GI

Question 1

Location

H pylori gastritis

Answer 1

usually antrum

Question 2

Location

Zollinger-Ellison

Answer 2

Ulcerations in the stomach (jejunal ulcer is the buzzword).
Duodenal bulb is actually the most common location for ulcers in ZE. Remember ZE is
from gastrinoma - and might be a way to test MEN syndromes.

Question 3

Location (stomach)

Crohns

Answer 3

Uncommon in the stomach, but when it is, it likes the antrum

Question 4

Location

Menetrier’s

Answer 4

Usually in the Fundus (classically spares the antrum)

Question 5

Location

Lymphoma

Answer 5

Crosses the Pylorus” - classically described as doing so, although in reality adenocarcinoma does it more.

Question 6

FAP

Answer 6

100s of polyps - 100% risk of Colon CA (usually before 40)

Hyperplastic Stomach Polyps , Adenomatous Bowel Polyps
Adenomatous

Locally invasive desmoid tumors are common at surgicai ls■i*tes post
colectomy (these actually kill 10%ofFAPers)

Question 7

HNPCC (Lynch)

Answer 7

As the name implies, this is not a disease of 100s of polyps. Instead it is DNA Mismatch Repair problem associated with lots of cancers.

Another difference between this and FAP is that the cancers of the colon are usually solitary (and right sided).

They also get lots of other cancers (endometrial being the second most common)

Question 8

Gardner Syndrome

Answer 8

FAP + Desmoid Tumors, Osteomas, Papillary Thyroid Cancer

Question 9

Turcots

Answer 9

FAP + Gliomas and Medulloblastomas

Question 10

Peutz-Jeghers

Answer 10

Hamartoma Style!

Mucocutaneous Pigmentation (gross Dalmatian dog lips)

Small and Large Bowel CA, Pancreatic CA, and GYN CA

Question 11

Cowden

Answer 11

Hamartoma Style!

BREAST CA, Thyroid CA,
Lhermitte-Duclos (posterior fossa noncancerous brain tumor)

Hamartoma Style!

Question 12

Cronkhite-Canada

Answer 12

Hamartoma Style!

Stomach, Small Bowel, Colon,

Ectodermal Stuff (skin, hair, nails, yuck)

Question 13

Juvenile Polyps

Answer 13

Hamartoma Style!

Increased risk for colorectal and gastric cancer (different than sporadic juvenile polyps -which are typically solitary and benign)

Question 14

Stomach ulcer

Malignant

Answer 14

Width > depth

located within lumen

nodular irregular edges

folds adjacent to ulcer

aunt minnie: carmen meniscus sign

can be anywhere

Question 15

Stomach Ulcers

benign

Answer 15

Depth>Width

Project beyond the expected lumen

sharp contour

folds radiate to ulcer

Aunt minnie: hamptons line

mostly on lesser curvature

Question 16

GIST

overview

Answer 16

This is the most common mesenchymal tumor of the GI tract (70% in stomach, duodenum is second most common — colon is actually the least common). Think about this in an old person (it’s rare before age 40).

Question 17

Gist

Tricks to know

Answer 17

• Lymph node enlargement is NOT a classic feature
• Malignant ones tend to be big angry mother fuckers (>10cm with ulceration - and possible perforation).
• If they do met - it is typically to the liver.
• Having said that, malignancy is rare with these.
They typically don’t met anywhere, which is why lymph node enlargement is uncommon.
• The association with Carney’s triad
• The association with NF-1

Question 18

Carneys triad

Answer 18

“Carney’s Eat Garbage”
Chondroma (pulmonary)
Extra Adrenal Pheo
GIST

Question 19

Gastric “Cancer” is either

Answer 19

Lymphoma (<5%) or Adenocarcinoma (95%)…. Rarely a malignant GIST.

Question 20

Gastric adenocarcinoma

overview

Answer 20

is usually a disease of an old person (median age 70).

H. Pylori is the most tested risk factor.

Question 21

Gastric adenocarcinoma

trivia to know

Answer 21

• Ulcerated carcinoma (or the “penetrating cancer”) has the
look of an advanced cancer
• Metastatic spread to the ovary is referred to as a Krukenberg Tumor.
• Gastroenterostomy performed for gastric ulcer disease
(old school - prior to PPIs) have a 2x - 6x- increased risk
for development of carcinoma within the gastric remnant.
• Step 1 trivia question: swollen left supraclavicular node = Virchow Node.

Question 22

Gastric Adenocarcinoma

The look

Answer 22

Gastric Adenocarcinoma looks very different (usually) than a GIST.

GIST (arrow) is usually smoothly marginated and exophytic

Gastric
Adenocarcinoma is usually a large, ulcerated, heterogenous mass

Question 23

Ulcer Trivia:

Answer 23

Duodenal Ulcers are 2-3x more common than Gastric Ulcers.

Gastric Ulcers - They have 5% chance o f being cancer.

Duodenal Ulcers - Are never cancer (on multiple choice)

Gastric Ulcers occurs from “altered mucosal resistance”, and favor the bulb

Duodenal Ulcers occur from….

Question 24

Gastric Lymphoma

overview

Answer 24

can be primary (MALT), or secondary (systemic lymphoma). The stomach is the
most common extranodal site for non-Hodgkin lymphoma.

Question 25

Gastric Lymphoma even when extensive

Answer 25

rarely causes gastric outlet obstruction. It was classically described as “crossins the pylorus ’’ , although since gastric carcinoma is like lOx more common, it is actually more likely to do that.

Question 26

Gastric Lymphoma looks like

Answer 26

Has multiple looks and can be big, little, ulcerative, polypoid, or look like target lesions. It can also look like Linitis Plastica

Question 27

Gastric Lymphoma Trivia

Answer 27

it can rupture with treatment

Question 28

Gastric Cancer is “More Likely” Than Lymphoma to...

Answer 28

* More Likely to Cause Gastric Outlet Obstruction * More Likely to be in the distal stomach * More Likely to extend beyond the serosa and obliterate adjacent fat plains * More Likely to be a focal mass (95% of primary gastric tumors are adenocarcinoma)

Question 29

Mets to the Stomach: This is actually very rare.

Answer 29

Melanoma Breast Lung

Question 30

Mets to the Stomach: Melanoma

Answer 30

Melanoma is probably the most common culprit, when it does occur. This obviously has a variable appearance but multiple button type soft tissue nodules is probably the most classic look.

Question 31

Mets to the Stomach: Breast and lung

Answer 31

these are known for producing a particular look of diffuse infiltration and a contracted desmoplastic deformity resembling a stiff leather bottle. This is the so called Linitis Plastica appearance

Question 32

Chronic Aspirin Therapy

Answer 32

“Multiple gastric ulcers” is the buzzword. Obviously this is nonspecific, but some sources say it occurs in 80% of patient’s with chronic aspirin use. As a point of trivia, aspirin does NOT cause duodenal ulcers.

Question 33

If you see multiple duodenal ulcers (most duodenal ulcers are solitary) you should think

Answer 33

ZE

Question 34

Areae Gastricae

Answer 34

This is a normal fine reticular pattern seen on double contrast. A favorite piece of trivia to ask is when does this “enlarge” ? The answer is that it enlarges in elderly and patient’s with H. Pylori. Also it can focally enlarge next to an ulcer. It becomes obliterated by cancer or atrophic gastritis.

Question 35

Menetrier’s Disease

Answer 35

Rare and has a French sounding name, so it’s almost guaranteed to be on the test. It’s an idiopathic gastropathy, with rugal thickening that classically involves the fundus and spares the antrum. Bimodal age distribution (childhood form thought to be CMV related). They end up with low albumin, from loss into gastric lumen.

Question 36

Menetrier’s Disease Essential trivia

Answer 36

inolves the fundus and spares the antrum

Question 37

Ram’s Horn Deformity (Pseudo Billroth I)

Answer 37

Tapering of the antrum causes the stomach to look like a Ram’s Horn. This is a differential case, and can be seen with Scarring via peptic ulcers, Granulomatous Disease (Crohns, Sarcoid, TB, Syphilis), or Scirrhous Carcinoma.

Question 38

Ram’s Horn Deformity (Pseudo Billroth I) Essentrial trivia

Answer 38

The stomach is the most common GI tract location for sarcoid.

Question 39

Gatric volvulus Organoaxial

Answer 39

the greater curvature flips over the lesser | curvature. This is seen in old ladies with paraesophageal hernias. It’s way more common.

Question 40

Gastric volvulus meseneroaxial

Answer 40

twisting over the mesentery. Can cause ischemia and needs to be fixed. Additionally this type causes obstruction. This type is more common in kids.

Question 41

Gastric Diverticulum

Answer 41

The way they always ask this is by trying to get you to call it an adrenal mass (it’s most commonly in the posterior fundus). Gamesmanship: Find the normal adrenal.

Question 42

Gastric Varices

Answer 42

Gastric Varices: This gets mentioned in the pancreas section, but I just want to hammer home that test writers love to ask splenic vein thrombus causing isolated gastric varices. Some sneaky ways they can ask this is by saying “pancreatic cancer” or “Pancreatitis” causes gastric varices. Which is true.... because they are associated with splenic vein thrombus. So, just watch out for that.

Question 43

Bilroth 1

Answer 43

Pylorus is removed and the proximal stomach is sewed directly to the duodenum. Done for Gastric CA, Pyloric Dysfunction, or Ulcers. Less Post Op Gastritis (relative to Billroth 2)

Question 44

Bilroth 2

Answer 44

Partial gastrectomy, but this time the stomach is attached to the jejunum. Done for Gastric CA, or Ulcers. Risks: • Dumping syndrome • Afferent loop syndrome • Increased risk of gastric CA 10-20 year after surgery

Question 45

Roux-en-y

Answer 45

Stomach is divided to make a “pouch.” This gastric pouch is attached to the jejunum. The excluded stomach attaches to the duodenum as per normal. The jejunum is attached to the other jejunum to form the bottom of the Y. can also be performed for gastric cancer as an alternative to Billroth if the primary lesion has directly invaded the duodenum or head of the pancreas. Supposedly these have less reflux, and less risk of recurrent gastric CA. They are at increased risk for gallstones, and they have all that internal hernia shit.

Question 46

Dumping syndrome

Answer 46

group of symptoms; diarrhea, nausea, and lightheaded / tired after a meal, - caused by rapid gastric emptying (seen classically with Billroth 2 and early in the post op period after Roux-en Y).

Question 47

Afferent Loop Syndrome

Answer 47

An uncommon complication post billroth 2. The most common cause is obstruction (adhesions, tumor, intestinal hernia) o f the afferent. The acute form may have a closed loop obstruction. The result o f this afferent obstruction is the build up of biliary, pancreatic, and intestinal secretions resulting in afferent limb dilation. The back pressure from all this back up dilates the gallbladder, and causes pancreatitis. A much less common cause is if the stomach preferentially drains into the afferent loop.

Question 48

Jejunogastric Intussusception

Answer 48

This is a rare complication o f gastroenterostomy. The Jejunum herniates back into the stomach (usually the efferent limb) and can cause gastric obstruction. High mortality is present with the acute form.

Question 49

Bile Reflex Gastritis:

Answer 49

Fold thickening and filling defects seen in the stomach after Billroth 1 or II are likely the result o f bile acid reflux.

Question 50

Gastro-Gastric Fistula

Answer 50

This is seen in Roux-en-Y patients who gain weight years later. The anastomotic breakdown is a chronic process, and often is not painful.

Question 51

Cancer after gastric surgery

Answer 51

With regard to these old peptic ulcer surgeries (Billroths), there is a 3-6 times increased risk o f getting adenocarcinoma in the gastric remnant (like 15 years after the surgery).

Question 52

Dumping Syndrome 2

Answer 52

Different than the “dumping syndrome” associated with late night Taco Bell. This type o f dumping is related to rapid transit o f undigested food from the stomach. Tc Gastric Emptying study is an option to diagnose this. The therapy is typically conversion o f Billroth to Roux-en-Y (and avoiding delicious carbs).

Question 53

Small bowel follow through Steps

Answer 53

Step 1 evaluate the folds Step 2a evaluate for loop seperation with t without tethering step 2b if nodules are present evaluate the distribution and secondary findings to help narrow diff step 3 trademark features

Question 54

SBFT step 1 thin <3mm, straight folds with dilation

Answer 54

Mechanical Obstruction Paralytic Ileus Scleroderma Sprue

Question 55

SBFT step 1 thick straight folds >3mm segmental distribution

Answer 55

Ischemia Radiation Hemorrhage Adjacent Inflammation

Question 56

SBFT step 1 thick straight folds >3 mm diffuse distribution

Answer 56

Low Protein Venous Congestion Cirrhosis

Question 57

SBFT step 1 thick folds with nodularity segmental distribution

Answer 57

Crohns Infection Lymphoma Mets

Question 58

SBFT step 1 thick folds with nodularity diffuse distribution

Answer 58

``` Whipples Lymphoid Hyperplasia Lymphoma Mets Intestinal Lymphangiectasia ```

Question 59

SBFT step 2a loop seperation without tethering

Answer 59

``` • Ascites, • Wall Thickening (Crohns, Lymphoma), • Adenopathy • Mesenteric Tumors ```

Question 60

SBFt step 2a loope separation with tethering

Answer 60

Tethering looks like someone is pinching and pulling the loops towards the displacing mass. • Carcinoid

Question 61

SBFT Step 2b sand like nodules

Answer 61

Diffuse nodules in the jejunum whipples (tropheryma whipplei) pseudo whipples (MAC)

Question 62

SBFT Step 2b uniform 2-4 mm nodules

Answer 62

Lymphoid Hyperplasia

Question 63

SBFT Step 2b nodules of larger or varying sizes

Answer 63

Cancer - th in k M e ts (M e la n om a )

Question 64

SBFT Step 2b cobblestoning

Answer 64

* Raised islands o f mucosa separated by linear streaks running perpendicular to the lumen o f the bowel. * These streaks represent ulceration. * This findings (especially when combined with areas o f stricture, and loop separation from fat proliferation) should make you think Crohns

Question 65

SBFT Step 3 ribbon bowel

Answer 65

bowel is featureless, atrophic, and has fold thickening (ribbon-like). Graft Vs Host

Question 66

SBFT Step 3 hidebound bowel

Answer 66

Narrow separation of normal folds with mild bowel dilation. Scleroderma

Question 67

SBFT Step 3 Moulage sign (tube of wax)

Answer 67

Dilated jejunal loop with complete loss of jejunal folds - opacified like a “tube o f wax” Celiac

Question 68

SBFT Step 3 Fold reversal

Answer 68

Jejunum loses folds to look more like the normal Ileum, Ileum gains folds (in the right lower quadrant) to look more like normal Jejunum Celiac

Question 69

SBFT Step 3 Freaking worm

Answer 69

Thread like defect in the barium column ascaris suum (demon worm)

Question 70

Small bowel path The target sign

Answer 70

’ Single Target: GIST, Primary Adenocarcinoma, Lymphoma, Ectopic Pancreatic Rest, Met (Melanoma). ’Multiple Target: Lymphoma, Met (Melanoma)

Question 71

Small bowel path clover leaf sign

Answer 71

This is an Aunt Minnie for Healed Peptic Ulcer of the Duodenal Bulb.

Question 72

Small bowel path Whipples

Answer 72

Just like a stripper - it prefers white men in their 50s. The bug infdtrates the lamina propria with large macrophages infected by intracellular whipple bacilli leading to marked swelling of intestinal villi and thickened irregular mucosal folds primarily in duodenum and proximal jejunum.

Question 73

Small bowel path Buzzword for whipples

Answer 73

“sand like nodules” referring to diffuse micronodules in the jejunum.

Question 74

Small bowel path Pseudo whipples

Answer 74

MAI (instead of T. Whipplei). This is seen in AIDS patients with CD4<100. The imaging findings of nodules in the jejunum and retroperitoneal nodes are similar to Whipples (hence the name). The distinction between the two is not done with imaging but instead via an acid fast stain (MAC is positive).

Question 75

Small bowel path Intestinal lymphangiectasia

Answer 75

Lymphangiectasia results from obstruction to the flow of lymph from the small intestine into the mesentery. This results in dilation of the intestinal and serosal lymphatic channels. This can be primary from lymphatic hypoplasia, or secondary from obstruction of the thoracic duct (or any place in between).

Question 76

Small bowel path Graft vs Host

Answer 76

It occurs in patients after bone marrow transplant. It’s less common with modem anti-rejection drugs. Skin, Liver, and GI tract get hit. Small bowel is usually the most severely affected. Bowel is featureless, atrophic, and has fold thickening (ribbonlike).

Question 77

Small bowel path graft vs host buzzword

Answer 77

ribbon bowel

Question 78

Small bowel path SMA Syndrome

Answer 78

This is an obstruction of the 3rd portion of the duodenum by the SMA (it pinches the duodenum in the midline). It is seen in patients who have recently lost a lot of weight.

Question 79

Small bowel path Celiac sprue

Answer 79

Small bowel malabsorption of gluten

Question 80

Small bowel path Celiac sprue high yeild points

Answer 80

* Can cause malabsorption of iron, and lead to iron deficiency anemia. * Associated with Idiopathic Pulmonary Hemosiderosis (Lane Hamilton Syndrome) * Increased Risk of bowel wall lymphoma * Gold standard is biopsy (surprisingly not barium) * Dermatitis Herpetiformis - some skin thing (remember that from step 1)

Question 81

Small bowel path Celiac sprue findings on CT/Barium

Answer 81

* Fold Reversal is the Buzzword (Jejunum like Ileum, Ileum like Jejunum) * Moulage Sign - dilated bowel with effaced folds (tube with wax poured in it) * Cavitary Lymph Nodes (low density) * Splenic Atrophy

Question 82

Small bowel path M e c k e l’s D iv erticu lum I D iv e rtic u litiss

Answer 82

This is a congenital true diverticulum of the distal ileum. A piece of total trivia is that it is a persistent piece of the omphalomesenteric duct. Step 1 style, “rule of 2s” occurs in 2% of the population, has 2 types of heterotopic mucosa (gastric and pancreatic), located 2 feet from the IC valve, it’s usually 2 inches long (and 2 cm in diameter), and usually has symptoms before the child is 2. If it has gastric mucosa (the ones that bleed typically do) it will take up Tc-Pertechnetate just like the stomach (hence the Meckel’s scan).

Question 83

Small bowel pathM e c k e l’s D iv erticu lum I D iv e rtic u litis high yield trivia

Answer 83

Can get diverticulitis in the Meckels (mimic appendix) GI Bleed from Gastric Mucosa (causes 30% of symptomatic cases) Can be a lead point for intussusception (seen with inverted diverticulum) Can cause Obstruction

Question 84

Small bowel path Duodenal In flam m a to ry Disease:

Answer 84

You can have fold thickening of the duodenum from adjacent inflammatory processes of the pancreas or gallbladder. You can also have thickening and fistula formation with Crohn’s (usually when the colon is the primary site). Primary duodenal Crohns can happen, but is super rare. Chronic dialysis patients may get severely thickened duodenal folds which can mimic the appearance of pancreatitis on barium.

Question 85

Small bowel path Jejunal diverticulosis

Answer 85

Less common than colonic diverticulosis, but does occur. They occur along the mesenteric border. Important association is bacterial overgrowth and malabsorption. They could show this with CT, but more likely will show it with barium (if they show it at all).

Question 86

Small bowel path Gallstone ileus

Answer 86

Not a true ileus, instead a mechanical obstruction secondary to the passage of a gallstone in the lumen of the bowel. Gallstones access the bowel by eroding through the duodenum (usually). As you can imagine, only elderly or weak patients (those unworthy of serving in the spartan infantry) are susceptible to this erosion.

Question 87

Small bowel path riglers triad

Answer 87

pneumobilia, obstruction, and an ectopic location o f a gallstone. The classic trick is to try and get you to say that free air - the “Riglers Sign" - is part of the Riglers Triad (it isn’t) — mumble to yourself “nice try assholes.”

Question 88

Direct signs of bowel trauma

Answer 88

Spilled oral contrast active mesentric bleed

Question 89

indirect signs of bowel trauma

Answer 89

fat stranding fluid layering along the bowel

Question 90

Shock Complex Features

Answer 90

• Thickened Enhancing Bowel Loops (small bowel involved more than larger bowel) • On Non-Contrast, bowel loops may appear denser than the psoas . Collapsed IVC • HYPO-enhancement of solid organs (liver and spleen) • Bilateral delayed nephrograms (persistence nephrograms) • HYPER-enhancement of the adrenals

Question 91

“Shock Bowel” “Hypovolemic Shock Complex”

Answer 91

This is typically seen with severe hypotension , although anything that gives you low volume - (cardiac arrest, septic shock, bacterial endocarditis, diabetic ketoacidosis, etc.. so on and so forth) can also cause it.

Question 92

Bowel Trauma vs shock bowel findings

Answer 92

Focal vs Diffuse Wall Thickening with High Attenuation Blood in the Submucosa vs Wall Thickening with Near Water Attenuation Edema Mucosa enhances normally (or less than normal) vs Mucosa demonstrates intense enhancement Secondary signs of injury (free air, leaked contrast, mesenteric hematoma, etc... etc... so on and so forth). vs Other signs of shock (bright adrenals, flat IVC, etc...)

Question 93

Small bowel cancer Adenocarcinoma

Answer 93

Most common in the proximal small bowel (usually duodenum). Increased incidence with celiac disease and regional enteritis. Focal circumferential bowel wall thickening in proximal small bowel is characteristic on CT. The duodenal web does NOT increase the risk.

Question 94

Small bowel cancer adenocarcinoma gamesmanship

Answer 94

Adenocarcinoma is more likely to obstruct relative to lymphoma.

Question 95

Small bowel cancer Lymphoma

Answer 95

It’s usually the non-Hodgkin flavor. Patients with celiac, Crohns, AIDS, and SLE are higher risk. It can look like anything (infiltrative, polypoid, multiple nodules etc....) The Hodgkin subtype is more likely to cause a desmoplastic reaction..

Question 96

Small bowel cancer lymphoma key triia

Answer 96

do not obstruct even with massive circum involvement

Question 97

Small bowel cancer trivia

Answer 97

favors the ileum

Question 98

Small bowel cancer gamesmanship

Answer 98

obstruction is rare

Question 99

Small bowel cancer Carcinoid aunt minnie

Answer 99

a mass + desmoplastic stranding. “Starburst” appearance of the mesenteric mass with calcifications.

Question 100

Small bowel cancer carcinoid

Answer 100

This tumor most commonly occurs in young adults. The primary tumor is often not seen. That calcified crap you are seeing is the desmoplastic reaction. Liver mets are often hyper vascular. Step 1 style, you don’t get carcinoid syndrome (flushing, diarrhea) until you met to the liver. The appendix, has the best prognosis of all G1 primary sites. Systemic serotonin degrades the heart valves (right sided), and classically causes tricuspid regurgitation. MIBG or Octreotide scans can assist with diagnosis

Question 101

Small bowel cancer carcinoid most common primary location

Answer 101

distal ileum

Question 102

Small bowel cancer Mets

Answer 102

This is usually melanoma (which hits the small bowel in 50% of fatal cases). You can also get hematogenous seeding of the small bowel with breast, lung, and Kaposi sarcoma. Melanoma will classically have multiple targets.

Question 103

Most common type of abdominalhernia

Answer 103

inguinal M>F (7:1)

Question 104

femoral hernia

Answer 104

Likely to obstruct. Seen in old ladies. They are medial to the femoral vein, and posterior to the inguinal ligament (usually on the right).

Question 105

Obturator hernia

Answer 105

Another old lady hernia. Often seen in patients with increased intra-abdominal pressure (Ascites, COPD - chronic cougher). Usually asymptomatic - but can strangulate.

Question 106

Direct inguinal hernia

Answer 106

Less common Medial to inferior epigastric artery Defect in Hesselbach’s Triangle NOT covered by internal spermatic fascia

Question 107

Indirect inguinal hernia

Answer 107

More Common Lateral to inferior epigastric artery Failure of processus vaginalis to close Covered by internal spermatic fascia

Question 108

Lumbar Hernia

Answer 108

Can be superior (Grynfeltt-Lesshaft) through the superior lumbar triangle, or inferior (Petit) through the inferior lumbar triangle. Superior is more common than inferior. Otherwise, they are very similar and usually discussed together. Causes are congenital or acquired (post-surgery).

Question 109

Spigelian Hernia

Answer 109

The question is probably the location along the Semilunar line ( “S ” fo r “S ”) through the transversus abdominis aponeurosis close to the level of the arcuate line.

Question 110

Littre hernia

Answer 110

hernia with a meckedl diverticulum in it

Question 111

amyand hernia

Answer 111

hernia with the appendix in it

Question 112

Richter hernia

Answer 112

Contains only one wall of bowel and therefore does not obstruct. This are actually at higher risk for strangulation.

Question 113

Hernias Post laparoscopic Roux-en-Y Gastric Bypass Factors that promote internal hernia after gastric bypass

Answer 113

(1) Laproscopic over Open - supposedly creates fewer adhesion, so you have more mobility (2) Degree of weight loss ; more weight loss = less protective, space occupying mesenteric fat.

Question 114

Hernias Post laparoscopic Roux-en-Y Gastric Bypass There are 3 potential sites

Answer 114

(1) At the defect in the transverse mesocolon, through which the Roux-Loop Passes (if it’s done in the retrocolic position). (2) At the mesenteric defect at the enteroenterostomy (3) Behind the Roux limb mesentery placed in a retrocolic or antecolic position (retrocolic Petersen and antecolic Petersen type). ** This is the one they will likely ask because it has an eponym with it.

Question 115

Internal Hernias overviews

Answer 115

The most common manifestation is closed loop obstruction (often with strangulation). There are 9 different subtypes, of which I refuse to cover. I will touch on the most common, and the general concept.

Question 116

Internal Hernias General concept

Answer 116

This is a herniation of viscera through the peritoneum or mesentery. The herniation takes place through a known anatomic foramina or recess, or one that has been created post operatively.

Question 117

Internal Hernias Paraduodenal overview

Answer 117

This is by far the most common type of internal hernia. They can occur in 5 different areas, but it’s much simpler to think of them as left or right. Actually, 75% of the time they are on the left.

Question 118

Paraduiodenal leftsided hernia

Answer 118

The exact location is the duodenojejunal junction (“fossa of Landzert”). Here is the trick; the herniated small bowel can become trapped in a “sac of bowel" between the pancreas and stomach to the left of the ligament of Treitz. The sac characteristically contains the IMV and the left colic artery.

Question 119

Paraduodenal right sided hernia

Answer 119

located just behind the SMA and just below the transverse segment of the duodenum, at the “Fossa of Waldeyer.” The classic setting for right-sided PDHs is nonrotated small bowel, with normally rotated large bowel.

Question 120

Crohns disease overview

Answer 120

Typically seen in a young adult (15-30), but has a second smaller peak later 60-70. Discontinuous involvement of the entire GI tract (mouth -> asshole). Stomach, usually involves antrum (Ram’s Horn Deformity). Duodenal involvement is rare, and NEVER occurs without antral involvement. Small bowel is involved 80% o f the time, with the terminal ileum almost always involved (Marked Narrowing = String Sign). After surgery the “neo-terminal ileum” will frequently be involved. The colon involvement is usually right sided, and often spares the rectum / sigmoid. Complications include fistulae, abscess, gallstones, fatty liver, and sacroiliitis.

Question 121

Crohns disease squaring of the folds

Answer 121

An early manifestation from obstructive lymphedema

Question 122

Crohns disease skip lesions

Answer 122

Discontinuous involvement o f the bowel

Question 123

Crohns disease proud loops

Answer 123

Separation of the loops caused by infiltration o f the mesentery, increase in mesenteric fat and enlarged lymph nodes

Question 124

Crohns disease cobblestoning

Answer 124

Irregular appearance to bowel wall caused by longitudinal and transverse ulcers separated by areas o f edema

Question 125

Crohns disease pseudopolyps

Answer 125

Islands of hyperplastic mucosa

Question 126

Crohns disease Filiform

Answer 126

Post-inflammatory polyps - long and worm-like

Question 127

Crohns disease pseudodiverticula

Answer 127

Found on anti-mesenteric side. From bulging area of normal wall opposite side o f scarring from disease

Question 128

Crohns disease string-sign

Answer 128

Marked narrowing of terminal ileum from a combination of edema, spasm, and fibrosis

Question 129

IBD trivia associating

Answer 129

increased risk of melanoma

Question 130

UC overview

Answer 130

Just like Crohns, it typically occurs in a “young adult” (age 15-40), with a second peak at 60-70. Favors the male gender. It involves the rectum 95% of the time, and has etrograde progression. Terminal ileum is involved 5-10% of the time via backwash ileitis (wide open appearance). It is continuous and does not “skip” like Crohns. It is associated with Colon Cancer, Primary Sclerosing Cholangitis, and Arthritis (similar to Ankylosing Spondylitis).

Question 131

UC Barium

Answer 131

On Barium, it is said that the colon is ahaustral, with a diffuse granular appearing mucosa. “Lead Pipe” is the buzzword (shortened from fibrosis).

Question 132

UC key clinical point

Answer 132

UC has an increased risk of cancer (probably higher than Crohns), and it doesn’t classically have enlarged lymph nodes (like Crohns does), so if you see a big lymph node in an UC patient (especially one with long standing disease), you have to think that it might be cancer.

Question 133

More common in crohns vs UC Gallstones PSC Hepatic Abscess Pancreatities

Answer 133

Gallstones Crohns PSC UC Hepatic Abscess Crohns Pancreatities Crohns

Question 134

Cronhs this vs that

Answer 134

``` Slightly less common in the USA Discontinuous “Skips” Terminal Ileum - String Sign Ileocecal Valve “Stenosed” Mesenteric Fat Increased "creepingfat” Lymph nodes are usually enlarged Makes Fistulae ```

Question 135

UC this vs that

Answer 135

``` Slightly more common in the USA Continuous Rectum Ileocecal Valve “Open” Perirectal fat Increased Lymph nodes are NOT usually enlarged Doesn’t Usually Make Fistulae ```

Question 136

Toxic Megacolon

Answer 136

Ulcerative colitis, and to a lesser degree Crohns, is the primary cause. C-Diff can also cause it. Gaseous dilation distends the transverse colon (on upright fdms), and the right and left colon on supine films. Lack of haustra and pseudopolyps are also seen. Some people say the presence of normal hausta excludes the diagnosis. Don’t do a barium enema because of the risk of perforation. Another piece of trivia is that peritonitis can occur without perforation.

Question 137

Behcets

Answer 137

Ulcers of the penis and mouth. Can also affect GI tract (and looks like Crohns) - most commonly affects the ileocecal region. It is also a cause of pulmonary artery aneurysms (test writers like to ask that).

Question 138

Diverticulosis/Dviverticulitis

Answer 138

Some trivia worth knowing is that diverticulosis actually bleeds more than diverticulitis. Right-sided is less common (but is seen in young Asians). Fistula fonnation is actually most common with diverticulitis, and can occur to anything around it (another piece of bowel, the bladder, etc..).

Question 139

Epiploic appendagitis

Answer 139

Epiploic appendages along the serosal surface of the colon can torse, most commonly on the left. There is not typically concentric bowel wall thickening (unlike diverticulitis). Omental infarction is typically a larger mass with a more oval shape and central low density. It is more common on the right (ROI - right omental infarct). Both entities are self-limiting.

Question 140

Appendicitis steps

Answer 140

The classic pathways are: obstmction (fecalith or reactive lymphoid tissue) -> mucinous fluid builds up increasing pressure -> venous supply is compressed -> necrosis starts -> wall breaks down -> bacteria get into wall -> inflammation causes vague pain (umbilicus) -> inflamed appendix gets larger and touches parietal peritoneum (pain shifts to RLQ).

Question 141

appendix mucocele

Answer 141

Mucinous cystadenomas are the most common mucinous tumor of the appendix. They produce mucin and can really dilate up and get big. They look similar to cystadenocarcinomas and can perforate leading to pseudomyxoma peritonei. On ultrasound the presence of an “onion sign” - layering within a cystic mass - is a suggestive feature of a mucocele.

Question 142

Omental infarction

Answer 142

Omental infarction is typically a larger mass with a more oval shape and central low density. It is more common on the right (ROI - right omental infarct). Both entities are self-limiting.

Question 143

Appenix ages

Answer 143

It occurs in an adolescent or young adult (or any age).

Question 144

appendix ct

Answer 144

The measurement of 6 mm was originally described with data from ultrasound compression, but people still generally use it for CT as well. Secondary signs of inflammation are probably more reliable for CT.

Question 145

appendix gamesmanship

Answer 145

In pregnancy MRI without contrast is the test of choice

Question 146

sigmoid colonic volvulus

Answer 146

Most common adult form. Seen in the nursing home patient (chronic constipation is a predisposing factor). This is the “Grandma” volvulus. Buzzword is coffee bean sign (or inverted 3 sign). Another less common buzzword is Frimann Dahl’s sign - which refers to 3 dense lines converging towards the site o f obstruction. Points to the RUQ. Recurrence rate after decompression = 50%.

Question 147

cecal colonic volvulus

Answer 147

Seen in a younger person (20-40). Associated with people with a “ long mesentery.” More often points to the LUQ. Much less common than sigmoid.

Question 148

Cecal bascule colonic volvulus

Answer 148

Anterior folding o f the cecum, without twisting. A lot o f surgical text books dispute this thing even being real (they think it’s a focal ileus). The finding is supposedly dilation o f the cecum in an ectopic position in the middle abdomen, without a mesenteric twist.

Question 149

Colonic Pseudo-Obstruction

Answer 149

(Colonic Ileus, Ogilvie Syndrome): Usually seen after serious medical conditions and in nursing home patients. It can persist for years, or progress to bowel necrosis and perforation. The classic look is marked diffuse dilation o f the large bowel, without a discrete transition point.

Question 150

Diversion colitis

Answer 150

Bacterial overgrowth in a blind loop through which stool does not pass (any surgery that does this).

Question 151

Colitis cystica superficial

Answer 151

The superficial kind consists of cysts that are small in the entire colon. It’s associated with vitamin deficiencies and tropical sprue. Can also be seen in terminal leukemia, uremia, thyroid toxicosis, and mercury poisoning.

Question 152

Colitis cystica deep

Answer 152

These cysts may be large and are seen in the pelvic colon and rectum.

Question 153

Rectal cavernous hemangioma

Answer 153

Obviously very rare. Just know it’s associated with a few syndromes; Klippel-Trenaunay-Weber, and Blue Rubber Bleb. They might show is. you a ton of phleboliths down there.

Question 154

Gossypiboma

Answer 154

It’s a retained cotton product or surgical sponge and it can elicit an inflammatory response.

Question 155

Entamoeba Histolytica

Answer 155

Parasite that causes bloody diarrhea. Can cause liver abscess, spleen abscess, or even brain abscess. Within the colon it is one of the causes of toxic megacolon. They are typically “flask-shaped ulcers” on endoscopy. It affects the cecum and ascending colon most commonly and unlike many other GI infections, spares the terminal ileum.

Question 156

Entamoeba histolytica barium

Answer 156

the buzzword is “conedcecum” referring to a change in the normal bulbous appearance of the cecum, to that of a cone.

Question 157

Colonic TB

Answer 157

Typically involves the terminal ileum, and is another cause of the “coned cecum” appearance. Causes both ulcers and areas of nanowing. Two other signs: (1) Fleischner sign - enlarged gaping IC valve, and (2) Stierlin sign - narrowing of the Tl.

Question 158

Infections tht like the duodenum and proximal small bowel

Answer 158

Giardia strongyloides

Question 159

infections that like the TI

Answer 159

TB Yersinia

Question 160

This vs that sigmoid vs cecal

Answer 160

sigmoid - old person, points to the RUQ cecal - younger person, points to the LUIQ

Question 161

colonic CMV

Answer 161

Seen in patients who are immunosuppressed. Causes deep ulcerations - which can lead to perforation. Step 1 question = Cowdry Type A intranuclear inclusion bodies

Question 162

C-DIFF

Answer 162

Classically seen after antibiotic therapy, the toxin leads to a super high WBC count. CT findings of the “accordion sign” with contrast trapped inside mucosal folds is always described in review books and is fair game for multiple choice. The barium findings include thumb printing, ulceration, and irregularity. Of course it can cause toxic megacolon as mentioned on the prior page.

Question 163

Neutropenic Colitis (Typhlitis):

Answer 163

Infection limited to the cecum occurring in severe neutropenia.

Question 164

Colon Cancer adenocarcinoma overview

Answer 164

Common cause of cancer death (#2 overall). Cancers on the right tend to bleed (present with bloody stools, anemia). Cancers on the left tend to obstruct. Apple core is a buzzword.

Question 165

Colon Cancer adenocarcinoma gamesmanship

Answer 165

Large bowel intussusception in adult = Malignancy

Question 166

Colon Cancer adenocarcinoma gamesmanship 2

Answer 166

Colon likes to Met to the Liver. Liver Mets will classically be T1 Dark, T2 Mildly Bright (“evil grey”), heterogenous non-progressive in enhancement, sometimes target.

Question 167

Colon Cancer squamos cell carcinoma

Answer 167

occasionally in the anus (HPV)

Question 168

Rectal Cancer Trivia

Answer 168

- Nearly always (98%) adenocarcinoma - If the path says Squamous - the cause was HPV (use your imagination on how it got there). - Lower rectal cancer (0-5 cm from the anorectal angle), have the highest recurrence rate. - MR1 is used to stage - and you really only need T2 weight imaging - contrast doesn’t matter - Stage T3 - called when tumor breaks out of the rectum and into the perirectal fat. This is the critical stage that changes management (they will get chemo/rads prior to surgery).

Question 169

nodes in perirectal fat are abnormal when

Answer 169

>5mm

Question 170

High rectal cancer

Answer 170

- Treated with Low Anterior Resection (LAR) - These patients will maintenance fecal continence post op

Question 171

Low rectal cancer

Answer 171

- Treated with Abdomino- Perineal Resection (APR) | - These poor bastards will end up with colostomies

Question 172

Rectal Cancer surgery

Answer 172

classically determined by the position of the tumor relative to the butthole. Most people will use the number “5 cm” above the anorectal angle to delineate “high” vs “low.” Both surgical approaches are performed with a total mesorectal excision (tumor, nodes, and blood supply).

Question 173

Colon lipomas

Answer 173

Second most common tumor in the colon

Question 174

Colon adenomas

Answer 174

The most common benign tumor of the colon and rectum. The villous adenoma has the largest risk fo r malignancy.

Question 175

McKittrick-Wheelock Syndrome:

Answer 175

This is a villous adenoma that causes a mucous diarrhea leading to severe fluid and electrolyte depletion. The clinical scenario would be something like “80 year old lady with diarrhea, hyponatremia, hypokalemia, hypochloremia... and this” and they show you a mass in the rectum / bowel.

Question 176

Pseudomyxoma Peritonei

Answer 176

This is a gelatinous ascites that results from either (a) ruptured mucocele (usually appendix), or intraperitoneal spread of a mucinous neoplasm (ovary, colon, appendix, and pancreas). It’s usually the appendix (least common is the pancreas). The buzzword is “scalloped appearance of the liver.” Recurrent bowel obstructions are common

Question 177

Peritoneal carcinomatosis

Answer 177

The main thing to know regarding peritoneal implants is that the natural flow of ascites dictates the locat ion of implants. This is why the retrovesical space is the most common spot, since it’s the most dependent part of the peritoneal cavity.

Question 178

Omental seeding/caking

Answer 178

The omental surface can get implanted by cancer and become thick (like a mass). The catch-phrase is “posterior displacement of the bowel from the anterior abdominal wall.”

Question 179

Primary peritoneal mesothelioma

Answer 179

This is super rare. People think about mesothelioma involving the pleura (and it does 75% of the time), but the other 25% of the time it involves the peritoneal surface. The thing to know is that it occurs 30-40 years after the initial asbestosis exposure.

Question 180

Cystic peritoneal mesothelioma

Answer 180

This is the even more rare benign mesothelioma, that is NOT associated with prior asbestos exposure. It usually involves a women of childbearing age (30s).

Question 181

Mesenteric Lymphoma

Answer 181

This is usually non-Hodgkin lymphoma, which supposedly involves the mesentery 50% of the time. The buzzword is “sandwich sign.” The typical appearance is a lobulated confluent soft tissue mass encasing the mesenteric vessels “sandwiching them.”

Question 182

Barium peritonitis

Answer 182

``` This is why you use water soluble contrast anytime you are worried about leak. The pathology is an attack of the peritoneal barium by the leukocytes which creates a monster inflammatory reaction (often with massive ascites and sometimes hypovolemia and resulting shock). If no “real doctor” is available, you should give IV fluids to reduce the risk of hypovolemic shock. The long tenn sequela of barium peritonitis is the development of granulomas and adhesions (causing obstructions and an eventual lawsuit). ```

Question 183

Barium intravasation

Answer 183

This is super rare, but can happen. If barium ends up in the systemic circulation it kills via pulmonary embolism about 50% of the time. Risk is increased in patients with inflammatory bowel or diverticulitis (altered mucosa).

Question 184

Liver bare area

Answer 184

The liver is covered by visceral peritoneum except at the porta hepatis, bare area, and the gallbladder fossa. An injury to the “bare area” can result in a retroperitoneal bleed.

Question 185

Couinaud system testable trivia

Answer 185

* Right Hepatic Vein Divides 7/8, and 6/5 * Middle Hepatic Vein Divides 4a/8, 4b/5 * Left Hepatic Vein / Fissure for the Ligamentum Teres (falciform) divides 4a/2, 4b/3 * The Portal Vein Divides the Liver into Upper and Lower Segments * The Caudate Lobe (Segment 1) is unique in that it drains directly to the IVC.

Question 186

Cantlies line

Answer 186

divides the liver into a functional left and right hepatic lobes. This line runs from the IVC to the middle of the gallbladder fossa.

Question 187

Caudate Lobe

Answer 187

The caudate lobe (segment 1) has a direct connection to the IVC through it’s own hepatic veins, which do not communicate with the primary hepatic veins. Additionally, the caudate is supplied by branches o f both the right and left portal veins - which matters because the caudate may be spared or hypertrophied as the result o f various pathologies such as Budd Chiari, etc...

Question 188

Liver trivia 1

Answer 188

Along the same lines of anatomy explaining pathology, the intra-hepatic course of the right portal vein is longer than the left, which is why it is more susceptible to fibrosis (this is why the right liver shrinks, and the left liver grows in cirrhotic morphology).

Question 189

Liver trivia 2

Answer 189

Most common vascular variant = Replaced right hepatic (origin from the SMA)

Question 190

Liver trivia 3

Answer 190

Most common biliary variant = Right posterior segmental into the left hepatic duct.

Question 191

Liver Normal MRI Signal Characteristics

Answer 191

I like to think of the spleen as a bag o f water/blood (T2 bright, T1 dark). The pancreas is the “brightest T1 structure in the body” because it has enzymes. The liver also has enzymes and is similar to the pancreas (T1 Brighter, T2 darker), just not as bright as the pancreas

Question 192

Liver fetal circulation

Answer 192

Placenta > Umbilical Vein > Liver > IVC Placenta > Umbilical vein > Ductus Venosus (remnant of ligamentum venosum) > IVC

Question 193

Liver us trivia

Answer 193

Pancreas should be more echogenic than liver

Question 194

classic liver ultrasound anatomy pic 1 Pancreas

Answer 194

Anterior to posterior ``` Pancreas Splenic vein SMA LRV to the IVC on the pts right Aorta Vert Body ```

Question 195

classic liver ultrasound anatomy pic 2 porta hepatis

Answer 195

Anterior to posterior CBD RHA PV

Question 196

Liver pic three porta hepatis mickey mouse

Answer 196

Left ear Bile duct Right hear hepatic artery Head portal vein

Question 197

``` Another consequences of the Longer Right Portal Vein Course is that Hepatic Abscess (often from ascending hematogenous sources) nearly always (75%+) involves ```

Answer 197

right hepatic lobe

Question 198

Cirrhosis most common cause us world

Answer 198

etoh schistosomiasis

Question 199

portal htn measurements

Answer 199

portal vein pressure 6-8 mmhg above hepatic veins variceal bleeding and ascites around >12mmhg

Question 200

prehepatic causes of portal htn

Answer 200

portal vein thrombosis | tumor compression

Question 201

hepatic causes of portal htn

Answer 201

cirrhosis | schistosomiasis

Question 202

posthepatic causes of portal htn

Answer 202

budd chiari

Question 203

prehepatic portal htn collateral

Answer 203

form above the diaphragm

Question 204

THAD overview

Answer 204

These Transient Hepatic Attenuation Differences are typically seen in the arterial / early portal phase - NOT on the equilibrium / delayed phases (hence the word “transient”). The easiest way to think about them is that they are focal “arterial buffer responses.” In other words, in that tiny little spot right there the liver feels like there isn’t enough portal flow, so it responses by increasing the arterial flow.

Question 205

Causes of THAD

Answer 205

Cirrhosis Clot Mass Abscess/Infection

Question 206

THAD Cirrhosis

Answer 206

A bunch o f scar / fibrosis deforms the hepatic sinusoids compressing the tiny little portal veins (think about arteries and veins in the neck or groin - pressure will compress the vein first) - people call this “shunting.” This is most typical in the subcapsular region.

Question 207

THAD Clot

Answer 207

Venous blood flow could be compromised from a clot in a portal vein branch (these enhancement patterns are typically larger, wedge shaped, and extend towards the periphery).

Question 208

THAD MAss

Answer 208

(B9 or Malignant): This can occur from two primary mechanisms. 1 - You could have the direct mass effect from the mass smashing the veins. 2 - The tumor could be recruiting /up-regulating arterial flow (VEGF etc...).

Question 209

THAD Abscess/Infection

Answer 209

Also probably a mixed mechanism. Some direct mass effect, but also some element o f “hyperemia” - causing a “siphon effect.” For clarity we aren’t just talking liver abscess here, cholecystitis can also have this region effect.

Question 210

parasitizing the portosystemic decompressive apparatus

Answer 210

So the artery does something else, it opens up tiny little connections to the portal system. The enlargement o f these tiny communications has been referred to as “parasitizing the portosystemic decompressive apparatus.”

Question 211

Portal hypertensive colopathy

Answer 211

With increased resistance in the liver to the portal circulation, you also start to have colonic venous stasis (worse on the right). This can lead to “Portal Hypertensive Colopathy, ” which is basically an edematous bowel that mimics colitis.

Question 212

Portal hypertensive colopathy why worse on the right

Answer 212

The short answer is that collateral pathways develop more on the left (splenorenal shunt, short gastrics, esophageal varices), and decompress that side.

Question 213

Portal hypertensive gastropathy

Answer 213

same things as portal hypertensive colopathy but in the stomach causing a thickened gastric wall on CT, as welt as cause upper GI bleeding in the absence of varices.

Question 214

HCC overview

Answer 214

This is how multi-focal HCC starts. Regenerative nodules -> Dysplastic nodules (increased size and ccilularity) -> HCC. As this process takes place, the nodule changes from preferring to drink portal blood to only wanting to drink arterial blood. This helps explain why HCC has arterial enhancement and rapid washout. The transformation also follows a progression from T2 dark (regenerative) -> T2 bright (HCC).

Question 215

HCC transformation buzzword

Answer 215

“nodule within nodule ’’ where a central bright T2 nodule has a T2 dark border. This is concerning for transformation to HCC.

Question 216

Regenerative nodules

Answer 216

Contains iron T1 dark T2 dark does not enhance

Question 217

Dysplastic nodules

Answer 217

Contains fat, glycoprotein T1 bright T2 Dark Usually does no enhance

Question 218

HCC nodules

Answer 218

T2 bright does enhance

Question 219

OATP

Answer 219

As hepatocytes become cancer they lose function in this transporter and become dark on the delayed phase. The exception (highly testable) is the well differentiated HCC which retains OATP function and is therefore bright on the 20 min delayed Eovist sequence.

Question 220

Hepatic contrast phase timing

Answer 220

arterial phase 25-30 seconds portal venous phase 70 seconds

Question 221

liver late arterial phase

Answer 221

This ("Late A rterial”) is the most critical phase for HCC evaluation. You can recognize this timing as contrast in the hepatic artery and portal vein (but none in the hepatic veins).

Question 222

Liver window

Answer 222

Center 100 | width 200

Question 223

MR Contrast Hepatobiliary Considerations How they work

Answer 223

Gadolinium (which is super toxic) is bound to some type of chelation agent to keep it from killing the patient. The shape and function of the chelation agent determine the class and brand name. The paramagnetic qualities of gadolinium cause a local shortening of the T1 relaxation time on neighboring molecules (remember short T1 time = bright image).

Question 224

MR Contrast Hepatobiliary Considerations Types of agents

Answer 224

I want you to think about MR1 contrast in two main flavors: (1) Extracellular (2) Hepatocyte Specific.

Question 225

MR Contrast Hepatobiliary Considerations Etracellular

Answer 225

These are nonspecific agents that are best thought of as Iodine contrast for CT. They stay outside the cell and are blood flow dependent (just like CT contrast). The imaging features in lesions will be the same as CT - although the reason they look bright is obviously different - CT contrast increases the density (attenuation), MR contrast shortens the T1 time locally - which makes T1 brighter. The classic imaging set up is a late hepatic arterial phase (15-30 seconds), portal venous phase (70 seconds), and a hepatic venous or interstitial phase (90 seconds - 5 mins) - just like CT. MAgnevist

Question 226

MR Contrast Hepatobiliary Considerations Hepatocyte specific

Answer 226

Certain chelates are excreted via the bile salt pathway. In other words, they are taken up by normal hepatocytes and excreted into the bile. This gives you great contrast between normal hepatocytes and things that aren’t normal hepatocytes (cancer). The 20 min delay is the imaging sequence that should give you a homogenous bright liver (dark holes are things that don’t contain normal liver cells / couldn't drink the contrast). The problem is that it’s pretty non-specific with a handful of benign things still taking it up (classical example is FNH), and at least one bad thing taking it up (well-differentiated HCC). Plus, a handful of benign things won’t take it up (cysts, etc..). There are at least three good reasons to use this kind of agent: (1) it’s great for proving an FNH is an FNH - as most lesions won’t hold onto the Gd at 20 mins, (2) it’s great for looking for bile leaks, and (3) once you’ve established a baseline MRI (characterized all those benign lesions) it’s excellent for picking up new mets (findings black holes on a white background is easy). Eovist

Question 227

Is Eovist a pure Hepatocyte Specific Agent

Answer 227

Nope - It also acts like a non-specific extracellular agent early on (although less intense). About 55% is excreted into the bile - and gives a nice intense look at 20 mins.

Question 228

What about Gd-BOPTA (Multihance)

Answer 228

This is mostly an extra-cellular agent, but has a small amount (5%) of biliary excretion. The implication is that you can use Multihance to look for a bile leak you just have to wait longer (45mins-3 hours) for the Gd to accumulate.

Question 229

What about Manganese instead o f Gd

Answer 229

This is the old school way to do biliary imaging. It works the same as Gd - by causing T1 shortening.

Question 230

Luver Hemangioma

Answer 230

This is the most common benign liver neoplasm. Favors women 5:1. They may enlarge with pregnancy. On US will be bright (unless it’s in a fatty liver, than can be relatively dark). On US, flow can be seen in vessels adjacent to the lesion but NOT in the lesion. On CT and MR1 tends to match the aorta in signal and have “peripheral nodular discontinuous enhancement”. Should totally fill in by 15 mins. Atypical hemangioma can have the “reverse target sign.”

Question 231

Liver Hemangioma Trivia

Answer 231

A hemangioma can change its sonographic appearance during the course of a single examination. No other hepatic lesion is known to do this.

Question 232

Hemangioma ultrasound pearls

Answer 232

Need to core for biopsy, FNA does not get enough tissue (only blood) Hyperechoic (65%) Enhanced thru transmission is common NO Doppler flow inside the lesion itself Atypical appearance - hyperechoic periphery, with hypoechoic center (reverse target) Calcifications are extremely rare

Question 233

FNH

Answer 233

This is the second most common benign liver neoplasm. Believed to start in utero as an AVM. It is NOT related to OCP use. It is composed of normal hepatocytes, abnormally arranged ducts, and Kupffer cells (reticuloendothelial cells). May show spoke wheel on US Doppler. On CT, should be“homogenous” on arterial phase. Can have a central scar. Scar will demonstrate delayed enhancement (like scars do). Sulfur Colloid is always the multiple choice test question (reality is that it’s only hot 30-40%). Unlike hepatic adenomas, they are not related to the use of birth control pills, although as a point of confusing trivia and possibly poor multiple choice test question writing, birth control pills may promote their growth.

Question 234

Focal Nodular Hyperplasia (FNH): Trivia

Answer 234

You have to hit the scar, otherwise path results will say normal hepatocytes.

Question 235

FNH stealth

Answer 235

a “Stealth” lesion on MRI - T1 and T2 isointense.

Question 236

Hepatic adenoma

Answer 236

Usually a solitary lesion seen in a female on OCPs. Alternatively could be seen in a man on anabolic steroids. When it’s multiple you should think about glycogen storage disease (von Gierke) or liver adenomatosis. No imaging methods can reliably differentiate hepatic adenoma from hepatocellular carcinoma. Rarely, they may degenerate into HCC after a long period of stability. They often regress after OCPs are stopped. Their propensity to bleed sometimes makes them a surgical lesion if they won’t regress.

Question 237

Hepatic adenoma gamesmanship

Answer 237

Signal Drop Out with in and out of phase can be used to show fat

Question 238

Hepatic adenoma Trivia

Answer 238

Q: Most common location for hepatic adenoma (75%) A: Right Lobe liver

Question 239

Hepatic adenoma management

Answer 239

You stop the OCPs and re-image, they should get smaller. Smaller than 5cm, watch them. Larger than 5cm they often resect because (1) they can bleed and (2) they can rarely turn into cancer.

Question 240

HCC

Answer 240

Occurs typically in the setting of cirrhosis and chronic liver disease; Hep B, Hep C, hemochromatosis, glycogen storage disease, Alpha 1 antitrypsin. AFP elevated in 80-95%. Will often invade the portal vein, although invasion of the hepatic vein is considered a more “specific finding.’’

Question 241

HCC Doubling time

Answer 241

the classic Multiple Choice Question. This is actually incredibly stupid to ask because there arc 3 described patterns of growth (slow, fast, and medium). To make it an even worse question, different papers say different stuff. Some say: Short is 150 days, Medium to 150-300, and Long is >300. I guess the answer is 300 - because it’s in the middle. Others define medium at around 100 days. A paper in Radiology {May 2008 Radiology, 247, 311-330) says 18-605 days. The real answer would be to say follow up in 3-4.5 months.

Question 242

HCC Other random trivia

Answer 242

HCCs like to explode and cause spontaneous hepatic bleeds.

Question 243

this vs that FNH vs Fibrolamellar HCC

Answer 243

FNH FL HCC T2 Bright T2 Dark (usually) Enhances on Delays Does NOT enhance Mass is Sulfur Colloid Avid (sometimes) Mass is Gallium Avid

Question 244

this vs that HCC vs FL HCC

Answer 244

``` HCC FL HCC Cirrhosis No Cirrhosis Older (50s-60s) Young (30s) Rarely Calcifies Calcifies Sometimes Elevated AFP Normal AFP ```

Question 245

Cholangiocarcinoma overview

Answer 245

Where HCC is a cancer of the hepatocyte, cholangiocarcinoma is a cancer of the bile duct. Cholangiocarcinoma believes in nothing Lebowski. It fucks you up, it takes the money (prognosis is poor).

Question 246

Cholangiocarcinoma gamesmanship

Answer 246

Gamesmanship - They could tell you the dude has ulcerative colitis, as a way to infer that he also has PSC.

Question 247

Cholangiocarcinoma buzzword

Answer 247

“Painless Jaundice.” (just like pancreatic head CA)

Question 248

Cholangiocarcinoma who gets it

Answer 248

The most classic multiple choice scenario would be an 80 year old man, with primary sclerosing cholangitis - PSC (main risk factor in the West), recurrent pyogenic “oriental” cholangitis (main risk factor in the East), Caroli Disease, Hepatitis, HIV, history of cholangitis, and fucking Liver Worms (Clonorchis). Oh who also had a semi-voluntary cerebral angiogram performed by a Nazi with a cleft asshole (in 1930s Germany, Thorotrast was the preferred angiographic contrast agent).

Question 249

Cholangiocarcinoma what does ti look like

Answer 249

It is variable and the described subtypes overlap. The easiest way to conceptualize this thing is as a scar generating cancer. Fibrosis (scar) is the main thing you are seeing - either primarily as a mass that enhances on delayed imaging (just like scar in the heart), or secondarily through the desmoplastic pulling of the scar (example capsular retraction and ductal dilation). The dilation of ducts is most likely to be shown as unilateral and peripheral, although if the lesion is central the entire system can obstruct.

Question 250

cCholangiocarcinoma classic features

Answer 250

Delayed Enhancement Peripheral Biliary Dilation Liver Capsular Retraction NO tumor capsule

Question 251

Klatskin tumor

Answer 251

Cholangiocarcinoma that occurs at the bifurcation of the right and left hepatic ducts. It’s usually small but still causes biliary obstruction (“shouldering / abrupt tapering” on MRCP). These things are mean as cat shit. It is a “named” subtype, so that increases the likelihood of it showing up on a multiple choice exam.

Question 252

Cholangiocarcinoma staging pearls

Answer 252

* Proximal extent of involvement is a key factor for surgical candidacy (more = bad). * Atrophy of a lobe implies biliary +/- vascular involvement o f that lobe (imaging often underestimates disease burden). * Typically combinations of bilateral involvement (veins on the right, ducts on the left - vice versa, etc.. etc... etc... ) is bad news.

Question 253

this vs that Cholangiocarcinoma vs hcc

Answer 253

HCC = Invades the Portal Vein Cholangiocarcinoma = Encases the Portal Vein

Question 254

ABD tumor markers

Answer 254

-Cholangio: CEA and Ca19-9 elevated Pancreatic Ca19-9 elevated Colon CA: CEA elevated

Question 255

Hepatic Angiosarcoma

Answer 255

This used to be the go to for thorotrast questions. Even though everyone who got thorotrast died 30 years ago, a few dinosaurs writing multiple choice test questions still might ask it. Hepatic Angiosarcoma is very rare, although technically the most common primary sarcoma o f the liver. It is associated with toxic exposure - arsenic use (latent period is about 25years), Polyvinyl chloride exposure, Radiation, and yes... thorotrast.

Question 256

Hepatic angiosarcoma addt trivia

Answer 256

Can see in hemochromatosis and NF patients

Question 257

biliary cystadenoma

Answer 257

Uncommon benign cystic neoplasm o f the liver. Usually seen in middle aged women. Can sometimes present with pain, or even jaundice. They can be unilocular or multilocular and there are no reliable methods for distinguishing from biliary cystadenocarcinoma (which is unfortunate).

Question 258

Mets to the Liver

Answer 258

If you see rnets in the liver, first think colon. Calcified mets are usually the result o f a mucinous neoplasm (colon, ovary, pancreas).

Question 259

Mets to the Liver US

Answer 259

Hyperechoic mets are often hypervascular (renal, melanoma, carcinoid, choriocarcinoma, thyroid, islet cell). Hypoechoic mets are often hypovascular (colon, lung, pancreas).

Question 260

Mets to the Liver too small to characterize

Answer 260

even in the setting of breast cancer (with no definite hepatic mets) tiny hypodensities have famously been shown to be benign 90-95% o f the time.

Question 261

Liver lymphoma

Answer 261

Hodgkins lymphoma involves the liver 60% o f the time (Non Hodgkins is around 50%), and may be hypoechoic.

Question 262

Kaposi sarcoma liver

Answer 262

Seen in patients with AIDS. Causes diffuse periportal hypoechoic infiltration. Looks similar to biliary duct dilation.

Question 263

Hemangioma Ultrasound

Answer 263

``` Hyperechoic with increased through transmission ```

Question 264

Hemangioma CT

Answer 264

Peripheral Nodular Discontinuous

Question 265

Hemangioma MR

Answer 265

T2 Bright

Question 266

Hemangioma Trivia 1

Answer 266

Rare in | Cirrhotics

Question 267

Hemangioma Trivia 2

Answer 267

``` Kasabach- Merritt; the sequestration of platelets from giant cavernous hemangioma ```

Question 268

FNH Ultrasound

Answer 268

Spoke | Wheel

Question 269

FNH CT

Answer 269

Homogenous Arterial Enhancement

Question 270

FNH MR

Answer 270

“Stealth Lesion - Iso on T1 and T2”

Question 271

FNH Trivia 1

Answer 271

Central | Scar

Question 272

FNH Trivia 2

Answer 272

Bright on Delayed Eovist (Gd-EOBDTPA)

Question 273

Hepatic Adenoma Ultrasound

Answer 273

Variable

Question 274

Hepatic Adenoma CT

Answer 274

Variable

Question 275

Hepatic Adenoma MR

Answer 275

Fat Containing on In/Out Phase```

Question 276

Hepatic Adenoma Trivia 1

Answer 276

OCP use, Glycogen Storage Disease

Question 277

Hepatic Adenoma Trivia 2

Answer 277

Can explode and bleed

Question 278

Hepatic angiomyolipoma Ultrasound

Answer 278

Hyperechoic

Question 279

Hepatic angiomyolipoma CT

Answer 279

gross fat

Question 280

Hepatic angiomyolipoma MR

Answer 280

t1 and t2 bright

Question 281

Hepatic angiomyolipoma Trivia 1

Answer 281

``` Unlike renal AML, 50% don’t have fat ```

Question 282

Hepatic angiomyolipoma Trivia 2

Answer 282

Tuberous sclerosis

Question 283

Congenital liver cystic kidney disease

Answer 283

Patient’s with AD polycystic kidney disease will also have cysts in the liver. This is in contrast to the AR form in which the liver tends to have fibrosis.

Question 284

Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu)

Answer 284

Autosomal dominant disorder characterized by multiple AVMs in the liver and lungs. It leads to cirrhosis and a massively dilated hepatic artery.

Question 285

Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu) trivia

Answer 285

The lung AVMs set you up for brain abscess.

Question 286

Liver infections where?

Answer 286

Most common in the right hepatic lobe bc of the longer R port vein

Question 287

Liver infection buzzwords viral hepatitis

Answer 287

starry sky (US)

Question 288

Liver infection buzzwords pyogenic abscess

Answer 288

double target (CT)

Question 289

Liver infection buzzwords Candida

Answer 289

Bulls eye (US)

Question 290

Liver infection buzzwords amoebic abscess

Answer 290

Extra hepatic extension

Question 291

Liver infection buzzwords Hydatid diesease

Answer 291

Water lily Ct sand storm US?

Question 292

Liver infection buzzwords Schistosomiasis

Answer 292

tortois shell

Question 293

Liver infections Viral

Answer 293

Hepatitis which is chronic in B and C, and acute with the rest. A point of trivia is that HCC in the setting of hepatitis can occur in the acute form of Hep B (as well as chronic). Obviously, chronic hep C increases risk for HCC. On ultrasound the “starry sky” appearance can be seen. Although, this is non-specific and basically just the result of liver edema making the fat surrounding the portal triads look brighter than normal.

Question 294

Liver infections Pyogenic overview

Answer 294

These can mimic cysts. For the purpose of multiple choice, a single abscess is Klebsiella, and multiple are E. Coli. The presence of gas is highly suggestive of pyogenic abscess.

Question 295

Liver infections double targert pyogenic

Answer 295

sign with central low density, rim enhancement, surrounded by more low density is the classic sign of a liver abscess on CT.

Question 296

Liver infections next step amebic abscess

Answer 296

A special situation (potentially testable) is the amebic abscess in the left lobe. Those needs to be emergently drained (they can rupture into the pericardium).

Question 297

Fitz-Hugh-Curtis Syndrome Overview

Answer 297

This syndrome is seen exclusively in women of questionable moral standard (“free spirits”). It manifests on multiple choice exams in the setting of known pelvic inflammatory disease (Gonococcal salpingitis and/or Chlamydia infection), with right upper quadrant pain

Question 298

Fitz-Hugh-Curtis Syndrome imaging

Answer 298

The classic imaging features are enhancement of the anterior liver capsule, perihepatic ascites, and peritoneal septations. They could show you a tubo-ovarian abscess in the pelvis to cue you in on the excessively promiscuous behaviors this young lady has been engaging in.

Question 299

Fatty liver overview

Answer 299

Very common in America. Can be focal (next to gallbladder or ligamentum teres), can be diffuse, or can be diffuse with sparing. You can call it a few different ways.

Question 300

Fatty liver CT

Answer 300

If it’s a non-contrast study, 40 HU is a slam dunk. If it’s contrasted, some people say you can NEVER call it. Others say it’s ok if (a) it’s a good portal venous phase (b) the HU is less than 100, and (c) it’s 25 H.U. less than the spleen.

Question 301

Fatty liver US

Answer 301

If the liver is brighter than the right kidney you can call it. Hepatosteatosis is a fat liver. NASH (hepatitis from a fat liver) has abnormal LFTs.

Question 302

Fatty liver MRI

Answer 302

Two standard deviation difference between in and out of phase imaging. Remember the drop out is on the out of phase images (india ink ones - done at T.E 2.2 ms - assuming 1.5T).

Question 303

Fatty liver Stuffery

Answer 303

This signal drop out assumes there is more water than fat in the liver. As such, the degree of signal loss is maximum when the fat infiltration is 50% (exactly 1:1 signal loss). When the percentage of fat grows larger than 50% you will actually see a less significant signal loss on out of phase imaging, relative to that maximum 50%.

Question 304

Fatty liver What causes it

Answer 304

McDonalds, Burger King, and Taco Bell. Additional causes include chemotherapy (breast cancer), steroids, cystic fibrosis.

Question 305

Hemochromatosis overview

Answer 305

Iron overload. They can show this two main ways: (1) The first is just liver and spleen being T 1 and T2 dark. (2) The second (and more likely) way this will be shown is in and out of phase changes the opposite of those seen in hepatic steatosis. Low signal on in phase, and high signal on out of phase (“Iron on In-phase”)

Question 306

Hemochromatosis innout

Answer 306

Watch out now — this is the opposite of the fat drop out * *FAT - Drop out on OUT of phase (india ink one - T.E. 2.2 ms) - 1.5 T * *IRON - Drop out on IN phase (non india ink one - T.E. 4.4 ms) - 1.5 T

Question 307

Hemochromatosis primary

Answer 307

the inherited type, caused by more GI uptake, with resulting iron overload. The key point is the pancreas is involved and the spleen is spared.

Question 308

Hemochromatosis secondary

Answer 308

the result of either chronic inflammation or multiple transfusions. The body reacts by trying the “Eat the Iron,” with the reticuloendothelial system. The key point is the pancreas is spared and the spleen is not.

Question 309

This vs that hemochromatosis primary vs secondary

Answer 309

Primary Secondary genetic elev absorption acquired trans liver and panc liver and spleen heart, thyroid, pituitary

Question 310

Budd Chiari Syndrome overview

Answer 310

Classic multiple choice scenario is a pregnant woman, but can occur in any situation where you are hypercoagulable (most common cause is idiopathic). The result of hepatic vein thrombosis.

Question 311

Budd Chiari Syndrome imaging findings

Answer 311

The characteristic findings of Budd-Chiari syndrome include hepatic venous outflow obstruction, intrahepatic and systemic collateral veins, and large regenerative (hyperplastic) nodules in a dysmorphic liver. The caudate lobe is often massively enlarged (spared from separate drainage into the IVC). In the acute phase, the liver will show the classic “flip-flop pattern ’’ on portal phase with low attenuation centrally, and high peripherally. The liver has been described as “nutmeg” with an inhomogeneous mottled appearance, and delayed enhancement of the periphery of the liver.

Question 312

who gets a nutmeg liver

Answer 312

* Budd Chiari * Hepatic Veno-occlusive disease * Right Heart Failure (Hepatic Congestion) * Constrictive Pericarditis

Question 313

Budd Chiari Syndrome arterial

Answer 313

Central Enhancement | Peripheral Minimal

Question 314

Budd Chiari Syndrome portal v

Answer 314

Central Washout | Peripheral Enhancement

Question 315

Budd Chiari Syndrome renerative nodules

Answer 315

Regenerative (hyperplastic) nodules can be difficult to distinguish from multifocal hepatocellular carcinoma. They are bright on T1 and typically dark or iso on T2. Multiple big (>10cm) and small (<4cm) nodules in the setting of Budd-Chiari suggest a benign process. T2 dark also helps (HCC is usually T2 bright).

Question 316

Budd Chiari Syndrome presentation

Answer 316

Presentation can be acute or chronic. Acute from thrombus into the hepatic vein or IVC. These guys will present with rapid onset ascites. Chronic from fibrosis of the intrahepatic veins, presumably from inflammation.

Question 317

who gets massive caudate lobe hypertrophy

Answer 317

* Budd Chiari * Primary Sclerosing Cholangitis * Primary Biliary Cirrhosis

Question 318

Hepatic Veno-occlusive Disease

Answer 318

This is a form of Budd Chiari that occurs from occlusion of the small hepatic venules. It is endemic in Jamaica (from Alkaloid bush tea). In the US it’s typically the result of XRT and chemotherapy. The main hepatic veins and IVC will be patent, but portal waveforms will be abnormal (slow, reversed, or to-and fro).

Question 319

Passive Congestion overview

Answer 319

Passive hepatic congestion is caused by stasis of blood within the liver due to compromise o f hepatic drainage. It is a common complication of congestive heart failure and constrictive pericarditis. It is essentially the result o f elevated CVP transmitted from the right atrium to the hepatic veins.

Question 320

Passive Congestion: Findings

Answer 320

Refluxed contrast into the hepatic veins Increased portal venous pulsatility Nutmeg liver

Question 321

Portal Vein Thrombosis

Answer 321

Occurs in hypercoaguable states (cancer, dehydration,e tc .. .)• Can lead to cavernous transformation, with the development of a bunch of serpiginous vessels in the porta hepatis which may reconstitute the right and left portal veins. This takes like 12 months to happen (it proves portal vein is chronically occluded).

Question 322

Pseudo Cirrhosis

Answer 322

Treated breast cancer mets to the liver can cause contour changes that mimic cirrhosis. Specifically, multifocal liver retraction and enlargement o f the caudate has been described. Why this is specific for breast cancer is not currently known, as other mets to the liver don’t produce this reaction.

Question 323

Cryptogenic Cirrhosis

Answer 323

Essentially cirrhosis o f unknown cause. Most o f these cases are probably the result of nonalcoholic fatty liver disease.

Question 324

Liver transplant overview

Answer 324

The liver has great ability to regenerate and may double in size in as little as 3 weeks, making it ideal for partial donation. Hepatitis C is the most common disease requiring transplantation (followed by EtOH liver disease and cryptogenic cirrhosis). In adults, right lobes (segments 5-8) are most commonly implants. This is the opposite o f pediatric transplants, which usually donates segments 2-3. The modem surgery has four connections (IVC, artery, portal vein, CBD).

Question 325

Liver transplant contraindications

Answer 325

Contraindications include, extrahepatic malignancy, advanced cardiac disease, advanced pulmonary disease, or active substance abuse. Portal HTN is NOT a true contraindication although it does increase the difficulty o f the surgery and increase mortality.

Question 326

Liver transplant normal us

Answer 326

Normal Doppler should have a RAPID systolic upstroke * Diastolic -> Systolic in less than 80msec (0.08 seconds) Resistive Index is Normally between 0.5 - 0.7 Hepatic Artery Peak Velocity should be < 200 cm/sec

Question 327

Liver transplant syndrome of impending thrombus

Answer 327

``` 3-10 days post transplant (1st) Initial Normal Waveform (2nd) No diastolic flow (3rd) Dampening Systolic flow Tardus Parvus R1 < 0.5 (4th) Loss o f Hepatic Waveform ```

Question 328

Liver transplant vessels

Answer 328

As mentioned before, the normal liver gets 70% blood flow from the portal vein, making it the key player. In the transplanted liver, the hepatic artery is the king and is the primary source of blood flow for the bile ducts (which undergo necrosis with hepatic artery failure). Hepatic artery thrombosis comes in two flavors: early (< 15 days), and later (years). The late form is associated with chronic rejection and sepsis

Question 329

Liver transplant trivia

Answer 329

Tardus Parvus is more likely secondary to stenosis than thrombosis

Question 330

Portal venous gaus vs pneumobilia

Answer 330

These are the two patterns of branching air in the liver. The classic way to distinguish between the two is Central (Pneumobilia) vs Peripheral (PVG). The way to remember this is that bile is draining out of the liver into the bowel - so it is flowing towards the porta-hepatis and should be central. Portal blood, on the other hand, is being pumped into the liver - so it will be traveling towards the periphery. The potential trivia question is how peripheral is peripheral — and that is 2cm. Within 2cm of the liver capsule = portal venous gas. Other things to remember - gas in the bile is usually related to a prior procedure (anything that fucks with the sphincter of Oddi). Gas in the portal system can be from lots of stuff (benign things like COPD or bad things - the most classic being bowel necrosis -look for pneumatosis*).

Question 331

Jaundice

Answer 331

You always think about common duct stone, but the most common etiology is actually from a benign stricture (post traumatic from surgery or biliary intervention).

Question 332

Bacterial Cholangitis

Answer 332

Hepatic abscess can develop secondary to cholangitis, usually as the result of stasis (so think stones). The triad of jaundice, fever, and right upper quadrant pain is the step 1 question.

Question 333

PSC overview

Answer 333

Chronic cholestatic liver disease of unknown etiology characterized by progressive inflammation which leads to multifocal strictures of the intra and /or extrahepatic bile ducts. The disease often results in cirrhosis, and is strongly associated with cholangiocarcinoma. The buzzword for the cirrhotic pattern is “central regenerative hypertrophy”. It is associated with inflammatory bowel disease (Ulcerative Colitis 80%, Crohn’s 20%). It is an indication for transplant, with a post transplant recurrence of about 20%.

Question 334

PSC Buzzwords

Answer 334

‘“Withered Tree” - The appearance on MRCP, from abrupt narrowing of the branches ‘“Beaded Appearance” - Strictures + Focal Dilations

Question 335

Dilated intrahepatic bile ducts are very rare in all forms of cirrhosis except

Answer 335

PSC

Question 336

AIDS Cholangiopathy

Answer 336

Infection of the biliary epithelium (classically Cryptosporidium) can cause ductal disease in patients with AIDS. The appearance mimics PSC with intrahepatic and/or extrahepatic multifocal strictures. The classic association/finding is papillary stenosis (which occurs 60% of the time).

Question 337

This vs that AIDS cholangioapathy

Answer 337

Focal Strictures of the extrahepatic duct > 2cm Absent saccular deformities o f the ducts Associated Papillary Stenosis

Question 338

This vs that PSC

Answer 338

Extrahepatic strictures rarely > 5mm Has saccular deformities o f the ducts

Question 339

Oriental Cholangitis overview

Answer 339

Recurrent pyogenic cholangitis): Common in Southeast Asia (hence the culturally insensitive name). They always show it as dilated ducts that are full of pigmented stones.

Question 340

Oriental Cholangitis buzzword

Answer 340

“straight rigid intrahepatic ducts.”

Question 341

Oriental Cholangitis location cuase

Answer 341

The cause o f the disease is not known, but it may be associated with clonorchiasis, ascariasis, and nutritional deficiency. These guys don’t do as well with endoscopic decompression and often need surgical decompression. Remember this is a major risk factor for cholangiocarcinoma in the East.

Question 342

Oriental Cholangitis location

Answer 342

The anatomically longer, flatter left biliary system | tends to make the disease burden left dominant (the opposite o f hematogenous processes which favor the right lobe).

Question 343

Primary Biliary Cirrhosis

Answer 343

An autoimmune disease that results in the destruction of small & medium bile ducts (intra not extra). It primarily affects middle-aged women, who are often asymptomatic. In the early disease, normal bile ducts help distinguish it from PSC. In later stages, there is irregular dilation o f the intrahepatic ducts, with normal extrahepatic ducts. There is increased risk of HCC. If caught early it has an excellent prognosis and responds to medical therapy with ursodeoxycholic acid. The step 1 trivia is “antimitochondrial antibodies (AMA)” which are present 95% o f the time.

Question 344

Long Common Channel

Answer 344

An anatomic variant in which the common bile and pancreatic duct fuse prematurely at the level o f the pancreatic head (prior to the sphincter o f Oddi complex). The testable consequence is the increased incidence o f pancreatitis - as reflux o f enzymes is more common. There is also an association with Type 1 choledochocysts.

Question 345

Choledocchal cysts types

Answer 345

type 1 is focal dilation o f the CBD Type 2 and 3 are super rare. Type 2 is basically a diverticulum o f the bile duct. Type 3 is a “choledochocele.” Type 4 is both intra and extra. Type 5 is Caroli’s, and is intrahepatic only

Question 346

Choledocchal cysts high yield trivia

Answer 346

type 1 is focal dilation o f the CBD and is by fa r the most common.

Question 347

Carolis overview

Answer 347

AR disease associated with polycystic kidney disease and medullary sponse kidney. The hallmark is intrahepatic duct dilation, that is large and saccular. Buzzword is “central dot sign” which corresponds to the portal vein surrounded by dilated bile ducts

Question 348

Carolis compications

Answer 348

Cholangiocarcinoma * Cirrhosis * Cholangitis * Intraductal Stones

Question 349

Carolis gamesmanship

Answer 349

If they give you imaging o f dilated biliary ducts and a history of repeated cholangitis, think choledocal cyst. These things get stones in them and can be recurrently infected.

Question 350

Ductal High Yield Summary Carolis

Answer 350

-Communicates with the ducts -Type 5 Cyst -Central Dot Sign (on CT, MR, US) -Associated with Polycystic Kidney, Medullary Sponge Kidney Cholangiocarcinoma

Question 351

Ductal High Yield Summary PSC

Answer 351

-40 year old Male with U.C. -Withering Tree -Beading -Mild Dilation -Strongly Associated with Ulcerative Colitis & Cholangiocarcinoma

Question 352

Ductal High Yield Summary Oriental cholangioheatitis (recurrent pyogenic)

Answer 352

``` -Associations with clonorchiasis, ascariasis -Lots of Stones -Favors the left ductal system - Strongly Associated with Cholangiocarcinoma ```

Question 353

Ductal High Yield Summary AIDS cholangiopathy

Answer 353

``` -Related to Cryptosporidium or cytomegalovirus. -Segmental Strictures (looks like PSC) -Ducts look like PSC + Papillary Stenosis - Associated with Cholangiocarcinoma ```

Question 354

Cholangiocarcinoma VS B9 Strictures

Answer 354

CA Strictures tends to be long, with “shouldering.’ | B9 strictures tend to be abrupt and short.

Question 355

Duct path association

Answer 355

If you can’t remember what the association is, and it’s ductal pathology, always guess Cholangiocarcinoma.``

Question 356

Normal Gallbladder

Answer 356

The normal gallbladder is found inferior to the interlobar fissure between the right and left lobe. The size varies depending on the last meal, but is supposed to be < 4 x < 10cm. The wall thickness should be < 3mm. The lumen should be anechoic.

Question 357

Gallbladder phyrgian cap

Answer 357

A phrygian cap is seen when the GB folds on itself. It means nothing.

Question 358

Gallbladder intrahepatic gallbladder

Answer 358

Variations in gallbladder location are rare, but the intrahepatic gallbladder is probably the most frequently recognized variant. Most are found right above the interlobar fissure.

Question 359

Gallbladder duplicated

Answer 359

it can happen

Question 360

Gallbladder duct of luschka

Answer 360

An accessory cystic duct. This can cause a big problem (persistent bile leak) after cholecystectomy. There are several subtypes which is not likely to be tested.

Question 361

GB Wall Thickening (> 3mm):

Answer 361

Very non-specific. Can occur from biliary (Cholecystitis, AIDS, PSC...) or non-biliary causes (hepatitis, heart failure, cirrhosis, etc....).

Question 362

Gallstones

Answer 362

Gallstones are found in 10% o f asymptomatic patients/ Most (75%) are cholesterol, the other 25% are pigmented. They cast shadows.

Question 363

Reasons a gallstone might not cast a shadow

Answer 363

* It’s not a stone * It’s a stone, but < 3mm in size * The sonographer is an amateur (Bush league psyche-out stuff. Laughable, man)

Question 364

Gallbladder shadowing

Answer 364

(1) Gallbladder full of stones * Clean shadowing. (2) Porcelain Gallbladder * Variable shadowing (3) Emphysematous Cholecystitis * Dirty shadowing.

Question 365

Mirrizzi syndrome

Answer 365

This occurs when the common hepatic duct is obstructed secondary to an impacted cystic duct stone. The stone can eventually erode into the CHD or GI tract.

Question 366

Mirrizzi syndrome key point

Answer 366

increased co-incidence o f gallbladder CA (5x more risk) with Mirizzi.

Question 367

Mirrizzi syndrome trivia

Answer 367

Mirizzi occurs more in people with a low cystic duct insertion (normal variant), allowing for a more parallel course and closer proximity to the CHD.

Question 368

Clinically Meaningless THIS vs THAT: Gallbladder Adenomyomatosis VS Cholesterolosis overview

Answer 368

Nothing makes an Academic Radiologist happier than spending time deploying intense focused concentration targeted at distinguishing between two very similar appearing completely benign (often incidental) processes. They believe this “adds value” and will save them from the eventual avalanche of reimbursement cuts with subsequent AI takeover.

Question 369

Clinically Meaningless THIS vs THAT: Gallbladder Adenomyomatosis VS Cholesterolosis classic example

Answer 369

Adenomyomatosis vs Gallbladder Cholesterolosis. These things are actually different - and even though it makes zero difference clinically, this is just the kind of thing people who write questions love to write questions about.

Question 370

Clinically Meaningless THIS vs THAT: Gallbladder Adenomyomatosis VS Cholesterolosis adenomyomatosis

Answer 370

You have hypertrophied mucosa and muscularis propria, with the cholesterol crystals deposited in an intraluminal location (within Rokitansky-Aschoff sinuses).

Question 371

Clinically Meaningless THIS vs THAT: Gallbladder Adenomyomatosis VS Cholesterolosis cholesterolosis

Answer 371

Cholesterol and triglyceride deposition is within the substance of the lamina propria, and associated with formation o f cholesterol polyps.

Question 372

Adenomyomatosis imaging

Answer 372

manifest from the unique acoustic signature as comet-tail artifact (highly specific for adenomyomatosis).

Question 373

Adenomyomatosis 3 types

Answer 373

Generalized (diffuse), Segmental (annular), and Fundal (localized or adenomyoma). The Localized form can’t be differentiated from GB cancer.

Question 374

Adenomyomatosis gamesmanship

Answer 374

Don’t be tricked into selecting “Adenomyosis” as a distractor. That shit is in the uterus. Remember the larger word is in the smaller organ. Or, you can think about the two Ms in MyoMat - turned inward sorta looks like a gallbladder.

Question 375

Porcelain gallbladder

Answer 375

* Extensive wall calcification. * The key point is increased risk o f GB Cancer. * These are surgically removed.

Question 376

Gallbladder polyps benign

Answer 376

< 5mm * these are nearly always cholesterol polyps Pedunculated Multiple Comet Tail Artifact on Ultrasound (seen in cholesterol polyps)

Question 377

Gallbladder polyps malignat

Answer 377

> 1cm *between 5mm-10mm usually get followed for growth Sessile Solitary Enhancement on CT/MRI greater than the adjacent gallbladder wall. Flow on Doppler.

Question 378

Gallbladder polyps overview

Answer 378

These can be cholesterol (by far the most common), or non cholesterol (adenomas, papillomas). Cholesterol polpys aren’t real polyps, but instead are essentially enlarged papillary fronds full o f lipid filled macrophages, that are attached to the wall by a stalk. The non-cholesterol subtypes are almost always solitary and are typically larger. The larger polyps may have Doppler flow. They are NOT mobile and do NOT shadow. Once they get to be 1 cm, people start taking them out.

Question 379

Gallbladder cancer classic vignette

Answer 379

elderly women with nonspecific RUQ pain, weight loss, anorexia and a long standing history o f gallstones, PSC, or large gallbladder polyps.

Question 380

Gallbladder cancer risk factors

Answer 380

* Mirizzi syndrome has a well described increased risk o f GB cancer * Other risk factors include smoldering inflammatory processes (PSC, Chronic Cholecystitis, Porcelain Gallbladder), and large polyps (“large” = bigger than 1cm)

Question 381

Gallbladder cancer presentation

Answer 381

Unless the cancer is in the fundus (which can cause biliary obstruction) they often present late and have horrible outcomes with 80% found with direct tumor invasion o f the liver or portal nodes at the time of diagnosis.

Question 382

Duplex

Answer 382

means color

Question 383

spectral

Answer 383

means color with a waveform

Question 384

Concept of arterial resistance

Answer 384

Some organs require continuous flow (brain), whereas others do not (muscles). The body is smart enough to understand this, and will make alterations in resistance / flow to preserve energy. When an organ needs to be “on,” its arteriolar bed dilates, and the waveform becomes low resistance. This allows the organ to be appropriately perfused. When an organ goes to “power save” mode, its arterioles constrict, the waveform switches to high resistance, and blood flow is diverted to other more vital organs.

Question 385

Continuous diastolic flow

Answer 385

low resistance

Question 386

RI

Answer 386

To help quantify this low resistance high resistance thing, we use this “Resistive Index (RI)” - which is defined as V1-V2 / VI. RI = PSV - EDV / PSV

Question 387

Tardus

Answer 387

``` Refers to a slowed systolic upstroke. This can be measured by acceleration time, the time from end diastole to the first systolic peak. An acceleration time > 0.07 sec correlates with >50% stenosis of the renal artery ```

Question 388

parvus

Answer 388

``` Refers to decreased systolic velocity. This can be measured by calculating the acceleration index, the change in velocity from end diastole to the first systolic peak. ```

Question 389

Upstream

Answer 389

Blood that has NOT yet passed through the stenosis

Question 390

Downstream

Answer 390

Blood that has passed through the area o f stenosis

Question 391

Stenosis direct sign

Answer 391

The direct signs are those found at the stenosis itself and they include elevated peak systolic velocity and spectral broadening (immediate post stenotic).

Question 392

Stenosis indirect sign

Answer 392

The indirect signs are going to be tardus parvus (downstream) - with time to peak (systolic acceleration) > 70msec. The RI downstream will be low (< 0.5) because the liver is starved for blood. The Rl upstream will be elevated (> 0.7) because that blood needs to overcome the area o f stenosis.

Question 393

Hepatic vein flow

Answer 393

Flow in the hepatic veins is complex, with alternating forward and backward flow. The bulk of the flow should be forward “antegrade” (liver -> heart). Things that mess with the waveform are going to be pressure changes in the right heart which are transmitted to the hepatic veins (CHF, Tricuspid Regurg) or compression o f the veins directly (cirrhosis). Anything that increases right atrial pressure (atrial contraction) will cause the wave to slope upward. “A” represents atrial contraction. Anything that decreases right atrial pressure will cause the wave to slope downward.

Question 394

Abnormal Flepatic Vein Waveforms can manifest in one o f three main categories:

Answer 394

1) More Pulsatile (2) Less Pulsatile (3) Absent = Budd Chiari

Question 395

Tricuspid regurg vs right sided chf on hepatic vein us

Answer 395

* Tricuspid Regurg - D deeper than S | * Right Heart Failure - S deeper than D

Question 396

Portal vein us

Answer 396

Flow in the portal vein should always be towards the liver (antegrade). You can see some normal cardiac variability from hepatic venous pulsatility transmitted through the hepatic sinusoids. Velocity in the normal portal vein is between 20-40 cm/s. The waveform should be a gentle undulation , always remaining above the baseline.

Question 397

portal vein us patterns

Answer 397

(1) Normal (2) Pulsatile (3) Reversed

Question 398

Causes o f Portal Vein Pulsatility

Answer 398

Right-sided CHF, Tricuspid Regurg, Cirrhosis with Vascular | AP shunting.

Question 399

Causes o f Portal Vein Reversed ¥\ow

Answer 399

The big one is Portal HTN (any cause).

Question 400

Portal vein absent flow

Answer 400

This could be considered a fourth pattern. It’s seen in thrombosis, tumor invasion, and stagnant flow from terrible portal HTN.

Question 401

Portal vein slow flow

Answer 401

Velocities less than 15 cm/s. Portal HTN is the most common cause. Additional causes are grouped by location: * Pre - Portal Vein Thrombosis * Intra - Cirrhosis (any cause) * Post - Right-sided Heart Failure, Tricuspid Regurg, Budd-Chiari

Question 402

Liver doppler trivia

Answer 402

An ultra-common quiz question is to ask “what should the Doppler angle be?” Now even though ultrasound physics is covered in more detail in the dedicated section o f the War Machine this is a high yield enough point to warrant repetition. The answer is “less than 60. ” Why? Doppler strength follows the cosine o f the angle. For example, Cos 90 = 0, Cos 60 = 0.5, Cos 0 = 1.0 - the doppler strength follows the Cos.

Question 403

Pancreas anatomy

Answer 403

The pancreas is a retroperitoneal structure (the tail may be intraperitoneal).

Question 404

Pancreas Classic US Trivia

Answer 404

The Pancreatic Echogenicity should be | GREATER than the normal liver.

Question 405

Pancrease CF

Answer 405

The pancreas is involved in 85-90% of CF patients. Inspissated secretions cause proximal duct obstruction leading to the two main changes in CF: (1) Fibrosis (decreased T1 and T2 signal) (2) Fatty replacement (increased T l) - the more common of the two Patients with CF, who are diagnosed as adults, tend to have more pancreas problems than those diagnosed as children. Just remember that those with residual pancreatic exocrine function tend to have bouts of recurrent acute pancreatitis (they keep getting clogged up with thick secretions). Small (1-3 mm) pancreatic cysts are common.

Question 406

Pancreas high yield trivia

Answer 406

• Complete fa tty replacement is the most common imaging finding in adult CF • Markedly enlarged with fatty replacement has been termed lipomatous pseudohypertrophy of the pancreas. *This is a buzzword. • Fibrosing Colonopathy: Wall thickening of the proximal colon as a complication of enzyme replacement therapy.

Question 407

Shwachman-Diamond Syndrome

Answer 407

The 2nd most common cause of pancreatic insufficiency in kids (CF #1). Basically, it’s a kid with diarrhea, short stature (metaphyseal chondroplasia), and eczema. Will also cause lipomatous pseudohypertrophy o f the pancreas.

Question 408

Pancreatic lipomatosis

Answer 408

Most common pathologic condition involving the pancreas. The most common cause in childhood is CF (in adults it’s Burger King). Additional causes worth knowing are Cushing Syndrome, Chronic Steroid Use, Hyperlipidemia, and Shwachman-Diamond Syndrome.

Question 409

Pancreatic agensis does not have a

Answer 409

duct

Question 410

Dorsal Pancreatic Agenesis

Answer 410

All you need to know is that (1) this sets you up for diabetes (most o f your beta cells are in the tail), and (2) it’s associated with polysplenia.

Question 411

Annular Pancreas

Answer 411

Essentially an embryologic screw up (failure o f ventral bud to rotate with the duodenum), that results in encasement o f the duodenum. Results in a rare cause o f duodenal obstruction (10%), that typically presents as duodenal obstruction in children and pancreatitis in adults. Can also be associated with other vague symptoms (postprandial fullness, “symptoms of peptic ulcer disease”, etc...).

Question 412

Annular pancreas adults vs kids

Answer 412

Remember in adults this can present with pancreatitis (the ones that present earlier - in kids - are the ones that obstruct).

Question 413

Annular pancreas imaging

Answer 413

look for an annular duct encircling the descending duodenum.

Question 414

Pancreatic Trauma overview

Answer 414

The pancreas sits in front o f the vertebral body, so it’s susceptible to getting smashed in blunt trauma. Basically, the only thing that matters is integrity of the duct. If the duct is damaged, they need to go to the OR. The most common delayed complication is pancreatic fistula (10-20%), followed by abscess formation. Signs of injury can be subtle, and may include focal pancreatic enlargement or adjacent stranding/fluid.

Question 415

Pancreatic Trauma imaging pearls

Answer 415

• Remember it can be subtle with just focal enlargement of the pancreas • If you see low attenuation fluid separating two portions o f the enhancing pancreatic parenchyma this is a laceration, NOT contusion. • The presence o f fluid surrounding the pancreas is not specific, it could be from injury or just aggressive hydration — on the test they will have to show you the liver and IVC to prove it’s aggressive fluid resuscitation.

Question 416

Pancreatic trauma high yield

Answer 416

Traumatic Pancreatitis in a kid too young to ride a bike = NAT.

Question 417

Suspected pancreatic duct injury?

Answer 417

Next Step - MRCP or ERCP

Question 418

Acute pancreatitis Etiology

Answer 418

By far the most common causes are gallstones and EtOH which combined makeup 80% o f the cases in the real world. However, for the purpose o f multiple choice tests, a bite from the native scorpion o f the island of Trinidad and Tobago is more likely to be the etiology. Additional causes include ERCP (which usually results in a mild course), medications (classically valproic acid), trauma (the most common cause in a child), pancreatic cancer, infectious (post viral in children), hypercalcemia, hyperlipidemia, autoimmune pancreatitis, pancreatic divisum, groove (para-duodenal) pancreatitis, tropic pancreatitis, and parasite induced.

Question 419

Acute pancreatitis clinical outcomes

Answer 419

Prognosis can be estimated with the “Balthazar Score.” Essentially, you can think about pancreatitis as “mild” (no necrosis) or “severe” (having necrosis). Patients with necrosis don’t start doing terrible until they get infected, then the mortality is like 50-70%

Question 420

Acute pancreatitis key point

Answer 420

Outcomes are directly correlated with the degree o f pancreatic necrosis

Question 421

Acute pancreatitis severe pancreatitis

Answer 421

Severe acute pancreatitis has a biphasic course. With the first two weeks being a proinflammatory phase. This is a sterile response in which infection rarely occurs. The third and fourth weeks transition to an anti-inflammatory period in which the risk of translocated intestinal flora and thesubsequent development o f infection increases.

Question 422

Acute pancreatitis words??

Answer 422

No necrosis < 4 week > acute peripancreatic fluid collection No necrosis > 4 weeks > pseudocyst Necrosis < 4 weeks > acute necrotic collection Necrosis > 4 weeks > Walled off necrosis

Question 423

Acute pancreatitis Vascular compications

Answer 423

* Splenic Vein and Portal Vein Thrombosis O Isolated gastric varices can be seen secondary to splenic vein occlusion * Pseudo-aneurysm o f the GDA and Splenic Artery

Question 424

Acute pancreatitis nonvascular compications

Answer 424

* Abscess, Infection, etc... as discussed * Gas, as a characteristic sign of an infected fluid collection, is detected in only 20% of cases o f pancreatic abscesses.

Question 425

Acute pancreatitis random imaging pearl

Answer 425

On Ultrasound, an inflamed pancreas will be hypoechoic (edematous) when compared to the liver (opposite o f normal).

Question 426

Pancreatic Divisum | anatomy

Answer 426

There are two ducts, a major (Wirsung), and a minor (Santorini). Under “normal” conditions the major duct will drain in the inferior of the two duodenal papilla (major papilla). The minor duct will drain into the superior of the two duodenal papilla (minor papilla). The way I remember this is that “Santorini drains Superior”, and “Santorini is Small,” i.e. the minor duct.

Question 427

Pancreatic Divisum | overview

Answer 427

Pancreatic Divisum is the most common anatomic variant of the human pancreas, and occurs when the main portion of the pancreas is drained by the minor or accessory papilla. The clinical relevance is an increased risk of pancreatitis.

Question 428

Chronic Pancreatitis Overview

Answer 428

CP represents the end result o f prolonged inflammatory change leading to irreversible fibrosis of the gland. Acute pancreatitis and chronic pancreatitis are thought o f as different disease processes, and most cases of acute pancreatitis do not result in chronic disease. So, acute doesn’t have to lead to chronic (and usually doesn’t), but chronic can still have recurrent acute.

Question 429

Chronic pancreatitis Etiology

Answer 429

Same as acute pancreatitis, the most common causes are chronic alcohol abuse and cholelithiasis which together result in about 90% of the cases. (EtOH is #1)

Question 430

Chronic pancreatitis imaging findings early

Answer 430

* Loss o f T1 signal (pancreas is normally the brightest T1 structure in the body) * Delayed Enhancement * Dilated Side Branches

Question 431

Chronic pancreatitis imaging findings late

Answer 431

* Commonly small, uniformly atrophic - but can have focal enlargement * Pseudocyst formation (30%) * Dilation and beading of the pancreatic duct with calcifications * * most characteristic finding o f CP.

Question 432

This vs that CP vs Cancer CP

Answer 432

Dilatation is irregular duct is <50% of the AP gland diameter

Question 433

This vs that CP vs Cancer Cancer

Answer 433

Dilation is uniform duct is >50% of the AP gland diameter

Question 434

Chronic pancreatitis complication

Answer 434

Pancreatic cancer (20 years o f CP = 6% risk o f Cancer) is the most crucial complication in CP and is the biggest diagnostic challenge because focal enlargement o f the gland induced by a fibrotic inflammatory pseudotumor may be indistinguishable from pancreatic carcinoma.

Question 435

Autoimmune pancreatitis

Answer 435

Associated with elevated IgG4 Absence of Attack Symptoms Responds to steroids Sausage Shaped Pancreas, capsule like delayed rim enhancement around gland (like a scar). No duct dilation. No calcifications.

Question 436

Groove pancreatitis

Answer 436

Looks like a pancreatic head Cancer - but with little or no biliary obstruction. Less likely to cause obstructive jaundice (relative to pancreatic CA) Duodenal stenosis and /or strictures of the CBD in 50% of the cases Soft tissue within the pancreaticoduodenal groove, with or without delayed enhancement

Question 437

Tropic pancreatitis

Answer 437

Young Age at onset, associated with malnutrition Increased risk of adenocarcinoma Multiple large calculi within a dilated pancreatic duct

Question 438

Hereditary Pancreatitis

Answer 438

Young Age at Onset Increased risk of adenocarcinoma SPINK-1 gene Similar to Tropic Pancreatitis

Question 439

Ascaris Induced

Answer 439

Most commonly implicated parasite in pancreatitis Worm may be seen within the bile ducts

Question 440

1 Say Autoimmune Pancreatitis

Answer 440

you say IGG4

Question 441

I Say IgG4

Answer 441

``` Autoimmune Pancreatitis Retroperitoneal Fibrosis Sclerosing Cholangitis Inflammatory Pseudotumor Riedel’s Thyroiditis ```

Question 442

THIS vs THAT: | Autoimmune Pancreatitis vs Chronic Pancreatitis

Answer 442

Autoimmune Pancreatitis Chronic Pancreatitis No ductal dilation Ductal Dilation No calcifications Ductal Calcifications

Question 443

Pancreatic pseudocyst

Answer 443

When you see a cystic lesion in the pancreas, by far the most common cause is going to be an inflammatory pseudocyst, either from acute pancreatitis or chronic pancreatitis.

Question 444

Pancreatic simple cyst

Answer 444

True epithelial lined cysts are rare, and tend to occur with syndromes such as VHL, Polycystic Kidney Disease, and Cystic Fibrosis.

Question 445

Pancreas serous cystadenoma demographics

Answer 445

(Grandma). The former term “microcystic adenoma” helps me think o f a little old lady, which is appropriate for a lesion primarily found in elderly ladies. The lesion is benign

Question 446

Pancreas serous cystadenoma imaging

Answer 446

classically described as a heterogeneous, mixed-density lesion made up o f multiple small cysts, which resembles a sponge. They are more commonly (70%) located in the pancreatic head (mucinous is almost always in the body or tail). An additional key distinction is that it does NOT communicate with the pancreatic duct (IPMNs do). About 20% of the time they will have the classic central scar, with or without central calcifications (mucinous calcifications are peripheral). Rarely, they can be unilocular. When you see a unilocular cyst with a lobulated contour located in the head o f the pancreas, you should think about this more rare unilocular macrocystic serous cystadenoma subtype.

Question 447

Pancreas serous cystadenoma trivia

Answer 447

Serous Cystadenoma is associated with Von Hippel Lindau

Question 448

Pancreas serous cystadenoma Memory aid

Answer 448

“GRANDMA Serous is the HEAD o f the household”

Question 449

Pancreas mucinous cystic neoplasm demographics

Answer 449

Mother. This pre-malignant lesion is “always” found in women, usually in their 50s. All are considered pre-malignant and need to come out.

Question 450

Pancreas mucinous cystic neoplasm imaging

Answer 450

They are found in the body and tail (serous was more common in the head). There is generally no communication with the pancreatic duct (IPMNs will communicate). Peripheral calcifications are seen in about 25% o f cases (serous was more central). They are typically unilocular. When mutlilocular, individual cystic spaces tend to be larger than 2 cm in diameter (serous spaces are typically smaller than 2 cm).

Question 451

Pancreas mucinous cystic neoplasm memory aid

Answer 451

Mucinous in the mother

Question 452

Solid Pseudopapillary Tumor of the Pancreas Demographics

Answer 452

(Daughter): Very rare, low grade malignant tumor that occurs almost exclusively in young (30s) females (usually Asian or Black).

Question 453

Solid Pseudopapillary Tumor of the Pancreas imaging findings

Answer 453

It is typically large at presentation, has a predilection for the tail, and has a “thick capsule.” Similar to a hemangioma it may demonstrate progressive fill-in o f the solid portions.

Question 454

IPMN - intraductal Papillary Mucinous Neoplasm Overview

Answer 454

These guys are mucin producing | tumors that arise from the duct epithelium. They can be either side branch, main branch, or both.

Question 455

IPMN - intraductal Papillary Mucinous Neoplasm side branch

Answer 455

"The pulmonary nodule of the pancreas" common and usually meaningless typically appear as a small cystic mass, often in the head or uncinate process if large amounts of mucin are produced it may result in main duct enlargement lesions less than 3 cm are usually benign

Question 456

IPMN - intraductal Papillary Mucinous Neoplasm main branch

Answer 456

produces diffuse dilation of the main duct atrophy of the gland and dystrophic calcs may be seen (mimicking chronic pancreatitis have a much higher%of malignancy compared to side branch all main ducts are considered malignany and resection should be considered

Question 457

IPMN - intraductal Papillary Mucinous Neoplasm Features concerning for malignancy

Answer 457

main duct >10mm (some sources say 1.5 cm) enhancing nodules solid hypovascular mass

Question 458

Main Branch IPMN summary

Answer 458

- “The Bad One” | - Has malignant potential

Question 459

Solid Pseudopapillary summary

Answer 459

- Daughter Lesion - Solid with Cystic parts, enhances like a hemangioma - Capsule

Question 460

Side Branch IPMN summary

Answer 460

- “Common One” - Has much less malignant potential - Often in head /uncinate - Communicates with duct

Question 461

Serous cystic summary

Answer 461

- Grandma Lesion - Benign - Microcystic, with central calcifications

Question 462

Mucinous cystic summary

Answer 462

- Mother Lesion - Premalignant - Body / Tail - 95% - Unilocular with thick wall septations

Question 463

Solid Pancreatic lesions overview

Answer 463

Pancreatic Cancer basically comes in two flavors. (1) Ductal Adenocarcinoma - which is hypovascular and (2) Islet Cell / Neuroendocrine which is hypervascular.

Question 464

Ductal Adenocarcinoma overview

Answer 464

In the setting of a multiple choice test, the finding o f an enlarged gallbladder with painless jaundice is highly suspicious for pancreatic adenocarcinoma, especially when combined with migratory thrombophlebitis (Trousseau’s syndrome). The peak incidence is in the 7th or 8th decade. The strongest risk factor is smoking.

Question 465

Ductal Adenocarcinoma imaging findings

Answer 465

Approximately two-thirds o f these cancers arise from the pancreatic head. On ultrasound, obstruction o f both the common bile duct and the pancreatic duct is referred to as the “double duct sign”. On CT, the findings are typically a hypo-enhancing mass which is poorly demarcated and low attenuation compared to the more brightly enhancing background parenchyma. The optimal timing is on a pancreatic phase (40 seconds).

Question 466

Ductal Adenocarcinoma staging

Answer 466

The key to staging is assessment o f the SMA and celiac axis, which if involved make the patient’s cancer unresectable. Involvement o f the GDA is ok, because it comes out with the Whipple.

Question 467

Ductal Adenocarcinoma trivia

Answer 467

``` • Tumor Marker = CA 19-9 # Hereditary Syndromes with Pancreatic CA: O HNPCC, BRCA Mutation, Ataxia-Telangiectasia, Peutz-Jeghers * Small Bowel Follow Through: Reverse impression on the duodenum “Frostburg’s Inverted 3 Sign” or a “Wide Duodenal Sweep.” They would have to actually find a case o f the inverted 3 to show it, but could ask it in words. The ‘Wide Duodenal Sweep ” could actually be shown. ```

Question 468

Periampullary Tumor overview

Answer 468

Defined as originating within 2cm of the major papilla. It can be difficult to differentiate from a conventional pancreatic adenocarcinoma as both obstruct the bile duct, and present as a mass in the pancreatic head. Basically, all you need to know about them is they can try and treat them with a Whipple and they have a better prognosis than pancreatic adenocarcinoma.

Question 469

Periampullary tumore trivia

Answer 469

There is an increased incidence o f ampullary carcinoma in Gardner’s Syndrome.

Question 470

Islet cell/neuroendocrine pancreatic tumors overview

Answer 470

Neuroendocrine tumors are uncommon tumors of the pancreas. Typically hypervascular, with brisk enhancement during arterial or pancreatic phase. They can be thought of as non-functional or functional, and then subsequently further divided based on the hormone they make. They can be associated with both MEN 1 and Von Hippel Lindau.

Question 471

Islet cell/neuroendocrine pancreatic tumors Insulinoma

Answer 471

The most common type (about 75%). They are almost always benign (90%), solitary, and small (< 2cm).

Question 472

Islet cell/neuroendocrine pancreatic tumors gastrinoma

Answer 472

The second most common type overall, but most common type associated with MEN 1. They are malignant like 30-60%. They can cause increased gastric acid output and ulcer formation - Zollinger-Ellison syndrome.

Question 473

Islet cell/neuroendocrine pancreatic tumors non-functional

Answer 473

The 3rd most common type, usually malignant (80%), and are usually large and metastatic at the time of diagnosis.

Question 474

Islet cell/neuroendocrine pancreatic tumors I say nonfunctional

Answer 474

you say large with calcification

Question 475

gastrinoma buzzword

Answer 475

Jejunal Ulcer = Zollinger-Ellison

Question 476

Gastrinoma triangle

Answer 476

The anatomical region where most (90%) of gastrinomas arise. Boundaries • Superior: Junction of the cystic and common bile ducts • Inferior: Start of the third portion of the duodenum • Medial: Start of the body of the pancreas

Question 477

Intrapancreatic Accessory Spleen Overview

Answer 477

It is possible to have a pancreatic mass that is actually just a piece of spleen. The typical scenario is that of post traumatic splenosis. Look for the question stem to say something like “history o f trauma. ” Another hint may be the absence of a normal spleen.

Question 478

Intrapancreatic Accessory Spleen Imaging Findings

Answer 478

- Follows spleen on all image sequences (dark on Tl, and bright on T2 - relative to the liver). - It will restrict diffusion (just like the spleen). - The classic give away, and most likely way it will be shown is as a tiger striped mass on arterial phase (tiger striped like the spleen on arterial phase).

Question 479

Intrapancreatic Accessory Spleen trivia

Answer 479

Nuclear medicine tests - (1) Heat Treated RBCs, and (2) Sulfur Colloid can be used to prove the mass is spleen (they both take up tracer— just like a spleen).

Question 480

The Whipple Procedure overview

Answer 480

The standard Whipple procedure involves resection of the pancreatic head, duodenum, gastric antrum, and almost always the gallbladder. A jejunal loop is brought up to the right upper quadrant for gastrojejunal, choledochojejunal or hepaticojejunal, and pancreatojejunal anastomosis.

Question 481

The Whipple Procedure alternative

Answer 481

An alternative method used by some surgeons is to perform a pancreatoduodenectomy and preserve the pylorus when possible. There is debate in the surgery literature with regard to which method should be the standard. In this pylorus-preserving pancreatoduodenectomy, the stomach is left intact and the proximal duodenum is used for a duodenojejunal anastomosis.

Question 482

The Whipple Procedure complications

Answer 482

Delayed gastric emptying (needfor NG tube longer than 1- day) and pancreatic fistula (amylase through the surgical drain >50 ml fo r longer than 7-10 days), are both clinical diagnoses and are the most common complications after pancreatoduodenectomy. Wound infection is the third most common complication, occurring in 5%-20% of patients.

Question 483

Pancreas transplant overview

Answer 483

Pancreas transplant (usually with a renal transplant) is an established therapy for severe type 1 diabetes - which is often complicated by renal failure. The vascular anatomy regarding this transplant is quite complicated and beyond the scope of this text. Just know that the pancreas transplant receives arterial inflow from two sources: the donor SMA, (which supplies the head via the inferior pancreaticoduodenal artery) and the donor splenic artery, (which supplies the body and tail). The venous drainage is via both the donor portal vein and the recipient SMV. Exocrine drainage is via the bowel (in older transplants via the bladder).

Question 484

Pancreas transplant graft failure

Answer 484

The number one cause of graft failure is acute rejection. The number two cause of graft failure is donor splenic vein thrombosis. Donor splenic vein thrombosis usually occurs within the first 6 weeks of transplant. Venous thrombosis is much more common than arterial thrombosis in the transplant pancreas, especially when compared to other transplants because the vessels are smaller and the clot frequently forms within and propagates from the tied-off stump vessels. Both venous thrombosis and acute rejection can appear as reversed diastolic flow. Arterial thrombosis is also less of a problem because of the dual supply to the pancreas (via the Y graft). A point of trivia is that the resistive indices are not of value in the pancreas, because the organ lacks a capsule. The graft is also susceptible to pancreatitis, which is common < 4 weeks after transplant and usually mild. Increased rates of pancreatitis were seen with the older bladder drained subtype.

Question 485

Pancreas transplant shrinking transplant

Answer 485

is a buzzword for chronic rejection, where the graft progressively gets smaller in size.

Question 486

Spleen normal trivia

Answer 486

By the age of 15 the spleen reaches its normal adult size. The spleen contains both “red pulp" and “white pulp” which contribute to its tiger striped appearance during arterial phase imaging. The red pulp is filled with blood (a lot o f blood), and can contain up to one liter of blood at any time. The spleen is usually about 20 HU less dense than the liver, and slightly more echogenic than the liver (equal to the left kidney). The splenic artery (which usually arises from the celiac trunk) is essentially an end vessel, with minimal collaterals. Occlusion o f the splenic artery will therefore result in splenic infarction. Pathology involving the spleen can be categorized as either congenital, acquired (as the sequela o f trauma or portal hypertension), or related to a “mass.” A general rule is that most things in the spleen are benign with exception o f lymphoma or the rare primary angiosarcoma.

Question 487

Normal Spleen on MRI:

Answer 487

Bright on T2, relative to the liver Dark on T1 relative to the liver Like a lymph node it restricts diffusion

Question 488

Accessory spleens

Answer 488

These are very common; we see them all the time. Some random trivia that might be testable includes the fact that sulfur colloid could be used to differentiate a splcnule from an enlarged pathologic lymph node. Additionally, in the scenario where a patient is post splenectomy for something like ITP or autoimmune hemolytic anemia, an accessory spleen could hypertrophy and present as a mass. Hypertrophy of an accessory spleen can also result in a recurrence of the original hematologic disease process.

Question 489

Wandering Spleen

Answer 489

A normal spleen that “wanders” off and is in an unexpected location. Because of the laxity in the peritoneal ligaments holding the spleen, a wandering spleen is associated with abnormalities of intestinal rotation. The other key piece of trivia is that unusual locations set the spleen up for torsion and subsequent infarction. A chronic partial torsion can actually lead to splenomegaly or gastric varices.

Question 490

Splenic Traums

Answer 490

The spleen is the most common solid organ injured in trauma. This combined with the fact that the spleen contains a unit or so of blood means splenic trauma can be life threatening. Remember the trauma scan is done in portal venous phase (70 second), otherwise you’d have to tell if that is the normal tiger-striped arterial-phase spleen or it is lacerated.

Question 491

Splenosis

Answer 491

This occurs post trauma where a smashed spleen implants and then recruits blood supply. The implants are usually multiple and grow into spherical nodules typically in the peritoneal cavity of the upper abdomen (but can be anywhere). It’s more common than you think and has been reported in 40-60% of trauma. Again, Tc Sulfur colloid (or heat-treated RBC) can confirm that the implants are spleen and not ovarian mets or some other terrible thing.

Question 492

Spleen Gamn Gandy Bodies (siderotic nodule)

Answer 492

These are small foci of hemorrhage in the splenic parenchyma that are usually associated with portal hypertension. They are T2 dark. Gradient is the most sensitive sequence.

Question 493

Spleen sarcoidosis

Answer 493

Sarcoid is a disease o f unknown etiology that results in noncaseating granulomas which form in various tissues o f the body (complete discussion in the chest section o f this text). The spleen is involved in 50% - 80% o f patients. Splenomegaly is usually the only sign. However, aggregates o f granulomatous splenic tissue in some patients may appear on CT as numerous discrete l-2cm hypodense nodules. Rarely, it can cause a massive splenomegaly and possibly rupture. Don’t forget that the gastric antrum is the most common site in the GI tract.

Question 494

Spleen Peliosis

Answer 494

This is a rare condition characterized by multiple blood filled cyst-like spaces in a solid organ (usually the liver - peliosis hepatitis). When you see it in the spleen it is usually also in the liver (isolated spleen is extremely rare). The etiology is not known, but for the purpose of multiple choice tests it occurs in women on OCPs, men on anabolic steroids, people with AIDS, renal transplant patients (up to 20%), and patients with Hodgkin lymphoma. It’s usually asymptomatic but can explode spontaneously.

Question 495

Splenic artery aneurysm

Answer 495

the most common visceral arterial aneurysm. Pseudoaneurysm can occur in the setting of trauma and pancreatitis. The incidence is higher in women o f child bearing age who have had two or more pregnancies (4x more likely to get them, 3x more likely to rupture). It’s usually saccular and in the mid-to-distal artery. They usually fix them when they get around 2-3cm. Colossal fu c k up to avoid: Don’t call them a hypervascular pancreatic islet cell mass and biopsy them.

Question 496

Splenic vein thrombosis

Answer 496

frequently occurs as the result o f pancreatitis. Can also occur in the setting o f diverticulitis or Crohn’s. Can lead to isolated gastric varices.

Question 497

Splenic infarction

Answer 497

can occur from a number of conditions. On a multiple choice test the answer is sickle cell. The imaging features are classically a wedge-shaped, peripheral, low attenuation defect.

Question 498

Splenic infections

Answer 498

Most common radiologically detected splenic infection is histoplasmosis (with multiple round calcifications). Splenic TB can have a similar appearance (but much less common in the US). Another possible cause of calcified granuloma in the spleen in brucellosis, but these are usually solitary and 2 cm or larger. They may have a low density center, encircled by calcification giving the lesion a "bull's eye” appearance. In the immunocompetent patient, splenic abscess is usually due to an aerobic organism. Salmonella is the classic bug - which develops in the setting of underlying splenic damage (trauma or sickle cell). In immunocompromised patients, unusual organisms such as fungi, TB, MAI, and PCP can occur and usually present as multiple micro-abscesses. Occasionally, fungal infections may show a “bulls-eye” appearance on ultrasound.

Question 499

Small spleen ddx

Answer 499

sickle cell post radiation post thorostras malabsorption syndromes (uc>crohns)

Question 500

Big spleen ddx

Answer 500

passive congestion (heart failure, portal HTN, Splenic vein thrombosis) lymphoma leukemia gauchers

Question 501

Feltys syndrome

Answer 501

abnormality o f granulocytes, with a triad of: | (1) Splenomegaly, (2) Rheumatoid Arthritis, (3) Neutropenia

Question 502

Splenic post traumatic cysts

Answer 502

(pseudocysts) are the most common cystic lesion in the spleen. They can occur secondary to infarction, infection, hemorrhage, or extension from a pancreatic pseudocyst. As a point o f trivia they are “pseudo” cysts because they have no epithelial lining. They may have a thick wall or prominent calcifications peripherally.

Question 503

Splenic epidermoid cysts

Answer 503

second most common cystic lesion in the spleen. They are congenital in origin. As a point o f absolutely worthless trivia, they are “true” cysts and have an epithelial lining. They typically grow slowly and are usually around 10cm at the time o f discovery. They can cause symptoms if they are large enough. They are solitary 80% o f the time, and have peripheral calcifications 25% o f the time.

Question 504

Hydatid or echinococcal cysts

Answer 504

third most common cystic lesion in the spleen. They are caused by the parasite Echinococcus Granulosus. Hydatid cysts consist o f a spherical “mother cyst” that usually contains smaller “daughter cysts.” Internal septations and debris are often referred to as “hydatid sand.” The “water lily sign” is seen when there is detachment o f the endocyst membrane resulting in floating membranes within the pericysts (looks like a water lily). This was classically described on CXR in pulmonary echinococcal disease.

Question 505

Splenic hemangiom

Answer 505

most common benign neoplasm in the spleen. This dude is usually smooth and well marginated demonstrating contrast uptake and delayed washout. The classic peripheral nodular discontinuous enhancement seen in hepatic lesions may not occur, especially if the tumor is smaller than 2 cm.

Question 506

Splenic lymphangiomas

Answer 506

rare entities in the spleen but can occur. Most occur in childhood. They may be solitary or multiple, although most occur in a subcapsular location. Diffuse lymphangiomas may occur (lymphangiomatosis).

Question 507

Splenic hamartomas

Answer 507

rare in the spleen, but can occur. Typically this is an incidental finding. Most are hypodense or isodense and show moderate heterogeneous enhancement. They can be hyperdense if there is hemosiderin deposition.

Question 508

Spleen littoral cell angiomas

Answer 508

zebra that shows up occasionally in books and possibly on multiple choice tests. Clinical hypersplenism is almost always present. Usually presents as multiple small foci which are hypoattenuating on late portal phase. MR shows hemosiderin : 5 ; : (low T1 & T2).

Question 509

Malignant Masses of the Spleen overview

Answer 509

Most things that occur in the spleen are benign. Other than lymphoma (discussed below) it is highly unlikely that you will encounter a primary malignancy of the spleen (but i f you do i t ’s likely to be vascular). For the purposes o f academic discussion (and possible multiple choice trivia), angiosarcoma is the most common.

Question 510

Splenic angiosarcoma

Answer 510

It is aggressive and has a poor prognosis. On CT it can manifest as a poorly defined area o f heterogeneity or low density in an enlarged spleen. They can contain necrosis and get big enough to rupture (spontaneous rupture occurs like 30% o f the time). Contrast enhancement is usually poor. Yes, these can occur from prior thorotrast exposure.

Question 511

Splenic lymphoma

Answer 511

is the most common malignant tumor o f the spleen, and is usually seen as a manifestation of systemic disease. Splenomegaly is the most common finding (and maybe the only finding in low-grade disease). Although both Hodgkins and Non-Hodgkins types can involve the spleen, Flodgkins type and high-grade lymphomas can show discrete nodules o f tumor. With regard to imaging, they are low density on CT, T1 dark, and are PET hot.

Question 512

Spleen mets

Answer 512

Metastatic Disease to the spleen is rare. When it does occur, it occurs via common things (Breast, Lung, Melanoma). Trivia: Melanoma is the most common primary neoplasm to met to the spleen.