Interactive Transcript
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Hello and welcome to Case Crunch, rapid case review
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for the core exam hosted by modality.
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In this rapid fire format,
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faculty will show key images along
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with a multiple choice question,
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and you'll respond with your best answer via
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the live polling feature.
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After a quick answer explanation, it's on to the next case.
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You'll be able to access the recording
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of today's case review
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and previous case reviews
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by creating a free account using the
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link provided in the chat.
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Today. We are honored to welcome Dr. Lindsay Negretti
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for a GI Imaging Board prep case review.
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Dr. Negretti completed her residency training
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at uc San Diego.
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She completed her abdominal imaging fellowship at Stanford
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and stayed on for an attending position after training.
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She is active in medical student mentorship
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and is the podcast creator
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of let's read out, in her spare time.
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She loves playing golf with her husband
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and spending time with her golden retriever.
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Willow questions will be covered at the end if time allows.
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Please remember to use the q
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and a feature to submit your questions.
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With that, we are ready to begin today's board review. Dr.
1:07
Negretti, please take it from here.
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Jackie, thank you so much for that warm welcome.
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I am really, truly honored to be here today.
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I wish I would've had this when I was a resident,
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um, or our fellows.
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So thank you so much. This is such a great resource,
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and you know, first of all, I just want everyone you know,
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who's tru tuning in.
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I know it's five o'clock,
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it's eight o'clock, it's, it's late.
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Um, so what really sets you guys apart is the effort you're
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taking when others are stopping.
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You're taking the time to study even after hours.
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And really that extra effort you put in today,
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I know it will make you stand out tomorrow.
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So keep up the great work.
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You should really, uh, you know, take some extra time,
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watch some extra TV tonight because you deserve it.
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Success really isn't just about talent, it's,
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it's about dedication.
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I have no disclosures today. Here's our agenda.
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And then to make things a little bit extra fun, um,
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I will sprinkle in some medical trivia as we switch topics.
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I'll probably show my age, um,
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but hopefully, uh,
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it'll make things a little bit more entertaining.
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But first, uh, let's just, uh, practice a little bit
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and are you a resident, an attending, just here
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for the cases or something else?
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Wonderful. So it looks like, um, the majority of you are
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residents studying for the court.
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Uh, so we'll start off with the pharynx and esophagus.
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So go ahead and just take a second.
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Uh, this is a 59-year-old male with HIV and thank you to Dr.
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Fiona Cassidy.
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Um, from, from the VA San Diego for this case.
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What is the most likely diagnosis based on these findings?
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Is it Canada? Is it a carcinoma?
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Is it eosinophilic esophagitis?
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Is it gerd or is it feline esophagus?
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Jaggy. Can, can they see the, the, the answers?
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They can see the answer options, yes.
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Okay, okay. Even though, okay.
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And they'll see the answer choice.
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Ah, they can, are you seeing the answer here?
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Nope. Not on, that's on the next slide, right?
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Oh, okay. Yes. And then that'll,
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the poll will show on the next slide, the,
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like they'll be able to see the, see the distribution.
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Yes, they should. Do you see it?
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I see your answer. Explanation slide. Yes.
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Okay. And the distribution, or do I maybe have to,
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We're seeing in the chat. Yes, we see it.
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Okay. Okay. Just making sure. Thank you.
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I just wasn't sure. Appreciate it.
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Um, so this is, uh, esophageal candidiasis.
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This is a shaggy esophagus.
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Uh, when Canada is severe, like it is in this case,
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it really appears shaggy herpes will have more
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of a small emus halo.
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CMV will be large, flat ovoid ulcers
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and eosinophilic esophagitis will have concentric rings.
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The history will be failing PPIs,
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but the patient will get better with steroids.
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And again, that will be a ringed appearance.
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So this is a 3-year-old female with dysphagia
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and I'll let you guys just sink in for that one.
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Which of the following statements is true
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regarding this condition?
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Uh, so if you said b, uh, you are correct.
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They are found in conjunction with hial hernias.
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Uh, so this is a,
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at Stanford we actually use a single contrast as opposed to,
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um, double contrast.
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Um, but the B line is a thin construction, uh,
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constriction at the GE junction.
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And again, the keyword here is going to be symptomatic, um,
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because the patient is symptomatic.
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This finding, um, may be, uh, more appropriately referred to
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as a chat skis ring.
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And again, this is gonna be circumferential as opposed
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to our esophageal carcinoma, which is asymmetric.
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And an irregular contour webs are typically more higher up
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in the cervical esophagus.
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And again, this one not only shows, um, the circumferential,
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but also the small hiatal hernia.
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Um, and again, symptomatic, so shaky s for symptomatic.
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So I don't have the, um, polling for the these questions,
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but if someone wants to just come off of, um,
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or sit, see in the chat, I can't see it in the chat.
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So hopefully Jackie can help me out here.
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Um, but I am a big Noah Wiley fan.
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I used to watch the er, uh, every Thursday night.
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Um, and the new show, the pit also on HBO,
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what is this character's name
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and the new drama, the pit, is it Forest?
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Is it Hunter? Is it Whitaker
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or is it Neil
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And Jackie, if you can help me out
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'cause I can't see the chat on my screen.
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We've got one person saying Whitaker.
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Nice. Excellent, excellent.
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I can tell, maybe it's not as popular
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as I thought it would be.
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So let's move on to the stomach. Uh, case three.
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I'll let this sink in with, um,
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a plain film that we have here.
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And moving on to the ct.
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And now moving on to the question.
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Which of the following is most likely the underlying
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cause of this condition?
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Seems like, um, interesting.
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So we got some peptic ulcer disease.
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Um, we got gastric perf, um, ischemic bowel.
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Um, so the answer I was looking for, kind
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of a difficult question, um,
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but I was looking for, um, more of
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mucosal disruption.
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So mucosal disruption from an ulcer
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or tumor that is really the entrance site, um, for, uh,
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gastric emphysema
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and gastric emphysema is what we're seeing here.
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And that's air in, uh, the wall of the stomach here.
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Um, it gastric perforation,
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you would typically see more free air in
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the peritoneal cavity.
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Um, and, and we also just don't have an NG tube.
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Um, that would probably be more of the clue here.
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Case four.
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So this patient presented, uh,
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for a staging exam for rectal cancer.
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What is the best next step
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for the finding in the upper abdomen?
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Good. I see a lot of do nothing.
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So there is a normal left adrenal here, um,
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and there is a posterior gastric diverticulum
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and posterior is the, uh, the most common spot.
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Um, for a gastric diverticulum. These can be confusing.
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Um, they can be mistaken, mistaken for an abscess
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'cause there, there can be gas, um,
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but oral contrast can really seal the deal here, uh,
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and doing nothing.
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This is, uh, a nothing burger as my attending would say.
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Okay, case five. I'll be honest, this is my favorite case,
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probably my favorite fluoro.
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Um, so let's hope, uh,
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that you love the question as much as I do.
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A 42-year-old female with a history of a lap, uh,
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ruin y bypass presents with abdominal pain.
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What is the diagnosis?
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Good. So this is a gastro gastric fistula.
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Um, there is prompt of ification of the gastric pouch
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as well as the hold on, um,
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as well as the, uh, GJ limb.
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And here we also see simultaneous filling
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of the excluded stomach.
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Uh, so this is a gastro gastric fistula.
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You can have some filling of the, um,
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excluded stomach by reflux.
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Um, but really here the key is, um,
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simultaneous filling.
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And these patients present with a poor post-op weight loss.
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And again, simultaneous filling
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reflux again will be in a delayed fashion.
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Beloved, Dr. Mark Green had a slightly rebellious daughter.
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What was her name? Also give you a hint.
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Uh, she shares the same character name as,
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uh, Jennifer Aniston's.
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Uh, character and friends
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we're getting a lot of Rachel's.
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Nice, nice everyone.
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Okay, moving on to, uh, bowel and colon. Uh, case six.
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This patient has a ulous esophagus and renos in her fingers.
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The left upper abdomen, small bowel can best be described as
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feathery ribbon, hide bound or featureless.
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So this is actually, uh, hide bound and good.
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Most of you, uh, the majority of you got that.
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Um, so this patient has, uh, scleroderma.
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So this is collagen deposition in multiple organs,
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including the GI muscular layers.
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Um, high bound really refers to that narrow closest, uh,
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close separation, um,
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with normal thickness despite d dilatation
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of the bowel lumen case, seven
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30-year-old female with chronic diarrhea,
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weight loss and fatigue.
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What does this finding suggest
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Excellent malabsorption due to celiac disease?
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So I guarantee you were probably expecting me
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to ask you in the form of a a abdominal plane film.
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Um, you see the normal
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al pattern here in the left upper abdomen,
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this feathery appearance.
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And here, um, in this patient on, uh, the, the right,
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there's a reversal of that full fold pattern.
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So I really tell people when they're studying
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for these tests, if you're expecting something to be, uh,
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given to you on plain film, expect
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to see it something some somehow, somewhere differently.
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If you're expecting it to see it.
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Uh, you normally always see it on MRI expect
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to see it in a different modality.
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So again, uh, this is celiac disease.
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It's an autoimmune proximal enteritis.
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It's T-cell mediated and it's malabsorption
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and is characterized by this fold reversal.
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On imaging, the al should have more fold than the ilium,
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but in celiacs you have a loss of the al folds
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and you'll have a compensatory increase in the IAL folds.
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Celiac has a number of different manifestations as well,
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including mesenteric adenopathy, engorgement
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of mesenteric vessels, splenic atrophy.
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It increases the risk of venous thromboembolism.
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And you can also get a dermatitis for pettifor rash.
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A 45-year-old male with a longstanding history
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of untreated celiac disease presents
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with worsening abdominal pain and weight loss.
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He undergoes an endoscopy which reveals a mass
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in the small intestine.
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What is the most common malignancy associated
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with untreated celiac disease?
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So if you said, uh, T-cell lymphoma, you would be right.
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I just said that celiac is a T-cell mediated.
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Um, so it is the most common malignancy associated
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with untreated celiac disease.
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You may see on CT some sort
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of exophytic mass valve thickening and really enlarged
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and pathologic, uh, mesenteric lymph nodes.
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Continuing, uh, with our celiac theme,
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a 30-year-old female presents with a history
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of chronic diarrhea, weight loss, and fatigue.
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She also reports recent episodes
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of cough and shortness of breath.
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And a chest x-ray reveals bilateral infiltrates in a
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bronchoscopy with lavage shows chemo citrin
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laden macrophages.
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Given her gastrointestinal symptoms
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and pulmonary findings,
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what is the most likely underlying condition?
15:04
Good. Wow, I didn't know the answer to this question, uh,
15:08
when I was a resident.
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So, excellent job.
15:11
So this is actually pulmonary, pulmonary hemo citrus, uh,
15:15
secondary to celiac disease, disease, um,
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and the syndrome is called lame Hamilton.
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Um, so celiac, uh, really can lead to a number
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of systemic complications,
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including pulmonary manifestations due to malabsorption
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and subsequent iron overload
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case 10, a 48-year-old male with left lower quadin.
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We'll go fast 'cause I hope that these are
15:49
easy ones for you.
15:57
Excellent. Um, so this is epi appendicitis.
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Um, these are small patches of fat that hang from the colon.
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I probably see this once a week
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and it truly does mimic diverticulitis.
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Um, and this will just be anti-inflammatory meds.
16:15
Um, many ask me what's the difference between this
16:18
and omental infarct?
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Um, very similar,
16:21
but usually, uh, omental infarct is a little bit larger,
16:24
the location is different
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and, uh, it doesn't have the char characteristic oval shape
16:30
of the epi poetic appendage.
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I love pathophys questions.
16:37
So you'll see several of those tonight.
16:39
What is the most common etiology of epi poetic appendicitis?
16:50
Excellent. Uh, so this is, uh, due to ischemia, uh,
16:55
in which the, there is, uh, torsion
16:57
or twisting of the appendage.
16:59
You can also have a thrombosis as well.
17:05
Okay. Case 12. Which of the following statements
17:09
regarding colonic diverticula is correct?
17:18
Excellent. So colonic diver ticus.
17:20
So this is a little bit of a trick question.
17:23
So, um, I think it said high animal protein.
17:27
Uh, it should have said, uh,
17:29
if it would've been the correct answer,
17:30
it would've said low fiber, um, but not high animal protein.
17:34
Um, so this diverticular usually occur, uh, adjacent
17:38
to the erecta,
17:39
and those are the small vessels
17:41
that extend into the submucosa
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and that that's the weakest area of the colon.
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I also thought of another question that would be, um,
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you know, where are diverticula maybe least likely to occur
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or unlikely to occur?
17:56
Um, and they actually are rare in the rectum
18:00
where the longitudinal muscle covers the entire
18:02
circumference of the bowel.
18:04
Um, so that's actually why you don't see
18:07
diverticulitis in, in the rectum.
18:12
Um, you might also get questions based on hepatic abscesses.
18:16
Um, I tell my residents also to, uh, look
18:19
for septic thrombo phlebitis.
18:21
You can actually get, um, in the vessels, uh,
18:24
mesenteric vessels, especially the veins, um, next
18:28
to the colon you can get a septic thrombo
18:30
phlebitis picture as well.
18:32
And if you see any question with a vesicular fistula, um,
18:36
that's usually a good look
18:37
for a diverticulitis question as well.
18:42
Okay, let me play this cine for you.
18:44
Uh, so this case, uh, coronal CT is not going to be about,
18:50
um, the hepatic metastases you see, um,
18:53
but it is going to be a question about, uh,
18:56
this large colonic mass in the pelvis here.
19:01
And the question is, which region
19:06
of the colon is most common site of perforation due
19:09
to an obstructing sigmoid colonic mass?
19:18
Um, so let's see, cecum, uh, let's see,
19:22
hepatic flexor proximal to the, the mass.
19:25
Um, all great guesses, um,
19:27
but seum is actually the correct answer.
19:30
So with a competent ileocecal valve,
19:32
an obstructing colonic lesion results in a closed loop
19:36
obstruction in the small bowel.
19:38
The most common site for perforation is just proximal
19:41
to the point of obstruction.
19:42
But in the colon, the most common site
19:45
for perforation is at the cecum.
19:47
Um, the risk of sequel perforation increases, um,
19:51
as the diameter gets bigger.
19:53
Um, but it's truly, um, from my readings, from my research,
19:57
the acuity of the onset of obstruction is equally important.
20:01
So if you're getting rapid onset of dilatation,
20:04
that actually poses a higher risk as well.
20:10
Okay. Case 14.
20:11
This is, uh, courtesy of my very good friend
20:14
and colleague, Dr. Rachel Patel.
20:16
And let me play this in for you.
20:24
So if you're picking up on this, uh,
20:28
this fistula here with the perianal fistula
20:32
and some concern about the terminal ilium,
20:35
then you're on the right track here.
20:40
Which of the following statements best describes the
20:43
characteristic histopathological feature of Crohn's?
20:53
Good. Um, so the transmural inflammation affecting all the
20:57
layers of the bowel.
20:59
And again, that can be granuloma in inflammation from mouth
21:03
to anus and again, transmural.
21:06
And this really sets you up for understanding why, uh, that
21:10
there's penetrating disease or fistula disease
21:14
because it's extending beyond, it's going
21:17
beyond that mucosa.
21:18
It's going beyond that submucosa.
21:20
And that's why you're not gonna see fistulas disease
21:22
or penetrating disease.
21:24
Um, with ulcerative colitis, it's again, uh,
21:27
transmural inflammation because of Crohn's.
21:33
Okay, I have, uh, some coronal MRI post contrast images.
21:39
So study these images here.
21:46
What type of polyp is most commonly associated
21:49
with pew Jager syndrome?
21:54
So these are all small bowel polyps, uh, enhancing polyps.
21:58
And uh, this patient does have pew. Ja,
22:08
excellent.
22:08
So this is hammer tous polyps.
22:10
Um, so, uh, individuals with p ja, um,
22:14
multiple hematomas polyps,
22:16
but not just in the proximal small bowel.
22:18
They can also occur in the stomach, the colon, um,
22:22
they can bleed, they can cause intestinal obstruction.
22:25
They can act as a lead point
22:26
and be intussusception causes as well.
22:29
And these individuals also really have an increased,
22:32
increased risk of, um, gynecological neoplasms,
22:35
but also colorectal rest, pancreatic ovarian ansular.
22:42
Um, this case or this trivia is courtesy of my husband.
22:47
Uh, he loved scrubs.
22:48
Um, so the stuffed laboratory dog's name,
22:52
was it Rex Shadow Rowdy or Lasy?
23:03
No, nobody's thrown an answer into the chat yet,
23:05
so you may have stumped them.
23:09
I'm really, uh oh,
23:11
Dre. Or we're
23:12
seeing D and Rex.
23:15
Yes, rowdy is correct.
23:17
I'll tell my husband it was, it was not a good question.
23:24
Okay, moving on to the pancreas.
23:27
Uh, case 16, again, these are all from my case collection
23:32
and this one is also one of my favorites.
23:36
So a 36-year-old male presents with a family history
23:38
of multiple tumors.
23:40
He has several pancreatic cysts, renal cysts,
23:43
eblast, and the cerebellum.
23:45
What is the most likely diagnosis?
23:53
So if you said, um, von Hippo Linde, you would be correct.
23:58
Um, I truly, uh, I actually do see this quite often.
24:02
Um, these patients, uh, get pheos.
24:04
They get pancreatic, pancreatic cyst, neuroendocrine tumors.
24:09
Um, they also, uh, we will talk about some
24:12
of their other manifestations as well, uh, such
24:15
as urogenital.
24:16
They get epididymal cysts.
24:18
Um, broad ligament, if you see a broad,
24:20
broad ligament cystadenoma
24:22
or papillary cystadenoma
24:23
of the epididymus all von Hippo window.
24:29
Um, this is also a case of mine.
24:32
And two things that are pathognomonic for VHL are going
24:37
to be endo lymphatic sac tumors.
24:39
I'm not a neuro person, so I don't have
24:41
one of those in my case files.
24:42
Um, but I do have, uh, one of these epi epidermal,
24:46
papillary cystadenomas.
24:48
And this patient, uh, did have, uh, von Hippo Lindo.
24:57
Okay, we're doing another Von Hippo Lindo case.
25:02
The most concerning lesion in a patient
25:04
with this syndrome is located in which organ.
25:13
Sorry if I was a little, little fast on this. Good.
25:16
Excellent. Um, so actually, um, RCC for, uh,
25:20
pe uh, people with vulnerable, Linda,
25:23
RCC is the most common cause of, of the mortality.
25:32
Okay. Uh, we have two patients here, um, with the same, um,
25:36
path here and Pancreat, both have pancreatic masses.
25:44
Um, and the question is, uh,
25:49
it's this 3-year-old male.
25:51
So this 3-year-old male presents with abdominal pain,
25:55
significant weight loss, painful subq nodules,
25:59
his serum lipase levels were high,
26:02
and biopsy confirms the diagnosis.
26:06
Which of the following, uh, uh, which
26:10
of the following pancreatic tumors is most likely associated
26:12
with secretion of digestive enzymes
26:15
and the development of these skin manifestations?
26:23
Yeah, it's gastro is a good thought.
26:26
Um, but this is actually going to be asner cell, um,
26:31
the asner cell.
26:32
Um, they can, uh, secrete lipase
26:35
and they can be associated with skin manifestations, um,
26:38
such as painful nodules.
26:46
Um, so which of the following we're gonna continue on that
26:50
is best explains the presence
26:51
of the painful nodules in this patient?
27:00
Good. Excellent, excellent.
27:03
Um, so these pain feral nodules are a result
27:06
of a peroneal plastic.
27:07
Um, peroneal plastic just means the tumoral systemic
27:11
effects, um, including hormones, cytokines,
27:15
other biologically active substances, um,
27:18
and not the actual local presence of the tumor.
27:22
And I, apo apologize, if you see some stirring
27:25
underneath my DS desk.
27:26
It is five 30 here
27:27
and my, my golden retriever, uh, is is hoping
27:30
for for dinner.
27:33
So how much was the check that Denny gave
27:36
to Izzy when he passed away?
27:44
I'm seeing C
27:46
Is popping. Wow.
27:47
Very good. Yes. 8.7 million. Excellent.
27:50
We have some Grey's Anatomy fans.
27:54
Okay, moving to the liver.
27:56
Um, we have a lot of questions here.
27:58
I think the liver is really, um, for us, abdominal imagers,
28:02
I think the liver is, is a good area of, um, a lot
28:07
of really source of questions.
28:11
So case 20, I'll let this sink in for a second.
28:21
A 28-year-old woman presents with intermittent,
28:24
intermittent right upper quadrant pain and a palpable mass.
28:27
Um, her MRI showed a a liver lesion consistent
28:31
with hepatic angio.
28:33
She developed thrombocytopenia
28:35
and a prolonged pt, which
28:36
of the following conditions is most likely responsible
28:39
for her abnormalities?
28:47
So if you said kaback mirror, which the majority of you did,
28:51
um, or nearly all of you did, uh, you would be right.
28:54
So these are actually, um, uh, uh, thrombocytopenia,
28:59
hemolytic anemia, subjective coagulopathy,
29:02
typically more common, um, in infants.
29:06
Um, but the classic question, uh, is again,
29:09
with these giant cavernous mandis, um, you will see
29:12
that they're really following the pattern here, um,
29:15
from arterial to delayed phase.
29:18
Um, the centripetal fillin patients, um,
29:21
typically they don't have symptoms, um,
29:23
but if the heman is large
29:25
or palpable, um, they can be, uh, removed
29:33
case 21.
29:40
And the question is, which
29:41
of the following organisms is responsible
29:43
for causing these findings?
29:51
So if you said AOC caucus, you'd be right.
29:54
Um, you see here those classic, uh, floating membranes, um,
29:59
the liver is most frequently, um,
30:01
but I have seen some questions as well as some colleagues
30:04
with cases, um, that show, uh,
30:07
show in the lungs are manifest in the lungs
30:09
and where it is the second most common location.
30:11
Humans are the accidental intermediate host.
30:15
After ingesting the ova passed in the dog species,
30:21
36-year-old male with liver mass,
30:28
what is the best diagnosis?
30:37
Uh, so if you said fibro Ella, HCC, you'd be correct.
30:41
Um, this patient actually came, uh, from an outside hospital
30:45
and they thought he had a pancreatic tumor.
30:48
Um, but this actually in the sins.
30:50
And, uh, when we looked at it,
30:51
his pancreas was completely normal.
30:54
He did have these large conglomerate lymph nodes, um,
30:58
and he had these large masses, um, in, in the liver.
31:02
So I just wanted to briefly talk about fibro HCC.
31:05
These are the patients, the young adults no as association
31:08
with Hep B or C, um, no, A FP elevation.
31:13
And the pneumonic here is psych, uh, pseudo capsule, uh,
31:17
scar, young patients, capsular retraction, huge
31:21
and heterogeneous.
31:22
Um, again, uh, f and Hs.
31:26
Uh, there'll be homogeneous,
31:27
but heterogeneous masses, those are gonna be filo meers.
31:33
And just to give you a little bit more background on FNH
31:35
versus fibro mear, um, typically, uh, the vus, the F
31:40
and Hs will take up, uh, VUS and the fibro mear.
31:43
Again, we'll have a T two dark scar
31:45
and lots of central cals.
31:50
Uh, here are a couple more five L
31:52
HCCs, one of them courtesy.
31:54
My, uh, good friend Dr. William Hong from UCSF.
31:57
And again, his images, his post con images with vis show,
32:01
no retention, no uptake.
32:03
These were very concerning for, again,
32:05
these central calcs here, A five LHCC
32:12
case 23.
32:15
What is the best diagnosis based on these findings?
32:25
Good. Um, so you'll see a heterogeneous, um,
32:30
mass, and then on more of the delayed images, um,
32:33
you can see it actually fills in and,
32:35
and shows increased enhancement.
32:38
Um, don't confuse this for fibrosis.
32:41
Um, fibrosis has hyperintensity T two reticulations,
32:45
it can have capsular retraction.
32:48
Um, cholangio can very closely mimic this.
32:52
Um, and adeno, we see a lot
32:54
of adenocarcinomas also show this pattern
32:56
of capsular retraction and delayed enhancement.
33:00
Um, but usually, uh, the lack
33:02
of upstream dilatation really favors confluent fibrosis
33:06
over, um, adeno.
33:10
And just to show that, again, capsular retraction
33:13
and delayed progressive enhancement.
33:16
Um, at SAR, not this past SAR, but the one
33:19
before that, it seems like the consensus that the 10
33:23
to 15 minute cholangio delays, um, may not be that helpful.
33:27
And we can really see the same things on three
33:30
to five minute liver delays.
33:31
So here at Stanford we're actually, uh, trying
33:33
to shorten our protocols, um, as well, uh,
33:37
to keep liver delays a little bit shorter.
33:43
Okay, case 24.
33:45
Which of the following images best represents a
33:47
late arterial phase?
33:56
Um, so a is actually, you do see some robust filling
33:59
of the portal, Venus, so it is not A
34:02
and B is more of our delayed.
34:04
Um, c uh, and we'll go into why this is.
34:08
Um, but you see the arterial enhancement, you see, uh,
34:12
the arterial, uh, enhancement here as well.
34:15
And you see slight filling of that portal venous phase.
34:22
Which of the following statements is true
34:24
regarding the late arterial phase in liver imaging?
34:34
Excellent. So it is crucial for identifying, um,
34:37
hypervascular lesions such as hepatocellular carcinoma.
34:41
So I do wanna talk just a little bit about the optimum liver
34:44
arterial enhancement.
34:45
And that is the late phase, late phase arterial enhancement,
34:49
not just an early phase arterial enhancement.
34:52
The optimal liver arterial enhancement is a
34:54
late arterial phase.
34:56
So how do you know when you're in that?
34:58
Um, well typically your hepatic veins are unenhanced.
35:02
You have a tiger stripe spleen,
35:04
and really I like to see slight just slight filling of
35:09
that portal vein.
35:10
Sometimes you can also see slight filling of
35:13
that left renal vein.
35:14
So in all my HCC workups, um, I ask myself,
35:18
is this um, an adequate liver arterial enhancement?
35:22
Um, and I go through this checklist.
35:29
Okay, case 26, we have a 21-year-old male
35:32
with elevated LFTs.
35:33
I'm giving you the ct, um, as well as the MRT images.
35:44
What is the diagnosis? Is this normal enhancement?
35:47
Is this lymphoma? Is this acute viral
35:49
or is this glycogen storage disease?
35:58
Good. So, um, the majority
35:59
of you did say it was acute viral.
36:01
Um, this particular patient had, uh, his A ST alt were, uh,
36:07
very elevated and he did end up going to on
36:10
to have severe active hepatitis.
36:12
Um, in the hetero in we just talked about an arterial phase.
36:17
As long as you have an adequate late arterial phase
36:19
and you see heterogeneous enhancement, um,
36:22
on this late arterial phase, um, then you should start,
36:27
you know, thinking about this diagnosis.
36:29
Um, on T two images you'll see periportal edema,
36:33
and this is another case of a patient with hepatitis.
36:35
Um, it's such severe thickening of the gallbladder wall.
36:43
Okay, case 27, uh, 46-year-old male with cirrhosis.
36:47
He's coming in, uh, being evaluated pre-transplant.
36:52
So a apologies for going fast.
36:54
This first one is his axi and his, uh, coronal imaging.
36:58
Um, and then here's his in and out of phase imaging.
37:07
Good. So, uh, primary hemochromatosis is the correct answer
37:11
and so let's talk a little bit about why that is.
37:14
Um, so in conventional chemical shift, MRI images, um,
37:18
when fat and water are out of phase
37:21
and in phase on out of phase,
37:22
fatty tissues will appear darker.
37:25
But on, um, in terms of iron, um, on out
37:30
of phase images that'll show,
37:31
or I'm sorry, on in phase, uh, this, uh,
37:34
show a decrease in signal
37:36
of the liver on the endphase images.
37:39
Um, again, that's on the loss
37:42
of signal on the endphase of images.
37:45
So primary hemochromatosis
37:47
and secondary P stands for primary, which stands
37:51
for pancreas.
37:52
Um, you'll see that same, uh, loss
37:55
of signal on the end phase for primary hemochromatosis
37:58
and for secondary hemochromatosis
38:01
or reticular endothelial system.
38:04
I know that's a little bit of a stretch,
38:05
but hemoch, secondary hemochromatosis involves the spleen,
38:09
uh, spleen and liver and the bone marrow.
38:12
Um, so you see that same, uh, loss of signal here
38:16
of the spleen on enphase images.
38:18
Um, but the pancreas is normal in signal
38:23
primary hemochromatosis.
38:25
Again, pancreas low T two, uh, pink signal, the spleen
38:30
and bone marrow will be normal.
38:33
Secondary hemochromatosis such as repeated transfusions,
38:37
thalassemia, they'll have a normal pancreas.
38:40
Um, but again, that, that spleen will be dark.
38:46
Okay, case 28, we have a 47-year-old female
38:49
with a liver lesion here.
38:51
I give you, uh, T two images post con arterial
38:54
as well as VUS images.
39:02
What is the diagnosis?
39:10
So this is a, a classic FNH.
39:13
So these guys are stealthy on T two,
39:16
you can really hardly see them.
39:19
Um, on vus, they're either going to be hyper or iso.
39:23
And on post con they really do avidly enhance.
39:27
So let's talk a little bit about FHS versus adenomas.
39:31
Um, young person, non-cirrhotic, no malignancy
39:35
or risk factors you see in arterially enhancing lesion.
39:38
Your differential, you're gonna be thinking FNH and adenoma.
39:42
Um, so on MRI, again, this is an FNH case.
39:46
Um, you're gonna see slightly increased
39:49
or iso again, it's that stealthy lesion.
39:52
Um, the MRI,
39:54
these FNH lesions are gonna enhance avidly
39:58
during the arterial phase.
39:59
And they typically tend to fade
40:01
or become a little bit more harder to see on portal venous
40:05
and delayed on vis, um,
40:07
they're usually hyper or iso.
40:11
And here fat and hemorrhage. Uh, are your friends here?
40:14
No fat, no hemorrhage.
40:17
Let's talk a little bit about adenomas,
40:19
which is this case here.
40:21
You see here it's not as stealthy, it's not as, um,
40:25
harder as hard to see.
40:27
It's a little bit more mild here.
40:29
Um, the MRI Avidity is gonna be actually a little bit less
40:33
than an F and h um, vis, it'll tend to be hypo or reduced.
40:38
And here fat is your friend.
40:40
Uh, there can be intralesional fat and they can hemorrhage.
40:44
I typically, I I often see a large subcapsular hematoma,
40:49
um, in a patient coming in, uh, with a ruptured adenoma
40:54
if you crave the details.
40:55
My colleague and good friend Dr.
40:57
Justin Shea has an amazing paper.
41:01
I would not read this right now.
41:02
Um, but if you are interested in body imaging, uh,
41:05
and you crave more details, uh,
41:08
he can give you a little bit more information about some
41:11
of these adenoma subtypes.
41:13
Uh, this is what you may look like when you read the paper.
41:15
It is, it is a hard, it is a difficult paper with a lot
41:19
of, uh, details.
41:20
But let me give you the bottom line.
41:22
Let me give you the cheat sheet.
41:24
Um, the inflammatory is gonna be tied for the most common
41:28
with the H and F1 alphas.
41:30
Um, the exon three ones,
41:33
those are gonna be the anabolic steroid ones,
41:36
the male sex ones.
41:37
Um, and then these last two are our hemorrhage risks.
41:45
Okay, case 29.
41:47
We have 13 minutes
41:48
or so to get through about 15 more questions.
41:51
So we'll hustle here. Um, which
41:53
of the following statements is true regarding Bud Chiari?
42:00
Is it caused by a portal vein, thro portal vein thrombus,
42:04
obstruction of hepatic vein outflow?
42:07
Is it commonly associated with chronic Hep B
42:10
or it typically presents
42:11
with isolated abdominal pain without any other symptoms?
42:21
Excellent. So the key word here is actually, um, a hepatic
42:25
venous outflow issue.
42:27
Um, and it can be at any point.
42:29
It can be at the small hepatic veins,
42:31
it can be the large hepatic veins, it can be at the IBC.
42:35
Um, there is a difference.
42:36
There is a primary and secondary form.
42:38
Primary are gonna be our endoluminal thrombosis,
42:42
our hypercoagulable states such as birth control.
42:45
And our secondary, uh,
42:47
venous outflow issues are gonna be typically due
42:50
to an extrinsic compression or tumor.
42:53
Here you see a really dysmorphic liver.
42:56
Um, you see an enlarged cacau, a lobe just heterogeneous,
43:00
um, and just heterogeneous enhancement are really,
43:03
this is not a, a normal liver.
43:08
Okay, case 30, which is the following,
43:13
what is the following syndrome called?
43:22
Uh, so this is Osler Weber Randu or HHT.
43:26
These cases are pretty incredible.
43:29
They have these very large ectatic, uh,
43:32
hepatic arteries just really, uh,
43:35
shunting throughout the liver.
43:36
They typically have, uh, nose bleeds
43:39
and you see the embolized AVMs here in the liver.
43:43
Um, here at Stanford, our hepatologists do, uh,
43:46
all these patients closely, um,
43:48
because they can have biliary ischemia and cardiac failure.
43:54
So why am I showing you this?
43:55
Well, here's where people make the mistakes,
43:58
their frequency, um, really diminishes the criteria
44:02
for HCC diagnosis.
44:04
So the critical aspect to remember here is, um,
44:07
HHT Bud Chiari, cardiac congestions.
44:11
Um, you know,
44:12
you'll get these benign arterial lesions called
44:15
FNH like lesions.
44:16
I see them all the time.
44:17
They mimic HCC
44:19
and their frequency really diminishes the specificity
44:22
criteria for HCC diagnosis.
44:24
So a question you may get, um, come June may be, which
44:29
of the following, uh, can you use for rads?
44:32
And if you see a liver that has HHC
44:35
or Bud Chiari, you will not select that one.
44:41
Okay, case 31,
44:46
are these abscesses, hematomas, hepatic cysts,
44:50
or polycystic liver disease?
44:55
Again, this kind of goes back to, uh,
44:57
you're probably expecting more of an MRI
45:00
to see this on an MRI.
45:02
Um, but here, uh, I'm giving it to you on ultrasound.
45:12
Good. So I didn't trick you. These are, um, biliary omas.
45:17
These are small cystic lesions.
45:18
They do not communicate with the biliary tree
45:22
and they tend to be a little bit more smaller
45:24
and more irregularly shaped than just simple cysts.
45:29
Okay, case 32.
45:31
Are these hepatic abscesses per biliary abscesses,
45:35
biliary hematomas, again, or per biliary cysts?
45:45
Good. Excellent. Uh, so these are per biliary cysts.
45:49
These are cystic formations
45:51
around the intra hepatic B ducts.
45:53
Um, they primarily are in a LAR distribution
45:57
and, um, they do not communicate with the biliary trait.
46:02
Which of the following is the most common etiology
46:05
associated with the development of per biliary cysts?
46:15
So if you, uh, try
46:17
to use everything you got when you're taking the test.
46:20
Um, so this is actually gonna be that, uh,
46:23
chronic liver disease, particularly cirrhosis.
46:26
So you can see the per bi ais here,
46:29
you can see the nodular contour of this liver.
46:32
Um, in this patient with cirrhosis, um, they can develop due
46:36
to changes in the surrounding liver tissue in the chronic
46:39
of just chronic liver disease or liver inter, uh, injury.
46:44
Um, and again, a per bis are more likely to be associated
46:47
with chronic liver disease.
46:52
Okay, uh, 70-year-old female with right upper quadrant pain.
46:56
Which of the following is a common risk factor
46:58
for developing this, this condition
47:07
X.
47:08
Um, so if you thought to yourself, this looks like
47:11
emphysemic cystitis, you'd be correct.
47:13
Um, again, you're probably looking to, uh, see it on ct,
47:17
but here I'm showing you to you on ultrasound
47:19
and this is all dirty shadowing.
47:21
Um, and cur lineer bands with bright echogenicity,
47:25
which again is gonna be air bubbles.
47:27
And this is emus cholecystitis. Okay?
47:32
This is a 48-year-old, uh, male with a history
47:34
of Wilson's disease.
47:36
He has p status post on orthotopic liver transplant.
47:40
He's presenting with fever, new LFT abnormalities,
47:43
which vessel should be closely interrogated on
47:46
Doppler ultrasound.
47:53
Good, the hepatic artery.
47:56
Um, so in the liver transplant,
47:59
the hepatic artery is the sole blood supply
48:02
to the biliary epithelium.
48:04
We, patients will,
48:06
we are a huge liver transplant center here at Stanford.
48:08
They get a transplant
48:10
and I would say within hours, um, we are checking,
48:13
we are checking the main portal vein,
48:15
but we're also checking the hepatic artery, the anastomosis,
48:19
the left and the right hepatic arteries.
48:21
If I don't see those, if my tech can't go get them, I ask,
48:25
I say, let's go find another tech.
48:27
Let's, let's try to get it again.
48:29
Um, 'cause that's what the surgeons want to know.
48:36
Uh, just showing you some, uh, uh, very similar cases.
48:39
Uh, this is a 71-year-old male
48:41
with a remote liver transplant presenting
48:43
with hyper bilirubin anemia.
48:46
Um, we see these large branching tubular structures, um,
48:50
here on these pret pret one images we see, uh, hemorrhage
48:55
or poor tenacious, um, material within it.
48:58
Um, and this is also, um, a patient, uh, with, uh,
49:04
um, biliary ischemia due to, um, the cutoff
49:08
of the hepatic artery.
49:09
And let me show you. So if you watch this video
49:12
with the sinning, um,
49:16
you'll see the celiac takeoff
49:17
and you see the stump here of the hepatic artery.
49:21
Um, and again, this, the hepatic artery is
49:25
what we are looking for.
49:28
Um, so the, again,
49:29
the int hepatic bile ducts are exclusively supplied, um,
49:34
by the per biliary plexus
49:36
or branches from the hepatic artery.
49:38
The extra hepatic ducts have multiple blood supplies.
49:42
And again, I really wanna emphasize that any cause leading
49:45
to hepatic artery occlusion can lead to biliary necrosis,
49:49
hyper coag states trauma, um, you know, cases,
49:55
um, I've seen it in patients who, um, get bili.
49:58
I've seen patients with a large tumor, um,
50:02
that causes mass effect
50:03
or compression on the hepatic artery,
50:05
and that also leads to biliary necrosis.
50:08
So the characteristic is gonna be the liver transplant.
50:12
Um, but again, biliary necrosis, um,
50:15
because of occlusion, uh, due to these other conditions,
50:18
be on the lookout for that as well.
50:23
Okay. Uh, another medical showed trivial.
50:25
We'll go fast if you don't, you don't like this question.
50:27
My husband also wrote this one. What was Dr.
50:31
Todd's original specialty before joining Dr. House's team?
50:40
We've got answers for B and there's a, someone said a,
50:45
A, we have some house fans.
50:47
So plastic surgery, uh, we have two minutes left.
50:51
Um, we'll just do this question
50:54
and then we will, we'll part, um,
50:57
so this patient is 36-year-old.
51:00
Uh, what is the typical histopathological finding in an auto
51:04
infarcted spleen?
51:12
Good, excellent, excellent.
51:13
Drop necrosis of, um, the red pulp.
51:17
Um, so, sorry, I'm just doing this.
51:21
Um, in case of auto infarct, particularly sickle cell,
51:25
the red pulp is primarily affected due
51:27
to vaso-occlusive events that can lead to ischemia.
51:31
Uh, the spleen infarcts, it shrinks in calcified, uh,
51:35
can be very, very small.
51:37
Um, sometimes you can't, you can barely see it.
51:39
It's so tiny. Um, but I just love this example
51:42
'cause it is, um, just so, uh, dense and calcified.
51:47
So I lied. Let's just do one more question.
51:51
Um, let's see, Jackie, if we could skip to, um,
51:57
let's go to case 44.
52:00
Got it. If you get this
52:05
question right, I think you're, uh, on your way,
52:08
you're doing really well.
52:09
Um, you're making really great progress.
52:11
So a 55-year-old male with epigastric pain,
52:14
his endoscopy revealed an ulcerated gastric mass.
52:18
The stains were diffusely positive for dog one as well
52:21
as CD 17.
52:22
What is the most likely tumor?
52:31
Excellent. So this is a true case of mine where I had
52:33
to read the, uh, path report.
52:35
And remember, uh, that gist, uh,
52:39
is defines, uh, CD one 17 defines GIST
52:44
and other mesenchymal tumors.
52:46
Um, and gist, uh, most commonly metastasized
52:51
to the liver and their malignant potential is really based
52:54
on size and, um, mitotic rate.
52:58
Um, let's just, I do wanna let, uh,
53:02
just end on this as well.
53:04
Neurofibromatosis type one, um,
53:07
they have manifestations such as gist, uh, tumors,
53:12
carcinoids, phe, uh, dural lac.
53:16
Um, in the gen population,
53:18
gists are more common in the stomach,
53:20
but for NF one patients, um, they're typically,
53:23
uh, in the small bowel.
53:24
And this was a patient of mine, um,
53:26
and she developed recurrence.
53:29
Um, you'll also see, uh, you can see these on ct.
53:33
This was a history of, uh, resected neck tumor.
53:36
It's a very complex multisystem disorder.
53:39
Um, but you can see these small papular projections
53:42
here on the ct.
53:43
And this patient with NF one,
53:45
you can even see it on this plain film here.
53:47
These pedunculated papillo nodules of NF one patient.
53:53
Um, so I'm sorry we didn't get to about five
53:55
or six questions, but just to give you a little bit
53:57
of a summary, um, expects a different presentation
54:01
of images than the typical.
54:03
Um, again, we're all looking for
54:05
that celiac on the plain film,
54:07
but make sure you're aware of
54:09
how it looks on other modalities such as CT
54:12
or MRI know your syndromes.
54:14
Uh, Von Hippel, Lindel and F1 HHT.
54:18
Uh, I do see them quite frequently here at Stanford.
54:21
They are a big part of my practice.
54:23
Um, it wasn't just when I was studying first, uh,
54:26
step one or boards.
54:28
Um, and really for, for these exams,
54:31
think horses not zebras.
54:33
Um, they're not gonna show you, you know, crazy cases of,
54:37
you know, really, uh, odd liver tumors.
54:41
No one's gonna, everyone wants you to just know an FNH,
54:44
uh, and an adenoma.
54:46
Um, and then just, uh, have a golden retriever mindset.
54:51
Um, my golden has taught me a lot, you know,
54:53
golden retrievers.
54:55
Uh, they don't get stuck in the past.
54:57
She knows she's not allowed to be on this furniture.
55:00
Um, but she doesn't, when when I scold her, she just,
55:04
she stays in the presence, she shakes it off,
55:06
she moves forward, they have so much enthusiasm, uh,
55:10
focus on what's next.
55:11
Chase that next opportunity.
55:13
Um, so thank you so much for joining.
55:16
If you have any questions, you wanna, you're, you're hungry.
55:19
For those last five questions that we didn't get to go over,
55:22
I'd be more than happy, uh, to go over them with you.
55:25
Um, best of luck
55:26
and please reach out to me if you're ever interested in, uh,
55:29
coming to Stanford for a fellowship.
55:31
Um, or just wanna learn more about the Bay
55:34
Area. Thank you so much.
55:36
Thank you so much Dr.
55:37
Negreti for taking us through that rapid case review.
55:40
It was so much fun. Um, it was a blast.
55:43
Thank you so much for taking your time to be here.
55:46
And thank you to all who are participating.
55:49
You can access the replays on previous reviews
55:51
by creating a free account.
55:53
And be sure to join us next Monday, March 31st with Dr.
55:57
Mahesh, who will lead us in a physics radiography,
56:00
fluoroscopy board review.
56:02
You can register for at the link provided in the chat
56:05
and follow us on social media
56:06
for updates on future meetings.
56:08
Thanks again for learning with us and we'll see you soon.