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46 Cards in this Set
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1. What is the etiology of Budd-Chiari Syndrome?
2. What is the difference between primary and secondary Budd-Chiari? 3. What can early Budd-Chiari syndrome mimic? 4. What are the imaging features of Budd-Chiari Syndrome? |
1. Obstruction of hepatic venous outflow at the level of the hepatic veins and/or IVC.
2. Primary Budd Chiari: - membranous obstruction of the hepatic veins. Secondary Budd-Chiari: - occlusion of the hepatic veins with thrombus. - affects small and large veins. - Small vein occlusion is seen with various drugs or treatments (chemotherapeutic and immunosuppressive drugs). - Large vein occlusion is seen with coagulopathy (hematologic disorders and coagulation abnormalities, including polycythemia rubra vera, paroxysmal nocturnal hemoglobinuria, pregnancy, and oral contraceptives are common causes). - Venous obstruction can also be 2/2 tumor growth (from renal cell carcinoma, hepatoma, or adrenal carcinoma) into the IVC or hepatic veins. 3. Passive hepatic congestion due to CHF (kind of like Budd-Chiari where there is obstruction of hepatic veins) 4. - Non-opacification of the hepatic veins/IVC. - Hypertrophy of the caudate lobe with peripheral atrophy resulting in a dysmorphic liver. - Intrahepatic and perihepatic venous collaterals. On hepatic venogram, you see narrowed or occluded hepatic veins with a characteristic pattern of tortuous web-like hepatic venous collaterals. - Large regenerative nodules (nodular regenerative hyperplasia) that have imaging features and histology similar to focal nodular hyperplasia. They can easily be confused with HCC. However, HCC has greater washout than nodular hyperplasia. |
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1. What are the morpholgic patterns of HCC?
2. What are the imaging findings of HCC on MRI? 3. What does the presence of a capsule indicate? |
1. May have a variety of morphologic appearances:
- Focal: internal fat, capsule, mosaic attenuation. - Mutlifocal: may simulate mets. Look fora dominant mass with satellite masses which are believed to occur from portal venous metastases that seed adjacent hepatic parenchyma. - Diffusely infiltrating neoplasm: innumerable masses 2. - Small lesions show early arterial enhancement with washout on portal venous and delayed images. - Larger lesions (>5 cm) tend to be heterogeneous,with necrosis. +/- tumoral capsule. - Non-enhanced T1WI: variable, iso to hyperintense; may be due to fatty metamorphosis, copper, or glycoproteins. - Non-enhanced T2WI: iso to hyperintense as HCC loses ability to concentrate iron. - Rarely, HCC can be primarily cystic mimicking abscess or cystic met. In these cases, look for secondary signs of HCC such as angioinvasion. NOTE: dysplastic and regenerative nodules can also show increased signal on T1WI. However, dysplastic and regerative nodules retain the ability to concentrate iron and are thus low SI on T2WI. 3. Presence of capsule is highly suggestive of focal HCC. Capsules are found in well-differentiated HCC and often indicate a favorable prognosis. |
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1. What is lipiodol and its role in detection and treatment of HCC?
2. What are the imaging findings after lipiodol treatment? 3. What is the appearance after successful ablation of a liver tumor? What findings suggest recurrent/residual tumor? |
1. Lipiodol is an iodinated oil that when injected into the hepatic artery localizes to HCC. It can be injected alone for diagnostic purposes or during chemoembolization with I-131 labeled lipiodol.
2. On NECT, lipiodol is hyperdense. If, on follow-up imaging, there is abnormal enhancement adjacent to the lipiodol, it represents recurrent tumor. 3. A successful ablation results in a water attenuation mass without evidence of enhancement. Enhancing nodules within or adjacent to the ablation zone are consistent with recurrent or residual HCC. |
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1. What is primary sclerosing cholangitis?
2. Does it affect intra- or extrahepatic ducts? 3. Is it more common in males or females? 4. Patients with PSC are at increased risk of developing what malignancy? 5. What are the MRI findings in PSC? |
1. Idiopathic progressive inflammatory disease causing multifocal strictures.
2. Involves both intra- and extrahepatic bile ducts. 3. More common in males 2:1. 4. High risk of developing cholangioCA 5. - Cirrhosis present in 87%. - Macronodular (>3cm) cirrhosis with nodules located in the central aspect of the liver. - Segmental intrahepatic ductal dilatation. - Peripheral wedge shaped atrophy. T2 characteristics of fibrosis changes with time, with acute fibrosis having higher signal due to higher water content. Chronic fibrosis has low signal on T2 weighted images. |
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1. What is the DDX of multiple hepatic masses in a pt with AML?
2. What are the imaging features of hepatic candidiasis? |
1. Leukemic nodules (chloromas) vs. Multiple hepatic abscesses, usu. candidiasis
2. - Generally occurs in immunocompromised pts. - Most common systemic fungal infection in immunocompromised - Uniformly hypoechoic, most common - “Wheel within a wheel”: periph hypoechoic zone with inner echogenic wheel and hypoechoic center “Bull’s Eye” Echogenic, due to calcification and scar formation. |
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What is the differential diagnosis of malignant neoplasms resulting in multiple hypodense liver lesions on CT?
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Malignant causes of multiple hypodense liver lesions:
- Metastases: Colon, pancreas, stomach, lung, breast, etc - Lymphoma (dessiminated dz or in immunocompromised pts) Hepatocellular Carcinoma - Usually in cirrhotic liver or one damaged by chronic hepatitis - Associated signs of portal hypertension, venous invasion - Most lesions are heterogeneously hypervascular on arterial phase CECT Epithelioid Hemangioendothelioma - Multiple, peripheral, confluent hepatic masses - Often with target appearance and overlying hepatic capsular retraction |
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What is the differential for multiple cystic/low attenuation liver lesions?
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- Simple Hepatic Cysts
- Biliary hamartoma - Peribiliary cyst - Polycystic liver disease - Caroli Disease - Infections: Candidiasis, pyogenic abscesses - Inflammatory: Sarcoidosis - Mets/lymphoma |
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What is the differential diagnosis of benign neoplasms resulting in multiple hypodense liver lesions on CT?
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Hepatic Cavernous Hemangioma
- Multiple lesions are not rare. - May be innumerable and in other organs and body wall (Kasabach-Merritt syndrome). Multifocal Fatty Infiltration - May closely simulate metastases. - Often has perivascular distribution or follows fissures - Blood vessels traverse lesion without mass effect Hepatic Adenoma - Uncommon disease but lesions are often multiple, may be innumerable (adenomatosis) - Larger lesions usually heterogeneous due to presence of fat, hemorrhage or necrosis. - Associated history of oral contraceptives, anabolic steroids, glycogen storage disease. Biliary Hamartoma - Usually multiple to innumerable, rarely more than 15 mm diameter - Fibrotic tissue in walls may cause peripheral enhancement on CECT or CEMR, and echogenicity on US Nodular Regenerative Hyperplasia - Usually occurs in Budd-Chiari syndrome - "Large regenerative nodules" - Benign hyperplastic nodules that resemble FNH on imaging and histology - Usually multiple, 1-4 cm diameter, may have hypodense halo or rim, central scar Hepatic Angiomyolipoma - Multiple lesions are seen almost exclusively in tuberous sclerosis syndrome - AMLs in kidney, cystic lesions in lungs Hepatic Sarcoidosis |
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What infections can present as multiple hypodense liver lesions.
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- Hepatic Pyogenic Abscess: more common and multiple than with amebic or hydatid. Associated pleural effusion, atelectasis, portal vein thrombophlebitis.
- Hepatic Amebic Abscess : usually isolated or no more than a few - Hepatic Hydatid Cyst: - Hepatic Candidiasis: innumerable "microabscesses" in immunocompromised patient |
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1. What are the imaging findings of hemochromotosis in the liver?
2. What is the etiology of primary hemochromatosis? secondary hemochromatosis? 3. How do you differentiate primary from secondary hemochromatosis? 4. Are pts with hemochromatosis at increased risk of HCC? What is the appearance of HCC with hemochromatosis? |
1.
- CT is not as sensitive as MRI in showing early findings of hemochromotosis. - On CT= increased attenuation (>75 HU on NECT). - On MRI= liver is markedly hypointense with hemochromotosis. 2. - Primary hemochromatosis: AR disorder characterized by excess absorption of iron from GI tract. - Secondary hemochromatosis (hemosiderosis): results in excess iron deposition in the reticuloendothelial tissues from repeated transfusions. 3. - Primary hemochromatosis: excess iron is deposited in the liver, heart, and pancreas, with sparing of the spleen. - Secondary hemochromastosis: iron is deposited in the RES of the liver, spleen, and bone marrow. 4. Yes. 1/3 of deaths from hemochromatosis are related to HCC. Look for a focal T2 hyperintense mass on a background of very low T2SI liver parenchyma. |
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1. What are the imaging findings of amiodarone therapy in the liver?
2. What findings are seen on MRI? |
1. Amiodarone therapy results in iodine deposition within the liver. Therefore, high attenuation on CT. There also can be hyperattenuation w/n the lung parenchyma and secondary interstitial lung disease.
2. MRI is normal. |
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1. What is the signal intensity of the spleen in relation to the liver on T1 and T2WI?
2. What is a good internal control of the T2 SI of the liver? |
1. On T1WI, the liver is brighter. On T2WI, the spleen is brighter.
2. Paraspinal muscles. The SI of the liver on T2WI is not lower than that of the paraspinal muscles. |
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1. What are the 2 morphologic types of cirrhosis?
2. What are they associated with? |
1. Micronodular and Macronodular. Micronodular cirrhosis has regenerative nodules less than 3 mm. Macronodular cirrhosis has regenerative nodules larger than 3mm.
2. Micronodular cirrhosis is associated with alcohol related cirrhosis. Macronodular cirrhosis is related to viral hepatitis. |
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1. What are the signal characteristics of regenerative nodules on MRI?
2. What are the signal characteristics of dysplastic nodules on MRI? 3. What are the signal characteristics of HCC on MRI? |
1. Regenerative nodules are usually T1 and T2 isointense becuase they still have to ability to concentrate iron (low SI on MRI).
2. Dysplastic nodules can be T1 hyperintense and T2 isointense with isointense to background liver on post-contrast images. T1 hyperintensity is due to fat or copper. In and out-of-phase imaging could help make this distinction. T2 hyperintensity suggests HCC. 3. HCC is T2 hyperintense with enhancement of the T2 hyperintense component. |
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1. What are the imaging features of confluent hepatic fibrosis?
2. What part of the liver is most commonly involved? 3. Is capsular retraction present? 2. What does it mimic and how can you differentiate among the possibilities? |
1. Confluent hepatic fibrosis manifests a wedge shaped region of low T1 and high T2SI extending from the liver capsule towards the porta hepatis.
2. Most commonly involves the anterior segment of the right hepatic lobe and medial segment of the left lobe. 3. Capsular retraction is seen in 90% of cases. 4. Confluent hepatic fibrosis can mimic diffuse or infiltrating HCC, cholangioCA, and treated mets. However, usually a tumor is expansive and bulges the hepatic contour. In confluent hepatic fibrosis, there is no venous invasion and size of the area does not change over time. The bile ducts are not dilated. |
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1. What is the pathogenesis of cardiac cirrhosis?
2. What are the imaging features of cardiac cirrhosis? 3. What effect does this have on the portal vein? |
1. Heart failure and/or constrictive percariditis lead to an increased central venous pressure resulting in increased hepatic venous pressure which diminishes hepatic arterial flow leading to hepatocellular hypoxia.
2. Mottled enhancement of the liver resembling early changes of Budd-Chiari syndrome. Dilated hepatic veins and IVC, intrahepatic periportal lucency, ascites, and pleural and pericardial effusions. 3. Doppler waveform of the portal vein becomes abnormal with loss of normal continuous flow pattern and increased pulsatility. |
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1. What are some of the causes of hepatic steatosis?
2. How do you confirm the presence of intrahepatic fat on MRI? 3. What is the underlying etiology of focal steatosis? |
1. Alcohol, obesity, TPN, diabetes, corticosteroids, NASH
2. Drop in signal intensity on out-of-phase images. 3. Focal steatosis is thought to be due to regional differences in hepatic blood flow. |
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1. What is the underlying abnormality in glycogen storage diseases?
2. Does the liver have increased or decreased attenuation as a result of glycogen deposition? 3. What hepatic neoplasm occurs in greater frequency in pts with glycogen storage disease? |
1. Abnormality in breaking down glycogen into glucose resulting in excess deposition of glycogen within the hepatocytes and proximal tubules of the kidney.
2. Although glycogen accumulation results in a hyperattenuating liver, in some people the effects of fatty infiltration predominate due to chronic hormonal stimulation of the liver. 3. Multiple hepatic adenomas. |
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1. What are the imaging findings of radiation induced liver disease?
2. What accounts for the low attenuation? |
1. Look for a straight sharply defined zone of low attenuation corresponding to the treatment port.
2. Edema and fatty infiltration |
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1. What are the demographics of fibrolamellar HCC?
2. What are the imaging features of fibrolamellar HCC? 3. What other lesions can contain a central scar? |
1. Fibrolamellar HCC occurs in young adults without underlying cirrhosis. Because these tumors are discovered late in the course of the disease, they are large and of advanaced stage at diagnosis.
2. Large heterogeneously enhancing mass (as opposed to FHN which demonstrates homogeneous enhancement) with centrcarotene calcified scar. The presence of nodal and distal metastases is also a common finding at presentation. 3. FNH and large hemangiomas 4. While fibrolamellar hepatocellular carcinoma (HCC) is said to have a better prognosis than conventional HCC, it is still a deadly disease and usually leads to death within months to a few years of the young patients that are most commonly affected. |
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What is the DDX of diffuse hyperattenuation of the liver?
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1. Amiodarone toxicity
2. Iron overload 3. Wilson's disease (Copper) 4. Gold therapy 5. Glycogen storage disease |
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1. What is the DDX of multiple liver cysts?
2. What is the appearance of peribiliary cysts and what are they associated with? 3. Do biliary hamartomas enhance? |
1. Multiple simple cysts, biliary hamatoma, cysts associated with polycystic liver disease, peribiliary cysts, cystic mets, Caroli's disease.
2. Multiple tiny cysts that can be clustered or strings of cysts that occur along the portal tracts. They represent dilated intrahepatic peribiliary glands. associated with cirrhosis. 3. Biliary hamartomas can have rim enhancement related to compressed liver parenchyma. They are usually small (<1cm). |
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1. What are the different types of liver abscesses?
2. What are some causes of hepatic abscesses? 3. What are the imaging characteristics of pyogenic abscess? 4. What are the imaging characteristics of an amebic abscess? 5. What are the imaging characteristics of echinococcal cysts? 6. What are the imaging characteristics of candidal abscess and what can they mimic? |
1. Pyogenic abscess, amebic abscess, echinococcal cysts, and fungal (candidal) abscess.
2. Diverticulitis, appendicitis, cholecystitis, biliary obstruction, penetrating trauma, surgery, adjacent infection. 3. Pyogenic abscess presents as a cluster of low attenuation cysts (cloverleaf appearance) with enhancing rim. 4. Amebic abscess is caused by Entamoeba histolytica. Look for a unilocular mass with a low density ring. Cecal thickening is often seen. 5. Echinococcal disease is caused by the tapeworm --Echinococcus granulosus/ multilocularis. Usually occurs in regions where dogs are used to herd livestock. Look for a cystic mass with multiple smaller cysts within it which may look like septations (mimicking cystadenoma). The walls of the large cyst may calcify. 6. Multiple small, low attenuation masses in liver and spleen in immunocompromised hosts. Bull's eye lesions at sonography. May look like leukemic infiltrates or lymphoma. |
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1. What are the imaging features of biliary cystadenoma?
2. What can mimic this appearance? 3. What are findings seen in cystadenoCA? |
1. Multilocular cystic mass with a thick capsule.
2. Echinococcal cysts. 3. Mural nodules or thick, irregular, enhancing septations. |
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1. What liver lesions may contain fat?
2. What is hepatic AML associated with? |
1. Angiomyolipoma, Lipoma, hepatic adenoma, HCC, metastatic liposarcoma.
2. AML may be solitary or multiple. Associated with tuberous sclerosis. |
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What are the primary malignancies that give hypervascular mets?
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Renal cell, neuroendocrine tumors (islet cell, pheochromocytoma, carcinoid), sarcoma, GIST, thyroid, breast
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What are the imaging features of intrahepatic cholangioCA?
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- Intrahepatic biliary obstrution
- Chronic obstruction of the bile ducts leads to lobar atrophy. |
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1. What is more common -- primary or secondary lymphoma?
2. What are the imaging features of secondary lymphoma? 3. What are the imaging features of primary lymphoma? |
1. Secondary lymphoma
2. Multiple small, hypoechoic and hypodense lesions. Sometimes lymphomatous involvement of the liver is often difficult to detect radiographically due to tiny and diffuse implants. Look for associated adenopathy. 3. Primary lymphoma of the liver is very rare. Usually presents as a solitary mass. Increased incidence in pts with chronic liver disease (hep C) and HIV. |
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1. What are the imaging features of biliary cystadenoCA?
2. How does the prognosis change if the cystadenoma/CA contains ovarian tissues? |
1. Thick septae, enhancing nodular components, and calcifications.
2. Biliary cystadenomas and cystadenoCA may contain ovarian stroma (found only in women). Those contaning ovarian stroma have a better prognosis. |
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What are the imaging features of epitheliod hemangioendothelioma?
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- Rare malignat tumor of vascular origin
- Multiple solitary masses that grow together to form a large confluent mass(es). Typically, the lesions are located in the periphery of the liver. - May have capsular retraction. |
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1. What is the significance of hypoechoic halo on US?
2. What is the appearance of most hypervascular mets on US? |
1. Hypoechoic halo around a liver mass is a ominous sign.
Usually seen with mets or HCC. 2. The more vascular a tumor, the more likely it is to be echogenic. |
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1. What is the etiology of portal vein thrombosis?
2. What are the causes of bland thrombosis? 3. What are the causes of malignant thrombosis? 4. What is chronic portal vein thrombosis with development of collateral veins in the porta hepatis called? 5. What happens to the hepatic artery as a result of portal vein thrombosis? |
1. Bland thombosis or malignant tumor thombosis.
2. Causes of bland thrombosis include: - Stasis from cirrhosis-related sinusoidal obstruction. - Acute pancreatitis - Seeding of PV by infected material (acute appendicitis, intraperitoneal abscess, inflammatory bowel disease) - Hypercoagulable states (primary or tumor-related) 3. Malignant portal vein thrombosis: - HCC: most common - Pancreatic carcinoma - Liver metastases 4. Cavernous transformation of the portal vein. 5. Hepatic artery enlarges as a result of portal vein thrombosis. |
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Which primaries give rise to echogenic metastases?
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Echogenic mets are seen with hypervascular tumors such as renal cell CA, carcinoid, and pancreatic islet cell tumors.
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Cystic mets
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Cystic metastases may come from primary cystic tumors (e.g., ovarian), sarcomas, gastrointestinal stromal tumor (GIST), and others, especially after treatment. They will usually have mural nodularity
GIST metastasis treated with Gleevec may appear exactly as a simple cyst (check history and prior studies). |
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What criteria are used to distinguish tumor thrombus from bland thrombosis?
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1. contiguity with parenchymal tumor
2. expansion of the lumen of the vein 3. enhancing thrombus |
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1. What is the cause of cirrhosis in cystic fibrosis?
2. Wha are the causes of fatty infiltration of the pancreas/fatty pseudohypertrophy of the pancreas. |
1. Chronic liver injury due to inspissated bile within small bile ducts that may result in a form of biliary cirrhosis.
2. - senescent change - cystic fibrosis - Shwachman-Diamond syndrome - diabetes/steroids/cushing's disease |
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What are the imaging findings in Caroli's disease?
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1. Cystic dilation of terminal intrahepatic ducts that results in multiple intrahepatic cysts. Calculi may form within these cysts. Look for a central dot sign which represents the portal vein branch surrounded by the dilated intrahepatic duct.
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Congenital fibropolycystic disease
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Findings in the liver:
- biliary hamartomas - polycystic liver disease - caroli's disease Findings in the kidneys: - arpkd - adpkd - medullary sponge kidney |
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What are the imaging findings in FNH following gadoxetate?
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1. On delayed images obtained 20 minutes after administration of gadoxetate, there will be retention of contrast in FNH.
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Inflammatory pseudotumor
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An inflammatory pseudotumor of the liver may be indistinguishable on imaging from peripheral or hilar cholangiocarcinoma. Peripheral lesions result in capsular retraction and show delayed enhancement.
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1. What are the imaging findings of arterioportal shunts in cirrhosis?
2. What are the imaging findings of regenerative or dysplastic nodles on ct? |
1. Peripheral, subcapsular location, small size, wedge shape, and no corresponding lesion on venous or delayed phase imaging.
2. Regenerative (cirrhotic) and dysplastic nodules are usually not detected on CECT. They may be detected as small hyperdense lesions on the NECT phase, but fade into the background cirrhotic liver on enhanced phases of imaging and are rarely hypervascular. They are not transiently hyperdense on arterial phase imaging. |
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Angiosarcoma of the liver
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- rare tumor, often with multiple lesions in the liver and spleen. Angiosarcoma can have peripheral and delayed enhancement, similar to hemangiomas. However, the bright, homogeneous T2 signal seen in hemangiomas is greater than the signal seen with angiosarcoma.
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1. What is oriental cholangiohepatitis?
2. What organisms are implicated? 3. What are the complications? |
1. Recurrent pyogenic cholangitis
2. Clonorchis and Ascaris lumbricoides. 3. Pigment stones obstruct intrahepatic ducts resulting in superimposed infection and abscess formation. Portal occlusion may be seen. |
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1. What are the causes of portal vein thrombosis?
2. What are the manifestations of subacute-chronic portal vein thrombosis? |
1. HCC, cirrhosis, inflammatory causes (pancreatitis, cholangitis), sepsis, dehydration, hypercoagulable state.
2. Cavernous transformation of the portal vein. Look for large enhancing serpiginous collateral veins in the porta hepatis with nonvisualization of the normal expected portal venous branching pattern. |
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hepatic adenoma
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histopathology of hepatic adenomas demonstrate mostly hepatocytes without portal triads or bile ducts.
multiple hepatic adenomas can be seen with glycogen storage disease. Complications include hemorrhage and rupture and occasional presence of malignant degeneration to hepatoma. - Peripherally draped vascular supply (rather than central for FNH). |
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Hepatic veno-ooclusive disease
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- Occurs in ~50% of pts with bone marrow transplant.
- Occurs within 20 days after BMT - Most cases resolve spontaneously - Acites, GB wall thickening, splenomegaly, portal HTN |
