Cirrhosis
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Cirrhosis

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Cirrhosis Cirrhosis Presentation Transcript

  • GI: 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
  • 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
  • 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 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
  • 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. 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
  • 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 *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
  • 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)
  • 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