Liver Disease

Submitted By Ivonne-Avitia
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Pages: 17
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Liver: Largest internal organ and gland
Gerontologic Consideration of Liver Disease
Increase liver disease rate with age because of liver structure changes with age
Decrease liver volume – Because liver size will change with age
Decrease in hepatobilary function
Decrease drug metabolism: which increases the vulnerability for drug-induced hepatitis and increase risk for drug interactions
Decrease ability to respond to injury
Hepatitis
Most common cause for liver inflammation is viral infection
Acute Infection:
Inflammation causes damage liver cell and may develop into hepatic cell necrosis.
If there are no complications, the liver cells can regenerate and regain its normal appearance and function.
Chronic Infection:
Last longer than 6 months
May persist for years
Continuous inflammation and damage done to the liver will slowly develop into liver cirrhosis, then liver failure, and then liver cancer.
Clinical Manifestations:
Acute Phase: 1-4 Months: Icteric Phase
Jaundice begins
Clay Color stools
Convalescence Phase: Post-Icteric phase (healing phase)
Jaundice starts to disappear
Last about 2-4 months.
Major complaint is easy fatigue and malaise.
Priority Nursing Diagnosis:
Activity Intolerance r/t decrease physical energy and strength.

Recovery Phase: Most patients recover completely
Chronic Infection/Condition:
Develops into: Chronic hepatitis, Cirrhosis, Hepatic Failure, Heptocellular cancer
Assessment:
Health History:
Medications: Some medications that can be toxic to the liver
Physical Assessment:
Normal liver cannot be palpated
Percussion is used to determine if the liver is normal size. (8 to 10cm)
Diagnosis:
Liver Enzyme:
Elevated ALT and GTT
Alk Phos will be elevated.
Damaged liver cells release alk. Phos. Enzymes
Protein will be decrased because the liver is unable to produce the proteins
Increase Bilirubin
Indirect or unconjugated bilirubin
Prolonged prothrombin time (increase clotting time): because the liver is unable to produce clotting factors.
*IMPORTANT CONCEPT* RBC are broken down, broken down in 3 pieces , globin, iron, heme. Heme will be further broken down into greenish pigment call biliverdin, quickly converted to yellow pigment call bilirubin. This bilirubin is known as indirect /Unconjugated bilirubin(In the blood). This bilirubin will go into the liver by binding with albumin(transporter), and once it enters the liver, it will mix with glucuronic acid. The glucuronic acid will make the indirect/unconjugated bilirubin into more solid form call direct/conjugated bilirubin. Will go back into the biliary system and mix with bile and use the biles for digestive process.
*If you understand the concept, then you understand how this works* That is why patients with hepatitis will have elevated indirect/unconjugated bilirubin because the liver cannot process all that unconjugated bilirubin, and that is also why the patient has clay color stools. This is also why the person looks jaundice.

Patient who have uncompatable blood transfusion will have pre-hepatic jaundice
Patient who has viral hepatitis or cirrhosis will have hepatic jaundice
Patient who problems with the biliary system(gallbladder and pancreas), they will have First-Hepatic Jaundice.
General Home Care:
Not everyone goes to hospital when they have mild or moderate case of hepatitis and go through home remedy.
Rest
Well Balanced Diet
Low Fat, High carbohydrate, High Protein
Maintain fluid & electrolyte balance
Vitamin supplement: B-Complex(help regenerate liver tissues)
Viral Hepatitis
6 types of hepatitis virus: A-E, & G
To determine which viral antibody a patient has, it will depend on what antigen and antibodies are found in the system.
Hepatitis A(HAV)
Transmitted through fecal to oral route (touching feces, putting it in the mouth)
37% of outbreaks of HepA are from eating contaminated food or drinking contaminated water.
Risk Factors:
Poor hygiene
Improper handling of foods
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