DIP Episode 186 - Updated USMLE Step 1 GI Review Series 2

Okay, welcome. My name is Divine, I'm a resident. This is episode 186 of the Divine Intervention Podcast. And in this podcast, I'm going to be continuing the comprehensive review series for GI for the USMELISTPON exam. So let's get ready into it. So what if you get a question about a child? Is it this child is 96 hours old? And this child has not pooped. What's your diagnosis there? That's herch-prone disease, right? That's herch-prone disease. And and this child right, likely has, I mean, because think about it, when are you supposed to pass your first poop by? Within the first 48 hours, right? So the thing that has essentially happened to this kid is this kid has like failure to pass my conium and there are many things that can cause this, right? Like you can have herch-prone disease cause this. Remember herch-prone disease is like a problem with like neurocressol migration, right? So like the albax plexi and the Meisner's plexi, you don't find them. Remember, the Meisner's plexis is what's known as the subucosal plexis. The albax plexis is what is known as the myenteric plexis. You'll find it between the inner circular and the outer longitudinal layers of the of the muscularis external, right? So if you have like those the Meisner's and albax plexi that are right from neurocressol. So if you have problems with neurocressol migration then you have herch-prone disease.

And remember that herch-prone disease is fairly common in kids that have a history of Down syndrome, right? And I guess since I'm kind of talking about Down syndrome, let me sort of mention some high-yield things, right? So they can give you a question about a kid with Down syndrome that's having like chronic small bowel obstruction. What do you think is causing that? Well that's an anula pancreas, right? I'll talk about that in a in a later podcast. What if they give you a question about a kid that has a history of Down syndrome and this kid has billions of omitted? Well I hope you're thinking about Dordinal atreisure. Remember that classically described double-bubble on imaging. Now what if they give you a question about a kid with a history of Down syndrome? And they tell you that this kid is at the fifth percentile for a weight and this kid has like secondary hyperparathy, or it is in from like a vitamin D deficiency. And then they tell you that this kid has like a rush on extensive surfaces of the upper extremities. A key in like dermatitis or perteforms. What are you thinking about? Well I hope you're thinking about celiac disease, right? And then what is the most common cardiac congenital anomaly in case with a history of Down syndrome? That's all that's a endocardial cushion defects, right? And then don't forget that Down syndrome is also associated with early onset Alzheimer's, okay? Very high yield to nodules fins. With Down syndrome, right?

It can also cause her spurns disease. And remember I also said in the podcast from yesterday that if a person has... I said yesterday that if a person has a history of triplosomacruzia, triplosomacruzia, can destroy the albax amizolous plexia that you find in the distal GI tract and that can also present as rush from disease. Now the thing is when people have rush from disease, right? Let me say okay, why does it matter if I don't have the amizolous plexia or the albax plexia? Well, if you don't have those fins, right? Then you have problems with peristosis, right? And if you don't have peristosis, then you're kind of screwed, right? You're kind of screwed because, essentially, the thing that will happen is food will just kind of hang out in that portion of your of your GI tract. So that's very important to understand. Now, one weird thing you want to keep at the back of your mind with, rush from disease is that it can also be caused by a rect gene mutation, right? So you see, how is that possible? Well, the thing is remember that most of your GI tract includes something known as the enteric nervous system. The thing is when you have like a loss of function mutation in the rect gene, that actually messes up with the proper development of the enteric nervous system. So that can increase the person's risk of, of herchpoint disease.

Although remember, reg gene mutations, you can also see them in the MEN2 symptoms, like MEN2 A, where people have like the parapyramory hyperparapyroidism, fiochromocytoma and medallary thyroid cancer, and also in MEN2 B, where people have like the fiochromocytomas, medallary thyroid cancers, you cause all neuromas, right? And then they have the marphorneid body habitus. Now, what did they give you a question about like six-day-old newborn, okay? And this child has been having like bilia's vomiting. And then let's say the MEN2 A kind of puts up like a picture for you. And the picture you notice that you don't see a double bubble in the picture and you don't see a triple bubble in the picture. What diagnosis should you be thinking about? Well, I would really hope you're thinking about some kind of marrotation with mid-gott volulose. That is the classic presentation on M Gaming Exams. They'll give you a question about a newborn that has bilia's vomiting. And then they will give you a picture that usually most met students cannot interpret. So the algorithm I give people for dealing with those kinds of questions is if you see bilia's vomiting in the newborn, there are three things you should have on your differential. Mid-golf volulose, Duanella trisia and Jijunella trisia, right? The thing is that my rotation with mid-golf volulose typically the image is not something you can interpret.

But I feel like most people can identify the double bubble that we find with Duanella trisia and a triple bubble that we find with Jijunella trisia, right? So if you look at the image they give you and you don't see a double bubble or you don't see a triple bubble, then go ahead and pick my rotation with mid-golf volulose. This algorithm works not just well for step one, it also works pretty well for step two CK, right? So that is one kind of volulose that you may find on in-game exams. Well, another kind of volulose you may find would be more in the elderly population. You can see things like sycovovulus, you can see things like sigmoid volulose, okay? So sycovovulus and sigmoid volulose. So you may see, oh, divine, how do I identify those on in-game? Well, the thing is it will present in an old person and the person will have like signs and symptoms of like a large bowel obstruction and typically one thing they will do on the exam is they will show you an image and illustrate something known as the coffee bean sign. In fact, for those of you that are studying for step one, there's a podcast actually have known as USML radiology. It's one of like the earlier podcasts on my website just again, good to the search box in my website and type in radiology. You find the podcast is like a 20, 30 minute podcast. It highlights many of the high-yield images that you do need to be able to identify for purposes of the USML exams.

So the thing is the coffee bean sign is pathonomonic on in-bim exams for sigmoid volulose and sycovovulus. But you may see, oh, divine, how do I differentiate between the coffee bean sign for sigmoid volulose versus the coffee bean sign for sycovovulus? Or here's the deal. When a person has sycovovulus, the typical part like the top of the coffee bean will be oriented towards the left upper quadrant. But if a person has a sigmoid volulose, the top of the head of the coffee bean will be oriented towards the right upper quadrant. Very high yield to know those things for you exams. And really what is a volulose? Well, because it's just twist in ring, basically the column kind of twists around the mid-entry and the thing is that will cause like a bowel obstruction. But another thing that can happen is remember that the blood vessels that feed the GI tract to run within the mid-entry. I will talk about the mid-entry when I do the GI embryology podcast. But basically, if you have the column kind of twisting around this mid-entry, that can kick off those blood vessels and that can cause a skimia like your skimic bowel disease. So just something to keep at the back of your mind for exams. Now, what if they give you a question about a patient and they tell you that, oh, this patient, you know, he was studying for like an organic chemistry exam.

And then this person presents with like studying on set severe abdominal pain around the umbilikus and then it's beginning to migrate down towards the right lower quadrant. What are you thinking about? Well, I hope you're thinking about appendicitis, right? Appendicitis. Remember, appendicitis, the appendix is actually high year for two pathologies on Indian exams. One pathology is appendicitis, right? And what causes appendicitis? Well, the thing is that if you have, at least there's this common concept that you've seen me talk about at Nazimim mini podcast, right? Whenever you have an obstruction, infection and inflammation can always build up behind that obstruction. So when a person has like the appendix obstructed by a thick lift, basically it's just like very thick, almost like, I think of it as like a feces like a poop stone, basically, when you have like the appendix are obstructed by a thick lift, right? Then that obstruction infection can build up behind it and then you get appendicitis. That's usually what happens in adults. But in kids, the thing is, kids can have like a GI like viral infection and then that GI viral infection will lead to like a hyperplasia of like the mucusa associated lymphoid tissue that you find in the appendix. And that hyperplasia can then almost serve as like a lip point for like a ton of inflammation and then those kids have appendicitis. And the thing is for appendicitis, right?

So big things you want to keep at the back of your mind at a physical exam findings, right? So you want to make sure for sure, remember your McBrennie's point. Remember, McBrennie's point is like two thirds of the way. So start at the umbilikus, right? It's two thirds of the way going from the umbilikus to the anterior superior iliac spine, okay? That's my brain's point. You typically have tenderness over that region in a person that has appendicitis. And then appendicitis, there's this thing known as soas sign, where if you like extend the person's hip, it causes severe pain, right? Soas sign is pathonomonic as well as a pathonomonic mbme physical exam finding for appendicitis. And then there is something also known as rough sin sign, right? Where if you press on the left lower quadrant, it exacerbates the right lower quadrant pain. That's pathonomonic for appendicitis. So those are all high yield things you want to know on your exam. Really for the most part like how do you make the diagnosis? If it's a child, you don't want to expose them to like significant amounts of radiation or I mean if you want to avoid radiation ultimately, right? You can do an ultrasound in kids, right? But if you see it in an adult, you know you go ahead and do a CT scan. Appendicitis is really pretty classic when a CT scan and then you go ahead and send the patient to surgery. And remember that when a person has appendicitis, they can have certain complications, right?

They can have like ruptured appendix or they can develop an abscess, right? A peri appendicitis, abscess. Usually for that you want to go ahead and drain that abscess and then you also do an appendectomy under those circumstances. Now the thing is when a person has appendicitis, when the surgery is done, it's actually very high yield to know for the purposes of the USMLA exams that when you do surgery for appendicitis, you can actually damage a nerve known as the iliohypogastric nerve. If you damage the iliohypogastric nerve, that will classically present the hotel you that oh you know, weeks after the person had surgery for like the appendicitis, they have like this burning sensation around the bladder or along the like around the inward origin. If you see that, think about damage to the iliohypogastric nerve. Now the other hyalurgy that you need to know in relation to the appendix for NVMA exams is that the most common location of carcinoid tumor in the GI tract is actually in the appendix, okay? That's a very high yield factor to know for exams. And then let me just take a small sidebar here and kind of talk about like the flora that's typically found in the colo. The thing is, your colonic flora is actually useful, right? They help you make things like vitamin K, right? And they also place some roles in the treatment of arthritis in a sense and the current disease. I'll talk about that in a bit.

But basically, the most common flora in your colon is actually B-frag, right? So bacteria's fragile is remembered as an anion. And then the second most common is actually E-coline, right? And then, there are many other things you find in the colon like CDF, CDB, it's actually part of your normal colonic flora. The area where you get into trouble is when CDF overgrows, right? But like proteors, savonella, shigella, clepsiela, those are all things that make up your normal colonic flora, okay? And these things, I mean if they overgrow again, they can cause like a big time lactic acidosis because they break down sugars into lactic acid, right? Because remember, many of these organisms are anaerurves, so they participate in fermentation. And one of the big end products of fermentation is lactic acid, right? So again, just all the important things to know for your exams. And then yesterday I kind of talked about the pectinic line, I think I should, you know, kind of highlight it again today. The thing is the pectinic line basically is a very high yield important line you want to keep at the back of your mind for the USMD exams. Sometimes you may see it referred to as the dentic line on MDM means, right? So what's what why do you need to know about the pectinic line? Well, the thing is the pectinic line cannot demarcates that it's like a line you'll find around the distal parts of your GI tract, right?

And the thing is above the pectinic line, everything that's around that region is derived from endoderm, what below the pectinic line, everything that is derived from there is derived from ectoderm, okay? So the thing is proximal to the pectinic line, everything there is derived from endoderm, and the thing is the t-shirt above the pectinic line tends to have visceral innervation. So because it has visceral innervation, those things tend to not be painful, okay? So if, for example, a person has like an internal hemorrhage, internal hemorrhage are above the pectinic line because they just have visceral sensation, they're not painful. So for those internal hemorrhages, you can kind of treat them in the office, it wouldn't be given any kind of anesthetic, and the patient will be fine, they will not feel any kind of pain, they'll just feel like a pressure like sensation. Now another high yield thing to know is when a person has like some kind of malignancy above the pectinic line, that will typically be an adnocarsinoma, right? Because again, it's endodermal t-shirt. Contrast this with a cancer below the pectinic line that will likely be a scrimous cell cancer. And one other thing your friends at the MVM, unfortunately, want you to know, is to know the difference between the arterial supply above the pectinic line and the arterial supply below the pectinic line. Above the pectinic line, the arterial supply is exactly from the superior rectal artery.

Remember that the superior rectal artery is actually a branch of the inferior mesenteric artery, right? Remember, inferior mesenteric artery is one of the big branches of the abdominal ear, right? And it's the blood supply to the hind leg. But in terms of venous drainage, if you remember the arterial supply, you automatically know the venous drainage. Basically for the area of the GI tract above the pectinic, at least the area of the rectum above the pectinic line, basically you have the superior rectal vein draining that region, right? And then that superior rectal vein dumps into the inferior mesenteric vein. And then the inferior mesenteric vein ultimately dumps into the poro vein. So again, very high you to know this. And again, like really the nerve supply for the most part is like the inferior hypogastric plexus. The inferior hypogastric plexus is the nerve supply to the region of the rectum above the pectinic line. Now, below the pectinic line, again, like I said, that's the right from actoderm, right? So if you see like cancers there, that'll be a scrimousel cancer. And typically those regions of the GI tract contain carateneized stratified scrimous epithelium. Contrast that with the non-carateneized stratified scrimous epithelium that we find in the asophagus. That's one. And the thing is, what is the biggest risk factor for homolognancy? Like the scrimousel cancers you'll find below the pectinic line. Well, I hope you're telling me HBV, right?

Huma and papilloma virus. Remember, HBV makes like E6 and E7. Those are like ubiquitin like easy. So those target like B53 for destruction. Right? So the HBV's like HBV like 16, 18, those in the 30s, those increase the presence risk of scrimousel cancer. Right? And the thing is the region of the rectum below the pectinic line actually has somatic sensations. So things are like super, super painful. So when a person has like an external hemorrhage, that you typically need to do some kind of anesthesia there so that the patient does not feel the pain as you're trying to like tie off the hemorrhage or whatever. And then in terms of a terrorist supplier, I remember I said, for the region of the rectum above the pectinic line, we had the superior rectal artery. Well, it's different for the region below the pectinic line. The region below the pectinic line gets a terrorist supply from the middle rectal artery and the inferior rectal artery. And those actually, at least I'll see probably the big ones remember for purposes of the USM Ls is the inferior rectal artery. The inferior rectal artery is actually a branch of the internal pudendal artery and internal pudendal artery is actually a branch of the internal iliac artery. Okay? So the inferior rectal artery is a blood supply to the region of the rectum that is below the pectinic line. And again, if you're like, oh, divide, how does venous drainage work? Well, just basically change all the arterial needs to venous names.

So the inferior rectal vein drains the region below the pectinic line, drains into the internal pudendal vein, we drain into the internal iliac vein, which then subsequently drains into the inferior vein giver. Okay? And again, because this region of the GI tract has somatic sensation, the thing that happens is if, for example, a person has like an inner feature, right? The classic endemic example should be a person that has blood on the toilet paper. If you see that, or the end, they usually have like some risk factor that increases their risk of having like very solid poop like chronic constipation or like their pregnant and all that stuff. If you see those things, think about an inner feature like blood on the toilet paper, right? Again, it's painful because inner features almost always arise right below the pectinic line. Okay? And really, the treatment for that is a seed spath. It's just like almost like a soothing bat. I think it's a little, essentially, just put your body like some kind of water or whatever. You can look at pictures or videos of that online. It's a very popular thing that's prescribed by many primary care physicians. And then the last thing I want to say is, for example, a person has inflammation of the rectum. What's the term used to describe the inflammation of the rectum? Especially in a patient that has like osteoarthritis. It's proctitis, right? So if you see the word procto, right? Think about the rectum. Okay? Think about the rectum.

So proctitis, think about the inflammation of the rectum. It's very classic in people that have osteoarthritis. In fact, most people that have UCD, a symptom start in the rectum. UC almost always begins as a proctitis. And really, the way you treat that is you treat that with with topical, critical steroids. You treat that with topical, critical steroids. Now, what if they give you a question about like a 55-year-old guy, you know, presents with like a like a micro-city canemia and they tell you that, oh, he stools, a hemocort positive. What are you worried about there? Well, I hope you're thinking about some kind of colon cancer, right? Remember, colon cancer is like the third most common cancer in meals and females in the US. And is actually the third most common cause of cancer in meals and females in the US as well. That's like a weird, high-yield epidemiological thing you want to know for purposes of the USMLA exams. So, you know, where do most colon cancers arise from? Well, they typically arise as colon polyps, right? And the thing is, for the purposes of the USMLA exams, you want to know the different kinds of colon polyps, right? So I'll put them in two major categories, right? There's the hyperplastic polyps and there's the other nomadous polyps. The thing is the hyperplastic polyps. They're actually the most common kind of polyps that you find in the colon. And for the most part, you find them around like the sigmoid colon and around the rectum. Okay?

The thing is, these things are not pre-cancerous. This is very high-yield to know. Hyperplastic polyps have no cancerous potential. Okay? And again, you typically find them on colonoscopy. And then when you find them, you typically have to remove them because you cannot say, oh, just based on the colonoscopy. You're like, oh, you know, this thing looks a lot like a hyperplastic polyp. No, you cannot see that, right? You can only confirm the diagnosis of a hyperplastic polyp after you take out tissue and then look at it under the microscope. Now, they are the nomadous polyps. Those are the nomadous polyps. These ones increase the presence risk of cancer. And the thing is, there are three types of adenovato polyps. So there are three types of adenovato polyps, right? And really, they're easy to remember. There is the tubular, there is the velus, and then if you kind of combine those two, there's the tubular velus. And the thing is, the velus ones are the worst, right? These ones have the highest malignancy potential. Oh, excuse me. And they typically contain like no glands, and they kind of look like finger-like projections on, on his stology, right? So tubular tubular velus and velus. tubular has some cancer potential, but it's not as bad as the velus adenomas. And then the tubular velus are kind of like in the middle, okay? So again, all important things to know, for example.

Now, one weird bizarre factoid that your friends at the NBME kind of expect you to know is that many of these velus adenomas can actually produce, or let me just say just for velus adenomas. These adenomadas polyps in general, some of them can produce a ton of mucus, and that mucus can actually cause diarrhea. So you can actually see a chronic diarrhea is actually a classic presentation of adenomadas polyposes on NBME exams, and also clinically in some people. Now, what are the different polyposes, the sodders that you want to be able to identify on exams? Well, there is something called a familiar adenomadas polyposes, right? The thing is FAP, right? It's inherited in an autosomal dominant fashion, and the big thing you want to remember in your exam is that it arises from an APC gene mutation, okay? Autosomal dominant inheritance, APC gene mutation. Remember that your APC gene is a tumor suppressor gene. So if you have one mutation in that, that can increase your risk. At least that basically makes your colon most susceptible to progressing towards becoming adenomadas, okay? So the APC gene is a tumor suppressor gene. If you have a mutation in that gene, that can predispose you to having colon cancer. Now, what are some other derivatives of this from APC gene mutation besides familiar adenomadas polyposes? Well, here's the deal.

If they give you a question about a person that has like an APC gene mutation, and then they tell you that this person has like a posterior fossa mass that's grown along the vermin of the cerebellum, and then they may want to tell you that oh, one image in the sea like some drop metastasis to the spinal cord. If you see that, you want to think about a medalloblastoma, right? The thing is, if you see an APC gene mutation, so a lot of like colonic polyposes in the setting of medalloblastoma, think about something known as torco syndrome, okay? Torco syndrome. And then if you see like an APC gene mutation, and then they tell you that oh, this person has like hyperplegia of the retina, so the person can have like visual difficulty, and they tell you that oh, this person has a lot of like soft tissue tumors, like sarcomas, and like pomas and things of that sort. Then you want to think about something known as Gardner syndrome, okay? Those are two high-yield associations with having an APC gene mutation. Now, there is another malig, like polyposes, the southern one has like juvenile polyposes syndrome.

It's just basically, if you see like a ton of polyps, especially like in kids, think about juvenile polyposes, the thing is for the most part, many of these polyps have normalignant potential, but in truth, if you actually review the literature, kids that have a juvenile polyposes syndrome, they have like a slightly increased risk of colon cancer compared to the general population, okay? But the thing is for the most part, most of those polyps actually don't have malignant potential. So kids with juvenile polyposes syndrome, they tend to have like a ton of polyps in the stomach, in the small intestine, in the large intestine. And then the final polyposes syndrome, I think I'll talk about is like a HNPCC, right? So like hereditary non-poliposis, colorectal cancer, right? So notice, in fact, I will see one unfortunate thing is many times, this disorder is discussed under the purview of polyposes syndrome. Now look at the name, hereditary non-poliposis colorectal cancer, HNPCC. This, sometimes you see a reverse as a linch syndrome, linch syndrome actually involves colon cancer not developing from a polyp, okay? Colon cancer not developing from a polyp. So typically, these people can have colon cancer and again, it would not develop from a polyp, and I will talk about something in a few seconds where there's this progression where you go from like APC gene mutation to a care expectation and they have a P53 mutation and then you get colon cancer.

That is actually not so with HNPCC. HNPCC, those people typically actually have a P53 mutation first as the very first mutation that occurs that predisposes them to get in a colorectal cancer, okay? So linch syndrome, remember, all those other dominant inheritance, it does not involve the formation of a polyp, okay? And P53 mutations kind of like, I'd like the first mutation that are arise in people that have a linch syndrome in the development of a colon cancer. And then you absolutely want to remember that linch syndrome is associated with DNA mismatch repair defects, okay? DNA mismatch repair defects. And the thing is, if you look at the colon, right, there's like the proximal colon and then there's the distal colon. About 50% of colon cancers are raised in the distal colon. About 50% of colon cancers are raised in the proximal colon. When you see a pressing have a proximal colon malignancy on MDM exams, think about linch syndrome as a potential etiology. That's very high you to know for for exams. So, and what are some other cancers you can find in people linch syndrome? Well, people linch syndrome. In addition to getting colon cancers, they can get endometrial cancers, they can get ovarian cancers, okay? So, I just think of it as like CEO cancers, like you know, like the CEO of a company. So, colon cancer, endometrial cancer, ovarian cancer, okay? Very high you to know those things for tests. So, let's talk about this adenomados polyp, adenoma carcinoma sequence, right?

So, the thing is typically when people have colon cancer, the first thing that typically happens is that they have like an APC gene mutation, okay? The thing is again, remember the APC gene is a tumor suppressor gene, right? And almost like not every, but pretty much every colon cancer begins as having an APC tumor suppressor gene mutation, right? The thing is after you have, when you have an APC gene mutation, that predisposes you to fobin, that basically makes your colon very high risk for developing adenomas, right? But the thing is on top of that APC gene mutation, if you're throwing a Keras mutation, Keras is not a tumor suppressor gene, Keras is an oncogene, it encourages cell proliferation. So, if you add a Keras mutation on top of an APC tumor suppressor gene mutation, that then turns your high risk of colon to an adenomados polyp, okay? And then if you then go down the route of having a P53 mutation, or you have like a DCC mutation, DCC stands for like deleting colon cancer, then that can get you from having an adenomados polyp to having full blown colorectal cancer, okay? So, again, this is again something that's very important to know for purposes of the USMLA exams. And remember again, I said that in people that have linked syndrome, they can typically have like a P53 mutation occurring first, okay? As like the pathway to them ultimately getting colon cancer.

Another high yield one to remember is that people that also have like colon cancer from like all three of colitis, those people also don't go through this normal like APC to Keras to P53 sequence. No, people would, you see that end up getting colon cancer, they typically start with like a P53 gene mutation that then gives rise to the colon cancer. And again, you'll see you generally would not find a polyp with people that have a colorectal cancer from all three of colitis. And when people have like a UC based colorectal cancer, typically physicians, at least surgeons choose to do like a procto-collectomy, they decide to just get rid of the entire rectum and the entire colon because the thing is when a person has colorectal cancer from UC in one region of their colon, they are more likely to have colorectal cancer from UC in other regions of the colon. It tends to be multifocal. That's a very high yield factoid. You want to remember for purposes of your exams. And one thing I actually forgot to mention with linked syndrome is that sometimes they may actually put like the specific genes, the specific like mismatch repair genes that I'm irritated in linked syndrome. Don't forget they are things you'll see like letters like MSH or MLH. Typically on exams you'll see like MSH2 or MSH6. Okay. Those are classic things that are associated with linked syndrome. And this notice, I kind of raised the dichotomy here.

I said that when you have an APC gene mutation and then you get KERAS and then you get P53, that increases your risk of like colon cancer. That's like the classic progression. But I also talked about this linked syndrome pathway. The thing is this APC pathway is classically known as the chromosomal instability pathway leading to colon cancer. Contrast this with the linked syndrome pathway that is known as the microsatellite instability pathway that ultimately leads to colon cancer. Now one last thing I want to mention here actually not one last in there. A few other things I want to say about colon cancer is that when people have overexpression, I mean you can actually see this, it's actually pretty prominently discussed in the literature. When people have overexpression of cycloxygenies that can actually increase a person's risk of colon cancer. So you can see divine. How does that make any sense? Well think about it. Cox leads to the production of Prosteglandins and Lychotriens. And the thing is Prosteglandins and Lychotriens, they are pro-inflammatory agents. The thing is when you have a ton of inflammation in the region of the body, that can ultimately increase the presence risk of developing a malignancy in that region of the body. Think about it. Why do people with ulcerative colitis have a high risk of colon cancer? Well because they have a ton of inflammation. So the thing is if you could actually inhibit Cox 2, specifically because there is Cox 1, there is Cox 2.

The big one you want to remember is Cox 2. If you can actually inhibit Cox 2, that can actually lower a person's risk of colon cancer. So that's why if a person has a history of colon cancer, some physicians actually recommend that they take like a Cox inhibitor, like an insect basically has like a chemo protection for against the future development of of colorectal cancer. Now some other quick things that I want to see with colon cancer is don't forget your puberty eager syndrome, right? Typically those people have like hyper pigmented like areas on like their lips, their mouth and stuff like that. And then it's an orosomal dominant disorder and these people actually had increased risk for like many different kinds of malignancy like pancreatic cancer, stomac cancer, colon cancer, ovarian cancer, endometrial cancer. I mean like they have a pretty high risk of many of these malignancies. But one other thing you want to remember with puziagres is that it's a hematoma-dost disorder. So what's a hematoma? A hematoma is just I cannot think about it as like crowded tissue, like crowded normal tissue. People that have put the eager syndrome, they tend to have hematomas in many parts of the GI tract, right? So they'll have no more tissue but there's just way too much of it in a given location, okay? But don't forget the association with the development of all the cancers and especially pancreatic cancer for whatever reason.

They even made me love that pancreatic cancer association with puziagres syndrome. And remember the pee in puziagres for the pee in pancreatic cancer. And then the last thing I want to say is what if they give you a question about a person that hasn't got a creditis and then you obtain blood cultures and you grow like strep bovis. What's your next step in management for those people? Well you want to go ahead and get a colonoscopy, right? Because remember strep bovis bacteremia has a very strong association with a concurrent a colorectoma-legancy, okay? Instead of putting strep bovis sometimes, let me try to mess up your head by putting like strep galoleticus. That's all that's like a strep bovis derivative. That's also again associated with the presence of a concurrent a colorectoma-legancy. And what are the colon cancers screening guidelines? I mean you want to start at the age of 50, right? When I start at the age of 50, probably like the gold standard is getting like a colonoscopy, start at the age of 50, do it every 10 years. I mean there are other things you can do like you can do like this, like this thing called like a fit test is like a fecal immunohistochemical test. And then there's this thing called like an FOBT like a fecalocoblot test. You can do that every year. Or sometimes you can do like the FOBT and like a flexible sigmoidoscopy. Those are things you can all do.

And then one other thing you can also do is CT colonography, but I will encourage you to not be CT colonography on your exam. Chances are it's going to be the wrong answer. It's just not something that has found mainstream acceptance. There's still a lot of studies that need to be done. So I will encourage you to not pick that answer choice on your exam. Now one weird scenario you may see on your test is oh a person has a history of Australian colitis. How do you screen them for colon cancer? Well here's the deal. If a person has a history of UC, you want to start screening them for colon cancer eight years after the initial diagnosis of all Australian colitis has been made. So let's say the diagnosis would use the age of 25. You want to start screening them for colon cancer at the age of 33. But one weird exception to that really is if a person has a history of I should probably not mention this. It's something that's more important for step two, step three. So let me let that go. Now one other thing you may see on your exam is what if a person has like a family member that was diagnosed with colon cancer at the age of 39? When should those people start getting screened? Well they just start getting screened for colon cancer at the age of 29. Remember if a person has a first degree of relative that has like you know like a history of colon cancer you want to start screening like 10 years before?

That person was like that first degree of relative was diagnosed with colon cancer or studying a age of 40. Whichever one comes first okay? Whichever one comes first. So if you have a first degree of relative that was diagnosed with colon cancer at the age of 52? You want to start screening them at the age of 40 because if you're backtracked 10 years from 52 that's 42. Well 40 comes before 42 right? It's an earlier number so it starts screening at the age of 40. So I really hope that that makes sense to you right? And then some other weird things you may see with colon cancer and exams is like that like a right side of colon cancer tends to obstruct. I mean sorry a left side of colon cancer tends to obstruct. So that's the one where people classically present with like pencil thin stools and then the right side of colon cancer tends to bleed. So that's the classic one where it will be like a person that's past the age of 50 and they'll present with like a micrositic anemia and like a hemocorpositive stool if you think if you see that think more about like a right side of that colon cancer and then there's this thing where they say oh you may see like an apple core lesion on a barium swallow. And I'll encourage you to look up like an image of that. That's a classic image that tends to show up on NV Me exams to kind of hint you towards the pressing potentially having colon cancer.

Okay now what if you get a question about like a 25 year old guy and this guy has you know like for the past six months and be having like bloody diarrhea a chronic bloody diarrhea if you see that what do you want to think about? Well I hope you're thinking about all three of colitis right? I hope you want to think about all three of colitis. So if you see a young male with chronic bloody diarrhea that is the classic NV Me exam presentation of all three of colitis. So what are some big things you want to know about all three of colitis? Well you want to know that it has an association with like primary stlerosing colinitis right? PSC remember PSC is where you have problems with like like inflammation and fibrosis of that intra and extra hepatic bowel ducts right? So it will cause a conjugated hyperbular banymia and it has this weird association with PNG on NV Me exams right? Now what parts of the GI tract are affected specifically by ulcerative colitis? Well think about it right? If it's a colitis that means it affects the colin and almost always you see affects the rectum it does not spare the rectum. The inflammation almost always starts at the rectum and then it begins to proceed proximate and the thing with ulcerative colitis that the lesions don't skip around right?

They are continuous lesions that's one high you thing to know and then one other thing you want to know is that ulcerative colitis remember I said the layers of the GI tract you have the mucosa and then you have the sobucosa and then you have the muscularis external. The thing is people that have UC it only involves the mucosa in some cases it can also involve the sobucosa so it is not a transmural problem or like what obtains in Croons disease and classically when you do like a barium NMR in these people that have ulcerative you see something called like the lead pipe pattern. The lead pipe pattern basically happens because we lose the house strap that are outlined like those fine wavy lines that are outlined that colon you lose those house strap right? That's the thing that gives rise to the lead pipe pattern on a barium NMR in a person that has a history of almost redif colitis and then some other boss frees you want to remember is because again it's an ulceration right?

It's like almost like a superficial ulcer so typically when you do a colonoscopy in a person that has a history of almost redif colitis you'll see things known as like crypt abscesses sometimes you may see them refer to as like what's this other term besides the crypt abscess it's not coming to mind so I'm going to keep going because again I want to keep this podcast under an hour but with crypt abscesses they are classic finding in people that have ulcerative colitis is just a kind of ulceration is just a term that gastroenterologies used to describe certain morphologies of ulcerations like you see in the colon in people that have you see now what if they give you a question about and they ask you like oh what's the most serious complication of a person having ulcerative colitis you actually want to think of something known as a toxic maker colon okay toxic maker colon classic your name being exempt they will show you an image and you see like massive massive massive distinction of the transverse colon if you see that think about toxic maker colon your next step in management for those people is to take them to surgery toxic maker colon has like a very high morbidity and mortality so it's something you need to fix and fix quick although remember that toxic maker colon can also be like a bad complication of c-difcolitis right and it can also be a pretty bad complication of tripanosomal cruziac okay those are Ohio things to remember and then don't forget that you see right also kind of like Crohn's disease can cause like a kind of arthritis right like one of those a seronegative spondylonethropythes that associated with HLEB27 right so remember right that there's this pair nomonic like PAR for the seronegative spondylonethropythes that HLEB27 associated right so they are things like psoriasic arthritis right that's the P the A stands for ankylose spondylitis and then t

he I stands for IBD associated arthritis well IBD right includes all seronegative colitis and Crohn's disease and then the R is what's known as reactive arthritis that was previously known as a rider syndrome okay so you see certainly has that association with IBD associated arthritis and then don't forget that you see can also cause like you know like with this like IBD associated arthritis you may see presenters like visual difficulty like like with like a U Vitis on MDM exams right or you may also see presenters like a sacred LIDIS right kind of like ankylose spondylitis in a sense on MDM exams and then don't forget that you see classically causes the skin finding known as pyrodermagandranosom contrast this with the erythema nodosom that is pathonomonic on MDM exams for Crohn's disease so erythema nodosom is more classically associated with Crohn's disease on MDM exams and then pyrodermagandranosom is more classically associated with all seronegative colitis on MDM exams but I know some of you may be saying oh divine I've heard about erythema nodosom in other contexts yes that is true erythema nodosom may also be found in stracoid doses on an MDM exam and erythema nodosom may also be found in coxidiumicosis on MDM exams remember coxidiumicosis has an association with like being from like Arizona on Nevada or California or New Mexico or Texas kind of deal so again those are probably the big things you want to keep at the back of your mind with all seronegative colitis and I mean how is all seronegative colitis treated well remember that thing I said earlier about like oh if a person has like a ton of form like cox 2 activity that increases the presence risk of colon cancer well if you inhibit a cycloxygenic that can again dumb down the inflammation and help with these symptoms of all seronegative colitis right so typically people that have UC typically use that with l

ike a compound known as a 5asa compound like sofa salazine sofa salazine basically is essentially an insect but the thing is it's an insect that for whatever reason actually I know the reason I was playing a second it tends to work primarily in the in the colon okay because the thing is those colonic bacteria remember I told you colonic bacteria they actually useful for something well one thing they can do is they can actually I mean besides making vitamin K and making lactic acid one thing they can do is that they can actually break down sofa salazine and relieves like the active agent in the colon so when you take sofa salazine nothing happens to eating the stomach nothing happens to eating the small intestine when you get to the large intestine the intestine large intestinal flora convert it to like the active agent that they inhibit cycloxygenies and helps with symptoms of all seronegative colitis right but some other things you can use for UC you can use like a is a thioprin or like six wake up to purine you can also use a tnf alpha inhibitor like adalimiumab or influximab and if you actually want to cure the person of all seronegative colitis you can actually do something called like a procto colectomy right so you get rid of the rectum you get rid of the colon and all the symptoms go away because oserative colitis only involves the colon right so if you get rid of the colon you get rid of the person's ulcerative colitis now um so I guess since I've kind of talked about UC let me I guess also talk about Crois disease so Crois disease again it's an inflammatory bowel disease um and unlike oserative colitis right that tends to be like a continuous lesion Crois disease tends to have lesions that's one thing to know and then unlike oserative colitis that usually just involves the mucusa or just like the mucusa and sub mucusa Crois disease tends to involve every of t

he GI tract so you can involve the mucusa you can involve the sub mucusa you can involve the musculitis externally right so it causes transmural inflammation in fact that is actually one of the primary reasons why people that have Crois disease can begin to form fissionals right so they can form like a fissional to the skin they can form like a fissional from the colon to the bladder they can form a fissional from the colon to the um from the colon to like the vagina right so um that fissional from the colon to the bladder is what's known as a colo vesicle fissional it's actually very high yield to remember for the purposes of the USM Ds that colo vesicle fissionals are not found only in oserative I mean only in Crois disease you can also find them in as a complication of diverticalitis I think diverticalitis will probably be the last topic I'll talk about or talk about in a couple of minutes so Crois disease transmural inflammation okay so it affects every year and Crois disease unlike you see that tends to involve the rectum Crois disease actually tends to spare the rectum the most common region of the GI tract that's torched by Crois disease is actually the terminal ilion okay is actually the terminal ilion and again like I said usually spares the rectum now the thing is Crois disease can affect any part of the GI tract it does not just affect the colon like you see in oserative colitis now in Crois disease if we take like a biopsy of the lesions what kind of granuloma will you find well I hope you're telling me that you tend to find out you tend to find non-case seeding granulomas basically let me give you a road I'll help your life on the USMD exams the only cause of a case seeding granuloma that you need to know for the USMD exams is TB every other granuloma you see on NBME exams it's gonna be a non-case seeding granuloma and then unlike the lead pipe sign that y

ou'll find on a barium swallow in a person that has oserative colitis in people that have Crois disease you tend to find this they known as a string sign the string sign just arises because people that have Crois disease you know they have like this segmental inflammation in the GI tract that can lead to development of structures and those structures almost give like a segmented pattern to the colon and the small intestine so that's why you observe something known as the string sign okay and because Crois disease tends to affect the terminal area it can present as a Fatmal absorption on NBME exams because remember your bowel salts right are absorbed in the terminal area people that also have Crois disease on NBME exams they can give you a question and show you that oh these people have like a megaloblastic anemia well that's arising from a B12 deficiency because remember B12 is also reabsorbed in the terminal area and then one other thing you may see on NBME exams in the context of Crois disease is those people having like you know like flat pain redid into the growing E.K.A like an effulothiasis the thing is when your terminal area is not working well you're not able to reabsorb by last six the thing that happens is you begin to have a lot of oxyly run free around the region of the terminal area so the area absorbs at a higher rate and that can increase your risk of having nephrolothiasis from calcium oxylyt crystals that's a very very high your thing to not the back of your mind for for the USM Ns and then don't forget again that again also Crois disease typically on NBME exams it will not present as a bloody diarrhea I think I've maybe only seen like one or two questions where the present has Crois disease and it presented as a bloody diarrhea bloody diarrhea usually forms one that the purview of all straight-of-collitis okay usually people that have Crois disease t

hey just tend to have like a chronic watery diarrhea okay chronic watery diarrhea and one I guess a few other quick things I should mention here in like in terms of treatment really the treatment of Crois disease kind of strongly parallels the treatment of all straight-of-collitis typically you give like the five like the ASC five ASC agents so like the salamine, sofa saline you can give those for for for Crois disease you can also give like a TNF inhibitor right so like infleximab at a limbumab a tanner septum, a tanner septus that's a classically described a decoy receptor and typically these TNF agents usually give it to people that have like an inflammatory bowel disease and then you have like an atherodic component to their disease as well and I mean obviously if the present has like an acute exacerbation of like Crois disease or UC you know you can give them like pulse steroids like very high doses of IV cortical steroids and that can help sort of calm down inflammation now one other thing you want to keep at the back of your mind with Crois disease is that Crois disease tends to be mediated by T-helper one cells remember those are the cells that ultimately mediates cell mediated immunity versus all straight-of-collitis that tends to be mediated by the T-helper two cells remember those T-helper two cells tend to focus more on like antibody or like your humoral mediated immunity and then remember I said that people that have all straight-of-collitis right they you know they can have PSC and they have like PSC has this association like P-Hanker Crois disease actually tends to have an association with something known as a positive ASC-A antibody so antibodies against saccharomyces are servicing okay that's like just one of these weird bizarre factoids I know I learned at least I know I certainly learned this during my my pre-med a curriculum in match I mean not my

pre-curricular at my med school or pre-clinical or curricula just one of those weird bizarre things that occasionally tends to pop up on the USMLE exams and then the final thing the final thing I'll mention with Crois disease is that Crois disease tends to cause I mean it can increase your risk of colon cancer but the risk is not as great as UC UC has a much higher risk of colon cancer compared with Crois disease and then the last thing I want to mention again I promise I'll give today's podcast on the run hour if they give you a question about like a 65 year old guy and this guy says oh he's been having like these painless bloody bowel movements and then they show you some labs and you see that oh this person has like a microcytic like iron deficiency beast andemia if you see that what you want to what do you want to think about when I hope you're thinking about diverticulosis okay diverticulosis remember diverticulosis is basically like an outpouching of like like a like a part of the GI tract usually at least that if you're thinking about like the colon usually it arises in the region of the like the sigmoid colon okay and you know you have these outpouchings there is symptomatic for the most part but one thing that your friends at the end of the end of the end of the end of the end of the end of the you want to know the risk factors for diverticulosis anything that causes like a chronic increase in intra abdominal pressure again like being in a career where you stand all the time or having a histro chronic constipation that can increase your risk of having diverticulosis and again diverticulosis there is symptomatic for the most part but occasionally we can cause like you know like left low quadrant discomfort and on end game is whatever is in the tend to present as painless bloody bowel movements in the elderly in fact I'll say this is very high you to know the m

ost common cause very high you the most common cause of painless not even painless like just most common cause of lower GI bleeds in the elderly is diverticulosis okay but for the most part again these things tend to be asymptomatic well what if one of these diverticul blah right like let's assume like a person has like a colony diverticulosis what if it's obstructed by like a fickleph right and then you have like infection and inflammation behind it well you then develop something known as diverticulitis okay that classic presentation of diverticulitis on an in-bim exam will be an old person that has fever and left lower quadrant pain okay fever and left lower quadrant pain in an elderly person is diverticulitis until proven otherwise on an in-bim exam and really the way you make the diagnosis of diverticulitis you know you use those C Ts kind of the abnormal like IV contrast that will typically help you make the diagnosis and really the way you feel you you know you just give antibiotics or so you can give like the classic cocktail on in-bim exams for most GI infections is like the combination of ampicillin gentamysin and metronidazole or you can give c-pro-fluxecin and metronidazole or you can give trimethoprimsofomethoxazole and metronidazole and the thing is when a person has diverticulitis well there's some bad things that can happen as a result of diverticulitis one thing that can happen is you can prefer it to the person's colon right so you have like three earndere diaphragm that's obviously like a surgical emergency that is why that is actually why a colonoscopy is contraindicated in a person that is having an acute episode of diverticulitis typically for presence of diverticulitis you do a colonoscopy but you do it like about six weeks after the inflammation has resolved okay so diverticulitis when a person is going through that acute episode you don't do a

colonoscopy because those people are very high risk with all that inflammation of your pepharate in the acolym right and then the thing is obviously the colon perforates right or you have like severe inflammation you can again begin to form fistulas from the colon to the bladder okay like a colovesicul fistula remember I said that a colovesicul fistula may also be found in Crohn's disease colovesicul fistulas may also be found in diverticulitis in fact I'll say at least in my mbmi test taking experience the most common cause of a colovesicul fistula on mbmi exams is diverticulitis okay the hotel that a person has no maturia basically you see gas bubbles and the person's urine if you see that think about a colovesicul fistula think about a colovesicul fistula and then I said that you use a CT scan with IV contrast to make the diagnosis of diverticulitis well if a person has diverticulosis you can actually make the diagnosis of the CT scan as well or classically on mbmi exams you want to go more with like a barium like a barium enema a barium enema is like pretty great for the diagnosis of a diverticulosis and I will encourage you to also look up an image of this you want to be able to identify diverticulosis on image on an mbmi exam now um to round this out I guess let me kind of talk about the differences between like you know like a true diverticulum and a false diverticulum the thing is for purposes of the USMLE exams they are only two true diverticula you need to know right attraction diverticulum that you find in the middle third of the esophagus and then mechols diverticula right remember mechols diverticulum will present as like painless bloody bowel movements in a child you'll be the diagnosis with like a mechol scan like the technician 99 mr scan those are the only two true diverticula that you should expect to see on an image exam so you may say okay divine w

hat is a true diverticulum well a true diverticulum is a diverticulum that includes all layers of the GI tract so the mucus the subucosa and the muscularis extruder every other diverticulum zenchres diverticulum if you friendly divert um epiphanics actually there's some that are true diverticula so let me be like I shouldn't say that with that but zenchres diverticulum the diverticula that you find in a person that has diverticulosis those are all examples of false diverticula they typically just involve like the mechols and the sub mechols right and these false diverticula are usually arise from regions of weakness in the muscularis external so if you have a regional weakness in the muscularis external then the mechols and the sub mechols can through it so you have this outpouching and then that creates a false diverticulum so I think since again it's almost an hour let me go ahead and pause here for today um you know again I'll pick up from here in a different podcast and as I do at the end of every podcast and I feel like the number of things I offer I just much so I'll just tell you this if you're taking any US semialexa step one two CK two CSTF three or you're taking any med school exam or you're taking the M cat or you're trying to apply for residency as a med student so like an iris application or plan to college as a a plan to med school as a college student so like an amca application or you're like a medicine resident that needs to do for like the intranin exam or the abi m board the abi m board exam offer to do it for all those things right over to do it for all those things like coaching and like iris personal statements, mocking, interviews, all that stuff I do all that stuff and then I actually offer like defined US Emily courses like for step one I do like this 20 hour course for step two CK step three I offer like a 10 hour course where if you have the

end of your day get it period or you kind of want to put everything together in a very like rapid review format um um um I can meet with you one on one online and then we kind of go through like the most no material for these uh respective exams and then if you need like a large group like a more comprehensive uh US Emily course again if you have a group of five just reach out to me either through the website or you send me an email at divineintervention podcasts with an sd and a gmail.com and then we can kind of make arrangements from there so have a wonderful rest of the day I hope you find this to be helpful thank you good bless you

Diverticulosis.

Chromosomal instability pathway (Adenoma-Carcinoma Sequence).

Obturator sign.

Villous adenomas (part of the adenomatous polyps).

The presence of outpouchings/diverticula.

Crohn's disease (CD).

Familial Adenomatous Polyposis (FAP) and Gardner syndrome.

UC lesions are continuous, starting at the rectum; CD lesions are often skip segments and can be transmural.

Mismatch repair genes (e.g., MSH2 or MLH1).

Lower GI bleeding, most commonly due to diverticulosis.

Meckel's diverticulum and rectal diverticulum (or sometimes specifically mentioned as the location of the true diverticula).

Above: Superior rectal artery (branch of IMA). Below: Inferior rectal artery (branch of internal pudendal artery).

Hyperplastic polyps.

Lead pipe pattern (due to loss of Haustra).

UC lesions are continuous, starting at the rectum; CD lesions are often skip segments and can be transmural.

Mismatch repair genes (e.g., MSH2 or MLH1).

Lower GI bleeding, most commonly due to diverticulosis.

Meckel's diverticulum and rectal diverticulum (or sometimes specifically mentioned as the location of the true diverticula).

Above: Superior rectal artery (branch of IMA). Below: Inferior rectal artery (branch of internal pudendal artery).

Hyperplastic polyps.

Lead pipe pattern (due to loss of Haustra).