GI diseases.pdf

Another exit, so officially I can't get to The skin may just form an Abscess collec<on in the in the abdomen or in the muscle wall for example. Crohn's disease can also look very, very different. Some<mes you just see at this ulcer just like you would see in oral cavity. Usually there's a lot of them....

Another exit, so officially I can't get to The skin may just form an Abscess collec<on in the in the abdomen or in the muscle wall for example. Crohn's disease can also look very, very different. Some<mes you just see at this ulcer just like you would see in oral cavity. Usually there's a lot of them. Many of us may have a few others officers in our GI tract of no consequence. But if we see a lot of them, even if they're small like this, we think about Crohn's disease. Here's this example of some larger ulcers in the Ileum. And here's an example of someone who has some ulcers as well as a narrowing or stricture there. This is a a resec<on specimen of someone who had Crohn's disease involving the terminal ileum. So this skin is skinny part here is the the the sole ilium where it connects to the colon is kind of flayed open now. But this had this one had a structure. Thickened walls there and under the microscope there's just some examples of what you might see. Phone disease in the inflamma<on not only kind of cuts through the mucosa here, but you can see it spills into the semi Cosa, this kind of lighter band of <ssue here. And so these are all inflammatory cells going into the summit Cosa. And actually you can see some<mes the pathologists describe these. Misery or knife like ulcers where it's you have kind of a cleM, like someone just took a knife and cut through the the wall. And this is an example of a granuloma. Granulomas are these kind of collec<on of immune cells, oMen<mes with these giant cells with mul<ple nuclei. These collec<ons are what we consider pathognomonic for chronic disease, meaning if you have someone with features sugges<ve of of chronic disease and you see granulomas. On the biopsies, this basically senses A diagnosis. Granulomas however will probably only seen in about 15 to 30% of pa<ents with Crohn's disease. So it will be the minority of of of pa<ents who diagnosed with chrones. But again if you see it in the right clinical context, we usually say this is kind of cinches of diagnosis or as pathogenic. I men<oned earlier that that IBD can present with extra test manifesta<ons will kind of go over these quickly, but. That the. The manifesta<ons can involve the skin. Some<mes you see these ulcera<ve lesions. This is an example of powder. In Americanism, pa<ents can present with these painful nodules, par<cularly on the shins. This is called endosome. Endosome can come, can come with other diseases as well. But in our world, GI we only. Think about with pose or inflammatory bowel disease. But it can be linked with things like some fungal infec<ons and present with even those and others as well. Down here is an example of sweet syndrome doesn't protect too well but these kind of almost like a pimple like rash on the on this pa<ents neck these are filled with these are basically liWle apples they're filled with neutrophils. ID can present in the liver and in the bile duct can present on the that you track of presen<ng with stones or even obstruc<on of the order. We recognize that pa<ents with IBD have a higher risk for clots so believe it's a hyper hyper printable state. And so there are risk for blood clots, pulmonary embolism, even strokes. They can move their eyes, the joints. So all these systems, again just indica<ng that these are systemic immune diseases, not just a GI specific disease. But then finally, geZng to what you might all care about, whether oral manifesta<ons go through a number of slides is showing some examples that have been published in the literature, but we'll cover kind of some of these manifesta<ons. Listed in this table here. So one thing to comment about oral manifesta<ons IBD, they tend to be more common in Crohn's disease compared to ulcera<ve coli<s and they will oMen correlate with perianal disease. So, but very oMen, you know we'll ask our our pa<ents about whether they're popping up in these sores in their mouth and we'll take a look in the old cavity. Because some<mes these manifesta<ons will come up a liWle bit before their GI, something really ac<ng up. So if we start hearing that pa<ents are cropping up a lot of sores in their mouth, even if they're not having a lot of diarrhea, bleeding or pain, we start geZng worried that their disease in the gut is actually ac<ve, more ac<ve than. May indicate. So usually these signs will kind of parallel ballot ac<vity. So if the ballot ac<vity is quite there's not much going on in the world cavity vice versa. So these were some some examples of lip swelling, some cobblestoning of the Big Buckle Macosa. So very well, but actually some other examples of linear ulcers because of tags and and gingival disease. In this case we go gingivi<s. So again some examples at this also is probably more common things that we see that could be large and mul<ple and recurrent. We'll see some examples in the subsequent slides, a lot of the labial disease swelling fissures. This example with late, you know, problems with the lips as well as the gingiva. This is aMer chemo and steroids, and we'll get this treatment in a moment. This is kind of a unique one. We don't see this very oMen, although this lower panel was published in. One of the pa<ents I care for in the clinic is something called postopera<ve. As vegetarians, you can make out these kind of white kind of inflammatory tracks. Is maybe? Another example of the kind of soM <ssue tag again the lip disease and in this case it was biopsies of the Macosa show granuloma. So this is same as you see in the in the gut biopsies. And so in this case, helps support the diagnosis that these two are oral manifesta<ons of Crohn's disease. Is a example that was supposed to fuse ago showing constantly disease being the prominent oral manifesta<on. You see this kind of ulcera<on and exit on the consoles pre treatment and this is post treatment of their disease. This is another example that was published a few years ago on personalized vegetarians. Again, kind of these kind of white tracks. This just is showing that on the example under the microscope, just to denson flammatory infiltrate. Again, example of significant lip swelling and also this was a biopsy from the lip showing granulomas inflamma<on. This might be the last one here showing very significant kind of tags and gingival hyperplasia again showing granulomas on biopsies. So those are some examples I we started the case with someone with at this stoma<<s. And just want to also men<oned that aMer some place obviously can occur for other reasons besides Crohn's disease. Most of us have at some point you've had you know aMer this ulcers in the mouth. It doesn't mean that we have <me to bowel disease may not even mean that we have any disease at all, but it can increase especially if there are mul<ple or recurrent or large it can indicate. Time through balances like you're talking about CSE, which we'll talk about in a moment or later in the lecture. It could indicate some type of vitamin or or might mineral deficiency. PreWy uncommon in people inges<ng a Western diet, but some<mes we see in pa<ents who are malnourished or have malabsorp<on disorder. There's a vascular disease called beset disease that can look very much like Crohn's disease and but the more common things are listed here, stress, hormonal factors, food sensi<vity, some<mes even minor trauma can induce it or a familial tendency as well. Now we've talked about some of the symptoms of inflammatory bowel disease. Some<mes problems greater than just symptoms can happen. These are some of the more severe complica<ons that can occur, including colon cancer. You know, we recognize that chronic inflamma<on in any organ can lead to cancer and that's true of the gut and so pa<ents who have. Like unchecked inflamma<on in the in the colon par<cularly. Are increase risk for colon cancer. So pa<ents with the with extensive or pancoli<s have about a 5 to 15 <mes the risk over the life<me of developing colon cancer compared to someone who has no inflammatory bowel disease. And this is something that's related to dura<on of disease as well. So it's about a half a percent per year within the first 10 to 20 years and. That beyond that about 1% per year. So this is a big deal for someone who's diagnosed in their teenage years, right with with, with pandas, with coli<s, you know by the <me they're 20 to 30 they're geZng annual call out or nearly annual colonoscopies to check for, for colon cancer and precancerous changes. Some<mes the corn ruptures, that's what we call perfora<on with small bowel ruptures as well. So that's called the perfora<on generally something that requires surgical interven<on. Pa<ents can bleed either acutely or just chronic blood loss that can lead to some<mes preWy significant anemia as I men<oned some of the companies in the chronic disease. And finally, there's something called toxic magic: This is something that we some<mes in hospitalized pa<ents with severe flare of ulcera<ve coli<s or Crohn's disease where they're column basically just stops func<oning. They stop having bowel movements that: distends. They're showing signs of sepsis and this is usually considered a surgical emergency. They have to get their: out otherwise. It's a preWy high mortality rate. We'll go over this kind of trimming. Very briefly. I just want to go over some of the major categories, some of which might be important for you to be familiar with as far as what they can do to the oral cavity or to managing pa<ents. GeZng with temporal procedures at the boWom of the pyramid are kind of what we use for mild disease, these are. Basically GI an< inflammatories. We call these mesalamine. They're good for mild, you know, mild to moderate chronic site ulcer coli<s, not so useful for chronic disease. This middle part of the pyramid is probably the most relevant potency for for you all. Because emphasis is again a immune dysregula<on or inappropriate immune response. When we treat moderate to severe chronic disease, we start using immune suppressing type medica<ons. And so in this category are steroids and immunomodulators steroids you might be familiar with these steroids for all sorts of type of. Inflammatory type diseases have in their body, but for the gut we can give it orally. You can give it as like an enema which is topical or for sick pa<ents we give it through the IV. This is very good for inducing remission, geZng these under control, but maintaining disease with steroids is usually not a good idea because of side effects. So things like diabetes, hypertension, increased risk for infec<on, weight gain, those are all kind of the long term steroid side effects that we're trying to avoid. So if you want to avoid steroids but someone I mean suppressed immune system, we oMen use something called the immunomodulator and these are medica<ons that were that are used you know for things like kidney transplant, immune suppression or or. As part of chemotherapy regimens for certain agencies that are kind of immune related. So we use it in GI to to suppress the immune response and IBD. But as a result, we recognize our poten<al consequences like suppressing them the modern marrow. So that can be to anemia, leukopenia thrombocytopenia, there's probably also. Increased risk for infec<on and malignancy in these pa<ents. So top of the permit are what we call the biologics. This is actually, even though it's a smaller part of the pyramid in my figure, this is probably the rapidly, most rapidly growing part of the human paradigm that we have. And so it it's, you know, most of the commercials that you see on TV today are things for, you know, moderate, severe chronic disease and those are using these biologics and there's so many of them, but and you don't really need to know the details of what kind of medica<ons are in this class. But the the, the most commonly used in the original biologic or things that are are called TNF antagonist, tumor necrosis factor antagonist. These antagonize the ac<vity of teen off which is a potent inflammatory cytokine in our body and so we want to suppress that trigger. And so again, these are going to suppress the immune system and probably just like immune modulators probably linked with increased risk for delinquency and definitely risk for infec<ons. So why does any of this maWer? So some poten<al implica<ons for Madison Dental pa<ents, One of them is just being cau<ous with NSAIDs. So I men<oned earlier on we'll talk about triggers and the causes of IBD and said can trigger a flare or even a new diagnosis. ID but typically in pa<ents who have pre-exis<ng disease. Insects can worsen ac<vity or cause a flare. This is doesn't happen current, you know. To most pa<ents. So generally speaking it's safe to use it insert and pa<ents inflammatory bowel disease but probably about 10 to 15% of pa<ents that can trigger or worsen their disease. So we want to be cau<ous about that or before recommending or prescribing and said for post procedure pain or dental pain you want to ask your ID pa<ents, have you ever taken it before. Has ever worsened your ID before because it says something that that can happen. And it's being familiar again with some of the poten<al toxicity or risk of the IBD medica<ons that we use as it relates to infec<ons including things like Canada is preWy common with people on steroids for any amount of <me. And then for those of you who will be doing procedures or dental procedures that can increase your. For bleeding. Speak at that and then have to take any ques<ons From these first two cases we have ques<ons. Yes, ques<on about N says Then why that? Yeah, no, it's not related to ACID. It's probably not known what why it is, why it can trigger. I believe but it's I don't. I don't believe anyone thinks it's ACID related issue. Is probably more related to kind of the effects that incest can have on inflamma<on in their body, Cox 2, Cox ONE produc<on, etcetera. But the actual mechanism, not sure. But it's not simply an acid thing, so you couldn't kind of counterbalance it by providing like an essence or ques<on for example. The ques<on. Right. So the ques<on about pre medica<ng? With an<bio<cs before invasive dental procedure. Right. Right. Generally not recommended, at least not I don't know if there's any specific guidelines in in kind of your guidelines segments, but as far as typical procedures like when we do a colonoscopy and someone RBD on the mission, we don't give an<bio<cs. So I think that would probably be similar. Move on the clinical scenario 2. This is a 36 month year old woman who presents with severe erosion of her molar enamel. She denied drinking a lot of sodas or or citrus inges<on, vitamin C supplementa<on. But she did, despite having very frequent heartburn. So we'll talk about GERD and this is someone with dental rose and secondary to GERD or gastroesophageal reflux disease. So we use we define GERD as the presence of symptoms or complica<ons that that are caused by abnormal reflux of gastric contents into these alphas and the most common gastric content that is reflux is going to be acid. So there are a number of things that contribute to the pathogenesis of third and most important is probably the func<on or dysfunc<on of the what we call the LS with the lower SoMail sphincter and we all have kind of a soM kiss at the boWom of the Socus. We have a stricter mechanism that is composed of both smooth muscle in our Sophus. As well as the suppor<ng structures around that area, the most important one is the diaphragm, kind of the big flat plate like muscle that separates our chest cavity from abdominal cavity. And usually those are usually the the stomach resides fully under the diaphragm, so the diaphragm kind of provides some physical support against reflux. But thi smooth muscle in our esophagus as well as the suppor<ng structures around that area, the most important one is the diaphragm, kind of the big flat plate like muscle that separates our chest cavity from abdominal cavity. And usually those are usually the. The stomach resides fully under the diaphragm, so the diaphragm kind of provides some physical support against reflux. But this LES is also very important. So that LES that we all have has to obviously has to relax when we swallow food so that food will pass and then we want to the the sphincter to <ghten aMer the food is passed so that it doesn't come back up. So throughout the day for all of us our LDS is relaxing and <ghtening, relaxing and <ghtening. And that's normal. But in pa<ents with with GERD symptoms, we recognize that this relaxa<on process happens too oMen or for too long a period of <me. And so for for that <me with the LS is relaxed, the stomach contents have greater opportuni<es to reflux up and this contributes significantly to gird. We also have a social clearance mechanisms to get things out of our socie<es including you know food that obviously that we we ate or drank as well as acid that can come up. And so pa<ents with GERD have problems may have problems clearing their Sophus, they're totally may be sluggish. Or they even things like having inadequate saliva. Can impair your social clearance mechanisms. Gastric emptying can contribute using Again, aMer we eat, our food kind of grinds up our stomach and this fits us some the contents out into the duodenum and the small bowel for absorp<on. But if the stomach doesn't empty properly and has been turning on diges<ng food and making acid, if the acid can't get out in a <mely fashion, it will find its way out one way or another. Either or pass into the small intes<ne eventually or or come up into this RPS during one of our LS relaxa<ons. And so some<mes you know pa<ents can have a primary problem with gastric emptying condi<on called gastroparesis and these pa<ents can have significant problems with reflux disease and finally just to me. Integra<ng the actual physical barrier of the sophus can be impaired in pa<ents with with GERD. There are some common condi<ons that are linked with your one of them I was looking to earlier is is a defect with again the the inner <e fam, which again is supposed to bolster that kind of LDS mechanism. But pa<ents with the hiatal hernia shown up in this cartoon where a liWle bit of the stomach touches up into the chest cavity. So usually a hernia. Within that iframe muscle, these pa<ents now no longer have that coordina<on of the LES muscle, inner sofas and the diaphragm muscle, and now they're separated and so. Things are more easily, can more easily reflect up to the sofas with the idle hernia. This is super common. Pregnancy, obesity, things that can increase just a maWer of pressure on the stomach can increase reflux. Pregnancy also has effect of progesterone being a relaxant of the LES. So very very common for pregnant pa<ents to have a worsening of reflux symptoms or even development of new reflux symptoms during pregnancy. And then a host of lifestyle and iatrogenic factors that I'll go over in the next few slides. So things that we that that can trigger GERD or contribu<ng to things that we eat. Common triggers include things like coffee, chocolates, mince, faWy and fried foods, citrus and black pepper. Some of these are just because they trigger symptoms, others because they increase gastric acid. And some can say because they relax LS including peppermints. There's move up to relaxing. Habits. You know, smoking, alcohol, been linked with bird, ea<ng late or ea<ng a large meal, going to bed and lying down aMer ea<ng late all can contribute to reflux. And some<mes we're giving things that contributed reflux. I don't think if to commit any of these medica<ons to memory, just recognize there's a whole host of medicines that we use and lots of different classes including you know, nitrates for heart disease, custom tobacco for blood pressure of these are kind of very important medica<ons that people need to be on when I see pa<ents in the clinic. With difficult to control reflux, I try to go through the list to see what might be changeable. For example, if someone on the custom channel back for blood pressure control, I might say you know let's talk to your primary care doctor about using it, ACE inhibitor or diure<c, something else that might be affected for blood pressure control but not affect the the risk for Gerber. Or reflux. That's talk about the actual symptoms themselves. The classic ones that you probably recognize would be that Harper and that burning sensa<on that comes up from the stomach upwards into the chest. Pa<ents some<mes actually get regurgita<on of acid all the way up to the oral cavity. Basis based salivate align something called water brash. Food may not go down smoothly. Some suc<on sensa<on that we call this phasia. And there are a host of extra intes<nal sorry, extra social manifesta<ons as well. Things like hoarseness, chronic cough, exacerba<on of asthma or chronic bronchi<s, noncardiac chest pain, and some oral manifesta<ons like dental erosion. So not only are symptoms annoying, but some<mes good can actually lead to real significant problems. These are some examples of endoscopies, so in the lower esophagus, and these are pa<ents who have actual erosions or ulcers in the esophagus. Umm. This is a nice example where the the ulcer recents have caused a stricture, so a narrowing of the esophagus so that can lead to food impac<ons or this phase like I scribed earlier. And so these are more severe complica<ons, but there's even more kind of significant complica<ons that can happen with your. Namely something called BarreWs metaplasia, which is a change in the the the cell type of the lower Sophus from a scream is epithelium. Normally the esophagus is squamous epithelium. It's just like our like our skin and endoscopic is should look like this, what we call a pearly Gray, kind of a pale whi<sh grayish color. Metaplasia is a change in the cell type from the squamous epithelium to something that resembles intes<ne, and so the intes<nal type metaplasia looks like this, what we call salmon pink. And so this is a risk factor for esophageal adenocarcinoma, in fact adenocarcinoma of Sophus. There's probably there has been recent years one of the most rapidly rising types of cancers in the US for a number of reasons. But GERD is kind of the, the underpinning behind it and so BarreWs esophagus can either. Feel adrenochrome which is shows up as a mass lesion shown there. So this can be a significant problem. You know more than just bothersome symptoms. Now as far as oral manifesta<ons, these tables show some of the the symptoms and signs have been described with with bird including, you know, symptoms like burning or <ckling, sensa<on in the mouth, sensi<ve tongue, bad breath. Impaired taste or water crashing in this excessive saliva<on. As for the of the 10th of the oral signs, dental erosion is probably the best described, but these other signs have also been reported with with their. Now studies looking at specifically at Orem sta<ons have defied dental erosion as the most common and it's found that up to 55% of pa<ents with George pa<ents at least in a few studies. And in this situa<on the mechanism of ac<on is acid is direct contact of acid on the dental enamel.s 5.5. One interes<ng thing in these days with sensory that guard may be silent. Pa<ents may not have the heartburn, the water brash, the acid regula<on. And so some<mes the dental version is the only sign. Now dental Rosen, as you'll know or probably have learned, is can be caused from a host of things, not just dirt. So the distribu<on and loca<on of the erosion can be helpful in determining what the cause is. Now GERD, because the acid they the the cosmic kind of contact comes from the back, right from our esophagus, the posterior teeth. Will be most severely involved and it will be the lingual and occlusal surfaces, as opposed to if someones inges<ng something that's causing their erosion through the anterior teeth and their labial surfaces will be most significantly involved and it will be less severe as you go posteriorly. Now management of GERD the aim to try to control symptoms. We want to prevent complica<ons like erosive esophagus, strictures and and and barreWs. And so we'll talk with the basins about their lifestyle, what are they ea<ng, drinking, when are they going to do aMer they they have their last meal. I'll show you go over his medica<ons By the <me pa<ents come to see gastroenterologist in the clinic, almost always they're going to need some type of medica<on because they have a frequent or severe symptoms and in some situa<ons surgery may be warranted. So we'll start with the lifestyle modifica<ons indicated earlier. You want to avoid lying down aMer your last meal. Usually we say about three to four hours aMer your last meal. Make sure you don't lie down for bed before then. Something must have allowed public trouble at night, because when relying supine, their sockets can't clear as well just because of gravity and so. It may be helpful to raise the head of the bed about 6 inches, provide that ton of that slant. Allow gravity to clear our sophus when we sleep. Obviously we talk about roo<ng dietary triggers and if applicable, you know, losing weight or maintaining a healthy body weight, avoiding the big meals, stopping smoking and drinking. All easier said than done, right? And so that's why by <me I see pa<ents, they've already kind of either ignored those recommenda<ons, try them and failed and now need some medica<on. And so there are three basic kind of categories of medica<ons that we use. The most simple are the end acids are things like Tums, Maalox, mylanta, basically just calcium is the most common ingredient where you can just pop it and neutralize. The acid provides the least immediate but temporary relief. So this is useful if pa<ents have very infrequent symptoms. Or they know that if I eat this, I'm going to get heartburn, so I'll take it commands or something like that at that <me. These two blockers, so histamine, which is the age there histamine is one of the important triggers for gastric acid secre<on. It's not the only one, but it's a big one and so if you give a histamine blocker, you can suppress that mechanism of acid secre<on. And so this is good for mild symptoms. Provides longer relief than antacids, which are very desperate temporary. So the common histamine blockers you see out there are things like Pepcid, AC. Which is for modera<ng. The biggest class or and really what most people pa<ents end up on at some point are the PPI or the proton pump inhibitors. These are best for frequent or severe symptoms and these are very potent an< acid secre<on medica<ons. They inhibit the final common pathway of all acid secre<on. So whether it's histamine or some other trigger. Causing our gastric acid pumps to make acid, the Ppis will block that final pathway and so. So these are very effec<ve but they have to be given in a very unique way which is not known to a lot of pa<ents even. Doctors and even some guests Realtors don't recognize that these are pro drugs. PPI's are inac<ve medica<ons. They're only ac<vated in our body in somewhere with a very, very acidic milieu. And the only part of our body with that not that acidic view is an ac<ve. Gastric acid pump. And So what that means is that you may need our stomach to be making acid while the while the drug is in circula<on for the drug to work. And so normally we we tell pa<ents that you have to eat something about 30 minutes aMer your aMer your dose otherwise the drug will circulate in their plasma looking for that acid pump. If it doesn't see it, our body eventually metabolize it. You see within 30 to 45 minutes for most of these guys and aMer that 34 to 5 minutes that PPI's gone and won't do anything. So this is something that we reinforce our pa<ents who you know are on a PPI but have ini<ally something control. We always say how are you taking in rela<on to your meal. So it's important to remember. And finally, some<mes surgery. Now the classic surgery, something called missing fundoplica<on, where the surgeon basically just physically wraps the upper stomach around the LES, so provides kind of a a physical barrier against reflux and regurgita<on. And so this is very effec<ve for something really now most pa<ents. Do with the hope of geZng off medica<ons. And s<ll having some control and and it can be achieved, but it's not a foolproof guarantee that they won't ever have to be on a medica<on again. And so we some<mes have to set our expecta<ons of pa<ents when they request you know surgery for their for their reflux that doesn't necessarily mean that they're going to get off medica<ons. This is just the before and aMer example of endoscopic appearance of someone who had this infla<on. This is before what we looking at here is the endoscope kind of coming in from the esophagus. This is upside down view. So we're have this scope kind of you turned up to look back at the entrance of the of the stomach. So this is the entrance area. And one thing you'll no<ce in this pa<ent is this big kind of shadow here. This is a gap around the scope and this is somewhere the large hiatal hernia. All this kind of <ssue around here with which is in the shaded area is above the diaphragm. So this person had to repair the hiatal hernia with basically a certain pull the stomach down and close up the hernia. And then did the RAP. And so now you see there's really no gap around the scope. This kind of <ssue here is the effect of the fund applica<on where now there's a physical kind of barrier to vengeance from the stomach to this opus. As far as managing dental pa<ents? These may or may not be too significant. I think these recommenda<ons came from preWy old literature, but NSAIDs with calcium we're geZng most common antacids will be calcium carbonate. These can interfere with Florida absorp<on, so there's a poten<al for some drug interac<on. Same is true with omeprazole risk for drug drug interac<on with diazepam. Omeprazole inhibits. The side from P450 system which is responsible for a lot of our metabolism of other medica<ons including in this case diazepam, benzodiazepine. So if you're using that medica<on for its seda<on effects, if you wear that, that that diabetes pen may be metabolized more slowly in the pa<ents who take omeprazole chronically and so you can have an increased set of effect. At a more kind of prac<cal or mundane level is that pa<ents with with bad girl, especially if they have a big hiatal hernia or very relaxed LES, they may have the trigger of symptoms and they're kind of puZng that supine posi<on for oral exam. So maybe something if it's possible to modify for the pa<ents that experience symptoms in the exam, just be aware of that. OK, what we'll do here, we're probably a liWle bit past the halfway point, so once we take like a 5 minute break. Happy to take some ques<ons while we're on the break, but when we plan on resuming at the. 855. So the first one is this 28 year old man who comes in with complaints of persistent swelling of his jaw and he can maybe appreciate a liWle bit of asymmetry on that picture there. He on the review systems men<oned that he's had some intermiWent rectal bleeding over the past eight months or so and. In this family history, he men<oned that his mother died of some type of intes<nal cancer in her 40s. He wasn't really sure of the details, but it was a GI tract type cancer. To get Xray, he shows that he has a large osteoma at the angle of his leM mandible. And underrated right canine. Of the mandible. As part of this work up for his family history and his rectal bleeding at a colonoscopy and this showed he had innumerable polyps, all these kind of round lumps. We have hundreds of them throughout this column, so this is someone who has familial adenomatous polyposis. Or FAP, and specifically what we call the Garner syndrome variant. We'll talk about what that means. So first slide about FAP. This is a gene<c condi<on, a single gene disorder. It's thankfully rare, but it's caused by a muta<on of a single gene called the APC gene on chromosome 5. APC gene is believed to be kind of like a gatekeeper gene. Where if it becomes mutated, it leads to the IT can. Need to pathway to colon cancer. It seems to be kind of one of the first important muta<ons that occurs from pa<ents develop colon cancer even without this syndrome. Pa<ents who develop colon cancer very oMen have muta<on of a CD and FAP. Pa<ents are born with FAP or APT muta<on. But every cellular body has a defec<ve ABC game. So this occurs in about 1 in 10,000 people in men and women. And the main clinical feature is in our our case is the presence of mul<ple, some<mes hundreds or even thousands of adenomas, which are the precursor polyps to call. Cancer. The average age of popula<on in in pa<ents with FAP is 16 years, so teenagers and if untreated, meaning if the colon is that removed, 100% of these pa<ents will develop colon cancer in their life<me, typically by the <me they're 40. This is just a gross resec<on specimen of someone who had FAP and all these kind of cherry red growths are adenomas. Now the term Garner syndrome is applied when we have some with that gene<c FAP with some type of prominent extra intes<nal manifesta<on, and so one of the most important ones, as in our case are present the Bony tumors. These are very common in the jaw, but can occur in the skull as well they can have problems with. That their their eyes. They can have tumors elsewhere, including in the brain. The pancreas and thyroid cysts in the skin can be seen with the syndrome and dental abnormali<es. And and the thing that's unique about this syndrome is that some<mes the dental abnormali<es may even proceed the colonic polyps. The main oral manifesta<ons of Gardner syndrome are listed here, including supernumerary teeth, unerupted teeth where these tumors of the of the jaw odontomas were osteomas. Um. So that pa<ent had FAP. I wanna talk just briefly about a couple other polyposis syndromes will <e it all together is what we talked about colon cancer. But there are two kind of named polyposis, hamartomatous polyposis syndromes that have unique oral manifesta<ons and are linked with the increased risk for some type of cancer. Uh, GI or otherwise. The pres<gious syndrome is is one of them. Here, this is again a single gene disorder, but this is A and this is also AutoZone dominant, so if the person gets one bad copy from either parent, they'll have the disease. As opposed to FAP where pa<ents had adenomas which are there again the precursors to colon cancer, pa<ents with push figures and Caltrans we'll talk about in a moment have hammered Thomas that hammer Tomas are just normal <ssue in abnormal spot And so technically these are not precancerous type growths, but they can s<ll cause a lot of problems including blockage. Feeding and something called intercep<on Where? Part of the this occurs in a small valve where a growth in the valve can kind of lead to telescoping of that valve down to another segment and that can lead to a ballot struc<on. Now even though hammer communist policy as I just said are not technically precancerous growths, pa<ents are push dagger syndrome are at very high risk for cancers both TI and non TI. And so these pa<ents by the <me they're in their mid 60s have over 90% chance of having some type of cancer. So when we iden<fy these. So typically you'll be as a teenager or young adult. These pa<ents aren't going surveillance or screening exams for all sorts of cancers. My specialty, we screen them for things like colon cancer. Pancreas cancer, small intes<nal cancer, but again non GI cancer risk is also significant increase in pa<ents with Postgres. The unique thing about procedures of the oral sign lines and this is something that we see in our specialty every couple years, but this, these are the kind of classic flat spots, very small typically around the lips or the perioral region, perioral region. But also inside on the buccal mucosa, and also at least un<l adolescence, on their hands and their feet. So you might be able to spot them there. But aMer puberty the these spots tend to fade, except for the buccal mucosa lesions. And so recognizing these kind of oral signs obviously would be very important, especially if there's no known family history. Of pres<gious or whatnot. This can lead to a very important diagnosis. Powder syndrome is the other kind of main hammer tomato syndrome. And in this case, the hammer combos can occur in different organs including skin or mucosa GI tract in their breast. The important thing about paWern syndrome is that that these pa<ents are at high risk for breast cancer and thyroid cancer. And the oral signs are shown here. They can include these papillomatous growths on the lips or the mucus membranes and this kind of cobblestoning of the tongue. So it's alluding to these all signs can be very important and some<mes the presen<ng sign of a syndrome that can carry a very significant risk for disease including cancer. And so if you see any of these signs or suspect them, you know, you make sure you get a thorough family history of cancer, full physical dam and perhaps it's the next consultant. There are, you know, blood tests can be done to like diagnosis gene<c disorders. Now. Thankfully these polyposis and Hammer home the syndrome overall are very rare and contribute just a very small piece of the pie. As far as what actually the overall colon cancer burden, the majority of pa<ents with colon cancer are shown in this big cyan wedge here where there's we call sporadic, there's no underlying. Known risk in a family, in the genes, et cetera. And so these polyposis and hammered promises emphasis these liWle slivers of the pie. And about 1/4 of pa<ents have some type of family history. So that's called familial colon cancer, even though it's not truly an inherited cancer syndrome. So I wanted to talk a liWle bit about colon cancer, Colon cancer because it is a a very common and can be poten<ally lethal but preventable cancer. Based on recent sta<s<cs, about 149,000 people will be diagnosed in the US each year with colon cancer, and about 53,000 those pa<ents will die each year in the US. So unless born today in the US, has about a 4% life<me risk for developing colon cancer. This has slowly trickled down, I think when I first started. In this lecture nearly 20 years ago, it was closer to like 6% and through screening, more awareness of things has come down a liWle bit. Although there is a liWle bit of disturbing trend in that recent trend show that increasing race and diagnosing young individuals very prominent. Colon cancer and a young individual recently was Chadwick Boseman, Black Panther, who had laces colon cancer in his 40s and for reasons that are not en<rely known yet, the hypothesis, which we'll get into, but for reasons that are not en<rely no, we're seeing increased risk or increased diagnosis of colon cancer in 40 year olds. Early 50s. And so even though the mee<ng age is s<ll, you know, kind of mid to late 60s, there's this bump which actually has led to changes in our screening recommenda<ons. Now this is the old slide, but the general trends are s<ll generally true that age. It's showing that age is the major risk factor for sporadic colon cancer. So again, pa<ents with no known gene<c inherited risk, age is the main risk factor. We can't do anything about that, right? And also just shows that for for at each age it's more common. In men than in women. The risk factors are calling cancer shown here. We talked about kind of AIDS being the main risk factor and it's a strong one. Long standing inflammatory bowel disease we talked about in our first case is a strong risk factor and polyposis syndromes like FAP which is strongest factor model risk factors include. Having a family history or personal history of these precursor polyps or adenomas, having radia<on, it seems to increase your risk. And then the thing that pa<ents are most kind of interested about, like diet, lifestyle, probably have some effect, but only a modest effect and so. Things like having a fiber rich diet, side high fat diet, red meat, a lot of red meat and diet probably increase the risk of colon cancer somewhat. Same things with obesity or sedentary lifestyles increase the risk somewhat. Smoking, definitely. We know alcohol is well. As has as far as how to protect what reduce risk for colon cancer. You know we believe again it's hard to show but high physical ac<vity, high fiber diet, lots of fruits and vegetables, some of these things probably affect our gut microbiome alluded to earlier and the microbiome may play a role in in colon cancer development, but these probably have modest effects on. Colon cancer. NSAIDs we talk about some of the poten<al harms for ends earlier, but NSAID use regularly has been also linked with the decrease risk for colon cancer, aspirin included. However, most medical societal guidelines fall short of recommending using these ancestral aspirin regularly for colon cancer preven<on because of the risk of side effects or toxicity. I see from these medica<ons. So there's no widespread blanket recogni<on right now that pa<ents should or should not be on and said we're aspirins for colon cancer preven<on. Now, concerning present in any number of ways, probably the most common presenta<on would be some degree of rectal bleeding. It could be minor, some<mes just spot of blood on this tool or intermixed in this tool. Some<mes there's no visible visible bleeding at all. Pa<ents can just present with iron deficiency as a result of chronic occult or invisible bleeding. In late stages it can cause a change in the bowel habit or in a stool caliber or even need to frank obstruc<on. But the most important thing is that it can be completely asymptoma<c un<l it's already advanced or metasta<c and therefore you know we put a a big emphasis on screening for colon cancer, so for preven<on. Now a couple of kind of interes<ng things about colon cancer as relates to to the oral cavity. First of all, colon cancer can metastasize or cavity. This is not a common metastasis paWern. Usually you can't colon cancer spreads or go to the liver first and oMen<mes nowhere else besides that. But there are case reports of. Metastasis to the oral cavity. So in these situa<ons they were described most commonly to the posterior mandible. This has to relate to the fact that it's hematologist. They spread so through the the blood flow, but can present with. Pain paresthesias or loosening of teeth or like a non healing extrac<on socket. And this is a situa<on where a biopsy of a non healing socket found this <ssue here which is. Not all, Kevin, because of this is metasta<c colon cancer. This one obviously had a prior, this pa<ent had a prior history of colon cancer, but the metastasis was found in oral cavity. The other thing that I think is kind of interes<ng is that there's an oral pathogen, Fusobacterium nucleatum. Which has been linked with colon cancer, increasing risk for colon cancer and adenomas and the pathway going from adenomas to colon cancer. So this this pathogen is found in abundance in the colon cancer <ssue and in the lining of ENCOSTA pa<ents with the precursor polyps or adenomas been talking about. In the in the in vitro, this pathogen has a pro carcinogenic effect. And clinically there's there was their view, very few studies kind of on the. Clinical, you know showing any clinical significance of this pathogen. But there was an abstract that was presented in one the GI mee<ngs a few years ago that found that more frequent dental visits was inversely associated with the the presence of autonomous Apollo. So these precursor polyps about a 30% risk reduc<on and so we talked about. You know, cold cancer screening and preven<on. One important aspect that we don't kind of talk about much is maintaining good oral hygiene and seeing dental personal regularly for cleanings etcetera. There may be a link there, there appears to be a link there. OK, we've got the clinical scenario 4. This is a young woman, 25 year old woman who presents with painful cracks at the corners of her lips and a burning sensa<on of her tongue. This is maybe a representa<on of what you look like, and on her review system she reports having very frequent loose, greasy, foul smelling stools. So she had some stool studies done by your primary care that said that you breaking abnormal and the fat in the stool and blood test unless you use anemic. Let's use low in both iron and folic acid. A blood test was done called the an< <ssue transglutaminase for TG an<body and she had elevated levels and so this all led to diagnosis of CVA disease. The civic disease is probably more common than we appreciate, but it's really the gluten. I know that gluten is like. Very. It's like Public Enemy number one, some<mes, right, as far as dietary GI symptoms, etcetera, etcetera. But gluten in pa<ents with celiac disease causes a real inflammatory problem. And so that's what celiac disease it's an inflammatory condi<on of a small intes<ne, someone who's gene<cally suscep<ble and is triggered by ingested gluten. So that's found commonly in wheat, rye, barley, but it can be found it can be found in other things, including certain medica<ons. Some<mes the coding or the capsule may. So those are the things that it could be kind of a lot of things, but dietary inges<on is the most common trigger. This is most commonly in in whites of Northern European ancestry, but we're star<ng to see in all sorts of popula<ons around the world now, but most of the <mes at least in kind of Europe and North America based on blood tes<ng found that. Influence of about one in 120 to one in 300. Most of us say rather recently have it about 1:00 and 1:50, so not uncommon. Now the presenta<on is very variable. It can present an embassy that's probably the classic presenta<on and I'm not a pediatric guest for all this, so I don't see these childhood diagnosis, but we certainly do make occasional diagnosis in adulthood. Pa<ents can present with Frank Mel Gibson, so this foul smelling greasy stools. A weight loss and perhaps even nutri<onal deficiencies. But more oMen, at least in in adult GI some<mes can be very mild or even asymptoma<c, some<mes just in the workup of iron deficiency. We find that there. And because they're just not absorbing the iron normally or they can have very mild symptoms like occasional loose stools or certain foods sugar. You know diarrhea. Those type of symptoms are preWy common. Some<mes connec<vity is symptom of of subclinical celiac disease. Now seeing disease most commonly presents in the gut, but it can present in other parts of the body, kind of like what we talked about with IBD. There are extra testament sta<ons of celiac disease as well. One of the most prominent on the skin is something called derma<<s repe<<ve formis, which is kind of a vesicular silica, blistering, itchy rash. Which is most commonly on the extensor surfaces of the arms, some<mes around the the trunk, but it has been reported to occur in the oral cavity as well, so that this picture down there is example of oral derma<<s herpe<formis. There are a whole host of other associa<ons. You don't have to commit any of these. Memory, some of that we pay aWen<on to in our prac<ce is actually increased risk for GI tract legacies. So it's something that we that we in our prac<ce are very aWuned to as well. And it's believed that these malignancy risks are increased in pa<ents who are poorly controlled, have poorly controlled celiac disease. So some of the oral manifesta<ons are shown here. The most common whether classic one or the the dental enamel defects or enamel hypoplasia you can see here it's typically bilateral and symmetrical to talk about. In the first case, civic disease is on the differen<al diagnosis for pa<ents who present with recurrent oral at this stoma<<s. And the other signs that have been reported including delayed 2-3 erup<on, smaller teeth or again less common in the in the US just because of how our food is kind of for<fied. But the tradi<onal deficiencies presen<ng with coli<s, this atrophic last si<s and gingivi<s can occur. The way we diagnosis this is first of all through a blood test. This was an<body that is checked in the blood and in pa<ents with C diseases they'll have a lot of this an<body. But the way we since the diagnosis is by doing a small bowel biopsy. So if we have someone with suspected CIA disease in the in a posi<ve TTG an<body, we'll do an upper endoscopy and take a biopsy of the small test. And now on the leM here are our normal examples of normal diascopy and normal biopsies. And you can see the normal biopsy we all have these villi, these liWle finger like projec<ons that these are the absorp<ve surfaces of our small intes<ne. And someone said that disease you can't really show that the endoscopy features don't show up on the slide. But oMen<mes you can see visually that the villi are kind of blunted the instead of looking like a like feathery lining like a normal <ssue. Some<mes it looks kind of scalloped or knobby or notched. But the really the the main thing we rely on is a. I'm just looking at a microscope of our small biopsies and in this case you see no more of those strangulate projec<ons. So these are disabili<es blunted or complete planning in some cases and there's a lot of inflammatory changes as well. Again, that's the immune, it's a sign of immune mediated effect that there's inflamma<on going on. The treatment is both easy and difficult and it really is just one main thing which is lifelong gluten free diet. They're really right now, no approved medica<ons for treatment of celiac disease. There are things obviously we do for counseling and educa<on and replacing the nutri<onal deficiencies at present, but really it's a lifelong avoidance of all gluten, so that means avoiding we rye malt barley bruises. That old oats are are generally don't have gluten, but some<mes they're contaminated by other products that do have gluten. So for celiac disease pa<ents, we always tell them even if you're ea<ng oats, make sure that it says on the labeling that is gluten free. And so we you know pa<ents are educated to kind of make sure they're reading all the labels on their the prepared foods or condiments. And when we prescribe medica<ons for for celiac disease pa<ents, we I always look on this online database for gluten free medica<ons just to make sure that when I'm prescribing won't be trigger. As far as dental pa<ents are involved in their management. Some<mes pa<ents can absorb malabsorbed so significantly that they may absorb malabsorbed iron and become anemic or their vitamin K and become a risk for bleeding and quite good pathic because vitamin K is one of the key factors in our coagula<on system. So prior to invasive dental procedures that may involve more than trivial bleeding, you want to make sure that you're dealing with the kind of normal coagula<on parameters. As someone who's not severely anemic that they would be at harm if they lost addi<onal blood. There's also recogni<on that some pa<ents may be very sensi<ve to even brief exposure to gluten, so some prophy, paste and fluoride humans may have gluten in them, so having a gluten free op<ons to be considered. I am last case here is a 65 year old male who presents with a chief complaint of bleeding gums he miss. He doesn't brush or floss or come to the den<st right oMen. His examina<on shows a severe periodontal disease. He looks a liWle bit yellow in his eyes, under his tongue and he's got these swollen prostate glands. He reports that he has a long standing history of alcohol use disorder. So this is someone who has cirrhosis from alcohol with periodontal disease in salad enosis. Just a word about dental and periodontal disease in pa<ents with alcoholic cirrhosis studies Tips from that alcohol abuse predisposes to kind of poor dental hygiene, carious teeth, oral cancers, and infrequent professional dental care. No, this isn't true of all obviously Alcoholics erra<cs or all ceramics from other causes, but something to be aware of in pa<ents who have this diagnosis. I just want to take a step back, Well, what do we mean by cirrhosis? So this this term we apply when someone has a late stage of progressive aZc fibrosis. For a liver scarring, this is an example of a a cirrho<c liver which is all knobby and and nodular and and bold. And the most common causes are shown in bold here. Alcohol abuse is probably one of the most common causes. While help head is BC worldwide are very common causes. Although you're now with the current humans, we can essen<ally cure Hepa<<s C with rela<vely, you know with rela<ve ease and Hepa<<s B you know we can vaccinate against and there are treatments for that as well. Although the can s<ll leave this rosis, but probably the. The most rapidly growing group of ceramics, especially in western popula<ons, are not non alcoholic faWy liver disease, so these are people who have don't drink excessively. But develop faWy liver disease as a result of what we call the metabolic syndrome. This usually includes things like high blood pressure, diabetes, high cholesterol, obesity. This kind of syndrome increases the risk for faWy liver disease and about 15% of pa<ents with faWy liver liver disease will go on to develop. Cirrhosis. So this is an important pa<ent popula<on that we're seeing more and more of, especially in our country. Now, sources some<mes can be completely asymptoma<c pa<ents may have sources and have no problems at all. When you start seeing problems, we see in in a number of categories, one of the the key kind of origin of problems is something called portal hypertension that refers to high 10 high pressure in the portal vein, which is one of the main kind of blood supplies to the liver, the portal vein. So when there's high pressure in the portal vein. Release the sides, which is fluid accumula<on in the belly. It can lead to varices in the Sophus, basically like varicose veins but in the food pipe, and these can cause massive gastrointes<nal bleeding. Pa<ents can get mental status changes, what we call hepa<c encephalopathy. Some<mes this is very trivial. At one extreme, cases may may be comatose from athle<cs clothing. Those are pa<ents who are in the hospital, obviously. But on the other end of the extreme, pa<ents may just be slightly inaWen<ve. They may have a liWle bit of forgenulness, They may have trouble sleeping at night, but kind of drowsy during the day. Those are kind of early signs of concep<on supply. The that could be related to cirrhosis. The other thing that results is that the spleen becomes hyperac<ve. We'll call hypersplenism. Spleen is basically like a filter of our blood. It kind of clears out blood cells, and one of the cells that it clears out are platelets. And so someone with a hyperac<ve spleen can get very, very thrombocytopenic, some<mes dangerously so. The liver is also responsible for making a lot of things in our body, a lot of proteins, including the things that caught our blood. And so pa<ents with impaired liver func<on can have problems with blood cloZng. And then finally, pa<ents with sources or increases were hepa<c cellular carcinoma. Again, this is probably related to chronic inflamma<on in the liver leading to cancer. So some of the oral and oral facial manifesta<ons are shown in the city here, including kind of a a jaundice that can be shown in the skin and eyes. But actually the first place that shows up before it shows up in the skin or the eyes is usually under the tongue or in the in the paleWe and so. This will be kind of the first place you know I'll look if someone I suspect might be joined this business showing up elsewhere and having that yellow discolora<on is is a telltale sign that there might be something wrong deliver. Um. This example of something like in plainness this is linked with Pepsi did not really alcohol related sources but hepsi is a very common cause for cirrhosis and and you can see this kind of the white Lacy kind lesion here on the on the Gingiva. This is an example of metasta<c liver cancer that went to the oral cavity. They're not very common paWern of spread for liver cancer, but it can happen. And then we'll just wrap up talking about kind of implica<ons for management of dental pa<ents, pa<ents with cirrhosis. The first one is kind of intui<ve, but for pa<ents with boWle HeMy Inc. Prac<<oners are at risk for infec<on. It's a bloodborne and body fluid spread, so obviously you take universal precau<ons. There's also kind of a. A very unfortunate situa<on years ago about oral surgeon Tuscaloosa who was had a he was prac<cing den<stry. He was not properly cleaning his. The supplies as he would, he would go from pa<ent to pa<ent without proper kind of steriliza<on of his equipment. And this is back in like 2013. Years later he was inves<gated because of. TransmiWed infec<ons of Pepsi, Pepsi even I think a case of HIV actually because of his prac<ce, the the very first human to human transmission of, I think it was Hep C was documented through all procedures. So obviously that doesn't apply if you prac<ce normally, but that's just kind of a sign that. You can spread disease through oral procedures, dental procedures. Again, relate to those who have severe thrombocytopenia or cirrhosis who may have severe thrombocytopenia. Quote allopathy. You want to assess their risk for bleeding prior to invasive dental procedures And then there's a whole host of medicines that the drug metabolizes and there's and so these are challenges in in selec<ng medica<ons for pa<ents with Pastoris. Some<mes pain control can be a difficult situa<on for us to italics. You have seen a minivan is generally safe when used at safe doses now for each one of us. With presumably healthy rivers, if we overdose on acetaminophen we can destroy the liver. It's one of the more common causes for drug suicide aWempts through drug overdose. Because you can't, you will dissuade the liberty if you overdose on on scene. So with cirrhosis can handle a liWle bit of a senior minivan but no more than using about one or two bands per day. So typical kind of extra strength tablet is about 500 milligrams. So we usually tell them no more than two to four exis<ng pound all in the 24 hour. And sets is the other major category generally safe, but again we have to be cau<ous because they can present, they can precipitate bleeding because they do impair platelet func<on a bit and some<mes it can precipitate kidney failure, which I didn't talk about when we talk about kind of complica<ons of liver disease but. Pa<ents with best roses some<mes are teetering on the edge of kidney failure. And so in those pa<ents that we iden<fied, we avoid NSAIDs and the other big category of opiates, again, generally safe for cirrho<cs, but in pa<ents with bad cirrhosis, especially if there's an element of pa<ence philosophy. Opioids can precipitate or worsen the supply apathy and so you have to make sure you limit your use to short term and perhaps increase your dose interval so so instead of like every 12 hours, you might say one a day Max, things like that. You've been anesthe<cs again, we're not going to go over every single one of these, but anesthe<cs can you metabolize the liver. So there are situa<ons we have limited dose and same is true with seda<ves. And this is going to be too much to commit to memory. But just recognize that there are a lot