RNSG 2432 ONLINE NOTES
Module 14: Gastrointestinal: Liver- Hepatitis/Cirrhosis of the liver
Marnie Quick, RN, MSN, CNRN (Revised 3/09)
*These notes are an expansion of the Lewis textbook and required
references. They are met to be used together.
Etiology/Pathophysiolgy
1.
Normal liver physiology as it relates to hepatitis/cirrhosis of the liver (Lewis
p. 931, Fig 39-4, Fig 39-5 and p. 932 Table 39-1)
a. Carbohydrate metabolism1)
Conversion of glucose to glycogen, breakdown of glycogen
to glucose, formation of glucose from protein and fats.
2)
Glucose level depends on livers’ ability to remove glucose
from blood, store it, break it down, and release it again.
b. Protein metabolism1)
Protein breakdown begins in the GI track where ammonia is
formed by the breakdown of protein (from food or blood in
the GI track) by the bacteria in the GI track. The ammonia
is normally converted by the liver to form urea.
2)
Liver synthesizes plasma proteins- prothrombin, fibrinogen,
and albumin (these alter blood clotting and serum osmotic
pressure) Increased calorie intake helps increase this
synthesis.
c. Fat metabolism1)
Synthesis of lipoptoteins and of fatty acids from amino acids
and glucose.
2)
Synthesis and breakdown of cholesterol.
3)
Breakdown of triglycerides into fatty acids and glycerol.
4)
Formation of ketone bodies
d. Steroid metabolism1)
Estrogens are unmetabolized and deactivated by the liver
and excreted in bile.
2)
Aldosterone metabolism- if liver not working get increased
levels and this causes Na and H2O retention.
3)
Steroids should be used with caution in patient with liver
disease.
e. Bile formation and secretion (1L/day)- (Lewis p 932 Fig 39-6)
1)
Bile is produced in liver and secreted into the biliary lobules
which in turn drain into the ducts to the gallbladder. The
gallbladder stores and concentrates the bile which aides in
the digestion of fats
2)
Formation of bile salts/pigments (bilirubin) which aids in
digestion and absorption of fats in small intestine.
3)
Unconjugated or indirect bilirubin is broken down to
urobilinogen (in small intestines) which is excreted in stool
and gives it it’s color
f. Storage1)
Fat soluble Vitamins A, D, E, and K and water soluble B’s,
minerals, amino-acids, and fatty acids
2)
Glucose in the form of glycogen
g. Regulates blood coagulation-
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1)
2.
3.
4.
Liver forms blood constituents and maintains flow of blood.
prothrombin, fibrinogen, and heparin.
2)
In liver disease have decrease of Vit K and fibrinogen which
causes increased fibrinolysis and decreased platelets which
leads to hemorrhage
h. Detoxification1)
Some drugs (such as sedatives, alcohol) are metabolized in
the liver
2)
In liver failure, endogenous products accumulate in blood,
lead to hepatic coma
i. Heat production- 2nd only to muscle tissue.
j. Phagocyte action- breakdown of old RBC’s (hemoglobin to bilirubin),
WBC’s, and bacteria.
Individual will begin to show symptoms when 80% liver destroyed
The liver can regenerate itself (depending on the amount of damage) and if
adequate nutrition and no hepatotoxins- alcohol/drugs
Liver has dual blood supply to lobules (Lewis p. 931 Fig 39-5)
a. Hepatic artery carries one third of oxygenated blood to liver
b. Portal vein from the stomach, intestines, spleen and pancreas carries
two thirds partly oxygenated blood to the liver. It also carries
absorbed products of digestion directly to the liver.
Hepatitis
Etiology/Pathophysiology of Hepatitis
1.
Hepatitis is inflammation of the liver caused by:
a. Viral- most common cause of inflammation of the liver.
1) Acute- HAV; HBV; HCV; HDV; HEV; HGV
2) Chronic- Hepatitis B, C, and D can cause a chronic form.
Chronic is the primary cause of liver damage leading to
cirrhosis and liver cancer
3) Only way to diagnosis viral type is presence of antigens and
antigenic subtypes and antibodies to them in blood.
b. Hepatotoxic: drugs and chemicals directly damage liver which result
in necrosis. Hepatotoxins include chronic alcohol abuse; drugs such
as acetaminophen, statins, sulfonamides, methotrexate; chemicals
such as benzene, carbon tetrachloride (Lewis 934 Table 39-6)
c. Hepatobillary- Disruption of the flow of bile out of the liver.
d. Other causes: autoimmune liver disease, bacterial, other viriuses.
e. Hepatitis can cause hepatic cell necrosis and can progress to liver
cancer, cirrhosis- end stage liver disease. Systemic effect: rash,
arthritis, fever, and malaise
2.
Viral hepatitis (Lewis 1090 Table 44-2)
a. Hepatitis A virus (Infectious hepatitis)(Lewis 1090 Fig 44-2)
1) Fecal-oral transmission. Ingestion of infected food/liquid.
2) Contaminated food, water, shelfish, unsanitary conditions,
direct contact with infected person, infected food handler.
3) Prevent spread by handwashing!!!!
4) Individual is contagious through stool up to 2 wks before
symptoms appear and 1-2 wks after.
5) Incubation period 2-7 weeks.
6) Onset abrupt, benign and self-limiting, symptoms last up to 2
months; liver usually repairs itself so no permanent effects.
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7) No chronic state of Hepatitis A and infected individual has
immunity to HAV. Blood test shows IgG anti-HAV in blood.
8) Vaccine- 2 doses IM
9) Postexposure prophylaxis- standard IG-immune globulin, IM
within 2 weeks of exposure.
10) 2/2/2/2 rule- 2 doses IM to prevent; S&S last 2 months;
contagious 2 wks before S&S; post exposure dose given IM
within 2 wks of exposure.
b. Hepatitis B (Lewis 1091 Fig 44-3)
1) Blood and body fluid transmission
2) Perinatally by mothers infected with HBV; percutaneously by
health care workers exposure to blood and needle sticks; IV
drug users; by exposure to infectious blood or other body
fluids (semen, vaginal secretions, saliva)- unprotected sex;
men who have sex with other men; body piercing, tattoos;
and individuals exposed to blood products as hemodialysis,
and with organ transplantation.
3) Onset symptoms slower and more severe than Hep A
4) Frequently seen with HIV. More infectious than HIV. Can live
on dry surface 7 days
5) Contagious before and after symptoms appear continues 4-6
months; in carriers continues for individual’s lifetime.
6) Incubation period 6-25 weeks
7) Liver damage is by immune response to ‘B’ antigen.
8) Increased risk for primary liver cancer; causes acute and
chronic hepatitis or fulminant hepatitis.
9) Vaccine- 3 doses IM, 4-6 weeks apart.
10) Post exposure- hepatitis B immune globulin, IM in 2 dosesdose 1st within 24 hrs-7 days post exposure; dose #2 28-30
days post exposure. Vaccine series should be started
11) May become chronic carrier. HBsAG positive two times 6
months apart. As a chronic carrier need to have liver
function monitored. Drugs used: (text 1094 Table 44-7)
a) Alpha-Interferon: multiple effects on the viral
replication cycle. Long-acting form given subq once
wk and has many side effects.
b) Nucleoside analogs: Lamivudine, Adefovir, and
Entecavir suppress HBV replication by inhibiting viral
DNA synthesis. Taken orally decreases viral load,
liver damage, and decreases liver enzymes. If stop
drugs may seroconvert and have liver inflammation.
Individual may develop resistant to drugs.
c. Hepatitis C (formerly known as non A, non B)
1) Blood and body fluid transmission
2) IV drug users (primary cause), tattoos, body piercing,
unprotected sex, perinatal contact, exposure to infected
blood/body fluid.
3) Symptoms mild and nonspecific
4) Primary worldwide cause of chronic hepatitis, cirrhosis, and
liver cancer. May be 10-20 year delay between infection and
clinical appearance of liver damage.
5) No vaccine
6) Greater risk of chronic HCV than HBV.
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7) Because there are many subtypes of HCV- genotyping of the
virus needs to be done before beginning drug therapy.
8) Drug therapy: pegylated alpha-interferon (subq) given alone
or with ribavirin (oral- has many side effects). Together
have synergistic effect. Can be treated as long as liver not
decompensated.
9) Many with HIV also have HCV- drug interactions may occur
d. Hepatitis D, E and G are other viral forms. (Text 1090 Table 44-2)
e. 80% of liver cancer are caused by Hepatitis B and C.
3. Fuminant Hepatitis- rapidly progressive form that causes severe impairment
of liver (possible liver failure) with hepatic encephalopathy. Most common
cause, drugs: acetaminophen/alcohol/INH/; HBV second; also caused by
mushroom poisoning
Common Manifestations/Complications of Hepatitis
1.
Many forms are asymptomatic
2.
Incubation Phase- after exposure to virus, no symptoms
3.
Acute phase of hepatitis (1-4 months)- Jaundice, ‘Flu-like’ symptoms,
general malaise, fatigue, muscle and body aches; GI symptomsnausea/vomiting, diarrhea/constipation; mild right upper abdominal pain;
chills and fever. (Text 1092, Table 44-3)
4.
Not all with viral hepatitis have jaundice. Jaundice is the result of bilirubin
diffusing into the tissue, urine dark for same reason, stool light color due to
blockage of bile release from liver. Pruritus with jaundice due to
accumulation bile salts.
5.
Convalescent phase begins as jaundice disappears (lasts wks to months)
Major problem is malaise and relapse may occur.
6.
There is some difference in symptoms with different types of Hepatitis.
7.
Local effect on liver: hepatic cell necrosis; Systemic effect: rash, arthritis,
fever, and malaise
8.
Physical assessment- palpable liver with hepatic tenderness, hepatomegaly,
and splenomegaly
9.
Most all cases of HAV resolve. HBV and HCV can result in chronic life-long
viral infection.
10. Healing generally within 3-16 wks. Uncomplicated cases recovery occurs
within 2 wks of jaundice
11. Complications of hepatitis include: fulminant hepatic failure, chronic
hepatitis, cirrhosis of the liver, hepatocellular carcinoma. Are dependent on
a variety of factors, such as type of virus and health of the individual.
Collaborative Care of Hepatitis (Lewis 1094 Table 44-6 Diagnostic/Collaborative)
1.
Diagnostic tests
a. Tests for viral hepatitis- Variety of blood tests for specific antigens,
antibodies (Text 1092 Table 44-4) and if acute infection, chronic
carrier. EIA and RIBA specific test for HCV.
b. Acute hepatitis (Lewis 1093 Table 44-5)
1) Liver function studies: Transaminase- ALT (specific to liver),
AST (liver and heart) Enzymes elevated because are released
into blood when liver cells are damaged.
2) Serum billrubin- elevated in viral hepatitis because of
impaired bilirubin metabolism. Elevated with obstructed
hepatobilary ducts due to inflammation and edema
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2.
3.
4.
5.
3) Prothombin time- prolonged PT due to decreased absorption
of vitamin K in intestine
c. Sonogram- to see degree of liver scarring.
d. Liver biopsy- May be done in chronic hepatitis- degree of
inflammation, fibrosis or cirrhosis (see nursing care for patient
undergoing biopsy with ‘Cirrhosis Notes’ below)
No specific treatment for acute viral hepatitis- rest and nutrition at home.
Drug Therapy (Lewis 1094 Table 44-6)
a. Antiemetic- Dramamine, Tigan
b. Sedative- Benadryl
c. HAV and HBV vaccines available. HBV given to high-risk group.
d. Post-exposure prophylaxis recommended for household and sexual
contacts of individuals with HAV or HBV
e. Chronic HBV: Interferon, Nucleoside analogs (See above HBV notes)
f. Chronic HCV: pegylated Alpha-interferon, Ribavirin (See HCV notes)
Prevention (Lewis 1098 Table 44-9 p. 1100 Table 44-10)
a. HAV: General measures, use of Immune Globulin
b. HBV/HCV: Percutaneous and sexual transmission, general measures
Nutritional Therapy
a. High-calorie, high-protein, high-CHO, low fat diet
b. Vitamin supplement
c. Avoid alcohol intake and drugs toxic to liver
Nursing Assessment Specific to Hepatitis
1.
Nursing Assessment (Lewis 1096 Table 44-8)
a. Subjective data
b. Objective data
Pertinent Nursing Problems and Interventions for Hepatitis
2. Nursing Care Plan (Lewis 1097-8 Table 44-1)
a. Imbalanced nutrition
b. Activity intolerance
c. Ineffective therapeutic regimen management
3. Nursing Implementation
a. Health promotion
b. Acute intervention- jaundice and rest
c. Ambulatory and Home care
4. Control of Hepatitis in Health care personnel - Hepatitis A, B, C
Cirrhosis of the Liver
Etiology/Pathophysiology of Cirrhosis
1.
2.
3.
4.
Cirrhosis is the end stage of chronic liver disease. It is progressive and
usually is irreversible and results in liver failure. (Lewis 1102 Fig 44-4)
Functional liver tissue is destroyed and replaced by fibrous scar tissue.
As hepatocytes are destroyed, metabolic functions are lost; blood and bile
flow within liver is disrupted and portal hypertension develops.
Alcoholic/nutritional cirrhosis- Most common cause
a. Alcohol is hepatotoxic; alcohol abuse with resultant lack of nutrition.
b. Stage 1: Metabolic changes affect fatty metabolism, fat accumulates
in liver- fatty liver. In this early stage, abstinence from alcohol could
allow liver to heal.
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5.
6.
7.
c. Stage 2: With continued alcohol use, inflammatory cells infiltrate the
liver causing necrosis, fibrosis and destruction of liver tissue.
d. Stage 3: Regenerative nodules form and the liver shrinks.
Postnecrotic cirrhosis
a. Post chronic hepatitis B or C, toxic substances or autoimmune cause
extensive liver cell loss and fibrosis.
Biliary cirrhosis
a. Chronic biliary obstruction causing fibrosis of the liver.
b. Jaundice primary symptom.
Cardiac cirrhosis
a. Severe long-standing rt-sided heart failure causes backup to portal
circ
Common Manifestations of Cirrhosis (Lewis 1104 Fig 44-6)
1. Early
a. Insidious onset, GI symptoms, abdominal pain, enlarged liver, weak
2. Late (Text 1103 Fig 44-5 p. 1104 Fig 44-6))
a. Jaundice- can’t form and excrete bilirubin
b. Skin lesions- spider angiomas with hormone changes
c. Hematologic problems caused by splenomegaly
d. Endocrine problems because liver can’t metabolize hormones
e. Peripheral neuropathy- tend to be sensory- from dietary deficiency
Complications of Cirrhosis/Treatment
1. Portal hypertension
a. Fibrous connective tissue in the liver disrupt blood and bile flow. This
causes restrictive blood flow from the inferior vena cava and
compression of the portal and hepatic veins- portal hypertension
b. Blood flow is obstructed, increasing pressure in the veins.
c. Major problems result from portal hypertension--d. Veins in the esophagus, rectum and abdomen become
engorged/congested, resulting in esophageal and gastric varices.
e. With this backup of blood, also have acites, splenomegaly, peripheral
edema, anemia and low WBC/platelet (increased blood cell
destruction) see below
f. Treatment: medications to control hypertension; diuretics to
decrease fluid retention and acites; TIPS procedure to shunt blood
2. Esophageal and gastric varices
a. Dilated tortuous veins at the lower end of esophagus (80%) and
upper portion of the stomach (20%) caused by portal hypertension.
b. Occurs in about 60% of individuals with cirrhosis.
c. Major concern- uncontrolled massive bleeding from fragile veins.
d. Treatment- Medications
1) IV Vasopressin to control bleeding.
2) Beta blockers- to prevent bleeding of varices. (Inderal)
3) H2 receptor blockers (Zantac); proton pump inhibitors
(Protonix); Antibiotics; Inderal prevent recurrent GI bleed
4) Blood replacement if bleeding- fresh frozen plasma to restore
clotting factors
5) Vitamin K for correction of clotting abnormalities.
e. Treatment1) Avoid alcohol, aspirin, irritating/course foods
2) Avoid coughing, anything that increases pressure on varices
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f.
Treatment1) Surgical ligation of varices
2) Endoscopic sclerotherapy-during endoscopy a sclerosing drug
is injected into the veins to thrombosis distended veins
3) Banding- during endoscopy small rubber bands placed on
sclerotic veins to occlude blood flow.
g. Treatment- Transjugular Intrahepatic Portosystemic Shunt (TIPS
procedure) (Lewis p 1109 Fig 44-11)
1) Balloon catheter is inserted through the jugular vein to the
hepatic vein
2) A channel made in the liver and the expandable stent is
inserted into channel
3) Allows blood to flow from portal vein into hepatic vein,
bypassing the cirrhotic liver
4) This relieves pressure in the esophageal veins and helps
control fluid retention.
5) Used as short term measure until liver transplant
h. Treatment- Sengstaken Blakemore tube- balloon tamponade (Lewis
1109 Fig 44-10) Applies direct pressure on bleeding varices.
1) Physician inserts tube down the mouth into the esophagus.
2) Three lumens- one for gastric aspiration; one inflates
esophageal balloon (25-30 mmHg); and third one inflates
gastric balloon (250 ml air)
3) Tension (traction) is needed to keep to tube in place.
4) Endotracheal tube may be inserted to maintain airway
5) Do not leave in place more than 48 hrs
6) Suction secretions- can not swallow- risk for aspiration.
3. Splenomegaly
a. Spleen enlarges as blood shunted into splenic vein
b. Blood cells destroyed- anemia, leukopenia, thrombocytopenia
c. Treatment- treat portal hypertension
4. Ascites and Peripheral edema (Lewis 1105 Fig 44-8; Table 44-11)
a. Ascites- accumulation of plasma-rich fluid in the abdominal cavity.
b. Portal hypertension causes an impairment of liver synthesis of
albumin (hypoalbuminemia) and the accumulation of albumin in
peritoneal cavity. Also with the decrease in renal blood flow have an
increase in aldosterone which results in sodium and water retention.
c. Assess- abdominal distention (girth) and weight gain
d. Peripheral edema can also occur because of portal hypertension, it is
seen in ankle and sacral areas.
e. Treatment- diet: high carbohydrate and protein, low-fat, low-sodium.
f. Treatment- Medications: diuretics (Aldactone); Salt-poor albumin to
help maintain intravascular volume and output
g. Treatment- Paracentesis
1) Considered a temporary treatment for acites
2) Physician inserts a needle into abdominal cavity to remove
large amounts of fluid (& protein)
3) Obtain weight, take VS, and patient void before
4) Watch for bleeding after procedure
5) Salt-poor albumin may be given after to replace lost protein
h. Treatment- Peritoneovenous Shunt
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1) Shunt with one-way valve inserted from the abdominal cavity
to the jugular vein (Lewis 1108 Fig 44-9)
5. Hepatic encephalopathy
a. Caused by accumulated neurotoxins in blood; ammonia produced in
gut is not converted to urea and accumulates in blood; medications
may not be metabolized and add to mental changes.
b. The ammonia is formed in the GI track by the breakdown of protein
(from food or blood in the GI track from varices) by the bacteria in
the GI track. The ammonia is normally converted by the liver to form
urea. Because the liver is nonfunctioning there is a buildup of
ammonia in the blood and ammonia crosses the blood brain barrier
and causes the symptoms of encephalopathy.
c. Grading scale for hepatic encephalopathy (Lewis 1106 Table 44-13)
1) From 0-4 and includes level of conscious, intellectural function
and neurologic findings such as asterixis (liver flap).
d. May also have fetor hepaticus- musty sweet odor on breath from
digestive by-products liver unable to digest.
e. Considered terminal complication of cirrhosis.
f. Treatment
1) Treatment aimed at decreasing ammonia level.
2) Enemas q 6 hrs to decrease ammonia absorption
3) Lactulose is a laxative and it also causes an acid environment
in the GI track. It decreases ammonia level by decreasing the
bacteria in bowel that normally convert protein to ammonia.
It also causes a more acid environment so that ammonia is
converted to ammonium-- which is a more nonabsorble form.
The ammonia and ammonium then are excreted in the stool
(3-4 stools a day). This decreases the ammonia in the blood,
decreasing the symptoms of hepatic encephalopathy. Given
orally or by enema.(p.591)
4) Neomycin- intestinal antiseptic to achieve sterile bowel- this
decreases the bacteria in bowel that normally convert protein
to ammonia. Given orally or enema. Other antibiotics- Flagyl,
Vancomycin may be used.
5) If the liver patient is experiencing severe symptoms of
encephalopathy then decrease protein intake. If he is not,
then encourage an increase in protein to help with repair of
the damaged liver.
6. Hepatorenal syndrome
a. Generally felt to be caused by decreased blood to the kidney as a
result of hepatic portal hypertension causing renal failure- decreased
urine output, increased BUN and creatine.
Collaborative Care for Cirrhosis (Lewis 1107 Table 44-15)
1. Diagnostic tests
a. Liver biopsy- determine liver cell changes
1) Pre biopsy nursing care: Check lab- PT, platelet count,
*coagulation studies, may need Vitamin K to correct
2) Explain procedure.
3) NPO 4-6 hrs and empty bladder prior.
4) Place in supine position on far right side of bed; turn head to
left and extend arm above head.
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5) Post biopsy- pressure applied to site, place on right side to
maintain site pressure, watch for bleeding
6) VS every 2 hrs
7) Food and fluid withheld for 2 hrs post test
8) Avoid coughing, lifting, or straining for 2 weeks
b. CT, liver ultrasound
c. Enzyme levels- ALT, AST elevated initially with the liver damage; in
end-stage may be normal
d. Total protein and albumin decreased in Cirrhosis
e. Serum bilirubin increased; prothrombin time prolonged
2. Drug Therapy (Text 1110 Table 44-16)
3. Nutritional therapy Diet
a. High calories with high CHO, low fat
b. High protein diet -only time not to is when in extreme hepatic
encephalopathy
c. May need NG feeding to meet body demands
4. Liver transplant
Nursing Assessment Specific for Cirrhosis
1. Nursing assessment (Lewis 1111 Table 44-17)
a. Subjective data
b. Objective data
Pertinent Nursing Problems and Interventions for Cirrhosis
2. Nursing implementation
a. Health promotion- educate regarding underlying cause
b. Patient/family teaching guide (Lewis 1115 Table 44-18)
c. Acute intervention
d. Ambulatory home care
3. Nursing Care Plan (Lewis 1112-3 NCP 44-2)
a. Imbalanced nutrition less than body requirements
b. Impaired skin integrity
c. Dysfunctional family process: alcoholism
d. Excess fluid volume
4. Collaborative problems (Lewis 1113 NCP 44-2 at bottom of page)
a. Potential complications- hemorrhage
b. Potential complications- hepatic encephalopathy
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