Assessment and Management of Liver Disorders Quiz

d. Most patients with primary sclerosing cholangitis (PSC) also have ulcerative colitis. The manifestations are otherwise similar to cirrhosis, and PSC may lead to cirrhosis, liver failure, and liver cancer.

d. HBV DNA quantitation is the best indicator of viral replication and effectiveness of therapy for chronic HBV. HBsAg is present in acute or chronic infection. HBeAg shows high infectivity and can be used to determine clinical management of patients with chronic HBV. Anti-HBc IgM occurs with acute infection. Anti-HBc IgG indicates ongoing infection. Anti-HDV is present in past or current infection with HDV and therefore HBV. Anti-HBs indicate previous infection with HBV or_x000d_immunization.

d. Liver transplantation is indicated for patients with cirrhosis as well as for many adults and children with other irreversible liver diseases._x000d_Liver transplantation is contraindicated with severe extrahepatic disease, cancers, ongoing drug or alcohol use, and inability to comprehend or comply with the rigorous posttransplant care._x000d__x000d_Nurses should be knowledgeable about the indications for transplantation and be able to discuss the patient’s questions and concerns related to transplantation. Rejection is less of a problem in liver transplants than with other organs, such as the kidney.

c. The patient may not be oriented or able to walk to the bathroom alone because of hyperreflexia, asterixis, or decreased motor coordination. Turning should be done every 2 hours to prevent skin breakdown. Activity is limited to decrease ammonia as a by-product of protein metabolism. Although constipation will be prevented, it will not
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d. The most common cause of acute liver failure is drugs, usually acetaminophen in combination with alcohol. HBV is the second most common cause. HAV is a less common cause.

d. Blood flow through the portal system is obstructed and causes portal hypertension that increases the BP in the portal venous system. Decreased albumin production leads to decreased serum colloidal oncotic pressure that contributes to ascites. Hyperaldosteronism increases sodium and water retention and contributes to increased fluid retention, hypokalemia, and decreased urinary output. The retained fluid has low oncotic colloidal pressure. It escapes into the interstitial spaces, causing_x000d_peripheral edema. Portal hypertension contributes to esophageal varices. Reduced renal blood flow and increased serum levels of antidiuretic hormone (ADH) contribute to impaired water excretion and ascites.

b. People who have been exposed to hepatitis A through household contact or foodborne outbreaks should be given IG within 1 to 2 weeks of exposure to prevent or modify the illness. Hepatitis A vaccine is used to provide pre-exposure immunity to the virus. Although hepatitis A may be spread by sexual contact, the risk is higher for transmission with the oral-fecal route

a. Oral hygiene may improve the patient’s taste sensation. Food preferences are important, but some foods may be restricted if the patient is on a low-sodium or low-fat diet. The patient will feel more independent with self-feeding and will be more likely to increase intake by having someone sit with the patient while the patient eats. Snacks and supplements should be available whenever the patient desires them but should not be forced on the patient.

d. HBV vaccine and hepatitis B immune globulin (HBIG) are used together prophylactically after a needle stick. Interferon is used to treat chronic HBV.

a. Adequate nutrition is especially important in promoting regeneration of liver cells, but the anorexia of viral hepatitis is often severe, requiring creative and innovative nursing interventions. Strict bed rest is not usually required, and the patient usually has only minor discomfort with hepatitis. Diversional activities may be required to promote psychologic rest but not during periods of fatigue.

D: Hemolytic jaundice from a blood transfusion reaction is from increased breakdown of red blood cells (RBCs) producing increased unconjugated bilirubin in the blood. Hepatocellular jaundice results from damaged hepatocytes leaking bilirubin. Hemolytic jaundice occurs with malaria. Obstructive jaundice is from obstructed bile flow through the liver or biliary duct system.

b, c. With diuretic therapy, fluid and electrolyte balance must be monitored; serum levels of sodium, potassium, chloride, and bicarbonate must be monitored, especially for hypokalemia. Renal function must be monitored with blood urea nitrogen and serum creatinine. Water excess is manifested by muscle cramping, weakness, lethargy, and confusion._x000d_Gastrointestinal (GI) bleeding, body image disturbances, and bleeding tendencies seen with cirrhosis are not related to diuretic therapy.

c. Esophageal varices occur when collateral channels of circulation develop inelastic fragile veins from portal hypertension. Portal hypertension is from scarring and nodular changes in the liver leading to compression of the veins and sinusoids, causing resistance of blood flow through the liver from the portal vein. It contributes to peripheral edema and ascites. Jaundice is from the inability of the liver to conjugate_x000d_bilirubin. Biliary cirrhosis causes the loss of small bile ducts and ultimate cholestasis in patients with other autoimmune disorders.

a, b, d. There is no treatment for nonalcoholic fatty liver disease (NAFLD) except to control the other diseases that are common in these persons. These measures include weight loss for obesity, control of blood glucose for diabetes, control of hyperlipidemia, and treating hypertension if it is present. Ulcerative colitis is unrelated to NAFLD.

b. During the incubation period, there are no symptoms, but serologic and enzyme markers of the disease are present. Earliest symptoms may include anorexia and discomfort in the upper right quadrant of the abdomen. Pruritus, dark urine, and light-colored stools occur with the onset of jaundice in the acute phase. Easy fatigability and malaise are seen in the convalescent phase as jaundice disappears.

b. The patient with acute hepatitis B is infectious for 4 to 6 months, and precautions to prevent transmission through percutaneous and sexual contact should be maintained until tests for Hbs Ag or anti-HBc IgM are negative. Close contact does not have to be avoided, but close contacts of the patient should be vaccinated. Alcohol should not be used for at least a year, and rest with increasing activity during convalescence is recommended.

c. Corneal Fleischer rings, brownish red rings in the cornea near the limbus, are the hallmark of Wilson’s disease. Pruritus (not seen with Wilson’s disease) is commonly seen with jaundice or primary biliary cirrhosis. Renal failure associated with hepatorenal syndrome is not seen with Wilson’s disease. High serum iron levels are seen with hemochromatosis.

c. Bleeding esophageal varices are a medical emergency. During an episode of bleeding, management of the airway and prevention of aspiration of blood are critical factors. Portal shunting surgery may be done for esophageal varices but not during an acute hemorrhage._x000d__x000d_Occult blood as well as fresh blood from the GI tract would be expected. Vasopressin causes vasoconstriction, decreased heart rate, and decreased coronary blood flow._x000d__x000d_IV nitroglycerin may be given with the vasopressin to counter these side effects.

c. Abstinence from alcohol is very important in alcoholic cirrhosis and may result in improvement if started when liver damage is limited. Although further liver damage may be reduced by rest and nutrition, most changes in the liver cannot be reversed. Exercise does not promote portal circulation, and very moderate exercise is recommended._x000d__x000d_Acetaminophen should not be used by the patient with alcoholic cirrhosis because this liver is more sensitive to the hepatotoxicity of acetaminophen.

d. Monitoring for viral, fungal, and bacterial infection after the liver transplant is essential, as only fever may be present with an infection. Alcohol will not be any better for the patient after the transplant than it was before the transplant. HBIG is given for postexposure protection from HBV. The head of the bed is elevated to improve ventilation with severe ascites.

b. HCV genotyping is done to determine HCV drug choice, duration, and response to drug therapy. Anti-HCV and HCV RNA quantitation are tests completed to diagnose HCV. FibroSure (FibroTest) is used to assess the extent of hepatic fibrosis.

c. Nucleoside and nucleotide analogs (e.g., lamivudine) and pegylated interferon are used to treat chronic hepatitis B. No specific drugs are effective in treating acute viral hepatitis, although supportive drugs, such as antiemetics, sedatives, or antipruritics, may be used for symptom control.

d. The systemic manifestations of rash, angioedema, arthritis, fever, and malaise in viral hepatitis are caused by the activation of the complement system by circulating immune complexes. Liver manifestations include jaundice from hepatic cell damage and cholestasis as well as anorexia. Impaired portal circulation usually does not occur in uncomplicated viral hepatitis but would be a liver manifestation.

c. Immunosuppressive agents are indicated in hepatitis associated with immune disorders to decrease liver damage caused by autoantibodies. Autoimmune hepatitis is similar to viral hepatitis in presenting signs and symptoms and may become chronic and lead to cirrhosis.

d. Anti-HAV IgM indicates acute HAV infection. Anti-HBc IgG indicates previous or ongoing infection with HBV. Anti-HBc IgM indicates acute HBV infection. Anti-HAV IgG indicates previous infection with HAV.

c. Ammonia must be reduced to treat hepatic encephalopathy. The laxative, lactulose, decreases ammonia by trapping the ammonia and eliminating it in the feces. A β adrenergic blocker will be used to decrease portal venous pressure and decrease variceal bleeding. The proton pump inhibitor will decrease gastric acidity but will not eliminate blood already in the GI tract. Rifaximin will decrease bacterial flora and therefore decrease ammonia formation from protein metabolism.

c. Because the prognosis for cancer of the liver is poor and treatment is largely palliative, supportive nursing care is appropriate. The patient exhibits clinical manifestations of liver failure, as seen in any patient with advanced liver failure. Whether the cancer is primary or metastatic, there is usually a poor response to chemotherapy and surgery is indicated in the few patients that have localization of the tumor when there is no evidence of invasion of hepatic blood vessels.

a, c, d. The anemia of cirrhosis is related to overactivity of the enlarged spleen that removes blood cells from circulation. Vitamin B deficiencies from altered intake and metabolism of nutrients and decreased prothrombin production can increase bleeding tendencies. The other options do not contribute to anemia in the patient with cirrhosis.

d. Early signs (grade 1) of this neurologic condition include impaired computational skills, short attention span, personality change, decreased short-term memory, mild confusion, depression, and incoordination. Loss of consciousness (grade 4) is usually preceded by asterixis, abnormal reflexes, and disoriented to time (grades 2 and 3); inappropriate behavior, deficient executive function, marked confusion, loss of meaningful conversation, and incomprehensible speech. Increasing oliguria is a sign of hepatorenal syndrome.

b. Serum bilirubin, both direct and indirect, would be expected to be increased in cirrhosis. Serum albumin and cholesterol are decreased and liver enzymes, such as aspartate aminotransferase (AST) and alanine aminotransferase (ALT), are initially increased but may be normal in end-stage liver disease.

B: Hepatitis B virus (HBV) is a DNA virus that is transmitted via infectious blood and body products and is required for hepatitis D virus (HDV) replication, and chronic HBV along with chronic hepatitis C virus (HCV) accounts for 80% of hepatocellular cancer cases. Hepatitis A virus (HAV), HCV, HDV, and HEV are all RNA viruses.

c. Immunization to HBV after vaccination is identified with the hepatitis B surface antibody (anti-HBs). Anti-HBc immunoglobulin (Ig)G indicates previous or ongoing HBV infection. Surface antigen HBsAg is present in acute and chronic infection. Core antigen anti-HBc IgM indicates acute infection and does not appear after vaccination.