GI

Question 1

Typical bugs of emphysematous cholecystitis?

Predisposing factor?

Answer 1

E. coli, klebsiella.

50% occur in diabetics. Look for intramural gas.

Question 2

Positive HIDA scan- how long wait to see GB?

Predisposing factors for acalculus cholecystitis?

Presentation?

Answer 2

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).

Question 3

What is a hepatic adenoma?

Who?

Complications?

Answer 3

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).

Question 4

Imaging findings of hepatic adenoma?

Answer 4

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.

Question 5

Differential diagnosis for linitis plastica?

Imaging appearance?

Answer 5

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.

Question 6

Imaging findings in graft vs host disease?

Symptoms?

Answer 6

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).

Question 7

Differential diagnosis for diffuse small bowel fold thickening?

Nodular SB folds?

Answer 7

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.

Question 8

Imaging appearance of whipple disease vs mycobacterium avium-intracellulare infection (pseudo whipple)?

Cause of each?

Answer 8

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.

Question 9

What is colonic urticaria?

Answer 9

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).

Question 10

Spectrum of disease in mesenteric panniculitis?

Typical age?

Association?

Answer 10

Mesenteric panniculitis (inflammation) -> mesenteric lipodystrophy (fat necrosis) -> retractile mesenteritis (fibrosis).

5-7th decades.

Small association with lymphoma.

Question 11

Differential diagnosis for splenic micronodularity?

Differentiating features?

Answer 11

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.

Question 12

What is Peutz-Jeghers syndrome?

Answer 12

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.

Question 13

What is Cronkhite-Canada syndrome?

Answer 13

Hyperplastic inflammatory polyps in the stomach, small bowel, and colon. Loss of hair and nails and hyperpigmentation. Protein-losing enteropathy. 5th-8th decades.

Question 14

What is Cowden syndrome?

Answer 14

Causes hamartomas of the GI tract, tongue, and skin. Autosomal dominant, extremely rare. Increased risk for thyroid and breast cancer.

Question 15

What is hyperplastic cholycystosis?

What are 2 subtypes?

Answer 15

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).

Question 16

Imaging findings in adenomyomatosis?

Differential?

Answer 16

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.

Question 17

Most common cause of proximal esophageal stricture?

Answer 17

Barrett’s. Caustic ingestion can also cause it (~1-3 months after event).

Question 18

Appearance of Barrett stricture?

Associated finding?

Cause?

Answer 18

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.

Question 19

Differential diagnosis for a noncalcified multilingual mass centered around the gallbladder and invading the liver?

Answer 19

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.

Question 20

What is the most common mesenchymal neoplasm?

Imaging features?

Association?

Answer 20

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.

Question 21

What is the most common small bowel neoplasm?

Typical presentation?

Answer 21

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).

Question 22

Differential diagnosis for a fat containing liver mass?

Answer 22

If growing: HCC (by far most common), liposarcoma (metastatic or less common primary), teratoma (met, direct invasion, rare primary).

If stable: angiomyolipoma, myelolipoma, lipoma.

Question 23

GI imaging findings in scleroderma (progressive systemic sclerosis)?

Differentiation from celiac?

Answer 23

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.

Question 24

Differential diagnosis for a cystic lesion in the spleen?

Answer 24

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.

Question 25

Portal venous gas vs biliary gas- which one seen more peripherally?

Answer 25

Portal venous gas goes to the periphery, biliary gas avoids it.

Question 26

Imaging appearance of toxic mega colon? Differential diagnosis?

Answer 26

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). #1: Ulcerative colitis (May see lack of haustral folds due to chronic UC). Also: Ischemic colitis, pseudomembranous colitis, Crohns, rarely TB (coned cecum more classic). Note: barium enema absolutely contraindicated due to high risk for rupture.

Question 27

Differential diagnosis for enlargement of the ileocecal valve?

Answer 27

Lipomatous infiltration, lipoma, adenoma. Yersinia infection, TB, amebiasis. Adenocarcinoma, lymphoma, carcinoid (prolapsing from terminal ilium). Crohn's disease, ulcerative colitis.

Question 28

What is cecal bascule?

Answer 28

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.

Question 29

What is the name of the congenital lateral abdominal wall hernia? Where does it occur?

Answer 29

Spigelian. At the linea semilunaris, between the rectus abdominis and transversalis abdominis / internal obliques. Overlying intact external oblique muscle.

Question 30

What is Mirizzi syndrome?

Answer 30

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.

Question 31

Diagnosis?

Answer 31

Linitis plastica. DIfferential: gastric adenocarcinoma, mets (breast, lung), lymphoma, inflammatory.

Question 32

Diagnosis?

Answer 32

Graft vs host disease. Edema in small bowel folds- "ribbon" appearance on barium studies. Wall thickening on CT.

Question 33

RLQ ultrasound, appendix is normal. Diagnosis? Other findings?

Answer 33

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.

Question 34

Diagnosis?

Answer 34

Epiploic appendagitis. Most common location is adjacent to the sigmoid colon. Differential includes segmental omental infarct.

Question 35

Diagnosis?

Answer 35

Adenomyomatosis.

Question 36

Diagnosis?

Answer 36

Scleroderma (stacks of thin, straight duodenal and jejunal folds).

Question 37

Diagnosis?

Answer 37

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.

Question 38

Differential diagnosis for retropharyngeal gas on a lateral radiograph? What is a Zenker diverticulum?

Answer 38

Zenker diverticulum, pharyngeal perforation, retrotracheal abscess. Consider ulceration due to infection or neoplasm. ZD- herniation of the mucosa and submucosa at the cricopharyngeus muscle in the midline of the Killian dehiscence. (versus a Killian-Jamieson diverticulum, smaller and occur laterally or anterolaterally).

Question 39

Differential diagnosis for a smoothly marginated mass in the mesentery?

Answer 39

#1: **GIST**. Smoothly marginated mass with heterogeneous enhancement. Can be a primary neoplasm or a met from stomach/small bowel. Treat with resection and KIT inhibitor. **Desmoid tumor** (mesenteric fibromatosis). Large, well-circumscribed with heterogeneous or homogeneous enhancement. Most common in younger women (20-40), may be sporatic, after trauma/pregnancy, or part of Gardner syndrome. **Soft-tissue sarcoma** (leiomyosarcoma, liposarcoma, fibrosarcoma). Could also consider lymphoma (would see other lymphadenopathy), mets (less likely well circumscribed.

Question 40

What are the types of pelvic external hernias?

Answer 40

**Inguinal hernia:** usually acquired. Indirect (lateral to inferior epigastric vessels) vs direct (medial, often through defect in Hesselbech triangle). **Femoral hernia:** through the femoral canal. **Obturator hernia:** usually right-sided in thin, elderly women. Through obturator canal between the pectineus and external obturator muscles. **Sciatic hernia:** Rare. Through the sciatic foramen to a potential space deep to the gluteus muscles. **Perineal hernia:** Rare. Through the pelvic floor musculature, herniated structures can be seen adjacent to the distal rectum.

Question 41

Diagnosis? Why might this patient have pain in the inner thigh?

Answer 41

**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).

Question 42

Diagnosis? What is this? Presentation? Complications?

Answer 42

**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.

Question 43

What is the most common congenital GI anomaly? Presentation?

Answer 43

**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.

Question 44

Imaging features of intrahepatic cholangiocarcinoma? Predisposing factors?

Answer 44

US: biliary ductal dilitation, may or may not see hyperechoic mass, abrupt transition from dilated to nondilated bile ducts. CT: mass with indistinct margins (no capsule), hypodense on noncontrast, enhancing mass with persistent enhancement on delayed imaging (vs HCC which washes out). May see retraction of the liver capsule (tends to cause fibrosis). This is an adenocarcinoma originating from biliary epithelial cells. Predisposing factors include chronic biliary infections or inflammation (infection, UC, choledochal cyst, cholangitis, PBC).

Question 45

Differential diagnosis for strictures of the terminal ileum and cecum?

Answer 45

Inflammatory bowel disease: **Crohn disease** (chronic stage. more acutely look for ulcers, skip lesions, cobblestoning, pseudodiverticula, pseudopolyps, creeping mesenteric fat- lots of fat b/t bowel loops, thickened bowel wall), **ulcerative colitis** with backwash ileitis. Infections that mimic CD: **TB** (mimics CD but no history of IBD, no polyps), ***Yersinia*** (similar, both have aphthous ulcers, resolves in 2-4 mo w/ abx, polyps rare), actinomycosis, histoplasmosis. Neoplasm: lymphoma (less likely to cause luminal narrowing).

Question 46

What is Caroli disease? Caroli syndrome? Association? Presentation?

Answer 46

Autosomal recessive, belongs to the spectrum of fibropolycystic liver disease, due to in utero malformation of the ductal plate (hepatic precursor cells). **Multifocal cystic dilatation of segmental intrahepatic bile ducts. **(Caroli syndrome when hepatic fibrosis too) Association with polycystic kidney disease, medullary sponge kidney. Increased risk ( Presentation is in childhood or young adulthood. Jaundice, elevated bilirubin and transaminases, RUQ pain, fever.

Question 47

Diagnosis?

Answer 47

Caroli disease. (with PKD)

Question 48

Diagnosis? Associations?

Answer 48

**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.

Question 49

Differential diagnosis for omental caking and peritoneal soft tissue infiltration?

Answer 49

Peritoneal carcinomatosis, primary peritoneal carcinoma (look at ovaries), peritoneal malignant mesothelioma. Consider pseudomyxoma peritonei if just low density material throughout the abdomen, look for semicircular calcifications and an ovarian, pancreatic, or colonic prinmary. Rarely disseminated infections such as TB and histoplasmosis can cause this. Leiomyomatosis peritonealis disseminata (diffuse abdominal soft-tissue infiltration, an incidental finding in young pregnant women with a history of contraceptive use and fibroids).

Question 50

Differences between sclerosing cholangitis and primary biliary cirrhosis?

Answer 50

Sclerosing cholangitis- men \< 45, involves intra and extra-hepatic bile ducts. Associated with UC. PBC- women, limited to intrahepatic ducts.

Question 51

Diagnosis? Imaging features? Presentation? Differential?

Answer 51

**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)

Question 52

What is primary biliary cirrhosis? Presentation? Lab test? Associations?

Answer 52

**PBC:** a chronic progressive cholestatic liver disease. _Destruction of small intrahepatic bile ducts, portal inflammation, and progressive scarring_- cause unknown, likely autoimmune. Middle-aged woman. Presentation: fatigue and pruritus, laboratory test evidence of cholestasis. _Serum anti-mitochondrial antibody_ tests are highly sensitive and specific for PBC Associations: other autoimmune diseases, such as thyroiditis, systemic sclerosis.

Question 53

Differential?

Answer 53

_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.

Question 54

Differential diagnosis for a duodenal polyp?

Answer 54

_Adenoma_ (usually periampullary, solitary unless FAP, can also be seen in the small bowel), _brunner gland hamartoma_ (proximal duodenum, may be heterogeneous on CT), _lipoma_, _leiomyoma_. If cystic: _duplication cyst_, _choledochocele_, hamartoma, cystic degeneration of neoplasm. Lymphoma, adenocarcinoma, GIST, carcinoid, met. Multiple: syndromes: FAP, brunner gland hyperplasia, peutz-jeghers, lymphoid hyperplasia.

Question 55

What is a gastrinoma? How often malignant? Imaging? Location?

Answer 55

A **functional islet cell tumor** that produces gastrin. Gastrin stimulates marked gastric hydrochloric acid release (Zollinger-Ellison syndrome) and causes hypersecretion and ulcers. Malignant in 60%. Imaging: small, homogeneously enhancing mass. Low T1, very high T2. Can localize with somatostatin receptor scintigraphy. Typical locations: pancreas \> duodenum \> liver \> lymph nodes. Rarely stomach, omentum, ovaries.

Question 56

29 yr old female. Diagnosis?

Answer 56

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.

Question 57

Most common type of gastric polyp? Cause?

Answer 57

**Hyperplsatic polyps** (up to 90%). A result of chronic gastritis. Can be seen in any age. Vary in size, may be multiple, can be anywhere but most in body.

Question 58

Diagnosis? What is it? Other imaging features?

Answer 58

**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.**

Question 59

What is the most common type of esophageal cancer?

Answer 59

Squamous cell carcinoma: 81-95% (secondary to smoking/alcohol). Adenocarcinoma: 4-19% (within barrett, typically lower). Other types: mucoepidermoid carcinoma, adenoid cystic carcinoma (ACC), spindle-cell (tends to expand lumen without obstructing), leiomyosarcoma, rhabdomyosarcoma, fibrosarcoma, lymphoma, melanoma.

Question 60

What is the most common cystic lesion in the pancreas?

Answer 60

Pseudocysts from pancreatitis (90%).

Question 61

Connects with the main pancreatic duct. Diagnosis? MRI appearance? Presentation?

Answer 61

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.

Question 62

What is an inflammatory esophagogastric polyp? Inflammatory myofibroblastic pseudotumor? Fibrovascular polyp?

Answer 62

**Inflammatory esophagogastric polyp:** Hyperplastic epithelium / inflamed stroma, originates from the gastric side of the squamocolumnar junction. Associated with reflux esophagitis. Smoothly marginated polyp near the squamoculumnar junction that appears to be a continuation of a linear gastric fold. _Inflammatory myofibroblastic pseudotumor_- arises from the mucosa and contains granulation tissue, a true neoplasm (not just hyperplastic), viral associated (EBV, HPV, herpes). _Fibrovascular polyp_- composed of connective tissue, adipose, and vascular structures, usually in the cervical esophagus. Can be large and pedunculated, rarely cause asphyxiation by regurgitation and impaction at the glottis. Cancer would typically be more nodular, irregular, and ulcerated than these lesions.

Question 63

What is the most common primary retroperitoneal neoplasm? Imaging features?

Answer 63

Liposarcoma. Also seen in the omentum and mesentery. Heterogeneous mass with fat and soft tissue. Often large at presentation. Mass effect predominates over local invasion. (next most common retroperitoneal soft tissue sarcomas are leiomyosarcoma \> malignant fibrous histiocytoma)

Question 64

Diagnosis?

Answer 64

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).

Question 65

Diagnosis? Cause?

Answer 65

Feline esophagus. Transient contraction of the longitudinal muscularis mucosa. Asymptomatic but may indicate gastroesophageal reflux. Distal 2/3 of esophagus.

Question 66

Diagnosis? Cause?

Answer 66

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).

Question 67

What is Ménétrier disease?

Answer 67

A form of rare idiopathic hypertrophic gastropathy. Bimodal in distribution, children \< 10, adults 30 - 60. Males. The juvenile form has been linked to CMV infection and usually resolves spontaneously. The adult form tends to progress with time. Clinical presentation: achlorhydria, hypoproteinemia and edema- classic triad. Gastric mucosal hypertrophy, marked rugal thickening. Most commonly affects the gastric fundal region, typically spares the antrum. Differential: gastric lymphoma, other forms of gastritis.

Question 68

Imaging features of FNH? How to differentiate from fibrolamellar HCC? Adenoma?

Answer 68

**FNH:** US: hypoechoic mass with hypoechoic center. CT: Hypodense on non-contrast CT with scar, enhances in arterial phase. Portal phase- isodense and may be missed. MRI: isointense on T1 with hypointense scar, slightly hyperintense on T2 with hyperintense scar. Enhances in arterial phase with delayed enhancement of scar. **VS**: _Fibrolamellar HCC_: is more commonly symptomatic. Usually presents with pain and weight loss. Scar can calcify. Scar is *usually* hypointense on T2. _Adenoma_: associated with OCPs, rupture common. Large at presentation. May drop signal on out-of-phase images b/c of fatty hepatocytes.

Question 69

Diagnosis? What is this? Who? Associations?

Answer 69

**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.

Question 70

Diagnosis? Presentation?

Answer 70

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.

Question 71

What causes Budd-Chiari syndrome? Imaging features?

Answer 71

Causes include hypercoagulable states, myeloproliferative disorders, oral contraceptives, pregnancy, venous webs, infection, and tumor infiltration / compression. Idiopathic. CT and MRI: early heterogeneous and delayed homogeneous peripheral enhancement ("nutmeg liver"). Obstructed hepatic veins. Venography may show spiderweb collaterals.

Question 72

What is carcinoid syndrome?

Answer 72

Usually occurs in the setting of carcinoid tumor with multiple liver metastases. The release of serotonin metabolites leads to flushing, cyanosis, sweating, and watery diarrhea. In severe cases, can cause right sided heart failure. Note- percutaneous biopsy of liver mets can cause hypotensive crisis.

Question 73

What are some causes of pseudomyxoma peritonei?

Answer 73

Ovarian mucinous cystadenocarcinoma (most common), appendiceal mucinous cystadenoma/cystadenocarcinoma. Rarely by adenocarcinoma of the stomach, colon, and mucinous tumors of the pancreas.

Question 74

Differential diagnosis for a cystic appendiceal mass?

Answer 74

Carcinoid of the appendix, appendiceal mucocele (mucosal hyperplasia), mucinous cystadenoma/cystadenocarcinoma. Rim calcifications seen in cystadenoma, not carcinoid.

Question 75

Imaging findings of GI melanoma? Main differential?

Answer 75

Classic: multiple submucosal polyps with central ulceration. Also: large, exophytic mass that is cavitary, necrotic, or ulcerated. Differential includes leiomyosarcoma of the small bowel (affects ileum \> jejunum \> duodenum, usually presents as a large, exophytic, centrally necrotic mass).

Question 76

What are some etiologies on the differential for gastric fold thickening?

Answer 76

**Gastritis (H. pylori)**- most common. Typically mild-moderate thickening and regular. May be focal (typically antral) or diffuse. **Chronic renal failure on dialysis** (hypergastrinemia)- gastritis, peptic ulcer disease, and/or GI bleeding. **Zollinger-Ellison syndrome** (look for gastrinoma). **Ménétrier disease** (massive and lobulated fold thickening, often spares antrum). **Lymphoma, adenocarcinoma.** Typically nodular. **Eosinophilic gastritis.** **Portal hypertensive gastropathy** (finely nodular). Also consider gastric varices (often fundal).

Question 77

Imaging features of fibrolamellar carcinoma? Differential diagnosis?

Answer 77

**CT**: large, lobulated mass with a dense capsule and a hypodense central scar from fibrosis. Heterogeneous enhancement in the arterial phase, early washout. Calcifications are common. **MRI**: Low T1, high T2. Scar has decreased signal on T1, T2, and post gad. Negative on sulfur colloid. AFP level is typically normal. Age 5-35 w/o cirrhosis. VS: Hepatic adenoma: can also be large with central scar and enhancing capsule. More homogeneous (unless it has hemorrhaged). Look for draped peripheral vessels. FNH: central scar has delayed enhancement. May be positive on sulfur colloid. No calcs. Cholangiocarcinoma: no dense capsule. Look for capsular retraction.

Question 78

What is the most common benign tumor of the esophagus? What are it's imaging features?

Answer 78

Leiomyoma. Smoothly marginated submucosal mass. Overlying mucosa usually intact. Most common location mid-lower esophagus (the location of the smooth muscle). On CT, diffuse enhancement and occasional calcs. Usually asymptomatic. Low risk for malignant degeneration to leiomyosarcoma. Nonspecicfic imaging features. Differential includes neural tumor, lipoma, fibroma, hamartoma, hemangioma, duplication cyst.

Question 79

What is Alport syndrome?

Answer 79

Genetic- deafness, glomerulonephritis, and renal failure. Predisposed to diffuse leiomyomatosis of the esophagus.

Question 80

No infectious signs, no primary malignancy. Diagnosis? Other imaging features? Differential?

Answer 80

**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.

Question 81

Diagnosis? US and CT findings? Differential?

Answer 81

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.

Question 82

What is the difference between primary and secondary hemochromatosis?

Answer 82

**Primary**- autosomal recessive intestinal disorder resulting in increased iron absorption and iron deposition in _hepatocytes_. Causes fibrosis, cirrhosis, increased risk of HCC. Associated with: hyperpigmentation, diabetes, OA, cardiomyopathy. Low T2 signal in liver and pancreas. **Secondary**- iron deposits in the _Kupffer cells_ with no associated hepatic damage. Rarely clinically significant. Causes include multiple blood transfusions, sickle cell, Bantu siderosis (excessive dietary intake of iron). Low T2 signal in liver and spleen, normal echogenicity on US.

Question 83

What is a telangiectatic hepatic adenoma?

Answer 83

Has prominent vascular features that cause focal areas of delayed contrast enhancement and washout. Random note... hepatocellular adenomatosis is multiple adenomas unrelated to estrogen levels and OCPs, can be seen in men and women.

Question 84

What are the two most common types of internal hernias and where do they occur?

Answer 84

1) **Paraduodenal**. Occurs through a rent between the mesentery and parietal peritoneum at the ligament of Treitz. Can herniate to the _left_ (most common, results in a mass of dilated small bowel in the LUQ, lateral to the 4th portion of the duodenum) or _right_ (fossa of Waldeyer, occurs w/ incomplete malrotation). 2) **Lesser sac**. Occurs through the foramen of Winslow. Results in herniated structures posteromedially along the lesser curvature of the stomach, displacing the stomach and transverse colon down and to the left. Surgical emergency due to impending strangulation.

Question 85

What are differentiating features between malignant and benign gastric ulcers?

Answer 85

**Malignant:** Can arise from several tumor types: adenocarcinoma, GIST, leiomyosarcoma, mets. Project within the confines of the gastric lumen. Surrounded by irregular, nodular soft tissue and featureless mucosa with absent areae gastricae. Lack barium-filled folds radiating to the edge of the crater. **Benign:** Usually located along the lesser curve or posterior wall of the body or antrum. Project beyond the gastric lumen. May be surrounded by a smooth rim of edematous folds (ulcer mound), prominent areae gastricae, and a radiolucent line (Hampton line) that separates the barium-filled crater from the stomach wall. May have barium-filled folds radiating to the edge of the ulcer crater.

Question 86

Diagnosis? Cause?

Answer 86

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.

Question 87

What should this lesion look like on sulfur colloid scan?

Answer 87

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)

Question 88

What does a hemangioma look like on tagged RBC scan?

Answer 88

99Tc RBC labelled SPECT can be sensitive for larger lesions. Typically demonstrate decreased activity on initial dynamic images followed by increased activity on delayed, blood pool images. (Hemangioma and tumor are both cold on sulfur colloid. Tagged RBC can help differentiate b/c tumor will also be cold on the tagged RBC)

Question 89

Which type of renal stone can conform to the shape of the calyx?

Answer 89

Matrix stone. This is a low density stone, made up of mucoprotein and mucopolysaccharides.

Question 90

What makes cervical cancer inoperable? In what stage would you see hydronephrosis?

Answer 90

Chemo/Radation is typically be used to treat: Bulky disease (\>4cm), parametrial invasion, or locally advanced disease (stage 3 and 4). Spread into the parametrium resulting in hydronephrosis is stage **IIIB**.

Question 91

What types of VHL do/don't get pheo?

Answer 91

**Type I** – Lower risk of pheo **Type II** – High risk of pheo... _IIA_: Low risk of RCC, _IIB_: High risk of RCC, _IIC_: Only gets pheo and does not get RCC or hemangioblastomas.

Question 92

What are the guidelines for metformin use with iodinated contrast?

Answer 92

_Normal renal function and no comorbidities_: no need to discontinue metformin or check renal function after procedure. _Multiple comorbidities and normal renal function_: discontinue metformin for 48 hours. Do not need to recheck renal function _Patients with renal dysfunction_: discontinue metformin and recheck renal function prior to resuming metformin therapy. Concern is due to (low) risk of lactic acidosis.

Question 93

What determines the T portion of the TMN staging for RCC?

Answer 93

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.

Question 94

What are the Bosniak criteria?

Answer 94

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.