NS3P1 Mod 2: Hepatitis & Cirrhosis

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NS3P1 Mod 2: Hepatitis & Cirrhosis
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2015-09-09 01:57:34
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NS3 NS3P1 Olga Cirrhosis Hepatitis Liver
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NS3P1 Mod 2: Hepatitis & Cirrhosis
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  1. **LIVER
    The liver is essential for life. It functions in the manufacture, storage, transformation, and excretion of a number of substances involved in metabolism and is the major site for drug and hormone metabolism.

    -Hepatocytes: arranged around a central vein

    -Capillaries (sinusoids) are located between the rows of hepatocytes are lined with kupffer cells: carry out phagocytic activty (removal of acteria and toxins from the blood)

    -Interlobular bile ducts form from bile capillaries

    Hepatic cells secrete bile into the canaliculi-Portal circulatory system: brings blood to the liver from the stomach, intestines, spleen and pancreas. Portal vein carries absorbed products of digestion directtly to the liver, where it branches and comes in contact with EACH lobule.

    • => Liver functions: manufacture, storage, transoormation, and excretion of a number of substances involved in metabolism.
    • -Kupffer cells: breakdown of old RBCs, wBCs, bacteria, and other particles. Breakdown of hemoglobin from old RBCs to bilirubin and biliverdin.
  2. **The biliary tract 
    -GallBladder
    -Bile
    consists of the gallbladder and the duct system.

    • Bile is produced in the liver and stored in the gallbladder. It consists of bilirubin, water, cholesterol, bile salts, electrolytes, and phospholipids

    • The exocrine function of the pancreas contributes to digestion. The endocrine function occurs in the islets of Langerhans, whose  cells secrete insulin,  cells secrete glucagon, and  cells secrete somatostatin.

    • => Gallbladder: pear shaped sac located BELOW the liver. Main function: to concentrate and STORE bile. It holds 45 mL of bile
    • -Bile: produced by hepatic cells and secreted into the biliary canaliculi of the lobules, then drains into the interlobular bile ducts, which unite into the two main left and light hepatic ducts --> merge with the cystic duct from the gallbladder to form the common bile duct. IT then enters the duodenum at the ampulla of Vater.
  3. **Bilirubin metabolism:
    In theintestines, it's reduced into stercobilinogen (this gives stool the brown color) and urobilinogen by bacterial action.Bilirubin is a pigement dervied from the breakdown of hemoglobin,. It is insolube in water, bound to albumin for transport to the liver (In this form: it's unconjugated"-Becomes conjugated in the Liver with glucoronic acid: soluble and is excreted in bile.Bile: consists of water, cholesterole, bile salsts, electrolytes, and phospholipids. BIle salts are needed for fat emulsification and digestion!
  4. Liver
    1. The largest gland in the body, weighing 3 to 4pounds

    2. Contains Kupffer’s cells, which remove bacteriain the portal venous blood

    3. Removes excess glucose and amino acids fromthe portal blood

    4. Synthesizes glucose, amino acids, and fats

    5. Aids in the digestion of fats, carbohydrates, andproteins

    6. Stores and filters blood (200 to 400 mL of bloodstored)

    7. Stores vitamins A, D, and B and iron8. The liver secretes bile to emulsify fats (500 to1000 mL of bile/day).

    • => Hepatic ducts
    • a. Deliver bile to the gallbladder via the cysticduct and to the duodenum via the commonbile duct
    • b. The common bile duct opens into the duodenum,with the pancreatic duct at the ampulla of Vater.
    • c. The sphincter prevents the reflux of intestinalcontents into the common bile duct and pancreaticduct.
  5. BLOOD SUPPLY TO AND FROM LIVER:
    1. Portal vein: brings nutrient rich blood from GI system (Food that's absorbed will end up in liver for metabolsim)

    2. Proper Hepatic Artery: Brings arteyr rich oxygen: arterial blood

    3. Hepatic Vein: Removes blood from the liver and moves to the IVC (both nutrient and oxygen POOR)

    4. Common Hepatic Duct: Removs bile
  6. Gallbladder
    1. Stores and concentrates bile and contracts to forcebile into the duodenumduring the digestion of fats2. The cystic duct joins the hepatic duct to form thecommon bile duct.3. The sphincter of Oddi is located at the entranceto the duodenum.4. The presence of fatty materials in the duodenumstimulates the liberation of cholecystokinin,which causes contraction of the gallbladderand relaxation of the sphincter of Oddi.
  7. Albumin
    • 1. Description
    • a. A main plasma protein of blood

    b. Maintains oncotic pressure and transportsbilirubin, fatty acids, medications, hormones,and other substances that are insoluble inwater

    c. Increased in conditions such as dehydration,diarrhea, and metastatic carcinoma; decreasedin conditions such as acute infection, ascites,and alcoholism

    d. Presence of detectable albumin, or protein, in theurine is indicative of abnormal renal function

    2. Value: 3.4 to 5 g/dL


    3. Nursing consideration: Fasting is not required.
  8. Alkaline phosphatase
    • 1. Description
    • a. Alkaline phosphatase is an enzyme normallyfound in bone, liver, intestine, and placenta.

    b. The level rises during periods of bone growth,liver disease, and bile duct obstruction.

    2. Value: 4.5 to 13 King-Armstrong units/dL

    • 3. Nursing considerations
    • a. The client may need to fast 12 hours beforethe test.b. Hepatotoxic medications administered within12 hours before specimen collection cancause a falsely elevated value.c. Transport the specimen to the laboratoryimmediately.
  9. Ammonia
    • 1. Description
    • a. Ammonia is a byproduct of protein catabolism;most of it is created by bacteria actingon proteins present in the gut.

    b. Ammonia is metabolized by the liver andexcreted by the kidneys as urea.

    c. Elevated levels resulting from hepatic dysfunctionmay lead to encephalopathy.

    d. Venous ammonia levels are not a reliableindicator of hepatic coma.


    2. Value: 10 to 80 mcg/dL

    3. Nursing considerationsa. Instruct the client to fast, except for water, andto refrain from smoking for 8 to 10 hoursbefore the test; smoking increases ammonialevels.b. Place the specimen on ice and transport tothe laboratory immediately.
  10. Alanine aminotransferase (ALT)
    1. Description: Used to identify hepatocellular diseaseof the liver and to monitor improvement orworsening of the disease.

    2. Value: 4 to 6 international units/L

    3. Nursing considerationsa. Previous intramuscular injections may causeelevated levels.b. No fasting is required.
  11. Aspartate aminotransferase (AST)
    1. Description: Used to evaluate a client with suspectedhepatocellular disease (may also be usedalong with other cardiac markers to evaluate coronaryartery occlusive disease)

    2. Value: 0 to 35 units/L

    • 3. Nursing considerations
    • a. Previous intramuscular injections may causeelevated levelsb. No fasting is required.
  12. Bilirubin
    1. Description

    a. Bilirubin is produced by the liver, spleen, andbone marrow and is also a byproduct ofhemoglobin breakdown.

    b. Total bilirubin levels can be broken downinto direct bilirubin, which is excreted primarilyvia the intestinal tract, and indirectbilirubin, which circulates primarily in thebloodstream.

    c. Total bilirubin levels increase with any type ofjaundice; direct and indirect bilirubin levelshelp differentiate the cause of the jaundice.

    • 2. Values
    • a. Bilirubin, direct (conjugated): 0 to 0.3 mg/dL
    • b. Bilirubin, indirect (unconjugated): 0.1 to1 mg/dL
    • c. Bilirubin, total: Lower than 1.5 mg/dL

    • 3. Nursing considerations
    • a. Instruct the client to eat a diet low in yellowfoods, avoiding foods such as carrots, yams,yellow beans, and pumpkins, for 3 to 4 daysbefore the blood is drawn.
    • b. Instruct the client to fast for 4 hours beforethe blood is drawn.
    • c. Note that results will be elevated with theingestion of alcohol or the administration ofmorphine sulfate, theophylline, ascorbic acid(vitamin C), or acetylsalicylic acid (aspirin).
    • d. Note that results are invalidated if the clienthas received a radioactive scan within 24 hoursbefore the test.
  13. Classification of Jaundice:
    Hemolytic
    Hepatocellular 
    Obstructive
    => Hemolytic Jaundice: Caused by Blood transustion reactions, sickle cell crisis, hemolytic anemia

    -Caused by increasedreadwon of RBCs, which produces an increased amount of unconjugated bilirubiin inblood. Live is unable to handle increased load.

    Dx: Increased unconjucated (indirect) serum bilirubin and urobilinogen increased in stool and urine

    • => Hepatocellular Jaundice
    • From hepatitis, cirrhosis, hepatocellular carcinoma
    • -Caused from liver's altered ability to take up bilirubin from the blood or to conjgate or excrete it. In hepatocellular disease, damaged hepatocyes leak bilirubin.

    • DX: increased unconjugated and conjugated bilirubin
    • -Severe disease caused decreased in direct bilirubin
    • -either normal stool OR Decreased urbilinogen in stool and increase in urine

    • => Obstructive Jaundice:
    • -Hepatitis, Cirrhosis, Hepatocellular Carcinoma. Common bile duct onstruction from stones, biliary strictures, scleromsing cholangitis, and pancreatic cancer.
    • -Results from decreased or obstructed flow of bilethrough liver or biliar y duct system. Obsstruction may occur in intrahepatic or extrahepatic bile ducts. Intrahepatic onstructons are due to swelling or fibrosis of the liv er's canaliculi and bile ducts.

    Dx: Increased serum ilirubin, urine bilierubin and Decreased uroblinogen in stool and urine.
  14. HEPATITIS & Patho
    -Manifestations
    • Hepatitis is a broad term that means “inflammation of the liver.”
    • Hepatitis is most commonly caused by viruses. Hepatitis can also be caused by drugs (alcohol), chemicals (see Table 39-6), autoimmune diseases, and metabolic abnormalities.

    • => Causes
    • Viral (most common)
    • Drugs (alcohol)
    • Chemicals
    • Autoimmune diseases
    • Metabolic abnormalities

    **Hepatitis Pathophysiology: During an acute viral hepatitis infection, liver damage is mediated by cytotoxic cytokines and natural killer cells that cause lysis of infected hepatocytes. Inflammation can interrupt bile flow (cholestasis). After resolution of an acute infection, liver cells can regenerate, and if no complications occur, they should resume their normal appearance and function.

    • A chronic viral hepatitis infection causes chronic inflammation and can cause fibrosis that (over decades) can progress to cirrhosis.
    • The antigen-antibody complexes between the virus and its corresponding antibody may form circulating immune complexes in the early phases of hepatitis.
    • The circulating immune complexes activate the complement system.

    • => The clinical manifestations of this activation are: rash, angioedema, arthritis, fever, and malaise.
    • Cryoglobulinemia (abnormal proteins found in the blood), glomerulonephritis, and vasculitis have also been found secondary to immune complex activation.
  15. **Hepatitis Clinical Manifestations:
    ACUTE vs CHRONIC
    • => ACUTE:
    • -Manifestations: Anorexia, n/v, Right upper quad discomfort, constipation/diarrhea, decreased sense of taste and smell, Malaise, Headache, Fever, Arthralgias, URticaria, Hepatomegaly, Splenomegaly, weigh loss,Jaundice, Pruritus, Dark urine, BIlirubinura, Light stools, Fatigue, continued hepatomegaly with tenderness

    The acute phase is the period of maximal infectivity.

    The acute phase usually lasts from 1 to 4 months.

    During the incubation period, symptoms may include malaise, anorexia and weight loss, fatigue, nausea, occasional vomiting, and abdominal (right upper quadrant) discomfort.

    The patient may find food repugnant and, if a smoker, may have distaste for cigarettes.

    Sense of smell is also decreased. Other symptoms may include headache, low-grade fever, arthralgias, and skin rashes.

    Physical examination may reveal hepatomegaly, lymphadenopathy, and sometimes splenomegaly.

    The acute phase may be icteric (jaundice) or anicteric

    Jaundice, a yellowish discoloration of body tissues, results from an alteration in normal bilirubin metabolism or flow of bile into the hepatic or biliary duct systems.

    The urine may darken because of excess bilirubin being excreted by the kidneys.

    If conjugated bilirubin cannot flow out of the liver because of obstruction or inflammation of the bile ducts, the stools will be light or clay-colored.

    Pruritus (intense chronic itching) sometimes accompanies jaundice. The pruritus occurs as a result of the accumulation of bile salts beneath the skin.

    • => CHRONIC:
    • Malaise, Easy fatigability, Hepatomegaly, Myalgias and or arthalgias, Elevated liver enzymes (aspartate aminotrasferase (AST) and Alanine Aminotransferase(ALT))
  16. **Hepatitis A:
    Causative Agent:HAV, RNA virus

    Transmission:Fecal-oral route

    Most common History: Contaminated food or H2O, travel, poor hygiene, day-care, croweded condtions, poor santitation, milk, water, shellfish, persons with subclinical infections, sexcual contact and IV drug user

    Diagnostics: Anti-HAV IgM = acute, Anti-HAV IgG = lifelong immunity

    Infectivity: most ionfectious during 2 wk before onset of symptoms. INfectious until 1-2 qwwk after the start of symptoms

    Carrier : No chronic carrier state

    Chronic Diagnosis: no

    Vaccination: YES

    Exposure? HAIGComplications:Can cause fulminant hepatic failure

    • => More notes:
    • Hepatitis A viral infection can cause a mild flu-like illness or an acute hepatitis with jaundice. It can also cause acute liver failure. It does not result in a chronic (long-term) infection. In the United States, the incidence of hepatitis A viral infection has declined since vaccination was recommended for at-risk persons and children (at the age of 1).Hepatitis A virus (HAV) is a ribonucleic acid (RNA) virus that is transmitted primarily through the fecal-oral route. It frequently occurs in small outbreaks caused by fecal contamination of food or drinking water. Poor hygiene, improper handling of food, crowded situations, and poor sanitary conditions are contributing factors. Transmission occurs between family members, institutionalized individuals, and children in day care centers. Foodborne hepatitis A outbreaks are usually due to food contaminated by an infected food handler.The virus is present in feces during the incubation period, so it can be carried and transmitted by persons who have undetectable, subclinical infections. The greatest risk of transmission occurs before clinical symptoms are apparent. HAV is found in feces 2 weeks or more before the onset of symptoms and up to 1 week after the onset of jaundice. It is present only briefly in blood. Anti-HAV (antibody to HAV) immunoglobulin M (IgM) appears in the serum as the stool becomes negative for the virus. Detection of hepatitis A IgM indicates acute hepatitis. Although not commonly assessed clinically, hepatitis A IgG indicates past infection. IgG antibody provides lifelong immunity. Hepatitis A vaccination and thorough hand washing are the best measures to prevent outbreaks.
  17. **Hepatitis B:
    Causative Agent: HBV, DNA virus

    Transmission:Perinatally, percutaneously, or sexually

    Most common History: Hemodialysis pts, health care workers, transplantation, BT, same as other STDs, tattoo, children from mothers with Hepatitis B, contaminated needles,

    Diagnostics: Anti-HBs = immunity from vaccine or HBV infection

    Infectivity: Before and after systmptoms appear (4-6 months), can be infectious for life. -_-

    Carrier: 6% become carriers, HBsAg positive

    Chronic Diagnosis: Yes, appr. 6%

    Vaccination: YES

    • Exposure? HBIG & vaccine seriesComplications:Acute HBV can cause fulminant hepatic failure. 12-25% of chronically infected die from chronic liver Dx
    • Chronic can progress to cirrhosis and is risk factor for liver CA

    • => Morenotes:
    • Hepatitis B virus (HBV) can cause either acute or chronic disease. Starting in the 1990s and continuing today, the incidence of HBV infection has decreased because of the widespread use of the HBV vaccine.About 12 million Americans have been infected with HBV. In the majority of adults with acute hepatitis B, the infection completely resolves. Of the more than 1 million Americans who develop chronic infections, the severity of liver impairment may range from none to severe liver disease. Approximately 15% to 25% of chronically infected persons die from chronic liver disease. HBV is a deoxyribonucleic acid (DNA) virus. It can be transmitted perinatally by mothers infected with HBV; percutaneously (e.g., IV drug use, accidental needle-stick punctures); or by mucosal exposure to infectious blood, blood products, or other body fluids (e.g., semen, vaginal secretions, saliva). In people with HBV, hepatitis B surface antigen (HBsAg) has been detected in almost every body fluid. Infected semen and saliva contain much lower concentrations of HBV than does blood, but the virus can be transmitted via these secretions. If gastrointestinal (GI) bleeding occurs, feces can be contaminated with the virus from the blood. There is no evidence that urine, feces (without GI bleeding), breast milk, tears, and sweat are infective. Sexual transmission is a common mode of HBV transmission. Men who have sex with men (especially those practicing unprotected anal intercourse) are at risk for HBV infection. Although there is a much lower risk of transmission with kissing and sharing of food items, these activities may spread the virus via saliva. Other at-risk individuals include those who have household contacts with chronically infected persons, patients undergoing hemodialysis, and health care and public safety workers. Organ and tissue transplantation is another potential source of infection. In some patients with acute hepatitis B, there is no readily identifiable risk factor.HBV can live on a dry surface for at least 7 days. HBV is much more infectious than HIV.HBV is a complex structure with three distinct antigens: the surface antigen (HBsAg), the core antigen (HBcAg), and the e antigen (HBeAg). HBsAg in the serum for 6 months or longer after infection indicates chronic HBV infection. Each antigen has a corresponding antibody that may develop in response to HBV infection. The presence of hepatitis B surface antibody (anti-HBs) in the blood indicates immunity from the HBV vaccine or from past HBV infection.
  18. **Hepatitis C:
    Causative Agent:HCV, RNA virus

    Transmission: Percutaneously

    Most common History: Sharing contaminated needles among IV drug users;High-risk sexual behavior, occupational exposure, hemodialysis, BT before 1992.

    Infectivity: 1-2 weeks before symptoms appear. Continues during clinical course 75-85% go on to develop chronic heaptiis C and remain infectious.

    Diagnostics: Anti-HCV

    Carrier : none

    Chronic Diagnosis: Majority of pts (75-85%)

    Vaccination: NO

    Exposure? No (CDC)

    Complications:20% develop cirrhosis and 20% of those develop liver failure

    => More notes: Infection with the hepatitis C virus (HCV) can result in both acute and chronic illness. Acute hepatitis C, which is usually asymptomatic, can be difficult to detect unless diagnosed with laboratory testing. The most common causes of acute hepatitis C are injection drug use and outbreaks among HIV-positive men who have sex with men.The majority of patients who acquire hepatitis C usually develop chronic infection. Most are unaware of their infection. Chronic HCV results in a potentially progressive liver disease; 20% to 30% of infected patients develop cirrhosis. Hepatitis C is the most common cause of chronic liver disease and the most common indication for liver transplantation in the United States.HCV is an RNA virus that is primarily transmitted percutaneously. The most common mode of HCV transmission is the sharing of contaminated needles and equipment among IV drug users. The proportion of cases attributed to high-risk sexual behavior (e.g., unprotected sex, multiple partners) has increased in recent years. In the United States, 10% of all cases of HCV infection are due to occupational exposure, hemodialysis, and perinatal transmission. Some patients with HCV cannot identify a source. The risk of perinatal HCV transmission is higher in women who are co-infected with both HIV and HCV.Patients given blood or blood products before 1992 (when blood product testing for HCV began) may be at risk for chronic HCV infection and should be tested. Because of the 15- to 20-year delay between infection and the clinical appearance of liver damage, long-term effects of HCV infection pose important future health care challenges. Chronic HBV and HCV account for 80% of the cases of hepatocellular cancer.Persons at risk for HCV infection are also at risk for HBV and HIV infections. About 30% to 40% of HIV-infected patients also have HCV. This high rate of co-infection is related primarily to IV drug use. Co-infection with HIV and HCV places the patient at greater risk for progression to cirrhosis.
  19. **Hepatitis Complications:
    Complications that can occur include acute liver failure, chronic hepatitis, cirrhosis of the liver, and hepatocellular carcinoma.

    Almost all cases of acute hepatitis A resolve, although a small number of patients may have a viral relapse in the first 2 to 3 months after the infection.

    The disappearance of jaundice does not mean the patient has totally recovered. Some HBV infections and the majority of HCV infections result in chronic (lifelong) viral infection.

    Alterations in the patient’s cellular immune response may be important in the development of the chronic HBsAg carrier state and the progression from acute to chronic HBV infection. These immune system alterations may explain why patients with chronic kidney disease who are undergoing dialysis when hepatitis B develops are more at risk for developing chronic infection. Persons with chronic kidney disease have a depressed cellular immune response.

    The risk for infection to become chronic is greater for HCV than for HBV.

    Many patients with chronic HCV infection will develop chronic liver disease, cirrhosis, and hepatocellular cancer.

    Risk factors for progression to cirrhosis include male gender, alcohol consumption, and excess iron deposition in the liver.

    Elevated cholesterol or triglyceride levels, obesity, and diabetes mellitus are also risk factors for the progression of HCV infection to cirrhosis.
  20. **Hepatitis Collaborative Care:

    => Hepatitis A

    => Hep C
    There is no specific treatment or therapy for acute viral hepatitis. Most patients can be managed at home.

    Emphasis is on measures to rest the body and assist the liver in regenerating. Adequate nutrition and rest seem to be most beneficial for healing and liver cell regeneration. No special diet is required in the treatment of viral hepatitis. Emphasis is placed on a well-balanced diet that the patient can tolerate.

    • During acute viral hepatitis, adequate calories are important because the patient usually loses weight. If fat content is poorly tolerated because of decreased bile production, it should be reduced.
    • Vitamin supplements, particularly B-complex vitamins and vitamin K, are frequently used. If anorexia, nausea, and vomiting are severe, IV solutions of glucose or supplemental enteral nutrition therapy may be used. Fluid and electrolyte balance must be maintained.Rest reduces the metabolic demands on the liver and promotes cell regeneration. The degree of rest ordered depends on the severity of symptoms, but alternating periods of activity and rest are usually adequate.Counseling should include the importance of avoiding alcohol and drugs detoxified by the liver. Also, the patient should notify possible contacts for testing and prophylaxis, if indicated.


    • ==> Hepatitis A:
    • Outbreaks of viral hepatitis are usually due to HAV. Preventive measures include personal and environmental hygiene and health education to promote good sanitation. Hand washing is essential and is probably the most important precaution. Teach about careful hand washing after bowel movements and before eating. Control and screening (signs, symptoms) of food handlers can also help to control outbreaks.Vaccination is the best protection against HAV. All children at 1 year of age should receive the vaccine.Adults at risk should also receive the vaccine. These include people who travel to areas with increased rates of hepatitis A, men who have sex with men, users of injection and noninjection drugs, persons with clotting factor disorders (e.g., hemophilia), and persons with chronic liver disease.Isolation is not required for HAV infection. For a patient with HAV infection, use infection control precautions. A private room is indicated if the patient is incontinent of stool or has poor personal hygiene.Both hepatitis A vaccine and immune globulin (IG) are used for prevention of HAV infection after exposure to an infected person (postexposure prophylaxis). The vaccine is used for preexposure prophylaxis, and IG can be used either before or after exposure. IG provides temporary (1 to 2 months) passive immunity and is effective for preventing hepatitis A if given within 2 weeks after exposure. IG is recommended for persons who do not have anti-HAV antibodies and are exposed as a result of close (household, day care center) contact with persons who have HAV or foodborne exposure. Because patients with HAV are most infectious just before the onset of symptoms (the preicteric phase), those exposed through household contact or foodborne outbreaks should receive IG. Although IG may not prevent infection in all persons, it may modify the illness to a subclinical infection.When hepatitis A occurs in a food handler, IG should be administered to all other food handlers at the establishment. Patrons may also need to be given IG.Persons who have received a dose of HAV vaccine more than 1 month previously or who have a history of laboratory-confirmed HAV infection do not require IG.

    • ==> Hepatitis C:
    • No vaccine is currently available for hepatitis C. The primary measures to prevent HCV transmission include screening of blood, organ, and tissue donors; use of infection control precautions; and modification of high-risk behavior. Because of the number of people with hepatitis C that has not been diagnosed, the CDC has recommended that all persons born between 1945 and 1965 undergo HCV testing regardless of risk factor status.The CDC does not recommend IG or antiviral agents such as interferon for postexposure prophylaxis (e.g., needle-stick exposure from an infected patient) for HCV infection. Following an acute exposure (e.g., needle stick), the person should have anti-HCV testing done. For the person exposed to HCV, baseline anti-HCV and ALT levels should be measured. Follow-up testing for anti-HCV and ALT should be done at 4 to 6 months. Testing for HCV RNA may be performed at 4 to 6 weeks.
  21. **Hep Drug Therapies:
    Chronic B
    Chronic C
    There are no drug therapies for the treatment of acute hepatitis A infection. Treatment of acute hepatitis B indicated only in patients with severe hepatitis and liver failure. Among persons with acute hepatitis C, treatment with pegylated interferon within the first 12 to 24 weeks of infection has markedly reduced the development of chronic hepatitis C.Supportive drug therapy may include antiemetics for nausea, such as prochlorperazine (Compazine), promethazine (Phenergan), or ondansetron (Zofran).

    For Chronic Hep B: Drug therapy for chronic HBV infection is focused on decreasing the viral load and liver enzyme levels and slowing the rate of disease progression.Long-term goals are the prevention of cirrhosis, hepatic failure, and hepatocellular cancer. Current drug therapies for chronic HBV do not eradicate the virus but work well to suppress viral replication and prevent complications of hepatitis B.

    --First-line therapies include pegylated interferon and nucleoside and nucleotide analogs.

    A. Interferon has multiple effects on the viral replication cycle. After binding to receptors on host cell membranes, the drug blocks viral entry into cells, synthesis of viral proteins, and viral assembly and release.There are two forms of interferon: standard (Intron A) and pegylated. Standard (conventional) interferon has a short half-life, necessitating frequent subcutaneous administrations (three times per week). In contrast, the long-acting preparations (pegylated interferons) are administered subcutaneously less frequently (just once per week), which makes them more convenient. In addition, with the long-acting preparations, blood levels remain high between doses, and therefore clinical responses are better.The long-acting preparations are made by conjugation of a standard interferon with polyethylene glycol (PEG), in a process known as pegylation. Therapeutic effects of the pegylated products (PEG-interferon alfa-2a [Pegasys] and PEG-interferon alfa-2b [Pegintron]) are due solely to its interferon component. The PEG component serves only to delay elimination of the drug. Because of their convenience and superior efficacy, these products are preferred over standard interferon and are used in treatment of both hepatitis B and hepatitis C.In patients with HBV receiving interferon, one third will have a significant reduction of serum HBV DNA levels, normalization of ALT levels, and loss of HBeAg. The response to treatment may vary on the basis of viral genotype. Interferon treatment is associated with a number of side effects. These side effects are dose related and tend to decrease in severity with continued treatment. Patients receiving interferon should have blood counts and liver function tests performed every 4 to 6 weeks.

    • B. Nucleoside/nucleotide analogs
    • Hepatitis B virus reproduces by making copies of its viral DNA nucleosides and nucleotides. The nucleoside/nucleotide analog drugs masquerade as normal building blocks for DNA, thereby “fooling” the hepatitis B virus. Thus the virus is unable to reproduce.Nucleoside/nucleotide analogs do not prevent all viral reproduction, but they can substantially lower the amount of virus in the body. These medications include lamivudine (Epivir), adefovir (Hepsera), entecavir (Baraclude), telbivudine (Tyzeka), and tenofovir (Viread). These oral medications are used in the treatment of chronic HBV when there is evidence of active viral replication. Nucleoside/nucleotide analogs have beneficial effects in terms of reducing viral load, decreasing liver damage, and decreasing liver enzymes. Most patients with HBV will require long-term treatment with these medications. When these drugs are stopped, the majority of patients (except those who have seroconverted) have HBV DNA and liver enzyme levels that return to pretreatment levels.Severe exacerbations of hepatitis B have developed following discontinuation of treatment. If these drugs are discontinued, liver function should be monitored closely for several months.



    • ==> For Chronic Hep C:
    • Treatment of chronic hepatitis C is individualized and based on the genotype, the severity of liver disease, potential side effects, presence of co-morbid conditions, patient’s readiness for treatment, and presence of other health problems (e.g., HIV). Drug therapy is directed at eradicating the virus and preventing HCV-related complications.Treatment for HCV includes pegylated interferon (PEG-Intron, Pegasys) given with ribavirin (Rebetol, Copegus). Pegylated interferon is injected once a week, and ribavirin is taken orally twice daily. Ribavirin, given in combination with peginterferon, has a synergistic effect and reduces the rate of relapse following hepatitis C treatment. Ribavirin has a number of side effects, including teratogenisis. During treatment, pregnancy must be avoided, both by women taking the drug and by women whose male partners are taking the drug.Patients who have HCV genotype 1 also receive either telaprevir (Incivek) or boceprevir (Victrelis), which are HCV protease inhibitors. Protease is an enzyme that is essential in viral replication. Both boceprevir and telaprevir are taken orally every 8 hours.
  22. **Nursing Assessment for Hep:
    Obtain the following health information from the patient:

    Past health history: hemophilia; exposure to infected persons; ingestion of contaminated food or water; exposure to benzene, carbon tetrachloride, or other hepatotoxic agents; crowded, unsanitary living conditions; exposure to contaminated needles; recent travel; organ transplantation; exposure to new drug regimens, hemodialysis, transfusion of blood or blood products before 1992, HIV status (if known)

    Medications: use and misuse of acetaminophen, new prescription, over-the-counter, or herbal medications or supplements

    Also obtain the following important health information related to pertinent functional health patterns:

    Health perception–health management: IV drug and alcohol abuse; malaise, distaste for cigarettes (in smokers), high-risk sexual behaviors

    Nutritional-metabolic: weight loss, anorexia, nausea, vomiting; feeling of fullness in right upper quadrant

    Elimination: dark urine; light-colored stools, constipation, or diarrhea; skin rashes, hivesActivity-exercise: fatigue, arthralgias, myalgias

    Cognitive-perceptual: right upper quadrant pain and liver tenderness; headache; pruritus

    Role-relationship: exposure as health care worker, as long-term care institution resident, through incarceration, through homelessness


    Perform a focused physical assessment for the following clinical manifestations:

    General: low-grade fever, lethargy, lymphadenopathy

    Integumentary: rash or other skin changes, jaundice, icteric sclera, injection sites

    Gastrointestinal: hepatomegaly, splenomegaly
  23. **Hep NDS & Planning :
    • Nursing diagnoses for the patient with viral hepatitis may include, but are not limited to, the following:
    • • Imbalanced nutrition: less than body requirements related to anorexia and nausea
    • • Activity intolerance related to fatigue and weakness
    • • Risk for impaired liver function related to viral infection

    The overall goals are that the patient with viral hepatitis will (1) have relief of discomfort, (2) be able to resume normal activities, and (3) have return to normal liver function without complications.
  24. **Nursing Implementation for Hepatitis: Acute Care

    Home Care

    Evalv: expected outcomes
    In patients with hepatitis, assess for the presence and degree of jaundice. In light-skinned persons, jaundice is usually observed first in the sclera of the eyes and later in the skin. In dark-skinned persons, jaundice is observed in the hard palate of the mouth and inner canthus of the eyes. The urine may have a dark brown or brownish red color because of the presence of bilirubin.Comfort measures to relieve pruritus (if present), headache, and arthralgias are helpful.Ensuring that the patient receives adequate nutrition is not always easy. The anorexia and distaste for food cause nutritional problems. Assess the patient’s tolerance of specific foods, as well as eating pattern. Small, frequent meals may be preferable to three large ones and may also help prevent nausea.Often, a patient with hepatitis finds that anorexia is not as severe in the morning, so it is easier to eat a good breakfast than a large dinner. Measures to stimulate the appetite, such as mouth care, antiemetics, and attractively served meals in pleasant surroundings, should be included in the nursing care plan. Carbonated beverages and avoidance of very hot or very cold foods may help alleviate anorexia. Adequate fluid intake (2500 to 3000 mL/day) is important.Rest is essential and is an important factor in promoting hepatocyte regeneration. Assess the patient’s response to the rest and activity plan, and modify it as needed. Liver function tests and symptoms are used as a guide to activity.Psychologic and emotional rest is as essential as physical rest. Limitation in activity may produce anxiety and extreme restlessness in some patients.Diversional activities, such as reading and hobbies, may help the patient.


    • => Home care:
    • Most patients with viral hepatitis are cared for at home, so you need to assess the patient’s knowledge of nutrition and provide the necessary dietary teaching. Caution the patient about overexertion and the need to follow the health care provider’s advice about when to return to work. Teach the patient and caregiver how to prevent transmission to other family members. Also teach what symptoms should be reported to the health care provider.Assess the patient for manifestations of complications. Bleeding tendencies with increasing prothrombin time values, symptoms of encephalopathy, or elevated liver function levels indicate problems.Instruct the patient to have regular follow-up for at least 1 year after the diagnosis of hepatitis. Because relapses occur with hepatitis B and C, teach the patient the symptoms of recurrence and the need for follow-up evaluations. All patients with chronic HBV or HCV should avoid alcohol, as it can accelerate disease progression.The patient who is receiving interferon for the treatment of HBV or HCV requires education regarding this drug. Because interferon is administered subcutaneously, the patient or caregiver needs to be taught how to administer the drug. The numerous side effects with the therapy, including flu-like symptoms (e.g., fever, malaise, fatigue), make adherence to therapy challenging for some patients. Patients who are positive for HBsAg (chronic carrier status) or HCV antibody should not be blood donors.

    • **Evaluation: Expected outcomes
    • Adequate nutritional intake Increased tolerance of activityPerforming daily activities with scheduled rest periodsAbility to explain methods of transmission and methods of preventing transmission
  25. CIRRHOSIS (Lewis)
    • Cirrhosis is a chronic progressive disease characterized by extensive degeneration and destruction of the liver parenchymal cells.

    • Any chronic (long-term) liver disease, most frequently excessive alcohol intake and viral hepatitis, can cause cirrhosis. Other causes include malnutrition, biliary obstruction, and right-sided heart failure.

    • => Clinical Manifestations and Complications
    • • Manifestations of cirrhosis include jaundice, skin lesions (spider angiomas), hematologic problems (thrombocytopenia, leucopenia, anemia, coagulation disorders), endocrine problems, and peripheral neuropathy.

    • Patients without complications of cirrhosis are said to have compensated cirrhosis; those who have more than one complication of their liver disease are described as having decompensated cirrhosis.

    • • Major complications of cirrhosis include portal hypertension, esophageal and gastric varices, peripheral edema and ascites, hepatic encephalopathy, and hepatorenal syndrome.
    • o Portal hypertension, a persistent increase in blood pressure in the portal venous system, is characterized by increased venous pressure in the portal circulation, as well as splenomegaly, large collateral veins, ascites, systemic hypertension, and esophageal varices.o Bleeding esophageal varices, tortuous veins at the lower end of the esophagus, are the most life-threatening complication of cirrhosis.
    • o Ascites is the accumulation of serous fluid in the peritoneal or abdominal cavity, and may be accompanied by dehydration, hypokalemia, and peritonitis.
    • o Hepatic encephalopathy is considered a terminal complication in liver disease. A characteristic symptom of hepatic encephalopathy is asterixis (flapping tremors).
    • o Hepatorenal syndrome is characterized by functional renal failure with advancing azotemia, oliguria, and intractable ascites.

    • => Diagnostic Studies
    • • Diagnostic test results in cirrhosis include elevations in liver enzymes, decreased total protein, fat metabolism abnormalities, liver fibrosis, and positive liver biopsy.

    • => Collaborative Care
    • • There is no specific therapy for cirrhosis.
    • • Management of ascites is focused on sodium restriction, diuretics, and fluid removal.

    • • The main therapeutic goal for esophageal and gastric varices is avoidance of bleeding and hemorrhage.
    • o If the patient has esophageal and/or gastric varices, observe for any signs of bleeding from the varices (e.g., hematemesis and melena).
    • o If bleeding occurs, the nurse must be prepared. The management of bleeding varices includes prophylactic, therapeutic, and emergency interventions.
    • o A transjugular intrahepatic portosystemic shunt (TIPS) may be created to redirect portal blood flow.
    • o Patients are monitored for spontaneous bacterial peritonitis, which can occur after variceal hemorrhage.

    • Management of hepatic encephalopathy is focused on reducing of ammonia formation and treating precipitating causes. The focus of nursing care of the patient with hepatic encephalopathy is on maintaining a safe environment, sustaining life, and assisting with measures to reduce the formation of ammonia.

    • The diet for the patient with cirrhosis without complications is high in calories (3000 cal/day) with high carbohydrate content and moderate to low fat levels. Sodium restrictions are placed on the patient with ascites and edema.

    • An important nursing focus is the prevention and early treatment of cirrhosis.
  26. CIrrhosis:
    • => Description
    • - Cirrhosis is a chronic progressive disease of the liver characterized by extensive degeneration and destruction of the liver cells.
    • - The liver cells attempt to regenerate, but the regenerative process is disorganized, resulting in abnormal blood vessel and bile duct architecture. VERY DISORGANIZED so non fuctional and enlarged. Therefore it cannot metabolize all the products that should be metab. in order to go into the blood stream.
    • -The overgrowth of new and fibrous connective tissue distorts the liver’s normal lobular structure, resulting in lobules of irregular size and shape with impeded blood flow.

    -Eventually, irregular and disorganized liver regeneration, poor cellular nutrition, and hypoxia (from inadequate blood flow and scar tissue) result in decreased functioning of the liver.

    -The development of cirrhosis is an insidious, prolonged course, usually after decades of chronic liver disease.

    -Cirrhosis (combined with chronic liver diseases) is ranked as the eighth leading cause of death in the United States.

    -Cirrhosis is twice as common in men as in women. Cirrhosis that developed secondary to alcoholism. The characteristic diffuse nodularity of the surface is due to the combination of regeneration and scarring of the liver.

    -symptoms due to portal HTN and inability to metabolize.


    Eventually the liver loses the ability to compensate. Transplants:
  27. **Cirrhosis Etiology and Pathophysiology
    Specific cause not always known

    Most common causes : alcohol abuse, second: United States are chronic hepatitis C and alcohol-induced liver disease

    Protein malnutrition

    Environmental factors

    Chronic inflammation and cell necrosis

    Synergistic factors accelerate damageenlarged liver is palpaple


    Note: Any chronic liver disease, including excessive alcohol intake and NAFLD, can cause cirrhosis. The specific cause of cirrhosis may not be determined in all patients. The most common causes of cirrhosis in the United States are chronic hepatitis C infection and alcohol-induced liver disease. In patients with alcohol-induced liver disease, some controversy exists as to whether the cause is the alcohol or the malnutrition that often coexists with chronic alcoholism. A common problem in alcoholic patients is protein malnutrition. There have been cases of nutrition-related cirrhosis resulting from extreme dieting, malabsorption, and obesity. Environmental factors and a genetic predisposition may also lead to the development of cirrhosis, regardless of dietary or alcohol intake.Approximately 20% of patients with chronic hepatitis C and 10% to 20% of those with chronic hepatitis B will develop cirrhosis. Chronic inflammation and cell necrosis result in fibrosis and, ultimately, cirrhosis. Chronic hepatitis combined with alcohol ingestion is synergistic in accelerating liver damage.

    => Biliary cirrhosis: Associated with chronic biliary inflammation and obstructionBiliary causes of cirrhosis include primary biliary cirrhosis and primary sclerosing cholangitis. Primary sclerosing cholangitis is a chronic inflammatory condition affecting the liver and bile ducts that is frequently found in men.


    => Cardiac cirrhosis: From long-standing severe right-sided heart failureCardiac cirrhosis includes a spectrum of hepatic derangements that result from long-standing, severe right-sided heart failure. The treatment is aimed at managing the patient’s underlying heart failure.
  28. **Cirrhosis: Clinical Manifestations
    • The onset of cirrhosis is usually insidious.
    • Early symptoms can include fatigue. Many patients with normal liver function (compensated cirrhosis) may not be aware of their liver condition. The diagnosis may not be discovered until later, when they present with symptoms of more advanced liver disease.

    Later symptoms may be severe and result from liver failure and portal hypertension.

    Jaundice, peripheral edema, and ascites develop gradually.

    Other late symptoms include skin lesions, hematologic disorders, endocrine disturbances, and peripheral neuropathies.

    In the advanced stages, the liver becomes small and nodular.

    SOB: ascities: fliuid accumulation pressuing on lung capacity. Lethargy.

    • => Jaundice
    • Functional derangement of liver cells
    • Compression of bile ducts by overgrowth of connective tissue
    • Decreased ability of liver cells to conjugate and excrete bilirubin
    • Severity varies: The jaundice may be minimal or severe, depending on the degree of liver damage. The bile cannot be excreted. Liver loses ability to conjugate so urine becomes dark and stool becomes clay colored. Not enough bile, then fatty stool may occur

    • => Skin lesions
    • Various skin manifestations are commonly seen in cirrhosis because of an increase in circulating estrogen as a result of the damaged liver’s inability to metabolize steroid hormones.
    • Spider angiomas (telangiectasia or spider nevi) are small, dilated blood vessels with a bright red center point and spider-like branches. They occur on the nose, cheeks, upper trunk, neck, and shoulders. due to (phospholase.. have to be metabolized in liver)
    • Palmar erythema (a red area that blanches with pressure) is located on the palms of the hands.

    • => Hematologic disorders
    • Hematologic problems include thrombocytopenia, leukopenia, anemia, and coagulation disorders.
    • Thrombocytopenia, leukopenia, and anemia are probably caused by the splenomegaly.
    • -Splenomegaly results from backup of blood from the portal vein into the spleen (portal hypertension). Overactivity of the enlarged spleen results in increased removal of blood cells from circulation. Low platelet production.
    • Anemia is also due to inadequate RBC production and survival, poor diet, poor absorption of folic acid, and bleeding from varices.
    • The coagulation problems result from the liver’s inability to produce prothrombin and other factors essential for blood clotting. Coagulation problems are manifested by hemorrhage or bleeding tendencies, such as epistaxis, purpura, petechiae, easy bruising, gingival bleeding, and heavy menstrual bleeding.
    • Liver produces albumin: RBC production is inhibited because albumin builds up any cell ): Also needed for coagulation factors.
    • INR High, PTT High.

    • => Endocrine disorders
    • Normally the liver is very important in the metabolism of adrenocortical hormones, estrogen, and testosterone. In men with cirrhosis, gynecomastia (benign growth of the glandular tissue of the male breast), loss of axillary and pubic hair, testicular atrophy, and impotence with loss of libido may occur because of increased estrogen levels.In younger women with cirrhosis, amenorrhea may occur, and in older women there may be vaginal bleeding. The liver fails to metabolize aldosterone adequately, resulting in hyperaldosteronism with subsequent sodium and water retention and potassium loss.aldosterone is cholesterol based: hyperaldosteronism occurs
    • --THerapy: Aldactone

    • => Peripheral neuropathy
    • Dietary deficiencies of thiamine, folic acid, and cobalamin (vitamin B12); worsened by alcoholism
    • Peripheral neuropathy is a common finding in alcoholic cirrhosis and is probably due to a dietary deficiency of thiamine, folic acid, and cobalamin.
    • The neuropathy usually results in mixed nervous system symptoms, but sensory symptoms may predominate.
    • Banana bags for alcohol abusers: folic acid, thiamine, potassium
    • Alcohol abuse at risk for low magnesium: at risk for dysrhytmias??
  29. **Cirrhosis Complications
    => Compensated cirrhosis: Patients without complications of cirrhosis have compensated cirrhosis.

    • => Decompensated cirrhosis
    • Portal hypertension
    • Esophageal and gastric varices
    • Peripheral edema and ascites
    • Hepatic encephalopathy
    • Hepatorenal syndromee-Those who have one or more complications of their liver disease have decompensated cirrhosis.
    • Major complications of cirrhosis are portal hypertension with resultant esophageal and/or gastric varices, peripheral edema and ascites, hepatic encephalopathy (mental status changes, including coma), and hepatorenal syndrome.
  30. **Complications Portal hypertension
    If there is abnormality of vascualar system of liver (sclerosis) then htn: because there is a back up and goes into the spleen, looks for other opportunities to shift the blood

    Increased portal venous pressure

    Splenomegaly

    Large collateral veins

    Ascites : portal htn, oncotic pressure contributes: Not enough albumin and pressure within the blood vessels, so fluid shifts outside into the tissue --> Peripheral edema and ascites.

    • Gastric (80%) and esophageal varicesespohageal: very fragile, blood vessels not made to accomodate a high amount of blood so their walls are very thin, so they bleed easily. In pts who are already at risk with poor coagulations.
    • #1 cause of death of cirrhosis: BLEEDING FROM VARICES! D:

    • =>> Portal hypertension results from obstruction to the normal flow of blood through the portal system, secondary to structural changes in the liver that cause compression and destruction of the veins and sinusoids.
    • Portal hypertension is characterized by increased venous pressure in the portal circulation, as well as splenomegaly, large collateral veins, ascites, and gastric and esophageal varices.

    Collateral circulation develops in an attempt to reduce high portal vein pressure and also to reduce the increased plasma volume and lymphatic flow. The common areas where the collateral channels form are in the lower esophagus (the anastomosis of the left gastric vein and the azygos veins), the anterior abdominal wall, the parietal peritoneum, and the rectum.

    Varicosities may develop in areas where the collateral and systemic circulations communicate, resulting in esophageal and gastric varices, caput medusae (ring of varices around the umbilicus), and hemorrhoids.
  31. **Complications : Esophageal and Gastric Varices
    • => Esophageal varices
    • Complex of tortuous veins at lower end of esophagus, Very fragile, Bleed easily; bleeding can be life-threatening
    • Esophageal varices are a complex of tortuous veins at the lower end of the esophagus, which are enlarged and swollen as a result of portal hypertension. These varices contain little elastic tissue and are quite fragile. They tolerate high pressure poorly, and the result is that these veins bleed easily. Large varices are more likely to bleed. Esophageal varices are responsible for approximately 80% of variceal hemorrhages. Bleeding esophageal varices are the most life-threatening complication of cirrhosis. The patient may have melena or hematemesis. There may be slow oozing or massive hemorrhage. Massive hemorrhage is a medical emergency.

    • => Gastric varices
    • Upper portion of stomach; Gastric varices are located in the upper portion (cardia, fundus) of the stomach. These account for 20% of all varices.
  32. **Complications Peripheral edema
    ↓ Colloidal oncotic pressure from impaired liver synthesis of albumin

    ↑ Portacaval pressure from portal hypertension

    Occurs as ankle/presacral edema

    Peripheral edema results from decreased colloidal oncotic pressure from impaired liver synthesis of albumin and increased portacaval pressure from portal hypertension.

    Peripheral edema occurs as ankle and presacral edema.
  33. **Complications Ascites
    Accumulation of serous fluid in peritoneal or abdominal cavity

    Abdominal distention with weight gain

    • Common manifestation of cirrhosisAscites is the accumulation of serous fluid in the peritoneal or abdominal cavity.
    • Ascites is manifested by abdominal distention with weight gain.It is a common manifestation of cirrhosis.

    • SOB-they have to sit up.-Fluid can build up to 10 L. Don't drain all at once, because you can put your patient at shock.
    • Temporary measure: Paracentesis. The body will just shift the fluid right back into the abdominal cavit so it's a comfort measure more than anything.

    Measure abdominal girth, weight fluctuates

    another sign: collateral veins start developing around the umbiliacal. The head of "medusa":

    • ==> Ascites Chart:
    • With portal hypertension, proteins shift from the blood vessels via the larger pores of the sinusoids (capillaries) into the lymph space. When the lymphatic system is unable to carry off the excess proteins and water, they leak through the liver capsule into the peritoneal cavity. The osmotic pressure of the proteins pulls additional fluid into the peritoneal cavity.

    A second mechanism of ascites formation is hypoalbuminemia, resulting from the inability of the liver to synthesize albumin. The hypoalbuminemia results in decreased colloidal oncotic pressure.

    A third mechanism is hyperaldosteronism, which occurs when aldosterone is not metabolized by damaged hepatocytes. The increased level of aldosterone causes increased sodium reabsorption by the renal tubules. This retention of sodium, as well as an increase in antidiuretic hormone, causes additional water retention.

    Because of edema formation, intravascular volume is decreased and, subsequently, renal blood flow and glomerular filtration are decreased. The patient has signs of dehydration (e.g., dry tongue and skin, sunken eyeballs, muscle weakness). There is also a decrease in urinary output. Hypokalemia is common and is due to an excessive loss of potassium caused by hyperaldosteronism. Low potassium levels can also result from diuretic therapy used to treat the ascites.Because of alterations in immune function associated with cirrhosis, patients with ascites are at risk for spontaneous bacterial peritonitis (SBP). SBP is a bacterial infection of the ascites fluid. This occurs in approximately 15% to 25% of hospitalized patients with cirrhosis and ascites, and it is particularly common after variceal hemorrhage. The bacteria most frequently found are gram-negative enteric pathogens such as E. coli.
  34. **Complications Hepatorenal syndrome
    Very late; as a result of liver failure, kidney perfusion occurs due to vasoconstriction of renal circulation sooo pt's kidneys fails! Main cause is liver, so kidney transplants don't help.

    Renal failure with azotemia, oliguria, and intractable ascitesNo structural abnormality of kidneys

    Portal hypertension → vasodilation → renal vasoconstriction

    -Notes: Hepatorenal syndrome can occur in patients with decompensated cirrhosis.It is a type of renal failure with advancing azotemia, oliguria, and intractable ascites. This syndrome is not characterized by structural abnormality of the kidneys. The etiology is complex, but the final common pathway is likely to be portal hypertension along with liver decompensation that results in splanchnic and systemic vasodilation and decreased arterial blood volume. As a result, renal vasoconstriction occurs, and renal failure follows. This renal failure can be reversed by liver transplantation. In the patient with cirrhosis, hepatorenal syndrome frequently follows diuretic therapy, GI hemorrhage, or paracentesis.
  35. **Complications Hepatic encephalopathy & CARE c:
    Ammonia should be excreted by liver, but not in failure: accumulates in blood: neurotoxin (can cross blood-brain barrier). Treat by getting rid of it! Ammonia is end product of protein, so restrict in the diet!

    • =>Neurotoxic effects of ammonia
    • =>Abnormal neurotransmission
    • =>Astrocyte swelling
    • =>Inflammatory cytokines
    • Liver unable to convert increased ammonia Ammonia crosses blood-brain barrier


    note: Hepatic encephalopathy is a neuropsychiatric manifestation of liver disease. The pathogenesis of hepatic encephalopathy is multifactorial and includes the neurotoxic effects of ammonia, abnormal neurotransmission, astrocyte swelling, and inflammatory cytokines. A major source of ammonia is the bacterial and enzymatic deamination of amino acids in the intestines. The ammonia that results from this deamination process normally goes to the liver via the portal circulation and is converted to urea, which is then excreted by the kidneys. When blood is shunted past the liver via the collateral vessels or the liver is unable to convert ammonia to urea, the levels of ammonia in the systemic circulation increase. The ammonia crosses the blood-brain barrier and produces neurologic toxic manifestations.

    => Changes in neurologic and mental responsiveness

    =>Impaired consciousness and/or inappropriate behavior

    =>Sleep disturbances to lethargy to coma

    =>Asterixis : when patient stretch hands, they have flapping tremor

    =>Fetor

    • note: Clinical manifestations of encephalopathy are changes in neurologic and mental responsiveness, impaired consciousness, and/or inappropriate behavior, ranging from sleep disturbances to lethargy to deep coma. Changes may occur suddenly because of an increase in ammonia in response to bleeding varices or infection, or it may arise gradually as blood ammonia levels slowly increase. A grading system is often used to classify the stages of hepatic encephalopathy: 0 to 4, 4 being most advanced.
    • A characteristic manifestation of hepatic encephalopathy is asterixis (flapping tremors). This may take several forms, the most common involving the arms and hands. When asked to hold the arms and hands stretched out, the patient is unable to hold this position, and there will be a series of rapid flexion and extension movements of the hands. Fetor hepaticus (musty, sweet odor of the patient’s breath) occurs in some patients with encephalopathy. This odor is from the accumulation of digestive by-products that the liver is unable to degrade.

    • =====================
    • **Collaborative Care Hepatic encephalopathy
    • Keeping ammonia level up can make damage permanent
    • => Reduce ammonia formation
    • Lactulose (Cephulac), which traps ammonia in gut and helps to excrete it.
    • Rifaximin (Xifaxan) antibioticPrevent constipation

    • => Treatment of precipitating cause
    • Control GI bleeding: Remove blood from GI tract by NG tube--suctioning and removing that source of the protein!

    • =========================
    • **Acute intervention: Hepatic encephalopathy

    Maintain safe environment=> Assess carefullyLevel of responsivenessSensory and motor abnormalitiesFluid/electrolyte imbalancesAcid-base balanceEffects of treatment measuresThe focus of nursing care of the patient with hepatic encephalopathy is on maintaining a safe environment, sustaining life, and assisting with measures to reduce the formation of ammonia. Assess (1) the patient’s level of responsiveness (e.g., reflexes, pupillary reactions, orientation), (2) sensory and motor abnormalities (e.g., hyperreflexia, asterixis, motor coordination), (3) fluid and electrolyte imbalances, (4) acid-base imbalances, and (5) the effect of treatment measures.Perform neurologic assessment every 2 hoursPrevent constipationEncourage fluidsControl factors known to precipitate encephalopathy=> Assess the neurologic status, including an exact description of the patient’s behavior, at least every 2 hours. Plan your care of the patient with neurologic problems according to the severity of the encephalopathy.Institute measures to prevent constipation to reduce ammonia production. Give drugs, laxatives, and enemas as ordered. Encourage fluids, if not contraindicated. Any GI bleeding may worsen encephalopathy. Assess the patient taking lactulose for diarrhea and excessive fluid and electrolyte losses.Control factors known to precipitate encephalopathy as much as possible, including anything that may cause constipation (e.g., dehydration, opioid medications).
  36. **Cirrhosis: Diagnostic Studies
    • Total protein, prealbumin LOW
    • Serum bilirubin HIGH
    • PT prolonged-bleeding
    • In cirrhosis, there are abnormalities in most of the liver function studies.
    • Enzyme levels, including alkaline phosphatase, AST, ALT, and γ-glutamyl transpeptidase (GGT), are initially elevated because of their release from damaged liver cells. However, in end-stage liver disease, AST and ALT levels may be normal. In cirrhosis, total protein and albumin levels are decreased, and serum bilirubin and globulin levels are increased.

    Fat metabolism abnormalities are reflected by decreased cholesterol levels.

    The prothrombin time is prolonged, and bilirubin metabolism is altered.

    A liver ultrasound study may be used to assess the severity of cirrhosis.

    A liver biopsy may be done to identify liver cell changes and alterations in the lobular structure.

    Differential analysis of ascitic fluid may help confirm the cause of cirrhosis.
  37. **Cirrhosis Collaborative Care FOR REST & ASCITES

    Tolvaptan

    Paracentesis

    Transjugular Intrahepatic Portosystemic Shunt (TIPS)
    • Rest: conserve energy, but mobility becomes an issue also
    • Administration of B-complex vitamins
    • Avoidance of alcohol (even it's not a reason why the patient developed it), aspirin, acetaminophen (hepatotoxicity!), and NSAIDs (risk for GI bleed-we're already worried about varices)

    • **Collaborative Care: Ascites
    • => Sodium restriction
    • The amount of sodium restriction is based on the degree of ascites. Initially the patient may be encouraged to limit sodium intake to 2 g/day. Patients with severe ascites may need to restrict their sodium intake to 250 to 500 mg/day. Very low sodium intake can result in reduced nutritional intake and subsequent problems associated with malnutrition. The patient is usually not on restricted fluids unless severe ascites develops.

    • => Albumin
    • Admin albumin and diuretics
    • Accurately assess and monitor fluid and electrolyte balance. Albumin infusion may be used to help maintain intravascular volume and adequate urinary output by increasing plasma colloid osmotic pressure.

    • => Diuretics
    • Diuretic therapy is an important part of management. Brings the fluid from outside of the BV INTO the blood vessels and the diuretics help excrete it!! Often a combination of drugs that work at multiple sites in the nephron is more effective. Spironolactone (Aldactone) is an effective diuretic, even in patients with severe sodium retention. Spironolactone is an antagonist of aldosterone and is potassium sparing. A high-potency loop diuretic, such as furosemide (Lasix), is frequently used in combination with a potassium-sparing drug.

    => Tolvaptan (Samsca): Tolvaptan (Samsca), a vasopressin-receptor antagonist, is used to correct hyponatremia in patients with cirrhosis. It causes an increase in water excretion, resulting in an increase in serum sodium concentrations.

    => Paracentesis A paracentesis (needle puncture of the abdominal cavity) may be performed to remove ascitic fluid or to test the fluid for infection (spontaneous bacterial peritonitis). Reserved for the patient with impaired respiration or abdominal pain caused by severe ascites. It is only a temporary measure because the fluid tends to reaccumulate.can be done at bed sideworry about bladder distension so we ask the patient to void before the procedure; worried about bladder perforaton.

    => Transjugular intrahepatic portosystemic shunt (TIPS): to shift the blood to avoid the portal system because that's the treatment, risk for hepatic encephalopathy b/c liver isn't metabolizing anythingTransjugular intrahepatic portosystemic shunt (TIPS) (discussed later) is used to alleviate ascites that does not respond to diuretics.Peritoneovenous shunt is a surgical procedure that provides continuous reinfusion of ascitic fluid into the venous system. Its use has almost been eliminated because of the high rate of complications.
  38. **Paracentesis
    Actions to Take in Caring for a Client With aParacentesis

    • 1. Ensure that the client understands the procedureand that informed consent has been obtained.
    • 2. Obtain vital signs, including weight.
    • 3. Have the client void.
    • 4. Position the client upright.
    • 5. Assist the physician, monitor vital signs, and providecomfort and support during the procedure.
    • 6. Apply a dressing to the site of puncture.
    • 7. Monitor vital signs, weigh the client, and maintainthe client on bedrest.
    • 8. Measure the amount of fluid removed.
    • 9. Label and send the fluid for laboratory analysis.
    • 10. Document the event, client’s response, appearanceand amount of fluid removed.

    Description: Paracentesis is the transabdominal removal of fluidfrom the peritoneal cavity. The nurse first ensures thatthe client understands the procedure and that informedconsent has been obtained because the procedure isinvasive. The nurse next obtains preprocedure vital signs,including weight so that a baseline is obtained. Weight istaken before and after the procedure to provide an indicationof the effectiveness of the procedure in fluidremoval. The client is positioned upright on the edge ofthe bed with the back supported and the feet resting ona stool or in a Fowler’s position in bed. The nurse assiststhe physician, monitors vital signs per protocol, and providescomfort and support to the client during the procedure.Once the procedure is complete the nurse applies adressing to the site of puncture and monitors for leakageor bleeding. The client is placed in a position of comfort,bedrest is maintained as prescribed, and vital signs aremonitored to assess for complications. The fluidremoved from the client is measured, labeled and sentto the laboratory for analysis. The nurse documents theevent, the client’s response, the appearance and amountof fluid removed, and any additional pertinent data.
  39. **Collaborative Care: Esophageal and gastric varices
    IMPORTANT B/C NUMBER ONE CAUSE OF DEATH. PREVENTION OF BLEEDING IS KEY THERAPY: Prevent bleeding/hemorrhage

    • Avoid alcohol, aspirin, and irritating foods
    • Screen for presence with endoscopy

    Nonselective β-blocker: propanolol and indralol: reduce portal htn, so varices don't result because no pressure causes bleeding. For hx of esophageal varices . Parameters are different. Systolic: hold if less than 80-Evaluate how: NOT BLEEDING. So CBCs. Occult blood. That is your evaluation. The main therapeutic goal for esophageal and gastric varices is to prevent bleeding and hemorrhage.The patient who has esophageal varices should avoid ingesting alcohol, aspirin, and nonsteroidal antiinflammatory drugs (NSAIDs). All patients with cirrhosis should have upper endoscopy (EGD) to screen for the presence of varices. The diagnosis of esophageal or gastric variceal bleeding needs to be made by endoscopic examination as soon as possible. Patients with varices at risk of bleeding are started on a nonselective β-blocker (nadolol [Corgard] or propranolol [Inderal]) to reduce the incidence of hemorrhage. β-blockers decrease high portal pressure.

    Sandostatin: hormones, causes vasoconstriction of blood vessels. Temporary 1-2 days. After the bleeding is controlled?

    • => If bleeding occurs, stabilize patient, manage airway, provide IV therapy and blood ; When variceal bleeding occurs, the first step is to stabilize the patient and manage the airway.
    • IV therapy is initiated and may include administration of blood products.


    • => Drug therapy : The main goal of drug therapy is to stop bleeding so that treatment measures can be initiated.
    • Octreotide (Sandostatin)

    • Vasopressin : IV administration of VP produces vasoconstriction of the splanchnic arterial bed, decreases portal blood flow, and decreases portal hypertension. However, VP has many side effects, including decreased coronary blood flow, dysrhythmias, and increased BP.
    • Because of this, IV nitroglycerin is often given in combination with VP. The nitroglycerin reduces the adverse effects of the VP while enhancing its beneficial effect. VP should be avoided or used cautiously in the older adult because of the risk of cardiac ischemia.

    • Endoscopic therapy: At the time of endoscopy, band ligation or sclerotherapy may be used to prevent re-bleeding. Endoscopic variceal ligation (EVL or “banding”) is placement of a small rubber band (elastic O-ring) around the base of the varix (enlarged vein).
    • -used for diagnosis and therapy.
    • -Can also do sclero: staple them. Patient isn't cured. The body will build other collateral blood vessels. So you're just patching the problem.

    Band ligation

    Sclerotherapy: Sclerotherapy involves injection of a sclerosant solution into the varices through an injection needle that is placed through the endoscope.

    Management that involves a combination of drug therapy and endoscopic therapy is more successful than either approach alone.

    Drug therapy for bleeding varices may include the somatostatin analog octreotide (Sandostatin) or vasopressin (VP, terlipressin [Teripress]).
  40. **Collaborative Care Balloon tamponade
    • Special type of NG tube with balloon: either gastric or esoph. Inflate balloon for pressure against varices.
    • There is a different port for esoph. and diff port for gastricMechanical compression of varices
    • Sengstaken-Blakemore tube ( Tube inserted into esophagus and stomach. SAFETY ALERT: Label each lumen to avoid confusion. Deflate balloons for 5 minutes every 8 to 12 hours per institutional policy to prevent tissue necrosis.)Minnesota tubeLinton-Nachlas tubeBalloon tamponade may be used in patients with acute esophageal or gastric variceal hemorrhage that cannot be controlled on initial endoscopy. Balloon tamponade controls the hemorrhage by mechanical compression of the varices.Different types of tubes are available. The Sengstaken-Blakemore tube has two balloons, gastric and esophageal, with three lumens: one for the gastric balloon, one for the esophageal balloon, and one for gastric aspiration.Two other types of balloons include the Minnesota tube (a modified Sengstaken-Blakemore tube with an esophageal suction port above the esophageal balloon), and the Linton-Nachlas tube.Risk of aspiration: have scissors to cut off the port!

    If the patient has esophageal and/or gastric varices, observe for any signs of bleeding from the varices, such as hematemesis and melena. If hematemesis occurs, assess the patient for hemorrhage, call the physician, and be ready to assist with treatment used to control the bleeding. The patient will be admitted to the intensive care unit (ICU). The patient’s airway must be maintained.Balloon tamponade may be used in patients who have refractory bleeding that is unresponsive to band ligation or sclerotherapy. When balloon tamponade is used, the initial nursing task is to explain the use of the tube and how it will be inserted. Check the balloons for patency. It is usually the physician’s responsibility to insert the tube, which may be inserted via the nose or the mouth. Then the gastric balloon is inflated with approximately 250 mL of air, and the tube is retracted until resistance (lower esophageal sphincter) is felt. The tube is secured by placement of a piece of sponge or foam rubber at the nostrils (nasal cuff). For continued bleeding, the esophageal balloon is then inflated. A sphygmomanometer is used to measure and maintain the desired pressure at 20 to 40 mm Hg. The position of the balloons is verified by x-ray.

    • => Balloon tamponade
    • Monitor for complications (i.e., aspiration pneumonia)
    • Scissors at bedsideSemi-Fowler’s positionOral/nasal care=Nursing care includes monitoring for complications of rupture or erosion of the esophagus, regurgitation and aspiration of gastric contents, and occlusion of the airway by the balloon. If the gastric balloon breaks or is deflated, the esophageal balloon will slip upward, obstructing the airway and causing asphyxiation. If this happens, cut the tube or deflate the esophageal balloon.Keep scissors at the bedside. Minimize regurgitation by oral and pharyngeal suctioning and by keeping the patient in a semi-Fowler’s position.The patient is unable to swallow saliva because the inflated esophageal balloon occludes the esophagus. Encourage the patient to expectorate, and provide an emesis basin and tissues. Frequent oral and nasal care provides relief from the taste of blood and irritation from mouth breathing.
  41. **Collaborative Care: Supportive measures for acute bleed
    Fresh frozen plasma: Then need clotting factors BUT this works quickly vs (vit k)

    Packed RBCs gives volume and rBC

    Vitamin K: clotting, but takes a while

    Proton pump inhibitors

    Lactulose (Cephulac) and rifaximin (Xifaxan): treating high ammonia levels

    Antibiotics


    => notes: Supportive measures during an acute variceal bleed include:Administration of fresh frozen plasma and packed RBCsVitamin K (AquaMEPHYTON) Proton pump inhibitors (e.g., pantoprazole [Protonix])Lactulose (Cephulac) and rifaximin (Xifaxan) administration may be started to prevent hepaticencephalopathy from breakdown of blood and the release of ammonia in the intestine. MUST have 3 bowel movements. NOT 1. It's not used as a laxativee!! Diarrhea is needed now. That's your goal. :) why is it given: part of blood is staying in GI AND it will digest, but protein is in the blood and, ammonia is a end result of metabolized protein..so esophageal bleeding puts the pt at risk for worseniing Hepatic encephalopathy because blood= protein. If the pt develops esoph bleeding, they're given lactulose. Complication of esoph varices is hepatic encephalopathy!!Antibiotics are given to prevent bacterial infection: Rifaxamin: works on intestian flora that is responsible for working on ammonia production
  42. **Collaborative Care Long-term management
    Nonselective β-adrenergic blockers

    Repeated band ligation

    Portosystemic shunts: decreases risk for hepatic encepho because you bypass the liver completel

    • Because there is a high incidence of recurrent bleeding with each bleeding episode, continued therapy is necessary.
    • Long-term management of patients who have had an episode of bleeding includes nonselective β-blockers, repeated band ligation of the varices, and portosystemic shunts in patients who develop recurrent bleeding.
  43. **Collaborative Care Shunting procedures
    Used more after second major bleeding episode

    Nonsurgical: transjugular intrahepatic portosystemic shunt (TIPS)

    Surgical: portacaval and distal splenorenal shunt

    • => Nonsurgical and surgical methods of shunting blood away from the varices are available.
    • Shunting procedures tend to be used more after a second major bleeding episode than an initial bleeding episode.
    • Transjugular intrahepatic portosystemic shunt (TIPS) is a nonsurgical procedure in which a tract (shunt) between the systemic and portal venous systems is created to redirect portal blood flow.
    • Various surgical shunting procedures may be used to decrease portal hypertension by diverting some of the portal blood flow and at the same time allowing adequate liver perfusion. Currently, the surgical shunts most commonly used are the portacaval shunt and the distal splenorenal shunt.
  44. **Total Portal Division after TIPS
    Total portal diversion after transjugular intrahepatic portosystemic shunt (TIPS).

    A. Portal venogram before TIPS shows filling of large esophageal varices (arrows).

    B. After insertion of a TIPS, flow to varices is eliminated. Intrahepatic portal vein flow is now reversed, with the direction of intrahepatic flow toward the TIPS. Procedure: A catheter is placed in the jugular vein and then threaded through the superior and inferior vena cava to the hepatic vein. The wall of the hepatic vein is punctured, and the catheter is directed to the portal vein. Stents are positioned along the passageway, overlapping in the liver tissue and extending into both veins.This procedure reduces portal venous pressure and decompresses the varices, thus controlling bleeding. TIPS does not interfere with a future liver transplantation. TIPS is contraindicated in patients with severe hepatic encephalopathy, hepatocellular carcinoma, severe hepatorenal syndrome, and portal vein thrombosis.
  45. **CIRRHOSIS DRUG THERAPY TABLE 44-13:
    Vasopressin (Pitressin): Hemostasis and conttrol of bleeding in esophageal and gastric vacrices, constriction of splanchnic arterial bed.

    Octreotide (Sandostatin):Hemostasis and conttrol of bleeding in esophageal and gastric vacrices, constriction of splanchnic arterial bed.

    Lactulose (Cephulac): Acidification of feces in bowel and trapping of ammonia, causing its elimination in feces.

    Rifaximin (Xifaxan): Decrease in bacterial flora, decreased formation of ammonia.

    Neomycin Sulfate:Decrease in bacterial flora, decreased formation of ammonia.

    Magesium Sulfate: Magnesium replacement, hypomagnesemia possible with liver dysfunction

    Vitamin K: correction of clotting abnormalities from decreased level of vitamin K.

    Protom Pump Inhibitors (Pantoprazole or Protonix): decreases gastric Acididty

    • Diuretics:
    • -> Sprinoloactone: blocks aldosterone effects, spares potassium

    -> Furosemide (lasix): Acts on distal tubule and loop of Henle to decase reabsorption of soddium and water.
  46. **Nutritional Therapy: Diet for patient without complications
    High in calories (3000 cal/day)

    ↑ Carbohydrate

    Moderate to low fat

    Protein restriction rarely justified: only if pt has hepatic encephalopathy!

    Protein supplements for protein-calorie malnutrition

    Low-sodium diet for patient with ascites and edema

    => The diet for the patient who has cirrhosis without complications is high in calories (3000 cal/day) with high carbohydrate content and moderate to low levels of fat. Protein restriction may be appropriate in some patients immediately following a severe flare of symptoms (i.e., episodic hepatic encephalopathy). However, protein restriction is rarely justified in patients with cirrhosis and persistent hepatic encephalopathy. Malnutrition is a more serious clinical problem than hepatic encephalopathy for many of these patients.

    => A patient with alcoholic cirrhosis frequently has protein-calorie malnutrition. For the patient with protein malnutrition, enteral formula supplements containing protein from branched-chain amino acids that are metabolized by the muscles may be recommended. These supplements provide protein that is more easily metabolized by the liver. Parenteral nutrition or enteral nutrition therapy may be required.

    The patient with ascites and edema is placed on a low-sodium diet. The degree of sodium restriction varies, depending on the patient’s condition. The patient needs instruction regarding the degree of restriction. Table salt is a well-known source of sodium, but sodium is also present in baking soda and baking powder. Foods that are high in sodium content include canned soups and vegetables, many frozen foods, salted snacks (e.g., potato chips), nuts, smoked meats and fish, crackers, breads, olives, pickles, ketchup, and beer. Advise the patient to read labels. The patient and the caregiver need assistance to make the diet more palatable by the use of seasonings such as garlic, parsley, onion, lemon juice, and other spices.
  47. Cirrhosis Subj Vs OBj
    • **Subjective data:
    • functional health patternsChronic alcoholismWeakness, fatigueAnorexia, weight lossDyspepsiaNausea and vomitingGingival bleeding=> Elimination: Dark urineDecreased outputLight-colored or black stoolsFlatulenceChange in bowel habitsDry, yellow skinBruisingRUQ or epigastric painNumbness, tinglingPruritusImpotenceAmenorrhea-Cognitive-perceptual: dull, right upper quadrant or epigastric pain; numbness, tingling of extremities; pruritusSexuality-reproductive: impotence, amenorrhea


    • Objective data
    • Fever, cachexia, wasting of extremitiesIcteric sclera, jaundicePetechiae, ecchymosesSpider angiomas, palmar erythema Alopecia, loss of axillary and pubic hairPeripheral edemaShallow, rapid respirationsEpistaxisAbdominal distention, ascitesDistended abdominal wall veinsPalpable liver and spleenFoul breathHematemesis; black, tarry stoolsHemorrhoidsAltered mentationAsterixisGynecomastiaTesticular atrophyImpotenceLoss of libidoAmenorrhea, vaginal bleeding
  48. ** Cirrhosis Labs:
    Anemia, thrombocytopenia, leukopenia↓ Serum albumin and potassium levels

    Abnormal liver function studies

    ↑ INR

    ↑ Ammonia and bilirubin levels

    Abnormal findings on abdominal ultrasonography or MRI

    = > Perform a focused physical assessment for the following clinical manifestations:

    Possible diagnostic findings: anemia, thrombocytopenia; leukopenia; ↓ serum albumin level, ↓ potassium level; abnormal liver function studies; ↑ INR, ↑ ammonia level, and ↑ bilirubin levels; abnormal abdominal ultrasound study or MRI
  49. CIRRHOSIS  ND & Plannng
    Imbalanced nutrition: less than body requirements related to anorexia, nausea, impaired utilization and storage of nutrients

    Impaired skin integrity related to peripheral edema, ascites, and pruritus

    Excess fluid volume related to portal hypertension and hyperaldosteronism

    Ineffective self-health management related to ineffective coping and abuse of alcohol

    Dysfunctional family processes related to abuse of alcohol and inadequate coping skills as evidenced by deterioration in family relationships, family denial, neglected obligations, inability to accept and receive help appropriately

    • **Nursing Management Planning
    • Overall goalsRelief of discomfortMinimal to no complicationsReturn to as normal a lifestyle as possible
  50. Cirrhosis Health promotion
    Reduce or eliminate risk factorsTreat alcoholismMaintain adequate nutritionIdentify and treat acute hepatitisBariatric surgery for morbidly obese==Common risk factors for cirrhosis include alcohol, malnutrition, viral hepatitis, biliary obstruction, obesity, and right-sided heart failure. Prevention and early treatment of cirrhosis must focus on reducing or eliminating these risk factors. Alcoholism must be treated. Urge patients to avoid alcohol ingestion, and support their efforts.Adequate nutrition, especially for alcoholic and other individuals at risk for cirrhosis, is essential to promote liver regeneration. Identify and treat acute hepatitis early so that it does not progress to chronic hepatitis and cirrhosis. Bariatric surgery for morbidly obese individuals has been shown to occurrences reduce liver disease.
  51. **Nursing Management: Acute intervention
    Rest needs:
    Prevent complications, Modify schedule -> Nutritional needsOral hygieneBetween-meal nourishmentFood preferencesExplanation of dietary restrictions

    => The focus of nursing care for the patient with cirrhosis is on conserving the patient’s strength while maintaining muscle strength and tone. When the patient requires complete bed rest, implement measures to prevent pneumonia, thromboembolic problems, and pressure ulcers. Modify the activity and rest schedule according to signs of clinical improvement (e.g., decreasing jaundice, improvement in liver function studies).Anorexia, nausea and vomiting, pressure from ascites, and poor eating habits all create problems in maintaining an adequate intake of nutrients. Oral hygiene before meals may improve the patient’s taste sensation. Make between-meal nourishments available so that they can be taken at times when the patient can best tolerate them. Provide food preferences whenever possible. Explain the reason for any dietary restrictions to the patient and caregiver.
  52. jaundice & paracentesis
    • => Measures to relieve pruritus
    • Cholestyramine or hydroxyzine
    • Baking soda or Alpha Keri baths
    • Lotions, soft or old linen
    • Temperature control
    • Short nails; rub with knuckles=> Monitor color of urine and stools

    NOTES: Nursing assessment and care should include the patient’s physiologic response to cirrhosis. Is jaundice present? Where is it observed: sclera, skin, hard palate? What is the progression of jaundice? If the jaundice is accompanied by pruritus, measures to relieve itching should be carried out. Cholestyramine (Questran) or hydroxyzine (Atarax) may be ordered to help relieve the pruritus. Measures to help alleviate pruritus include baking soda or Alpha Keri baths; applying lotions containing calamine; antihistamines; soft or old linen; and control of the temperature (not too hot and not too cold). Keep the patient’s nails short and clean. Teach patients to rub with their knuckles rather than scratch with their nails when they cannot resist scratching.Note the color of the urine and stools. When jaundice is present, the urine is often dark brown and foamy when shaken. The stool is gray or tan.

    • Accurate I/O recording
    • Daily weight measurementExtremities measurementAbdominal girth measurement

    => Edema and ascites are frequent manifestations of cirrhosis and necessitate nursing assessments and interventions. Accurate calculation and recording of intake and output, daily weights, and measurements of extremities and abdominal girth help in the ongoing assessment of the location and extent of the edema. The abdomen should be marked with a permanent marker so that girth is measured at the same location.

    • **Paracentesis
    • Patient voids immediately before
    • High Fowler’s position or sitting on side of bed
    • Monitor for fluid and electrolyte imbalances
    • Monitor dressing for bleeding/leakage
    • => Immediately before a paracentesis, have the patient void to prevent a puncture of the bladder. When a paracentesis is done, the patient sits on the side of the bed or is placed in high Fowler’s position. Following the procedure, monitor for hypovolemia and electrolyte imbalances, and check the dressing for bleeding and leakage.
  53. **LIVER BIOPSY:
    1. Description: A needle is inserted through theabdominal wall to the liver to obtain a tissuesample for biopsy and microscopic examination.

    • 2. Preprocedure
    • a. Assess results of coagulation tests (prothrombintime, partial thromboplastin time, plateletcount).b. Administer a sedative as prescribed.c. Note that the client is placed in the supine orleft lateral position during the procedure toexpose the right side of the upper abdomen.

    • 3. Postprocedure
    • a. Assess vital signs.b. Assess biopsy site for bleeding.c. Monitor for peritonitis (see Box 56-3).d. Maintain bedrest for several hours.e. Place the client on the right side with a pillowunder the costal margin to decrease therisk of hemorrhage, and instruct the clientto avoid coughing and straining.f. Instruct the client to avoid heavy lifting andstrenuous exercise for 1 week.
  54. **LIVER CANCER (HEPATOCELLULAR CARCINOMA)
    • Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer.

    • The manifestations are similar to cirrhosis, making it difficult to diagnose in its early stage.

    • Prevention of liver cancer is focused on identification and treatment of chronic viral hepatitis (B and C). Treatment of chronic alcohol ingestion may also lower the risk of liver cancer.

    • Treatment of liver cancer depends on the size and number of tumors, presence of spread beyond the liver, and age and overall health of the patient. Overall the management is similar to that for cirrhosis.
  55. **LIVER TRANSPLANTATION
    • Indications for liver transplant include chronic viral hepatitis, alcoholic liver disease, congenital biliary abnormalities (biliary atresia), inborn errors of metabolism, HCC (confined to the liver), NAFLD, and acute hepatic failure.

    • Postoperative complications of liver transplant include bleeding, rejection, and infection.

    • The patient who has had a liver transplant requires highly skilled nursing

    Liver disease related to chronic viral hepatitis is the leading dindication for liver transplantation. Other indications: congential biliary abnormalities (biliary atresia), inborn errors of metabolism, livercancer, sclerosing cholangitis, acute liver failure and chronic end stage liver disease.

    Liver transplant candidates must o through a rigiourous presurgery screening: to confirm diagnosis of endstage liver disease and to assess for other comorbdidies (cardioascular disease, chronic kkidney diseas)

    Contradindications for liver transplant incllude severe extrahepatic disease, advanced hepatocellular carcinoma or other cancer, ongoing drug or alcohol abuse, and inability to comprehend or ocmply with the rigourous postransplant course. because of the scarcity of abialable livers, a donor liver may be divided into two parts (split liver transplant) and implanted into two recipeients.

    Immunosuppressive therapy generally involves a combination of corticosteroids (prednisone), a calcineurin inhibitor (cyclsprine or tacrolimus) and an antiproliferative agnt (azathioprine).

    Tacrolimus appears to be superior to cyclosporine in liver traansplantantion.

    • The pt who has had a transplant requires highly skilled nursing care (ICU): post op nursing care: asssessing neuro status, monitoring for signs of hemorrhage, preventing pulmonary complications, monitoring drainage, electolyte lev es, urine output, and monitoring for signs and symptoms of infection and rejection.
    • => commong resp problems: pneumonia, atelectasis, pleural effusions. TCDB, IS, repositioning.
    • => measuring the drainage
    • =First two months critical for montitoring infection. Can be viral, fungal or bacterial.

    Approximately 78% of pts survive more than 5 years after a liver transplant. Describe the collaborative care of the patients undergoing liver transplant.

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