97-02' WRITTENS GI

Views:
 
Category: Education
     
 

Presentation Description

No description available.

Comments

Presentation Transcript

GIRadiology Recalls From ’97 to ‘02 Writtens(181 Questions Including Repeats) : 

GIRadiology Recalls From ’97 to ‘02 Writtens(181 Questions Including Repeats)

2002 : 

2002 CT shows a large spleen and hyperdense liver and pancreas:a. Fatty infiltrationb. Cystic fibrosisc. Hemochromatosisd. Iron overloade. Gaucher’s disease

Slide 3: 

C. Hemochromatosis= excess iron deposition in various organs (liver, pancreas, spleen, kidneys, heart) leading to cirrhosis with portal htn. Males > Females 10:1. Iron is Dense on CT, Low signal on T2WI[hemosiderosis=increased iron deposition without organ damage] Primary hemochromatosis: ab. Increased absorption of dietary iron:auto recess; “Bronze DM”; Pancreas, heart, pituitary involved, less spleen; Iron deposited in hepatocytes (not Kupffer cells); increased risk of HCC. Tx: repeated phlebotomy Secondary hemochromatosis: seen in pts with hemolytic anemias requiring transfusions.(actually represents hemosiderosis):no pancreas involvement; iron deposited in Kupffer (and other RE cells); more splenic involvement; no risk of HCC; requires no txFatty infiltration of the liver is decreased density on CT. See reversal of liver-spleen density relationship (spleen normally 6-12 HU below liverCystic fibrosis: 30% have steatosis of liver, secondary to untxed malabsorpt., dietary def, meds. See signs of portal htnSources: Dähhnert 5th p. 706-707

Slide 4: 

What are the T1 signal characteristics of pancreatic ductal adenocarcinoma pre- and post-contrast compared to normal pancreatic parenchyma?a. T1:hyperintense / T1 with contrast: hyperintenseb. T1:hyperintense / T1 with contrast: hypointensec. T1:hypointense / T1 with contrast: hypointensed. T1:hypointense / T1 with contrast: hyperintense

Slide 5: 

C. T1: hypointense / T1 with contrast: hypointenseHypointense lesion on fat-suppressed T1WI; diminished enhancement on dynamic contrast imaging.5th leading cause of cancer death in the US!; 62% in pancreatic headSource: Dähhnert 5th p. 724

Slide 6: 

Conjugated bile salts are resorbed where?a. terminal ileum by active transportb. terminal ileum by passive diffusionc. jejunum by active transportd. jejunum by passive diffusione. colon

Slide 7: 

A. ileum by active transportPossible variant on this question: free bile acids (as in bacterial overgrowth) are absorbed in the jejunum.Source: Dähhnert 5th p. 724

Slide 8: 

What is the most common complication of ERCP?a. perforationb. pancreatitisc. sepsisd. abscess

Slide 9: 

B. pancreatitisComplications of ERCP: pancreatitis 5%; duodenal perforation; GI bleeding Source: Primer 3rd p. 221.* Gore & Levine, Table 87-5 p. 1602 lists complications of ERCP: Pancreatits 1%; cholangitis 0.8%; drug side effects 0.6%; pancreatic abscess 0.3%; GI injury 0.2%; mortality 0.2%

Slide 10: 

What is the most likely cause of isolated gastric varices? a. splenic vein thrombosisb. portal hypertensionc. Budd-Chiari syndromed. other

Slide 11: 

A. Splenic Vein ThrombosisIsolated gastric varices is a specific sign for splenic vein occlusion. Gastric varices are usually associated with esophageal varices and are secondary to portal hypertension [seen in 2-78%]. The presence of isolated gastric (gastric without accompanying esophageal) varices is specific for splenic vein occlusion. Most commonly, this is secondary to pancreatitis or pancreatic carcinoma. Gastric varices are usually noted in the fundus, and vary in size with respiration or positioning. Source: Eisenberg, page 611.; Dähhnert 5th p. 827

Slide 12: 

During endoscopy of the esophagus, a sac-like structure is seen at anterior /lateral aspect, near cricopharyngeus musclea. Zenker’sb. Killian-Jamieson diverticulumc. Lateral pharyngeal diverticulumd. Brachial cleft cyst

Slide 13: 

B. Killian-Jamieson diverticulumKillian-Jamieson diverticulum: = lateral pharyngoesophageal diverticulum or lateral cervical diverticulum--Emerges in a lateral or anterolateral direction through a weak area in the anterolateral aspect of the pharyngoesophageal junction, just below the transverse portion of the cricopharyngeus muscle; small, with narrow neck, usually several mm in diameter; most found incidentally, rarely cause Sx; may be unilateral or bilateral; protrude through defect probably where inf. Laryngeal nerve and vessels pass Eisenberg 3rd p. 121;. GI Case Studies p 148 Pharyngeal pouches: large wide-mouth bulges along lateral contours of the hypopharynx; common among elderly and wind-playing musicians; do not retain swallowed food (Felson Gamuts 3rd p 447) Zenker’s Diverticulum: pulsion diverticulum; herniation through area of weakness at Killian’s dehiscence; above cricopharyngeus, midline & posterior (C5/C6); should see barium-filled sac extending caudally behind, and usually to left of esophagus. Risk of perforation at endoscopy. Dähnert 5th p. 866 Branchial cleft cyst: 95% arise from 2nd bronchial apparatus; located in parotid space near angle of mandible; history: usually of multiple abscesses unresponsive to tx; may insinuate between Internal and external carotid artery (pathognomonic)

Slide 14: 

The most common type of choledochal cysta. choledochoceleb. diverticulum of CBDc. fusiform dilitation of CBDd. Caroli’s Disease

Slide 15: 

C. fusiform dilatation of the CBDTypes of choledochal cysts:1. fusiform dilatation: CBD + CHD ( ~85%)2. diverticulum of extrahepatic ducts (1-3%) originating from CBD/CHD3. choledochocele (1-6%): cystic dilatation of distal CBD with herniation of CBD into duodenum (similar to ureterocele)4. multiple segmental cysts: in intra- and extra- hepatic ducts (19%)5. extrahepatic ducts only (rare)6. intrahepatic cysts = Caroli’s disease Source: Dähnert pp 554, 575

Slide 16: 

Which of the following is the most likely cause of a liver with increased attenuation on non-contrasted CT?a. steatosisb. chemotherapy (e.g., cyclophosphamide)c. radiationd. amiodaronee. amyloidf. lymphoma

Slide 17: 

D. AmiodaroneAmiodarone: 37% Iodine by weight; affinity for accum. In liver; on CT: 95-145 HU (range of nl liver is 30-70 HU). It is the only antiarrhythmic drug without cardiodepressive effects, so is very popular sources: Dahnert 5th p 547 Steatosis: fatty infiltration of liver = low density liveron CT see -reversed liver-spleen density relationship (spleen normally 6-12 HU below liver density); hyperdense intrahepatic vessels. source: Dahnert 5th p. 582Causes—Obesity (most commonly), alcohol, hyperalimentation, debilitation, chemotherapy (see below), steroids Radiation: increased attenuation from chronic hepatitis – no fatty infiltration (Dahnert 5th p. 713) [* the inclusion of this option may be an inaccurate recall, as there is a similar question from past years that lists amyloid as a possible choice] Chemotherapy: fatty / low-density liver (Primer 3rd p. 207) Amyloid: hepatomegally, with regions of low attenuation + decreased contrast enhancement. Dahnert 5th p. 582 Lymphoma: detection rate < 10% (usually autopsy) Dahnert 5th p. 718

Slide 18: 

Which is true regarding pancreatic adenocarcinoma?a. attenuation similar to normal Pancreas on CECTb. typically hyperchoic to normal pancreas on USc. displaces normal vesselsd. causes atrophy of pancreas proximal to masse. well encapsulated on CT

Slide 19: 

A. attenuation similar to normal pancreas on CECT[This is the most likely answer, by default. The others are all false]“On CECT 95% are of low attenuation. Typically the masses are nonenhancing but they may appear isoattenuating postcontrast”.(direct quote from Duke Case Review, p. 159); Eisenberg Fig. 28-31hypoechoic on US (Dahnert 5th p. 724)causes atrophy distally (atrophy of body/tail in 20%)pancreatic adenocarcinoma grows in a fibrous or schirrous manner. It tends to grow along tissue planes, and replaces the normal tissues in the region. It does not grow into a welldefined mass, but has poor margins. It also encases (rather than displaces) vessels [SMA, portal vein, etc.], which can make it non-resectable Primer 3rd p. 240; GI Case Review p. 12

Slide 20: 

A patient has intrahepatic and extrahepatic dilatations and strictures along with stricture of the sphincter of Oddi. Most likely diagnosis:a. primary sclerosing cholangitisb. secondary sclerosing cholangitisc. ascending cholangitisd. recurrent pyogenic cholangitise. Caroli’s disease

Slide 21: 

A. primary sclerosing cholangitisRare, chronic dx of bile ducts; Characterized by patchy, progressive fibrosis of intra-, extra-hepatic ducts, or both (60%-90%)- Multiple segmental strictures involving the intrahepatic and extrahepatic bile ducts are the hallmark finding; outpouchings 24%. CBD always involved; 60% have ulcerative colitis, 5% have Crohn’s secondary sclerosing cholangitis: cause: chronic bact. Cholangitis from a variety of causes including surgery, cong. Biliary tree anomalies, floxuridine tx, choledocholithiasis, etc. ascending cholangitis: recurrent (sporadic) episodes of sepsis + RUQ pain. acute: two types (nonsuppurative and nonsuppurative) - charcot triad 70% (fever+ chills+ jaundice); 100% mortality if not decompressed recurrent pyogenic (= Oriental) cholangitis: in the differential, but uncommon in the U.S. (see related question from 2002 GI) Caroli’s disease: beaded appearance of intrahepatic ductsSource: Dähnert 5th p. 689

Slide 22: 

Oriental cholangiohepatitis is NOT associated with--a. jaundiceb. biliary stonesc. biliary duct dilatationd. elderly orientalse. RUQ pain

Slide 23: 

D. elderly orientalsOriental cholangiohepatitis = recurrent pyogenic cholangitisAge range: 20 – 50 years (Dahnert 5th p. 689)Characteristic features: (?) clonorchis infestation, endemic to S.E. Asia; recurrent attacks of fever, chills, abdominal pain, jaundice; marked dilatation of proximal intrahepatic ducts in 100%; nonshadowing (Ca++ bilirubinate) stones (74%)

Slide 24: 

Meckel Diverticulum is remnant of what structure?a. omphalomesenteric ductb. Müllerian ductc. Wolffian ductd. urachus

Slide 25: 

A. omphalomesenteric duct (= vitelline duct)Meckel’s diverticulum is the most common congenital abnormality of GI tract (.3-3% of population); found within 30-90 cm of IC valve; on antimesemteric border- contains ectopic mucosa in 50% (gastric or pancreatic or bowel)- > 95% of GI hemorrhage have ectopic gastric mucosa- rule of 2s: in 2% of population; symptomatic usu. Before age 2; located within 2 feet of ICV; two inches long- Meckel scan > 85% sensitive, > 95% specific Mullerian duct: forms entire female genitalia except distal 1/3 of vagina; anomalies include uterine agenesis, hypoplasia, uterus didelphys, bicornuate uterus, etc.; degenerates in males. Wolffian duct: analog for vas deferens, seminal vesicles, epididymis; induces kidney devel.+ Mullerian dev. In females. Urachus: median umbilical ligament (remnant of allantois) sources: Primer 769; Dahnert 5th pp 750, 882, 976

Slide 26: 

Elderly male with severe abdominal pain and hematochezia. Plain film shows thickened folds of transverse colon. Likely cause--a. pseudomembranous colitis with hx antibiotic useb. ischemic colitisc. Crohn’s colitisd. Ulcerative Colitis

Slide 27: 

B. Ischemic colitisIschemic colitis--best answer for information given:- Thumbprinting seen on plain film in about 20% of patients with ischemic colitis (Eisenberg 3rd, p. 773; conflicts with Dähnert)”In an older patient presenting with abdominal pain and rectal bleeding, the detection of multiple smooth soft-tissue densities protruding into the lumen of the bowel permits a provisional diagnosis of ischemia” Eisenberg 3rd p. 773; GI Requ. pp 218, 232- Age > 50 yrs, M = F. - precipitated by obstruction, thrombosis, trauma, idiopathic Pseudomembranous colitis: caused by overgrowth of Clostridium difficile in response to decrease in no intestional flora. Predisposed, among others, are pts on antibioic therapy- certainly in the differential here, but is “rarely associated with significant rectal bleeding…” Eisenberg 3rd p. 779.- thumbprinting may be most prominent in the transverse colon (18%), but it is usually generalized rather than segmental Crohns and UC: diseases of younger pts; UC would usually involve the rectum; Crohn’s might show skip areas & SB disease.

Slide 28: 

Elderly male patient with diabetes has acute onset colicky abdominal pain and tarry stools. CT showing single loop of air dilated small bowel associated with a segment of straightened, thick-walled small bowel. What is the likely diagnosis?a. short segment (focal) ischemiab. generalized ischemic colitisc. Regional enteritis (Crohn's)d. C. difficile colitis

Slide 29: 

A. short segment (focal) ischemiaCaused by acute occlusive SMA embolus (> 50%); crampy ? continuous abdominal pain; gross rectal bleeding; in patients with cardiac disease predisposing to embolization- any segment of small bowel- CT: circumferential bowel wall thickening- focal or diffuse bowel dilatation from interruption of peristaltic activity CT findings (i.e., focal) are not consistent with generalized ischemic colitis; age group makes Crohn’s less likely; C. difficile would more likely involve the colon. Eisenberg 3rd p. 469, Dähnert 5th p. 848

Slide 30: 

Regarding Crohn’s diseasea. commonly affects gastroduodenal regionsb. commonly affects jejunumc. frequently affects colon and small bowel simultaneouslyd. asymmetric mural involvemente. continuous involvement

Slide 31: 

D. asymmetric involvementCrohn’s disease is characterized by discontinuous & asymmetric involvement of entire GI tract (“mouth to anus”). It affects the stomach in 1-2%- Colon in 22-55% = granulomatous colitis - Small bowel (80%, TI) = regional enteritis- TI (alone/ in combo. 95%); Jejunum / ileum (15-55%)- Affects duodenum in 3-10% [Source: Dahnert 5th pp 809]

Slide 32: 

Most common cause of colonic-vesicular fistulaa. diverticulitisb. IBDc. Crohnd. Ebola cystitis

Slide 33: 

A. DiverticulitisBladder fistulas: types and common causes- vesicoenteric: diverticulitis (most common cause),Crohn’s, ca- vesicovaginal: surgery, catheters,ca.., rads- vesicocutaneous: trauma, surgery- vesicouterine: C-section- vesicoureteral: hysterectomy source: Primer p 285

Slide 34: 

30 y/o female with pedunculated mass in the ileuma. lymphomab. adenocarcinomac. carcinoidd. leiomyosarcomae. lipoma

Slide 35: 

E. LipomaLipoma is the 3rd most common benign tumor of the SB (after leiomyoma and adenoma); most found in TI and IC valve area; arise in submucosa but protrude into lumen; pedunculated lipomas can be assoc. with intussusception. source: Eisenberg pp 484-8 lymphoma of SB: arise from Peyer’s patches (deposits of lymphoid tissue, which are more concentrated in the ileum); among the most common malig. Tumors of the SB, but somewhat less common than adenocarcinoma.- location: DISTAL SB (ileum>jejunum> duodenum- 2%)- types: single/multiple polypoid mucosal masses; endoexoenteric mass; infiltrating with plaquelike wall involvementsource: Dahnert 4th p 700 Adenocarcinoma of SB: 2nd most common primary SB malignancy (25%): location: PROXIMAL SB (duodenum-50% > jejunum> ileum 10%); presents as: annular stricture (60%); lobulated ovoid polypoid sessile mass (41%); ulcerated mass (27%); rarely, present as pedunculated polypsources: Dahnert 5th p 654; Eisenberg p 486,Alimentary Tract Radiology 3rd pp 972 Leiomyosarcoma: Location: ileum> jejunum> duodenum; Usually >6cm in size; Nodular mass: intraluminal (10%),pedunculated (5%),intramural (15%), chiefly extrinsic (66%).Source: Dahnert 4th p 698

Slide 36: 

Most commonly associated with the terminal ileuma. Giardiasisb. Yersinia enterocolitisc. ?d. ?

Slide 37: 

B. Yersinia enterocolitisGram neg.; fever, diarrhea, RLQ pain; location: terminal ileum; thickened folds, + ulceration. source: Dahnert 4th p 639 Giardiasis: Giardia lamblia (flagellated protpzoan); Pain, wt loss, failure to thrive (esp. in children); Location: most pronounced in duodenum, jejunum; Hypersecretion, segmentation, of barium, spasm, mucosal edema. Source: Dahnert 4th p 689

Slide 38: 

The caudate lobe of the liver does not abut which of the following:a. IVCb. Right lobe of the liverc. Left lobe of the liverd. Ligamentum venosume. Ligamentum teres

Slide 39: 

C. Ligamentum teres (= round ligament)The ligamentum teres forms the border between the medial and lateral segments of the left lobe of the liver.IVC= The caudate lobe lies anteromedial to the IVCRight lobe of liver = is contiguous with the caudate lobeLeft lobe of liver = abuts caudate, separated by ligamentum venosumLigamentum venosum = the fissure for the lig. Venosum forms the anterior border of the caudate, and separates it from the left lobeLigamentum teres = forms the border between the medial and lateral segments of the left lobe of the liverSource: ACR GI Teaching File (CD) , Liver section, case 801* Clemente 4th Plate 207 shows this relationship well.

Slide 40: 

What are typical esophogram findings of HIV infection of esophagus?a. shaggy mucosab. plaquesc. Giant ulcersd. Cobblestoning

Slide 41: 

C. Giant UlcersHIV Esophagitis: One or more giant (> 1cm) flat ulcers (esp. at time of seroconversion); satellite ulcers may be present; - indistinguishable from CMV esophagitis. Dahnert 5th p. 823.Herpes simplex: abnormal motility; small ulcers (initially blisters), < 5mmCandidiasis: Most common cause of infectious esophagitis- plaquelike, reticular; abnormal motility- also ”Cobblestone” and/or “Shaggy” appearance, esp. fulminant candidiasis (as in HIV)* This is a very popular topic, seen in various forms on many old writtens * Other sources: Dahnert 4th pp 624,682-3; Eisenberg 3rd p 58

Slide 42: 

Gastroesophageal reflux is associated with all except:a. thickened longitudinal foldsb. pseudodiverticulaec. plaque-like lesionsd. aperistalsis in lower esophaguse. granular appearing mucosaf. stricture

Slide 43: 

C. plaque-like lesionsGI reflux: earliest findings on Xray = superficial ulcerations, granular / finely nodular folds- more severe disease = widening and coarsening of esophageal folds; nonperistaltic waves in distal esophagus; segmental esophageal narrowing ( edema/spasm/stricture)- esophageal intramural diverticulosis = dilated excretory ducts of deep eophageal mucosal glands--in 90% assoc. with any severe esophagitis (most often reflux / candida)- Stricture may be a consequence of chronic reflux (Barrett’s)Plaques are associated with Candida esophagitissources: Dahnert 4th pp 680,2,3; Primer p 154; Dahnert 5th p. 822

Slide 44: 

Muscosa-Associated Lymphoid Tissue (MALT) lymphoma is most closely associated with :a. Helicobacter pylorib. Zollenger-Ellison syndromec. Nodular hyperplasiad. ?

Slide 45: 

A. Helicobacter pyloriMALT is lymphoid tissue scattered along mucosal linings of the body. It protects against antigens entering along mucosal surfaces. MALT is one of the major secondary lymphoid organs, along with nodes and spleen. Tonsils, Peyer’s patches and apendix are examples of MALT. Source: www.emedicine.com/med/topic 3204H. pylori is the main cause of gastritis, responsible for up to 80% of gastric and 95% of duodenal ulcers, and is implicated in the pathogenesis of gastric adenocarcinoma and MALT lymphoma. MALT is associated with H. pylori gastritis in 90% (may regress completely after antibiotic therapy).Sources : Dähnert 5th p 841; British Medical Journal Aug. 28,1999

Slide 46: 

Which is least likely to metastasize to the esophagus?a. melanomab. Kaposi’s sarcomac. Carcinoidd. Leiomyosarcomae. Breast

Slide 47: 

C. Carcinoid Mets to esophagus: melanoma, lymphoma, leiomyosarcoma, stomach, lung, breast Dähnert 4th p 626; Dähnert 5th p. 818. Kaposi now considered asystemic multifocal progressive tumor of the GI tract. Visceral involvement thought to be an expression of the multicentric potential of the tumor, rather than metastatic dissemination. “Infrequent esophageal involvement appears as nonspecific single or multiple polypoid filling defects” Eisenberg p 104; see also GI Requ. p. 258. Carcinoid is said to metastasize to lymph nodes, liver, lung, and bone (not esophagus); given this & the choices, it is probably the best answer. (Dähnert 5th p. 801).

Slide 48: 

Which of the following does not cause gastric ulcers?a. Zollinger-Ellisonb. Aspirinc. H. pylorid. Ménétrier dx

Slide 49: 

D. Ménétrier’s Disease Menetrier Dx: = Giant mucosal hypertrophy; characterized by excessive mucus production and triad of:-giant mucosal hypertrophy -hypoproteinemia-hypochlorhydria (decreased or absent acid output in 75%)There is also gastric pain (gastritis) and a possible association with gastric carcinoma Eisenberg 3rd p. 234; Gore & Levine[** Dähnert 5th p. 847 cites an association with gastric ulcers, however, review of several GI imaging texts suggests that Ménétrier’s is rarely, if ever, associated with gastric ulcers; the other choices clearly are **] Gastric ulcers: benign gastric ulcers = 95% of all gastric ulcers;path: disrupted mucosal barrier (H. pylori) multiple in 2-8%, esp. in pts. on aspirin (source: Dahnert 4th p 687) Zollinger-Ellison: = PUD assoc. with marked hypersecretion of gastric ulcer + non-b islet cell tumor of pancreas. cause:1. gastrinoma (90%) =non-beta islet cell tumor with continuous gastrin production2. pseudo Z-E syn=Cowley Syn=antral G-cell hyperplasia (10%)Location: Duodenal bulb (65%) + stomach (20%); Near lig of Treitz (25%); C-loop (5%); Distal esophagus (5%) Source Dahnert 4th p 720-1

Slide 50: 

Which of the following causes the greatest amount of pancreatic secretions?a. gastrinb. secretinc. cckd. trypsin

Slide 51: 

A. gastrinGastrin: 17 amino acid peptide amideproduced in antral cells + G-cells of pancreaseffects on pancreas: strong increase in enzyme output[source: Dahnert 4th p 646]secretin: produced in duodenal mucosa; effects on pancreas: weakly stimulates enzyme secretionCCK: produced in duodenal + upper intestinal mucosaeffects on pancreas: stimulates pancreatic enzyme secretionsource: Dahnert 4th p 646

Slide 52: 

Which of the following is most likely to be hypoechoic on US?a. lymphomab. breast metsc. colon metsd. hepatoma

Slide 53: 

A. lymphomaLymphoma is classically hypoechoic or anechoic due to the homogeneous cell population & paucity of of acoustic interfaces. Hyperechoic mets to the liver tend to arise from the colonDähnert p. 597: Echogenic liver mets:colon cancer (municous adenoca) 54%; hepatoma 25%; treated breast ca 21%.Dähnert p 507: Echopenic liver mets:lymphoma 44%; pancreas 36%; cervical ca 20%; lung (adenoca)

Slide 54: 

Which metastatic liver lesion is most likely to be hypervascular?a. breastb. colonc. bronchogenic carcinomad. pheochromocytoma

Slide 55: 

D. Pheochromocytoma Hypervascular liver metastases—“CHIMP”- Carcinoid, Hypernephroma, Islet cell carcinoma, Melanoma, Pheochromocytoma- also thyroid, choriocarcinoma, ovarian, sarcomasHypovascular liver metastases:- Stomach, colon, pancreas, lung, breastDähnert 5th p. 720-721

Slide 56: 

A patient has ulcers in the ileum on mesenteric border with sacculations on the antimesenteric border. Most likely dx:a. Crohnb. Yersiniac. TBd. Ischemia

Slide 57: 

A. Crohn’s DiseaseSee pseudodiverticulae = pseudosacculations = bulging areas of normal wall opposite scarred wall on antimesenteric side of SB. No other pathology will show this type of appearanceSource: Dähnert 4th p 670, ACR TF, GI, case 515 TB: Most commonly affects ileocecal area (80-90%)Rigid cone-shaped cecum Yersinia: Can resemble Crohn’s ileitis. Fold thickening, aphthous ulcers,coarsened mucosal surface, and inflamm. nodules are usual. Deep ulceration is unlikely; disease is self-limited. Ischemia: thickened folds, thumbprinting on mesenteric borderSources: Dahnert 4th p 670; ACR Learning File, GI, cases 514,515

Slide 58: 

Hypervascular on CECTa. microcystic adenomab. insulinomac. gastrinoma d. glucagonoma

Slide 59: 

A. Microcystic adenomaBenign lobulated neoplasm composed of innumerable small cysts. F:M 4:1. well demarcated lobulated mass, with characteristic central stellate scar. Contrast enhancement on CT.Source: Dähnert 4th p 579 Islet cell tumors of pancreas Small tumors characteristically enhnce transietly on bolus scan. Larger tumors may have calc. and central necrosis.Source: ACR TF GI case 809

Slide 60: 

Which is not true regarding pancreatitis?a. fluid collection often seen with acute pancreatitisb. focal involvement is commonly seen in acute pancreatitisc. gallstones are commonly associated with chronic pancreatitisd.

Slide 61: 

C. Gallstones commonly associated with chronic pancreatitis Acute pancreatitis most often occurs secondary to ETOH or gallstones. Chronic pancreatitis causes include ETOH, hyperparathyroidism, hyperlipidemia, genetic. Fluid collections (formerly called phlegmons) are collections of enzyme-rich pancreatic fluid that occur in 40% of patients. Acute pancreatitis most often causes diffuse or focal enlargement of the pancreas secondary to inflammation and edema.Source: GI Requisites 2nd pp 142-3

Slide 62: 

Which is not associated with colon cancer?a. breast cancerb. prostate cancerc. bronchogenic carcinomad. ovarian cancer

Slide 63: 

C. Bronchogenic Carcinoma (* probably) Breast, Colon, and ovarian cancer are all clearly associated; Dähnert 5th p. 804 – “…personal History of ovarian / endometrial / breast cancer… [are associated with Colon CA]” In fact, “early colorectal cancer” is listed as increasing the risk of ovarian cancer by 3.5x.A clearly listed association of either prostate or bronchogenic cancer with colon cancer was not found. However, Dähnert 5th p. 939 lists animal fat intake as a risk for prostate cancer; as this is also a well-known risk factor for Colon cancer, they are probably associated.Note that risk factors for Bronchogenic cancer include cigarette smoking, radon, asbestos, uranium, arsenic, and chlormethyl ether [Dähnert 5th p. 467]

2001 : 

2001 Which is most sensitive for bowel malrotation?a. duodenojejenal junction is inferomedially positionedb. cecum is in the right upper quadrantc. jejenum is to the right of the spined.

Slide 65: 

A. duodenaljejunal junction is inferiorly positioned(= Ligament of Trietz)“Location of Lig. Of Treitz is key to making diagnosis of midgut malrotation. The ligament is located inferiorly and medial to its expected position. In cases of complete malrotation it is located to the right of the spine. The position of the cecum is variable but in complete malrotation, it is located largely in the left abdomen.”Source GI Requisites p 93

Slide 66: 

Regarding the cricopharyngeus muscle, which is true?a. located at the C1-C2 levelb. indicates the inferior extent of the cervical esophagusc. is located just inferior to the mouth of a Zenker’s diverticulumd. posterior impression on the esophagus is an abnormal finding

Slide 67: 

C. is located just inferior to the mouth of a Zenker’s diverticulum. From the Primer 3rd p. 160: “[Zenker’s] … is located at Killian’s dehiscence (above cricopharyngeus at fiber divergence with inferior pharyngeal constrictor).” - The mechanism of formation for a Zenker’s is premature closure of the cricopharyngeus resulting in increased intraluminal pressure. Dähnert 5th p. 866.A Zenker’s is located at C5/C6, which means the cricopharyngeus is at least that low.The cervical esophagus extends from the lower border of cricoid cartilage to suprasternal notch. GI Req. 2nd p. 20; Brant & Helms 2nd p. 713.

Slide 68: 

Regarding esophageal leiomyomas--a. Often bleedb. Are the most common neoplasm of the esophagusc. Occur in mid to distal esophagusd. obstruct the esophagus

Slide 69: 

C. Occur in mid to distal esophagus.Site: frequently lower + mid 1/3 of esophagus. Dähnert 5th p. 839.- Hematemesis may occur if large (rare)Esophageal neoplasms, especially squamous cell carcinoma, are common causes of focal esophageal narrowing. GI Req. p. 21.- the majority of esophageal neoplasms, excluding lesions arising at the esophagogastric junction, are squamous cell carcinomas. B&H 2nd p. 332.- but leiomyoma is the most common benign submucosal tumor of the esophagus.Symptoms are commonly dysphagia, odynophagia, and dyspepsia. Obstruction is uncommon. Only calcifying tumor of the esophagus.

Slide 70: 

Smooth lobulated mass at level of the gastroesophageal junction and the gastric fundus with left upper quadrant pancreatic calcifications: a. Gastric varicesb. Gastric carcinomac. lymphomad. leiomyosarcoma

Slide 71: 

A. Gastric varices“Presence of isolated gastric varices, without esophageal varices, is often caused by splenic vein obstruction and is most commonly secondary to pancreatitis [= calcifications] or pancreatic carcinoma. Gastric varices appear as multiple, smooth, serpiginous filling defects. Occasionally, a conglomerate of varices may simulate a fundal mass.” Primer 3rd p. 174.“…splenic vein obstruction is most commonly caused by chronic pancreatitis, pancreatic pseudocysts, or pancreatic carcinoma… Large gastric varices may occasionally be recognized on chest or abdominal radiographs as one or more lobulated soft tissue densities in the gas-filled fundus. Depending on the cause of the varices (portal hypertension or splenic vein obstruction), abdominal plain films may also demonstrate splenomegaly, ascites, or pancreatic calcifications.” Gore & Levine p. 507.The other choices do not adequately explain both the “lobulated” nature of the mass and pancreatic calcifications.

Slide 72: 

Large esophageal ulcers are not seen ina. Melanoma metastasisb. CMVc. HIVd. Herpes simplex esophagitis

Slide 73: 

D. Herpes Simplex EsophagitisClassically Herpes begins as discrete vesicles that rupture to form discrete mucosal ulcers. The ulcers may be linear, puntate, or ringlike and have a characteristic radiolucent halo. Discrete ulcers on a background of normal mucosa involving the midesophagus is most characteristic of herpes. Nodules and plaques are usually absent. Dähnert p. 823.Cytomegalovirus (CMV) is a cause of fulminant esophagitis in patients with AIDS. CMV esophagitis causes giant ulcers and severe odynophagia. HIV esophagitis cause giant ulcers and severe odynophagia. Electron microscopy reveals HIV particles in the ulcers. The ulcers are large and usually in the midesopaghus.Metastatic melanoma: GI tract + mesentery (4-8%)- multiple submucosal nodules ± “bull’s-eye / target” appearance = central ulceration Brant and Helms 395, 714; Dähnert 5th p. 822-823; 843.

Slide 74: 

Cronkhite-Canda syndrome is associated witha. Oral pigmentationb. Nail abnormalityc. d.

Slide 75: 

B. Nail abnormalityDisease of older patients with a mean age of 60 years. Polyps are distributed throughout the stomach, small bowel, and colon. - Associated skin findings include nail atrophy, brownish skin pigmentation and alopecia. Patients present with watery diarrhea and protein-losing enteropathy Nonneoplastic nonhereditary inflammatory polyps. Hamartomatous polyps resembling juvenile/ retention polyps. Brant and Helms 755, Dähnert 671

Slide 76: 

On CT, Whipple’s disease is often associated witha. hyperdense spleenb. scattered calcifications in the liverc. Low density para-aortic lymph nodesd.

Slide 77: 

C. low density lymph nodesWhipple’s disease is an uncommon systemic disorder affecting the GI tract, joints, central nervous system, and lymph nodes. The disease is caused by Tropheryma whippelii, a gram-positive, rod shaped bacteria that are found within macrophages in many organs and tissues. Patients may present with arthritis, neurological symptoms or steatorrhea. Generalized lymphadenopathy is usually present. Enteroclysis demonstrates irregularly thickened folds most prominent in the jejunum. Demonstration of tiny (1 mm) sand-like nodules spread diffusely over the mucosa or in small groups is strong evidence of disease. Increased luminal fluid is usual. CT reveals enlarged mesenteric lymph nodes that may have fat density (due to extracellular neutral fat + fatty acids).Other findings: bowel wall thickening; splenomegaly; ascites; pleuropericarditis; sacroiliitis. Brant and Helms p. 746; Dähnert 5th p. 865.

Slide 78: 

Linitis plastica is caused bya. Menetrier's diseaseb. Breast carcinomac. H. pylorid. Zollinger Ellison syndrome

Slide 79: 

B. breast carcinoma“Linitis plastica and water-bottle stomach” are terms that may be used to describe the resulting stiff narrowed stomach usually from stomach wall thickening and rigidity. Can be caused by malignancy, inflammation, infection, trauma and others. Malignant causes include: 1. Scirrhous gastric carcinoma < not a choice >2. Hodgkins lymphoma < not a choice >3. Metastatic carcinoma--breast, pancreatic and colonic. Dähnert 5th p. 760.H. pylori: major cause of chronic gastritis, duodenitis, benign gastric and duodenal ulcers, gastric adenocarcinoma and gastric lymphoma. Zollinger Ellison syndrome caused by gastric-secreting islet cell tumor. UGI studies show peptic ulcers in the stomach, duodenal bulb and postbulbar duodenum. It also shows thickened gastric folds. Menetrier’s disease is also called heant hypertrophic gastritis. It is a rare condition characterized by excessive mucus production, giant mucosal hypertrophy and hypochlorydra. UGI findings include enlarged, pliable, thickened folds in the fundus and body with antrum sparing. Brant and Helms 725, 731

Slide 80: 

Gastric MALT lymphoma is associated with--a. Helicobacter pylorib. Campylobacter jejunic. Gastric carcinomad.

Slide 81: 

A. Helicobacter pylori.Helicobacter pylori infection has been associated with gastric ulcers (60-80% prevalence) and duodenal ulcers (90-100% prevalence). Helicobacter pylori has also associated with gastric lymphoma (MALT) in 90%, and gastric carcinoma. Dähnert 5th p. 841; Dähnert p. 690, B&H p.724-6Campylobacter jejuni can cause food poisoning.

Slide 82: 

Which of the following is false regarding ultrasound features of bowel cysts?a. They more common in the ileocolic regionb. They may not communicate with the bowel lumenc. Muscular layer is more hyperechoic than the mucosal layerd.

Slide 83: 

C. Muscular layer is more hyperechoic than the mucosal layer. (FALSE)A “muscular rim” sign is seen in 47% of duplications cysts (= echogenic inner mucosal lining & hypoechoic outer rim). Dähnert 5th p. 815.Commonly seen in the ileum (30-33%) > esophagus (17-20%) > colon (13-30%) > jejunum (10-13%) > stomach (7%) > pylorus (4%) > duodenum (4-5%)- 15% of pediatric abdominal masses are GI duplication cysts- on mesenteric aspect of alimentary canal- frequently (but not always) communicate with the lumen of the adjacent gut- gastric and pancreatic tissue are the only ectopic tissues of clinical importance

Slide 84: 

Screening for colon carcinoma should be performed in--a. Everyone after 35 years of ageb. Everyone after 40 years of agec. Everyone after 50 years of aged. Everyone after 60 years of age

Slide 85: 

C. Everyone after 50 years of ageFor persons > 50 years of age: annual fecal occult blood test + sigmoidoscopy / BE every 3 to 5 years (per American Cancer Society)Screening recommendations: as/more effective than mammographic screening- for first degree relatives of patients with colon cancer screening should start at age 40. Dähnert 5th p. 804.

Slide 86: 

Clonorchis sinensis most commonly associated with--a. Gall Stone b. Cholangiocarcinomac. Sclerosing cholangitisd.

Slide 87: 

B. CholangiocarcinomaExtrahepatic cholangiocarcinoma (65%) causes stenosis or obstruction of the common bile duct in most (95%) cases and presents as an intraductal polypoid mass in 5%. - Predisposing conditions include choledochal cyst, ulcerative colitis, Caroli’s disease, Clonorchis sinesis infection, and primary sclerosis cholangitis. -The tumor may be infiltrative, desmoplastic, and small, making imaging detection was well as needle biopsy difficult. Abrupt stricture with thickening of duct wall may be the only findings. Cross sectional imaging is used to detect adenopathy and hepatic metastases. -Prognosis is poor, with less than 30% resectable. Dähnert 5th p. 698.

Slide 88: 

Pulsatile flow in portal vein with enlarged liver--a. Budd chiari syndromeb. Cirrhotic liverc. CHFd.

Slide 89: 

C. CHFDef.: waveform pulsatility with > 2/3 change from peak to minimal velocity1. CHF: in cases of passive congestion associated with right-sided cardiac failure and/or tricuspid regurgitation, the pulsatility of right atrial and systemic hepatic venous flow is transmitted by the congested hepatic sinusoidal bed to the portal side of the circulation2. Hepatic artery-portal vein fistula3. Arteriovenous shunt in cirrhosis4. Portal-to-hepatic vein fistula Dähnert 5th p. 661; see also www.biosound.com

Slide 90: 

Pt with very large cholangiocarcinoma at the hepatic ducts confluence--- what is the cause of atrophy of the left lobe of the liver--a. portal vein compressionb. biliary ductal dilatationc. hepatic artery compressiond. hepatic vein compression

Slide 91: 

A. biliary ductal dilatation.This is the Klatskin tumor. Per the Duke Case Review (p. 151),”…there is marked biliary dilatation above the obstruction and hepatic atrophy of the segments involved…”- also note that biliary obstruction by other causes (e.g., stones) can cause atrophy“Focally stenotic or papillary cholangiocarcinomas often cause segmental bile duct dilatation and may induce lobar atrophy if the location of the tumor is central…” Gore and Levine p. 1719.On the other hand, portal vein occlusion (e.g., chronic portal vein thrombosis) does not seem to cause liver atrophy. Dähnert 5th p. 736.

Slide 92: 

Which statement is false about hepatic adenoma--a. increased incidence of hemorrhageb. pt present with painc. core biopsy can reliably differentiate between adenoma and carcinomad. associated with birth control pillse. characteristic appearance on 99mTc-sulfur colloid scans

Slide 93: 

C. core biopsy can reliably differentiate between adenoma and carcinoma This is probably the “best” answer, especially given the word “reliably,” and seems to be the consensus on old exams- adenoma shows benign hepatocytes, and well-differentiated HCC can appear similar. Dähnert 5th p. 714- [concerning anabolic-steroid associated HCA] “…this is due to its distinctive histologic appearance, which often resembles that of hepatocellular carcinoma…”; “Microscopically, the cells of HCC resemble normal liver cells and it is often difficult to distinguish normal hepatocytes from cells of HCC and/or hepatocellular adenoma…” Gore & Levine Textbook of GI radiology p. 1873, 1899.Dähnert [p. 708] describes the 99mTc-sulfur colloid appearance as follows: focal photopenic lesion surrounded by a rim of increased uptake (compression of normal liver). However, be aware that some other references were not quite this clear:- NM Req. says undifferentiated HCC refuses to fill in (p. 247). Further, there is a fairly broad differential for photopenic defects on 99mTc-sulfur colloid imaging (metastases, cavernous hemangioma, etc.) such that the appearance of hepatic adenoma is not completely characteristic. see Mettler 4th p. 241-242.The other choices are clearly true (Dahnert 5th p. 708):- Propensity to bleed: Intratumor or intraperitoneal hemorrhage (40%)- RUQ pain as a sign of mass effect (40%)- most frequent hepatic tumor in young women after use of contraceptive steroids (2.5x risk over 5 years)

Slide 94: 

Lipoma in colon , which is true--a. most common nonepithelial tumorb. more common in elderly obese patientsc. present with obstructiond. originates from epithelial cells

Slide 95: 

A. Most common nonepithelial tumorLipomas of the colon are not common but do represent the next most common benign tumor of the large bowel after adenomas. GI Req. 2nd p. 348.- Adenomas / Adenocarcinoma are epithelial in origin (adenomatous polyp = epithelial polyp). Dähnert 5th p. 787.- Most common submucosal tumor in the colon. - Usually in cecum and ascending colon- Typically asymptomatic but may have crampy pain.- Rarely causes intussusception (not obstruction). Dähnert 5th p. 840

Slide 96: 

In a previously healthy 28 yr old man an 8 cm mass is found in liver. CT shows heterogeneous enhancement with central scar. Most Likely diagnosis--a. FNHb. Fibrolamellar carcinomac. Adenomad.

Slide 97: 

B. Fibrolamellar carcinomaMean age is 23 years with a M:F of 1:2. No underlying cirrhosis or known risk factors, alpha-fetal protein is negative. Well-circumscribed strikingly desmoplastic tumor with calcifications + fibrous central scar. Partially/completely encapsulated solitary mass 4 – 17 cm in diameter. Prominent central fibrous scar (45-60%). CT: mass of low attenuation with varying degrees of enhancement. Dähnert 5th p. 715.FNH: rare benign congenital hamartomatous. Oral contraceptives do not cause FNH, but does have a trophic effect on its growth. More common in females in 3rd or 4th decades. Has a cental scar. Different phases of enhancement.Hepatic Adenoma: rare benign neoplasm, young women after contraceptive steroids (not seen in males unless anabolic steroids).

Slide 98: 

Large intraductal papillary mucinous neoplasm in pancreas—most common radiologic finding--a. Calcificationb. Unifocal large cystic massc. Dilatation of pancreatic duct(s)d. single large cyst

Slide 99: 

C. Dilatation of pancreatic duct(s).Intraductal Papillary Mucinous Neoplasm (IPMN):- has been called ductectatic mucinous tumor in the past (Dähnert 4th CD-ROM)- it distends the ductal system producing an apparent multiloculated mass (“cluster of grapes”) http://www.ijri.org/articles/current_issue/abdominal_501.htm- 1-2% of all exocrine tumors of the pancreas- elderly males (~ 65 yrs.); relatively good prognosisConsidered premalignant pancreatic lesions, and histologically may demonstrate areas ranging from hyperplasia to carcinoma within a single tumor (11). Although extensive longitudinal intraductal growth can be observed, they are slow to invade periductal tissues radially and slow to metastasize. see also Lichtenstein D, Carr-Locke D, Mucin-secreting tumors of the pancreas. Gastrointestinal Endoscopy Clinics of N America, 1995;5:237-258

Slide 100: 

Concerning the microcystic pancreatic neoplasm, which is false?a. occur in elderly femaleb. has malignant potentialc. shows contrast enhancementd.

Slide 101: 

B. has malignant potential (FALSE)Microcystic pancreatic neoplasm has no malignant potential. Dähnert 5th p. 721.It is a benign lobulated neoplasm composed of innumabable small cysts (1-20 mm) containing proteinaceous fluid separated by thin connective tissue. 82% occurs in over 60 years of age (M:F 1:4), therefore a is true. CT shows attenuation values close to water and contrast enhancement (C is true). US shows predominantly echogenic mass with mixed hypoechoic + echogenic arease. It is associated with von Hippel-Lindau syndrome. Angio shows hypervascular mas with dilated feeding arteries, dense tumor blush, prominent draining veins, neovascularity, occasional AV shunting, and No vascular encasement. Treatment is surgical excision/ follow up examinations.

Slide 102: 

Which of the following is the most common type of choledochal cyst--a. choledochoceleb. fusiform dilatation of the extrahepatic ductc. extrahepatic duct diverticulumd. Caroli’s disease

Slide 103: 

B. fusiform dilatation of the CBDTypes of choledochal cysts:1. fusiform dilatation: CBD + CHD ( ~85%)2. diverticulum of extrahepatic ducts (1-3%) originating from CBD/CHD3. choledochocele (1-6%): cystic dilatation of distal CBD with herniation of CBD into duodenum (similar to ureterocele)4. multiple segmental cysts: in intra- and extra- hepatic ducts (19%)5. extrahepatic ducts only (rare)6. intrahepatic cysts = Caroli’s disease Source: Dähnert pp 554, 575

Slide 104: 

Which of the following is true regarding Zenker’s diverticulum--a. muscular contractions lead to emptyingb. posterior midline of the lower pharynxc. inferior to cricopharyngeusd. traction diverticulum

Slide 105: 

B. posterior midline of the lower pharynxZenkers diverticulum arises in the hypopharynx just proximal to the UES. It is located in the posterior midline at the cleavage plane, known as Killian’s dehiscence, between the circular and oblique fibers of the cricopharyngeus muscle. It is located at C5-C6 and its neck is more cephalad than its base, encouraging the trapping of food and liquid. Barium examination shows a partially barium-filled outpouching at the junction fo the hypopharynx and cervical esophagus. A picture in Brant and Helms (pg 713) shows that it is near the junction of the upper cervical esophagus and hypopharynx, but not confirmed in the literature. Brant and Helms pg 713; Dähnert 5th p. 866.

Slide 106: 

The most common complication of ERCP isa. hemorrhageb. pancreatitisc. bile leakd. bowel perforation

Slide 107: 

B. pancreatitisComplications of ERCP: pancreatitis 5%; duodenal perforation; GI bleeding Source: Primer 3rd p. 221.* Gore & Levine, Table 87-5 p. 1602 lists complications of ERCP: Pancreatits 1%; cholangitis 0.8%; drug side effects 0.6%; pancreatic abscess 0.3%; GI injury 0.2%; mortality 0.2%

Slide 108: 

Which is the most common cause of pre-sinusoidal portal hypertensiona. passive venous congestionb. budd-chiari syndromec. cirrhosisd. schistosomiasis

Slide 109: 

D. SchistosomiasisPortal Hypertension is defined as a portal pressure > 5-10 mm Hg. Most commonly caused by hepatic cirrhosis. Clinical manifestations occur because of altered flow dynamics; GI variceal bleeding is the most common presentation. Dähnert 5th p. 733.Causes:- Presinusoidal – Schistosomiasis (most common cause worldwide), portal vein obstruction (thrombosis, tumor)- Sinusoidal – Cirrhosis- Postsinusoidal – Budd-Chiari syndrome, Hepatic vein or IVC obstruction. Primer 3rd p. 681

Slide 110: 

Primary sclerosing cholangitis – what is it most associated with? a. ulcerative colitisb. stones and surgery (are causes for secondary cholangitis)c. Crohn’s diseased. clonorchis infection

Slide 111: 

A. ulcerative colitsAssociated with UC in 50-74%- Crohn’s in 13% (Dähnert 5th p. 688)Characterized by insidious onset of jaundice with progressive disease affecting both intrahepatic and extrahepatic bile ducts. Alternating dilation and stenosis produces a characteristic beaded pattern of intrahepatic cts. Small saccular outpouching (duct diverticula), demonstrating on cholangiography, are considered to be pathognomonic. Brant and Helms 682

Slide 112: 

At the ileocecal region, which of the following organisms are least likely?a. TBb. salmonellac. giardiad. campylobactere. yersinia

Slide 113: 

C. GiardiaGiardia Lamblia may cause narrowing secondary to thickening of folds in the duodenum and proximal jejunum. TB causes narrowing and sometimes marked distortion of the ileocecal region. Other infections in which fold thickening and luminal narrowing are usually localized to the distal ileum include Camplyobacter, Yersinia, and Salmonella. GI Requistes 107

Slide 114: 

Which of the following is not associated with delayed gastric emptying?a. hyperglycemiab. Gastrinoma (Zollinger-Ellison syndrome)c. hypothyroidismd.

Slide 115: 

B. Gastrinoma (Zollinger-Ellison Syndrome)In Nuclear Medicine Requisites they have a chart which list causes of Rapid Gastric Emptying and Gastrinoma is one of them. - Hypothyroidism and Diabetes are listed as causes of Gastric Stasis. (pg 275).

2000 : 

2000 Which of the following is not a feature of Oriental Cholangitis?a. Stonesb. Jaundicec. RUQ paind. Elderly Asianse. Feverf. Causes biliary dilatation

Slide 117: 

D. Elderly AsiansRecurrent pyogenic cholangitis (also known as intrahepatic stone disease or oriental cholangiohepatitis) is a unique form of gallstone disease usually found in patients from Southeast Asian countries. These patients have large stones scattered through out the intrahepatic biliary system with marked dilation of proximal intrahepatic ducts. These patients are 20-50 years old and present with recurrent fever, chills, abdominal pain, and jaundice. [Dähnert p. 689]

Slide 118: 

30 year old female with multiple liver lesions on CECT. One is of water density. Some have central hyperdensity with enhancement. What is the most likely diagnosis?a. Caroli’s diseaseb. Cholangitisc. Multiple cavernous hemangiomasd. Multiple abscessese. Polycystic liver diseasef. Multiple adenomasg. Mets

Slide 119: 

B. Caroli’s disease Caroli’s disease is a Type 5 choledochal cystic disease limited to the intra-hepatic ductal system and manifests as segmental saccular dilatation . The portal vein is completely surrounded by the dilated bile ducts= the “central dot sign” on CT. This finding when present increases the specificity for the diagnosis on CT. Seen in the first 3 decades.Polycystic liver disease is a differential and sometimes need to do a luminal contrast study- ERCP/ PTC to differentiate it from Caroli’s. [Dähnert 5th ed p. 685, GI Req p. 183]

Slide 120: 

Multiple cystic lesions in the liver, high attenuation with peripheral enhancement.a. Caroli’s diseaseb. infectionc. hemangiomasd.

Slide 121: 

C. hemangiomas Cavernous hemangiomas of the liver are the most common benign liver tumors and the second most common liver tumors after metastases. female/male ratio of 5:1. multiple in 10-20%. CT - well circumscribed spherical/ovoid low density mass May have areas of higher/lower density within mass. Typical pattern on low density on NECT and centripedal enhancement and complete fill-in on delayed images 3-30 minutes post IV contrast bolus. Peripheral (72%)/central (8%)/diffusely dense (8%) enhancement Complete(75%), partial(24%), no(2%) fill-in to isodensity in delayed phase.Pyogenic liver abscesses on CT are imhomogenous , hypodense single/multiloculated cavities with a double target sign consisting of wall-enhancement and a surround hypodense zone of edema. Caroli’s has contrast centrally. see Dähnert 5th p. 710.

Slide 122: 

What tumor is most likely to be hypovascular in the pancreatico-duodenal region?a. Leiomyosarcomab. Microcystic adenomac. Adenocarcinomad. Glucagonomae. Insulinomaf. Mets

Slide 123: 

C. AdenocarcinomaPancreatic ductal adenocarcinoma:- mass with central zone of diminished attenuation (75-83%)- Incidence: 27,000 per yr., 5th leading cause of CA death Dähnert 5th p. 724.AdenoCA, lymphoma, mucinous cystic neoplasms, solid and papillary epithelial neoplasm, mets and focal pancreatitis are hypovascular pancreatic masses.- Note that Adeno CA, mucinous cystic neoplasms, solid and papillary neoplasm, etc. are of Epithelial Origin. Dähnert 5th p. 668.Islet cell tumors, serous / microcystic adenoma, mets from melanoma, and RCC are Hypervascular pancreatic masses. [GI Req p. 147]

Slide 124: 

Areae gastricae in the stomach represents which of the following:a. Clusters of gastric glandsb. Pre-malignant conditionc. Pepsin producing cellsd. Response to hyperacidity/hypertrophic gastritise. Pariental cells

Slide 125: 

A. Clusters of gastric glandsWhen examining the surface of the gastric mucosa with a magnifying lens in the fresh specimen, it is seen to be divided into a multitude of small, slightly elevated polygonal areas by numerous linear depressions. These raised areas, which measure from 1.0 to 6.0 mm in diameter, are called the areae gastricae (= Latin for gastric folds). On the surface of the areae gastricae numerous small tubular invaginations, the gastric pits or foveolae, are seen. It is into the bottom of these pits that the gastric glands open. Double contrast radiographic examination demonstrates the areae gastricae Macintosh CE, Kreel L. Anatomy and radiology of the areae gastricae. Gut l977, l8, 855-864.

Slide 126: 

What is the least likely location of intraperitoneal mets to the colon?a. Superior aspect of the transverse colonb. Superior aspect of the sigmoid colonc. Lateral aspect of the cecumd. Medical aspect of the cecume. Anterior aspect of the recto-sigmoid

Slide 127: 

C. Lateral aspect of the cecumTumor cells in ascitic fluid tend to implant in four locations:1) superior border of the sigmoid colon, where the sigmoid mesocolon temporarily traps fluid in the left inframesocolic compartment2) anterior wall of the rectosigmoid, where the rectovaginal or rectovesical pouches constitute the most dependent portions of the peritoneal cavity3) right paracolic gutter, via which most excess fluid in the pelvis flows superiorly4) ileocecal region, which is the most dependent portion of the right inframesocolic compartment. ACR GI CD-Rom. and Brant and helms p. 673 Cancers of ovary, pancreas, stomach and colon most commonly seed the intraperitoneal space. The retrouterine and retrovesicular space is the most common areas effected. Other areas include right lower quadrant small bowel loop (terminal ileum), the MEDIAL border of the cecum, the sigmoid colon, the right paracolic gutter, and the transcerse colon. Peritoneal mets involving the greater omentum invade the transverse colon. Ref. Chapter 12 Double contrast GI radiology, Levine and Laufer

Slide 128: 

Gastric acid is produced by which cells?a. Argentaffinb. Parietalc. Columnard. Goblete. Mucous cellf. Kupffer cell

Slide 129: 

B. ParietalParietal cells are stimulated to secrete acid by vagal stimulation, endocrine (primarily gastrin), and local histamine release from mast cells. Goblet cells are found in bronchi, bronchioles, and small intestine and secrete mucin. Columnar cells are absorptive cells found in the small bowel. [Robbins p. 688, 768, 784] Argentaffin pertains to cells or tissue elements that reduce silver ions in solution, thereby becoming stained brown or black (argentaffinoma – syn. Carcinoid tumor). [Taber’s cyclopedic Medical Dictionary p. 146]

Slide 130: 

Gastric acid is produced by which cells?a. Argentaffinb. Parietalc. Columnard. Goblete. Mucous cellf. Kupffer cell

Slide 131: 

B. ParietalParietal cells are stimulated to secrete acid by vagal stimulation, endocrine (primarily gastrin), and local histamine release from mast cells. Goblet cells are found in bronchi, bronchioles, and small intestine and secrete mucin. Columnar cells are absorptive cells found in the small bowel. [Robbins p. 688, 768, 784] Argentaffin pertains to cells or tissue elements that reduce silver ions in solution, thereby becoming stained brown or black (argentaffinoma – syn. Carcinoid tumor). [Taber’s cyclopedic Medical Dictionary p. 146]

Slide 132: 

Regarding hepatic abscesses, which is true?a. Echinococcus granulosus causes hydatid cystsb. Multi-locular abscesses respond to percutaneous drainagec. Amebic abscesses require surgical or percutaneous drainaged. 80% of pyogenic abscesses are cryptogenic

Slide 133: 

A. Echinococcus granulosus causes hydatid cystsEchinococcus granulosus causes liver and lung cysts among other organs (Brandt/Helms, p. 410, 2nd ed., Dähnert p. 699-700 Answer B is false: multiloculated collections are better managed surgically.Answer C is false; these are treated with Flagyl and chloroquine. Answer D is false; about half are caused by Staph, strep, and anerobes. 45% are cryptogenic.

Slide 134: 

Which is the most specific ultrasound sign of portal venous hypertension?a. Splenomegalyb. Portal vein enlargementc. Hepatic vein enlargementd. Ascitiese. Porto-systemic collateralsf. Enlarged hepatic vein

Slide 135: 

B. Portal vein enlargementThe most specific sign for portal hypertension is enlargement of the portal vein. In fact, a diameter of greater than 1.3 cm is 100% specific for portal hypertension (Gore and Levine 1620).Recanalization of umbilical vein and hepatofugal flow are diagnostic. [Primer p. 681]The most specific sonographic signs of portal hypertension is dilatation of the portal vein > 13 mm (100% specificity, 57% sensitivity) and loss of respiratory increase of splanchnic vein diameters (100% specificity, 80% sensitivity). Dähnert , p.733

Slide 136: 

No flow is detected in the portal vein on Doppler-pulse wave imaging. What can you do?a. Change the angleb. Increase pulse repetition frequency (PRF)c. Add a wall filterd. Change to a lower frequency transducere. Increase the sample volume

Slide 137: 

A. Change the angleThe duplex system allows estimation of the flow velocity directly from the Doppler shift frequency, since the velocity of sound and the transducer frequency are known, while the Doppler angle can be estimated from the B-mode image by the user and input into the scanner computer for calculation.Errors in the flow volume may occur. The vessel axis might not lie totally within the scanned plane, the vessel might be curved or flow might be altered from the perceived direction. The Doppler angle could be in error, which is much more problematic for very large angles, particularly those greater than 60 degrees. The Doppler gate (sample area) could e mispositioned or of inappropriate size, such that the velocities are overestimated (usually too small) or underestimated (usually too large) of the average velocity. Source: Bushberg 2nd ed. p. 538Remember, cos(90°) = 0, so if the transducer is perpendicular to the vessel, no flow can be detected.

Slide 138: 

Which would least likely affect small bowel in AIDS?a. MAIb. CMVc. Candidad. Cryptosporidium

Slide 139: 

C. CandidaAll of the other choices can affect the entire bowel. Candida presents with mucosal ulceration most commonly in the esophagus. It can affect the stomach and rarely the colon, and although the SB can be affected, it is least common. [GI Req p 309, Primer p. 272, B&H 714]

Slide 140: 

Which is most likely infection of the esophagus in HIV:a. Viralb. Candidac. d.

Slide 141: 

B. CandidaThe most common cause of infectious esophagitis is Candida. This is highly prevalent in AIDS patients. Usually, these demonstrate long, linear filling defects from raised plaques. However, with AIDS, the disease is more fulminant and results in the classic “shaggy esophagus” appearance (Brant/Helms 714).

Slide 142: 

What is the most likely cause of multiple target lesions in the spleen on CECT in an immunocompromised patient?a. Lymphomab. Multiple fungal microabscessesc. Disseminated PCPd. Multiple infarcts

Slide 143: 

B. Multiple fungal microabcessesFungal infection is the most common in an immunocompromised patient. US Req p. 146Splenic microabscesses are caused by fungus, and represent 26% of splenic abscesses- multiple round hypoechoic / hypoattenuating “target” lesions of 5-10 mm. Dähnert 5th p. 670.

Slide 144: 

Regarding islet cell tumor of pancreas:a. insulinomas are usually malignantb. non-functioning tumor usually have not metastasized at the time of diagnosisc. glucagonomas are the most commond. associated with VHLe. usually hypovascular

Slide 145: 

D. associated with VHLvon Hippel-LIndau Disease: > 1 hemangioblastoma in the CNS, or 1 hemangioblastoma & visceral manifestation, or 1 manifestation & family history- Type I: renal/pancreatic cysts, no pheochromocytoma- Type IIA: pheo. & pancreatic islet cell tumor (typically no cysts)- Type IIB: pheo. & renal & pancreatic disease Dähnert 5th p. 328.Insulinomas – 90% are benign. Non-functioning tumors grow large and metastasize before being diagnosed. Insulinomas are most common; gastrinomas are 2nd most common. Glucagonomas are uncommon. ICT’s are found in 20% of patients with VHL. They are usually hypervascular. [GI Requisites pp. 146-148]Only 10% of insulinomas are malignant, compared to 60% of gastrinomas and 80% of non-functioning tumors. VHL does have an association with islet cell tumors as well as pancreatic cysts and cystadenoma/cystadenocarcinoma. Non-functioning tumors are associated with coarse calcifications, large size, cystic degeneration, necrosis, local and vascular invasion, and metastases (BH 695-7; Dähnert 601, 276).

Slide 146: 

Most common pancreatic islet cell tumora glucagonomab insulimomac somatinstomad vipoma

Slide 147: 

B. insulinomaIslet cell tumors: 85% are functional- Insulinoma – most common; may be associated with MEN 1- Gastrinoma – 2nd most common, MEN 1 in 10-40%- Glucagonoma - rare

Slide 148: 

A 70 year-old female presents with a pancreatic mass with a central calcification.  The calcification was noted on a CT scan 5 years earlier.  What is the most likely diagnosis?a. Serous cystadenomab. Adenocarcinomac. Pseudocystd. Chronic pancreatitis

Slide 149: 

A. Serous cystadenomaMicrocystic adenomas of the pancreas (aka serous cystadenoma) are benign lobulated neoplasm composed of unnumerable small cysts (1-20mm) containing proteinaceous fluid separated by thin connective septa. They represent 50% of all cystic pancreatic neoplasms. The mean age of patients are 65 and 82% of patients are over 60. Females predominate with a ratio of 4:1 over males.Location: anywhere in the pancreas but have a slight predominance in the head. Appearance: well demarcated lobulated mass 1-25 cm (mean 5 cm) in diameter with smooth nodular contour. Innumerable small <2 cm cysts. Prominent central stellate scar (Characteristic)Amorphous central calcifications in dystrophic area of scar. Pancreatic duct/CBD may be displaced, encased or obstructed. On CT: attenuation values close to water, enhance with contrast. Source: Dahnet 4th ed, p. 597; Gastrointestinal Radiology The Requisites p - 152

Slide 150: 

What is the chance of malignancy in a 1.5cm colonic polyp in a 50 yo male?a. 1%b. 10%c. 35%d. 60%e. 90%

Slide 151: 

B. 10%Depends on the type of polyp. The neoplastic polyps are usually adenomas. Epithelial polyps are tubular (75%), tubulovillous (15%), or villous adenoma (10%). FYI, the most common is a nonneoplastic hyperplastic polyp (90%). The malignant potential is based on SIZE. Tubular Tubulovillous Villous< 1 cm 1% 5% 10%1-2 cm 10%, 7% 10%> 2 cm 30%; 40% 50%[Dähnert p. 787]

Slide 152: 

Which has the highest risk of malignancy?a. Juvenile polyposisb. Barrett’s esophagusc. Ulcerative colitisd. Gardner syndromee. Menetrier’s diseasef. Granulomatous enteritis

Slide 153: 

D. Gardner’s syndromeGardner’s syndrome is a polyposis syndrome which affects the colon 100% of the time and the duodenum 90% of the time. Malignant transformation is 100% if untreated. Dähnert 5th p. 824.Peutz-Jegher (other exam choice) consists of hamartomatous polyps which typically affect the small bowel more than the colon and stomach. These are non-neoplastic but may be associated with pre-malignant adenomatous polyps. Juvenille polyposis consists of large polyps in the rectum which can prolapse or obstruct, but are of unknown malignant potential. Barrett’s esophagus is progressive columnar metaplasiaof the distal esophagus second to chronic GERD and with a 15% incidence of adenocarcinoma. Ulcerative Colitis is associated with a 1%/year risk of colorectal adenocarcinoma (Brant and Helms 714, 741, 757; Weissleder 181-82). Menetrier’s disease: This is also called hypertrophic gastropathy and is a condition of large folds in the stomach associated with changes in the stomach lining and low acid production. Because this disease is very rare, the exact risk of stomach cancer is not known. Granulomatous enteritis = Crohn’s disease

Slide 154: 

Which Of The Following Is Not Inherited ?a. Cronkite-Canadab. Peutz-Jagerc. Juvenile Polyposisd. Multiple Hamartomase. Gardnersf. Turcot’s

Slide 155: 

A. Cronkite-Canada Nonneoplastic nonhereditary polyps--Associated with ectodermal abnormalities. Age 42-75, Protein losing enteropathy, diarrhea, wgt. loss, anorexia M>F, abd. pain, nail atrophy, macules hands and feet, alopecia,thickened gastric rugae, multiple polyps Dähnert p. 810-811; Gastrointestinal Radiology The Requisites p – 253

Slide 156: 

A 20 y/o male presents with a skin rash, diffuse sclerosis of bone, flushing, tarry stools, and a gastric ulcer. What is the most likely diagnosis?a. Gardner’s syndromeb. carcinoidc. mastocytosisd. sickle cell anemiae. lymphoma

Slide 157: 

C. mastocytosisThe right answer is Mastocytosis - systemic disease with mast cell proliferation in skin + RES (lamina propria of small bowel; bone; lymph nodes; liver; spleen) associated with eosinophils + lymphocytes- Epidemiology - Age: <6 months old (in 50%)- Signs/symptoms: nausea, vomiting, diarrhea, steatorrhea, urticaria, • abdominal pain, anorexia,alcohol intolerance, tachycardia, asthma, flushing, headaches, pruritus - Small bowel - generalized irregular distorted thickened folds ± wall thickening, diffuse pattern of 2 - 3 mm sandlike mucosal nodules, urticaria-like lesions of gastric + intestinal mucosa Small bowel, generalized irregular distorted thickened folds ± wall thickening, diffuse pattern of 2 - 3 mm sandlike mucosal nodules, urticaria-like lesions of gastric + intestinal mucosa- Liver & spleen – hepatosplenomegaly- Bone - sclerotic bone lesions [Dähnert p. 844-845]; (Brant and Helms 746, 755; Weissleder 170).

Slide 158: 

Which of the following are not always seen with sprue?a. hypersecretionb. folds > 4 mmc. villous atrophy on biopsyd. asymptomatic intussusceptions seen during examinatione. Moulage pattern on barium study

Slide 159: 

B. folds > 4mmMucosal folds can be normal / thickened / effaced (depending on hypoproteinemia). Typically not thick Hypersecretion-related artifacts are seen in Sprue. .Disease is characterized by malabsorption resulting from atrophy of small intestinal villi.Transient intussceptions are commonly observed during fluoroscopy. It is best seen in mid + distal jejunum (due to intestinal hypomotility). Small bowel dilatation is HALLMARK in untreated celiac disease (70 - 95%). The degree of dilatation is related to severity of disease.- “Moulage sign" is seen in app. 50% smooth contour with effaced featureless folds resembling tubular wax mold.- CHARACTERISTIC of sprue if seen in duodenum + jejunum. Not seen today due to improved BA solns.- "jejunization" of ileal loops (= adaptive response to decreased jejunal mucosal surface) = SPECIFIC [Dähnert p.859-860]

Slide 160: 

A 30yo female presents with diarrhea, a serum protein of 4.5ng/100dl, a small bowel follow through demonstrates dilated bowel, hypersecretion, variable thickened folds with an intussuception appearance.a. Sprueb. Sclerodermac. Whipple’s diseased. Gardner’se. Familial polyposis

Slide 161: 

A. SprueSprue is characterized by dilated small bowel loops, hypersecretion, and malabsorption. Transient intussusceptions are typical. The jejunal fold pattern is decreased (ilealization of the jejunum) and the ileal fold pattern becomes prominent (jejunization of the ileum). Scleroderma is characterized by atrophy of the muscularis layer resulting in flaccid, dilated bowel. A “hidebound” appearance of the small bowel folds is present, as the thinned folds are tethered together. Excessive contraction of the mesenteric border results in antimesenteric sacculations.Whipple’s disease is caused by Gram-positive rods. Irregularly thickened folds are present, most prominent in the jejunum, with tiny nodules spread throughout the mucosa. CT demonstrates enlarged low density mesenteric lymph nodes (Weissleder171; Brant and Helms 744-46). GI manifestations of Scleroderma do not demonstrate fold thickening but can rather demonstrate a hidebound appearance. Alternatively, folds may appear normal (Dähnert p. 859-860)

Slide 162: 

Which segment of the colon is most prone to ischemiaa. ascendingb. transversec. splenic flextured. sigmoide. rectum

Slide 163: 

C. splenic flextureLocation: left colon 46-90%, all colon 11%, right colon 30%, transverse 9%, sigmoid 4%, rectum spared.Most commonly affected segments: (watershed areas):- Griffith point(80%) – jx SMA/IMA – splenic fx.- Point of Sudeck – jx IMA/hypogastric – rectosigmoid jx Etiology: diminished blood flow within bowel wall (mucosa + submucosa most sensitive to ischemia); major mesenteric vessels usually patent.Precipitating factors:(a) bowel obstruction: volvulus, carcinoma (proximal bowel segment affected)(b) thrombosis: cardiovascular disease, collagen vascular disease, sickle cell disease, hemolytic- uremic syndrome, oral contraceptives(c) trauma: history of aortoiliac reconstruction (2%) with ligation of IMA. [Dähnert p. 837]

Slide 164: 

A 50 yo man presents with bloody stools after acute onset of abdominal pain. Films shows thickened folds of the transverse colon. Diagnosis?a. Ischemic colitisb. Pseudomembranous colitisc. Ulcerative colitisd. Granulomatous colitise. Colon cancerf. IBDg. Diverticulitish. Yersinial Colitis i. Embolic

Slide 165: 

A. Ischemic colitis Mesenteric ischemia classically presents with abdominal pain, rectal bleeding, and thumbprinting. UC is a mucosal disease which typically starts in the rectum.- Peak incidence is between 20 and 40 years of age.Pseudomembranous colitis is caused by overgrowth of C. difficile after long-term antibiotics. The clinical presentation consists of diarrhea, fever, pain, and leukocytosis (Dähnert p. 696; Brant and Helms p. 757; Weissleder p. 185-86).“Nonocclusive ischemia is characterized by slow flow in the SMA, diffuse narrowing of SMA branches and arcades, segements of alternating spasm and dilatation of these branches, and poor filling of the vasa recta. Contrast persists in intestinal branches for >2 seconds after the injection has ended. Profound systemic hypotension and certain vasoconstricting drugs can produce similar findings. Valji, Vascular and Interventional Radiology 1999 p.189

Slide 166: 

Regarding Barrett’s esophagus:a. usually seen in the upper 1/3b. cannot distinguish normal from Barrett’s on EGD c. UGI can differentiate normal from Barrett’sd. If untreated can lead to SCCe. Associated with reflux

Slide 167: 

E. Associated with refluxReplacement of squamous epithelium to columnar epithelium- Location –lower esophagus> middle > upper- Leads to adenocarcinoma (not squamous cell!)- Results from chronic reflux esophagitis- UGI findings are nonspecific and must be followed up by EGD- Diagnosis made with endoscopy and endoscopic biopsy to r/o adenocarcinoma [Dähnert p. 796, GI Req p. 17]

Slide 168: 

Regarding viral esophagitis:a. more common than monolialb. associated with immunocompromised patientc. common cause of strictured. assoc. w/ reflux dze. can occur inferior to the crico-pharyngeal muscle

Slide 169: 

B. associated with immunocompromised patientViral esophagitis tends to occur most commonly in AIDS patients and include that of herpes esophagitis, CMV esophagitis, and HIV esophagitis. These infections are not associated with reflux disease. The hallmark of these lesions are ulcers surrounded by a radiolucent rim of edematous mucosa not strictures. Many of these lesions can occur in the oropharynx. Ref. Chapter 5 Double contrast GI radiology, Levine and LauferCandida albicans is the most common cause of infectious esophagitis. Viral esophagitis most often affects immunocompromised patients, particularly those with AIDS. Reflux is the most common cause of esophageal stricture. Other causes include Barrett’s, corrosives, radiation, neoplasm, webs. [GI Requisites p. 14. Brant & Helms p. 714-715].

Slide 170: 

Viral esophagitis presents asa. shaggy ulcersb. stricturesc. large ulcersd. annular lesions

Slide 171: 

C. Large UlcersThese lesion tend to present as discrete, superficial ulcers---they are not shaggy. (* shaggy ulcers would be more typical for candida)Ref. Chapter 5 Double contrast GI radiology, Levine and Laufer

Slide 172: 

What is the most common cause of benign gastric ulcer along the greater curvature?a. antacidsb. morphinec. tetracyclined. KCle. Prednisonef. C. diffg. ASA

Slide 173: 

G. ASAThe classic location of NSAID ulcers is in the antrum along the greater curvature. In addition, the incidence of PUD from H.pylori is increased in patients on NSAIDS.Tetracycline along with Bisthmuth and Flagyl are used to treat H.Pylori. [GI Requisites p. 17, Dähnert p. 826, 830]

Slide 174: 

Regarding intussusception:a. the most common site of perforation is the intussusceptumb. ileocolic is the most common typec. a lead point is more likely in a recurrent intussusceptiond. it most commonly occurs in 18 m/o - 5 y/o.e. a lead point is found in 50% of recurrent intussusceptions

Slide 175: 

B. ileocolic is the most common type95% occur in children and 75-95% of these are ileocolic (ileoileal is more common in adults). Peak incidence is 5-9 months (40%), 60% occur before the 1st year 90% before the 2nd. [GI Requisites pp. 88-91.] Regarding perforation: it occurs either at the inner most wall(the intesusceptum) or at the outer most wall(the intususcepiens

Slide 176: 

Which of the following would appear as a large cavitary lesion in the bowel?a. Adenocarcinomab. Lymphomac. Leiomyosarcomad. Melanoma

Slide 177: 

C. LeiomyosarcomaLeiomyosarcoma of small bowel: duodenum 26%, jejunum 34%, ileum 40%- may show central ulcer pit / fistula communicating with a large necrotic center. Dähnert 5th p. 840.Adenocarcinoma: - annular stricture with overhanging edges (60%)- lobulated / ovoid polypoid sessile mass (41%)- ulcerated mass (27%) Dähnert 5th p. 788.Lymphoma of GI tract: Radiographic types--- Polypoid / nodular (47%)- Ulcerative (42%); may be complicated by perforation- Diffusely infiltrating (11%)Melanoma of GI tract: small intestine 35-50%- multiple submucosal nodules ± “bull’s eye / target” appearance = central ulceration. Dähnert 5th p. 843

Slide 178: 

Which of the following is not seen with leiomyosarcoma of stomach?a. larger tumor may show cystic area of necrosisb. usually broad based intramural massc. treated with chemo and XRTd. spread hemotogenouslye. better prognosis than other gastric cancers

Slide 179: 

C. Treated with CXT and XRTLeiomyosarcomas are large submucosal lesions with single, multiple, or cavitary ulcerations. These masses tend to grow silently to a very large size and have central hemorrhage and necrosis. They may be pedunculated or exogastric. They metastasize hematogenously.Histologic differentiation from leiomyoma is difficult and differentiation is based on size, gross appearance, and behavior of the tumor. Chemo and XRT have not proven useful. (Brant and Helms p. 727, Dähnert 840) http://www.emedicine.com/med/topic1180.htm

Slide 180: 

Giardiasis in small bowel causes?a. GI blood loss/chronic GI bleedingb. chronic malabsorptionc. ulcers in ileumd. most commonly jejunale. negative stool exam rules outf. most commonly gastroduodenalg. most commonly ileal h. Usually seen in immunocompromisedi. Causes strictures

Slide 181: 

B. chronic malabsorptionGiardiasis causes malabsoption (Dähnert p.829). Giardia typically involves the duodenum and jejunum. - Symptoms include abdominal pain, diarrhea, and malabsorption. The diagnosis is made upon finding cysts or trophozoites in the feces, although this is variable so multiple samples should be taken. No association with GI bleeding is mentioned. (Brant and Helms 733; Harrison’s Int. Med. 910-12).1.5 – 2% US population, 4-16% tropical countries, 3-20% - children in southern US. Immunocompromised are predisposed.

Slide 182: 

Regarding aphthous ulcers in Crohn’s disease:a. are usually specific for the diseaseb. usually painfulc. irreversibled. bleede. denote involvement of the circular muscle layer

Slide 183: 

B. usually painfulAphthous ulcers are not specific - ddx is long - amebic colitis, TB, Behcets. (Dähnert , p.766)Aphthous ulcers are caused by mucosal edema and erosions over lymphoid follicles, and are the earliest radiographic sign of Crohns (AFIP notes)

Slide 184: 

What is true re Crohn disease?a. asymmetrical mural involvement/ simultaneous involvement of colon and SBb. continuous involvement of colon and SBc. most often involves SB and colond. frequently involves gastroduodenume. most commonly involves jejunum

Slide 185: 

A. asymmetric mural involvementCrohn’s disease involves the colon and TI 55% of the time, only small bowel 30%, and only colon 15%. There is typically asymmetric involvement both longitudinally and around the lumen. Skip areas represent normal intervening bowel. The duodenum is involved 20% of the time (Brant and Helms 747; Weissleder 184-85).

Slide 186: 

The following statements regarding Glucophage (metformin) are false except:a. Combines with iodine and causes nephrotoxicityb. Can’t give iodinated contrast if taken within 48hrs of the studyc. Causes lactic acidosis in patients with impaired renal functiond.

Slide 187: 

C. Causes lactic acidosis in patients with impaired renal function Metformin may cause lactic acidosis, mainly in patients with impaired renal function. If a patient is to have iodinated contrast, metformin should be withheld for 48 hours after the examination, but metformin may be taken up to the examination. Renal function should be checked before reinstituting metformin. (Bristol-Squibb, metformin package insert).

Slide 188: 

A man undergoes a SBFT and has an excavating, freely mobile mass in the region of the TI. Most likely cause--a. Carcinoidb. Crohns dzc. Lymphomad. Adenocarcinomae. TBf. Leiomyosarcomag. melanoma

Slide 189: 

C. Lymphoma (most likely choice)Lymphoma of GI tract: Radiographic types-- [Dähnert 5th p. 841-842]- Polypoid / nodular (47%); Ulcerative (42%)--may be complicated by perforation; Diffusely infiltrating (11%)- most common malignant SB tumor (20% of SB malignancies); 51% in ileum- may present as a large mass with only a small intramural component- Lymphoma affects the TI most often due to the amount of lymphoid tissue normally found thereLeiomyosarcoma of small bowel: duodenum 26%, jejunum 34%, ileum 40%- may show central ulcer pit / fistula communicating with a large necrotic center. Dähnert 5th p. 840.- Leiomyosarcoma is more common in the ileum than jejunum. Most are exophytic and grow to large size. Ulceration and bleeding are common[* probably less common overall than lymphoma, however]Carcinoid is the most common small bowel tumor and usually occurs in the TI. However, this tumor tends to be very desmoplastic and “fixed,” not freely mobile as mentioned in the root. .Adenocarcinoma affects the duodenum and jejunum, but is uncommon in the TI. (Brant and Helms 738-40, GI Req p. 117).

Slide 190: 

A large, well defined homogeneous mass in the ileum of an otherwise asymptomatic adult female is most likely what?a. lymphangiomab. hemangiomac. adenomad. lipomae. leiomyoma

Slide 191: 

E. Leiomyoma.The differential diagnosis for benign small bowel tumors are in order of decreasing frequency are 1) leiomyoma, 2) lipoma, 3) adenoma 4) hemangioma and 5) lymphangioma and 6)neurogenic tumors (usually neurofibromatosis). Leiomyomas are scattered evenly throughout the small intestine. Leiomyomas, which originate predominantly in the submucosa, manifest as oval or rounded, smooth filling defects. They may occasionally present as pedunculated intraluminal defects or intussusception may occur. Leiomyomas, which grow predominantly in the subserosal layer with little or no protrusion into the lumen, show displacement of bowel loops by the extrinsic mass. Dumbbell-shaped lesions occur. In the latter instance, a bilobed tumor protrudes both extraluminally and intraluminally. On CT, leiomyomas are sharply defined, spherical masses that display homogeneous tissue density and occasionally contain calcifications. Adenomas comprise about one-fourth of benign small bowel tumors. They occur more frequently in the duodenum than in the jejunum or ileum. Adenomas appear as intraluminal filling defects that are usually pedunculated and may have a lobulated surface. Lipomas usually arise in the ileum and occur less frequently than adenomas or leiomyomas. They also occur with an increased incidence in patients with Turner's syndrome. Similar to other benign small bowel tumors, lipomas appear as smooth or oval, predominantly intramural defect.The softness or fatty nature of the lesion may be inferred by the changes in shape during compression radiography or determined directly by showing attenuation values consistent with fat (-80 to -120 HU) on CT images.Small intestinal hemangiomas are not usually detected by barium studies, but when they are of sufficient size, they present as intraluminal or intramural polypoid defect. Their association with other syndromes increases suspicion. Patients with Osler-Weber-Rendu disease (hereditary hemorrhagic telangiectasia) may have cavernous hemangiomas of the small bowel in addition to the telangiectatic lesions. Occasionally, the plain film may show multiple mobile calcific deposits representing calcification of thrombosed hemangiomas. Dähnert , 4th ed. P. 770-771, Taveras and Ferrucci Radiology

Slide 192: 

The right and left hepatic lobes are divided by the :a. RHVb. LHVc. MHVd. falciform ligament

Slide 193: 

C. MHVThe middle hepatic vein divides the left and right hepatic lobes. The left hepatic vein divides the medial and lateral segments of the left lobe, and the right hepatic vein divides the anterior and posterior segments of the right lobe (Dähnert 561).

Slide 194: 

The following are true of transrectal/transvaginal drainage except:a. Crohn’s disease is a relative contraindicationb. Coagulopathy is a relative contraindicationc. Antibiotics should be withheld until a sample is obtainedd. Self-locking catheter should be usede. Medications should be administered for pain and anxiety

Slide 195: 

C. Antibiotics should be withheld until a sample is obtainedWithholding antibiotics to avoid compromising culture results is a dangerous practice that has been abandoned; if infection is suspected, broad-spectrum antibiotics should be administered before the procedure to prevent sepsis. Relative contraindications to percutaneous drainage include significant coagulopathy or inability to evacuate contents through a drainage tube (ie. Necrotic debris, hematoma, or infected tumor). The only absolute contraindication is the necessity to traverse a vital structure. A self-locking catheter should be placed in order to secure the drainage tube, since suturing is not possible (LaBerge 318; Valji 407).

Slide 196: 

Inflammatory bowel disease is more commonly associated with which of the following:a. Ureteral calculib. Bladder calculic. Enterocutaneous fistulad.

Slide 197: 

C. Enterocutaneous fistulaGU complications of Crohn’s disease include urolithiasis (oxalate and urate), hydronephrosis, renal amyloidosis, focal cystitis, ileouretal and ileovesical fistula (5-20%) patients with ulcerative Colitis tend not to have GU complications. Ref. Dähnert pg 670 Source: Gastrointestinal Radiology The Requisites p – 263

Slide 198: 

Aneurysmal dilatation of the small bowel is a feature most likely to be seen in which of thefollowing:a. Hodgkin's diseaseb. Carcinomac. Carcinoidd. Lipoma

Slide 199: 

A. Hodgkin’s diseaseRadiographic types: Ulcerative 42%- may have aneurysmal configuration.Dähnert 5th p. 841. Source: Gastrointestinal Radiology The Requisites p - 275

1999 : 

1999 45 Yo Male With Increased Serum Glucose, Unusual Skin Pigmentation, Portal Htn And Inc Liver Attenuation On Ct --- (Q: A Repeat Question On An Elderly Gentleman With Pancreatic Insufficiency, Hyperglycemia, High Attenuation Of Liver And Skin Pigmentation) Gauchers Wilsons Hemosiderosis Amyloid Steatottic Liver Diabetes Mellitus Hemochromatosis

Slide 201: 

G. HemochromatosisHemochromatosis- T. Excessive absorption and parenchymal retention of iron within non-RES organs (liver, pancreas, heart, pituitary gland). Diffuse increased liver attenuation is noted, and 90% of patients exhibit hyperpigmentation. Complications include diabetes mellitus and periportal fibrosis leading to cirrhosis Primary form due to defect in intestinal mucosa, inc. Fe absorp); Clinical- bronze diabetes (due to insulin resistance by hepatocytes and pancreatic beta-cell damage from Fe deposition), cirrhosis, DM, hyperpigmentation. Secondary: due to mult transfusions, bleeders. Imaging:US: hyperechoic liver; CT: dense liver, relative “low density” intrahepatic vessels; MR: liver and spleen low intens on T2W; in primary form, panc is also hypointense; CX: HCC (Dähnert 585-6 and Weissleder)Gaucher’s-F. This is an inborn error of metabolism with deficiency of glucocerebrosidase, resulting in intracellular accumulation of glucosylceramide in predominantly the RES cells. This results in HSM, impaired liver fxn, hemachromatosis, anemia, leukokemia, thrombocytopenia, bone pain. Imaging Findings: HSM (marked splenomeg), focal infarcts are low dens on CT and hyperechoic on US; MSK findings- Erlenmeyer flask deformity of femur, generalized osteopenia, mult lytic lesions, aseptic necrosis of femoral head(Weissleder 197).Wilson’s- F. A hereditary disorder of copper metabolism which results in deposition within the liver and brain. Liver attenuation is increased, but there is no mention of skin or electrolyte abnormalities (GI Requisites 133). (Dähnert 3rd e) “hepatolenticular degeneration”, autosomal recessive w/ excessive copper retention; Sxs- tremor, rigidity, dysarthria, dysphagia, intellectual impairment, emotional disturbance, cirrhosis; skeletal findings in 2/3; neuro findings w/ hypodensity and inc T1, T2 in BG and rarely thalamus, cerebral WM atrophy DIAGNOSTIC: Kayser-Fleischer ring (green pigmentation around limbus cornea)Hemosiderosis-F This is a milder form of hemachromatosis which increased iron deposition which does not result in organ damage (Dähnert 585).Amyloid-F. (Dähnert 3rd e) deposition of protein-polysaccharide in various organs with mult findings: GI findings include malabsorption, occult GI bleed, obstruction, macroglossia, splenomeg, splenic masses This disorder affects the stomach, small bowel, and esophagus. There is no mention of liver involvement (Dähnert 657-8).Steatottic Liver-F. Synonymous for diffuse fatty infiltration, which results in decreased attenuation of liver parenchyma (Dähnert 582-3).Diabetes Mellitus- F. No association with diabetes mellitus in my sources.

Slide 202: 

Most common esophageal ulcer finding in a patient with HIV: Giant esophageal ulcer Shaggy esophagus. Small ulcerations. Pseudodiverticulitis. Leiomyoma Nodules

Slide 203: 

B. Shaggy EsophagusShaggy esophagus- Probably T. The most common cause of infectious esophagitis is Candida. This is highly prevalent in AIDS patients. Usually, these demonstrate long, linear filling defects from raised plaques. However, with AIDS, the disease is more fulminant and results in the classic “shaggy esophagus” appearance (Brant/Helms 714)."Shaggy" esophagus. Fulminant form of esophageal candidiasis encountered in patients with AIDS who may present with a grossly irregular or "shaggy" esophagus due to innumerable coalescent plaques and pseudomembranes with trapping of barium between these lesions. Some of these plaques and pseudomembranes may eventually slough, producing one or more deep ulcers superimposed on a background of diffuse plaque formation. Occasionally, these AIDS patients may present with the shaggy esophagus of candidiasis as the initial manifestation of their disease.Giant esophageal ulcer- Probably F. HIV has been reported to produce giant esophageal ulcers identical to those produced by CMV. However, see shaggy esophagus below (GI Reqs 12).Small ulcerations – F. Non-specific, this could represent anything from Candida, HSV (discrete mucosal ulcers), or Crohn’s disease (aphthous ulcers) (BH 714-5).Pseudodiverticulitis- F. Esophageal pseudodiverticulosis is exceedingly rare, and 90% of cases are associated with any severe esophagitis. Multiple tiny, rounded barium collections are seen in long rows paralleling the long axis of the esophagus. No mention of pseudodiverticulitis (Dähnert 680).Leiomyoma- F. Most common benign esophageal neoplasm. No association with AIDS mentioned (BH 714).Nodules- F. The raised plaques seen in Candida may resemble small mucosal nodules. Otherwise, this is a non-specific finding (BH 714).RADIOGRAPHIC FINDINGS HIV esophagitis is characterized on esophagography by the development of one or more giant, flat ulcers in the esophagus, sometimes associated with small, satellite ulcers. These giant ulcers are indistinguishable on barium studies from CMV ulcers in the esophagus. In fact, recent data suggest that most giant esophageal ulcers in HIV-positive patients are caused by HIV rather than CMV and that it is not possible to differentiate these infections either by clinical or radiographic criteria. Endoscopy is therefore required for a definitive diagnosis prior to initiating therapy in these patients. (Marc S. Levine, Esophagitis, Volume 4 Ch 13 in Radiology: Diagnosis, Imaging and Intervention, Taveras, J. Ed. 1998)

Slide 204: 

Which Of The Following Is Not Inherited? Cronkite-Canada Peutz-Jager Juvenile Polyposis Multiple Hamartomas Gardners Turcot’s Familial polyposis

Slide 205: 

A. Cronkite-CanadaCronkite-Canada-T. This disease has no familial predisposition. Multiple hamartomatous polyps are seen in the stomach and colon 100% of the time, and small bowel >50% of the time (Dähnert 671).Peutz-Jager- F. Peutz-Jegher consists of hamartomatous polyps which typically affect the small bowel more than the colon and stomach. These are non-neoplastic but may be associated with pre-malignant adenomatous polyps. Autosomal dominant inheritance pattern (BH 74`).Juvenille Polyposis-F. Juvenille polyposis consists of large polyps in the rectum which can prolapse or obstruct, but are of unknown malignant potential. Rare autosomal dominant disease (BH 742; Dähnert 696-7).Multiple Hamartomas- F. Also known as Cowden disease, this is an autosomal dominant condition characterized by multiple hamartomatous polyps, commonly in the sigmoid. Exceedingly rare condition (Dähnert 669).Gardner’s syndrome- F. Gardner’s syndrome refers to familial polyposis (tubovillous polyps) with the following extracolonic manifestations: osteomas of the skull, supernumerary teeth, exostoses of the mandible, dermal fibromas, desmoids, and epidermoid inclusion cysts (phew!). Autosomal dominant inheritance (BH 755; Dähnert 685).Turcot’s syndrome- F. Again, a familial polyposis syndrome variant with associated CNS tumors, especially suptratentorial GBM and occasionally medulloblastoma. Like Gardner’s syndrome, AD (BH 754-5; Dähnert 717).Familial polyposis F. Vanilla familial polyposis syndrome consisting of tubovillous polyps. Colorectal CA will develop in nearly all patients. Like Gardner’s and Turcot’s, AD (BH 754-55).

Slide 206: 

Most Common Cause Of Linitis Plastica Breast Ca Thyroid Ca Melanoma Prostate Ca Leimyosarcoma Kaposis Carcinoid

Slide 207: 

A. Breast Cancer*Note: Weissleder lists scirrhous carcinoma of the stomach as the most common cause of linitis plastica. It is conveniently missing from the above list (Weissleder 238).Breast CA- T. Metastatic disease can cause linitis plastica, and breast CA is the most common culprit. Lung CA is also a common cause (Weissleder 238).Thyroid CA- F. Does not metastasize to stomach. Papillary CA spreads to regional lymph nodes and lung; Follicular CA spreads to lung and bone; Anaplastic CA locally invades the thorax, internal carotid a., jugular v., or larynx; Medullary CA spreads to nodes, lung, liver, and bone (Dähnert 334).Melanoma- F. Metastasizes to the submucosal portion of the stomach, causing a target lesion. Not associated with linitis plastica (Aids to Radiologic Differential Diagnosis, Chapman, 3rd. ed., 220).Prostate CA- F. Prostate CA spreads via local extension and regional nodes. The disease spreads hematogenously to the axial skeleton, and lungs, liver, and kidneys late in the disease (BH 825).Leiomyosarcoma – F get GI bleeding from ulceration and mets to liver, lung, peritoneum; rarely to bone. Findings: geterogeneous exogastric mass with central zones of low density (necrosis with liquefaction) and ulceration (Dähnert 5th p840)Kaposi’s Sarcoma- F. Epidemic KS is disseminated, aggressive, and requires treatment. This affects the GI tract 40-50% of the time causing nodules, plaques, polypoid lesions, and thickened folds. Bulky lymphadenopathy can be seen in the retroperitoneum and mesentery (BH 667). Carcinoid- F. Carcinoid metastasizes to the liver and regional nodes. No mention of stomach involvement (BH 739).

Slide 208: 

Regarding GI bleeds: UGI bleeds account for 65% Small bowel bleeds account for 25% Need a rate of 0.1cc/min for detection with angio

Slide 209: 

A. UGI Bleeds Account For 65%Upper GI bleeds account for >65% TSmall bowel bleeds account for 24% F (actually lower GI bleeds account for 24%)Need a rate of 0.1cc/min for detection with angio- F. (Angiography requires 0.5 cc/min rate of bleeding for detection (BH 600). And Scintigraphy can detect 0.1 cc/min of bleeding.(Dähnert 5th p1111)Refer to AFIP GI notes from Dr. Bruce Brown (Iowa).

Slide 210: 

Zenker’s diverticula: Occur below the cricopharyngeus Occur at the posterior and inferior aspect of the pharynx Can contract due to the presence of a muscular wall Are traction diverticula

Slide 211: 

B. Occur At The Osterior And Inferior Aspect Of The PnarynxOccur at the posterior and inferior aspect of the pharynx- T. This herniation occurs posteriorly at the pharyngeoesophageal junction, in an area of potential weakness (Killian’s dehiscence) (GI Reqs 2nd p30).Occur below the cricopharyngeus- F. Zenker’s diverticula are pseudodiverticula and represent herniation of mucosa and submucosa. This occurs superior to the cricopharyngeus muscle (GI Reqs 22-23).Can contract due to the presence of a muscular wall- F. Only mucosa and submucosa herniate through the defect (GI Reqs 22-23).Are traction diverticula- F. Traction diverticula result from fibrous adhesions following lymph node infection, such as TB, and contain all 3 esophageal layers (Dähnert 625).

Slide 212: 

All these structures abut the caudate lobe except: IVC Ligamentum venosum Right lobe live Left lobe liver Ligamentum teres

Slide 213: 

A. IVCIVC- T. The IVC is directly posterior to the caudate lobe (BH 669).Ligamentum venosum- T. The ligamentum venosum is directly anterior to the caudate lobe (BH 669).Right lobe of liver- T. The caudate lobe is contiguous with the right lobe of the liver (BH 669).Left lobe of liver- T. Superior to the ligamentum venosum, the caudate lobe abuts the left liver lobe (Dähnert 562).Ligamentum teres- F. The ligamentum teres is the embryologic remnant of the obliterated umbilical vein. This structure is anteriorly located and runs into the ligamentum venosum, is not directly adjacent to the caudate lobe (Dähnert 562; Netter Atlas 270).

Slide 214: 

The most common cause of colovesicular fistula: Crohn’s Diverticulitis Lymphogranularium venereum Ulcerative colitis cancer

Slide 215: 

B. DiverticulitisDiverticulitis- T. Can fistulize to the urinary bladder as well as small bowel or vagina (Dähnert 673).Crohn’s- F. Tends to affect the right colon, sparing the sigmoid and rectum. Long fistulous tracts tend to parallel the bowel lumen (Dähnert 670).Lymphogranuloma venereum- F. STD caused by Chlamydia trachomatis causing a non-specific granulomatous response. Starts at the rectum and may spread to the sigmoid and descending colon. Can fistulize to pericolic regions, rectum, and vagina. Urinary bladder not mentioned (Dähnert 699).UC- F. UC is a mucosal and sucmucosal disease and does not form fistulas (Dähnert 728).Cancer- F. Complicutions include obstruction, perforation, instussusception, pneumatosis, and pseudomyxoma peritonei. No fistulas (Dähnert 668).

Slide 216: 

In gallstone ileus: Two/thirds or more of patients you see pneumobilia Most of the time you can see the gallstone on plain film You need to a percutaneous transhepatic cholangiogram in order to identify the fistula The most common location for the stone to stick is in the mid jejunum It is most likely to erode into the transverse colon

Slide 217: 

A. 2/3 Or More Of Patients Have Pneumobilia 2/3 or more of patients have pneumobilia- T. In 67% of patients, air is seen in the biliary system or gallbladder (BH 660).Most of the time you can see the gallstone on plain film- F. Ectopic calcified gallstone is only seen about 50% of the time (BH 660). 25% of the time according to GI Reqs 2nd p124PTC necessary to identify fistula- F. Barium study is adequate to image fistula. Duodenum should be injected specifically to evaluate for opacification of the biliary tree (BH 660).Most common location for stone to stick is mid-jejunum- F. The stone most commonly lodges in the distal ileum - at the ileocecal valve(BH 660 and GI reqs 2nd p124).It is most likely to erode into the transverse colon- F. The most common fistulization occurs between the duodenum and gallbladder, hence the import of injecting the duodenum specifically as stated above (BH 660).Gallstone ileus is a mechanical obstruction of the bowel from a passed or fistulized gallstone (usually > 2cm). It has the following characteristics: Incidence: 0.4 - 5% of all intestinal obstructions (20% of obstruction in patients >65 years; 24% of obstructions in patients >70 years); develops in <1% of patients with cholelithiasis; in 1 of 6 perforations; risk increases with age Age: average 65 - 75 years; M:F = 1:4 -7 Symptoms/History: previous history of gallbladder disease, intermittent episodes of ACUTE colicky abdominal pain (20 - 30%), nausea, vomiting, fever, distension, obstipation Radiographic Findings: Rigler triad on plain film: 1. Partial / complete intestinal obstruction (usually small bowel), "string of rosary beads" = multiple small amounts of air trapped between dilated + stretched valvulae conniventes (in 86%) 2. Gas in biliary tree (in 69%) 3. Ectopic calcified gallstone (in 25%): stones are commonly >2.5 cm in diameter Change in position of previously identified gallstone UGI / BE: 1. Well-contained localized barium collection lateral to first portion of duodenum (barium-filled collapsed GB + possibly biliary ducts) 2. Fistulous communication: cholecystoduodenal (60%), choledochoduodenal, cholecystocolic, choledochocolic, cholecystogastric 3. Identification of site of obstruction: terminal ileum (60 - 70%), proximal ileum (25%), distal ileum (10%), pylorus, sigmoid, duodenum (Bouveret syndrome) Recurrent gallstone ileus in 5 - 10% (additional silent calculi more proximally) Prognosis: high mortality (Gore, Levine, and Laufer, Textbook of Gastrointestinal Radiology, 1994: 1651-2.) and (Dähnert , Dähnert ’s Electronic Radiology Review, 1998)

Slide 218: 

Which is least likely to cause a gastric ulcer Zollinger Ellison Helicobacter gastritis Menetrier’s

Slide 219: 

C. Menetrier’sMenetrier’s disease: Large gastric rugal folds (hypertrophic gastritis) with protein-losing enteropathy. Clinical triad: achlorhydria, hypoproteinemia, edema. Typically occurs in middle-aged men. Complication: gastric carcinoma, 10%. Not usually associated with ulcers. Radiographic features: Giant gastric rugal folds, usually proximal half of stomach; Hypersecretion: poor coating, dilution of barium; Gastric wall thickening; Small intestinal foId thickening due to hypoproteinemia; Peptic ulcers are uncommon (Dähnert )Ménétrier's disease is the eponym for large gastric rugal folds with protein-losing enteropathy. This is an uncommon but not rare condition that is surrounded by confusion. At least 37 alternative terms exist for this disease process. The most common synonyms include hypertrophic gastritis, hyperplastic gastropathy, and giant hypertrophy of the gastric mucosa. Hyperplasia, which is present in the mucous or glandular tissues, results in prominence of the normally present gastric folds, especially along the greater curvature . However, thickening of folds may be seen in any region of the stomach. Variations in the clinical features and pathologic findings have led to a variety of classifications. Patients may have pain, vomiting, peripheral edema, gastrointestinal tract bleeding, and weight loss. More than half of patients have absent or decreased secretion of gastric acid, but many have normal and a few have increased secretion of acid. Protein-losing enteropathy is considered to be the sine qua non for classifying large gastric folds as Menetrier's Ménétrier's disease. Case reports cite carcinoma of the stomach occurring in patients with Menetrier's Ménétrier's disease, and a causal relationship may exist. As with all unexplained diseases of the stomach, a relationship between Menetrier's Ménétrier's disease and H. pylori infection is being sought. Patients who have no symptoms of gastric disease and no clinical evidence of any other abnormality occasionally are seen with large gastric folds. The term hyperplastic gastropathy is a useful, albeit meaningless, term for a benign increase in the pattern of rugal folds within the stomach. Francis J. Scholz, Gastritis, Volume 4 Ch 19 in Radiology: Diagnosis, Imaging and Intervention, Taveras, J. Ed. 1998Zollinger-Ellison- T. Gastrinoma causes ZE, and this results in multiple ulcers in the duodenum, stomach, and jejunum (BH 733).Helicobacter gastritis- T. 70% of benign gastric ulcers are caused by H. pylori (BH 724).Menetrier’s- F. Also known as hypertrophic gastritis, this condition is characterized by increased mucus production, hypoproteinemia, hypochlorhydria, and giant rugal folds in the proximal half of the stomach. Benign gastric ulcers are rare (Weissleder 163).

Slide 220: 

The origin of the superior hemorrhoidal artery Internal iliac External iliac IMA SMA

Slide 221: 

C. IMAThe IMA originates at the L3 level and gives rise to 3 branches: left colic, sigmoid, and superior hemorrhoidal (rectal) arteries (BH 598).

Slide 222: 

Pt with splenic v thrombosis and bleeding gastric varices. You should do: Splenorenal shunt Mesocaval shunt Portocaval shunt Spleno-? Shunt [ Splenectomy ]

Slide 223: 

E. SplenectomyThe appropriate therapy is to do a splenectomy. Contrary to belief most patients with isolated gastric varices may have generalized portal hypertension rather than splenic vein obstruction as the cause and hence should be treated by a more extensive procedure than just splenectomy. Nagral et al. Indian J Gastroenterol 1999 Apr-Jun;18(2):69-72Splenorenal shunt- F. Distal splenorenal (Warren) shunt is a selective conduit that diverts blood flow from GE varices but maintains intestinal portal venous flow. However, the splenic v is thrombosed so this is not a viable option (Valji Vascular and Interventional Radiology, 215).Mesocaval shunt- F. Non-selective conduit that directs all portal blood flow away from the liver and reduces PV pressure to normal levels if there is portal hypertension, but here the splenic vein is thrombosed, i.e. the portal pressure is normal. Prevents long-term variceal hemorrhage due to decreased PV pressure (Valji 214-5). Portocaval shunt- F, Also, non-selective conduit directing all portal blood flow away from the liver and reduce PV pressure to normal levels (Valji 214-5).Spleno-?- F. Splenic v is thrombosed.

Slide 224: 

What is assoc with echinococcal splenic cysts Wall trebeculation Most are symptomatic by age 20 Are congenital cysts Are due to trauma

Slide 225: 

B. Most Are Symptomatic By Age 20Most are symptomatic by age 20- Probably T. Clinical manifestations are non-specific, but usually consist of abdominal pain, splenomegaly, and fever. No age is mentioned (Dachman, Radiology of the Spleen, 156-7).Wall trabeculation- F. These cysts contain a sharp marginal wall of reactive parenchyma (ectocyst) and multilocular internal structure (endocyst) (Dachman, Radiology of the Spleen, 156).Are congenital cysts- F. Are due to Echinococcus granulosus. Epidermoid cysts are congneital (Webb, Fundamentals of Body CT, 165).Are due to trauma- F. Are due to echinococcus granulosus .

Slide 226: 

The changes in Cystic Fibrosis in the bowel in an adult is a risk factor for meconium ileus SBO Diverticulitis Cancer

Slide 227: 

B. SBOSBO- T. Adults can have bouts of low grade SBO whether or not they experienced meconium ileus as children. The adult form is called “meconium ileus equivalent” and symptoms include right lower quadrant pain, loss of appetite, occasionally with emesis and palpable mass (Harrison’s 1450).Meconium ileus- F. This complication of CF is seen in neonates, as well as meconium peritonitis or intussusception (Weissleder 52).Diverticulitis- F. No mention of diverticulitis in any of my sources.CA- F. No mention of CA in any of my sources.Cystic fibrosis is a multisystem disease that affects the exocrine glands of the pancreas, lungs, and GI tract. It is the most common cause of exocrine pancreatic deficiency in children. It is an autosomal dominant trait and is the most serious inherited disease of whites (1 in 2000). It is rare in asians and blacks. I have included the text from Dähnert to describe all of the radiographic findings. In Older children and adults with CF, a number of radiographic abnormalities in the GI tract can be seen. These include: 1. Thick duodenal folds with nodular indentations of the duodenal wall along with redundancy, kinking, or distortion of the duodenum in 85 % 2. Thickening of the mucosal folds of the proximal jejunum and a nonspecific malabsoption pattern in up to 33 % 3. “Jejunalization of the colon”- the colonic mucossa appears lacy and redundant owing to thick mucoid secretions and mucossal hypertrophy from clogged goblet cells. 4. Pneumatosis coli from dissection of pneumomediastinum into the colon 5. meconium ileus equivalent syndrome: mechanical obstruction of the distal small bowel by thick stool which usually occurs in adults who do not take their pancreatic enzyme replacement therapy. This presents with the typical radiographic features of SBO with a bubbly soft tissue mass in the distal ileum and cecum. It is best treated with a water soluable enema with N-acetylcysteine (Mucomyst).(Gore, Levine, and Laufer, Textbook of Gastrointestinal Radiology, 1994: 2187-2191.)

Slide 228: 

Regarding epidermoid cysts of the spleen (this may be recalled very imperfectely!) secondary to blunt trauma contain proteinaceous contents can be hyperdense on NECT has a cuboidal cell lining Septated

Slide 229: 

E. SeptatedSeptated- T. Peripheral septations are present in 86% of cases (Dähnert 582).Secondary to blunt trauma- F. These are congenital cysts which are caused by infolding of the peritoneal mesothelium (Dähnert 582).Contain proteinaceous contents- F. These cysts may contain cholesterol, fat, or blood. There is no mention of protein (Dähnert 582).Can be hyperdense on NECT- F. These cysts have the same appearance as post-traumatic cysts, and are hypodense (BH 703).Has a cuboidal lining- F. A mesothelial or squamous epithelium is present (Dähnert 582).

Slide 230: 

Solid and papillary tumors of the pancreas are most associated with: Young women. Head of pancreas. Benign lesion. Lack of calcification Hypervascular Homogeneously hypoechoic

Slide 231: 

A. Young WomenYoung women- T. The mean age of patients is 25 years, and the female:male ratio is 9:1Head of pancreas- F. Solid and papillary tumors of the pancreas typically are located in the tailBenign lesion- F. These masses have metastatic potential. Targets include lymph nodes, omentum, and the liverCalcification – F: 33% have stippled/punctuate/ or amorphous calcificationHypervascular – F: lesion are hypovascular with no contrast enhancement sometimes see ehnancementof sloid tissue projectging toward center of massHypoechoic – F: lesions are echogenic with a necrotic center (Dähnert 5th p738)

Slide 232: 

Cause for hyperdense liver on CT scanning. Amiodarone Fatty liver Amyloid Cyclophosphamide toxicity

Slide 233: 

A. AmiodaroneAmiodarone- T. Amiodarone consists of 37% iodine by weight and is a cause of hyperdense liver parenchyma on CT (Dähnert 2nd p658).Fatty liver- F. Fatty liver decreases attenuation (Dähnert 583, years of personal study).Amyloid F. Amyloid deposition causes hepatosplenomegaly. However, there is no mention of density change (Weissleder 173).Cyclophosphamide toxicity- F. Conversely, chemotherapy tends to decrease liver attenuation. Cyclophosphamide toxicity is primarily pulmonary, causing a basal reticular pattern (BH 484; Weissleder 249).Mnemonic: GG CHAT (Dähnert 2nd p658): Gold therapy, Glycogen storage disease, Cyclophosphanide, Hemochromatosis/hemosiderosis, Amiodarone, Thorotrast.

Slide 234: 

Which liver lesions would not be hyperdense on contrast CT melanoma renal cell CA thyroid CA

Slide 235: 

B. Renal Cell CaRCC- F. RCC mets are hypervascular, although may become iso-dense on contrast CT. (Dähnert 596).Melanoma- T. Melanoma metastases are hypervascular, and would be hyperdense on contrast CT (Dähnert 596).Thyroid CA- T. You guessed it, thyroid CA mets are also hypervascular (Weissleder 249).Editors Note: The concept here appears to be, “what is to be gained by non-contrast CT of the liver, when evaluating metastatic disease.” There are certain mets which become iso-dense with contrast enhancement, thus obscurring their presence if only a contrast study is done. These include: 1.Renal cell CA 2.Carcinoid 3. Islet cell CA (Dähnert p.596, GI Requisites p.138, GU Requisites p.95)

Slide 236: 

Which of the following is not a hypervascular metastases within the liver? Carcinoid Thyroid Renal Bronchogenic carcinoma melanoma

Slide 237: 

D. Bronchogenic CarcinomaBronchogenic carcinoma- F. Metastases from bronchogenic carcinoma are hypovascular (Weissleder 249; Dähnert 596).Carcinoid- T. Hypervacular liver metastases (Dähnert 596).Thyroid CA- T. You guessed it, thyroid CA mets are also hypervascular (Weissleder 249).RCC- F. RCC mets are hypervascular, although may become iso-dense on contrast CT. (Dähnert 596).Melanoma- T. Melanoma metastases are hypervascular, and would be hyperdense on contrast CT (Dähnert 596).

Slide 238: 

Least likely malignancy to metastasize to the liver Bronchogenic carcinoma Melanoma Breast Thyroid Renal ca

Slide 239: 

D. Thyroid CaThyroid CA- T. Thyroid does not usually metastasize to the liver. Prostate CA and skin cancers also have a low likelihood of spreading to the liver (Harrison’s 580).Bronchogenic carcinoma- F. Commonly metastasizes to the liver. Also tends to spread to lymph nodes, adrenal glands, bone, and brain, as well as the contralateral lung (BH 394).Melanoma- F. Melanoma commonly metastasizes to the liver. Interestingly, melanoma is the most common to metastasize to breast (Harrison’s 580; Weissleder 670).Breast- F. Breast commonly metastasizes to the liver. Also spreads to skin, lymph nodes, lungs, bones, and CNS (Harrison’s 1848).RCC- F. RCC liver mets are common, seen in approximately 33% of cases (Dähnert 795).

Slide 240: 

A three cm hemangioma of the liver is most likely to have this appearance. posterior acoustic enhancement iregular margins hypoechoeic doppler flow centrally

Slide 241: 

A. Posterior Acoustic EnhancementPosterior acoustic enhancement- T. Posterior acoustic enhancement is common, even in hypoechoic lesions (Weissleder 201).Irregular margins- F. The classic US appearance of a cavernous hemangioma is well-defined, echogenic mass (BH 835).Hypoechoic- F. Classically echogenic lesions (BH 835).Doppler flow centrally- F. Doppler usually demonstrates no central flow. On occasion, there may be slow flow detected with very high sensitivity settings (BH 835).Hemangiomas are thought to be m/c non-neoplastic lesion of liver (2-5%), 2nd m/c after mets, predilection for post right hepatic lobe, usually subcapsular. Classic sonographic appearance of hemangiomas is homogenous and hyperechoic, usually < 3cm. Atypical appearances tend to occur in larger lesions due to fibrosis, thrombosis and necrosis. In up to 40% of larger hemangiomas, inhomogenoeous hypoechoic mass w/ well-defined thick/thin echogenic lobulated border. Hypoechoic center possible. May show acoustic enhancement in 37-77% (Dähnert 3rd e, p520) Add’l finding occas seen is increased through transmission. Blood flow usu too slow to be detected by Doppler. Most hemangiomas are stable in size and echogenicity, but approx 10% regress partially or completely, only 2% enlarge. Can change sonographic appearance during the exam! General recommendation: low risk for malignancy pts should have 6 mo f/u (Requisites, US-p9-11 and GI-p169)

Slide 242: 

Complications of liver transplant include the following EXCEPT… GVHD Hepatic venous occlusive disease Pancreatitis Splenic abscess Adrenal hemorrhage

Slide 243: 

A. GVHDGVHD – F- : Liver transplants can be rejected but it is not due to GVHD. GVHD is specific description for the T lymphocytes from DONOR BONE MARROW causing selected epithelial damage of RECIPIENT targed organs. Occurs in 30-70% pts w/ allogeneic bone marrow txplt when immune-competent cells from donor react against immune-incompetent tissues or recipientHepatic venous occlusive disease – T – aka Budd-Chiari (5p’s PNH, plts, pill, pregnancy, polycythemia rubra vera), also caused by injury to vessel wall which I would think inherent in a transplant surgery(Dähnert 5th p683 and 718) and listed as a complication in (Primer 2nd p206)Pancreatitis - T- common postoperative especially kids – for more specifics medline search of liver TX and pancreatitis yields pages of resultsSplenic abscess – T - CT findings post liver transplant include abscesses including splenic (Primer 2nd p207)Adrenal hemorrhage occurs more commonly in neonates than adults. Listed specifically with orthotopic liver transplantation in (Dähnert 5th p909) Causes: severe trauma, shock, post-op – all these essentially inherent in liver transplant (Weissleder, p296)

Slide 244: 

Bone marrow transplant least likely to be associated with: Hepatoveno occlusive disease Graft-versus-host disease Adrenal hemorrhage Splenic abscess CMV pneumonia

Slide 245: 

C. Adrenal HemorrhageHepatoveno occlusive disease- T- can get Budd-Chiari due to immunosuppressive drugs in patients with BMT (Dähnert 5th p683)Graft-versus-host disease –T - GVHD is specific description for the T lymphocytes from DONOR BONE MARROW causing selected epithelial damage of RECIPIENT targed organs. Occurs in 30-70% pts w/ allogeneic bone marrow txplt when immune-competent cells from donor react against immune-incompetent tissues or recipientAdrenal hemorrhage – F - Could not find specific reference for or against this oneSplenic abscess- T – could not find specific reference but assume immunosuppressive drugs and subsequent compromised state would predispose to abscessCMV pneumonia- T – listed as early phase pulmonary complication (up to 100 days after tx) of BMT (Dähnert 5th p462)

Slide 246: 

Most reliable indicator of portal hypertension: Retrograde flow in the splenic vein. Slow flow in the splenic vein. Absence of flow in the splenic vein.

Slide 247: 

A. Retrograde Flow In The Splenic VeinSonographic findings: enlarged PV, splenomeg, ascites; portosystemic collaterals is the most specific sign, easiest to detect is recanalized paraumbilical vein that runs thru lig teres and communicates with umb segment of left portal vein bet medial and lat segments of left lobe. Next easiest to see is coronary vein behind the left lobe extending superiorly from splenic vein, normally has flow directed into splenic v but may have flow directed away from splenic v in pts w/ portal HTN (US Requisites p21).

Slide 248: 

Regarding portal venous pressure: Equals wedged hepatic pressure. Equals hepatic vein pressure. Equals hepatic vein pressure minus hepatic wedge pressure. Equals hepatic wedge pressure minus hepatic vein pressure.

Slide 249: 

A. Equals Wedged Hepatic Pressure.Hepatic wedge pressure = portal venous pressure (nl<10 mm Hg) (Dähnert 5th p733) Elevated hepatic wedge pressure = portal HTN.

Slide 250: 

There is a noncalcified 2 cm colonic polyp. The risk that this is a malignancy or the chance that this is a malignancy is: 0% 10% 50% 90%

Slide 251: 

B. 10%An adenomatous polyp measuring < 5 mm has a 0% chance of malignancy. 5-9 mm equals 1% chance. 10-20 mm = 10% chance. > 20 mm = 46% chance of malignancy.It is recommended that all polyps greater than 10 mm he removed. The patient may have a synchronous adenoma 50% of the time. Metachronous adenoma is seen 30-40% of the time. Synchronous adenocarcinoma is seen 1.5-5% of the time. Metachronous adenocarcinoma is seen 5-10% of the time. Most are asymptomatic References: B&H p.754, Dähnert 3rd e, p.575

Slide 252: 

Patient status post laparoscopic cholecystectomy. Now with right upper quadrant pain and ultrasound showing two echogenic calculi within the common duct. What is the best choice: ERCP with papillotomy Chemo dissolution Lithotripsy. Open cholecystectomy/stone removal Other choices not well remembered.

Slide 253: 

A. ERCP With PapillotomyERCP: Patients with common duct stones who have had a previous cholecystectomy are best treated by endoscopic sphincterotomy. The opening created in the sphincter permits stones to pass from the duct into the duodenum. Endoscopic sphincterotomy is unlikely to be successful in patients with large stones (>2cm), and it is contraindicated in the presence of stenosis of the bile duct proximal to the sphincter. Endoscopic removal of large impacted stones may be facilitated by preliminary lithotripsy. (Current Surgical Diagnosis and Treatment P557) and Harrisons 13th e, p 1513 [1994])Lithotripsy- T - Alternatives to Endoscopic Sphincterotomy for Stone Removal Other methods are being used for removal of common bile duct stones once ERCP has been performed. Endoscopic balloon dilation has shown success rates similar to endoscopic sphincterotomy with a lower occurrence of complications. Using this procedure, a deflated balloon at the end of the endoscope is moved up the bile duct beyond the stone; the balloon is then inflated and pulled back, pushing the stone out the small intestine as it moves. Endoscopic balloon dilation causes less trauma to the biliary sphincter. Occasionally, however, it is not wholly effective and follow-up procedures, such as lithotripsy, must be performed. This procedure is only appropriate when common bile duct stones measure less than eight to ten millimeters in diameter. Endoscopy with a technique called mechanical lithotripsy is also sometimes used for common bile duct stones. In this procedure, a tiny steel crushing basket is inserted through the endoscope into the bile duct; the basket expands to trap and then crush the stone. It is capable of crushing and removing very large stones. Laser and electric probes are also being used which send shock waves against the stone to crush it.FYI: Cholodocholithiasis occurs in 3-4% of post-cholecystectomy pts. Most common cause of bile duct obstruction! Get recurrent episodes of jaundice, chills, and fever (25-50%) (Dähnert 5th p695)

Slide 254: 

Which process is most likely to be responsible for lymphoid hyperplasia of the small bowel dysgammaglobinemia Crohn’s disease Sprue Scleroderma Peptic ulcer disease

Slide 255: 

A. DysgammaglobinemiaNormal lymphoid nodules are 1-3 mm and can be seen in the colon normally. Lymphoid hyperplasia is found in 1) nl variant in 13% of BE’s, (esp kids in the TI where lymphoid tissue is most abundant) 2) self-limiting local/systemic inflamm/infxn/allergy 3) may be related to immunodef/dysgammaglobulinemia w/ SB involvement. Location is primarily jejunum but may involve entire SB, asc colon & hep flexure, seldom in sigmoid/rectum. Mucosa studded w/ innumerable 1-3 mm small uniform polypoid lesions, may be umbilicated (uncommon) SB folds are nl when no underlying disease, may see fold thickening in pts w/ Ig deficiency or giardiasis. There has been suggestion that lymphoid hyperplasia may represent the earliest changes of IBD or lymphatic disease but this is, according to Requisites, “quite speculative and has never been proved.” (Dähnert 5th p841, GI Requisites, p115-16, 256-57)

Slide 256: 

Patient presents with thickening of the cecum, what clinical information would most make you think of typhlitis Pt is immunocomprimised Pt is on antiobiotics Pt is on chemo Pt has history of lymphoma

Slide 257: 

A. ImmunocompromisedCould be any of the choices but from many old recalls immunocimpromised is the best answer – I wonder about the accuracy of the other recalled answer choices.Ileocecal syndrome, neutropenic colitis aka typhlitis. Acute inflamm of cecum, appx and occas TI, initially described in kids w/ leukemia and severe neutropenia. Causes: leukemic/lymphomatous infiltrate, ischemia, focal pseudomembraneous colitis (abx use), infxn. Predisposed: common in childhood leukemia, aplastic anemia, lymphoma, immunosuppressive tx, clinical AIDS; Location: cecum and asc colon, appx and distal ileum may be secondarily involved. CT is preferred exam – circumferential wall thick, bowel wall edema, pericolonic inflammation, +/- pericolonic fluid and intramural pneumatosis. DDx: 1) leukemic/lymphomatous deposits, appy w/ periappendiceal abscess, diverticulitis, IBD. (Dähnert 5th p863)

Slide 258: 

Which organ is less likely responsive to glucogon injection? Esophagus Stomach Duodenum Small bowel Large bowel

Slide 259: 

A. EsophagusGlucagon is a useful hypotonic agent for the stomach and duodenum w/ no effect on esophageal peristalsis. It does relax the LES and increases the freq of reflux. (Levine, Double Contrast GI Radiology, p 48)Hypotonic effect on duodenum>jejunum>stomach>colon (Dähnert 5th p779)

Slide 260: 

Which does not affect pancreatic secretions: Secretin Cholecystokinen Glucogon Gastrin

Slide 261: 

C. GLUCAGONGlucagon – F - : produced in islet cells of pancreas and target organ is intestinesSecretin – T - : produced in duodenal mucosa; released by H+ with pH < 4.5. In pancreas: increases alkaline pancreatic secretions, weakly stimulates enzyme secretion, stimulates insulin releaseCCK – T - : produced in duodenal & upper intestinal mucosa; released by FA, some aa’s, H+ In pancreas: simulates secretion of pancreatic enzymes (Pancreozyman), stin bicarb secretion (partly via secretin effect), stim insulin releaseGastrin – T - : produced in antral cells and G cells of pancreas; release mediated by neuroendocrine cholinergic reflexes. In pancreas: strong increase in enzyme output, weakly stim fluid and bicarb output, stim insulin releaseInformation:4 Basic Stimuli of pancreatic secretion: acetylcholine released from parasympathetic vagus nerve endings and other cholinergic nerves, gastrin, CCK, and secretin.Pancreas secretes proteolytic enzymes: trypsin, chymotrypsin, carboxypolypeptidase and elastases and nucleases; enzymes for carb digestion: pancreatic amylase; enzymes for fat digestion: pancreatic lipase, cholesterol esterase, and phospholipase. Also secretes trypsin inhibitor which prevents activation of the proteolytic enzymes that would result in autodigestion of the pancreas. With pancreatic damage or duct blockage, the inhibitor can be overwhelmed and the enzymes become activated and can digest the pancreas within a few hours = Acute Pancreatitis. The pancreas also secretes bicarb and water by the epithelial cells of ductules and ducts leading from the acini.

Slide 262: 

Concerning GI bleeding Permanent occlusion is the preferred method with coils for Colonic bleed Selective vasopressin has same efficacy as IV vasopressin Hemorrhagic gastritis has good results with vasopressin PUD has good results with vasopressin

Slide 263: 

C. Hemorrhagic Gastritis Has Good Results With Vasopressinc. T: Intra-arterial vasopressin successfully controls bleeding from hemorrhagic gastritis in 84%, with recurrences in 16%. Control of colorectal bleeding is successful in 80-100% w/recurrence in up to 25%. (Kadir, pp61-3)a. F: “Gomes et al. advocated embolization as the tx of choice for UGI bleeding that is evaluated by angiography and vasopressin for lower tract bleeding followed by embolization if necessary (Gore& Levine 1994 p2529) Indications for arteriography and transcatheter tx are bleeding refractory to aggressive med mgmt, failed endoscopic tx, and >500ml/8hr transfusion requirement. According to Dähnert it is the method of choice (Dähnert 5th p743)b. F: The main indications for intra-arterial vasopressin infusion are colonic diverticular bleeding, diffuse mucosal hemorrhage (hemorrhagic gastritis, inflammatory lesions), or failed IV infusion, and also SB lesions not accessible to embolization. d. F: PUD: embolization is the primary tx from bleeding from peptic ulcers and other UGI sources (Gore& Levine 1994 p2529)

Slide 264: 

Which of these does not present as a cavitary small bowel lesion: melanoma lymphoma adenoCA leiomyosarcoma

Slide 265: 

C. Adenocarcinoma – Probably Best Answer – In Reality Ulceration Is Seen In All Of The ChoicesMelanoma: seen in GI tract and mesentery in 4-8% w/ abd pain and bleeding; SB (35-50%), colon (14-20%), stomach (7-20%); multiple submucosal nodules +/- “bull’s-eye/target” appearance = central ulceration; irregular amorphous cavity (exoenteric growth) (Dähnert 3rd e, p614)Lymphoma: 1/5 all SB malignancies; m/c SB malignant SB tumor; mult sites of involvement in 1/5; m/c cause of intussuception in kids >6yrs; ileum 51%, jejunum 47%, duodenum 2 % 4 types: 1) infiltrating w/ plaquelike involve of wall > 5 cm (80%)/ > 10 cm (20%), +/- ulceration; 2) single/mult polypoid mucosal/submucosal masses: may ulcerate 3) endoexoenteric mass: large mass w/ small intramural component; +/- ulcer, fistulae, and aneurysmatic dilatation 4) mesenteric/retroperitoneal adenopathy (Dähnert 3rd e, p613)AdenoCA: 25-26% malignant SB tumors; duodenum 48%, jejunum 44%, ileum 8%; see annular stricture 60%, lobulated/ovoid polypoid sessile mass 41%; ulceration 27% (Dähnert 3rd e, p561)Leiomyosarc: duodenum (26%), jejunum (24%), ileum (40%); usu > 6cm; nodular mass may be intraluminal, intraluminal and pedunculated, intramural, but mostly extrinsic; mucosa may be stretched and ulcerated (50%); may show central ulcer pit/fistula communicatin w/ large necrotic center; intussuception (Dähnert 3rd e p612)According to Dähnert , the differential diagnosis of cavitary small bowel lesions includes Primary adenocarcinoma Exocentric lymphoma Exocentric leiomyosarcoma Exocentric metastatic melanomaA search of the literature reveals a total of four articles on this subject which mainly talk about lymphoma.In Gore, Levine and Laufer, each of these tumor types is known to cavitate usually secondary to central necrosis. However, lymphoma (usually non-hodgkin’s) can fistulize through the small bowel and get walled off to form a cavity on the mesenteric side of the small bowel.

Slide 266: 

Which one of the following is least likely to be ischemic? sigmoid cecum hepatic flexure splenic flexure rectum

Slide 267: 

E. RectumLocation: left colon 46-90%, all colon 11%, right colon 30%, transverse 9%, sigmoid 4%, rectum spared.Most commonly affected segments: (watershed areas)Griffith point(80%) – jx SMA/IMA – splenic fx.Point of Sudeck – jx IMA/hypogastric – rectosigmoid jx Etiology: diminished blood flow within bowel wall (mucosa + submucosa most sensitive to ischemia); major mesenteric vessels usually patent.Precipitating factors:(a) bowel obstruction: volvulus, carcinoma (proximal bowel segment affected)(b) thrombosis: cardiovascular disease, collagen vascular disease, sickle cell disease, hemolytic- uremic syndrome, oral contraceptives(c) trauma: history of aortoiliac reconstruction (2%) with ligation of IMA. [Dähnert p. 837]Ischemic colitis is a specific vascular disorder of the large bowel, usually present within the supply of the inferior mesenteric artery but often observed in the splenic flexure and sometimes more proximally. Plain film and barium enema examination provide important information on its site and extent. Angiography is of less importance because it does not provide a therapeutic implication. The pathoanatomic abnormalities are mucosal necrosis and submucosal edema and hemorrhage. Compared with other types of ischemic disease, ischemic colitis has a relatively good outcome, with recovery in about two-thirds of the cases without acute resection. The lesion may heal completely or cause a fibrous narrowing that later requires resection. The etiology may be an arterial occlusion brought about by atherosclerosis, vasculitis, aortic surgery, or catheterization for angiography. Often, however, no vascular occlusion is observed, but instead increased blood flow with dilated arteries and early venous filling. This type of ischemic colitis should not be confused with the very serious forms of colitis that occur in nonocclusive ischemia, which usually include the small bowel as well as the right part of the large bowel. (Abrams Angiography)

Slide 268: 

Regarding angiodysplasia which is false: majority seen in elderly usually see active bleeding on Angio early draining of ileocolic vein seen predominantly R-sided increased arterial vessels on antimesenteric border

Slide 269: 

B. Usually See Active Bleeding On Angioa. T: majority > 55 b. F: see “arterial tuft” = cluster ov vessels during arterial phase but “contrast extravasation is unusual” c. T: see early opacification of draining ileocolic vein and a densely opacified dilated tortuous ileocolic vein into late cenous phased. T: Majority are cecum and ascending colone. T: see cluster of vessels during arterial phase along antimesenteric border – see the “arterial tuft” (a –e all from Dähnert 5th p792)Angiodysplasia is ectasia and kinking of mucosal and submucosal veins of colon wall and is thought to represent acquired vascular anomaly, m/c in cecum or rt colon along the antimesenteric border. Results from chronic intermittent obstruction of the veins where they penetrate the circular muscle layer manifested by maze of distorted, dilated vascular channels replacing nl mucosal structures and separated from lumen by layer of epithelium. Common cause of chronic lower GI bleeding in pts over age 50 (avg age is 65 yrs), rarely presents as acute GI bleed Radiographic: only detectable by mesenteric arteriography, vascular tuft on antimesenteric border, early or persistent draining vein, active bleeding usually not seen. (Weissleder p628, B & H 1994, p654, p760, Dähnert 5th p792)

Slide 270: 

A patient presents with hypotension and hematemesis. What is the next choice? Angiography Endoscopy CT scan

Slide 271: 

B. EndoscopyPatients with significant upper gastrointestinal bleeding have bright red or coffee ground hematemesis or melena. About 75% of patients with acute GI bleeding respond to supportive measures and minor blood transfusions.After resuscitaton and NG tube placement, endoscopy is used to identify and possibly treat the source of bleeding. Imaging is only carried out when the bleeding site cannot be identified or catheter directed treatment is contemplated.However, continuous rapid bleeding is signaled by passage of large amounts of blood, transfusion of greater than 4-6 units of blood in 24 hr, or hemodynamic instability. These patients should undergo angiographic evaluation. (Valji, Vascular and Interventional Radiology, p. 192.)

1998 : 

1998 Concerning pancreatic islet cell tumors which is true:1. Metastasis to the liver is hypervascular2. 50% insulinomas are malignant3. Gastrinoma may be intra and extra pancreatic

Slide 273: 

1=T 2=F 3=T1= T. Most islet cell tumors tend to be hypervascular. (Fundamentals of Diagnostic Radiology, Brant & Helms, p. 704)2 = F. Malignant potential 10% insulinoma; 60% gastrinoma; 80% glucagonoma. (Fundamentals of Diagnostic Radiology, Brant & Helms, p. 704)3 = T. Gastrinoma - solitary 25%; multiple 5%; ectopic 10% (stomach, duodenum) Primer, 3rd, 242

Slide 274: 

Pt. comes in with nonobstructing freely mobile mass in the ileum.a. Adenocarcinomab. Leiomyosarcomac. Metastasisd. Carcinoide. Lymphoma

Slide 275: 

E. Lymphoma.Lymphoma affects the small bowel more often than any other portion of the GI tract. Ileum most common portion involved due to the predominance of lymphoid tissue there. Non-Hodgkin’s lymphoma more common than Hodgkin’s. Solitary or multiple focal mural masses can be seen in addition to the usually appearance of fold thickening, luminal narrowing, aneurismal dilatation, diffuse nodularity, and extrinsic compression by mesenteric masses. With continued enlargement these masses may become exoenteric, undergo excavation and ulceration, or endoenteric, producing an intraluminal polypoid mass with the potential for intussusception. GI Requisites, 2nd, 117

Slide 276: 

Pt. with pancreatic VIPoma most likely to present with:a. Necrolytic erythema migransb. Hyperchlorhydriac. Hypokalemia

Slide 277: 

C. hypokalemia.VIPoma (vasoactive intestinal peptide). WDHA syndrome (Watery diarrhea, Hypokalemia, Achlorhydria) Causes hypokalemia 2 to loss of bicarb and K+ into the gut. Primer, 3rd, 243

Slide 278: 

True/False50% of insulinomas are malignantGlucogonaomas most commonly present with incresed gastric acid secretionGastrinomas can be found outside the pancreasLiver metastases are typically hypervascular

Slide 279: 

1=F 2=F 3=T 4=F10% of Insulinomas are malignant.Gastrinomas most commonly present with increased gastric acid secretion; glucogonomas present with diarrhea, diabetes, glossitis, necrolytic erythema migrans. Have 80% transformation.Gastrinomas can occur in stomach, duodenum, etc.Most liver mets are HYPOvascular. Primer, 3rd, 216, 243

Slide 280: 

71 y/o female with a large, low-attenuation pancreatic head mass with central calcification. Lesion has not changed in 5 years.islet cell tumorpancreatic ductal adenocarcinomamicrocystic adenomamacrocystic adenocarcinomasolid and papillary tumor

Slide 281: 

D. macrocystic adenocarcinoma.A microcystic adenoma is usually serous, benign, prefers the pancreatic head, has 1-20mm cysts, and a calcified stellate scar. It is hypervascular, and usually occurs in >60y/o. A macrocystic adenocarcinoma is mucinous, prefers the body and tail, has >20mm cysts, occurs 40-60y/o, has papillary excrescences, and is hypovascular. Macrocystic lesions may be benign or malignant, but all must be removed because benign ones can transform. Islet cell tumors are aggressive, and may secrete gastrin, glucagon, insulin, somatostatin, but may be non-functional. Part of MEN-I. Metastasizes to liver.Pancreatic ductal adenocarcinoma – most common pancreatic tumor, preferentially affects the head – very aggressive with poor prognosis. Primer, 3rd, 240-241

Slide 282: 

In patients undergoing laparoscopic cholecystectomy, the most common cause of bile leak is:Aberrant anatomyImproperly positioned surgical clip

Slide 283: 

B. Improperly positioned surgical clip. “Bile leaks tend to occur due to incomplete clipping of the cystic duct stump. Duct transections and lacerations usually occur because of failure to identify the cystic artery and cystic duct correctly. Therefore, common hepatic duct and hepatic artery may be transected and/or clipped inadvertently.” Ref: Laberge, et al, SCVIR Syllabus Biliary Interventions, 1995, p. 234 Davidoff AM, et al. Clinical features and mechanisms of major laparoscopic biliary injury. Semin Ultrasound CT MR. 1993 Oct;14(5):338-345

Slide 284: 

Pt. with Whipple’s, what is the most likely associated CT findingLow density para-aortic lymph nodesScattered calcifications in the liverHyperdense spleen

Slide 285: 

A. Low density para-aortic lymph nodes.Whipple’s is a rare multisystem disease. Organs primarily involved: SI joints, joint capsule, heart valves, CNS, jejunem.Radiographic features: micornodules in jejunem, no dilatation or increased secretions, nodal masses in mesentery, sacroileitis. Primer, 3rd, 184

Slide 286: 

Regarding focal fatty infiltration of the liver: (T/F)located around GB fossadoes not displace vesselshyperechoic on UShyperattenuation of CT confirms disease of lesion that is hyperechoic on US

Slide 287: 

1=T 2=T 3=T 4=FThere are two forms of hepatic steatosis: diffuse and focal.Diffuse: Most commonly caused by alcohol and diabetes. Chemotherapy is another important cause; the complete list is long. LFTs are normal, but diffuse steatosis can stretch the capsule and cause pain. On US, the liver is echogenic with poor penetration. Portal branches are not well visualized because their surrounding fat, normally echogenic, is obscured. On CT, the liver is lower in density than the spleen, but enhancement is normal. On Nucs, liver uptake is seen on Xe ventillation scans. Sulfur colloid scans are heterogeneous.Focal: caused by vascular insult. Wedge-shaped, peripheral. No mass effect. Echogenic on US, low density on CT, high signal on T1 and T2 (but drops out on fat-sat). Areas of unusual blood supply are more prone: subcapsular region, caudate lobe, GB fossa. Primer, 3rd, 207-208

Slide 288: 

What is the least likely complication from pancreatic biopsy?a. Hematomab. Hemorrhagec. Pancreatic-cutaneous fistulad. Abscesse. Seeding of the tract

Slide 289: 

E. seeding of the tract. a = Hematoma: b = Hemorrhage: 3% in pancreas tx bx. c = Pancreatic-cutaneous fistula: d = Abscess: E = Seeding of the tract: very rare. 23 cases seeding, 10 of 23 from bx malignancy.(Diagnostic Ultrasound. 2nd ed. Rumack et al., p. 608; Pancreatic Transplant biopsy. Radiology 201(3): Dec. 1996. Trenkner, Walsh.)

Slide 290: 

Large cavitary mass is noted in the distal ileum on SB follow through.a. Adenocarcinomab. Leiomyosarcomac. Metastasisd. Amebiasise. Lymphoma

Slide 291: 

E. Lymphoma.Adenocarcinoma: 25% of malignant SB tumors. 48% duodenum, 44% jejunum, 8% ileum.Leiomyosarcoma: 10%. 40% ileum, >6 cm, central ulcer, large necrotic center.Metastasis: rareAmebiasis: 90% right colon & cecum > flexures >rectosigmoid.10% distal ileum.collar button ulcers.Ameboma. annular & constricting/intramural mass/cavity.Lymphoma: 16-17%, 51% ileum, 47% jejunum, 2% duodenum, Peyer’s patchesLymphoma affects the small bowel more often than any other portion of the GI tract, most frequently the distal ileum. This is due to the preponderance of lympoid tissue there.Gastrointestinal Requisites, 2nd, 117 and Primer, 3rd, 183

Slide 292: 

What can be seen with leiomyosarcoma of the stomach?a. Necrosis and cystic areas can be seen on CT with large tumorsb. Typically mucosal polypoid massc. Worse prognosis than gastric carcinoma

Slide 293: 

A. Necrosis and cystic areas can be seen on CT with large tumors.Necrosis and cystic areas can be seen on CT with large tumors. Typically mucosal polypoid mass: large intramural pedunculated mass but not mucosal polypoid mass. Submucosal, subserosal or exophytic mass, ulcerated overlying mucosa. Survival is poor but not as bad as in gastric ca: 5-18% overall 5 yr survival, mean survival 7-8 mos for gastric ca. (Radiology Review Manual 3rd. ed. Dahnert, p. 612; Fundamentals of Diagnostic Radiology. Brant & Helms, p. 728.) GI Requisites, 2nd, 116-117

Slide 294: 

Matching:A. HIVB. CandidaC. NG tubeD. tuberculosis1, pseudodiverticulosis2. large ulcer3. long stricture4. traction diverticulum

Slide 295: 

1=B 2=A 3=C 4=DPseudodiverticulosis is dilated mucus glands which appear as small outpouchings of the esophageal lumen. It results from any severe esophagitis, particularly candida esophagitis. Large ulcers are most commonly the result of peptic disease and reflux, but viral infections such as herpes and CMV can also cause large ulcers. HIV patients are at risk for CMV esophagitis.Long strictures result from congenital stenosis, post-surgical strictures, caustic agents, reflux, intubation, radiation, and candida esophagitis. Traction diverticulum = interbronchial diverticulum. Contains all three esophageal layers. Results from fibrosis of adjacent lymph nodes, as in TB.CMV esophagitis most commonly results in superficial ulcers that may become confluent to form large ulcers. This is seen most commonly in HIV patients.Candida causes dysphagia, longitudinal plaques (“cobblestoning”), shaggy contour, narrowed lumen, strictures, and “intramural diverticulosis”, which I think is another name for pseudodiverticulosis. Although candida would be a decent answer, intubation is the more classic association with a long stricture. GI Requisites, 2nd, 14-19, 32

Slide 296: 

Concerning hernias:1. Spigelian2. Richter3. Paraduodenal4. Obturatora. only one side of bowel wall involvedb. congenital and diaphragmaticc. semilunar lined. with flexion and adduction of the leg there is pain in the lower extremitye. inferior mesenteric vein

Slide 297: 

1=C 2=A 3=E 4=DSpigelian: external hernia, hernia through internal oblique, beneath external oblique at lateral margin of rectus sheath(linea semilunaris). Richter: external hernia, entrapment of one wall in hernia orifice usually in older women with femoral hernias. Paraduodenal:(ligament of treitz) internal hernia, through fossa of landzert on left side (75%), lateral to 4th portion of duodenum behind descending colon & transverse mesocolon, 25% caudal to SMA & inferior to 3rd portion of duodenum. Obturator: external hernia GI Requisites, 2nd, 293-299 and Primer, 3rd, 249-250

Slide 298: 

Cause of presinusoidal cirrhosis (T/F): Budd-Chiari Schistosomiasis Laennec’s cirrhosis Biliary cirrhosis

Slide 299: 

B. Schistosomiasis.Normal pressure in the portal vein is low because vascular resistance in the hepatic sinusoids is minimal. Portal hypertension commonly results from increased resistance to portal blood flow. Increased resistance can occur at three levels relative to the hepatic sinusoids: 1) presinusoidal , 2) sinusoidal, and 3) postsinusoidal (Harrison’s Principles of Internal Medicine, p. 1489). False. Budd-Chiari syndrome is a form of postsinusoidal venous obstruction which occurs outside the liver resulting from thrombosis of the hepatic veins. Postsinusoidal obstruction can also occur outside the liver secondary to IVC thrombosis or, less commonly, within the liver as a result of venoocclusive disease which targets the central hepatic venules True. Schistosomiasis causes presinusoidal venous obstruction within the liver characterized by periportal fibrosis. Prolonged intestinal infection with schistosomiasis leads to the development of macroscopic bands of fibrosis which replace the portal venous tracts. This may lead to presinusoidal obstruction and portal hypertension. Because the obstruction is presinusoidal, intrahepatic pressure is normal and hepatic function is generally well preserved. Presinusoidal obstruction may occur outside the liver in the form of portal vein thrombosis False. Laennec’s cirrhosis a.ka. alcoholic cirrhosis is the most common type of cirrhosis encountered in the U.S. The obstruction occurs at the level of sinusoids as the liver parenchyma itself is being destroyed. Prolonged alcoholic intake induces hepatocyte destruction and collagen deposition by fibroblasts in the periportal and pericentral zones, eventually connecting portal triads and central veins. A fine connective tissue network surrounds small masses of remaining liver cells which regenerate and form nodules. This is a form of micronodular cirrhosis False. This is a form of sinusoidal cirrhosis. Biliary cirrhosis results from injury to or prolonged obstruction of either the intrahepatic or extrahepatic biliary system. It results in impaired biliary excretion, destruction of hepatic parenchyma, and progressive fibrosis. PBC is characterized by chronic inflammation and fibrous obliteration of the intrahepatic bile ductules. SBC results from long-standing obstruction of the larger extrahepatic ducts. Regeneration of residual parencyma also occurs resulting in a micronodular cirrhosis Primer, 3d, 218, 305 and GI Requisites ,167

Slide 300: 

TE fistula most commonly associated with:ileal atresiaanal atresiamalrotationrenal agenesissyndactyly/polydactyly

Slide 301: 

1=F 2=T 3=F 4=T 5=FTE fistula usually associated with VACTERL, cardiac anomalies, and other atresias/stenoses.Vertebral anomaliesAnorectal anomaliesCardiovascular anomaliesTracheal anomaliesEsophageal fistulaRenal anomalies: renal agenesisLimb anomalies: radial ray hypoplasia (not syndactyly)Cardiac anomalies: VSD, ductus arteriosus, right aortic arch. Other atresias: duodenal atresia, imperforate anus. Primer, 3rd, 816-817

Slide 302: 

Concerning Crohn’s disease (T/F):Mural asymmetry is a hallmark.Colon and ileum equally involvedJejunum commonly involvedDuodenum commonly involved

Slide 303: 

1=T 2= F 3=F 4=F“Extensive inflammatory changes in the terminal ileum, asymmetric ulceration, and the presence of fistulas and sinus tracts are characteristic of Crohn’s disease.” Especially useful for its distinction from ulcerative colitis.Ileum is the most commonly involved GI part in Crohn’s (85%), followed by colon (“2nd most common”). It doesn’t give the specific % for colon; but it says colon + t.i. in 55%, isolated small bowel in 31% and isolated colon in 18%. Dahnert, 3rd ed., p. 587, says jejunum/ileum in 15-55 %, so jejunum alone is not common; duodenum: 4-10%.Radiographic hallmarks of Crohn’s: aphthous ? confluent deep ulceration, thickened and distorted folds, fibrosis with thickened walls, contractures and stenosis, involvement of mesentary, asymmetric involvement both longitudinally and around the lumen, skip areas and fistulas / sinus tracts.Crohns Ulcerative ColitisTransmural ulcers superficial ulcersSkip lesions continuous15-30y/o 20-40 and 60-70 y/odistal ileum rectosigmoid“cobblestoning” “lead pipe colon”separated loops “thumbprinting”asymmetric wall thickening symmetric fold thickeningCrohn’s disease affects the distal ileum in 90% of cases, colon 40%, jejunum 15%, Duodenum 5%, and stomach 1%, although crohn’s can present with continuous involvement.Primer, 3rd, 194-196

Slide 304: 

What is the most likely complication in a Crohn’s patient s/p partial small bowel resection:obstructive uropathyrenal calculi

Slide 305: 

B. renal calculi.Extraintestinal complications of Crohn’s include: gallstones, osseous complications (spondylitis, sacroileitis, steroid complications), renal stones (7%). Primer, 3rd, 196

Slide 306: 

H. pylori is associated with all of the following except:gastric ulcerduodenal ulcertZollinger-Ellison syndromeGastric carcinomaLymphoma

Slide 307: 

C. Zollinger-Ellison syndrome.There is extensive literature associating Heliobacter pylori with gastric ulcers, and this is now well-accepted. The association with duodenal ulcers is weaker. H. pylori has been shown in MALT lymphomas, but causality is still lacking. H. pylori most commonly causes a castritis. The resulting fold thickening may mimic lymphoma or gastric carcinoma. Primer, 3rd, 169-170.

Slide 308: 

Plain film of the abdomen show calcification in the gastric fundus:a) Splenic vein thrombosis with gastric varicesb) Gastric carcinomac) Leiomyomad)

Slide 309: 

C. Leiomyoma.Leiomyoma--Between 85% and 90% of all neoplasms in the stomach are benign, the majority of which are leiomyomas. Approximately 50% of gastric leiomyomas develop in the body of the stomach, with the remainder equally distributed between the fundus and antrum. About 5% of leiomyomas of the stomach demonstrate some radiographic evidence of calcification. These are usually arranged in irregular streaks or clumps similar to uterine fibroids. Mucinous adenocarcinomas of the stomach may also calcify, but the calcification in these lesions tends to have a punctate, granular, or finely stippled appearance. Based on the statistical occurrence of these tumors, a leiomyoma would be the most likely diagnosis. Although splenic vein thrombosis is commonly associated with gastric varices, the incidence of variceal calcifications is extremely low. The differential diagnosis for left upper quadrant calcification also includes calcified adrenal, renal, or splenic lesions. GI Requisites, 2nd, 68-71

1997 : 

1997 A neonate that is two days post cardiac catheterization presents with abdominal distension and pneumatosis. Most appropriate imaging modality is (single best answer): cross table lateral plain film of abdomen for pneumoperitoneum abdominal ultrasound for aortic thrombosis barium enema contrast enhanced CT

Slide 311: 

A. Cross table lateral plain film of the abdomen for pneumoperitonneum.This was a hard one with really nowhere to look it up. Felt that with neonates you should try to do the least invasive exam. Cross table lateral for evaluation of pneumoperitoneum would be the first. This is because free air would indicate perforation and dictate an immediate trip to the O.R.. Abdominal US could then be performed subsequently to evaluate for thrombus/embolus. CT would be reserved for problem solving.

Slide 312: 

A small amount of free air is most likely to be seen in the following locations on a supine film (single best answer): cupola perihepatic around the falciform ligament around the umbilical veins (inverted V-shaped) Rigler’s sign

Slide 313: 

B. perihepaticAccording to Baker, The Abdominal Plain Film, p. 79, small collections of air can be seen as oval lucencies located just below the right hemidiaphram. Dähnert describes lucencies over the liver. Cupola is a domelike structure and refers to the dome of the diaprhagm. Moderate amounts of free air may be seen around the faliciform ligament. Free air around the umbilical veins is only seen with large volume pneumoperitoneum. Rigler’s sign aka serosal sign (gas outlining both sides of the bowel wall as a thin linear stripe on the non-luminal side Gore and Levine p180

Slide 314: 

A woman in her thirties presents with a distended abdomen and diarrhea. Albumin is normal. On small bowel exam multiple intussusceptions are seen, as well as multiple thick loops of bowel. The most likely etiology is (single best answer):a. Whipple’s diseaseb. sclerodermac. sprued. mastocytosis

Slide 315: 

C. SprueSprue also assoc transient intussus, more common the 30-40 yo range. May have normal/thickened/effaced mucosal folds depending on hypoproteinemia. However, this patient has normal albumin. Small bowel dilatation is hallmark in untreated celiac disease, also see moulage sign – smooth contour with effaced featureless folds resembling tubular wax mold. See mucosal thickening on CTWhipple's disease affects mainly adult male (see answer to next question for more information on Whipple’s) caucasians (M:F = 9:1), this patient is a female. Mastocytosis is a systemic disease with mast cell proliferation in skin and RES. Patients are < 6 monthes old in 50%. The small bowel will have generalized distorted thickened folds and nodules. Associated with sclerotic bone lesions. Thus both Whipple’s and mastocytosis are eliminated as choices.Scleroderma is a multisystem connective tissue disorder affecting smooth muscle and is M<F (1:3) and is common in the 30-50 year range. GI manifestations include diarrhea and abdominal pain. The first GI location is usually the esophogus with decreased peristalsis in the distal 2/3. In the small bowel may cause marked dilatation of the duodenum; may give a “hidebound” pattern to the small bowel. Normal bowel fold thickness. Small bowel intussusception is a complication. (Dähnert 5th p854) Dähnert 5th p859

Slide 316: 

Concerning filiform polyps (multiple true/false): associated with ulcerative colitis associated with Crohns associated with Turcots premalignant

Slide 317: 

A. T B. T C. F D. FFiliform polyps / Polyposis (also known as postinflammatory polyps and pseudopolyps) are a benign condition, not associated with cancer, and seen in the colon.These “polyps” are associated with inflammatory/infectious conditions, seen with ulcerative colitis, crohn’s disease and other granulomatous colitis, proximal to an obstruction, and occasionally with schistosomiasis and amebic colitis. Danhert 5th p775Imaging - thin, short, branching structures, “fingerlike”, and frondlike.- most common in the left colonFiliform polyposis (pseudopolyposis) Polypsisdifferent sizes uniform sizesY-shaped, irrgular, filiform shape round, stalked, sessilefuzzy margins (inflammation) well delineateddistorted colonic haustra (inflammation) preserved haustraTurcots: a autosomal recessive disese with colonic polyposis and CNS tumors that lead to death from brain tumor in 2nd or 3rd decade Dähnert 5th p863

Slide 318: 

Following bone marrow transplant, all of the listed complications occur except (single best answer):a. hepatic veno-occlusive diseaseb. CMV pneumoniac. splenic abscessd. graft versus host diseasee. sepsis

Slide 319: 

C. splenic abscessSplenic abscess - this can occur as a complication of splenic infarction secondary to a lymphoproliferative disease (CML most common). I think this is the answer to the question just because it is the least likely complication, and I've never heard of splenic abscess as a complication of BMT. I do think it is theoretically possible, though.Hepatic veno-occlusive disease - we all know that this can happen in BMT patients. (Primer CD-rom)CMV pneumonia - the virus that most commonly causes pneumonia in immunocompromised patients. Infection is typically related to a defect in cell-mediated immunity, and therefore occurs in patients with lymphoma or transplants. CMV pneumonia may coexist with or predispose to other pneumonias, especially PCP. The radiographic appearances are of diffuse interstitial shadows with basal predominance, extending from the bases to give a diffuse, patchy, often slightly nodular pattern. (Armstrong, Imaging of Diseases of the Chest, 1995) Graft vs. Host Disease - obviously this occurs when the immune-competent cells from the donor bone marrow react against immune-incompetent host tissues. It occurs in 30-70% of allogenic BMT patients. Radiologically, see in the GI tract shaggy fold thickening, toothpaste or ribbon bowel, loss of haustration, spasm, edema, ulceration, and granular mucosal pattern of the colon. Complications include opportunistic infections (Candida, herpes, invasive fungal, CMV, VZV, EBV, Coxsackie, hepatitis, rotaviruses A & B, PCP, and pneumococcus). (Dähnert)Sepsis - of course this can happen in BMT patients.

Slide 320: 

GI Match concerning the anatomy of the liver:1. Divides the left lobe into lateral and medial segments2. Divides the right lobe into anterior and posterior segments3. Divides the liver into right and left hepatic lobes . common bile duct umbilical vein ligamentum teres hepatis middle hepatic vein right hepatic vein running in the plane between the gallbladder and the IVC

Slide 321: 

Functional segmental liver anatomy is based on the distribution of the 3 major hepatic veins.1. Divides the left lobe into lateral and medial segments - c.The fissure for the ligamentum teres (obliterated umbilical vein connecting the placental venous blood to the left portal vein) is located at the free margin of the falciform ligament and divides the LEFT hepatic lobe into medial and lateral segments (divides subsegment 3 from 4).2. Divides the right lobe into anterior and posterior segments - e.The right hepatic vein separates the anterior and posterior segments of the right hepatic lobe.3. Divides the liver into right and left hepatic lobes - d.The middle hepatic vein separates the right from the left hepatic lobes.The left hepatic vein separates the medial from lateral segments of the left hepatic lobe.The fissure for the ligamentum venosum (obliterated ductus venosus, connection of left portal vein with the left hepatic vein) separates the caudate lobe from the left lobe of the liver.The fissure for the gallbladder divides the right from the left lobe. (Clinical Anatomy, Morris, 1994)The major portal veins are intrasegmental (within the segment), while the major hepatic veins are intersegmental (between the segments).

Slide 322: 

Match the following hormones with their syndromes (matching):1. VIP2. Bradykinin3. Calcitonina. Diarrhea syndrome b. MEN 3c. carcinoidd. ZE syndrome

Slide 323: 

1. VIP: a. Diarrhea Syndrome VIP is found in nerves in the GI tract, also in blood vessels. Its half-life is 2 min. It stimulates intestinal secretion of electrolytes, drawing water out. It also dilates peripheral blood vessels and inhibits gastric acid secretion. Pancreatic cholera syndrome: elevated VIP leads to large volume diarrhea. In adults it’s usually due to a VIPoma, a pancreatic islet cell adenoma; in children it’s often from ganglioneuromas or ganglioneuroblastomas. A.k.a. Verner-Morrison Synd., VIPoma syndrome, WDHH (watery diarrhea, hypokalemia, hypochlorhidria) Source:Ganong’s Physiology, Cecil’s text of medicine and Dähnert 5th p7262. Bradykinin: c. carcinoid syndrome carcinoid tumors come from enterochromaffin (Kulchitsky) cells, esp. in GI mucosa. They produce serotonin (most important factor in carcinoid synd), bradykinin, histamine, tachykinins, and prostaglandins carcinoid syndrome: flushing (90%), with diarrhea (3/4), hypotension, tachycardia, +/- wheezing (20%), cardiac failure (rare). Usually it’s associated with an ileal carcinoid which has metastasized to the liver bradykinin: is like histamine: it contracts visceral smooth muscle, relaxes vascular smooth mm.—decreased BP; increases capillary permeability, attracts WBCs3. Calcitonin: b. MEN 3 calcitonin: secreted by thyroid C-cells. Effect: lowers plasma Ca++ levels by blocking resorption of bone Ca++ by osteoclasts; also has a calciuric effect. Used to treat hyperresorptive disease—Paget’s, osteoporosis, and hypercalcemia Medullary thyroid carcinoma: may be sporadic or part of MEN syndromes; Tumor of thyroid C-cells; Behavior—intermediate betw. Indolent papillary and follicular CA vs. aggressive anaplastic thyroid CA; Does not concentrate I-131; Characteristics—thyroid mass; 10% calcify; early spread to adjacent organs and chest, LAN; may see fibrosis/bullae in lungs due to desmoplastic rxn Source: Cecil’sMEN: Autosomal dominant; cells from neural crest origin—APUD cells IIa: Sipple dz.; Medullary carcinoma of the thyroid; Pheochromocytoma: 50% ; bilateral, 3% malignant; +/- hyperparathyroidism; may be associated with carcinoid, cushing dz. III = IIb: Mucosal neuroma syndrome; medullary carcinoma of the thyroid; pheo; oral and intestinal ganglioneuromatosis; also see: long extremities (Marfanoid); thick lips (submucosal nodules); nodular deformity of the tongue; prognathism; constipation and diarrhea; GI studies: thick colon wall; dilated colon with abnormal haustra; alternating colon spasm and dilatation; submucosal neuromas—intussusception Source: DähnertBonus: Zollinger-Ellison Syndrome: usu. middle-aged (35-65); M>FClinical: pain/ulcers; diarrhea, fat malabsorption; 10-30% associated with MEN I; 90% caused by gastrinoma—90% of these are in the pancreas; most of the others in the duodenal wall; 50% malignant 10% caused by antral G-cell hyperplasia

Slide 324: 

Match the following with regard to anatomic relationship (matching):1. Caudate lobe2. Uncinate process of the pancreas3. Right renal arterya. cephalad to portal veinb. lateral to IVCc. posterior to IVCd. posterior to SMV

Slide 325: 

1. probably a, 2. d3. c. Caudate lobe is anterolateral to IVC and cephalad to portal vein. Uncinate process posterior to SMV. Right renal artery posterior to IVC.

Slide 326: 

Match the liver lesions with their associations (matching):1. Prone to bleeding2. Cystic3. Prolonged uptake on Tc99m RBC study4. Pedunculateda. hepatic adenoma b. hemangiomac. mesenchymalhamartomad. biliary cystadenoma

Slide 327: 

1. Prone To Bleeding - AHepatic adenoma is a benign proliferation of hepatocytes. This uncommon tumor is found most often in women on oral contraception, but has association with type 1 glycogen storage disease. Usually solitary and well demarcated, hepatic adenomas contain no bile ducts or kupffer cells. Imaging U/S - nonspecific, encompasses all echogenecity patterns Angiography - also nonspecific, may be hypo or hypervascular CT - may see peripheral hypodensity, or area of hemorrhage Tc sulfur colloid scan - cold (has no kupffer cells) MR - varies. Usually isointense on T1 and hyperintense on T2 Complications - hemorrhage ( 30-40% present with hemorrhage) - infarction - rare malignant degeneration 2. Cystic – C And DMesenchymal hamartoma is a rare developmental cystic liver tumor usually presenting in the first two years of life. Male to female ratio is 2:1. This tumor represents a disordered arrangement of primitive mesenchyme, bile ducts, hepatic parenchyma with a cystic predominance. The right hepatic lobe is preferentially involved 6:1 compared to the left lobe. 20% are pedunculated, with average size being 16 cm. 80% of these tumors have grossly discernable cysts. Imaging U/S - multiple rounded cystic areas in an echogenic background. May be solid in younger childrenCT - multiple cystic mass Tc sulfur colloid scan - decreased uptakeAngiography - hypovascular mass with enlarged tortuous vesselsBiliary cystadenoma is a rare slow-growing benign lesion resembling mucinous cystic neoplasms of the pancreas. These lesions are multiloculated, usually solitary and cystic. These can range from 1.5 – 30 cm in size. Age affected is usually over 30 years old, with a male:female ratio of 1:4. These lesions have papillary excrescences and mural nodules, and may be pedunculated. Imaging U/S - complex mass with iregular margins and single/multiple septations. May have fluid/fluid levels. CT - multiloculated mass with septations Angiography - avascular mass Diff DX - complicated congenital cysts, hematoma, cystic mets, abscess, echinoccocal cyst; Surgery is performed if a biliary cystadenoma is suspected, because these cannot be reliably differentiated from cystadenocarcinoma. Rare malignant degeneration can occur in these lesions.3. Prolonged Uptake On Tc99m RBC Study – BHepatic hemangioma or “cavernous hemangioma” is the most common benign liver tumor (78%) and second most common tumor after metastatic disease. Hemangiomas are large vascular channels filled with slowly circulating blood. No bile ducts are present. Thrombosis of these vascular channels can lead to central fibrosis and calcifications. Hemangiomas are asymptomatic if small (50-70%) Tc RBC scan - useful if lesion is > 2 cm in size - delayed fill-in with increased activity on delayed images at 1-2 hours4. Pedunculated – All

Slide 328: 

Most common cause of unilateral lymphangitic spread of carcinoma (single best answer):a. lung cancerb. breast cancerc. cervical cancerd. gastric cancer

Slide 329: 

A. Lung cancer. Characterized by tumor growth along lymphatics, thought to be hematogenous in origin, rather than due to retrograde dissemination (associated lymphadenopathy in <50%). Most commonly due to breast, lung, colon, stomach and pancreas. If unilateral, most often due to lung ( in 21/28 cases in one study ) or breast (unilateral in 2/3). HRCT findings include nodular interlobular septal thickening and thickening of bronchovascular bundles. On plain film may see increased coarse interstitial opacities and Kerley B lines as well as decreased lung volumes. Frequently dyspnea out of proportion to radiograph findings. (May also have smooth interlobular septal thickening and be difficult to distinguish from edema.) Fraser & Pare, p. 1632-1640. Radiology of Chest Disease, Lange & Walsh, p. 176-182.

Slide 330: 

GI Necrotizing migratory erythema is characteristic of which of the following diseases (single best answer):a. Verner Morrisonb. glucagonomac. gastrinomad. somatosatinoma

Slide 331: 

B glucagonomaAll the choices refer to pancreatic diseases. (Dähnert 5th p725)Glucagonaoma is an uncommon tumor, M< F. Usually located in pancreatic body/tail and is from 2-25 cm at diagnosis and arises from alpha cells. Hypervascular in 90%. Associated with necrolytic migratory erythema aka necrolytic erythema migrans (macules/papules of lower extremety, groin, buttocks, face); diabetes mellitus; anemia; wt loss. In 80% malignant transformation - usually large & liver mets at time of Dx. Gastrinomas – 2nd most common islet cell tumor, in alpha/delta cells. Associated with MEN I, Zollinger-Ellison syndrome and GI bleeding. 90% in pancreas, 50% solitary in head/tail, 50% malignant, 10% in duodenal wall, 70% are hypervascular.Somatostatinoma is from the delta cells of the pancreatic head. It is hypervascular; malignant trasformation in 50-90%. Verner Morrison syndrome is due to a VIPoma which are usually solitary and arise from delta cells in pancreatic body/tail. Can occasionaly be extrapancreatic: ganglioblastoma, pheochromocytoma, lung, neuroblstoma). Produces watery diarrhea, hypokalemia, hypochlorhydria (WDHH syndrome).

Slide 332: 

Regarding diseases involving the colon (matching):1. Lymphogranuloma venereum2. Ulcerative colitis3. Behçet disease 4. Amebiasisa. fistulab. aphthous ulcersc. granular mucosa d. toxic megacolon

Slide 333: 

1. Lymphogranuloma Venereum A. Fistulae. This condition results from a granulomatous inflammatory response to a STD caused by chlamydia. Usually starts in the rectum and works proximally resulting in abscess and fistula formation, often between rectum and vagina. Radiographic findings include increased presacral space and narrow, short, straight rectosigmoid. Dähnert 5th p8412. Ulcerative Colitis D. Toxic Megacolon. Complication of common, idiopathic condition with bimodal age distribution (20-40yrs, 60-70yrs). Usually first affects the rectum and progresses proximally. Can cause “backwash” ileitis. Usual radiographic findings include foreshortened featureless “leadpipe” colon with granular mucosa and shallow confluent ulcerations. With megacolon can see deep ulcerations, intraperitoneal gas.3. Behçet disease b. aphthous ulcers (stomatitis), genital ulcers, and ocular inflammation make up the TRIAD associated with this idiopathic, multisystem inflammatory condition. Relapsing course of mucocutaneaus and ocular symptoms. High mortality due to tendency for multiple intestinal perforations including esophageal. Colonic findings include deep ulcerations in otherwise normal mucosa. Other associations – migratory thrombophlebitis, chronic meningoencephalitis. DDx: crohn’s and UC. Dähnert 5th p7964. Amebiasis c. granular mucosa is seen in this condition due to mucosal edema and punctate ulcers. Ulceration is followed by sloughing of the mucosa and often secondary bacterial infection. Toxic megacolon can result here as well (note overlap of granular mucosa and toxic megacolon with UC). Usually affects areas of relative stasis (right colon and cecum), less frequently more distal areas. Etiology: Entamoeba histolytica. Other radiographic findings: loss of haustration, “collar-button” ulcers, and a cone-shaped cecum.

Slide 334: 

Regarding diseases of the gallbladder (matching):1. Mirrizi syndrome2. Kawasaki disease3. Adeonomyomatosisa. hydrops of the gallbladderb. cystic duct stone with intrahepatic biliary duct dilationc. segmental gallbladder wall thickeningd. hyperechoic foci, without shadowing which project into the lumen of the gallbladder

Slide 335: 

1. Mirrizi Syndrome b. cystic duct stone with intrahepatic ductal dilatation… due to extrinsic compression on right side of common hepatic duct by large cystic duct stone and chronic inflammation, can create fistula between cystic and common hepatic ducts. TRIAD:impacted gallstone, dilatation of proximal hepatic ducts, smooth segmental stenosis. DDx: lymphadenopathy, neoplasm.2. Kawasaki disease a. gallbladder hydrops (transient), also intestinal pseudo-obstruction. This is a mucocutaneous lymph node syndrome that presents as an acute febrile multisystem vasculitis with a predilection for the coronaries. Strikes children <5yrs, rash, conjunctivitis. Dähnert 5th p6343. Adenomyomatosis c. segmental gall bladder wall thickening, or can be diffuse. Benign proliferation of normal tissues, associated with gallstones (25-75%), >35yrs. Can see dilated Rokitansky-Aschoff sinus that project into the thickened wall (not into the lumen as in choice d.) Dähnert 5th p715Choice d. likely refers to cholesterol polyps – fixed non-shadowing polypoid echogenic lesions. If diffuse surface deposition of small polyps, gives the appearance of a “strawberry gallbladder.”

Slide 336: 

Regarding focal nodular hyperplasia (Multiple T/F)Prone to bleeding Strong association with oral contraceptivesMay be complicated by malignant transformationDemonstrates increased uptake on sulfur-colloid exam

Slide 337: 

Focal nodular hyperplasia (RARE – 357 cases ever, benign congenital hamartomatous condition, probably hyperplastic response to congenital AVM or other insult, multiple in 20%, specific diagnosis RARELY POSSIBLE, commonly multiple, R>L lobe)A.True. Rupture with hemoperitoneum. Likelihood of bleeding increases with OCP usage.B. False. No association of OCP’s with occurrence of FNH. Association: Twenty-three percent of patients on OCP’s have cavernous hemangiomas with FNH.C. False. One source said rarely undergoes malignant degeneration; others did not mention it, or said no degeneration. I go with false.D. True. Depends on what they mean by increased uptake on sulfur colloid exam. Sources said normal uptake (58-70%), cold (30-35%), hot (7-10%). However, of the common liver lesions, only FNH contains a sufficient number of Kupffer cells to take up sulfur colloid at all. Maybe that’s the distinction they are trying to make.DDx: regenerative nodules of cirrhosis, hepatocellular adenoma

Slide 338: 

Regarding GI bleeds which of the following is true Greater than 1.5 ml per minute necessary for identification on nuclear medicine scan Sulfur colloid is equally sensitive to in vitro RBC study A new focus of activity must move on subsequent images in order to be definitively positive Twenty-four-hour images will help to localize the site of bleed

Slide 339: 

C. A New Focus Must Move To Be PositiveA. False. For detection on tagged RBC scan there must be at least 0.2ml/min (another source said 2ml/hr). Angio needs at least 1.0ml/min.B. False. Sulfur colloid can be used, but it is less sensitive because of quicker clearance from blood pool. Therefore, intermittent bleeding can be missed. Also liver and spleen uptake obscures the upper abdomen. Lower abdomen views are clearer because faster clearance means better target to background ratio.C. True. If focus of activity does not move, may be angiodysplasia or aneurysm.D. False. Twenty-four hour images may see the blood, but it is impossible to tell where it originated, i.e. upper v. lower.

Slide 340: 

Regarding glucagon all are false excepta. Mediates its effects via the vagal nerveb. Does not relax the sphincter of Oddic. Contraindicated in pheochromocytomad. Contraindicated in patients with glaucoma

Slide 341: 

C. contraindicated in pheochromocytomaGlucagon is produced by alpha cells of the pancreas. The main stimulus for its release is hypoglycemia. It is an insulin antagonist, thus it increases blood blucose levels. It causes the relaxation of smooth muscle cells, it relaxes the gallbladder sphincter and the sphincter of Oddi thus increasing bile flow. Contraindications include pheochromocytoma and insulinoma.

Slide 342: 

Regarding internal hernias all are false excepta. Paraduodenal hernias are greater on the right than the leftb. Right paraduodenal hernias go through the fossa of the Lanzertc. Transmesocolic hernias are congenitald. Paraduodenal hernias are usually supracolic

Slide 343: 

C. transmesocolic hernias are congenitalParaduodenal (mesocolic) hernias may be regarded as developmental anamolies caused by trapping of bowel loops in colonic mesentery before completion of fixation and obliteration. The hernia sacs are thus formed by mesocolon. They represent 50% of internal hernias (5% of all hernias). When on the left side (3/4), they are through the fossa of Landzer. When on the right side (1/4), they are through the fossa of Waldeyer.Internal hernia incidence 0.5 - 3% of intestinal obstruction- paraduodenal hernias most common (75% left - 25% right)- left hernias occur through congenital fossa of Landzert to the left of ascending colon and extends down into descending mesocolonLook for: SB loops in left abdomen - lateral to 4th part of duodenumOn the right, herniation is through fossa of Waldeyer and then extends down into ascending mesocolon.Look for: SB loops in lower right abdomen (inf. to descending duodenum) often associated with partial intestinal malrotation.Both right and left hernias depress the transverse colon.Angiogram may be helpful in demonstrating reverse course of jejunal branches of SMA. Source: Ravin p. 775

Slide 344: 

Regarding liver lesions (matching):1. Adenoma2. FNH3. Hemangioma 4. Mesenchymal hamartomaa. often bleedsb. prolonged activity with Tc RBC scan c. pre-malignant d. associated with hepatitis B

Slide 345: 

1. Adenoma A. Hepatocellular adenomas are often resected to avoid hemorrhage2. FNH A. FNH also hemorrhages. Possibly also d. I found no definite association with hepatitis B but if FNH is a hyperplastic response to an insult, maybe “insult” would apply to hepatitis. (If HCC was one of the questions, this would be the match.) Hemangioma B. Classic nuclear medicine appearance is slow uptake and delayed washout of tagged RBC’sMesenchymal Hamartoma C. Found no definite allusion to premalignancy, but it was the only one left. Most sources said FNH definitely was not premalignant. This entity is a multicystic developmental liver abnormality that can be multiple and presents by two years of age as an aggressively enlarging abdominal mass.

Slide 346: 

Regarding primary hemochromatosis which is falsea. Associated with Keiser-Fleicher ringsb. Ten times greater in males than femalesc. Involvement of the heart and pancreas is characteristic

Slide 347: 

A: F (Kayser-Fleisher rings are assoc with Wilson’s disease Primary hemochromatosis is an autosomal recessive disorder characterized by an unexplained increased GI absorption of dietary iron. The iron is deposited in the heart, pancreas, and other organs. In the liver the iron is deposited in hepatocytes not Kupffer cells. Untreated patients will ultimately develop cirrhosis. Males are affected more than females (10:1). Patients develop hepatomegaly (early), cirrhosis, skin pigmentation, & diabetes mellitus (“bronze diabetes”). They have elevated serum iron, TIBC, and ferritin levels. Complications include an increased risk for hepatoma, hepatic failure, diabetes mellitus (due to pancreatic involvement), cardiac conduction disturbances, and CPPD deposition disease (most commonly involves the hands, especially the 2d and 3d metacarpal heads). Treatment consists of repeated phlebotomy. On CT there is generalized increased liver density. The spleen, pancreas, and pericardium may also increase in density due to reticuloendothelial uptake in these locations. On MRI there is classically a "black" liver with low signal on T1 (usually the liver is higher in signal than the spleen) and low on T2 (liver is usually of low signal on T2, spleen is very bright). Loss of signal may also be seen in the pancreas and myocardium (findings which are not seen in secondary hepatic iron overload). The spleen is typically of normal, or in some cases decreased, signal intensity. Secondary hemochromatosis is characterized by the loss of signal in both the liver and spleen, while the pancreas maintains a normal signal intensity. Other radiographic findings: Skeletal findings in hemochromatosis include generalized osteoporosis, chondrocalcinosis (found in over 60% of patients- the knee is the most common site), hook-like osteophytes from the metacarpal heads, and subchondral cysts (metacarpal heads). Secondary hemochomatosis is seen in patients with beta-thalassemia or other hemolytic anemias that require multiple transfusions and actually represents hemosiderosis as iron is deposited in Kupffer cells and other RES (reticuloendothelial cell system) cells alone. The condition requires no treatment. Iron may eventually be deposited within parenchymal cells once the reticuloendothelial cells become iron saturated (usually after transfusion of greater than 40 units of blood). M:F = 10:1

Slide 348: 

Regarding small bowel disease (multiple matching):1. Whipple’s disease2. Sprue3. Mastocytosisa. dense bonesb. lymphoma of the small bowelc. greater in Caucasian males

Slide 349: 

C. Whipple's disease is characterized by extensive infiltration of the lamina propria by large macrophages filled with glycoprotein granules that are PAS-stain positive. These PAS (+) macrophages can be found in every organ. The intestinal villi are distended and blunted which produces a "shaggy-rug" appearance. The duodenum and proximal jejunum are the most common sites of involvement. The condition affects mainly adult male caucasians (M:F = 9:1) and is considered by some to be familial. Patients present with malabsorption and extraintestinal complaints such as migratory polyarthritis, fever, weight loss, adenopathy, and skin pigmentation (similar to Addison's disease). The arthritis is noted in 65-95% of cases, is migratory and usually non-deforming and precedes the bowel disease in 10% of patients. Treatment consists of antibiotic therapy with TCN. B. Celiac Sprue (Non-tropical): The disorder occurs due to a genetically controlled enzymatic defect which is characterized by an intolerance to gluten (found in wheat, barley, and rye). The villi in the small intestine become short, flat, and atrophic. The condition improves with a gluten free diet. On UGI there is small bowel dilatation seen in up to 95% of cases, particularly involving the mid/distal jejunum, however, the duodenum is involved in 80%. The small bowel folds are normal (2-3mm in size) to decreased in size and there is poor peristalsis. Hypersecretion results in excessive fluid in bowel lumen. The "moulage" sign refers to the tubular appearance of the small bowel due to atrophy and effacement of the jejunal folds (characteristic of sprue). There may be jejunalization of the ileum in which the mucosal pattern in the ileum resembles the feathery appearance of the jejunum. This is actually a compensatory mechanism due to the decreased jejunal mucosal surface Complications include: An increased risk of diffuse small bowel lymphoma in long-standing disease (up to 20% of cases). The lesion most commonly arises in the jejunum which is typically the site of greatest inflammation/damage. Lymphoma in these patients most commonly produces a segment of bowel with thickened, nodular folds. A. Mastocytosis is of unknown etiology. In this condition there is mast cell proliferation in the RES which infiltrates the lamina propria of the small bowel. Over 50% of the cases are in patients < 6 months old. Symptoms are due to release of histamine from the mast cells and include pruritis, flushing, tachycardia, asthma, headache, abdominal pain, diarrhea, and malabsorption. The condition is associated with leukemia, urticaria pigmentosa, and peptic ulcer disease- possibly secondary to histamine mediated acid secretion. Patients may also develop sclerotic bone lesions. On UGI there is diffuse, irregular, distorted, thickened small bowel folds. Numerous tiny nodules may be superimposed upon this fold pattern. Urticaria-like lesions of the gastric/intestinal mucosa have also been described. CT may demonstrate other features of the disorder such as hepatosplenomegaly, retroperitoneal, periportal, and mesenteric adenopathy, thickening of the omentum and mesentery, and ascites. [Radiology 1997; 202: 367-372]

Slide 350: 

GI Regarding small bowel obstruction which is truea. Etiology is tumor > hernia > adhesions (i.e., in decreasing frequency)b. Midgut volvulus represents a closed loop obstructionc. CT scan is not useful to distinguish ileus from mechanical obstruction

Slide 351: 

B. midgut volvulus is a closed loopA. F. Small bowel obstruction is the most common surgical condition of the small bowel. Causes of SBO inclue: adhesions (60%) > hernias (20%) > neoplasms (15%) > other (5%) (regional enteritis, volvulus, gallstone ileus, intussusception). (Essentials of General Surgery, 2nd edition)B. T. Midgut volvulus is torsion of entire gut around SMA due to a short mesenteric attachment. It presents as a medical emergency in the newborn with biliuos vomiting. In an older child, may have intermittent obstructive symptoms. On plain film will see “double bubble sign” of air in stomach and duodenum. On barium stuies, Lig of Trietz inferior to duodenal bulb & to the right of expected position; may also see a “corkscrew” appearance of the midgut loops. On CT will see spiral loops on right side. (Dähnert, 3rd edition, p.618).C. F - who knows

Slide 352: 

The following is most useful in establishing the diagnosis of typhlitis (single best answer):a. thumb printingb. pneumatosisc. thickened folds in the distal ileumd. history of immunocompromised status

Slide 353: 

D. History of immunocompromised statusTyphlitis is a transmural inflammatory and/or necrotizing process involving the cecum and/or terminal ileum and appendix in close association with neutropenia. This is also been called ileocecal syndrome or neutropenic typhlitis.Predisposed - leukemia, lymphoma, aplastic anemia, immunosupressive drug therapy, organ transplantation, and AIDS.Findings:fluid filled mass-like density in RLQthumbprinting of colon/cecum edema/ulceration of entire bowel wallcircumferential cecal wall thickening (also on CT)occasional pneumotosisAgents involved - Pseudomonas, CMV, E. coli, B. fragalis, EnterobacterComplications - Perforation and abscess formation.Therefore early diagnosis and treatment is essential because of the rapid progression to transmural perforation, which carries a high mortality rate. Note that a barium enema carries increased risk of perforation and is not performed for diagnosisTreatment - high dose antibiotic and iv fluidsDiff Dx+ leukemic/lymphomatous infiltration (can exist simultaneously with typhlitis. Infiltration with leukemia/lymphoma is more eccentric in the bowel wall usually.+ intramural hemorrhage+ ischemia+ segmental pseudomembranous colitis+ appendicitis / right sided diverticulitis+ inflammatory bowel disease Reference: Dähnert, 3rd Edition, page 628.

Slide 354: 

The following is not part of the esophagus (single best answer):a. serosab. mucosac. longitudinal muscle layerd. muscularis mucosa

Slide 355: 

A. serosa The esophogus is composed of an inner mucosal layer, a circular muscle layer and a longitudinal muscle layer. The musculature of the upper 1/3 is skeletal muscle while the lower 2/3 is smooth muscle. In contrast to the rest of the GI tract, there is no serosal layer. This is significant because it explains the ease of extension of neoplasms that originate in the esophogus and the ease at which esophogeal perforation occurs. (Essentials of General Surgery, 2nd edition)

Slide 356: 

GI The following is true regarding Zenker’s diverticulum (single best answer): associated with cancer in 5% empties by contraction of its muscular walls is a traction diverticulum occurs below the level of the crichopharymgus muscle occurs in the posterior midline

Slide 357: 

E. occurs in the posterior midlineA. False. According to Gore, Levine and Laufer, it is associated with cancer in 0.3%.B. False. Remember, it is a mucosal herniation, so it contains no muscular walls.C. False. It is a pulsion type diverticulum. – does not have a muscular wall d. False. It occurs just above the cricopharyngeus. It occurs as a herniation of mucosa and submucosa through a defect in the posterior aspect of the pharyngoesophageal junction. It occurs through an area of potential weakness (Killian’s dehiscence) in the midline between horizontal and oblique fibers of the inferior constrictor muscle. May occur due to incomplete relaxation of the cricopharyngeus, although this is controversial. E. True. At least when they are small. When they are larger, they may project laterally, usually to the left. GI REQ 2nd p32

Slide 358: 

The following polyposis syndrome(s) is/are NOT inherited (single best answer):a. Gardner's syndromeb. Turcot's syndromec. Cronkhite-Canada syndromed. Peutz-Jeghers syndromee. multiple hamartomas

Slide 359: 

C. Cronkhite-Canada syndrome.Discriminators are as follows:Gardner's syndrome - Autosomal dominant, characteristic triad: (1) adenomatous colonic polyposis, (2) osteomas, (3) soft tissue tumors. Age 15-30. May be associated with MEA complex (). Location of polyposis in 100% colon, 90% duodenum (12% periampullary/duodenal carcinoma), 5-68% stomach (hamartomas), and <5% small intestine. Soft tissue tumors include sebaceous/epidermoid inclusion cysts (scull, back, face, extremities), fibromas, lipomas, leiomas, neurofibromas, and/or desmoid tumors, i.e., desmoplastic fibroses (retroperitoneal, mesenteric, mammary, keloid, etc. Osteomas are of membranous bone - calvarium, mandible (81%), maxilla, ribs, long bones. Malignant transformation in 100% with avg age of death 41. Prophylactic total colectomy at age 20. (+)skin pigmentation. Turcot's syndrome - Autosomal recessive. (1) adenomatous colonic polyposis, (2) CNS tumors (especially supratentorial glioblastoma, occasionally medulloblastoma). See multiple 1-30 mm polyps in colon and rectum, with 100% malignant transformation. Patients usually die from brain tumor in 2nd & third decade.Cronkhite-Canada syndrome - non-neoplastic, non-hereditary inflammatory polyps associated with ectodermal abnormalities. Histologically resemble juvenile/retention polyps with multiple cystic spaces filled with mucin secondary to degenerative changes See multiple polyps in stomach and colon (100%), >50% in small bowel. Rapidly fatal in women in 6-18 months. Tends to remit in men. Peutz-Jeghers syndrome - Autosomal dominant, characterized by hamartomatous intestinal polyposis and mucocutaneous pigmentation. Avg age 25 (10-30). Associated with GI tract carcinoma (2-3%), carcinoma of pancreas and breast (13%), ovary (5%); adenoma of bronchus and bladder. See freckles around lips, gums, palate, nose, cheeks, around eyes, and along volar aspect of toes and fingers. 47% with crampy abdominal pain/small bowel intussusception, 30% with rectal bleeding/melena, prolapse through anus. s. Life expectancy is decreased due to development of cancer. Multiple hamartoma syndrome = Cowden disease - Autosomal dominant, (1) Cutaneous + oral verrucous papules (lips, gingiva, tongue, (2) Endodermal, ectodermal, mesodermal dysplasia with tumors of skin, breast, GI tract, thyroid gland, (3) Malignant tumors of breast and thyroid. It is characterized by multiple benign facial tricholemmomas (localized proliferation of pale pink, glassy cells that resemble the uppermost portion of the hair follicle), The polyps are not dysplastic, and the risk of GI malignancy is not increased.Hereditary: AD = Familial (multiple) polyposis, Gardner's, Peutz-Jeghers', Cowden's syndrome.AR = Turcot's syndrome Non-Hereditary: Cronkhite-Canada, Juvenile polyposis.

Slide 360: 

Which of the following will increase the density of the liver as seen on contrast CT?a. amyloidb. amiodaronec. steatosisd. chemotherapy

Slide 361: 

B. amiodaroneSubstances which cause increased density of the liver on CT scanning include substances with high atomic number, such as:- Iron: Primary hemochromatosis, Transfusional hemosiderosis, Bantu siderosis (excessive dietary iron from food prep in iron containers)-Copper: Wilson’s disease = hepatolenticular degeneration-Iodine: Amioderone = antiarrhythmic drug with 37% iodine by weight (liver 95-145 HU)-Gold: Colloidal form of gold therapy of rheumatoid arthritis-Thorotrast®: included for historical purposes (not used since ~1960) a 25% colloidal suspension of 232ThO2 , physical half-life, 1.4 x 1010 yrs (= 14 billion years); this may somewhat overestimate its deleterious effects, as the biological half life is “only” 400 years. Hard Alpha emitter with atomic number of 90 Caused increased incidence of Hepatic CA, etc. (see here for more info)-Thallium: Accidental/suicidal ingestion of rodenticides (lethal dose is 0.2 -1.0 g)-Acute massive protein deposits - ?amyloid-Glycogen storage diseasemnemonic: "GG CHAT": Gold therapy, Glycogen storage disease, Cyclophosphamide (most chemotherapy causes decreased density of the liver), Hemochromatosis/hemosiderosis, Amioderone, Thorotrast

Slide 362: 

Concerning gastric varices (single best answer):a. communicate with the coronary veinb. may resemble leiomyosarcomac. d.

Slide 363: 

A communicate with the coronary veinThe gastric fundus contains a venous plexus that is normally drained by numerous short gastric veins that anastomose distally with the splenic vein and proximally with branches of the coronary vein as well as by venous channels surrounding the distal esophagus. Blood in the short gastric veins normally empty via the splenic vein into the portal venous system.The two main causes of gastric varices are Portal HTN causes reversal of blood through the splenic veins into the short gastric veins producing fundal varices. Portal HTN also causes reversal of blood flow through the coronary vein causing esophageal varices. Classically, portal HTN causes both esophageal and gastric varices, but isolated esophageal varices are common, with isolated gastric varices less often seen. Varices are more likely to form in the esophagus and be seen because the gastric fundal veins have thicker and better connective tissue support than thin esophageal veins, and because gastric varices are many times obscured by gastric folds/rugae.Splenic vein obstruction causes isolated gastric varices without uphill esophageal varices. Obstruction can occur from intrinsic thrombosis, or more commonly from extrinsic compression (especially pancreatic processes). Gastric varices have a propensity to bleed, although less likely than esophageal varices. Imaging - On barium studies, double contrast should be used as single contrast is unreliable. Gastric varices appear as thickened tortuous “folds” or lobulated filling defects in the fundus of the stomach. On CT, enhancing varices can usually be readily appreciated, as well as the stigmata of cirrhosis/portal HTN or splenic vein obstruction. On angiography, dilated enlarged gastric veins are seen.Dff DX - Thickened nodular folds on barium studies also may represent hypertrophic gastritis, menetrier’s dz, ZE syndrome, pancreatitis, lymphoma, or polypoid fundal carcinoma. Gastric varices may be changeable during the exam.Treatment - simple splenectomy for splenic vein obstruction/thrombosis.- porto-systemic shunt for portal HTN

authorStream Live Help