patient comes in with watery diarrhea, hypokalemia, and achlorhydria, what are you concerned about?
>> So that is the WH, or sorry, WDHA syndrome, and that's a VIPoma, otherwise known as Verner Morrison Syndrome. And these are the other ones that are rare, very rare, so rare goes along with malignancy, and these are located in the distal pancreas. So just briefly, so again, overview, neuroendocrine tumors, location, insulinoma, throughout the pancreas. Your ones in the head of the pancreas are your gastrinoma, your somatostatinoma.
Distal pancreas are your glucagonoma and your VIPomas. Malignancy potential, insulinomas normally benign. Gastrinoma, 50/50. The rest of them, usually malignant. >> And for the handful of you that are still listening, we're going to talk about one last painful category, and that is nutrition relating to calories and formulating TPN for patients. This is guaranteed to be on the test. So, Jason, just quickly, how many calories per gram are there for fat, protein, and carbs?
>> So, fat has 9 kilocals per gram, protein 4, carbohydrates 4, and then dextrose is the only kind of weird one, 3.4. >> And why is that important? Like who cares? Are they going to ask us what is the calories per gram? >> They are actually in a roundabout way. So invariably there is a question where you have to calculate the TPN calories. So, they'll give you somebody who has a thousand cc bag of TPN with 20 percent dextrose, 7 percent protein, and 250 cc's of 20 percent fat emulsion, and they're going to ask you how many calories are in there.
So, how should we go about tackling that question, Kevin? >> Right, so you know that it's a liter bag or 1000 cc's, and so 20 percent of it is dextrose. They told you that, they gave you that. So you do what is 20 percent of 1000? That is 200. So you're going to have 200 grams of dextrose in the bag, and Jason, what did you say? How many calories per gram of dextrose there is? >> So dextrose has 3.4. >> So 3.4 times 200 will give you 640 calories for dextrose, and you do the same for protein, which is 4 kcals per gram.
>> So they tell you you have seven percent of protein. So you take, you know, 0.07 times 1000 and that gives you 7 grams. And then you multiply that, your grams times your kilocals per gram at 4, and that gives you 280. So, yeah, you know, the fat emulsion is where things get a little tricky. So they're going to give you, either, you know, 250 cc's of either a 10 percent or a 20 percent fat emulsion, and you'll just have to know that that fat emulsion either has 1 kcal per cc or 2 kcals per cc depending on how [inaudible] 10 percent or 20 percent.
So you just multiply that by the number of cc's they tell you. If it's 250, if it's 500, you know, whatever. So in our little example we give of a 20 percent fat emulsion, 2 kcals per cc times 250 cc's, that's 500 calories. >> And one thing to remember, they'll sometimes have peripheral TPN versus central TPN. So TPN will actually have high percentages of fat in the solution. So you get the calories up because the carbohydrates are actually venotoxic and can cause sclerosis of the veins.
So the carbohydrate content will be lower in the peripheral solutions. >> So these are invariably on there every year. I would advise everybody to just go through a couple sample problems. You can find them online, of just calculating the number of calories in TPN, because that's an easy, it's a painful point to miss if you don't do it, and it's an easy point to pick up. >> And so, Jason, first of all, how many calories does a patient need per person per day? >> So, for a normal person 25 kcals per kilogram per day.
>> So a patient undergoes a colectomy, how would you adjust their calorie needs? >> So, for, that's a, you know, a moderate stress, so, you know, they don't need much of an adjustment. So those patients typically get 25 to 30 kcals per kilogram per day in calculating the caloric need, and about 1.5 grams of protein per kilogram per day. >> And we actually didn't say that. What is the normal amount of protein a patient needs at-- >> Typically one. >> Yeah 1 gram of protein per kilogram per day.
And so, let's say that actually you personally did their colectomy, and now they're critically ill. >> Oh gosh. >> What is their caloric need for a critically ill patient? >> So critically ill patients are a little bit more. So that's about 30 to 35 kcals per kilogram today, and that'll bump them up to the 2 grams of protein per kilogram a day range. >> Yeah, so think about 150 percent up to almost 200 percent of the need for a critically ill patient, and then the burn patient, this is the patient that's going to need heavy amounts of nutrition.
They're going to need the 30 kcals per kilogram per day times the percent burn onto their normal caloric need of 25 kcal per kilogram per day. So, Jason, what if a patient has a 20 percent burn, how many more calories are you going to give them? >> So, for a, so I'm going to give them, first I'm going to calculate their just normal intake, their 25 kcals per kilogram per day, and then I'm going to add on top of that 30 kcals per day times a 20 percent burn, which, I don't know, that math, what does that math come out to be, Kevin?
>> Six hundred. >> So, yeah, so and that's an extra 600, you know, calories per day added to that. And then you add 3 grams of protein per percent burn, again, added on. So they have very high caloric and very high protein needs. >> And normally these are those questions that'll have like four questions based off one, and you have to adjust for each individual patient. So, you think of just normal really not much increase at all for the lap chole patient. The patient that's critically ill, you're going to go about 150 percent, and then the burn patient you're going to go at least 200 percent plus of their normal needs.
And there are multiple requests out there for us to go over statistics. That would first require us to understand statistics and then second to be able to describe it over the radio. >> Yeah, you do not want us teaching you statistics, I promise you. >> Yeah. So the only thing I'll tell you guys about that is at least 80 percent of the statistic questions it's going to be based off that little quad table, and you just have to know how to calculate the positive predictive value, the negative predictive value, sensitivity, specificity. If you know that and you've done some other practice questions in statistics, you'll do okay.
>> Yeah, the stats on the ABSITE are not that involved. So typically if you can navigate a two by two table rather proficiently, you'll be alright. >> And then the one other thing that we've heard from some of our listeners and what they do to prepare for the ABSITE is some of this painful stuff that we just talked about, you should probably listen to it on your way to the ABSITE, so it's fresh in your mind, but you can also kind of draw out a little cheat sheet for lack of better words, but you do not bring into the test, but you look at right before the test.
So, Jason, what kind of things would you put on that cheat sheet? >> So, again, the, you know, there's always that graph, the pulmonary volume, what do you call it? The pulmonary volume-- >> Chart. >> Chart. Where you have to, you know, the inspiratory volume, the expiratory volume-- >> Volumes and capacities. >> Yeah, volumes and capacities, that's always on there. And it's something we don't really deal with on a day-to-day basis.
So I would just look over that chart and make sure I have my different volumes and capacities and the different formulas for, you know, what goes into the different capacities, what volumes go into each different capacity. >> That would get your question right on the test. >> That would give you a couple points. >> And then like we just talked about the calculating caloric needs for patients, and then, you know, look over the GI hormones, and then look over the staging for colon and breast cancer. That'll certainly get you a couple of points, and thyroid cancer is pretty commonly knowing about patients under 45 and how that makes their cancer treatment different.
Yeah, so just basically anything that is sort of rote memorization, and that way you can go into the test having it fresh in your mind. Well, thanks for listening this long, and we're going to start sending out our pins again after the ABSITE. We have had some requests. So just send us an email if you want one of our cool Behind the Knife pins to wear on your white coat or whatever you wear at your hospital. And we'll start getting those out after the ABSITE. And we look forward to, we have a great year of podcasts coming up for you in 2016.
>> Until next time, thank you for joining us on Behind the Knife, The Surgery Podcast. Dominate the day. [ Music ]