Liver Flashcards
carbohydrate metabolism
Glycogen to glucose (glycogenolysis)
glucose to glycogen (glycogenesis)
New glucose from AA&FA (gluconeogenesis)
protein metabolism
synthesis of amino acids and clotting factors
fat metabolism
synthesis of lipoproteins
breakdown of triglycerides and cholesterol
steroid metabolism
conjugation and excretion of gonadal and adrenal corticosteroid hormones
Assessment of viral hepatitis
Usually manifests initially with Influenza-like symptoms
HA, fatigue, low grade fever, RUQ abd pn, N/V
HBV can present with additional symptoms such as hepatomegaly, signs of billiary obstruction Clay colored stools,(b/c conjugated bilirubin can’t flow out of liver d/t obstruction or inflammation of the bile ducts) dark urine (bilirubin excreted into kidneys), jaundice,
elevated bilirubin & liver enzyme levels
Petichie
puritis b/c bile salts
icterus yellowing of eyes
ascites
digestion will be hard
forms of jundace
- Prehepatic– cause- massive hemolysis
Transfusion reactions, sickle cell anemia - Hepatic – cause – liver unable to conjugate or excrete bilirubin
Hepatitis, cirrhosis, metastatic CA, prolonged use of drugs metabolized by liver - Post Hepatic– in biliary & pancreatic disorders
Nursing interventions viral hepatitis
A. 10. Nursing Interventions
Implement Contact Isolation Precautions
Education re: Prevention of transmission
Assess activity intolerance – Bedrest promotes hepatic healing
Assess fluid & electrolyte status
Nutrition – increase calories & carbohydrates, low fat
Alcohol use?
causes of cirrhosis
Alcohol Abuse
Chronic Viral Hepatitis
Autoimmune Hepatitis
Staetohepatitis
Damage to the liver by drugs, toxins, and other infections
Chronic biliary cirrhosis (bile duct obstruction, bile stasis, and hepatic fibrosis)
Cardiac cirrhosis- Cause?
A - secondary to severe R sided heart failure inc. necrosis & fibrosis d/t lack of blood flow
S&S Cirrhosis
Early: Fatigue, Wt loss, N/V, diarrhea, RUQ abdominal pain
Late: Pruirtis build up of bile salts, Confusion( build up of ammonia in blood liver is unable to get rid of) GI bleeding (varices develop and bleed causing vomiting blood and passing blood in stool, Ascites(fluid in abdomen),Jaundice, Petechiae and spider angiomas, dependent peripheral edema(red pin point lesions from decreased synthesis of PT d/t deteriorating liver function) neuro changes(Asterixis(liver flapping tremor) Fetor Hepaticus (liver breath) is a fruity or musty odor
Cirrhosis diagnosis
Liver biopsy is most definitive
Abdominal films may show hepatomegaly, enlarged spleen and ascites
Serum enzymes- ALT, AST, ALP elevate- ALT and AST are elevated initially due to hepatic inflammation and then normal when liver cells are no longer able to create an inflammatory response . ALP increases in cirrhosis due to intrahepatic biliary obstruction.
Bilirubin levels are elevated in cirrhosis due to the inability of the liver to excrete bilirubin.
Serum proteins and serum albumin are lowered due to the lack of hepatic synthesis
Ammonia increases d/t hepatocellular injury(cirrhosis) prevents the conversion of ammonia to urea for excretion
CBC, WBC and platelets decreased secondary to anemia
PT/INR prolonged due to decreased synthesis of prothrombin
complication of cirrhosis Portal Hypertension
Portal Hypertension is elevated venous pressure in the PORTAL vein, which is part of the PORTAL circulation.
Blood flow meets increased resistance within portal or hepatic vascular system secondary to hepatic damage.
Caused by compression, mechanical obstruction/occlusion of hepatic veins. (portal or hepatic vascular system).
other complications of cirrhosis
Esophageal submucosal venous channels become enormously dilated secondary to portal HTN
May protrude into the esophageal lumen
If ruptures or overlying mucosa ulcerates then torrential hemorrrhage onto esophagus & stomach with hematemesis
other complications of cirrhosis Fulminating Hepatitis-
Fulminating Hepatitis- fatal form of hepatitis due to the inability of the liver cells to regenerate with increased progression of the necrotic process.
Hepatic Encephalopathy – increased ammonia enters circulation
Portal systemic encephalopathy (PSE) and death
Monitor for: neuro changes,Fluids & Electrolytes,comfort measures
Result is hepatic encephalopathy and death
Treatment of Hepatic Encephalopathy- a complication of cirrhosis- a terminal condition whereby liver damage causes increased ammonia to enter circulation. Without liver detoxification function, ammonia crosses blood brain barrier & produces neurologic toxic manifestations(lethargy,stupor,coma)
Give Lactulose-therapeutic effect- creates quick passage of stool
Eliminates ammonia-decreases serum ammonia levels
Treatment for Hepatic Encephalopathy
Damaged liver unable to detox and convert ammonia to less toxic form, ammonia enters circulation & ammonia crosses blood brain barrier & produces neurologic toxic manifestations
Give Lactulose
Give Neomycin & Flagyl
CirrhosisNursing Interventions
Comfort measures
What diet is needed? High kcal/mod. Fat/ low Na/low pro
Supplements-Boost,Ensure
Vitamins because liver can’t store them
If serum sodium is low fluids may be restricted
What about alcohol? Can I have just one drink?-AA-Diuretics-monitor for hypokalemia and hypotension
Medications sparingly (opiods, sedatives, barbituates) – metabolism of med in liver
Monitor bleeding complications- Labs & adm blood
Replaces blood volume and clotting factors.
Comfort measures
What diet is needed? High kcal/mod. Fat/ low Na/low pro
Supplements-Boost,Ensure
Vitamins because liver can’t store them
If serum sodium is low fluids may be restricted
What about alcohol? Can I have just one drink?-AA-Diuretics-monitor for hypokalemia and hypotension
Medications sparingly (opiods, sedatives, barbituates) – metabolism of med in liver
Monitor bleeding complications- Labs & adm blood
Replaces blood volume and clotting factors.
