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HEPATIC DISORDERS NUR – 224
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LEARNING OUTCOMES Explain liver function tests. Relate jaundice, portal hypertension, ascites, varices, nutritional deficiencies to the pathophysiology of the liver. Use the nursing process as the framework for the care of the patient with cirrhosis of the liver
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LIVER Largest gland in the body /complex organ Located on the right side of the abdomen – anterior to the stomach Highly vascular organ Circulation of blood to the liver is of major importance. Multiple metabolic and regulatory functions
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ESSENTIAL FUNCTIONS Secretes bile Stores fat-soluble vitamins (A, B,D, and several B- complex vitamins) Metabolizes medication – barbiturates, opioids, sedatives, amphetamines, anesthetics Active in fat/protein metabolism. Releases glucose during times of hypoglycemia Takes up glucose during times of hyperglycemia and stores it as glycogen or converts it to fat Store iron as ferritin – which is released as needed for the production of RBC’s Converts ammonia to urea
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DIAGNOSTIC STUDIES Liver Function test Liver biopsy
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LIVER BIOPSY Performed to r/o metastatic cancer, detect cyst, or cirrhosis of the liver Considered minor surgery Results of coagulation test – PTT, PT, platelet count Signed consent Withhold any anticoagulants, ibuprofen, ASA – for a week prior to the procedure Food/fluids withheld 4-6 hours before the procedure Void prior to the procedure
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LIVER BIOPSY Post procedure Client lies on the right side, immobile for several hours Avoid coughing and straining Monitor vital signs Avoid heavy lifting, strenuous activity for 1 week
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COMMON MANIFESTATIONS OF LIVER DISORDERS Jaundice Ascites Portal hypertension Esophageal varices Hepatic encephalopathy
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Jaundice Disrupted metabolism/excretion of bilirubin accumulates in the tissues --jaundice yellow staining of the body tissues First noticeable in the sclera of the eyes, then the skin Concentration of bilirubin in the blood is abnormally increased Types Hemolytic Hepatocellular Obstructive
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Portal Hypertension Impaired/obstruction blood flow through the liver increases pressure in the portal venous system drains into the GI system, spleen and surface veins of the abdomen. Leads to: ascites esophageal varices
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Ascites Accumulation of serous fluid in the peritoneal/abdominal cavity Contributing factors portal hypertension, increase flow of hepatic lymph system, and hyperaldosteronism. Common manifestation of cirrhosis Large amounts albumin-rich fluid fills the peritoneal cavity (12-15 L)
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Manifestations of Ascites Abdominal distention Rapid weight gain Signs of dehydration Decrease in urine output Hypokalemia
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Treatment of Ascites Sodium restriction Diuretics Fluid removal - paracentesis Bedrest Shunt procedures – transjugular intrahepatic portosystemic shunt (TIPS)
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Esophageal Varices Develop on a majority of patients with cirrhosis Dilated, tortuous vessels that develop at the lower end of the esophagus Enlarged and swollen as a result portal hypertension Are responsible for approx 80% of variceal hemorrhages
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Bleeding Esophageal Varices Life threatening and led to shock Varices rupture and bleed in response to ulceration and irritation Contributing factors Clinical manifestations – hematemesis, melena, hx of alcohol abuse, s/s of shock may be present Diagnostic findings - endoscopy
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Treatment of Bleeding Varices Treatment of shock Oxygen IV fluids with electrolytes Vasopressin, somatostatin, octreotide Beta-blocker agents Balloon tamponade Endoscopic therapies
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Treatment
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Nursing Management Monitor patient condition physical, emotional and cognitive status Assess nutritional and neurologic status – increase ammonia levels drowsiness, confusion Monitor tube care and GI suction Oral care Quiet calm environment
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Hepatic Encephalopathy Impaired consciousness and mental status accumulation of toxic waste products in the blood blood bypasses the congested liver Ammonia is considered the major etiologic factor in the development of encephalopathy. Life threatening complication of liver disease Associated with portal hypertension and the shunting of blood from the portal venous into the systemic circulation
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Hepatic Encephalopathy Onset insidious Clinical manifestations early symptoms – minor mental changes/motor disturbances late symptoms – incomprehensible speech, marked confusion Asterixis Apraxia Fetor hepaticus
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Management Hepatic Encephalopathy Eliminate precipitating factors Administer lactulose as ordered Assess neurologic status frequently Monitor mental status Administer antibiotics Discontinue sedatives, analgesics and tranquilizers Prevent development of respiratory complications
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Cirrhosis Chronic progressive disease Normal liver tissue is replaced by fibrous liver tissue that disrupts the structure and function of the liver 12 th leading cause of death in the US Death rate is twice as high in men than women Native American men have the highest incidence and mortality rate from cirrhosis
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Pathophysiology Functional tissue is destroyed and replaced by fibrous tissue. Hepatocytes and liver lobules are destroyed, metabolic function of the liver is lost. Fibrous connective tissue forms constructive bands that disrupt blood and bile flow within the liver lobules Blood no longer flows freely through the liver to the IVC Restricted blood flow portal hypertension, increased pressure in the portal system
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Cirrhosis Types alcoholic – end result of alcoholic liver disease postnecrotic – results from chronic hepatitis B or C, NAFLD biliary – retained bile damages and destroys liver cells
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Clinical Manifestations Onset insidious Early signs Dull aching pain – epigastric area/RUQ Weight loss, weakness, Bowel function disrupted – diarrhea/constipation Late signs Impaired metabolism bleeding, ascites, jaundice, neurological changes, splenomeagly GI varices, edema, vitamin deficiency, and anemia
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Assessment & Diagnostic Findings Liver function tests Coagulation studies Serum electrolytes Serum ammonia levels CBC with platelets Abdominal ultra sound Liver biopsy
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Collaborative Care Medications Fluid Management/Nutrition
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Nursing Process Excess Fluid Volume Risk for Bleeding Impaired Skin Integrity Risk for Acute Confusion
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Practice Alert Monitor for signs of impaired renal function oliguria, central edema and increase in serum Crt/BUN. Closely monitor patient who have GI bleeding assess for signs of hepatic encephalopathy. Monitor the respiratory status of the patient with a Blakemore/Minnesota tube.
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