|
| A) | Storage and release of bile | ||
| B) | Storage and filtration of blood | ||
| C) | Storage of vitamins A, D, and B12 | ||
| D) | Metabolism of carbohydrates, fats, and protein |
The principal function of the gallbladder is to store and release bile [3].
| A) | As blood passes through the liver, unconjugated bilirubin is added. | ||
| B) | Conjugated bilirubin is less soluble and more toxic than unconjugated bilirubin. | ||
| C) | Conjugated bilirubin is continually present in the bloodstream in small quantities. | ||
| D) | In the intestines, conjugated bilirubin is converted into a highly soluble substance called urobilinogen. |
Bilirubin (bile pigment), a major waste product of hemoglobin metabolism, is excreted by the liver. Normally, erythrocytes have a lifespan of about 120 days. They are then broken down by the reticuloendothelial cells, and the iron (heme) from the worn-out red cells is conserved for reuse in the synthesis of fresh hemoglobin. The remaining iron-free pigment is free (unconjugated) bilirubin, which is continually present in the bloodstream in small quantities. As blood passes through the liver, unconjugated bilirubin is removed. It is then combined (conjugated) with other substances and excreted via the bile ducts; a small amount of conjugated bilirubin returns to the blood [1,7].
Conjugated bilirubin is more soluble and less toxic than unconjugated bilirubin. In the intestines, conjugated bilirubin is converted into a highly soluble substance called urobilinogen, which is excreted primarily in the feces in an oxidized form known as stercobilin. About 5% of urobilinogen is absorbed into the bloodstream and excreted via the kidneys in an oxidized form called urobilin. Because stercobilin gives feces their brownish color, clay-colored stools are a classic sign of biliary tract abnormalities [1,7].
| A) | vitamin A. | ||
| B) | vitamin D. | ||
| C) | vitamin B12. | ||
| D) | vitamin K. |
The liver is capable of storing up to a four-month supply of vitamins B12and D and up to a 10-year supply of vitamin A for release as needed. Because of this storage capacity, excessive ingestion of vitamin A can have toxic effects on liver function [3,4].
| A) | Hepatomegaly due to persistent pathogenic influences is unrelated to fibrosis or impaired blood flow from the hepatic veins. | ||
| B) | The liver can regenerate normally after an acute condition, but persistent pathogenic influences will always lead to a complete restoration of normal liver function. | ||
| C) | Under normal circumstances, the liver will regenerate by replacing damaged cells with neoplastic tissue, leading to reduced liver size and minimal discomfort. | ||
| D) | Persistent pathogenic influences result in the liver replacing dead or diseased cells with fibrous tissue, causing hepatomegaly and potentially impeding blood flow from the hepatic veins. |
Under normal circumstances, the liver is capable of regeneration following alleviation of an acute condition (e.g., drug toxicity, abscess, inflammation). If the pathogenic influence persists, however, regeneration will be of fibrotic origin [7].
When dead or diseased cells are replaced by fibrous tissue, the liver becomes enlarged (hepatomegaly). Fibrotic scar tissue may impede emptying of blood from the hepatic veins, causing the liver lobules to become engorged. This engorgement leads to further enlargement. Pressure exerted on abdominal nerves by the enlarged liver or displacement of other abdominal organs may cause discomfort or pain. Hepatomegaly may also be related to invasion and multiplication of neoplastic cells [7].
| A) | Enhanced phagocytosis | ||
| B) | Increased production of lymphocytes | ||
| C) | Decreased circulation of micro-organisms | ||
| D) | Impaired phagocytosis and increased susceptibility to infection |
Injury to the liver is accompanied by damage to or destruction of the Kupffer cells. Phagocytosis is impaired. Micro-organisms enter the general circulation and may form abscesses in the liver tissue itself. Whereas the normal liver accounts of 25% of the body's production of lymphocytes, the diseased liver is incapable of lymphocyte production. Lymphocytopenia increases the body's susceptibility to infection [7,8].
| A) | Enhanced production of albumin | ||
| B) | Decreased retention of sodium and water | ||
| C) | Increased detoxification of alcohol and drugs | ||
| D) | Increased levels of circulating aldosterone and ADH |
The diminished detoxification capacity of the compromised liver may compound problems related to hypoalbuminemia. Increased levels of circulating aldosterone and ADH increase retention of sodium and water, respectively, further complicating the patient's edema. Intravascular dehydration (lack of plasma in the blood vessels) related to hypoalbuminuria, may mask erythrocytopenia, because the dilution state of the blood has been altered [10,11].
Alteration in detoxification may also induce other problems related to excessive levels of hormones, chemicals, or drugs. Changes associated with an excess of estrogen may occur, including loss of axillary, pubic, and body hair; soft skin; and gynecomastia and testicular atrophy in men. Decreased libido, impotence, spider angiomas, and palmar erythema are also associated with increased estrogen levels. Alcohol, antibiotics, psychotropic drugs, and some antihypertensive medications may also accumulate in toxic levels when liver function is impaired [10,11].
| A) | face. | ||
| B) | trunk. | ||
| C) | hands and around the eyes. | ||
| D) | extremities, especially the feet and toes. |
Xanthomas and xanthelasmas may occur in patients with biliary problems in whom serum cholesterol levels are high. These foamy, cholesterol-filled cells may appear anywhere on the body but are commonly seen on the hands and around the eyes [11].
| A) | Increased number of pregnancies | ||
| B) | Lower cholesterol saturation of bile | ||
| C) | Decreased action of estrogen and progesterone | ||
| D) | Decreased cholesterol saturation of bile due to estrogen and progesterone |
Cholelithiasis (gallstones) occurs in women four to five times as often as it does in men. This increased incidence is thought to be related to the action of estrogen and progesterone, which increase the cholesterol saturation of bile. The higher the cholesterol saturation, the greater the risk that gallstones will form. Pregnant women and those taking oral contraceptives are at even higher risk of developing cholelithiasis, especially those who have had several pregnancies or who have been on oral contraceptives for several years [12].
| A) | Limited contact with body fluids | ||
| B) | Minimal risk in laboratory settings | ||
| C) | Strict adherence to asepsis and isolation principles | ||
| D) | Exposure to virus-contaminated blood or secretions |
Exposure to all types of hepatitis is a special risk for healthcare professionals, who may be exposed to virus-contaminated blood or secretions. Laboratory and operating room personnel and those who work in hemodialysis units are at particular risk of contact through exposure to body fluids. Nurses administering intravenous therapy or disposing of secretions may be exposed to hepatitis if strict asepsis and isolation principles are not followed. In addition, dentists may be exposed to the hepatitis virus in the saliva of a hepatitis carrier or a person with active disease [18].
| A) | Radiologists | ||
| B) | Physical therapists | ||
| C) | Administrative staff | ||
| D) | Laboratory and operating room personnel |
Exposure to all types of hepatitis is a special risk for healthcare professionals, who may be exposed to virus-contaminated blood or secretions. Laboratory and operating room personnel and those who work in hemodialysis units are at particular risk of contact through exposure to body fluids. Nurses administering intravenous therapy or disposing of secretions may be exposed to hepatitis if strict asepsis and isolation principles are not followed. In addition, dentists may be exposed to the hepatitis virus in the saliva of a hepatitis carrier or a person with active disease [18].
| A) | Increased appetite and weight gain | ||
| B) | High energy levels and improved mood | ||
| C) | Loss of weight or loss of interest in food | ||
| D) | Enhanced blood clotting and reduced bruising |
Has the patient lost weight or lost interest in food? A positive reply might suggest the development of hepatitis or hepatic cancer, depending on other symptoms and signs elicited during the assessment. What does the patient usually eat? High fat intake might suggest cholelithiasis. Does the patient bruise easily or bleed for a long time after a minor cut? Decreased absorption of vitamin K may be associated with hyperbilirubinemia, which can affect blood coagulation and the clotting cascade [20,21,22].
| A) | Hirsutism | ||
| B) | Ecchymosis | ||
| C) | Muscle bulking | ||
| D) | Atrophied periumbilical veins |
Physical assessment of the patient with hepatobiliary dysfunction involves careful inspection of the skin, nails, and hair. Physical findings that suggest cirrhosis include:
Ascites
Ankle edema
Muscle wasting
Dilated periumbilical veins (caput medusa)
Ecchymosis
Spider angiomas
Loss of body hair
Gynecomastia (breast enlargement in males)
Jaundice (yellow coloration to skin and sclera)
Clubbing of the fingers
| A) | Alkaline phosphatase | ||
| B) | Lactic dehydrogenase (LDH) | ||
| C) | Aspartate aminotransferase (AST) | ||
| D) | All of the above |
Elevated serum enzyme levels occur when hepatic cells are damaged and enzymes are released into the blood. Specific values that are likely to be elevated with liver or gallbladder disease include:
Lactic dehydrogenase (LDH)
Aspartate aminotransferase (AST)
Alanine aminotransferase (ALT)
Alkaline phosphatase
Gamma-glutamyl transpeptidase (GGT)
| A) | The patient can eat normally before the test. | ||
| B) | Blood is drawn immediately after dye injection. | ||
| C) | The indocyanine green (ICG) clearance test is rarely used. | ||
| D) | The presence of more than 5% of dye in the serum indicates liver cell damage. |
For dye clearance studies, the patient fasts for 12 hours prior to the test. Dye is injected intravenously (about 5 mg/kg of body weight). Blood is drawn 45 minutes after the injection and inspected for the presence of dye. Normally, less than 5% of the dye will be found in the serum; the presence of a greater proportion of the dye indicates liver cell damage, as the impaired cells cannot absorb the dye from the blood. If hepatic damage is known to exist, lower dosages of dye are administered. The indocyanine green (ICG) clearance test is the most widely used quantitative liver function test [23,28,30].
| A) | ERCP is performed using a colonoscope. | ||
| B) | No antibiotics are needed during the procedure. | ||
| C) | ERCP is safe for all patients, including combative ones. | ||
| D) | The duodenum is immobilized using intravenously administered secretin. |
With ERCP, a type of fibrotic endoscope termed a duodenoscope is inserted into the duodenum via the esophagus. Intravenously administered secretin immobilizes the duodenum, facilitating visualization of the ampulla of Vater. Contrast material combined with a broad-spectrum antibiotic are administered through a small cannula inserted into the ampulla, and films are taken periodically for approximately an hour. The antibiotic is given to prevent gram-negative sepsis that may occur if bacteria are forced in the bloodstream by the pressure of the dye injections. Perforation of the esophagus, stomach, or duodenum is another possible complication of ERCP, so this technique is not used for combative patients [23,32,33].
| A) | Ensuring the patient remains NPO after midnight. | ||
| B) | Allowing the patient to eat a light meal before the procedure. | ||
| C) | Encouraging the patient to perform light exercise before the procedure. | ||
| D) | Administering a sedative to the patient without checking coagulation studies. |
These procedures require a consent form. The patient is kept NPO after midnight. Nursing responsibilities include:
Checking coagulation studies and consent form.
Maintaining NPO status.
Recording preprocedure vital signs.
Providing emotional support for the patient; this procedure can be frightening and uncomfortable.
Explaining the procedure to the patient, emphasizing the importance of holding still.
Immediately prior to needle insertion asking the patient to inhale deeply, exhale completely, and hold the breath at the end of expiration. This immobilizes the chest wall and keeps the diaphragm at its upper level during the procedure (which takes 5 to 10 seconds).
Appling pressure to the biopsy site after needle removal.
Turning patient onto right side with a pillow under the costal martin to maintain pressure to the site.
Observing for bile-colored drainage on the patient's dressing. This could indicate that a biliary vessel has been penetrated.
Monitoring post-procedure vital signs (every 15 minutes for an hour, then every 30 minutes for two hours, then every four hours), and administering comfort measures after the procedure.
| A) | A low-carbohydrate diet to prevent weight gain | ||
| B) | A diet high in fats and proteins to support muscle mass | ||
| C) | A balanced diet high in carbohydrates, vitamins, and proteins | ||
| D) | A diet high in fat-soluble vitamins A, D, E, and K to compensate for deficiencies |
Hepatic dysfunction is associated with impaired metabolism of proteins, fats, carbohydrates, and vitamins. Weight loss, fatigue, negative nitrogen balance, vitamin B deficiency, and deficiencies of fat-soluble vitamins A, D, E, and K are common. The patient should be encouraged to consume a balanced diet high in carbohydrates, vitamins, and (unless ammonia toxicity is present) protein. Abdominal pressure from ascites may cause a constant feeling of fullness as well as flatulence and constipation. These conditions may also diminish appetite, further depleting nutritional status. Patients with cirrhosis experience muscle wasting and significant weight loss [36,37].
In cholelithiasis or cholestasis, a low-fat, low-protein diet should be consumed because fat metabolism is reduced by disturbances in biliary function. Deficiency of vitamin K may also accompany these disorders [17,21].
| A) | NSAIDs | ||
| B) | Morphine | ||
| C) | Nitroglycerin | ||
| D) | Antispasmodics |
For pain associated with cholelithiasis, nonsteroidal anti-inflammatory drugs (NSAIDs) provide greater relief of biliary pain and are considered first-line management [38]. NSAIDs have been reported as superior to antispasmodics for pain control. For narcotic management, meperidine is usually the drug of choice; butorphanol or hydromorphone can also be utilized, especially if NSAIDs are contraindicated [39]. Morphine is rarely administered. Nitroglycerin or phenobarbital may promote comfort by relaxing smooth muscle. Nursing measures, such as giving a backrub, assisting the patient in changing position, providing distraction, and offering emotional support, may supplement analgesic medication [27].
| A) | Potassium supplementation to improve cerebral metabolism of ammonia. | ||
| B) | Intravenous administration of glucose to provide protein-conserving carbohydrates. | ||
| C) | Oral or enema administration of neomycin to reduce ammonia-synthesizing bacteria in the gut. | ||
| D) | All of the above |
Various therapeutic measures may be prescribed to decrease serum ammonia levels. Intravenous administration of glucose may provide protein-conserving carbohydrates. Rest can decrease release of ammonia associated with muscle contraction [27].
Pharmacologic measures may also be employed. Potassium may be given to improve cerebral metabolism of ammonia. Hypokalemia has been identified as being a contributing factor for the increased risk of hepatic encephalopathy. Studies have shown that supplementing and correcting hypokalemia in patients with cirrhosis can decrease ammonia levels [42,43]. Antibiotics such as neomycin may be administered orally or by enema to reduce the number of ammonia-synthesizing bacteria in the gut. Because neomycin is poorly absorbed from the intestine, its bactericidal action in the intestine is prolonged; however, this antibiotic may cause ototoxicity of nephrotoxicity if administered for more than six days [41,44]. Metronidazole and rifampin are alternative choices.
Lactulose may be given orally or by nasogastric tube. This acts by acidifying the colon, so ammonia couples with hydrogen ions and is excreted in the feces. Improvement may be seen within 24 hours, with serum ammonia levels being reduced by 25% to 50% in most patients. Diarrhea is common with lactulose therapy, so electrolyte levels should be monitored. In some cases, hemodialysis may be necessary to reduce serum ammonia levels [41,44].
Nurses should routinely check stools for occult blood and monitor vital signs for changes that might indicate gastrointestinal hemorrhage. If esophageal varices are bleeding, treatments include beta blockers and medical procedures to stop bleeding [27].
| A) | Decreased skin turgor | ||
| B) | Appropriate intake and output | ||
| C) | Rapid correction of hypertension | ||
| D) | Increased circumference of abdominal girth |
Expected outcomes related to fluid volume include good skin turgor, decreased circumference of edematous extremities or abdominal girth, and intake and output measurements are indications of correction of a fluid alteration. Correcting fluid volume alterations may take a long time, and several plans and revisions may be required [37].
| A) | Anxiety | ||
| B) | Cholestasis | ||
| C) | Normal liver function studies | ||
| D) | Bile duct abundance on liver biopsy |
Alagille syndrome is a genetic disorder with manifestations in multiple systems throughout the body. Variability in presentation is seen even among individuals from the same family [48]. The major clinical manifestations of this disorder are bile duct paucity on liver biopsy, cholestasis, congenital cardiac defects (primarily involving the pulmonary arteries), butterfly vertebrae, ophthalmologic abnormalities, and characteristic facial features. The diagnosis is made through positive genetic testing and/or clinical diagnostic criteria.
| A) | Malaria | ||
| B) | Tuberculosis | ||
| C) | Hepatitis A infection | ||
| D) | Nonalcoholic fatty liver disease |
Cirrhosis is the end stage of any chronic liver disease. In developed countries, the most common causes include nonalcoholic fatty liver disease, hepatitis infection, and excessive alcohol intake; in developing counties, hepatitis A and B infections are the most likely causes. There are two clinical categories of cirrhosis: compensated and decompensated. Patients who have compensated cirrhosis can be further categorized as:
Stage 1: No varices, no ascites
Stage 2: Varices, no ascites
| A) | Portal-systemic shunting is the only method required to manage bleeding from esophageal varices, with no need for medication or blood infusion. | ||
| B) | Hemorrhage from esophageal varices is best controlled by the administration of antibiotics alone, with no need for vasoconstrictor medications or blood transfusions. | ||
| C) | Infusions of medications such as vasopressin, somatostatin, or octreotide provide long-term control of variceal hemorrhage and are not associated with any significant complications. | ||
| D) | Temporary control of hemorrhage from esophageal varices can be achieved by infusions of vasopressin, somatostatin, octreotide, or terlipressin to induce arterial vasoconstriction and lower portal pressure. |
Hemorrhage of esophageal varices may be controlled temporarily by administering infusions of vasopressin, somatostatin, octreotide, or terlipressin to promote diffuse arterial vasoconstriction and to lower portal pressure by constricting the splanchnic arterial bed. The infusion may be given systemically or via the superior mesenteric artery and administered for five days, according to current guidelines [52]. This provides only temporary control and is associated with complications, including systemic arterial hypertension and coronary vasoconstriction, possibly leading to myocardial infarction. Whole blood should be available for immediate infusion [52,53,54]. If medication administration is unsuccessful, gastric lavage with ice-cold saline, use of the Minnesota tube or Sengstaken-Blakemore tube, or portal-systemic shunting may be implemented to control bleeding temporarily.
| A) | 40 g/day | ||
| B) | 60 g/day | ||
| C) | 80 g/day | ||
| D) | 100 g/day |
The amount of alcohol required to produce chronic liver disease varies widely, depending on body size, age, sex, and ethnicity, but the high end of the range is about 80 g/day for 10 to 12 years. This amount of alcohol can be in the form of 8 ounces of 86 proof (41% alcohol) whiskey, two bottles of wine, or six 12-ounce bottles of beer. Even after alcohol intake has stopped and all alcohol has been metabolized, the processes that damage liver cells may continue for many weeks and months. Clinical and chemical effects often become worse before the disease resolves. The accumulation of fat usually disappears within a few weeks, and cholestasis and inflammation also subside with time. However, fibrosis and scarring remain. The liver lobules become distorted as new liver cells regenerate and form nodules [64,65].
| A) | Hepatic steatosis | ||
| B) | Alcoholic cirrhosis | ||
| C) | Alcoholic hepatitis | ||
| D) | Portal hypertension |
Alcoholic cirrhosis and malnutrition is the end result of repeated bouts of drinking-related liver injury and designates the onset of end-stage alcoholic liver disease. The gross appearance of the early cirrhotic liver is one of fine, uniform nodules on its surface. The condition has traditionally been called monocular or Laënnec cirrhosis. With more advanced cirrhosis, regenerative processes cause the nodules to become larger and more irregular in size and shape. As this occurs, the nodules cause the liver to become relobulized through the formation of new portal tracts and venous outflow channels. The nodules may compress the hepatic veins, curtailing blood flow out of the liver and producing portal hypertension, extrahepatic portosystemic shunts, and cholestasis [64,65,69].
| A) | MASLD reflects a range of liver conditions caused by metabolic dysfunction. | ||
| B) | The condition has no association with rapid weight loss, parenteral nutrition, or surgical procedures such as jejunoileal bypass. | ||
| C) | MASLD is a rare form of liver disease that primarily results from excessive alcohol consumption and is unrelated to metabolic dysfunction or obesity. | ||
| D) | MASLD, formerly known as nonalcoholic fatty liver disease (NAFLD), is a condition characterized solely by fatty liver infiltration and is not associated with any other health conditions. |
Metabolic dysfunction-associated steatotic liver disease (MASLD) was previously referred to as nonalcoholic fatty liver disease (NAFLD) but was renamed in 2023 to better reflect the underlying pathophysiology and embrace affirmative, non-stigmatizing terminology [70]. It is caused by metabolic dysfunction that affects the liver. As noted, in the United States, it is the most frequently occurring form of chronic liver disease. The condition can range from simple steatosis (fatty infiltration of the liver) to nonalcoholic steatohepatitis (steatosis with inflammation and hepatocyte necrosis). Although steatosis alone does not appear to be progressive, approximately 10% to 15% of people with nonalcoholic steatohepatitis progress to cirrhosis. Obesity, type 2 diabetes, metabolic syndrome, and hyperlipidemia are coexisting conditions frequently associated with fatty liver disease. The condition is also associated with other nutritional abnormalities, surgical conditions, drugs, and occupational exposure to toxins. Both rapid weight loss and parenteral nutrition may lead to MASLD. Jejunoileal bypass, a surgical procedure historically used for weight loss, has largely been abandoned for this reason [65,71].
| A) | To rapidly cure the disease | ||
| B) | To eliminate the need for liver transplantation | ||
| C) | To increase alcohol consumption for better liver function | ||
| D) | To slow progression of the disease and prevent liver-related illness |
The aim of treatment is to slow progression of MASLD and to prevent liver-related illness. Weight loss and exercise improve insulin resistance and are recommended in conjunction with treatment of associated metabolic disturbances. Alcohol use should be avoided. Disease progression is slow and the magnitude of disease-related morbidity and mortality is uncertain. One study has shown the use of statins and antioxidants such as vitamins A and E have been effective in reducing the odds of hepatic steatosis in patients with MASLD. Liver transplantation is an alternative for some with end-stage liver disease, but MASLD may reoccur in up to 39% of people post-liver transplantation [65,72,73,74].
| A) | Jaundice and liver failure | ||
| B) | Dark urine and pale stools | ||
| C) | Unexplained pruritus, weight loss, and fatigue | ||
| D) | Osteoporosis and elevated serum alkaline phosphatase levels |
Primary biliary cholangitis is characterized by an insidious onset and progressive scarring and destruction of liver tissue. The liver becomes enlarged and takes on a green hue because of the accumulated bile. The earliest symptoms are unexplained pruritus, weight loss, and fatigue, followed by dark urine and pale stools. Osteoporosis occurs in 51% of women with the disorder. Jaundice is a late manifestation of the disorder, as are other signs of liver failure. Serum alkaline phosphatase levels are typically elevated [63].
| A) | hepatitis. | ||
| B) | cholestasis. | ||
| C) | granulomas within the liver. | ||
| D) | intrahepatic cholestasis with jaundice. |
Varying patterns of hepatic dysfunction are seen in response to use of other drugs and anesthetic agents. For example, halothane, methyldopa, and isoniazid can produce hepatitis. Chlorpromazine, erythromycin estolate, and methimazole can cause intrahepatic cholestasis with jaundice. Phenylbutazone and the sulfonamides can produce granulomas within the liver [76,78].
| A) | A benign tumor in the liver | ||
| B) | A non-infectious inflammation of the liver | ||
| C) | A type of liver cancer caused by viral infection | ||
| D) | An invasion of the liver by micro-organisms producing a localized collection of pus |
Hepatic abscess is an invasion of the liver by micro-organisms producing a localized collection of pus in a cavity formed by destruction of tissue. Hepatic abscess may be caused by fungal, bacterial, or even protozoan infection. An infection anywhere in the body can lead to formation of an hepatic abscess, but gastrointestinal infections are especially likely to do so [75,76,82,83].
| A) | Fecal-oral route | ||
| B) | Airborne droplets | ||
| C) | Blood transfusion | ||
| D) | Direct skin contact |
Hepatitis A is transmitted via the fecal-oral route, most commonly from contaminated water or food. After the virus is ingested, it is transported from the intestines to the liver, where it invades the hepatocytes. The virus uses the hepatocytes for viral replication and is then released into the bloodstream and excreted in the stool. HAV that is acquired percutaneously travels directly from the bloodstream to the liver to invade the hepatocytes; viral replication and excretion follow the same pattern as in fecal-oral transmission.
| A) | A single dose of 1 mL intramuscularly | ||
| B) | Two doses of 1 mL intramuscularly, one month apart | ||
| C) | Three doses of 1 mL intramuscularly, with boosters at one and six months | ||
| D) | Four doses of 0.5 mL intramuscularly, with boosters at one, three, and six months |
The U.S. Food and Drug Administration (FDA) has approved two single-antigen HAV vaccines and one combination vaccine for use in the United States, all of which are inactivated vaccines. The single-antigen vaccines are Havrix and VAQTA. Both are administered to adults in a dose of 1 mL intramuscularly. The dose for children is 0.5 mL [90]. Single-antigen vaccines are considered interchangeable. A second dose of either vaccine can be administered, regardless of which vaccine was administered as the first dose.
| A) | 15 to 30 days | ||
| B) | 30 to 45 days | ||
| C) | 45 to 180 days | ||
| D) | 180 to 365 days |
The incubation period for HBV can be as little as 45 days or as long as 180 days, but most commonly is 60 to 90 days. The severity of primary HBV infection varies from subclinical to fulminant illness. The age of the patient, the integrity of the immune system, and the infecting dose of the virus influence the severity of acute disease. Persons younger than 5 years of age exhibit mild symptoms or no symptoms, while 70% of infected adults exhibit significant clinical symptoms [99].
| A) | Treatment is recommended only for patients with cirrhosis. | ||
| B) | Treatment is recommended only for patients with advanced liver disease. | ||
| C) | Treatment is recommended only for patients who have not previously been treated for HCV. | ||
| D) | Treatment is recommended for all patients, except those with a short life expectancy that cannot be remediated. |
The IDSA/AASLD 2023 guidelines emphasize that treatment is recommended for all patients with chronic HCV infection, except those with a short life expectancy that cannot be remediated by HCV therapy, liver transplantation, or another directed therapy [115]. Prior to treatment, patients should be educated regarding proper administration of medications, adherence, and prevention of reinfection. Pretreatment assessment to facilitate decision making regarding the treatment strategy and to determine the need for initiating additional measures for the management of cirrhosis (e.g., hepatocellular carcinoma screening) is recommended in all patients.
| A) | Predominantly affects men | ||
| B) | Increased levels of anti-mitochondrial antibodies | ||
| C) | Susceptibility resides mainly with the HLA-DQ2 gene | ||
| D) | Increased levels of anti-smooth muscle and antinuclear autoantibodies |
Two distinct types of autoimmune hepatitis have been identified. Type 1 autoimmune hepatitis, the most common form of the disease, is characterized by increased levels of anti-smooth muscle and antinuciler autoantibodies. Approximately 78% of cases occur in women, and 38% of patients with autoimmune hepatitis also have other autoimmune diseases. Susceptibility to type 1 autoimmune hepatitis resides mainly with the HLA-DRBI gene.
| A) | Smoking | ||
| B) | Cirrhosis | ||
| C) | Chronic viral hepatitis | ||
| D) | All of the above |
Among the factors identified as etiologic agents in liver cancer are chronic viral hepatitis (HBV, HCV, HDV), cirrhosis, smoking, heavy alcohol consumption, obesity, and long-term exposure to environmental agents (e.g., aflatoxin). The exact pathogenesis is unclear. With HBV and HCV, both of which become integrated into the host DNA, repeated cycles of cell death and regeneration afford the potential for development of cancer-producing mutations. Aflatoxin, produced by food spoilage molds (e.g., Aspergillus flavus and Aspergillus parasiticus), is a known human carcinogen and is endemic in certain areas. A particularly susceptible site for aflatoxin mutation is the TP53 tumor suppressor gene [125].
| A) | Best survival rates are achieved when the HCC can be removed either by surgical resection or liver transplant. | ||
| B) | There are comprehensive studies showing that ablation is superior to surgical resection and liver transplant for early-stage HCC. | ||
| C) | Surgical resection is the only effective treatment for early-stage HCC, and liver transplant is only considered if surgical resection is not feasible. | ||
| D) | Randomized studies have robustly compared the effectiveness of surgical resection, liver transplant, and ablation for early-stage HCC, showing that liver transplant is universally preferred. |
Several treatments for HCC are associated with long-term survival, including surgical resection, liver transplant, and ablation. There are no large, robust, randomized studies that compare treatments considered effective for early-stage disease, nor are there studies comparing these treatments with best supportive care. Often, patients with HCC are evaluated by a multidisciplinary team that includes hepatologists, radiologists, interventional radiologists, radiation oncologists, transplant surgeons, surgical oncologists, pathologists, and medical oncologists.
Best survival rates are achieved when the HCC can be removed either by surgical resection or liver transplant. Surgical resection is usually performed in patients with localized HCC and enough functional hepatic reserve. For patients with decompensated cirrhosis and a solitary lesion (<5 cm) or early multifocal disease (up to three lesions, ≤3 cm in diameter), the best option is liver transplant, but the limited availability of liver donors restricts the use of this approach.
| A) | Alcohol use disorder | ||
| B) | Hepatitis B and C infections | ||
| C) | Obesity and type 2 diabetes mellitus | ||
| D) | Chronic inflammation and injury of the bile duct epithelium |
Cholangiocarcinoma is not associated with the same risk factors as hepatocellular carcinoma. Instead, most of the risk factors revolve around long-standing inflammation and injury of the bile duct epithelium. Bile duct cancer may occur more frequently in patients with a history of primary sclerosing cholangitis, chronic ulcerative colitis, choledochal cysts, or infections with the liver fluke Clonorchis sinensis [137].
| A) | Colicky pain | ||
| B) | Chronic diarrhea | ||
| C) | Persistent nausea and vomiting | ||
| D) | Constant dull ache in the lower abdomen |
The most common symptom of cholelithiasis is colicky pain believed to be related to spasms of the sphincter of Oddi. Pain may also be related to obstruction and distention of a bile duct. Usually, the pain is felt in the epigastrium or the right upper quadrants of the abdomen, but it may radiate up the back between the scapulae to the right shoulder or around the abdomen to the back, making it difficult for the patient to assume a comfortable position. Some patients will report laying in the supine position often worsens the discomfort. Biliary colic may occur at varying intervals following meals or may wake the patient from sleep. Usually, symptoms occur at progressively shorter intervals after ingestion of almost any food. Occasionally, however, a single pain episode will never be repeated [129,139,140,141].
| A) | Calcineurin inhibitor, digoxin, corticosteroids, and a diuretic | ||
| B) | Monoclonal antibody, aspirin, corticosteroids, and a beta blocker | ||
| C) | Mycophenolate mofetil, vitamin D, corticosteroids, and a calcium channel blocker | ||
| D) | Monoclonal antibody, mycophenolate mofetil, corticosteroids, and a calcineurin inhibitor |
Various combinations of immunosuppressive drugs (monoclonal and polyclonal antibodies) have been used to reduce the probability of post-transplant rejection. It is desirable to try to prevent or minimize the adverse effects of these drugs, including infections, malignancy, and general drug toxicity. In the immediate post-transplant period, a common drug regimen includes a combination of a monoclonal antibody, mycophenolate mofetil, corticosteroids, and a calcineurin inhibitor such as cyclosporine or tacrolimus [148]. According to Hanto, the addition of an anti-IL-2 receptor monoclonal antibody (basiliximab or daclizumab) can result in a decrease in rejection rate from 43.5% to 35.1% [156]. Sirolimus is a newer drug that appears to be useful, especially in patients with renal insufficiency.