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

2. Normal Liver

6. Label:

7. 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

8. Liver

9. 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)

10. 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

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

14. Liver disease

15. 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

16. 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

17. Jaundice- Note yellow eyes

18. 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 days

20. 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)

21. Hepatitis C

24. 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

25. Acute and chronic hepatitis

26. 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

27. 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

28. 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

29. 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

30. 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)

31. Cirrhosis of the liver

32. Cirrhosis

33. Cirrhosis

34. Cirrhosis

35. 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

36. 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)

38. 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

39. 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

40. Ascites with dilated veins

41. Ascites

42. Ascites

44. 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)

45. Esophageal varices

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

49. 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

50. 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

51. Asterixis- liver flap

52. 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

53. Cirrhosis Therapeutic Interventions cont
Medications:
Avoid toxic drugs- sedatives, hynotics, actaminophen, and alcohol
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

54. Cirrhosis: Therapeutic interventions cont
Dietary and fluid
Restricted fluid Na intake based on response to diuretic therapy, urine output and electrolyte values
Surgery
Surgery to treat complications
Liver transplant (p 593)

55. Liver biopsy

56. Liver transplant

57. Liver transplant

58. 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

59. Cirrhosis: Pertinent Nursing problems
Excess fluid volume
Disturbed thought process
Ineffective protection
Impaired skin integrity
Imbalanced nutrition: less than body requirements
Home care

60. Liver Failure