Med Surg Chapt 39: Hepatic Disorders

Created by ElizabethRVazquez 

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35 terms · Assessment and Management of Patients with Hepatic Disorders

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

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