GI: Liver Hepatitis and Cirrhosis

Marnie Quick, RN, MSN, CNRN

Normal Liver

Label:

Answers from previous slide A. Liver B. Hepatic vein- blood from liver C. Hepatic artery- oxygenated blood to liver D. Portal vein- partly O2 blood to liver E. Common bile duct F. Stomach G. Cystic duct H. Gallbladder

Liver

Liver functions

1. Metabolic functions CHO- liver removes glucose from blood, stores it as

glycogen, breaks it down to release glucose PRN Protein- converts ammonia to urea**

Protein (food/blood) is 1st broken down by bacteria in GI to form ammonia. Ammonia to liver which converts to urea.

Fat- ketogenesis. (see next slide- bile) Steriod- aldosterone metabolism (liver damage= inc

levels aldosterone causing Na & H2O retention)

Liver functions continued: 2. Bile synthesis & secretion-

Bile aids digestion/absorption fats in small intestine Indirect bilirubin broken down & excreted stool

3. Storage- Vitamin A, all B’s, D, E, and K 4. Regulates blood coagulation**

Forms prothrombin, fibrinogen, heparin If decrease Vit K & fibrinogen= increase fibrinolysis, &

decrease platelets> hemorrhage

5. Detoxification** Rids body of endogenous waste- drugs, bacteria, etc

Symptoms of liver failure appear when 80% liver destroyed

Liver can regenerate itself if adequate nutrition and no alcohol

Liver disease

Hepatitis- inflammation of the liver Etiology/pathophysiology

Viral- most common cause Hepatitis A,B,C,D, E Chronic- Hep B,C,D primary cause liver damage Fuminant- rapidly progressive form- Hep B, D

Toxic- hepatotoxins directly damage liver chronic alcohol abuse, drugs- acetaminophen,

chemicals

Hepatobillary- disruption flow bile out liver

Viral hepatitis Hepatitis A Fecal-oral transmission Contaminated food, unsanitary conditions, water,

shelfish, direct contact with infected person Onset abrupt, flu-like symptoms before jaundice Liver repairs itself- no chronic state 2/2/2/2 Rule: 2 doses vaccine IM to prevent;

contagious 2 wks before S&S; S&S last 2 months; post exposure dose IG-immune globulin given IM within 2 wks of exposure

Jaundice- Note yellow eyes

Viral Hepatitis Hepatitis B Blood and body fluid transmission Health care workers, IV drug users, multiple sex partners,

men who have sex each other, body piercing, tattoos, exposure to blood products (hemodialysis). Freq seen HIV. Hep B is more infectious

Incubation 6-24 months Risk for liver cancer, chronic & fulminant hepatitis and

becoming a chronic carrier Vaccine 3 doses IM 4-6 wks apart Post exposure- hep B immune globulin IM 2 doses: 1st

dose 1-7 days post exposure; 2nd 28-30 days

Viral Hepatitis: Hepatitis C (formally non A, non B) Blood and body fluid transmission IV drug users (primary); body piercing, tattoos Worldwide cause of chronic hepatitis, cirrhosis

and liver cancer Initial symptoms mild, nonspecific 10-20 year delay between infection and clinical

appearance of liver damage Interferon alpha to reduce risk of chronic C with

Ribavirin (oral antiviral)

Hepatitis C

Viral Hepatitis: Hepatitis D and E

Hepatitis D Blood body fluid transmission Transmitted with Hepatitis B Causes acute and chronic hepatitis

Hepatitis E Oral-fecal transmission Contaminated water supply in developing countries Rare in USA

Acute and chronic hepatitis

Hepatitis Common manifestations/complications

Incubation phase- no symptoms Preicteric- Flu-like sym & N&V Icteric- 5-7 days post preicteric- jaundice sclera,

skin, & mucous; pruitius; clay colored stools; brown urine (elevated bilirubin)

Posticteric (convalescent)- serum bilirubin & enzymes return normal; energy level inc; no pain

Complications some hepatitis- cirrhosis, liver failure

Hepatitis: Therapeutic Interventions Diagnostic tests

ALT (specific liver); AST (liver/heart)- enzymes released into blood liver cell damaged

Bilirubin- elevated from impaired metabolism or obstruction hepatobiliary ducts

Viral antigens & specific antibioties Liver biopsy- chronic hepatitis (590)

Medications- vaccines; post exp prophylaxis Acute hepatits treatments- BR; adeq nutrition; avoid

toxic substances as alcohol

Hepatitis: Nursing Assessment specific to Hepatitis

Health history- current symptoms, exposure to hepatitis, high risk

activities; current medications

Physical assessment- vital signs (temperature); color sclera/skin/stool;

abdominal tenderness; GI- N&V

Hepatitis: Pertinent Nursing Problems & Interventions Risk for infection (transmission)

Educate:vaccines;handwashing,body fluid precaution Report health department food handlers and child

care workers with Hepatitis A Fatigue- adeq rest- maybe up to 4 wks Imbalanced nutrition-less: small,freq,calorieCHO Disturbed body image- jaundice, itching Home care

Educate; avoid hepatic toxins, need for follow-up

Cirrhosis of the liver: Etiology/pathophysiology

End stage of chronic liver disease Functional liver tissue destroyed and replaced by

fibrous scar tissue Metabolic functions are lost; blood and bile flow

in liver is disrupted, portal hypertension develops Types: Alcoholic/nutritional (common); biliary

(chronic biliary obstruction) and posthepatic (hepatitis B or C; toxic substances)

Cirrhosis of the liver

Cirrhosis

Cirrhosis

Cirrhosis

Alcoholic/nutritional cirrhosis Most common cause of cirrhosis with resultant

lack of nutrition Stage 1: metabolic changes affect fatty

metabolism, fat accumulates in liver. In this stage abstinence from alcohol could allow liver to heal

Stage 2: With continued use of alcohol, inflammatory cells infiltrate the liver causing necrosis, fibrosis and destruction of liver

Stage 3: regenerative nodules form liver shrinks

Cirrhosis of the liver:Common manifestations, complications and treatment of complications

Early sings – enlarged, tender liver. Dull ache in RUQ, weight loss, weakness, anorexia

Progress to all systems effected (p. 587)

Cirrhosis of liver: Complication & treatment Portal hypertension

Fibrous connective tissue in liver disrupt blood and bile flow. Portal and hepatic veins become compressed.

With backup of blood have acites, splenomegaly, peripheral edema, increase blood cell destruction- anemia, low WBC and low platelets

Treatment: medication to control hypertension, diuretics to decrease fluid retention/acites and TIPS procedure (p. 593) to increase blood flow

Cirrhosis: Complications and treatment Splenomegaly, acites and peripheral edema

Spleen enlarges from blood shunted from portal hypertension. Blood cells destroyed

As liver impairment of synthesis of albuium occurs have accumulation plasma-rich fluid in abd cavity- acites (abd distention & wt gain)

Treat acites- diuretics (aldactone), paracentesis, diet (hi CHO, hi protein (stage?), low fat, low Na

Ascites with dilated veins

Ascites

Ascites

Cirrhosis: complication & treatment Esophageal varices As a result of portal hypertension, veins in esophagus,

rectum and abdomen become engorged/congested resulting in esophageal and gastric varices (major concern- can bleed out)

60% esophageal varices occur with cirrhosis Treat-

Medications: vasopressin (control bleeding), beta blockers (prevent bleeding), blood replace, Vit K

Surgery: shunt (TIPS), ligation varices, banding Sengstaken-Blakemeore tube (tamponade bleeding)

Esophageal varices

Sengstaken Blackmore tube:Inflate gastric balloon; Esophageal balloon; and third one to aspirate stomach

Cirrhosis: Complications & treatment Hepatic encephalopathy

Protein (from food or blood in GI) is broken down (with the aid of bacteria) in GI to ammonia

Liver then converts ammonia to urea and is excreted by kidneys

With liver failure have accumulation of ammonia in blood. Ammonia then enters brain and interferes with function of brain- encephalopathy

Hepatic encephalopathy continued

Stages:1. personality changes, irritability 2. hyper reflexia (liver flap) violent/abusive beh 3. coma

Treat: Enemas decrease ammonia absorption Lactulose- a laxative that decreases ammonia by

decreasing the bacteria in bowel that normally converts protein to ammonia. Causes 3-4 stools/day

Neomycin- intestinal antiseptic to decrease bacteria Decrease protein intake

Asterixis- liver flap

Cirrhosis: Therapeutic intervention Diagnostic tests-

Liver function test ALT, AST- not as high as hepatitis; CBC platelets (anemia, thrombocytopenia) Coagulation studies (lack Vit K- prolonged PT) Bilirubin (elevated); ammonia (elevated) Serum albumin (hypoalbuminemia) Abdominal ultrasound (liver size/nodular, ascitis) Esophagoscopy- varices Liver biopsy(p 590) not done if bleeding time elevated

Cirrhosis Therapeutic Interventions cont Medications:

Avoid toxic drugs- sedatives, hynotics, actaminophen, and alcohol

Diuretics to reduce ascites Lactulose (laxative) and neomycin (antibiotic) to dec ammonia-

hepatic encephalopathy Vit K to reduce risk bleeding Beta-blockers to prevent esophegeal varices from rebleeding Ferrous sulfate and folic acid to treat anemia Antacids decrease acute gastritis

Cirrhosis: Therapeutic interventions cont

Dietary and fluid Restricted fluid Na intake based on response to

diuretic therapy, urine output and electrolyte values

Surgery Surgery to treat complications Liver transplant (p 593)

Liver biopsy

Liver transplant

Liver transplant

Cirrhosis: Nursing Assessment specific to Cirrhosis

Health history Current symptoms, altered bowel; excess bleeding;

abdominal distention; jaundice; pruritus; history liver or gallbladder disease; alchohol history

Physical assessment VS; mental status, color skin; peripheral pulses and

edema; abd assessment; bowel sounds; abd girth; tenderness and liver size

Cirrhosis: Pertinent Nursing problems

Excess fluid volume Disturbed thought process Ineffective protection Impaired skin integrity Imbalanced nutrition: less than body

requirements Home care

Liver Failure