Digestive System review: March 13, 2025

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Stacey Ostrin: Okay, well, Hello, everyone. This is Dr. Ostrin coming to you first. I want to say thank you for your flexibility with me. I apologize that I needed to pivot. I had something come up with my family that I needed to take care of. So this session had been intend to be in person, so I’ll do my best to make it something you can follow along like a conversation, and then certainly, if there’s anything in here that you have questions about

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Stacey Ostrin: or want to talk through, please email me. And I can certainly meet as set up a meeting time as well to talk through things, so that is available to you. This was intended to be given on March 12, th but I’m not sure when this is when you all be watching this, but I hope you enjoy

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Stacey Ostrin: right.

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Stacey Ostrin: So once again, nothing to disclose. Normally I would have wanted this to be collaborative, but it certainly can be just asynchronously. But if you could remember, these are the 3 little stars that I would put on my notes. I actually put a red star on my notes whenever I heard of something that was either really applicable to boards or very common on wards. So just keep that in mind as you’re looking through these slides.

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Stacey Ostrin: So the objective is today to recall highly tested disorders, the gastrointestinal system or digestive system and bridge connections with other systems.

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Stacey Ostrin: All right, we’ll start with the 1st question, a 59 year old, male patient, with a history of alcohol use disorder, presents to the emergency room. With severe retrosternal pain and hematemesis. He reports he had a night of heavy drinking, followed by repetitive, forceful vomiting that contained bright red blood. On physical examination he has midepigastric tenderness and subcutaneous Emphysema as noted which of the following is the most likely diagnosis.

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Stacey Ostrin: Right? Let you look through and think.

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Stacey Ostrin: Pause it here, if you need.

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Stacey Ostrin: The answer is Borjabi syndrome.

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Stacey Ostrin: So I’m going to go through each of these questions and kind of talk about kind of the big takeaways. So with this question.

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Stacey Ostrin: really, I was hoping to get at the differences between Borjavis and Mallory. Weiss, and I heard this once that Bohr Javies is bad. Mallory Weiss is nice as a way to try to remember the differences. And you can kind of see here, you know, this patient did have hematemesis, which means bright red blood that they’re vomiting. But what may happen on questions is they will show a patient with normal vital signs

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Stacey Ostrin: or abnormal, and with Bora hobbies. Since this is not a good thing to have. They will often have abnormal vital signs

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Stacey Ostrin: that wasn’t included on this exam. But what was included was this kind of crepitus that was palpated. And so what that was to signify is that there’s been a rupture often, or perforation at the ge junction of the esophagus. And there’s some subcutaneous Emphysema. And so, if you have a patient with Bohr hobbies, it is an emergency. It is bad. And so, recognizing that right away is really important

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Stacey Ostrin: with Mallory Weiss. They may still have hematemesis, but often their vital signs were normal. They won’t have any crepitus or subcutaneous emphysema majority of those cases can heal with conservative management.

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Stacey Ostrin: What might you see on a chest? Radiograph? So on. Chest radiographs. They may show this, but you might see, I’m not sure if you can tell. But this kind of radiolucency here, this is showing some pneumo mediastinum. And this is kind of the subcutaneous emphysema. You can kind of also see it up here at the Cervical thoracic Junction. So be mindful. They may show an X-ray. That kind of asks you to look at that and see what they’re see what might be going on.

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Stacey Ostrin: So I put this in here, because, as you know, I try to talk fast. My goal is for folks not to be able to listen to me at twice speed. But no, I’m just kidding, but if you are listening to high speed, maybe that this resonates with you. I thought it was fun

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Stacey Ostrin: all right. Next question. A 53 year old female patient presents with a several month history of difficulty, swallowing solid foods and a 6 month history of fatigue. She has no significant past medical history. She denies fevers or weight loss. Physical examination reveals conjunctival pallor and fingernails as shown below. Which of the following additional findings is most likely in this patient. So pause here to think.

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Stacey Ostrin: and when you’re ready.

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Stacey Ostrin: so I wanted to talk through some of the things to highlight before answering. But this patient has difficulty swallowing solid foods.

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Stacey Ostrin: It’s been going on for 6 months. They have fatigue, they also they have not had any fevers or weight loss, so malignancy is probably less likely. They have conjunctival pallor, and these nails, which I would normally ask you what you’re thinking in class. But this is to try to point you to the direction that this patient has anemia, particularly iron deficiency, anemia. And so the answer here is esophageal web. And the goal of this question was really for folks to

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Stacey Ostrin: think about Plummer vinson Syndrome. So this is a really rare syndrome, but it’s something to keep in mind, and they often present with this trial of iron deficiency, anemia, dysphagia, and a cervical esophageal web.

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Stacey Ostrin: So boards loves this thought, I’d throw this in there very rare. As I said before, the other thing to think about is that this is a pre malignant disease. So these folks have an increased risk of squamous cell carcinoma of the esophagus, and so they might say, they might give the same scenario and just say, what’s the most likely complication, or what’s the most not likely. Excuse me, what’s a severe complication of this disease? So keep that in mind as you’re studying.

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Stacey Ostrin: What would you expect to see on a Cbc in this patient?

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Stacey Ostrin: So if you were to get a Cbc. What would you expect the hemoglobin and hematocrit to be.

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Stacey Ostrin: Look, what would you expect the mean corpuscle volume to be

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Stacey Ostrin: low? So this would be a microcytic anemia. What would you expect? The red cell distribution with to be or Rdw.

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Stacey Ostrin: Hi, iron studies. So think about iron studies with an iron deficiency. Is the Ferritin low, high, or normal.

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Stacey Ostrin: low? What about the iron level

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Stacey Ostrin: low. And how about the Tibc, the total iron iron binding capacity?

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Stacey Ostrin: Hi, so this is just a refresher to think about. The second thing is, you know, anytime in the digestive system, when we see somebody with iron deficiency anemia, we should be thinking about that critically. Why are they losing blood. Okay? Or why are they anemic? Is it absorption issue? But any men and postmenopausal women should be evaluated

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Stacey Ostrin: with gastrointestinal endoscopy? If they’re diagnosed with iron deficiency anemia. Because if they’re not menstruating, then we and we don’t really have a reason why they are iron deficient. That should be investigated further.

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Stacey Ostrin: Okay, this is just a reminder of what it looks like under a microscope. I’m not sure how long it’s been since you all have had heme, but they’ll have this microcytic, hypochromic looking cells, the platelets can be increased, and they can have a variation in the size of the Rbcs.

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Stacey Ostrin: Alright.

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Stacey Ostrin: all right. Next question. A 59 year old, male patient, with a history of gastroesophageal reflux disease or gerd presents with ongoing dyspepsia. For the past 15 years he’s never been able to stop the Pantoprazole proton pump inhibitor he takes without continuing to have severe symptoms. He is a non-smoker. An upper endoscopy is performed and revealed a 3 cm long segment of salmon colored mucosa. In the distal esophagus

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Stacey Ostrin: biopsy of this area is most likely to show which of the following cells

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Stacey Ostrin: pause it here, if you need to think on this for a second, I’m gonna answer.

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Stacey Ostrin: Well, before we get to the answer, I wanted to highlight just the things that kind of pick up. So oftentimes on boards or standardized types of tests, they’re really trying to highlight the really pertinent information. So this person has gastroesophageal reflux disease or Gerd. They’ve had it for a while, so they’ve had it for 15 years. Other thing is that they weren’t able to stop their protonics or excuse me, Pantoprazole.

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Stacey Ostrin: that he takes he’s a non-smoker. He was noted to have this salmon colored mucosa. That’s a pretty kind of

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Stacey Ostrin: common thing for someone with this disorder to have it. This be described, and it’s in the distal esophagus. So the answer here would be goblet cells. Okay?

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Stacey Ostrin: And so just to try to talk through this a little bit metaplastic, squamous cells that would be seen with something like squamous cell carcinoma, the neuroendocrine cells that’s more hormone producing cells, ciliated columnar that’s going to be primarily found in the respiratory system and multinucleated giant cells. Those can be seen in more of a granulomatous process or granulomatous diseases like tuberculosis and sarcoidosis. So just an fyi.

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Stacey Ostrin: So Barrett’s esophagus is really what this was getting at. So this person has had a long standing acid reflux, and I always think as they’re swallowing

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Stacey Ostrin: food, and if they’re reflexing that acid into the distal esophagus frequently for a long period of time, I always think about the body is trying to protect itself. Right? So it’s going to start making these kind of mucus secreting cells to try to protect it from the acid. Well, those mucus secreting cells. They’re actually metaplastic. So normal lining of the esophagus is going to be the stratified squamous cells.

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Stacey Ostrin: And so kind of this constant damage makes these cells change, and whenever you have kind of a changing of the cell that can be problematic, so regarding the previous patient, which of the following conditions are they at greatest risk of developing? Is it Achalasia, esophageal adenocarcinoma, gastric adenocarcinoma malt lymphoma, or squamous cell carcinoma of the esophagus so I’ll let you pause here to think.

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Stacey Ostrin: And the answer is, esophageal adenocarcinoma. Okay? So chronic. Gerd increases the risk of esophageal adenocarcinoma. You know other things. That can sometimes contribute to this having a hiatal hernia. Sometimes obesity can contribute to this. So it’s something to keep in mind. This is the most common esophageal cancer in the United States. So keep that kind of epidemiology piece in mind.

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Stacey Ostrin: Okay, so here’s the other things to think about. I wanted to include this here, just to briefly talk about some of the other things that were listed so, Achalasia, that if you remember, this is the one that has the bird’s beak.

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Stacey Ostrin: And so Achalasia is a failure of the les lower esophageal sphincter to relax. And it’s often caused by this degeneration of neurons in the myenteric plexus has this bird’s beak. Finding on barium swallow. Secondary Achylasia boards, loves this. Okay can arise from Chaga disease. So a reminder that came from the

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Stacey Ostrin: Trypanosoma Cruzi protozoa infection from the kissing bugs. I always kind of try to remind folks that it comes from the kissing bugs because I’ve seen that come up. I don’t know where, but on testings somewhere.

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Stacey Ostrin: esophageal atocarcinoma, the risk factors for that are chronic. Gerd

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Stacey Ostrin: Barrett’s esophagus and tobacco use gastric adenocarcinoma risk factors, are helicobacter, pylori, infection, smoking history, heavy alcohol, use dietary, nitrosamines, hot liquids, and chronic atrophic gastritis. Malt lymphoma that’s the one that we always think about in association with helicobacter pylori, and then squamous cell carcinoma of the esophagus. This is typically in the upper two-thirds of the esophagus. So keep that in mind

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Stacey Ostrin: okay.

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Stacey Ostrin: so just some more information about Barrett’s esophagus to try to remind. And you can kind of see here the salmon colored patch on endoscopy.

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Stacey Ostrin: Normally, this is the slide for questions. So if questions email me, the next one, this 10 year old female is Brad

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Stacey Ostrin: in by her parents with weight, loss, recurrent diarrhea, and Arthralgias. She has tried eating the brat diet, so bananas, rice, applesauce, toast, and eliminating dairy products without improvement. She has a 4 year history of type, one diabetes mellitus that is well controlled on an insulin pump. On examination she appears thin with bloated abdomen. Laboratory studies reveal a hemoglobin, a 1 c of 7.0 macrocytic anemia and a positive

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Stacey Ostrin: Sudan. Excuse me, stools Sudan. 3. Test. So

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Stacey Ostrin: give you a moment to think about this. But what are you thinking this might be.

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Stacey Ostrin: and what would be the next best test to order.

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Stacey Ostrin: So

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Stacey Ostrin: as you’re thinking on this, this is a patient with weight, loss, recurrent diarrhea and arthralgia. So we’re thinking, okay.

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Stacey Ostrin: something’s going on. And they also have arthralgia. So this is systemic. Okay, they have type one diabetes

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Stacey Ostrin: which you know, can be seen as an autoimmune process, a bloated abdomen, their hemoglomy. And see. What do you think about that normal, abnormal, high, low

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Stacey Ostrin: for type, one diabetic that’s a pretty fair range. It’s not normal, but it’s definitely near the goal where we want them and macrocytic anemia. So they have macrocytosis for some reason.

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Stacey Ostrin: and then the stool. Sudan. 3. Test being positive, the stool sudam 3. Test is a qualitative diagnostic test. So it’s used to detect the presence of fat in the stool, so they have fat in their stool. So they’re not absorbing. So

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Stacey Ostrin: what are you thinking?

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Stacey Ostrin: All right? Well, this was a classic description of hope of celiac disease. So celiac disease. The way that we test it typically in clinic is this anti-tissue transglutaminase antibodies. Okay, so this iga based transglutaminase antibodies

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Stacey Ostrin: so, therefore, in this patient we want to check the Iga tissue transglutaminate antibody. Excuse me, I said, that a bunch of times, and also the total iga levels because there are folks with celiac who have an iga deficiency about 2 to 3%. So make sure to think about both of those 2 tests. Okay.

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Stacey Ostrin: So now you have the same patient. I’m not going to read through the top. But this new part here is oops. Excuse me. A small bowel. Biopsy shows villus, atrophy, crypt, hyperplasia, and intraepithelial lymphocytosis.

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Stacey Ostrin: You decide to ask her about a possible rash which rash is most likely to be associated with her underlying diagnosis.

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Stacey Ostrin: I’ll give you a moment to think about it, even though I already gave it away.

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Stacey Ostrin: All right. So dermatitis ripatiformis. Okay, now, I wanted to bring your attention to this one as well. Necrobiosis lipotica diabeticorum. So I’m not sure if your dermatology

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Stacey Ostrin: lectures contain this. But this is a common board question. At least it was for me. And so I’m going to talk about both of these. And there’s a possibility that one could argue. Could that be present in this patient. So

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Stacey Ostrin: I’m going to go through each of these rashes. Malar rash. Typically, we think about that with systemic lupus erythematosus. It also can be seen a few others. I’m not going to go through them, but the list is here. Erythema nodosum. You just came off of rheumatology, so something that we do see most common, identifiable causes. We think about streptococcal infections, but it certainly can be present in inflammatory bowel disease and other disorders. So it’s not specific

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Stacey Ostrin: to any one piece. Dermatitis herpatiformis. This is pretty much like

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Stacey Ostrin: seen in celiac disease. It’s not very common, and it’s not always seen, but when you do see it. It’s often celiac. Okay. Psoriatic plaques psoriasis can be. Excuse me. Associated with celiac, but dramatically

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Stacey Ostrin: hepatiformis is more specific and then this necrobiosis lipotica diabeticorum this can be seen in diabetic patients which this patient is. And it’s typically in type one diabetic. So I’m going to talk about that and show you what that looks like in case it wasn’t brought up. So here’s the malar rash.

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Stacey Ostrin: You probably have seen this as you just came off of rheumatology. But here’s the diabetic dermatitis, dermatitis, herpetiformis. And the key here is to think about these kind of characteristic vesicles. That’s often the word that they will use but they also will talk about being on the extensor services. So and it’s very. And it’s itchy.

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Stacey Ostrin: Okay, here’s classic pictures of erythema nodosum. Okay? Again, this is one that we can also see in sarcoidosis

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Stacey Ostrin: and strep infections. This is psoriatic plaques, so they will often describe this as being raised skin patches or plaques covered with silvery scales.

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Stacey Ostrin: And here’s the necrobiosis lipotica diabeticorum. So this isn’t very common, but it’s a rare chronic condition, and they often describe it as being this yellow, brown, atrophic, talangectitic

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Stacey Ostrin: plaques. And it can have this. It can form an ulcer. So I think it’s just something to be aware of. It’s often present in the pre tibial surface. So you can see both here. It’s pre-tibial. So just wanted to bring that up. Okay. Which of the following genetic variants would likely be present

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Stacey Ostrin: in the previous patient.

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Stacey Ostrin: All right, Hla, Dq. 8. And, as someone told me in the last time I gave you this session, you know. Think of Dairy Queen. So heading off to Dairy Queen to Dairy Queen. So Dq. 8.

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Stacey Ostrin: Okay, I think there’s some sort of other mnemonic. So forgive me if I can’t remember it offhand.

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Stacey Ostrin: Which of the following genetic variants would likely be present. So Hla. B. 27, you know, we think about a lot with reactive arthritis or ankylosing spondylitis can be positive in inflammatory bowel disease, associated arthritis, Hladq. 2 or sorry D 2 and Dq. 8 associated with Celiac. Hladr. 3.

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Stacey Ostrin: Dr. 3 is associated with type, one. Diabetes, lupus, graves, Hashimoto’s and Addison’s, and Hla-dr. 4 is associated with rheumatoid arthritis diabetes type. One and Addison’s.

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Stacey Ostrin: Okay.

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Stacey Ostrin: I put this in here just because this patient did have, you know, stool fatty stools noted. And so just a reminder to think back to those vitamins that

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Stacey Ostrin: are absorbed are fat, soluble vitamins, so that vitamins A, DE, and K, and this is just kind of highlighting, you know some things to think about or remember what happens when they’re deficient in those. So an exam might give a patient with celiac and say, You know, they’ve been noticed to have these fatty stools or the stools are floating in the toilet, and maybe they might have some of these findings that point towards a vitamin deficiency.

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Stacey Ostrin: Next question, a 46 year old. Patient presents to the clinic because of 3 month history of intermittent abdominal pain that worsens with eating on exam. They are noted to have mild epigastric tenderness. Their stool is weakly positive. On hemocult.

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Stacey Ostrin: Upper gastrointestinal endoscopy reveals an ulcer near the gastric antrum culture of the specimen reveals gram-negative microelophylic organisms. Which of the following virulence factors helps this organism survive in the acidic environment of the stomach?

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Stacey Ostrin: Give me a moment to pause

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Stacey Ostrin: your rease. So way back, when when we were talking about how this how this

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Stacey Ostrin: bacteria can survive in the stomach, we learned that this bacteria had container

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Stacey Ostrin: contain this urease, and it would break the ammonia down into carbon dioxide and excuse me, it would break the ammonia down, and it would go into this Nh, 3 and carbon dioxide. And so that would neutralize the acidic environment. Okay, the flagella helps it swim. The Caga helps induce the inflammatory immune response and then the vaca causes epithelial cell death or ulcers. So

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Stacey Ostrin: this was I brought this up, because, if you remember, this is how we developed the Urea breath test which we use in clinic to see if folks have H. Pylori. So it’s based on the science. The urea is labeled with carbon isotope given by mouth, and H. Pylori. If present, liberate the carbon dioxide that can be detected on the breast samples.

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Stacey Ostrin: and this is just kind of a reminder of those vac A and cag a associated genes. And then the

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Stacey Ostrin: how that longstanding can lead to this malt lymphoma, or adenocarcinoma.

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Stacey Ostrin: And again, H. Pylori does not technically infect the cells. So just keep that in mind.

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Stacey Ostrin: this was just put in as a reminder of how do we treat this so? Boards loves to ask about how to treat this. So it’s a proton pump inhibitor. If it’s triple therapy, it’s proton pump inhibitor with Amoxicillin and carthemycin

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Stacey Ostrin: because of resistance we’re starting to see quadruple therapy used more often now in some areas. So kind of knowing what’s in your area, they might recommend a proton pump inhibitor, metronidazole, tetracycline and bismuth.

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Stacey Ostrin: Okay. Next question. Imagine the same 46 year old patient presented instead to the emergency room with a 3 month history of intermittent abdominal pain that worsens with eating now with an acute onset of hematimisis. So they’re vomiting blood. Upper, gastrointestinal endoscopy reveals an eroding gastric ulcer in the lesser curvature of the stomach, which of the following arteries is most likely the source of bleeding.

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Stacey Ostrin: I’ll give you a moment to think.

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Stacey Ostrin: Left gastric artery.

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Stacey Ostrin: so complications can happen with peptic ulcers. If they erode through the stomach lining, they can erode and depending on where they’re located. They can erode into some of the surrounding structures. And if you remember here the lesser curvature of the stomach, this is where this ulcer was. It can erode into the left gastric artery.

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Stacey Ostrin: Okay, if it’s on the posterior wall of the duodenum. It can erode into the gastroduodenal artery, and if it’s in the anterior wall of the duodenum they can have perforation. So what might you see on chef’s radiographs if there was a perforation of the anterior wall of the duodenum.

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Stacey Ostrin: So here is a radiograph, and what you might see, are these signs. So the red you can kind of see here, this kind of space here, this is air under the diaphragm, and then the yellow. This is actually called the Ringler, the regular sign, and it’s a double wall sign. So you can see both sides of the intestine here. And so that’s that’s really what we’re kind of looking for. Okay.

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Stacey Ostrin: pneumoperitoneum.

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Stacey Ostrin: All right. This is a reminder to the compare and contrast gastric versus duodenal ulcers. These are really important kind of things to remember. Whoops. Excuse me. The epigastric pain often is worse with eating and gastric ulcers, where it’s often

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Stacey Ostrin: eating relieves the pain in duodenal ulcers, and the thought is here is that when they’re eating with a gastric ulcer it releases the gastric acid, and it just the gastric acid. Just kind of stings. Okay? And the duodenal ulcers. The eating actually relieves pain because the food can kind of come down here where it’s more neutralized and it can make it can be soothing.

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Stacey Ostrin: Okay.

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Stacey Ostrin: darn it, I know better than to have a cup of coffee after October. How are we doing? Okay? Are you ready for more? Here we go.

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Stacey Ostrin: a 45 year old female presents with recurrent gastric and duodenal ulcers. She’s been taking ranitidine and omeprazole for the last year she has completed treatment for Helicobacter pylori in the past and had a test documenting eradication. She undergoes another endoscopy and a distal duodenal, and jejunal ulcer is noted which of the following additional serum tests may help uncover her most likely diagnosis.

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Stacey Ostrin: So here fasting gastrin levels. So here you have a patient with recurrent gastric and duodenal ulcers. Okay, so they have multiple. She has been taking therapy an H. 2 blocker and a Premton pump inhibitor for a while.

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Stacey Ostrin: and also the other kind of buzzword here is that she had both duodenal and jejunal ulcers. So when you’re starting to see these more distal ulcers think Zolinger, Ellison syndrome. Okay. And Zollinger-elison syndrome is caused by a gastroinsecheding tumor or gastronoma. The tumors can be found in the pancreas it can be found other places.

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Stacey Ostrin: but that gastronoma releases gastrin, which stimulates the parietal cells to secrete stomach acid. And so they can get these kind of treatment resistant

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Stacey Ostrin: or recurrent peptic ulcers. And so that’s something to keep in mind

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Stacey Ostrin: what additional finding or findings on the previous patient’s blood test evaluation might be concerning for an associated syndrome. So 1st I would think, what syndrome are you thinking? And then

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Stacey Ostrin: given that syndrome what also might be abnormal on their blood work?

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Stacey Ostrin: So the 1st one to think about I would think about would be hypercalcemia from a primary hyperparathyroidism. So.

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Stacey Ostrin: and then the second one that could be also elevated is hyperglycemia from a gluconoma glucagonoma. So I was trying to reference here. This is a slide from

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Stacey Ostrin: the endocrine lectures, thinking about the mem. One so multiple endocrine neoplasia type one you think about. The 3 P’s right. So you’ve got parathyroid tumors, pancreatic islet tumors, and pituitary tumors, and so the zolinger-ellison syndrome is an example of the gastronoma right? And so they might also have a parathyroid or pituitary problem. And so please keep that in mind. So the characteristic findings with

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Stacey Ostrin: right here with primary hyperparathyroidism, you see an elevated parathyroid hormone level, elevated, seric calcium levels low to normal serum phosphate concentration

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Stacey Ostrin: and with a glucagonoma you might see elevated glucose levels. Hyperglycemia.

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Stacey Ostrin: Next question, 49 year old. Male presents to his primary care physician’s office with intermittent abdominal pain and bloody stools. He’s lost 10 pounds in the last 3 months. Stool, hemocult, and fecal calprotectin is positive. A colonoscopy reveals diffuse continuous ulcers of the intestinal mucosa extending proximately from the rectum to the splenic flexure.

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Stacey Ostrin: Which of the following disorders is most likely associated with this patient’s condition. So the 1st process to think about is, there’s some clues here they have bloody stools, they’ve lost weight, and their fecal calprotectin is positive. So we’re thinking

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Stacey Ostrin: inflammatory bowel. Okay?

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Stacey Ostrin: Possibly there’s other things that can cause that to be positive. But that’s concerning for an inflammatory bowel disease. And then they have continuous ulcerations from the intestinal mucosa of the intestinal mucosa that start approximately from the rectum to the splenic fixture. So my hope is this, triggers folks to think about ulcerative colitis.

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Stacey Ostrin: Okay? And then I now next, I’m thinking, what’s associated with that. So of these which is associated with that. And my hope is that folks think about primary sclerosing Chloe Langitis to be one of their extra intestinal manifestations. So

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Stacey Ostrin: which of the following disorders associated with it? Well, primary biliary cholangitis, I don’t know about you, but I always got the 2 confused so primary biliary cholangitis is associated with other autoimmune conditions.

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Stacey Ostrin: Primary sclerosing cholangitis is associated with ulcerative colitis. The enterovsicular fistula I think would more likely to be seen with Crohn’s osteoarthritis is not associated with ulcerative colitis, or not, like the common association, and then vitamin b. 12. Deficiency, I think about that more if the terminal ileum is involved, which we think about more with Crohn’s disease.

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Stacey Ostrin: So kind of review back on primary, sclerosing cholangitis, so primary meaning. It’s not caused by something else. Sclerosing kind of, we think about hardening of the tissue, and then the cholangitis of the bile ducts. Okay? And so a key here is to remember it involves the intrahepatic and extrahepatic.

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Stacey Ostrin: and that it will often appear as this beads on the string. So that’s kind of the classic finding is this, these alternating strictures that actually make it look like beads on the string. You might see this kind of rings of fibrosis, so they might talk about that

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Stacey Ostrin: and the lab findings. So the lab findings, you’ll see with this, it’s going to be more of an obstructive pattern. Okay? And since those beads kind of pinch off the areas that can obstruct the flow of bile. And so the Bilirubin is going to be conjugated. Okay, and the alkphosph will be elevated and potentially the Ggt as well. And then the other finding on here that folks often think about is the P. Inca being positive

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Stacey Ostrin: or perinuclear anti-neutrophil cytoplasmic antibodies.

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Stacey Ostrin: Okay.

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Stacey Ostrin: these folks will have pruritus. They’re going to get like a lot of itching, so that might be something that they might also test on.

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Stacey Ostrin: or at least clue you into that.

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Stacey Ostrin: This is a reminder to go back and look at the table. This is a few. This is the table that Dr. Johnson and Dr. Kumar put together, and this is available in eflow under the inflammatory bowel disease session.

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Stacey Ostrin: So go back and look at if you can. It’s a really nice compare and contrast table. There’s more than what’s on this slide. Okay? But it’s just kind of a good reminder, because differentiating ulcerative colitis from Crohn’s is really really important, clinically. And it’s really really important on testing. So

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Stacey Ostrin: right down here, these are talking about the extra intestinal manifestations. So part of his session he gave this kind of nice diagram of some of the extra intestinal manifestations of inflammatory bowel disease. Okay? And I wanted to highlight this one here so pyoderma gangrennosum. This is often tested super rare. So it’s kind of an it’s not super common, but it’s not often seen outside of inflammatory bowel disease. And so.

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Stacey Ostrin: for whatever reason, this is something they like to ask about on board so rapidly enlarging very painful ulcer. It’s not an infection, and so just keep that in mind. It’s more commonly a complication of ulcerative colitis compared to Crohn’s. But you can see them in both. Okay, so keep that in mind.

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Stacey Ostrin: So if Crohn’s disease likes to affect the terminal ileum as kind of shown in that past slide, what vitamin deficiency should you keep in mind?

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Stacey Ostrin: Vitamin B. 12. So vitamin b. 12 is stored in the terminal ileum. So then they might say, what are you most likely to see on labs? Or how do you differentiate this from folic acid deficiency? And so the key here is that you’re going to see a megaloblastic anemia which is going to be that large. Mcv. It’s going to be greater than 100.

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Stacey Ostrin: Both will have hypersegmented neutrophils, so both folate and vitamin B 12 will have hypersegmented neutrophils. Both will have elevated homocysteine levels. But here’s the way to differentiate it. So, looking at methylmalonic acid levels, it’ll be normal in a folate deficiency, and it’ll be elevated in the vitamin B, 12. Deficiency. So that’s something to keep in mind that folks like to test about it. Also about these hypersegmented neutrophils.

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Stacey Ostrin: lots of stars. There they love B 12. Deficiency.

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Stacey Ostrin: Okay, so by the time you get this it’ll be pi day. And I saw this, and I thought this was fun. So maybe maybe this is how they named Pi, who knows? But anyway, thought it was fun

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Stacey Ostrin: all right. Next question 45 year old, male patient, with a history of heavy alcohol use presents with fatigue and right upper quadrant, abdominal pain. Laboratory tests show elevated liver enzymes

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Stacey Ostrin: a liver, biopsy reveals macrovesicular steatosis and inflammation. What would be a unique histologic finding suggests that this is alcoholic hepatitis. So, looking on the slides, what would be a unique histologic finding?

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Stacey Ostrin: So I don’t know if you remember this slide, but alcoholic hepatitis. There are these things right here. So this is a Mallory body, and they really like to ask about it. It used to be thought that this was pathognomonic for alcoholic hepatitis, but then, now we’re starting to see it in some other disorders, but

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Stacey Ostrin: it’s still one of those things to kind of keep in mind these Mallory bodies. They’re they’ve kind of. It’s an intracytoplasmic eosinophilic inclusion of damaged keratin filaments. Okay, so these damaged intermediate filaments. So

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Stacey Ostrin: keep that in mind. Think about alcoholic hepatitis. When you see that

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Stacey Ostrin: what lab abnormalities might you expect in someone with alcoholic hepatitis.

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Stacey Ostrin: So in most liver diseases, we’re going to think about the alt be greater than the ast. I always think of alt for liver, right? So in most liver diseases. Alt is going to be higher than ast, except

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Stacey Ostrin: and alcoholic hepatitis. So the ast to alt ratio is this, 2 to one. Okay, and also the alkphos can be elevated, and the Gamma Gt can be elevated, and sometimes the Mcb will be elevated. Given the alcohol use. So keep those things in mind. But it’s this ratio is really going for is that the ast is higher?

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Stacey Ostrin: Okay?

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Stacey Ostrin: New question. You’ve seen this before. I talked about this in one of the sessions. But I’m going to bring it up again, because I think this is a really high yield question more so on the why not? Are the other questions not correct? Are the other answer options not correct? So you have a 59 year old man, with a history of alcoholic cirrhosis brought to the physician by his wife for a 1 week history of progressive abdominal distension

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Stacey Ostrin: and yellowing of the eyes. For the past month he has been irritable, had difficulty falling asleep, becomes clumsy, and fallen frequently.

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Stacey Ostrin: 2 months ago he underwent banding for esophageal varices. Excuse me after an episode of vomiting blood. His vital signs are within normal limits. Physical exam shows, jaundice, multiple bruises, pedal, edema, gynecomastia, loss of pubic hair

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Stacey Ostrin: and small, firm testes. There are multiple small vascular lesions on his chest and neck that blanch with pressure, his hands are erythematous and warm. There is a flexion contracture of his left 4th finger, a flapping tremor is seen when extending the forearms and wrist.

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Stacey Ostrin: Abdominal examination shows dilated veins over the anterior abdominal wall. The spleen tip is palpated, 4 cm below the left costal margin, and there’s shifting dullness to percussion. Which of the following pairs of physical exam findings are caused by the same underlying Pathophysiology. So

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Stacey Ostrin: who this patient. This is an example of a patient with portal hypertension. Okay, and ascites, you know, and consequences of end, stage liver disease. And so the answer, here is Palma, Erythema, and Gynecomastia. Okay, but this is this is what the

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Stacey Ostrin: the goal of this slide is is really to think about. Why does this patient have splenomegaly. Well, they have splenomegaly because of the portal hypertension, and then the duplicate contracture. The mechanism is not really well understood, so they’re not likely, and it’s not likely from portal hypertension. So that’s why A is not correct.

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Stacey Ostrin: B is not correct, because the jaundice is the inability of the liver to conjugate bilirubin. Okay? So these folks would have an increased, unconjugated bilirubin, okay or indirect.

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Stacey Ostrin: And they have this flapping tremor or asteristics due to the increased pneumonia

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Stacey Ostrin: as far as option. D the esophageal varices that’s from portal hypertension and the pedal edema that can be from the decreased hepatic synthesis of albumin. So they can a different process. The Kaput medusa that

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Stacey Ostrin: kaput medusa we see from portal hypertension, the spider Angiomata. That’s from the hyperestrogenism, the testicular atrophy can be from multiple factors. Really, the thought is the suppression of the hypothalamic pituitary function. The abdominal distension is from ascites

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Stacey Ostrin: plus minus the decreased albumin, plus the portal hypertension. So.

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Stacey Ostrin: and then multiple bruises. So the liver’s not producing the coagulation factors. And so they. But they can also get decreased platelets, too, from sequestration from the spleen, and then the loss of pubic hair is from the hyperestrogenism. So I think this is a really good

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Stacey Ostrin: question to kind of make sure thinking about how

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Stacey Ostrin: with the liver not working very well. What’s the mechanism of of these findings?

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Stacey Ostrin: This is just another reminder of kind of what we see symptoms. This actually came from the American family physician. This isn’t always alcoholic hepatitis. Excuse me, but we see with ascites and portal hypertension and end stage liver disease.

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Stacey Ostrin: This is the mnemonic. This is Osmosis’s way of remembering this. So in portal hypertension you have ascites, you have bleeding varices. You have C for medusa d for diminished liver function, and E for enlarged spleen or encephalopathy or high estrogen.

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Stacey Ostrin: Okay.

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Stacey Ostrin: Same patient described above now presents to the emergency department. After a sudden onset of hemotemasis. His vital signs show a temperature of 98.7°F, heart rate of 1 15 blood pressure of 92, or 48. What vessel anastomosis is most likely responsible for this patient’s bleeding. So the thought here is this person is vomiting. They appear to be tachycardic and have a low blood pressure so hypotensive. What’s the most likely cause of bleeding?

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Stacey Ostrin: That’s the 1st question.

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Stacey Ostrin: Esophageal varices is most likely. Okay. And so then we think about well what vessel anastomoses make up esophageal varices, and we think about the left gastric vein, which is the portal system with the esophageal vein or the cable system.

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Stacey Ostrin: And this is just a reminder. I took this from Amboss. I thought it was a nice kind of diagram that talks about the different place, the different anastomosis.

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Stacey Ostrin: And so you have esophageal varices. We have kaput medusa, and on this slide colonic varices and anal rectal varices. So these 2 slides can be a really nice high yield of trying to remember the portal and cable systems.

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Stacey Ostrin: And then, if you have a patient who has too much has encephalopathy, sometimes they will do this procedure, if you remember the tips procedure. And so, remembering the 2 veins that the tips procedure connects can be a high yield thing to remember.

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Stacey Ostrin: And that’s the portal vein to the hepatic vein.

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Stacey Ostrin: Okay, moving on, doing great

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Stacey Ostrin: 55 year old. Female patient presents the emergency department with a 2 day history of left lower quadrant, abdominal pain, fever, and nausea. She has a history of hypothyroidism and chronic constipation for which she typically controls with polyethylene Glycol.

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Stacey Ostrin: On examination there is tenderness in the left lower quadrant, a Ct. Scan of the abdomen and pelvis shows colonic wall thickening and pericolonic fat stranding, which of the following is the most likely diagnosis.

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Stacey Ostrin: so this person has left lower quadrant, abdominal pain, fever, history of chronic constipation.

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Stacey Ostrin: What are you thinking?

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Stacey Ostrin: Oh, and this finding on Ct scan. This is a pretty classic description of this finding

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Stacey Ostrin: diverticulitis. Okay, so I just want to put this on here because that’s that kind of

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Stacey Ostrin: constellation of symptoms. They like to ask about quite a bit

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Stacey Ostrin: next question. I’m just moving quickly here. A 37 year old. Female patient presents to the emergency room with a history of progressive constipation and worsening abdominal pain. For the last 3 years

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Stacey Ostrin: she has previously been healthy. Her father died at age 31 in an automobile accident, and her mother was 62 0, sorry. Her mother is 62 has hypothyroidism, but is otherwise healthy. She was diagnosed with a bowel obstruction and was taken to the operating room for exploratory laparotomy. The gross appearance of this patient’s colonic tissue is shown histologic exam shows tubular, tubular villus and villus adenomas. What is the inheritance pattern of the most likely syndrome?

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Stacey Ostrin: So thinking about what this syndrome most likely is.

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Stacey Ostrin: So this patient most likely has familial, adenomatous polyposis or fap. Okay, which is caused by

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Stacey Ostrin: well, first, st it’s autosomal, dominant. That’s the inheritance pattern. This disorder is caused by a mutation in the Apc tumor suppressor gene.

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Stacey Ostrin: What is the likelihood that the previous patient’s children will develop their condition if their partner is not a carrier

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Stacey Ostrin: 50%.

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Stacey Ostrin: Okay, so kind of going back and kind of remembering that autosomal, these these trees just kind of being able to recognize when something is autosomal dominant.

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Stacey Ostrin: Why did I ask this? So most of the polyposis syndromes have autosomal, dominant inheritance so like when in doubt? If you’re thinking they have a polyposis syndrome. It’s going to be autosomal, dominant except for this one. So the muti associated polyposis syndrome has a different inheritance pattern can you remember which one that is

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Stacey Ostrin: autosomal recessive. So Dr. Kumar put together this really nice compare Contrast table in her polyps polyposis and inherited syndrome. So I’d highly suggest going back to look at that, and you’ll see here that the only one that doesn’t have it is that Mudy?

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Stacey Ostrin: Okay.

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Stacey Ostrin: 42 year old female patient undergoes elective cholecystectomy for recurrent biliary colic. During her laparoscopy it is noted that she had a black appearing liver after the operation. You review her preoperative lab work that was completed when she didn’t have any symptoms. The results were an ast of 25 alt of 30 alkphos of 52 total bilirumin of 1.9 direct bilirumin of 1.3.

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Stacey Ostrin: Upon further questioning, she does recall that she had periodic yellowing of her skin and eyes during times of stress. Which of the following is most excuse. Forgive me, I have a typo. There is her most likely confounding diagnosis.

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Stacey Ostrin: so

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Stacey Ostrin: she has a black appearing liver. Her Bilirubin is elevated, as is her direct Bilirubin. Okay? And periodic yellowing of her skin during times of stress.

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Stacey Ostrin: answers Dubin Johnson. So, looking here, Craigler Nahar, this one is usually seen in really young persons these folks can be. They have a really high indirect hyperbiliruminemia. It’s seen in newborns. It can cause that awful chronic dress. Okay? And that’s usually due to decreased or no Udp or flucarronal transferase synthesis.

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Stacey Ostrin: Dubin-johnson, which this patient has usually due to a deficient Mrp 2 protein transporter. Here’s the key. With this one. They have the direct hyperbilirubinemia, and they have the hyperpigmented liver as opposed to rotor syndrome. They have impaired biliary excretion they have a direct hyperbilirubinemia, but they don’t have the hyperpigmented liver. So kind of look at those 2 comparatively

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Stacey Ostrin: Gilbert Syndrome is another one that boards loves to ask about. It’s the most common inherited hyperbilirubinemia. It’s usually an indirect hyperbilirubinemia. Okay? And

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Stacey Ostrin: it has that mild decreased udp glucuronyltransferase can never say it a Udp. Thank you.

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Stacey Ostrin: Here’s a picture of the liver on the patient that I took this case from. It was published in the New England Journal of Medicine.

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Stacey Ostrin: and then this is the just a reminder to go back. Dr. Bowman put together this really great kind of compare Contrast Table. These are the remember, these are going to be the indirect hyperbilirubinemias. These are the direct hyperbilirubinemias, and they kind of have just like the nice compare contrast of each of these

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Stacey Ostrin: all right. You made it finally. So let you read through this.

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Stacey Ostrin: So just reminder.

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Stacey Ostrin: You do matter to all of us here. We’re excited for you to to take this exam. I know you’re going to do. Great.

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Stacey Ostrin: You’ve really got this. Okay. You’ve got a team behind you. So please reach out. If you have any questions email me, especially if I said anything here that you have questions about or just, you know, want to work through. And finally, if you’ve made it this far in the session. Please stop by Dr. Rachel Larson’s office before 3, 1825. I had meant to give you all a surprise, you know during class.

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Stacey Ostrin: but since I had to leave so urgently I left them there. So it was a way for me to share it with y’all remotely so stop by for a small surprise to take with you. And I wish you all the best on this exam. And here’s the resources.

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Stacey Ostrin: And again, email me if you have any questions. Thank you all so much.