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GI: Liver Hepatitis and Cirrhosis

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

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GI: Liver Hepatitis and Cirrhosis

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

  2. Normal Liver

  3. Label:

  4. 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

  5. Liver

  6. 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)

  7. Liver functions continued: • 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

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

  9. Liver disease

  10. 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

  11. 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

  12. Jaundice- Note yellow eyes

  13. 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 • Incubation 6-24 months • 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

  14. 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)

  15. Hepatitis C

  16. Viral Hepatitis: Hepatitis D and E • Hepatitis D • 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

  17. Acute and chronic hepatitis

  18. 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

  19. Hepatitis: Therapeutic Interventions • Diagnostic tests • ALT (specific liver); AST (liver/heart)- enzymes released into blood liver cell damaged • Bilirubin- elevated from impaired metabolism or obstruction hepatobiliary ducts • Viral antigens & specific antibioties • Liver biopsy- chronic hepatitis (590) • Medications- vaccines; post exp prophylaxis • Acute hepatits treatments- BR; adeq nutrition; avoid toxic substances as alcohol

  20. Hepatitis: Nursing Assessment specific to Hepatitis • Health history- • current symptoms, exposure to hepatitis, high risk activities; current medications • Physical assessment- • vital signs (temperature); color sclera/skin/stool; abdominal tenderness; GI- N&V

  21. Hepatitis: Pertinent Nursing Problems & Interventions • Risk for infection (transmission) • Educate:vaccines;handwashing,body fluid precaution • Report health department food handlers and child care workers with Hepatitis A • Fatigue- adeq rest- maybe up to 4 wks • Imbalanced nutrition-less: small,freq,calorieCHO • Disturbed body image- jaundice, itching • Home care • Educate; avoid hepatic toxins, need for follow-up

  22. 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) and posthepatic (hepatitis B or C; toxic substances)

  23. Cirrhosis of the liver

  24. Cirrhosis

  25. Cirrhosis

  26. Cirrhosis

  27. 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

  28. Cirrhosis of the liver:Common manifestations, complications and treatment of complications • Early sings – enlarged, tender liver. Dull ache in RUQ, weight loss, weakness, anorexia • Progress to all systems effected (p. 587)

  29. 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 (p. 593) to increase blood flow

  30. 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

  31. Ascites with dilated veins

  32. Ascites

  33. Ascites

  34. 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)

  35. Esophageal varices

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

  37. 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

  38. 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

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