GI: Liver Hepatitis and Cirrhosis Marnie Quick, RN, MSN, CNRN

Normal Liver

Label:

Answers from previous slide A. Liver B. Hepatic vein- blood from liver C. Hepatic artery- oxygenated blood to liver D. Portal vein- partly O2 blood to liver E. Common bile duct F. Stomach G. Cystic duct H. Gallbladder

Liver

Symptoms of liver failure appear when 80% liver destroyed Liver can regenerate itself if adequate nutrition and no alcohol

Liver functions 1. Metabolic functions CHO- liver removes glucose from blood, stores it as glycogen, breaks it down to release glucose PRN Protein- converts ammonia to urea** Protein (food/blood) is 1st broken down by bacteria in GI to form ammonia. Ammonia to liver which converts to urea. Fat- ketogenesis. (see next slide- bile) Steriod- aldosterone metabolism (liver damage= inc levels aldosterone causing Na & H2O retention)

2. Bile synthesis & secretion- Bile aids digestion/absorption fats in small intestine. Indirect bilirubin broken down & excreted stool 3. Storage- Vitamin A, all B’s, D, E, and K 4. Regulates blood coagulation**-Forms prothrombin, fibrinogen, heparin If decrease Vit K & fibrinogen= increase fibrinolysis, & decrease platelets> hemorrhage 5. Detoxification** -Rids body of endogenous waste- drugs, bacteria, etc 6. Heat production 7. Phagocyte action- breakdown old RBC, WBC, bacteria

Hepatitis- inflammation of the liver Etiology/pathophysiology Viral- most common cause Hepatitis A,B,C,D, E Chronic- Hep B,C,D primary cause liver damage Fuminant- rapidly progressive form- Hep B, D Toxic- hepatotoxins directly damage liver chronic alcohol abuse, drugs- acetaminophen, chemicals Hepatobillary- disruption flow bile out liver

Viral hepatitis Hepatitis A Fecal-oral transmission Contaminated food, unsanitary conditions, water, shelfish, direct contact with infected person Onset abrupt, flu-like symptoms before jaundice Liver repairs itself- no chronic state 2/2/2/2 Rule: 2 doses vaccine IM to prevent; contagious 2 wks before S&S; S&S last 2 months; post exposure dose IG-immune globulin given IM within 2 wks of exposure Prevent by handwashing!

Viral Hepatitis Hepatitis B Blood and body fluid transmission Health care workers*, IV drug users, multiple sex partners, men who have sex each other, body piercing, tattoos, exposure to blood products (hemodialysis). Freq seen HIV. Hep B is more infectious than HIV Incubation 6-25 wks Risk for liver cancer, chronic & fulminant hepatitis and becoming a chronic carrier Vaccine 3 doses IM 4-6 wks apart Post exposure- hep B immune globulin IM 2 doses: 1st dose 1-7 days post exposure; 2nd 28-30 days

Viral Hepatitis: Hepatitis C (formally non A, non B) Blood and body fluid transmission IV drug users (primary); body piercing, tattoos Worldwide cause of chronic hepatitis, cirrhosis and liver cancer Initial symptoms mild, nonspecific 10-20 year delay between infection and clinical appearance of liver damage Interferon alpha to reduce risk of chronic C with Ribavirin (oral antiviral)

Hepatitis C

Viral Hepatitis: Hepatitis D and E Blood body fluid transmission Transmitted with Hepatitis B Causes acute and chronic hepatitis Hepatitis E Oral-fecal transmission Contaminated water supply in developing countries Rare in USA

Hepatitis Common manifestations/complications Incubation phase- no symptoms Preicteric- Flu-like sym & N&V Icteric- 5-7 days post preicteric- jaundice sclera, skin, & mucous; pruitius; clay colored stools; brown urine (elevated bilirubin) Posticteric (convalescent)- serum bilirubin & enzymes return normal; energy level inc; no pain Complications some hepatitis- cirrhosis, liver failure

Jaundice- Note yellow eyes

Acute and chronic hepatitis

Hepatitis: Collaborative care Diagnostic tests ALT (specific liver); AST (liver/heart)- elevated- enzymes released into blood liver cell damaged Bilirubin- elevated from impaired metabolism or obstruction hepatobiliary ducts Albumin- decreased in liver damage; affects clotting Viral antigens & specific antibioties Liver biopsy- chronic hepatitis Medications- vaccines; post exp prophylaxis Acute hepatits treatments- BR; adeq nutrition; avoid toxic substances as alcohol

Hepatitis: Pertinent Nursing Problems & Interventions Lewis 1097 Table 44-1 Risk for infection (transmission) Educate:vaccines;handwashing,body fluid precaution Report health department food handlers and child care workers with Hepatitis A Activity intolerance- adeq rest- maybe > 4 wks Imbalanced nutrition-less: small,freq,calorieCHO Ineffective therapeutic regimen management Home care Educate; avoid hepatic toxins, need for follow-up

Cirrhosis of the liver: Etiology/pathophysiology End stage of chronic liver disease Functional liver tissue destroyed and replaced by fibrous scar tissue Metabolic functions are lost; blood and bile flow in liver is disrupted, portal hypertension develops Types: Alcoholic/nutritional (common); biliary (chronic biliary obstruction); postnecrotic (hepatitis B or C; toxic substances); cardiac

Stages of alcohol-induced liver damage

Cirrhosis

Alcoholic/nutritional cirrhosis Most common cause of cirrhosis with resultant lack of nutrition Stage 1: metabolic changes affect fatty metabolism, fat accumulates in liver. In this stage abstinence from alcohol could allow liver to heal Stage 2: With continued use of alcohol, inflammatory cells infiltrate the liver causing necrosis, fibrosis and destruction of liver Stage 3: regenerative nodules form liver shrinks

Cirrhosis of liver: Complication & treatment Portal hypertension Fibrous connective tissue in liver disrupt blood and bile flow. Portal and hepatic veins become compressed. With backup of blood have acites, splenomegaly, peripheral edema, increase blood cell destruction- anemia, low WBC and low platelets Treatment: medication to control hypertension, diuretics to decrease fluid retention/acites and TIPS procedure to increase blood flow

TIPS procedure- Note shunt that will divert blood- relieving hypertension & esophegeal varcies

Cirrhosis: complication & treatment Esophageal varices As a result of portal hypertension, veins in esophagus, rectum and abdomen become engorged/congested resulting in esophageal and gastric varices (major concern- can bleed out) 60% esophageal varices occur with cirrhosis Treat- Medications: vasopressin (control bleeding), beta blockers (prevent bleeding), blood replace, Vit K Surgery: shunt (TIPS), ligation varices, banding Sengstaken-Blakemeore tube (tamponade bleeding)

Esophageal varices

Esophageal varcies

Sengstaken Blackmore tube: Inflate gastric balloon; Esophageal balloon; and third one to aspirate stomach

Cirrhosis: Complications and treatment Splenomegaly, acites and peripheral edema Spleen enlarges from blood shunted from portal hypertension. Blood cells destroyed As liver impairment of synthesis of albuium occurs have accumulation plasma-rich fluid in abd cavity- acites (abd distention & wt gain) Treat acites- diuretics (aldactone), paracentesis, diet (hi CHO, hi protein (stage?), low fat, low Na

Ascites with dilated veins

Ascites

Cirrhosis: Complications & treatment Hepatic encephalopathy Protein (from food or blood in GI) is broken down (with the aid of bacteria) in GI to ammonia Liver then converts ammonia to urea and is excreted by kidneys With liver failure have accumulation of ammonia in blood. Ammonia then enters brain and interferes with function of brain- encephalopathy

Hepatic encephalopathy continued Stages:1. personality changes, irritability 2. hyper reflexia (liver flap) violent/abusive beh 3. coma Treat: Enemas decrease ammonia absorption Lactulose- a laxative that decreases ammonia by decreasing the bacteria in bowel that normally converts protein to ammonia. Causes 3-4 stools/day Neomycin- intestinal antiseptic to decrease bacteria Decrease protein intake

Asterixis- liver flap

Liver Failure

Cirrhosis: Therapeutic intervention Diagnostic tests- Liver function test ALT, AST- not as high as hepatitis; CBC platelets (anemia, thrombocytopenia) Coagulation studies (lack Vit K- prolonged PT) Bilirubin (elevated); ammonia (elevated) Serum albumin (hypoalbuminemia) Abdominal ultrasound (liver size/nodular, ascitis) Esophagoscopy- varices Liver biopsy(p 590) not done if bleeding time elevated

Liver biopsy

Cirrhosis Therapeutic Interventions cont Medications: Avoid toxic drugs- sedatives, hynotics, actaminophen, and alcohol. Drugs metabolized by the liver. Diuretics to reduce ascites Lactulose (laxative) and neomycin (antibiotic) to dec ammonia- hepatic encephalopathy Vit K to reduce risk bleeding Beta-blockers to prevent esophegeal varices from rebleeding Ferrous sulfate and folic acid to treat anemia Antacids decrease acute gastritis

Cirrhosis: Therapeutic interventions cont Dietary and fluid Restricted fluid/Na intake based on response to diuretic therapy, urine output and electrolyte values Hi calories; Hi CHO; low fat Surgery Surgery to treat complications Liver transplant (p 593)

Liver transplant

Cirrhosis: Nursing Assessment specific to Cirrhosis Health history Current symptoms, altered bowel; excess bleeding; abdominal distention; jaundice; pruritus; history liver or gallbladder disease; alchohol history Physical assessment VS; mental status, color skin; peripheral pulses and edema; abd assessment; bowel sounds; abd girth; tenderness and liver size

Cirrhosis: Pertinent Nursing problems/Care Health promotion Patient family teaching guides Acute intervention Ambulatory home care Imbalance nutrition less than body reequirements Dysfunctional family process: alcoholism Excess fluid volume Potential complication: hemorrhage; hepatic encephalopathy