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Med Surg Chapt 39: Hepatic Disorders

Assessment and Management of Patients with Hepatic Disorders
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asterixis
involuntary flapping movements of the hands associated with metabolic liver dysfunction
fetor hepaticus
sweet, slightly fecal odor of the breath; intestinal origin; seen with extensive collateral portal circulation in chronic liver disease
hepatic encephalopathy
CNS dysfunction d/t liver disease; associated with elevated ammonia levels that produce changes in mental status, altered LOC and coma
liver regulates?
glucose and protein metabolism
liver manufactures and secretes?
bile--important in the digestion and absorption of fats in the GI tract; stored in gallbladder
anatomy of the liver
largest gland in body; located in the upper right abdomen; 4 lobes; highly vascular, receives blood from GI tract via portal vein (80%, nutrient rich but low in O2) and hepatic artery (20%, rich in O2)
metabolic functions
glucose metabolism; ammonia conversion; protein metabolism; fat metabolism; vitamin and iron storage
bile formation; bilirubin excretion; drug metabolism
liver function studies
used to asses pts with liver disease. more than 70% of the parenchyma of the liver may be damaged before LFT results become abnormal
serum aminotransferases
sensitive indicators of injury to the liver cells, useful in detecting acute liver disease (hepatitis). AST (aspartate aminotransferase); ALT (alanine aminotransferase); GGT (gamma-glutamyl transferase); GGTP (G-glutamyl transpeptidase); LDH
additional diagnostic studies
liver biopsy, ultrasonography, CT, MRI
hepatic dysfunction
results from damage to the liver's parenchymal cells. can be acute or chronic (more common)
chronic liver disease
includes cirrhosis of the liver, twice as high in men, more common in Asian and African countries; compensated cirrhosis (liver able to perform normal function) goes undetected
causes of chronic liver disease
malnutrition r/t alcoholism (most common), infection, anoxia, metabolic disorders, nutritional deficiencies, hypersensitivity states
manifestations of chronic liver disease
jaundice; portal hypertension, ascites, varices (distended veins); hepatic encephalopathy or coma; nutritional deficiencies
jaundice
yellow or green tinged body tissues; sclera and skin d/t increased serum bilirubin levels
types of jaundice
hepatocellular and obstructive most associated with liver disease; hemolytic and hereditary hyperbilirubinemia
s/s associated with hepatocellular jaudice
may appear mild or severely ill
lack of appetite, nausea, weight loss
malaise, fatigue, weakness
headache, chills and fever if infectious in origin
s/s associated with obstructive jaundice
dark orange-brown urine and light clay-colored stools
dyspepsia (upset stomach) and intolerance of fats, impaired digestion
pruritis
portal hypertension
elevated pressure in the portal circulation d/t obstruction of venous flow into and through the liver. Results in ascites and esophageal varices
assessment of ascites
record abdominal girth and weight daily
pt may have straie, distended veins, umbilical hernia
percuss for shifting dullness or by fluid wave
monitor for fluid/electrolyte imbalances
treatment of ascites
low sodium diet; diuretics (spironolactone is 1st line); bed rest; paracentesis; adm salt-poor albumin; tranjugular intrahepatic portosystemic shunt (TIPS)
post paracentesis patient discharge teaching
monitor for bleeding/excessive drainage from puncture site, avoid heavy lifting/straining to allow puncture site to close, change position slowly d/t risk of hypovolemia r/t fluid removal, monitor for fever to detect infection.
hepatic encephalopathy and coma
life threatening complication; d/t accumulation of ammonia and other toxic metabolites in blood
assessment of hepatic encephalopathy and coma
EEG, changes in LOC (assess neuro status freq.), potential seizures, fector hepaticus, monitor fluid, electrolyte, ammonia levels
medical management of hepatic encephalopathy and coma
lactulose (reduce serum ammonia levels), IV glucose (minimize protein catabolism), protein restriction, gastric suction, enemas, oral antibx (reduce ammonia from GI tract), d/c sedatives, analgesics, tranquilizers
bleeding esophageal varices
occurs in 1/3 of pts with cirrhosis and varices; 1st bleed mortality rate of 30-50%; life-threatening, results in hemorrhagic shock that produces decreased cerebral, hepatic, renal profusion
bleeding esophageal varices: clinical manifestations
hematemesis, melana (black tarry feces), shock (cool clammy skin, hypotension, tachycardia), general deterioration, hx of alcoholism common, pts with cirrhosis should be screened via endoscopy q 2 yrs.
management of patient with bleeding esophageal varices
monitor emotional response, cognitive status, hepatic encephalopathy (d/t blood breakdown in the GI tract), delirium (r/t alcohol WD). monitor tube care, GI suction, oral care
hepatitis
viral hep: systemic viral infection, causes necrosis and inflammation of liver cells
nonviral hep: toxic and drug induced
Hep A (HAV)
fecal-oral transmission; incubation 15-50 days; last 4-8 weeks; manifestations: mild flu like symptoms, low grade fever, anorexia, later stage: jaundice and dark urine, indigestion, epigastric distress, enlarged liver and spleen. anti-HAV antibody in serum after symptoms appear
Hep B (HBV)
transmitted through blood, saliva, semen, vaginal secretions, sexually transmitted, to infant at birth. cause of cirrhosis and liver cancer
management: prevention via vaccines, passive immunization, standard precautions, screen blood and blood products
Hep C
transmitted via blood, sex, needles; most common blood borne infection, cause of 1/3 cases of liver cancer and common reason for liver transplant.
avoid alcohol and meds that effect liver as causes disease progression
Hep D
Only persons with Hep B at risk for Hep D; transmit through blood and sex; more likely to develop fulminant liver failure and chronic active hepatitis and cirrhosis
Hep E
transmit via fecal oral route, resembles Hep A
fulminant hepatic failure
rare, fatal in 1-2% of cases, fatality increase >60 yo, sudden, severe onset of acute liver failure, occurs w/i 8 weeks after the fist symptoms of jaundice