GI imaging Flashcards
(115 cards)
1
Q
How many liver segments are there?
What separates superior and inferior segments?
What forms the segmental borders in the axial plain?
A
Portal veins divide superior from inferior segments
Hepatic veins form the segmental borders in the axial plane
2
Q
A
3
Q
How to remember which segments are superior/inferior and left/right?
A
- Mnemonic for remembering the segments:
Superior segments, from left to right: 2, 4, 8, 7, 1 (caudate). 2 doubled is 4; 4 doubled is 8; 8 minus 1 is 7. Inferior segments, from left to right: 3, 4, 5, 6. - Segments 2, 3, and 4 are in the left lobe of the liver.
- Segments 5, 6, 7, 8 are in the right lobe of the liver.
4
Q
Where does the caudate lobe of the liver drain and how does this affect it in cirrhosis?
A
Caudate lobe drains directly to the IVC, not into the hepatic veins
The caudate lobe hence is not affected in early cirrhosis since the direct drainage to the IVC spares the caudate from increased venous pressures due to portal hypertension. This leads to compensatory hypertrophy of the caudate lobe.
Direct venous drainage to the IVC allows the caudate lobe to bypass the increased hepatic venous pressures seen in Budd-Chiara syndrome. Compensatory hypertrophy of the caudate lobe may preserve liver function in these patients.
5
Q
Liver USG, what is seen?
A
Hepatic steatosis causes increased sound attenuation, leading to poor visualization of deeper structures
6
Q
What is seen and dx?
Treatment?
A
Primary haemochromatosis is the most common cause of iron overload, due to a genetic defect causing increased iron absorption through the GIT
Excess iron is deposited in hepatocytes (not the Kupffer cells that make up the intrahepatic reticuloendothelial system or RES), pancreas, myocardium, skin and joints. Excess iron in hepatocytes can cause cirrhosis.
Liver and pancreas are markedly T2 hypointense an show signal dropout on in phase images. The spleen and bone marrow are normal since the RES is not involved.
Treatment of primary hemochromatosis is phlebotomy
7
Q
Which organs are effected in secondary haemochromatosis?
What are the causes of secondary haemochromatisis?
A
Secondary haemochromatosis is seen in diseases that cause haemosiderosis, where excess iron accumulates within the RES. This may be due to frequent blood transfusions or defective erythrocytosis. Treatment of haemosiderosis is with iron chelators.
RES has large capacity for iron and iron stored in RES is not harmful until it becomes in excess where just as in primary haemochromatosis, hepatocyte iron uptake may lead to cirrhosis.
Image: Secondary hemochromatosis: Multisequence MRI shows diffuse low T2 signal in the liver and spleen with associated signal loss on in-phase imaging compared to out-of-phase imaging, consistent with iron deposition from hemosiderosis in this patient with transfusion-dependent anemia.
8
Q
What are the causes of hypoattenuating and hyperattenuating liver?
A
Hypoattenuating liver: fatty liver (hepatic steatosis), hepatic amyloid
Hyperattenuating liver: iron overload is the most common cause of hyperattenuating liver, medications (amiodarone, gold and methotrexate), wilson disease (copper overload), glycogen disease
9
Q
What are the causs of liver cirrhosis?
A
Metabolic (alcohol, steatohepatitis, hemochromatosis, or Wilson disease)
Infectious (chornic hep B/C)
inflammatory (primary biliary cirrhosis or wilson disease)
10
Q
What are the intrahepatic signs of cirrhosis?
A
11
Q
What are early signs of cirrhosis?
A
Expansion of the periportal spaces
Atrophy of the medial segment of the left hepatic lobe in early cirrhosis causes increased fat anterior to the right main portal vein.
Enlargement of caudate lobe is a specific sign of cirrhosis. Specifically, a caudate to right lobe size ratio of >0.65 highly suggests cirrhosis.
The empty gallbladder fossa sign results when hepatic parenchyma surrounding the gallbladder is replaced with periportal fat.
12
Q
What are the secondary manifestations of cirrhosis?
A
- Portal hypertension causes splenomegaly and formation of portosystemic collaterals/varices, including recanalization of the paraumbilical vein
Gamna-Gandy bodies are splenic microhemorrhages secondary to portal hypertension. These appear as tiny echogenic foci on US, tiny hypo or hypoattenuating on CT - Gallbladder wall thickening us due to hypoalbuminemia and resultant edema
- Micronodular cirrhosis <3mm (normally associated with alcoholism)
- Macronodular cirrhosis features nodules (>3mm) separated by wide scars and fibrous septae. Macronodular cirrhosis caused by fulminant viral hepatitis which does uniformly affect the liver.
13
Q
What is the classical appearance of cirrhosis?
What is seen below?
What investigations can be done to test for cirrhosis?
A
Segmental atrophy and hypertrophy with nodular contour and parenchyma
Axial T2-weighted MR images show nodular contour of the liver with hypertrophy of the left lobe, atrophy of the right lobe, widened periportal space (yellow arrow), and right posterior hepatic notch sign (red arrow) in keeping with cirrhosis. This patient had a history of hepatitis C.
MR elastography: non invasive technique in which the patient wears a device resting over the right hepatic lobe which transmits mechanical waves
Sonoelastography: degree of fiibrosis on chronic liver disease
14
Q
What is seen and expected results for dx?
A
Encapsulated mass that enhances on arterial phase and washes out on portal venous phase with an enhancing capsule.
HCC is often locally invasive and tends to invade into the portal and hepatic veins, IVC and bile ducts.
In contrast, cholangiocarcinoma and metastases to the liver area much less likely to do so.
15
Q
What is the LI-RADS scoring system for HCC on CT and MRI?
A
Ranges from LR-1 (favoring benignity) to LR-5 (favoring malignancy)
Major criteria
* Arterial enhancement
* Non peripheral washout on portal venous and delayed phases
* Enhancing capsule/pseudocapsule seen in portal venous or delayed phases
* Threshold growth with diameter increase of >50% in <6 months
Ancillary findings favoring HCC including non enhancing capsule, nodule in nodule architecture, mossaic architecture, fat in mass, blood products in mass.
Treatmnet options: partial hepatectomy, orthotopic liver trnasplantation, radiation therapy, percutaneous ablation, and transcatheter embolization
16
Q
A
Fibrolamellar carcinoma is a rare subtype of HCC that occurs in young patients without cirrhosis. Better prognosis than HCC. AFP is not elevated.
A fibrotic central scar is classic, which is hypointense on T1 and T2W MRI. Does not have capsule.
17
Q
What is the appearance of hepatic metastases, which phase of imaging is best used to visualize?
Appearance on ultrasound?
A
Metastases supplied by branches of the hepatic artery. Most metastases are hypovascular and best appreciated on portal venous phase.
On MRI, metastatic lesions tend to be hypointense on T1W and hyperintense on T2W.
Ultrasound: hypoechoic rim producing a target sign.
18
Q
What are hypovascular and hypervascular hepatic metastases?
A
Hypovascular: breast, pancreas, lung, lymphoma
Hypervascular: melanoma, renal cell carcinoma, carcinoid/choriocarcinoma, thyroid
19
Q
What are calcified and cystic hepatic metastases?
A
Calcified: mucinous cancers (colon, gastric, ovarian), osteosarcoma, treated lymphoma
Cystic: ovarian cystadenocarcinoma, GI sarcoma
20
Q
What is dx?
DDx?
A
Dx: epithelioid hemangioendothlioma is a rare vascular malignancy that causes multiple spherical subscapular masses. It is a cause of capsular retraction.
ddx:
* Mass forming cholangiocarcinoma
* Fibrolamellar HCC
* Epithelioid hemangioendothlioma
* Pseudocirrhosis (Macronodular liver contour with capsular retraction due to treated metastases)
* Confluent hepatic fibrosis
21
Q
A
Hemangioma: Dynamic contrast-enhanced T1-weighted MRI (early arterial top left image to delayed bottom left image) shows a segment 8 lesion (yellow arrows) demonstrating peripheral discontinuous nodular enhancement. There is progressively increasing centripetal enhancement towards the center of the lesion on delayed images. The signal intensity of the peripheral enhancement is similar to that of the aorta.
The hemangioma is hyperintense on the T2-weighted image (bottom right image).
IMPORTANT: hepatic cavernous haemangioma is the most common benign hepatic neoplasm. It is composed or disorganized endothelial cell lined pockets of blood vessels, supplied by a peripheral branch of the hepatic artery
22
Q
A
23
Q
What is seen and dx?
What other nuclear imaging used to confirm?
A
- Hepatic adenoma is a benign hepatic neoplasm containing hepatocytes, scattered Kupffer cells, and no bile ducts.
The absence of bile ducts makes a nuclear medicine HIDA scan a useful test to distinguish between focal nodular hyperplasia (which contains bile ducts and would be positive on HIDA) verses a hepatic adenoma, which does not contain bile ducts and will show a paucity of uptake on HIDA.
24
Q
What are the enhancement patterns of common hepatic masses (HCC, FNH, hepatic adenoma, hypervascular metastasis, non-hypervascular metastasis)
A
25
Hepatic abscess most commonly caused by a bowel process (through portal system to the liver). Common causes include diverticulitis, appendicitis, crohns disease, and bowel surgery. Ecoli is the most common causative organism.
Others: entamoeba histolytica (parasitic) with 99% presentation of pain (dome of right lobe)
26
Apart from pyogenic abscess in the liver what other infections are possible?
TB
Fungal infection
Histoplasmosis
Pneumocystis jirovecii
Candidiasis
27
Liver
Hepatic echinococcus: Ultrasound (left image) shows a complex, primarily hypoechoic mass in the superior aspect of the liver containing a hyperechoic undulating membrane (red arrow). Contrast-enhanced CT (right image) shows a fluid-attenuating cystic mass (yellow arrows) containing an undulating membrane (red arrow).
* On CT and MRI, a hydatid cyst is a well-defined hypoenhancing cystic mass featuring a characteristic floating membrane or an associated daughter cyst. Peripheral calcification may be seen on CT.
* Classic ultrasound appearance is a large liver cyst with numerous peripheral daughter cysts. A highly suggestive finding is the change in position of daughter cysts as the patient is repositioned.
The water-lily sign is an undulating membrane within the hydatid cyst.
Hydatid sand is a fine sediment caused by separation of the membranes from the endocyst.
28
What are fat containing lesions in the liver?
Focal fat
Adenoma
HCC
Angiomyolipoma, lipoma, pseudolipoma of the Glissons capsule
29
What are central scar lesions in liver ultrasound?
FNH
Fibrolamellar HCC
Giant haemangioma
30
What is the AAST liver injury scale grading scale?
31
What criteria is used for consideration of liver transplantation?
Milan criteria is used to assess appropriateness of liver transpantation in those with HCC/cirrhosis
3 criterias
* Single tumor <5cm or up with 3 tumors, each with diameter <3cm
* No extrahepatic involvement
* No major vascular involvement
32
What are post operative appearance after liver transplant?
Periportal edema, minimal ascites, right sided pleural effusion, and a small perihepatic haematoma
33
What are complications of liver transplantation?
* Vascular: hepatic artery thrombosis is the most common vascular complication. Others include hepatic artery stenosis and pseudoaneurysm, IVC or hepatic vein stenosis or thrombosis and portal vein stenosis or thrombosis
* Biliary: ductal stricture is the most common biliary complication. Leaks and obstruction due to choledocholithiasis is also possible
* Other complications: haematoma, abscess, hepatitis, splenic infarct, recurrent malignancy or primary sclerosing cholangitis (depending on the indication for transplant) and PTLD (lymphoma caused by EBV which can arise after solid organ or bone marrow transplant)
34
Congenital Budd-Chiari: Axial contrast- enhanced CT shows massive enlargement of the caudate lobe (yellow arrows) and the right posterior segment. There is atrophy of the left lobe and right anterior segments of the liver. Collateral venous drainage in the periphery of the liver is seen as geographic peripheral hyperenhancement (red arrows).
Budd-Chiari is hepatic venous outflow obstruction, which can be thrombotic or non-thrombotic. Thrombotic Budd-Chiari may be due to hypercoagulative states including haematological disorders, pregnancy, oral contraceptive use, malignancy, infection and trauma.
Acute Budd chiari presents with the clinical triad of hepatomegaly, ascites and abd pain.
35
What is the direction of blood flow to the liver?
36
What is the normal hepatic vein waveform?
37
What is blood flow to the liver during portal hypertension?
38
What are secondary findings of portal hypertension?
* Dilated portal vein
* Splenomegaly
* Gamna-Gandy bodies
* Varices
* Portosystemic shunts (gastroesophageal, paraumbilical or splenorenal)
39
What is the treatment for portal hypertension?
Transjugular intrahepatic portosystemic shunt (TIPS), which connects a branch of the portal vein to a systemic hepatic vein.
Ultrasound for surveillance of TIPs patency with routine follow up in 1 month, every 3 months for 1st year, and then every 6 to 12 months.
40
What is the evaluation for TIPS stenosis?
What value is high intraTIPS velocity and low main portal vein velocity?
TIPS stenosis: Spectral Doppler of a TIPS shows a velocity of 45 cm/sec, indicative of stenosis due to slow flow.
High intra-TIPS velocity >190 cm/sec or low intra-TIPS velocity of <90 cm/sec suggests stenosis.
Intra-TIPS velocity change of ± >50 cm/sec since the baseline study is also concerning for stenosis.
Low main portal vein velocity (<30 cm/sec) suggests TIPS stenosis.
41
What are the causes for increased hepatic vein pulsaility?
What would you expect in ultrasound waveform?
42
Gallbladder dx and appearnce?
43
What is the ddx of echogenic macterial within the gallbladder?
Gallstone
Gallbladder sludge
Gallbladder polyp (echogenic, non mobile)
Hyperplastuc cholecystoses (echogenic, non mobile, multiple polyps)
Porcelain gallbladder (echogenic wall, shadowing)
Adjacent bowel (echogenic wall, dirty shadowing)
44
US findings and expected results for dx?
Acute calculus cholecystitis: Oblique sagittal ultrasound through the gallbladder demonstrates a thickened, echogenic gallbladder wall (arrows). The gallbladder contains numerous echogenic gallstones (red arrow).
Positive sonographic Murphs sign (RUQ pain with pressure from the transducer during inspiration)
Gallbladder wall thickening >3mm
Distended gallbladder >4cm in diameter
Pericholecystic fluid or inflammatory changes in the pericholecystic fat
Color doppler showing hyperemic gallbladder wall
45
What are the serious complications of acute cholecystitis?
Emphysematous cholecystitis
Gangrenous cholecystitis
Gallbladder perforation
46
Who is mainly affected by acalculous cholecystitis?
Cholecystitis without gallstones, typically seen in very sick patients such as those in the ICU thought to be due to stasis and hypoperfusion. RIsk factors include sepsis, prolonged total parenteral nutrition, and trauma.
Treatment of acalculous cholecystitis in typically percutaneous cholecystostomy by interventional radiology.
47
Gallbladder what is seen?
Grayscale ultrasound (left image) shows diffuse echogenic foci within the gallbladder wall corresponding to intramural foci of gas on axial CT (right image; arrows).
Emphysematous cholecystitis caused by gas forming bacteria (clostridium, e.coli)
48
What is dx and imaging seen?
Gangrenous cholecystitis due to increased intraluminal pressure, leading to gallbladder wall ischemia and necrosis with high risk for gallbladder perforation.
Axial and coronal contrast-enhanced CT shows gallbladder wall edema and pericholecystic fluid. There is discontinuous mucosal enhancement of the medial gallbladder wall (red arrow) due to necrosis and perforation with spillage of contents into the right subhepatic space.
49
What is the most severe complication of cholecystitis?
Gallbladder perforation has high mortality due to generalized bile peritonitis.
Subacute perfroation may lead to a pericholecystic abscess and chronic perforation may cause a cholecystoenteric fistula.
50
What are the 6S's that increase the risk of a gallbladder polyp being malignant?
**S**ize >10mm or rapid growth.
**S**ingle: solitary polyp is more suspcious for malignancy. In contrast, benign cholesterol polyps tend to be multiple
**S**essile (broad based)
**S**tones: presence of stones may induce chronic inflammation, which can predispose towards malignancy
Primary **s**clerosing cholangitis increases risk of maignancy
**S**ixty (age) or greater
In patients with several of these high risk features, cholecystectomy should be considered in the presence of a polyp greater than 10mm in size.
51
What are the causes of diffuse gallbladder wall thickening >3mm?
Fluid overload/edematous tates: **cirrhosis** (hypoalbuminemia leads to diffuse gallbladder wall thickening), **congestive heart failure**, protein wasting nephropathy
Inflammatory/infectious: **cholecystitis, hepatitis**, pancreatitis
Infiltrative neoplastic disease: gallbladder carcinoma (rare)
52
What are the causes of focal gallbladder wall thickening?
Hyperplastic cholecystoses: adenomyatosis and cholesterol polyp
Vascualr: varices
53
54
What mode of imaging for MRCP?
What are its adv and disadv over ERCP?
T2W preferred for contrasting the T2 hyperintense stationary fluid in the biliary tract and surrounding structures.
Adv: MRCP is non invasive, does not require sedation, has ability to visualize surrounding anatomy.
Disadv: MRCP cannot simultaneously diagnose and treat abnormalities
Contrast enhanced MRCP can also be performed with fat saturated T1W imaging after injection of gadolinium contrast agents that have biliary excretion, such as gadoxetic acid disodium (Eovist)
55
What is the Todani classification of choledochal cysts and their location?
56
57
Liver and bile duct
58
Biliary duct
Choledocholithiasis: Sagittal ultrasound (left image) of the porta hepatis demonstrates common bile duct dilation (calipers) to 1.1 cm. Transverse scan (right image) through the region of the head of the pancreas shows an echogenic gallstone within the distal common bile duct (arrow).
* Choledocholithiasis is a stone in the common bile duct, generally treated with ERCP.
* Patients may be asymptomatic, but more often have right upper quadrant pain, nausea,
vomiting and cholestatic pattern of LFT abnormalities secondary to obstructed bile outflow.
59
* Mirizzi syndrome is inflammation and external compression of the common hepatic duct (CHD) caused by a stone in the adjacent cystic duct. It is essential for the surgeon to know about preoperatively because the CHD may be mistakenly ligated instead of the cystic duct. Additionally, inflammation can cause the gallstone to erode into the CHD and cause a cholecystocholedochal fistula and biliary obstruction.
* On ultrasound, a stone is typically impacted in the distal cystic duct and the CHD is dilated. The cystic duct tends to run in parallel with the CHD.
60
What aer the causes of below?
Commonly seen after sphincterotomy or biliary to enteric anastomosis, but rarely may be due to cholecystoenteric fistula or emphysematous cholecystitis
61
What is the normal diameter of common bile duct?
CBD should be 6mm or less before age 60, but may still be normal if 1mm larger per decade after that age.
e.g. an 8mm duct in an 80 year old patient may be considered normal.
Common bile duct is often mildly dilated in patients who have undergone cholecystectomy, usually 10mm or less
62
What is seen and associated disease?
What are the long term complications of disease?
Primary sclerosing cholangitis is idiopathic inflammation and destruction of bile ducts
PSC associated with ulcerative colitis (UC) and to a lesser extent crohns disease, and is more common in males.
Biliary imaging shows classical beaded, irregular appearance of the common bile duct and intrahepatic bile ducts
Long term complications: cirrhosis (prominent caudate lobe hypertrophy), cholangiocarcinoma and recurrent biliary infections. Cross sectional imaging is better at evaluating for these complications compared to ERCP.
63
What is the cause of recurrent pyogenic cholangitis?
What is the imaging triad?
What is the long term risk factor?
Caused by the parasite clonorchis sinensis, which leads to pigment stone formation, biliary stasis and cholangitis. Clinically, patients present with recurrent jaundice and fevers
Imaging triad
* Pneumobilia
* Lamellated bile duct filling defects
* Intrahepatic and extrahepatic bile duct dilatation and strictures
Patients with recurrent pyogenic cholangitis have an increased risk of cholangiocarcinoma
64
Biliary cystoadenoma: benign cystic neoplasm
65
What is classical presentation?
What is dx and seen?
Painless jaundice
Klatskin tumor: Coronal contrast-enhanced CT and T2-weighted MRI show an enhancing, mildly T2 hyperintense tumor (arrows) at the common hepatic duct bifurcation, resulting in moderate intrahepatic biliary ductal dilatation.
Cholangiocarcinoma tends to obstruct bile ducts and lead to intrahepatic ductal dilation and capsular retractiion.
66
What are the 3 main subtypes of cholangiocarcinoma?
* Mass forming cholangiocarcinoma
* Periductal cholangiocarcinoma: most often at the confluence of the right and left hepatic biliary ducts (Klatskin tumor)
* Intraductal cholangiocarcinoma: has variable imaging appearance
67
What are the RF for cholangiocarcinoma?
* Choledochal cyst
* Primary sclerosing cholangitis
* Familial adenomatous polyposis syndrome
* Clonorchis sinensis infection
* Thorium dioxide (alpha emitter contrast agent) not used since 1950s.
68
What are the RF for gallbladder cancer?
Gallstones and chronic cholecystitis.
Porcelain gallbladder (somewhat controversial).
Primary sclerosing cholangitis.
Inflammatory bowel disease (ulcerative colitis more frequently than Crohn's disease). Adenomatous polyp >10 mm or with multiple risk factors, as described above.
69
What is the normal pancreatic ductal anatomy?
70
What is the drainage for pancreatic divisum?
What is treatment?
71
What is seen in MRCP
The crossing duct sign describes the common bile duct crossing over the main duct to join the duct or Wirsung.
72
What is the different sequences in MRI and MRCP for pancreatic abnormalities?
73
Acute pancreatitis on CT and ultrasound, what is seen?
Contrast-enhanced axial CT (left image) demonstrates diffuse pancreatic enlargement and peripancreatic edema. The pancreatic parenchyma enhances uniformly, without evidence for necrosis.
Transverse ultrasound (right image) of the head and body of the pancreas shows a diffusely enlarged, heterogeneous pancreas (arrows) due to pancreatic edema.
Commonly caused by alcohol use or an obstructing gallstone
2 morphologic subtypes: interstitial edematous pancreatitis, necrotizing pancreatitis
74
What are the pancreatic and peripancreatic complications of pancreatitis?
What duration are they seen?
Extrapancreatic complications
Perihilar renal inflammation which may lead to venous compression or thrombosis
Bowel involvement: may see ileus or even a fistula
Secondary inflammation of adjacent vessels: pseudoaneurysm, venous thrombosis (splenic vein thrombisis which may lead to portal hypertension)
75
Abdominal radiograph (left image) and contrast-enhanced axial CT (right image) show numerous coarse calcifications in the pancreas (arrows).
Chronic pancreatitis: most commonly from long term alcohol abuse
76
What are the categories of pancreatic neopalsms: solid epithelial neoplasm, cystic epithelial neoplasm, endocrine neoplasm?
77
Pancreatic adenocarcinoma of the head causing the double duct sign: Two coronal images from a contrast- enhanced CT show marked dilation of the common bile duct (CBD), moderate dilation of the pancreatic duct (PD), and the obstructing, ill-defined hypoattenuating mass in the pancreatic head (red arrows).
78
What is the pancreatic mass protocal CT?
Where does pancreatic cancer normally occur and what sign?
A pancreatic mass protocol CT includes early arterial phase, late arterial phase (pancreatic phase), and portal venous phase images. The late arterial phase (pancreatic parenchymal phase) has the greatest conspicuity for detecting the hypoenhancing tumor against the background enhancing pancreas.
Commonly arises from pancreatic duct where it often causes ductal obstruction. The double duct sign describes dilation of both the pancreatic duct and the CBD due to obstruction by the pancreatic head mass.
79
Since pancreatic adenocarinoma is almost always associated with a dilated pancreatic duct, an alternative dx should be considered if not dilated?
80
What are the comparisons of solid pseudopapillary tumor, mucinous cystic neoplasm and cystadenoma (pancreas)?
81
What are the 2 categories of intraductal papillary mucinous neoplasms?
Elderly males mostly: grandfather tumor
Premalignant neoplasm
82
What is the Whipples triad for pancreatic endocrine neoplasm?
Prognosis?
Insulinoma: hypoglycemia, clinical symptoms of hypoglycemia, and allevation of symptoms are admin of glucose.
Due to symptoms of hypoglycemia, insulinomas tend to present early
83
What is the associated secondary syndrome with gastrinoma?
What component of disease is it part of?
Where is it commonly found?
Gastrinoma is 2nd most common pancreatic endocrine tumor. Liver metastases are present at time of dx in 60% of patients.
Zollinger-Ellison syndrome is a clinical syndrome that occurs secondary to a gastrinoma. Hypersecretion of gastrin leads to gastritis, diarrhea, peptic ulcer disease and even GERD.
Gastrinoma associated with MEN type 1 (tends to be multiople and located in the duodenum rather than the pancreas)
Gastrinoma triangle describes the typical location of gastrinomas in area bounded by the junction of the cystic duct and the CBD, the duodenum inferiorly and the neck/body of the pancreas medially.
84
Apart from insulinoma, gastroma what other pancreatic endocrine tumors are there? What is prognosis?
* Glucagonoma: 3rd most common pancreatic endocrine tumor with migratory rash, diabetes and glossitis
* VIPoma: profuse watery diarrhea and hypokalemia. Most are malignant and have metastases at dx
* Somatostatinoma very rare
85
What is the effect of von Hippel Lindau syndrome in pancreas?
Inherited multisystemic disease
Pancreatic neoplasms in VHL include serous cystadenoma and pancreatic neuroendocrine tumors
86
What is ddx for hypervascular lesions, cystic lesions, diffuse enlargement, atrophy, fatty infiltration in pancreas?
87
What is the overview of splenic lesions: cystic, cystic and solid, solid (hypervascular/non-hypervascular), infectious/inflammatory?
88
What is the most common splenic lymphoma?
Splenic lymphoma is the most common splenic malignancy
Secondary splenic involvement of systemic lymphoma is much more common than primary splenic lymphoma (rare <1% of cases)
89
Axial contrast-enhanced CT shows a posterior peripheral wedge-shaped region of splenic non-enhancement (arrows), consistent with infarct.
* Splenic infarcts are most commonly due to emboli (in older patients) and thrombosis (in younger patients with hematologic disease).
* Splenic infarct classically manifests as a wedge-shaped peripheral region of nonenhancement, but a more heterogeneous, mass-like appearance can also be seen.
90
* Gamna-Gandy bodies are multiple tiny foci of hemosiderin deposition and are a sequela of portal hypertension.
* Other signs of portal hypertension and cirrhosis are usually apparent on imaging, such as splenomegaly, varices, recanalized umbilical vein, ascites, and a nodular liver contour.
* The hemosiderin deposits demonstrate low signal on all sequences. On in- and out-of-phase gradient-echo sequences, the longer TE of the in-phase images demonstrates blooming (relatively decreased signal on in-phase images), due to longer dephasing time and exaggeration of T2* effect.
Numerous low signal foci in the splen which demonstrate blooming on in ohase imaging (right image) compared to out of phase imaging (left image)
Cirrhotic morphology of the liver (nodular contour, widened fissures, multiple regenerative nodules)
91
What is the AAST splenic injury scale?
When multiple injuries are present, advance one grade up to a grade III
92
What is the landmarks for nasopharynx, oropharynx and hypopharynx?
* Nasopharynx: Extends from the base of the skull to the soft palate.
* Oropharynx: Located behind the mouth and extends from the uvula to the hyoid bone.
* Hypopharynx: Extends from the hyoid bone to the cricopharyngeus muscle, which is located at the lower end of the cricoid cartilage, usually between C5–6.
93
Double-contrast barium swallow showing normal impressions on the esophagus by the aortic arch (Ao, yellow arrows) and left mainstem bronchus (red arrow).
94
What is seen and dx?
What are the potential ddx?
Schatzki ring is a focal pathologic narrowing of the B (mucosal) ring of the distal esophagus less than 13mm causing intermittent dyspashgia.
Key imaging feature is focal, thin circumferential constriction near the GE junction almost always associated with a hiatual hernia, best seen in the RAO/prone position.
ddx:
* Focal stricture
* Muscular esophageal ring above the GE junction (also known as an A ring)
* Esophageal cancer (assocatde with irregular mucosal contour and an apple core appearance)
* Esophageal. web (rarely circumferential, usually in cervical esophagus)
95
What is seen?
What is the 2 most common ddx?
Refluex esophagitis caused by GERD
but also seen in:
* Zollinger Ellison syndrome (gastrinoma) due to increased acid production
* Scleroderma: due to gastroesophageal sphincter fibrosis and resultant incompetence
Fluoroscopic findings of reflux esophagitis
* Mucosal granularity
* Thickened folds
* Erosions (may be solitary or multiple, typically on posterior wall).
* Strictures
96
dx: esophageal candidiasis --> spot image from double contrast esophagram shows a diffuse, shaggy appearance
ddx:
* herpes esophagitis: small, discrete ulcerations scattered randomly
* CMV/HIV esophagitis
* medication esophagitis
* Crohns esophagitis
* Eosinophilic esophagitis: idiopathic inflammatory condition leading to strictures, webs and spasm
* Chemotherapy associated mucositis
97
Define splenomegaly and causes (mild to moderate/marked/massive)
97
Causes of hypervascular or hypoechoic splenic lesion?
Haemangioma (can also be hypoechoic)
Hamartoma
Lymphangioma
Angiosarcoma
97
What is dx and sign?
Malignant stricture (due to esophageal carcinoma)
Barium swallow (left image) demonstrates abrupt narrowing (arrows) of the distal esophagus with subtle mucosal irregularity. Sagittal CT (right image) shows mass-like soft tissue thickening in the same region.
* The key imaging finding is irregular narrowing with shouldered margins (apple-core appearance).
97
Splenic injury, what grade (2 different patients) and seen?
Left image: Coronal contrast-enhanced CT demonstrates a large subcapsular hematoma (arrows) compressing the spleen, without evidence of active extravasation, in keeping with grade III splenic injury.
Right image: Axial contrast-enhanced CT shows a shattered spleen (grade V) with surrounding hematoma.
98
Apart from malignant strictures, what other strictures can be present in the esophagus?
* Peptic stricture (secondary to chronic reflux)
* Barrets esophagus stricture (mid esophagus above the metaplastic adenomotous transition because adenomatous tissue is acid resistant and unaffected by gastric secretions)
* Caustic stricture (secondary to NG tube placement)
* Radiation stricture (long, smooth and narrow and occur in the radiation field)
* Extrinsic compression from mediastinal afenopathy (CT/MRI best to confirm)
99
How to tell what layer of esophageal mass by the angle?
100
What are the ddx of benign esophageal masses?
* Mesenchymal tumor (most common submucosal esophageal tumor): leiomyoma, lipoma, hemangioma
* Adenoma
* Fibrovascular polyp
* Inflammatory polyp
* Varices: on fluoscopy easily distinguished as change in size and shape with peristalsis and valsalva manouvre. Uphill varices are most common (distal esophagus): portal vein --> left gastric (coronary vein) --> periesophageal venoux plexus --> azygos/hemiazygos collaterals --> SVC)
* Foregut duplication cysts
* Esophageal foreign body
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Esophageal carcinoma: Oblique fluoroscopic spot image from a barium swallow (left image) shows an irregular stricture (yellow arrows) with proximal dilation of the esophagus. Two linear ulcerations (red arrows) project into the mural mass.
Contrast-enhanced axial CT (right image) shows irregular thickening of the esophagus (arrows).
ddx:
* Metastasis: direct invasion of the esophagus most commonly from gastric, lung or breast primaries
* Lymphoma
* Malignant GIST
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What is seen and the signs?
What is dx and complication?
What is a disease that mimics the dx?
Achalasia: Fluoroscopic spot image from an upper GI series (left image) shows a **markedly dilated esophagus terminating in a bird’s beak **(yellow arrow) at the GE junction, due to failure of the distal esophageal sphincter to relax. Axial non-contrast CT confirms the markedly dilated, debris-filled esophagus (red arrows).
Achalasia caused by the inability of the distal esophagus to relax because of abnormal myenteric ganglia in the Auerbach plexus.
Complications: esophageal cancer
Treatment: pneumatic dilatation, surgical myotomy (Heller myotomy), or peroral endoscopic myotomy (POEM) and pharmacologic interventions such as botulinum toxin injection
Pseudoachalasia caused by obstructing GEJ cancer mimicking primary achalsia. This can be differentiated on fluoroscopy because in achalasias there is eventual transient relaxation of the narrowing when the patient stands but the fixed obstruction of pseudoachalasia will not relax with standing.
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What is appearance sign and dx?
What symptoms may present?
Single-contrast esophagram demonstrates delayed passage of barium through the esophagus, with multiple tertiary contractions in a **corkscrew esophagus** configuration, and subsequent esophageal reflux
Chest pain or dysphagia cuased by repetitive, non propulsive esophageal contraction.
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What are the 2 types of diverticula?
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What is seen and dx?
What is it caused by?
What are the symptoms and location of disease?
Lateral and right anterior oblique barium esophagram images demonstrate contrast filling a blind-ending pouch (arrows) arising posteriorly from the pharyngoesophageal junction at level of C5, in keeping with a Zenker diverticulum.
Zenker diverticulum caused by failure of the cricopharyngeus muscle to relax, leading to elevated hypopharyngeal pressure and resultant outpouching.
Symptoms: halitosis, aspiration and regurgitation or undigested food.
Located in the hypopharynx, just above the upper esophageal sphincter (cricopharyngeus muscle)
Zenker diverticulum is best seen on lateral view
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Frontal view from a barium esophagram shows a 3 cm Killian-Jamieson diverticulum on the left (arrow).
* A Killian-Jamieson (KJ) diverticulum is located in the proximal cervical esophagus, at the Killian-Jamieson space, which is an area of weakness below the attachment of the cricopharyngeus muscle.
* A KJ diverticulum protrudes anterolaterally, best seen on the AP view and is more often bilateral.
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What is seen and dx?
Aberrant right subclavian artery
Oblique single-contrast barium esophagram (left image) demonstrates a smooth posterior indentation of the proximal thoracic esophagus (arrow). Aortogram in the same patient (right image) demonstrates the aberrant right subclavian artery (aRS, * at origin) crossing midline before heading towards the right arm. This patient has an additional aortic branching anomaly, with the left vertebral artery (LV) arising directly from the aorta. The right vertebral artery (RV), arising from the aberrant right subclavian, is hypoplastic. The right and left common carotid arteries (RCC and LCC), and left subclavian (LS) are normal.
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What are the 4 types of hiatal hernias?
* Type I – Sliding hiatal hernia (most common). A sliding hiatal hernia is present when the gastroesophageal junction (GEJ) slides up into the posterior mediastinum and gastric folds are seen above the diaphragm.
* Type II – Paraesophageal with GEJ in normal position (least common). A type II hiatal hernia is herniation of the gastric fundus, with a normally positioned GEJ (below diaphragm).
* Type III – Paraesophageal with GEJ above the diaphragm (second most common). In a type II hiatal hernia, both the GEJ and fundus/body of the stomach protrude into the lower mediastinum.
* Type IV – Associated with herniation of other organs above the diaphragm. A type IV hiatal hernia is displacement of the stomach and other organs (spleen, pancreas, small bowel, colon) above the diaphragm.
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What is dx and tyoe?
Paraesophageal hernia: Frontal and oblique single-contrast barium upper GI study shows intrathoracic herniation of the gastric fundus (yellow arrows), consistent with a recurrent paraesophageal hernia in this patient with prior history of hernia repair. The GE junction (red arrow) remains below the diaphragm, consistent with a type II hiatal hernia.
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What is seen and dx?
What are the possible causes?
Contrast filling thickened gastric folds (arrows) on a double contrast barium study, thought to represent gastritis in this patient.
* H.pylori gastritis (H.pylori is a major cause of gastritis, gastric ulcers and duodenal ulcers)
* Zollinger-Ellison (ZE) syndrome: gastrinoma (elevated gastrinv level and a paradoxical increase in gastrin after secretin administration)
* Eosinophilic gastritis
* Menetrier disease (hypertrophic gastropathy)
* Crohns disease (rarely isolated site: mainly distal half of stomach affected)
* Other causes of thickened gastric folds: gastric varices, sarcoidosis, gastric lymphoma and submucosal carcinoma
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