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
bilirubin. Biliary cirrhosis causes the loss of small bile ducts and ultimate cholestasis in patients with other autoimmune disorders.

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.

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. 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.

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.

IV nitroglycerin may be given with the vasopressin to counter these side effects.

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.

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.

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.

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.

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.
Gastrointestinal (GI) bleeding, body image disturbances, and bleeding tendencies seen with cirrhosis are not related to diuretic therapy.

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.

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.

d. Liver transplantation is indicated for patients with cirrhosis as well as for many adults and children with other irreversible liver diseases.
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.

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.

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
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.

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
keep the patient safe.

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.

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.

Acetaminophen should not be used by the patient with alcoholic cirrhosis because this liver is more sensitive to the hepatotoxicity of acetaminophen.

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.