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GI: Liver Hepatitis and Cirrhosis

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Title: Changes in Peripheral Nervous System Author: Marnie Quick Last modified by: msquick Created Date: 10/2/2001 1:16:26 AM Document presentation format – PowerPoint PPT presentation

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Title: GI: Liver Hepatitis and Cirrhosis


1
GI Liver Hepatitis and Cirrhosis
  • Marnie Quick, RN, MSN, CNRN

2
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

29
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

36
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

43
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

46
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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