GI Flashcards
Location
H pylori gastritis
usually antrum
Location
Zollinger-Ellison
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.
Location (stomach)
Crohns
Uncommon in the stomach, but when it is, it likes the antrum
Location
Menetrier’s
Usually in the Fundus (classically spares the antrum)
Location
Lymphoma
Crosses the Pylorus” - classically described as doing so, although in reality adenocarcinoma does it more.
FAP
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)
HNPCC (Lynch)
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)
Gardner Syndrome
FAP + Desmoid Tumors, Osteomas, Papillary Thyroid Cancer
Turcots
FAP + Gliomas and Medulloblastomas
Peutz-Jeghers
Hamartoma Style!
Mucocutaneous Pigmentation (gross Dalmatian dog lips)
Small and Large Bowel CA, Pancreatic CA, and GYN CA
Cowden
Hamartoma Style!
BREAST CA, Thyroid CA,
Lhermitte-Duclos (posterior fossa noncancerous brain tumor)
Hamartoma Style!
Cronkhite-Canada
Hamartoma Style!
Stomach, Small Bowel, Colon,
Ectodermal Stuff (skin, hair, nails, yuck)
Juvenile Polyps
Hamartoma Style!
Increased risk for colorectal and gastric cancer (different than sporadic juvenile polyps -which are typically solitary and benign)
Stomach ulcer
Malignant
Width > depth
located within lumen
nodular irregular edges
folds adjacent to ulcer
aunt minnie: carmen meniscus sign
can be anywhere
Stomach Ulcers
benign
Depth>Width
Project beyond the expected lumen
sharp contour
folds radiate to ulcer
Aunt minnie: hamptons line
mostly on lesser curvature
GIST
overview
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).
Gist
Tricks to know
• 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
Carneys triad
“Carney’s Eat Garbage”
Chondroma (pulmonary)
Extra Adrenal Pheo
GIST
Gastric “Cancer” is either
Lymphoma (<5%) or Adenocarcinoma (95%)…. Rarely a malignant GIST.
Gastric adenocarcinoma
overview
is usually a disease of an old person (median age 70).
H. Pylori is the most tested risk factor.
Gastric adenocarcinoma
trivia to know
• 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.
Gastric Adenocarcinoma
The look
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
Ulcer Trivia:
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….
Gastric Lymphoma
overview
can be primary (MALT), or secondary (systemic lymphoma). The stomach is the
most common extranodal site for non-Hodgkin lymphoma.
Gastric Lymphoma
even when extensive
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.
Gastric Lymphoma
looks like
Has multiple looks and can be big, little, ulcerative, polypoid, or look like target lesions. It can also look like Linitis Plastica
Gastric Lymphoma
Trivia
it can rupture with treatment
Gastric Cancer is “More Likely” Than Lymphoma to…
- 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)
Mets to the Stomach: This is actually very rare.
Melanoma
Breast
Lung
Mets to the Stomach:
Melanoma
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.
Mets to the Stomach:
Breast and lung
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
Chronic Aspirin Therapy
“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.
If you see multiple duodenal ulcers (most duodenal ulcers are solitary) you should think
ZE
Areae Gastricae
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.
Menetrier’s Disease
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.
Menetrier’s Disease
Essential trivia
inolves the fundus and spares the antrum
Ram’s Horn Deformity (Pseudo Billroth I)
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.
Ram’s Horn Deformity (Pseudo Billroth I)
Essentrial trivia
The stomach is the most common GI tract location for sarcoid.
Gatric volvulus
Organoaxial
the greater curvature flips over the lesser
curvature. This is seen in old ladies with paraesophageal hernias. It’s way more common.
Gastric volvulus
meseneroaxial
twisting over the mesentery. Can cause ischemia and needs to be fixed. Additionally this type causes obstruction. This type is more common in kids.
Gastric Diverticulum
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.
Gastric Varices
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.
Bilroth 1
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)
Bilroth 2
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
Roux-en-y
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.
Dumping syndrome
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).
Afferent Loop Syndrome
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.
Jejunogastric Intussusception
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.
Bile Reflex Gastritis:
Fold thickening and filling defects seen in the stomach after Billroth 1 or II are likely the result o f bile acid reflux.
Gastro-Gastric Fistula
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.
Cancer after gastric surgery
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).
Dumping Syndrome 2
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).
Small bowel follow through
Steps
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
SBFT step 1
thin <3mm, straight folds with dilation
Mechanical Obstruction
Paralytic Ileus
Scleroderma
Sprue
SBFT step 1
thick straight folds >3mm
segmental distribution
Ischemia
Radiation
Hemorrhage
Adjacent Inflammation
SBFT step 1
thick straight folds >3 mm
diffuse distribution
Low Protein
Venous Congestion
Cirrhosis
SBFT step 1
thick folds with nodularity
segmental distribution
Crohns
Infection
Lymphoma
Mets
SBFT step 1
thick folds with nodularity diffuse distribution
Whipples Lymphoid Hyperplasia Lymphoma Mets Intestinal Lymphangiectasia
SBFT step 2a
loop seperation without tethering
• Ascites, • Wall Thickening (Crohns, Lymphoma), • Adenopathy • Mesenteric Tumors
SBFt step 2a
loope separation with tethering
Tethering looks like someone is pinching and pulling the loops towards the displacing mass.
• Carcinoid
SBFT Step 2b
sand like nodules
Diffuse nodules in the jejunum
whipples (tropheryma whipplei)
pseudo whipples (MAC)
SBFT Step 2b
uniform 2-4 mm nodules
Lymphoid Hyperplasia
SBFT Step 2b
nodules of larger or varying sizes
Cancer - th in k M e ts (M e la n om a )
SBFT Step 2b
cobblestoning
- 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
SBFT Step 3
ribbon bowel
bowel is featureless, atrophic, and has fold thickening (ribbon-like).
Graft Vs Host
SBFT Step 3
hidebound bowel
Narrow separation of normal folds with mild bowel dilation.
Scleroderma
SBFT Step 3
Moulage sign (tube of wax)
Dilated jejunal loop with complete loss of
jejunal folds - opacified like a “tube o f wax”
Celiac
SBFT Step 3
Fold reversal
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
SBFT Step 3
Freaking worm
Thread like defect in the barium column
ascaris suum (demon worm)
Small bowel path
The target sign
’ Single Target: GIST, Primary Adenocarcinoma, Lymphoma, Ectopic Pancreatic Rest, Met (Melanoma).
’Multiple Target: Lymphoma, Met (Melanoma)
Small bowel path
clover leaf sign
This is an Aunt Minnie for Healed Peptic Ulcer of the Duodenal Bulb.
Small bowel path
Whipples
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.
Small bowel path
Buzzword for whipples
“sand like nodules” referring to diffuse micronodules in the jejunum.
Small bowel path
Pseudo whipples
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).
Small bowel path
Intestinal lymphangiectasia
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).
Small bowel path
Graft vs Host
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).
Small bowel path
graft vs host buzzword
ribbon bowel
Small bowel path
SMA Syndrome
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.
Small bowel path
Celiac sprue
Small bowel malabsorption of gluten
Small bowel path
Celiac sprue high yeild points
- 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)
Small bowel path
Celiac sprue findings on CT/Barium
- 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
Small bowel path
M e c k e l’s D iv erticu lum I D iv e rtic u litiss
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).
Small bowel pathM e c k e l’s D iv erticu lum I D iv e rtic u litis
high yield trivia
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
Small bowel path
Duodenal In flam m a to ry Disease:
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.
Small bowel path
Jejunal diverticulosis
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).
Small bowel path
Gallstone ileus
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.
Small bowel path riglers triad
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.”
Direct signs of bowel trauma
Spilled oral contrast
active mesentric bleed
indirect signs of bowel trauma
fat stranding
fluid layering along the bowel
Shock Complex Features
• 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
“Shock Bowel” “Hypovolemic Shock Complex”
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.
Bowel Trauma vs shock bowel findings
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…)
Small bowel cancer
Adenocarcinoma
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.
Small bowel cancer
adenocarcinoma gamesmanship
Adenocarcinoma is more likely to obstruct relative to lymphoma.
Small bowel cancer
Lymphoma
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..
Small bowel cancer
lymphoma key triia
do not obstruct even with massive circum involvement
Small bowel cancer
trivia
favors the ileum
Small bowel cancer
gamesmanship
obstruction is rare
Small bowel cancer
Carcinoid
aunt minnie
a mass + desmoplastic stranding. “Starburst” appearance of the mesenteric mass with calcifications.
Small bowel cancer
carcinoid
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
Small bowel cancer
carcinoid most common primary location
distal ileum
Small bowel cancer
Mets
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.
Most common type of abdominalhernia
inguinal M>F (7:1)
femoral hernia
Likely to obstruct. Seen in old ladies. They are medial to the femoral vein, and posterior to the inguinal ligament (usually on the right).
Obturator hernia
Another old lady hernia. Often seen in patients with increased intra-abdominal pressure (Ascites, COPD - chronic cougher). Usually asymptomatic - but can strangulate.
Direct inguinal hernia
Less common
Medial to inferior epigastric artery
Defect in Hesselbach’s Triangle
NOT covered by internal spermatic fascia
Indirect inguinal hernia
More Common
Lateral to inferior epigastric artery
Failure of processus vaginalis to close
Covered by internal spermatic fascia
Lumbar Hernia
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).
Spigelian Hernia
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.
Littre hernia
hernia with a meckedl diverticulum in it
amyand hernia
hernia with the appendix in it
Richter hernia
Contains only one wall of bowel and therefore does not obstruct. This are actually at higher risk for strangulation.
Hernias Post laparoscopic Roux-en-Y Gastric Bypass
Factors that promote internal hernia after gastric bypass
(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.
Hernias Post laparoscopic Roux-en-Y Gastric Bypass
There are 3 potential sites
(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.
Internal Hernias
overviews
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.
Internal Hernias
General concept
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.
Internal Hernias
Paraduodenal
overview
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.
Paraduiodenal leftsided hernia
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.
Paraduodenal right sided hernia
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.
Crohns disease
overview
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.
Crohns disease
squaring of the folds
An early manifestation from obstructive lymphedema
Crohns disease
skip lesions
Discontinuous involvement o f the bowel
Crohns disease
proud loops
Separation of the loops caused by infiltration o f the mesentery, increase in mesenteric fat and enlarged lymph nodes
Crohns disease
cobblestoning
Irregular appearance to bowel wall caused by longitudinal and
transverse ulcers separated by areas o f edema
Crohns disease
pseudopolyps
Islands of hyperplastic mucosa
Crohns disease
Filiform
Post-inflammatory polyps - long and worm-like
Crohns disease
pseudodiverticula
Found on anti-mesenteric side. From bulging area of normal wall opposite side o f scarring from disease
Crohns disease
string-sign
Marked narrowing of terminal ileum from a combination of edema, spasm, and fibrosis
IBD trivia associating
increased risk of melanoma
UC overview
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).
UC Barium
On Barium, it is said that the colon is ahaustral, with a diffuse granular appearing mucosa. “Lead Pipe” is the buzzword (shortened from fibrosis).
UC key clinical point
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.
More common in crohns vs UC
Gallstones
PSC
Hepatic Abscess
Pancreatities
Gallstones Crohns
PSC UC
Hepatic Abscess Crohns
Pancreatities Crohns
Cronhs this vs that
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
UC this vs that
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
Toxic Megacolon
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.
Behcets
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).
Diverticulosis/Dviverticulitis
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..).
Epiploic appendagitis
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.
Appendicitis
steps
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).
appendix mucocele
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.
Omental infarction
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.
Appenix ages
It occurs in an adolescent or young adult (or any age).
appendix ct
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.
appendix gamesmanship
In pregnancy MRI without contrast is the test of choice
sigmoid colonic volvulus
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%.
cecal colonic volvulus
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.
Cecal bascule colonic volvulus
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.
Colonic Pseudo-Obstruction
(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.
Diversion colitis
Bacterial overgrowth in a blind loop through which stool does not pass (any surgery that does this).
Colitis cystica
superficial
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.
Colitis cystica
deep
These cysts may be large and are seen in the pelvic colon and rectum.
Rectal cavernous hemangioma
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.
Gossypiboma
It’s a retained cotton product or surgical sponge and it can elicit an inflammatory response.
Entamoeba Histolytica
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.
Entamoeba histolytica
barium
the buzzword is “conedcecum” referring to a change in the normal bulbous appearance of the cecum, to that of a cone.
Colonic TB
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.
Infections tht like the duodenum and proximal small bowel
Giardia
strongyloides
infections that like the TI
TB
Yersinia
This vs that sigmoid vs cecal
sigmoid - old person, points to the RUQ
cecal - younger person, points to the LUIQ
colonic CMV
Seen in patients who are immunosuppressed. Causes deep ulcerations - which can lead to perforation. Step 1 question = Cowdry Type A intranuclear inclusion bodies
C-DIFF
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.
Neutropenic Colitis (Typhlitis):
Infection limited to the cecum occurring in severe neutropenia.
Colon Cancer
adenocarcinoma
overview
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.
Colon Cancer
adenocarcinoma
gamesmanship
Large bowel intussusception in adult = Malignancy
Colon Cancer
adenocarcinoma
gamesmanship 2
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.
Colon Cancer
squamos cell carcinoma
occasionally in the anus (HPV)
Rectal Cancer Trivia
- 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).
nodes in perirectal fat are abnormal when
> 5mm
High rectal cancer
- Treated with Low Anterior Resection (LAR)
- These patients will maintenance fecal
continence post op
Low rectal cancer
- Treated with Abdomino- Perineal Resection (APR)
- These poor bastards will end up with colostomies
Rectal Cancer surgery
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).
Colon lipomas
Second most common tumor in the colon
Colon adenomas
The most common benign tumor of the colon and rectum. The villous adenoma has the largest risk fo r malignancy.
McKittrick-Wheelock Syndrome:
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.
Pseudomyxoma Peritonei
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
Peritoneal carcinomatosis
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.
Omental seeding/caking
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.”
Primary peritoneal mesothelioma
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.
Cystic peritoneal mesothelioma
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).
Mesenteric Lymphoma
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.”
Barium peritonitis
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).
Barium intravasation
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).
Liver bare area
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.
Couinaud system
testable trivia
- 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.
Cantlies line
divides the liver into a functional left and right hepatic lobes.
This line runs from the IVC to the middle of the gallbladder fossa.
Caudate Lobe
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…
Liver trivia 1
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).
Liver trivia 2
Most common vascular variant = Replaced right hepatic (origin from the SMA)
Liver trivia 3
Most common biliary variant = Right posterior segmental into the left hepatic duct.
Liver Normal MRI Signal Characteristics
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
Liver fetal circulation
Placenta > Umbilical Vein > Liver > IVC
Placenta > Umbilical vein > Ductus Venosus (remnant of ligamentum venosum) > IVC
Liver us trivia
Pancreas should be more echogenic than liver
classic liver ultrasound anatomy
pic 1 Pancreas
Anterior to posterior
Pancreas Splenic vein SMA LRV to the IVC on the pts right Aorta Vert Body
classic liver ultrasound anatomy
pic 2 porta hepatis
Anterior to posterior
CBD
RHA
PV
Liver pic three porta hepatis mickey mouse
Left ear Bile duct
Right hear hepatic artery
Head portal vein
Another consequences of the Longer Right Portal Vein Course is that Hepatic Abscess (often from ascending hematogenous sources) nearly always (75%+) involves
right hepatic lobe
Cirrhosis most common cause
us
world
etoh
schistosomiasis
portal htn measurements
portal vein pressure 6-8 mmhg above hepatic veins
variceal bleeding and ascites around >12mmhg
prehepatic causes of portal htn
portal vein thrombosis
tumor compression
hepatic causes of portal htn
cirrhosis
schistosomiasis
posthepatic causes of portal htn
budd chiari
prehepatic portal htn collateral
form above the diaphragm
THAD overview
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.
