The gold standard for identifying liver lesions by imaging is:
The use of intraoperative ultrasound of the liver has rapidly expanded over the years with the increasing number and complexity of hepatic resections being performed. It has the ability to provide the surgeon with real-time accurate information useful for surgical planning. Intraoperative ultrasound is considered the gold standard for detecting liver lesions, and studies have shown that it can identify 20% to 30% more lesions than other preoperative imaging modalities. Importantly, it has been shown to influence surgical management in almost 50% of planned liver resections for malignancies. Applications for intraoperative ultrasound of the liver include tumor staging, visualization of intrahepatic vascular structures, and guidance of resections plane by assessment of the relationship of a mass to the vessels. In addition, biopsy oflesions and ablation of tumors can be guided by intraoperative ultrasound.
The most common cause of acute liver failure (ALF) in the United States is:
Acute liver failure (ALF) is defined as development of hepatic encephalopathy within 26 weeks of severe liver injury in a patient with no history ofliver disease or portal hypertension. In developing countries, the most common etiology of ALF is viral infections, including hepatitis B, A, and E. In the West (including the United States, Australia, United Kingdom, and most of Europe), 65% of ALF cases are related to drugs and toxins, especially acetaminophen.
A patient presents with painless jaundice, and is found to have cirrhosis. They have no history of alcohol abuse, but do note a history of diabetes mellitus and pseudogout. They also mention that multiple members of their family have suffered from cirrhosis. What is the most likely etiology for their cirrhosis?
Chronic hepatitis C infection is the most common cause of chronic liver disease in the United States. Other etiologies include alcohol abuse, nonalcoholic steatohepatitis (NASH), and autoimmune diseases (primary biliary cirrhosis, primary sclerosing cholangitis, and autoimmune hepatitis). Hereditary hemochromatosis is the most common metabolic cause of cirrhosis, and should be suspected if a patient presents with skin hyperpigmentation, diabetes mellitus, pseudogout, cardiomyopathy, or a family history of cirrhosis.
Which of the following is not one of the physiologic changes noted in patients with cirrhosis?
The clinical manifestations of cirrhosis are the result of numerous physiologic changes associated with a patient's progressive liver failure. Hypoalbuminemia results in finger clubbing, while spider angiomata and palmar erythema are thought to be caused by alterations in sex hormones. The physiologic basis for feminization of males (gynecomastia, loss of chest/axillary hair, testicular atrophy) with cirrhosis is less well understood. Portal hypertension manifests as caput medusa and varices. Cirrhotic patients suffer from chronic malnutrition, which may be associated with weakness, weight loss, and decreased fat and muscle stores. Despite this fact, patients with cirrhosis have elevated resting energy expenditure. Also noted are increased cardiac output and heart rate with decreased systemic vascular resistance and blood pressure.
Clinically significant portal hypertension is evident when the___ exceeds ___ mm Hg.
Portal hypertension occurs when the pressure in the portal system is increased due to factors that may be divided into three categories. Presinusoidal causes of portal hypertension include sinistral/extrahepatic (splenic vein thrombosis, splenomegaly, splenic atrioventricular fistula) and intrahepatic (schistosomiasis, congenital hepatic fibrosis, idiopathic portal fibrosis, myeloproliferative disorder, sarcoid, graftversus-host disease) etiologies. Sinusoidal portal hypertension is a consequence of cirrhosis of any etiology. Postsinusoidal hypertension can also be divided into intrahepatic (vascular occlusive disease) and posthepatic (Budd-Chiari, congestive heart failure [CHF], IVC webs) etiologies. In evaluating patients with suspected portal hypertension, an enlarged portal vein on routine abdominal ultrasonography may suggest portal hypertension but this is not diagnostic. Doppler ultrasound allows identification of vascular occlusion and the direction of portal venous flow. CT and MR angiography are useful for evaluating portal venous patency and anatomy. The most accurate method for measuring portal hypertension is hepatic venography. This procedure introduces a balloon catheter directly into the hepatic vein where free hepatic venous pressure (FHVP) is measured. The hepatic vein is then occluded by inflation of the balloon allowing measurement of the wedged hepatic venous pressure (WHVP). The hepatic venous pressure gradient (HVPG) may then be calculated by subtracting the FHVP from the WHVP (HVPG = WHVP - FHVP). Clinically significant portal hypertension is defined as HVPG greater than 10 mm Hg.
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