livercirrhosis-100728074944-phpapp02.pptx

Very simple

1. Liver Cirrhosis DR. HARSH JOSHI

2. Liver Cirrhosis a chronic, degenerative disease characterized by replacement of normal liver tissue with diffuse fibrosis that disrupts the structure and function of the liver MTCAT '10

3. Liver Cirrhosis Types: Alcoholic Cirrhosis ( Laennec’s Cirrhosis) Most common type of liver cirrhosis Caused by chronic alcoholism Postnecrotic cirrhosis Late result of a previous bout of acute viral hepatitis Biliary cirrhosis Resulted from chronic biliary obstruction and infection Least common type MTCAT '10

4. Liver Cirrhosis Predisposing/ Precipitating factors: malnutrition effects of alcohol abuse chronic impairment of bile excretion – biliary obstruction in the liver and common bile duct (gallbladder stones) necrosis from hepatotoxins or viral hepatitis Congestive heart failure MTCAT '10

5. Liver Cirrhosis Pathophysiology : liver cell damage result in inflammation & hepatomegaly attempts at regeneration eventually result to fibrosis and a small nodular liver hepatic function is slowly impaired obstruction of venous channels blocks hepatic blood flow and cause portal hypertension MTCAT '10

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9. Clinical Manifestations S/ Sx - early : anorexia, nausea, indigestion aching or heaviness in right upper quadrant weakness & fatigue Assessment: MTCAT '10

10. Clinical Manifestations Late signs : abnormal liver function tests:  bilirubin (N= 0-0.9 mg/dl) , AST (N=4.8-19U/L) ALT (N= 2.4-17U/L) Serum alkaline phosphatase (N=30-40U/L) Ammonia (plasma) (N= 15-45umol/L) intermittent jaundice, pruritus edema, ascites , prominent abdominal wall veins Ecchymosis , bleeding tendencies anemia Infection Gynecomastia , testicular atrophy Neurologic changes MTCAT '10

11. Complications of Liver Cirrhosis 1. Ascites abnormal intraperitoneal accumulation of watery fluid containing small amounts of protein due to : intravascular colloidal pressure  capillary hydrostatic pressure Na and H 2 O retention Failure of the liver to metabolize aldosterone MTCAT '10

12. Ascites S/ sx : abdominal enlargement,  wt. fatigue abdominal discomfort, respiratory difficulty Med. Mgt. (depending on severity of ascites ) Na+ & fluid restriction (500-1000 ml/day) diuretic therapy ( furosemide / spironolactone ) Paracentesis – for diagnosis or when fluid volume compromise comfort & breathing MTCAT '10

13. Nursing Interventions to  ascites & increase/promote comfort maintain on bed rest fluid & Na restriction monitor I/O, daily wt. measure abd . girth every shift maintain on high-Fowlers for max. respiration support abdomen with pillows administer diuretics, salt-poor albumin IV as ordered - monitor for signs of CHF, pulmonary edema, dehydration, electrolyte imbalance, hypersensitivity reaction Assist with Paracentesis have the client void before the procedure high –fowlers position during the procedure monitor pt. for hypovolemia & electrolyte imbalance observe puncture wound for leakage & signs of infection Ascites MTCAT '10

14. . Hepatic Encephalopathy cerebral dysfunction assoc. with severe liver disease inability of the liver to metabolize substances that can be toxic to the brain such as ammonia , which is produced by the breakdown of protein in the intestinal tract Complications of Liver Cirrhosis MTCAT '10

15. BRAIN LIVER Toxic N2 metabolites From Intestines Pathogenesis of Hepatic Encephalopathy MTCAT '10

16. Hepatic Encephalopathy S/ Sx : Asterixis - flapping hand tremors ---early sign  LOC – lethargy progressing to coma  mental status, confusion, disorientation dullness, slurred speech behavioral changes, lack of interest in grooming/ appearance twitching, muscular incoordination , tremors Fetor hepaticus elevated serum ammonia level MTCAT '10

17. Hepatic Encephalopathy Interventions: a. )  ammonia production  dietary protein to 20-40 g/day, maintain adequate calories  ammonia formation in the intestine – give laxative, enema as ordered and Neomycin -  bacterial ammonia production b.) Protect pt. from injury side rails up turning to side assess mental status, LOC proper positioning (semi-Fowler’s) prevent aspiration c.) Prevent further episodes of encephalopathy low protein diet prescribed medications avoid constipation ( to  ammonia production by bacteria in the GIT) early signs of encephalopathy (restlessness, slurred speech, dec . attention span) MTCAT '10

18. 2 . Esophageal Varices distention of the smaller blood vessels of the esophagus as a result of portal hypertension – due to obstruction of venous circulation w/in the damaged liver the  portal venous pressure causes blood to be forced into these vessels – become tortous and fragile blood vessel become prone to injury by mechanical trauma from ingestion of coarse food and acid pepsin erosion which may result in bleeding Complications of Liver Cirrhosis MTCAT '10

19. Esophageal Varices S/ Sx : upper GI bleeding ( hematemesis ) - melena massive hemorrhage signs/symptoms of hypovolemic shock MTCAT '10