This document provides information about cirrhosis of the liver including its causes, stages of progression, complications, treatment, and nursing care considerations. Cirrhosis is the end stage of chronic liver disease where liver tissue is replaced by scar tissue, disrupting blood flow and metabolic functions. Common causes include alcoholism and hepatitis. Complications include portal hypertension, esophageal varices, ascites, and hepatic encephalopathy. Treatment focuses on managing complications, medications to reduce bleeding risk and ammonia levels, dietary changes, and potentially liver transplantation. Nursing care involves monitoring for symptoms, providing education, managing fluid balance and medications, and preventing complications.

1. GI: Cirrhosis
Marnie Quick, RN, MSN, CNRN

2. Normal Liver

5. Label:

6. 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

7. Liver

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

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. 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

12. 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

14. Stages of alcohol-induced liver damage

15. Cirrhosis

16. 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

18. 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

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

20. 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)

22. Esophageal varices

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

25. 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 albumin
occurs have accumulation plasma-rich fluid in
abd cavity- ascites (abd distention & wt gain)
 Treat ascites- diuretics (aldactone), paracentesis,
diet (hi CHO, low fat, low Na

26. Ascites with dilated veins

27. Ascites

28. 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

29. Hepatic encephalopathy-- continued
 Stages: 1. personality changes, irritability
2. hyperreflexia (liver flap-asterixis) violent/abusive
behavior 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

30. Asterixis- liver flap

31. Liver Failure

33. 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

34. Liver biopsy

35. Cirrhosis
Therapeutic Interventions cont
 Medications:
 Avoid *drugs metabolized by the liver and drugs toxic to liver-
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

36. 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 (Lewis p 1087)

37. Liver transplant

38. 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

39. 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