GI: Liver Hepatitis and Cirrhosis

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GI Liver Hepatitis and Cirrhosis

• Marnie Quick, RN, MSN, CNRN

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Normal Liver
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Label
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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

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Liver
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• Symptoms of liver failure appear when 80 liver
  destroyed
• Liver can regenerate itself if adequate nutrition
  and no alcohol

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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)

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2. Bile synthesis secretion- Bile aids
digestion/absorption fats in small intestine.
Indirect bilirubin broken down excreted
stool 3. Storage- Vitamin A, all Bs, D, E, and
K 4. Regulates blood coagulation-Forms
prothrombin, fibrinogen, heparin If decrease Vit
K fibrinogen increase fibrinolysis, decrease
plateletsgt hemorrhage 5. Detoxification -Rids
body of endogenous waste- drugs, bacteria, etc 6.
Heat production 7. Phagocyte action- breakdown
old RBC, WBC, bacteria
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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

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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 SS SS last 2 months
  post exposure dose IG-immune globulin given IM
  within 2 wks of exposure
• Prevent by handwashing!

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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 than HIV
• Incubation 6-25 wks
• 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

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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)

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Hepatitis C
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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

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Hepatitis Common manifestations/complications

• Incubation phase- no symptoms
• Preicteric- Flu-like sym NV
• 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

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Jaundice- Note yellow eyes
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Acute and chronic hepatitis
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Hepatitis Collaborative care

• Diagnostic tests
• ALT (specific liver) AST (liver/heart)-
  elevated- enzymes released into blood liver cell
  damaged
• Bilirubin- elevated from impaired metabolism or
  obstruction hepatobiliary ducts
• Albumin- decreased in liver damage affects
  clotting
• Viral antigens specific antibioties
• Liver biopsy- chronic hepatitis
• Medications- vaccines post exp prophylaxis
• Acute hepatits treatments- BR adeq nutrition
  avoid toxic substances as alcohol

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Hepatitis Pertinent Nursing Problems
Interventions

• Risk for infection (transmission)
• Educatevaccineshandwashing,body fluid
  precaution
• Report health department food handlers and child
  care workers with Hepatitis A
• Activity intolerance- adeq rest- maybe gt 4 wks
• Imbalanced nutrition-less small,freq,calorieCHO
• Ineffective therapeutic regimen management
• Home care
• Educate avoid hepatic toxins, need for follow-up

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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) postnecrotic
  (hepatitis B or C toxic substances) cardiac

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Stages of alcohol-induced liver damage
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Cirrhosis
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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

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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 to increase blood flow

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TIPS procedure- Note shunt that will divert
blood- relieving hypertension esophegeal varcies
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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)

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Esophageal varices
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Sengstaken Blackmore tubeInflate gastric
balloon Esophageal balloon and third one to
aspirate stomach
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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

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Ascites with dilated veins
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Ascites
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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

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Hepatic encephalopathy-- continued

• Stages 1. personality changes, irritability
  2. hyperreflexia (liver
  flap-asterixis) violent/abusive behavior 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

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Asterixis- liver flap
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Liver Failure
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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

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Liver biopsy
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Cirrhosis Therapeutic
Interventions cont

• Medications
• Avoid drugs metabolized by the liver and drugs
  toxic to liver- 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

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Cirrhosis Therapeutic
interventions cont

• Dietary and fluid
• Restricted fluid/Na intake based on response to
  diuretic therapy, urine output and electrolyte
  values
• Hi calories Hi CHO low fat
• Surgery
• Surgery to treat complications
• Liver transplant (Lewis p 1087)

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Liver transplant
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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

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Cirrhosis Pertinent Nursing
problems/Care

• Health promotion
• Patient family teaching guides
• Acute intervention
• Ambulatory home care
• Imbalance nutrition less than body reequirements
• Dysfunctional family process alcoholism
• Excess fluid volume
• Potential complication hemorrhage hepatic
  encephalopathy

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