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Gastrointestinal Imaging Case Review with Dr. Lindsey Negrete (3-24-25)

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0:02

Hello and welcome to Case Crunch, rapid case review

0:05

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

0:11

with a multiple choice question,

0:13

and you'll respond with your best answer via

0:15

the live polling feature.

0:17

After a quick answer explanation, it's on to the next case.

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You'll be able to access the recording

0:22

of today's case review

0:23

and previous case reviews

0:25

by creating a free account using the

0:27

link provided in the chat.

0:29

Today. We are honored to welcome Dr. Lindsay Negretti

0:32

for a GI Imaging Board prep case review.

0:35

Dr. Negretti completed her residency training

0:38

at uc San Diego.

0:39

She completed her abdominal imaging fellowship at Stanford

0:43

and stayed on for an attending position after training.

0:46

She is active in medical student mentorship

0:49

and is the podcast creator

0:50

of let's read out, in her spare time.

0:53

She loves playing golf with her husband

0:54

and spending time with her golden retriever.

0:56

Willow questions will be covered at the end if time allows.

1:01

Please remember to use the q

1:02

and a feature to submit your questions.

1:04

With that, we are ready to begin today's board review. Dr.

1:07

Negretti, please take it from here.

1:10

Jackie, thank you so much for that warm welcome.

1:13

I am really, truly honored to be here today.

1:15

I wish I would've had this when I was a resident,

1:18

um, or our fellows.

1:19

So thank you so much. This is such a great resource,

1:21

and you know, first of all, I just want everyone you know,

1:24

who's tru tuning in.

1:26

I know it's five o'clock,

1:28

it's eight o'clock, it's, it's late.

1:30

Um, so what really sets you guys apart is the effort you're

1:33

taking when others are stopping.

1:35

You're taking the time to study even after hours.

1:39

And really that extra effort you put in today,

1:41

I know it will make you stand out tomorrow.

1:43

So keep up the great work.

1:45

You should really, uh, you know, take some extra time,

1:47

watch some extra TV tonight because you deserve it.

1:51

Success really isn't just about talent, it's,

1:53

it's about dedication.

1:59

I have no disclosures today. Here's our agenda.

2:04

And then to make things a little bit extra fun, um,

2:08

I will sprinkle in some medical trivia as we switch topics.

2:13

I'll probably show my age, um,

2:15

but hopefully, uh,

2:17

it'll make things a little bit more entertaining.

2:19

But first, uh, let's just, uh, practice a little bit

2:23

and are you a resident, an attending, just here

2:27

for the cases or something else?

2:36

Wonderful. So it looks like, um, the majority of you are

2:40

residents studying for the court.

2:47

Uh, so we'll start off with the pharynx and esophagus.

2:51

So go ahead and just take a second.

2:53

Uh, this is a 59-year-old male with HIV and thank you to Dr.

2:58

Fiona Cassidy.

2:59

Um, from, from the VA San Diego for this case.

3:06

What is the most likely diagnosis based on these findings?

3:10

Is it Canada? Is it a carcinoma?

3:13

Is it eosinophilic esophagitis?

3:15

Is it gerd or is it feline esophagus?

3:22

Jaggy. Can, can they see the, the, the answers?

3:28

They can see the answer options, yes.

3:30

Okay, okay. Even though, okay.

3:33

And they'll see the answer choice.

3:37

Ah, they can, are you seeing the answer here?

3:41

Nope. Not on, that's on the next slide, right?

3:44

Oh, okay. Yes. And then that'll,

3:46

the poll will show on the next slide, the,

3:48

like they'll be able to see the, see the distribution.

3:52

Yes, they should. Do you see it?

3:57

I see your answer. Explanation slide. Yes.

3:59

Okay. And the distribution, or do I maybe have to,

4:06

We're seeing in the chat. Yes, we see it.

4:08

Okay. Okay. Just making sure. Thank you.

4:10

I just wasn't sure. Appreciate it.

4:12

Um, so this is, uh, esophageal candidiasis.

4:16

This is a shaggy esophagus.

4:18

Uh, when Canada is severe, like it is in this case,

4:21

it really appears shaggy herpes will have more

4:24

of a small emus halo.

4:27

CMV will be large, flat ovoid ulcers

4:31

and eosinophilic esophagitis will have concentric rings.

4:35

The history will be failing PPIs,

4:37

but the patient will get better with steroids.

4:39

And again, that will be a ringed appearance.

4:46

So this is a 3-year-old female with dysphagia

4:50

and I'll let you guys just sink in for that one.

4:57

Which of the following statements is true

4:59

regarding this condition?

5:07

Uh, so if you said b, uh, you are correct.

5:10

They are found in conjunction with hial hernias.

5:14

Uh, so this is a,

5:16

at Stanford we actually use a single contrast as opposed to,

5:19

um, double contrast.

5:21

Um, but the B line is a thin construction, uh,

5:24

constriction at the GE junction.

5:27

And again, the keyword here is going to be symptomatic, um,

5:31

because the patient is symptomatic.

5:34

This finding, um, may be, uh, more appropriately referred to

5:37

as a chat skis ring.

5:39

And again, this is gonna be circumferential as opposed

5:42

to our esophageal carcinoma, which is asymmetric.

5:46

And an irregular contour webs are typically more higher up

5:50

in the cervical esophagus.

5:51

And again, this one not only shows, um, the circumferential,

5:55

but also the small hiatal hernia.

5:57

Um, and again, symptomatic, so shaky s for symptomatic.

6:05

So I don't have the, um, polling for the these questions,

6:09

but if someone wants to just come off of, um,

6:12

or sit, see in the chat, I can't see it in the chat.

6:14

So hopefully Jackie can help me out here.

6:17

Um, but I am a big Noah Wiley fan.

6:19

I used to watch the er, uh, every Thursday night.

6:23

Um, and the new show, the pit also on HBO,

6:27

what is this character's name

6:28

and the new drama, the pit, is it Forest?

6:32

Is it Hunter? Is it Whitaker

6:34

or is it Neil

6:40

And Jackie, if you can help me out

6:42

'cause I can't see the chat on my screen.

6:44

We've got one person saying Whitaker.

6:47

Nice. Excellent, excellent.

6:49

I can tell, maybe it's not as popular

6:51

as I thought it would be.

6:55

So let's move on to the stomach. Uh, case three.

6:58

I'll let this sink in with, um,

7:00

a plain film that we have here.

7:07

And moving on to the ct.

7:12

And now moving on to the question.

7:14

Which of the following is most likely the underlying

7:16

cause of this condition?

7:25

Seems like, um, interesting.

7:27

So we got some peptic ulcer disease.

7:29

Um, we got gastric perf, um, ischemic bowel.

7:33

Um, so the answer I was looking for, kind

7:35

of a difficult question, um,

7:37

but I was looking for, um, more of

7:42

mucosal disruption.

7:43

So mucosal disruption from an ulcer

7:45

or tumor that is really the entrance site, um, for, uh,

7:51

gastric emphysema

7:52

and gastric emphysema is what we're seeing here.

7:54

And that's air in, uh, the wall of the stomach here.

7:58

Um, it gastric perforation,

8:00

you would typically see more free air in

8:02

the peritoneal cavity.

8:04

Um, and, and we also just don't have an NG tube.

8:07

Um, that would probably be more of the clue here.

8:14

Case four.

8:21

So this patient presented, uh,

8:23

for a staging exam for rectal cancer.

8:26

What is the best next step

8:27

for the finding in the upper abdomen?

8:36

Good. I see a lot of do nothing.

8:39

So there is a normal left adrenal here, um,

8:42

and there is a posterior gastric diverticulum

8:46

and posterior is the, uh, the most common spot.

8:50

Um, for a gastric diverticulum. These can be confusing.

8:53

Um, they can be mistaken, mistaken for an abscess

8:56

'cause there, there can be gas, um,

8:59

but oral contrast can really seal the deal here, uh,

9:02

and doing nothing.

9:04

This is, uh, a nothing burger as my attending would say.

9:10

Okay, case five. I'll be honest, this is my favorite case,

9:14

probably my favorite fluoro.

9:16

Um, so let's hope, uh,

9:17

that you love the question as much as I do.

9:21

A 42-year-old female with a history of a lap, uh,

9:25

ruin y bypass presents with abdominal pain.

9:28

What is the diagnosis?

9:36

Good. So this is a gastro gastric fistula.

9:39

Um, there is prompt of ification of the gastric pouch

9:44

as well as the hold on, um,

9:49

as well as the, uh, GJ limb.

9:53

And here we also see simultaneous filling

9:55

of the excluded stomach.

9:57

Uh, so this is a gastro gastric fistula.

10:01

You can have some filling of the, um,

10:04

excluded stomach by reflux.

10:06

Um, but really here the key is, um,

10:10

simultaneous filling.

10:12

And these patients present with a poor post-op weight loss.

10:16

And again, simultaneous filling

10:19

reflux again will be in a delayed fashion.

10:25

Beloved, Dr. Mark Green had a slightly rebellious daughter.

10:29

What was her name? Also give you a hint.

10:32

Uh, she shares the same character name as,

10:36

uh, Jennifer Aniston's.

10:38

Uh, character and friends

10:48

we're getting a lot of Rachel's.

10:50

Nice, nice everyone.

10:54

Okay, moving on to, uh, bowel and colon. Uh, case six.

10:58

This patient has a ulous esophagus and renos in her fingers.

11:04

The left upper abdomen, small bowel can best be described as

11:09

feathery ribbon, hide bound or featureless.

11:21

So this is actually, uh, hide bound and good.

11:24

Most of you, uh, the majority of you got that.

11:27

Um, so this patient has, uh, scleroderma.

11:30

So this is collagen deposition in multiple organs,

11:34

including the GI muscular layers.

11:37

Um, high bound really refers to that narrow closest, uh,

11:41

close separation, um,

11:44

with normal thickness despite d dilatation

11:46

of the bowel lumen case, seven

11:52

30-year-old female with chronic diarrhea,

11:55

weight loss and fatigue.

12:00

What does this finding suggest

12:10

Excellent malabsorption due to celiac disease?

12:14

So I guarantee you were probably expecting me

12:17

to ask you in the form of a a abdominal plane film.

12:21

Um, you see the normal

12:23

al pattern here in the left upper abdomen,

12:25

this feathery appearance.

12:27

And here, um, in this patient on, uh, the, the right,

12:31

there's a reversal of that full fold pattern.

12:35

So I really tell people when they're studying

12:37

for these tests, if you're expecting something to be, uh,

12:41

given to you on plain film, expect

12:44

to see it something some somehow, somewhere differently.

12:47

If you're expecting it to see it.

12:48

Uh, you normally always see it on MRI expect

12:52

to see it in a different modality.

12:53

So again, uh, this is celiac disease.

12:56

It's an autoimmune proximal enteritis.

12:59

It's T-cell mediated and it's malabsorption

13:03

and is characterized by this fold reversal.

13:06

On imaging, the al should have more fold than the ilium,

13:10

but in celiacs you have a loss of the al folds

13:13

and you'll have a compensatory increase in the IAL folds.

13:18

Celiac has a number of different manifestations as well,

13:21

including mesenteric adenopathy, engorgement

13:24

of mesenteric vessels, splenic atrophy.

13:27

It increases the risk of venous thromboembolism.

13:30

And you can also get a dermatitis for pettifor rash.

13:37

A 45-year-old male with a longstanding history

13:40

of untreated celiac disease presents

13:42

with worsening abdominal pain and weight loss.

13:45

He undergoes an endoscopy which reveals a mass

13:47

in the small intestine.

13:51

What is the most common malignancy associated

13:53

with untreated celiac disease?

14:03

So if you said, uh, T-cell lymphoma, you would be right.

14:07

I just said that celiac is a T-cell mediated.

14:10

Um, so it is the most common malignancy associated

14:14

with untreated celiac disease.

14:15

You may see on CT some sort

14:17

of exophytic mass valve thickening and really enlarged

14:21

and pathologic, uh, mesenteric lymph nodes.

14:28

Continuing, uh, with our celiac theme,

14:32

a 30-year-old female presents with a history

14:34

of chronic diarrhea, weight loss, and fatigue.

14:37

She also reports recent episodes

14:39

of cough and shortness of breath.

14:40

And a chest x-ray reveals bilateral infiltrates in a

14:44

bronchoscopy with lavage shows chemo citrin

14:48

laden macrophages.

14:52

Given her gastrointestinal symptoms

14:54

and pulmonary findings,

14:56

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.

15:09

So, excellent job.

15:11

So this is actually pulmonary, pulmonary hemo citrus, uh,

15:15

secondary to celiac disease, disease, um,

15:17

and the syndrome is called lame Hamilton.

15:20

Um, so celiac, uh, really can lead to a number

15:24

of systemic complications,

15:25

including pulmonary manifestations due to malabsorption

15:29

and subsequent iron overload

15:35

case 10, a 48-year-old male with left lower quadin.

15:45

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.

16:00

Um, these are small patches of fat that hang from the colon.

16:06

I probably see this once a week

16:08

and it truly does mimic diverticulitis.

16:11

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?

16:19

Um, very similar,

16:21

but usually, uh, omental infarct is a little bit larger,

16:24

the location is different

16:26

and, uh, it doesn't have the char characteristic oval shape

16:30

of the epi poetic appendage.

16:35

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

17:43

and that that's the weakest area of the colon.

17:47

I also thought of another question that would be, um,

17:49

you know, where are diverticula maybe least likely to occur

17:54

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.

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Tags

Vascular Imaging

Pediatrics

Nuclear Medicine

Neuroradiology

Musculoskeletal (MSK)

Interventional

Head and Neck

Genitourinary (GU)

Gastrointestinal (GI)

Chest

Cardiac

Breast

Body