GI Flashcards
Typical bugs of emphysematous cholecystitis?
Predisposing factor?
E. coli, klebsiella.
50% occur in diabetics. Look for intramural gas.
Positive HIDA scan- how long wait to see GB?
Predisposing factors for acalculus cholecystitis?
Presentation?
4 hours or IV morphine and no Tc99m in GB is positive.
AC- diabetes, malignancy, recent surgery or trauma, cardiac disease, ventilated, TPN.
Severity of disease often out of proportion to amount of pain (no-min pain).
What is a hepatic adenoma?
Who?
Complications?
Benign hormone-induced neoplasm- mainly hepatocytes without portal triads or bile ducts.
Young women on OCPs. Also in glycogen storage disease, steroids.
Hemorrhage / rupture. Rare malignant degeneration to hepatoma (so these come out. FNH doesn’t).
Imaging findings of hepatic adenoma?
CT: large solitary mass. Early heterogenous enhancement on arterial phase, isodense on portal phase. Rare calcs. Vascular supply tends to be peripheral (central in FNH). Hyperdense if fresh hemorrhage.
MRI: iso to hyperintense on T1, mildly hyperintense on T2. Drop signal on out of phase GRE images due to fatty hepatocytes or hemorrhage. Early enhancement with gad.
US: Well demarcated heterogenous mass.
Variable uptake on Tc99m sulfur colloid.
Differential diagnosis for linitis plastica?
Imaging appearance?
Scirrhous gastric adenocarcinoma (#1 cause, but gastric ca more often presents as ulcerated mass or polyploid lesion), lymphoma (marked mural thickening), metastatic disease (breast).
Also consider TB, radiation enteritis if history, local invasion by pancreatic ca, Crohns (rams horn with tubular Antrum narrowed pylorus).
Non-distensible stomach, featureless mucosa.
Imaging findings in graft vs host disease?
Symptoms?
Barium: marked fold and mural thickening progressing to narrow featureless ileum (ribbon like), marked separation of bowel loops.
CT: marked diffuse small vowel and colon wall thickening, +/- pneumatosis, surrounding edema.
Cramping and watery diarrhea within 100 days of BMT. It is a severe, acute enteritis. Similar appearance in radiation enteritis (often more focal, history) and UC (featureless colon, no SB).
Differential diagnosis for diffuse small bowel fold thickening?
Nodular SB folds?
Thick: MAI infection, whipple disease, lymphoma, CHF, lymphangectasia, hypoproteinemia, amyloid, mastocysosis. (Localized think infection, ischemia, neoplasm).
Nodular folds: MAI infection, whipple disease, lymphoma, lymphangectasia, eosinophilic gastroenteritis, amyloid.
Imaging appearance of whipple disease vs mycobacterium avium-intracellulare infection (pseudo whipple)?
Cause of each?
Both appear as nodular thickened small bowel folds (jejunum), mesenteric lymphadenopathy, +/- hepatosplenomegaly. In whipple disease, the nodes are usually more bulky and low attenuation (fatty). MAI, can get microabscesses in liver and spleen.
MAI infection- late complication of AIDS. Whipple- tropheryma whippelii infection. Both cause diarrhea due to malabsorption.
What is colonic urticaria?
An abnormal reticular mucosal pattern due to mucosal or submucosal edema and ischemia. Important to recognize due to ischemia.
Seen in allergic reaction to medications (normal sized colon) or in a markedly dilated colonic segment (distal obstruction, ileus).
Spectrum of disease in mesenteric panniculitis?
Typical age?
Association?
Mesenteric panniculitis (inflammation) -> mesenteric lipodystrophy (fat necrosis) -> retractile mesenteritis (fibrosis).
5-7th decades.
Small association with lymphoma.
Differential diagnosis for splenic micronodularity?
Differentiating features?
Lymphoma/leukemia- homogenous and hypoechoic on ultrasound. Fungal infections (candida in immunocompromised, histoplasmosis)- hypoechoic on us, later target appearance due to central necrosis. TB. Sarcoidosis (rare).
Mets, hemangiomas, lymphangiomas- typically fewer larger nodules. Pyogenic infections- macroabscesses.
What is Peutz-Jeghers syndrome?
Autosomal dominant with incomplete penetrance- multiple GI hamartomas (anywhere but esophagus). Presents 2nd-3rd decades.
Increased risk for GI malignancy (often distant from site of polyps, younger than usual colon CA), breast, ovarian, testicular, pancreatic cancer.
Complications- intussusception and GI bleeding. Orocutaneous hyperpigmentation.
On CT can appear as a consolidated mass in the duodenal lumen due to multiple large polyps.
What is Cronkhite-Canada syndrome?
Hyperplastic inflammatory polyps in the stomach, small bowel, and colon. Loss of hair and nails and hyperpigmentation. Protein-losing enteropathy. 5th-8th decades.
What is Cowden syndrome?
Causes hamartomas of the GI tract, tongue, and skin. Autosomal dominant, extremely rare. Increased risk for thyroid and breast cancer.
What is hyperplastic cholycystosis?
What are 2 subtypes?
Benign tissue proliferation affecting the gallbladder.
Includes adenomyomatosis (mural hyperplasia of the muscular layer and epithelial mucosa with the development of mucosa-lined diverticula Rokitansky-Aschoff sinuses) and cholesterolosis (cholesterol and triglyceride deposits in the lamina propria, aka strawberry gb).
Imaging findings in adenomyomatosis?
Differential?
Can be focal (usually in the fundus), segmental (usually in body), or diffuse.
Enhancing mural thickening plus: US: immobile, echogenic Rokitansky-Aschoff sinuses, with comet tail reverberation artifact if cholesterol crystals are present (specific).
CT: RAs are low density, surrounded by enhancing mucosa. MRI: non enhancing RAs with low T1 high T2.
Differential is gallbladder adenocarcinoma, mets (melanoma most common), polyp.
Most common cause of proximal esophageal stricture?
Barrett’s. Caustic ingestion can also cause it (~1-3 months after event).
Appearance of Barrett stricture?
Associated finding?
Cause?
More commonly distal but can be proximal. Are long, smoothly marginated, circumferential.
Associated with intramural pseudodiverticulosis (barium in dilated mucous excretory glands. Seen with other conditions too such as candida, alcohol abuse, and diabetes.)
Metaplasia of the epithelium from squamous to columnar by reflux. 10% malignant degeneration to adenocarcinoma.
Differential diagnosis for a noncalcified multilingual mass centered around the gallbladder and invading the liver?
Gallbladder adenocarcinoma vs xanthogranulomatous cholecystitis. Often associated. Both most common in women age 60-70.
Rarely, could see colon cancer invading into the gallbladder.
Ca tends to have more lymphadenopathy. XC tends to have multiple masslike loculi with thick septa around pockets of fluid density material. On ultrasound, hypoechoic mural nodules or streaks.
What is the most common mesenchymal neoplasm?
Imaging features?
Association?
Gastrointestinal stromal tumor (GIST).
Often smoothly marginated, enhancing intraluminal polypoid mass with cavitary, cystic, hemorrhagic, and/or exophytic components. Stomach most common, small bowel second. Look for irregular margination, invasion, mets in malignant degeneration.
Neurofibromatosis type 1.
What is the most common small bowel neoplasm?
Typical presentation?
Metastatic disease, often as multiple masses (melanoma).
More common than primary tumors: most common primaries are adenocarcinoma, carcinoid tumor, leiomyosarcoma, lymphoma (fyi… more commonly causes decreased peristalsis and dilation rather than stricture due to distruption of the autonomic plexus).
Differential diagnosis for a fat containing liver mass?
If growing: HCC (by far most common), liposarcoma (metastatic or less common primary), teratoma (met, direct invasion, rare primary).
If stable: angiomyolipoma, myelolipoma, lipoma.
GI imaging findings in scleroderma (progressive systemic sclerosis)?
Differentiation from celiac?
Most commonly affects esophagus, small bowel.
Esophageal dilation due to decreased peristalsis. ‘Hidebound’ small bowel: increased frequency of thin, straight folds, typically jejunal (after the onset of skin changes). Marked small bowel dilation, duodenum and jejunum. Pseudosacculations on antimesenteric side if small bowel. Can have benign pneumatosis (pneumatosis cystoides coli) and/or free air. Constipation/fecal retention.
VS celiac disease- increased number of thin folds in the ileum, decreased folds in the jejunum. Hypersecretion in celiac, not PSS.
Differential diagnosis for a cystic lesion in the spleen?
Simple cyst (commonly result of past trauma, can get rim calcifications), epidermis cysts (congenital, less commonly calcify), echinococcal cysts (often eggshell calcs, budding daughter cysts, internal septa, more common in liver), pancreatic pseudocysts (can rarely invade splenic parenchyma), abscess.
Consider pseudoaneurysm if shown round peripherally calcified structure on radiograph.
Portal venous gas vs biliary gas- which one seen more peripherally?
Portal venous gas goes to the periphery, biliary gas avoids it.
Imaging appearance of toxic mega colon?
Differential diagnosis?
1: Ulcerative colitis (May see lack of haustral folds due to chronic UC).
Pseudopolyps (remnant patches of mucosa surrounded by severely ulcerated and denuded bowel wall), thumbprinting, and marked colonic dilatation (although lack of dilatation doesn’t rule it out).
Also: Ischemic colitis, pseudomembranous colitis, Crohns, rarely TB (coned cecum more classic).
Note: barium enema absolutely contraindicated due to high risk for rupture.
Differential diagnosis for enlargement of the ileocecal valve?
Lipomatous infiltration, lipoma, adenoma. Yersinia infection, TB, amebiasis. Adenocarcinoma, lymphoma, carcinoid (prolapsing from terminal ilium). Crohn’s disease, ulcerative colitis.
What is cecal bascule?
The more rare type of cecal volvulus. A result of cranial folding of the cecum.
Radiographs show a gas collection separated from the ascending colon by a transverse fold. Less prone to rupture.
Other (usual) cecal volvulus is called axial, due to rotation around the mesentery. Only see twirl sign and beak sign with this type.
What is the name of the congenital lateral abdominal wall hernia?
Where does it occur?
Spigelian.
At the linea semilunaris, between the rectus abdominis and transversalis abdominis / internal obliques. Overlying intact external oblique muscle.
What is Mirizzi syndrome?
Gallstone lodged in the neck of the gallbladder or cystic duct, resulting in compression of the CBD.
See: Bilateral intrahepatic biliary dilatation, jaundice with acute RUQ pain, and the stone. CBD diameter normal at or below the level of the cystic duct.
Diagnosis?
Linitis plastica.
DIfferential: gastric adenocarcinoma, mets (breast, lung), lymphoma, inflammatory.
Diagnosis?
Graft vs host disease.
Edema in small bowel folds- “ribbon” appearance on barium studies. Wall thickening on CT.
RLQ ultrasound, appendix is normal. Diagnosis? Other findings?
Mesenteric adenitis (3+ nodes with diameter of at least 5 mm).
May see ileal or ileocecal wall thickening.
When mesenteric adenitis or appendicitis occurs in childhood or adolescence, therer is a significantly reduced risk of ulcerative colitis later in life.
Diagnosis?
Epiploic appendagitis. Most common location is adjacent to the sigmoid colon.
Differential includes segmental omental infarct.
Diagnosis?
Adenomyomatosis.
Diagnosis?
Scleroderma (stacks of thin, straight duodenal and jejunal folds).
Diagnosis?
Toxic megacolon- a complication of UC/Crohn’s, infectious colitis, other types of colitis.
Colon (typically transverse) becomes markedly dilated with loss of haustral markings, pseudopolyps extending into the lumen. Thumbprinting from mucosal edema may be present.
Barium studies should be avoided, due to the risk of perforation.
Diagnosis? Why might this patient have pain in the inner thigh?
Obturator foramen hernia. Bowel through the obturator canal between the pectineus and external obturator muscle. Compression of the obturator nerve can cause pain along the inner thigh (Howship-Romberg sign).
Diagnosis? What is this?
Presentation?
Complications?
Choledocal cyst. Congenital defect caused by an anomalous unction of the common bile duct and pancreatic duct proximal to the normal location at the papilla. Reflux of digestive pancreatic enzymes into the CBD results in gradual bile duct distention.
More common in women. Usually presents in infancy or childhood. May see RUQ pain/colic, jaundice, fever, palpable RUQ mass. Surgical treatement with construction of a biliary-enteric anastomosis.
Complications- rupture, bleeding, cholangitis, pancreatitis, stones, malignancy (gallbladder adenocarcinoma, cholangiocarcinoma).
Broken down into multiple types (1 most common) based on location and types of dilitation.
What is the most common congenital GI anomaly?
Presentation?
Meckel diverticulum. Rule of 2s: 2 (-3)% of the population, 2 ft from the ileocecal valve, 2 in long, 2 years old (but can present later).
A true diverticulum (all layers of GI tract)- an antimesenteric ileal outpouching caused by failure of the omphalomesenteric duct to completely close. Bleeding can result from ectopic gastric mucosa causing ulceration (seen on technetium-99m pertechnetate scans). Often presents with bleeding in kids, diverticulitis (see pic below) or obstruction in adults.
Diagnosis?
Caroli disease. (with PKD)
Diagnosis?
Associations?
Multiple biliary hamartomas (von Meyenburg complexes). Small disorganised clusters of dilated cystic bile ducts (smal ductal plate malformations- the same thing that gets messed up in Caroli disease). Generally do not communicate w/ biliary tree. Asymptomatic and usually found incidentally.
Associated with autosomal dominant polycystic kidney disease, polycystic liver disease.
Radiographic findings can be non-specific and may be hard to differentiate from metastases and micro-abscesses. CT- hypoattenuating and often show no enhancement. MRI- T1 hypo, T2 hyperintense, usually no enhancement.
Diagnosis?
Imaging features?
Presentation?
Differential?
Sclerosing cholangitis (primary if idiopathic). Inflammation and sclerosis of the intra- and extrahepatic bile ducts.
Multifocal ductal stenoses (beaded appearance), pruning of peripheral ducts, ductal pseudo-diverticula, filling defects, wall thickening.
Presentation- men
Differential: acute pyogenic cholangitis (acute presentation, w/ obstruction), recurrent pyogenic cholangitis, AIDS-related cholangiopathy, PBC (only affects intrahepatic ducts though)
Differential?
Cone shaped cecum.
Infectious: blastomycosis, amebiasis, Yersinia enterocolitis, tuberculosis, typhoid fever, cytomegalovirus (CMV).
Inflammatory: inflammatory bowel disease (IBD), appendicitis w/ abscess, typhilitis, diverticulitis.
Tumoral: lymphoma, colonic adenocarcinoma, metastasis.
29 yr old female. Diagnosis?
Endometriosis.
Rectosigmoid colon is the most common location for bowel involvement, but can see small bowel, cecum, appendix.
Also consider abscess, serosal metastatic implants, or adjacent pelvic tumor.
Diagnosis?
What is it?
Other imaging features?
Serous cystadenoma (aka microcystic adenoma).
A benign tumor made up of small epithelial-lined cysts that contain protein rich fluid. No malignant potential. Females > 60, often asymptomatic. Association with von Hippel-Lindau.
Well-circumscribed pancreatic mass made up of multiple very small cysts. Honeycomb-like formation / central scar. Rarely can be macrocystic (oligocystic variant). Occasional punctate calcifications. Moderate enhancement.
Connects with the main pancreatic duct. Diagnosis?
MRI appearance?
Presentation?
Intraductal papillary mucinous neoplasm (IPMN), branch type. (Diffuse affects long segment of the main duct- diffuse ductal dilitation)
T1 hypointense, T2 hyperintense, no enhancement. Can have amorphous calcifications at the periphery of the lesion on CT.
More common in men. If symptoms, due to pancreatic duct obstruction (diarrhea, back pain, diabetes, pancreatitis). Differential includes pancreatic pseudocyst, mucinous cystic neoplasm. Malignant potential- mass component, enhancement.
Diagnosis?
Retroperitoneal fibrosis.
Most commonly idiopathic, postulated to be immune-mediated. Treatment- surgical lysis of the fibrous tissue causing symptoms.
Tends to encase structures rather than invading or displacing them (like soft tissue sarcomas would).
Diagnosis?
Cause?
Feline esophagus.
Transient contraction of the longitudinal muscularis mucosa. Asymptomatic but may indicate gastroesophageal reflux. Distal 2/3 of esophagus.
Diagnosis?
Cause?
Hypertrophic gastritis- enlarged areae gastricae and thickened rugal folds.
Hyperplasia of the gastric glandular epithelium, thought to be caused by chronic inflammation (ex h pylori).
Diagnosis? What is this?
Who?
Associations?
FNH.Disorganized, non-neoplastic liver tissue with central arteries (scar) and no portal supply. Benign. Growth can cause pain.
Younger women (20-40).
Small association with hemangiomas, intracranial berry aneurysms, and sickle cell anemia.
Diagnosis?
Presentation?
Spider web collaterals in Budd-Chiari syndrome.
Depends on acuity. Acute: no collaterals yet, nausea, vomiting, abdominal pain, abdominal distention from rapid onset ascites. Subacute: less marked ascites. Chronic: present with features of cirrhosis and portal HTN.
No infectious signs, no primary malignancy. Diagnosis?
Other imaging features?
Differential?
Biliary cystadenoma. Benign tumor of bile duct origin with mucin-containing cysts, usually presents in middle age. Rare degeneration to mucinous cystadenocarcinoma.
Uni- or multiloculated, smoothly marginated, cystic mass. Can get quite large. Variable internal characteristics depending on the amount of mucin, bile, or blood. MRI: T1 hypo, T2 hyperintense.
Differential: simple cyst, echinococcal cyst (“water lily sign” on MRI- curvilinear internal membranes, may be rim calcs, budding daughter cysts), abscess, mesenchymal hamartoma (presents in childhood), cystic HCC or mets.
Diagnosis?
US and CT findings?
Differential?
Hemochromatosis. Markedly decreased T2 signal intensity in the liver (and pancreas if primary, and spleen if secondary)
On US, the liver would appear coarse if primary, normal if secondary. CT- nonspecific diffuse hyperattenuation in the liver.
Differential: Differentiate from fatty infiltration on T2 fat sat images by looking for characteristic fat-sparing regions and less marked T2 signal loss. CT appearance of hyperattenuation is nonspecific, and can be seen in glycogen storage diseases, amiodarone, Wilson disease, and gold treatment for RA.
Diagnosis?
Cause?
Pseudomyxoma peritonei. Ruptrue of mucinous adenocarcinoma or peritoneal carcinomatosis leading to gradual filling of the peritoneum with gelatinous material.
Scalloping of the liver, diffuse, septated low-density material throughout the abdomen. May see curvilinear calcification (pathognomonic).
Cuases: ovarian mucinous cystadenocarcinoma (most common), appendiceal mucinous adenocarcinoma, adenocarcinoma of the stomach or colon, mucinous tumors of the pancreas.
What should this lesion look like on sulfur colloid scan?
FNH- The presence of Kupffer cells allows these lesions to take up Tc-99m sulphur colloid. Positive scans in 80% of lesions. This is helpful in distinguishing them from hepatic adenomas, HCC and hepatic metastases which do not contain Kupffer cells. (may be especially helpful in atypical FNH which doesn’t have the central scar b/c no central artery)
What determines the T portion of the TMN staging for RCC?
Note- involvement of the adrenal gland (T4) gives you stage 4 disease.
3b vs 3c is very important… because 3c involves the IVC above the diaphragm, thoracic surgeons will need to be involved.
What are the Bosniak criteria?
Management recommendations for patients with cystic renal mass.
Examples of Bosniak 3 lesions: multilocular cystic nephroma, cystic RCC. In Kids: cystic Wilms, clear cell sarcoma, cystic mesoblastic nephroma, segmental multicystic dysplastic kidney (ectopic ureterocele).
Bosniak 4 lesions… think cystic or necrotic RCC.
