Liver Disorders
John Nation, RN, MSN
Fall 2011
From the notes of
Charlene Morris, RN, MSN
Austin Community College
Overview of Today’s Lecture
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A & P Review
Hepatitis A
Hepatitis B
Hepatitis C
Cirrhosis
Portal Hypertension
Esophageal Varices
Hepatic Encephalopathy
Hepatorenal Syndrome
Liver Transplant
A and P Review
A and P Review
Largest internal organweighs around 3 lbs!
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A
B
C
D
E
Liver
Hepatic vein
Hepatic artery
Portal vein
Common bile
duct
F Stomach
G Cystic duct
H Gallbladder
Blood Supply – 2 sources

Hepatic artery:
– 500ml/min of oxygenated blood.
– 30% of Cardiac output goes to the liver
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Portal vein – 1000ml/min
– partly oxygenated blood supplies 50 - 60% O2
plus rich supply of nutrients, toxins, drugs
– from stomach, small and large intestines,
pancreas and spleen
Hepatic Blood Supply
(Cont’d)
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Both empty into
capillaries/sinusoids
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Liver filters the blood
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Hepatic vein to inferior vena cava
Lobule –
Functional unit of the liver
Capillaries
Metabolic Functions of
the liver
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“Body’s Refinery” Over 400 functions
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Primary role in anabolism and catabolism
Metabolic Functions of the Liver
1. Metabolism of Glucose
2. Protein Storage
3.
Fatty acids
4. Cholesterol
Other functions
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Immunologic
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Blood storage
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Plasma protein synthesis
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Clotting
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Waste products of hemoglobin
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Formation and secretion of bile
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Steroids and hormones
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Ammonia
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Drugs, alcohol and toxins metabolism
To Summarize….
The liver:
– changes food into energy
– removes alcohol and poisons from the
blood
– makes bile, a yellowish-green liquid that
helps with digestion
Hepatitis

Simply means inflammation of the liver
– “itis” means inflammation, “hepa” means
liver.

Viral hepatitis
– Most common cause
– Viral types include A, B, C, D, E, and G
Hepatitis

Other possible causes
– Drugs (alcohol)
– Chemicals
– Autoimmune liver disease
– Bacteria (rarely)
Hepatitis
Etiology

Causes
– A, B, C, D, E, and G virus
– Cytomegalovirus
– Epstein-Barr virus
– Herpes virus
– Coxsackie virus
– Rubella virus
Hepatitis A

Hepatitis A virus (HAV)
– RNA virus
– Transmitted fecal–oral route, parenteral
(rarely)
– Frequently occurs in small outbreaks
Hepatitis A


61,000 cases of hepatitis A occur
annually in the United States
10 million cases of hepatitis A occur
worldwide
– Nearly universal during childhood in
developing countries
Hepatitis A

Hepatitis A virus (HAV)
– Found in feces 2 or more weeks before
the onset of symptoms and up to 1 week
after the onset of jaundice
– Present in blood briefly
– No chronic carrier state
Hepatitis A:
Incubation Period
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2-6 weeks
Acute onset
Mild flu-like manifestations
Symptoms last up to 2 months
Liver usually repairs itself, so no
permanent effects
Hepatitis A

Hepatitis A virus (HAV)
– Anti-HAV immunoglobulin M (IgM)
Appears in the serum as the stool becomes
negative for the virus
 Detection of IgM anti-HAV indicates acute
hepatitis
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Hepatitis A

Hepatitis A virus (HAV)
– Anti-HAV immunoglobulin G (IgG)
IgG anti-HAV: Indicator of past infection
 Presence of IgG antibody provides lifelong
immunity

Hepatitis A:
Mode of Transmission

Mainly by ingestion of food or
liquid infected with the virus
–Poor hygiene, improper handling
of food, crowding housing, poor
sanitation conditions are all
factors related to Hepatitis A
Hepatitis A:
Mode of Transmission (Cont’d)
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Occurs more frequently in
underdeveloped countries
Contaminated waters
–Drinking water, contaminated
seafood
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Food-borne Hepatitis A outbreaks
usually due to infected food handler
–Contamination of food during
preparation
Hepatitis A:
Vaccine
2
doses IM
–Initial dose
–Booster in 6 to 12
months
Post-exposure
Prophylaxis
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Standard IG-immune globulin
– Given IM within 2 weeks of exposure
Hepatitis A Vaccine
IG is recommended for persons who do not have
anti-HAV antibodies and have had food borne
exposure or close contact with HAV-infected person
Remember 2/2/2/2 Rule
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2 doses IM for vaccination
Signs & symptoms last 2 months
Contagious 2 weeks before signs &
symptoms
Post-exposure dose given IM within 2 weeks
of exposure
Must report within one day
Hepatitis B

Nearly 400 million people infected with
Hepatitis B
– 50% to 75% active viral replication

73,000 new cases of Hepatitis B
annually in United States
– Incidence decreased due to HBV vaccine
Hepatitis B

Hepatitis B virus (HBV)
– DNA virus
– Transmission of HBV
Perinatally by mothers infected
 Percutaneously (IV drug use)
 Mucosal exposure to infectious blood, blood
products, or other body fluids

Hepatitis B
 Hepatitis
B virus (HBV)
–Transmission occurs when
infected blood or other body
fluids enter the body of a
person who is not immune to
the virus
Hepatitis B
 Hepatitis
B virus (HBV)
– Sexually transmitted disease
– Can live on a dry surface for 7 days
– More infectious than HIV
Hepatitis B- Precautions
Source: Uptodate
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PREVENT INFECTION OF FAMILY — Acute and chronic
hepatitis B are contagious. Thus, people with hepatitis B
should discuss measures to reduce the risk of infecting close
contacts. This includes the following:
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Discuss the infection with any sexual partners and use a latex
condom with every sexual encounter.
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Do not share razors, toothbrushes, or anything that has blood
on it.
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Cover open sores and cuts with a bandage.
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Do not donate blood, body organs, other tissues, or sperm.
Hepatitis B- Precautions
Source: Uptodate
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Immediate family and household members should
have testing for hepatitis B. Anyone who is at risk
of hepatitis B infection should be vaccinated, if not
done previously. (See "Patient information: Adult
immunizations".)
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Do not share any injection drug equipment
(needles, syringes).
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Clean blood spills with a mixture of 1 part
household bleach to 9 parts water.
Hepatitis B- Prevention
Hepatitis B cannot be spread by:
 Hugging or kissing* (some disagreement)
 Sharing eating utensils or cups
 Sneezing or coughing
 Breastfeeding
Source: Uptodate
Hep B Incubation Period
 6-24
weeks
 Prevention
–Vaccine-3 doses
Initial
dose
Dose at 4 weeks
Dose 5 months later
Post-exposure Hep B
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Hepatitis B Immune globulin
IM in 2 doses
– First dose within 24 hours to 7 days of
exposure
– Second dose 20 to 30 days post-exposure
Provides short-term immunity
Give HBV vaccine concurrently- vaccine can
be beneficial post- exposure
Hepatitis B

Hepatitis B virus (HBV)
– Complex structure with three antigens
 Surface antigen (HBsAg)
 Core antigen (HBcAg)
 E antigen (HBeAg)
– Each antigen—a corresponding antibody
may develop in response to acute viral
Hepatitis B
Hepatitis B Virus

Presence of Hepatitis B Surface
Antibodies
– Indicates immunity from HBV vaccine
– Past HBV infection
– With chronic infection, liver enzyme
values may be normal or ↑
– 15% to 25% of chronically infected
persons die from chronic liver disease
Hepatitis C
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Approximately 170 million people are
infected with the hepatitis C virus
(HCV)
Estimated 30,000 new cases
diagnosed annually
Hepatitis C
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8000 to 10,000 people in the
United States die each year from
complications of end-stage liver
disease secondary to HCV
Approximately 30% to 40% of
HIV-infected patients also have
HCV
Hepatitis C

Hepatitis C virus (HCV)
– Transmitted primarily
percutaneously
– Risk factors
 IV drug use
–Most common mode of
transmission in United States
and Canada
 Blood transfusions
Hepatitis C
 Hepatitis
C virus (HCV)
–Risk factors (cont’d)
– High-risk sexual behavior
 Hemodialysis
 Occupational
exposure
 Perinatal transmission
Hepatitis C:
Transmission
 Hepatitis
C virus (HCV)
– Up to 10% of patients with HCV cannot
identify a source
– Risk of body piercings, tattooing, and
intranasal drug use in transmission of
HCV
Hepatitis C
Diagnostic Studies
Anti-HCV
HCV
RNA
antibody
Hepatitis C Interventions
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Harm Reduction - Austin Harm
Reduction Coalition
Hepatitis D
 Hepatitis
D virus (HDV)
– Also called delta virus
– Defective single-stranded RNA virus
– Cannot survive on its own
– Requires the helper function of HBV
to replicate
Hepatitis D
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Hepatitis D virus (HDV) (cont’d)
–HBV-HDV co-infection
 ↑ Risk of fulminant hepatitis
More severe acute disease
Hepatitis E
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Hepatitis E virus (HEV)
– RNA virus
– Transmitted fecal–oral route
– Most common mode of transmission
is drinking contaminated water
– Occurs primarily in developing
countries
Hepatitis G
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Hepatitis G virus (HGV)
–RNA virus
–Poorly characterized parenterally
and sexually transmitted virus
–Found in some blood donors
–Can be transmitted by blood
transfusion
Hepatitis G
 Hepatitis
(cont’d)
G virus (HGV)
–Coexists with other hepatitis
viruses and HIV
–Does not appear to cause liver
damage
Pathophysiology of
Hepatitis
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Acute infection- widespread
inflammation of liver tissue
– Liver damage mediated by
 Cytotoxic cytokines
 Natural killer cells
– Liver cell damage results in hepatic
cell necrosis
Common Manifestations
of Acute Hepatitis
 Predictable
course among all
the viruses
 Incubation Phase: after
exposure to virus, no
symptoms
Preicteric Phase of
Hepatitis
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Flu-like symptoms
–General malaise
–Fatigue
–Body aches, headache
–GI symptoms- nausea/vomiting,
diarrhea, abdominal discomfort
–Chills, low grade fever
Icteric or Jaundice Phase
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Usually 5-10 days after pre-icteric symptoms
Jaundice results when bilirubin diffuses into
tissues
Sclera jaundiced
Urine darkens due to excess bilirubin being
excreted
If bilirubin cannot flow out of liver, stool will
be light or clay-colored
Severe Jaundice
Hepatitis
Clinical Manifestations
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Pruritus can accompany jaundice
– Accumulation of bile salts beneath the
skin
When jaundice occurs, fever subsides
Liver usually enlarged and tender
Convalescent Phase
Healing generally within 3-16
weeks
 Begins as jaundice is disappearing
 GI symptoms minimal
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Hepatitis
 Liver
cells can regenerate with
time and if no complications
occur, resume their normal
appearance and function
Hepatitis
Complications
 Fulminant
Hepatic Failure
 Chronic Hepatitis
 Cirrhosis
 Hepatocellular Carcinoma
Fulminant Hepatitis
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Results in severe impairment or necrosis of
liver cells and potential liver failure
Develops in small percentage of patients
Occurs because of
 Complications of Hepatitis B
 Toxic reactions to drugs and congenital
metabolic disorders
Diagnostic tests
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Liver function studies
– ALT (Alanine aminotransferase) – elevates: enzyme in
liver cells released into bloodstream with injury or disease
(0 – 50) normal
– AST (Aspartate aminotransferase) – elevates: enzyme in
liver & heart cells released into bloodstream (0 -41)
– GGT – gamma glutamyltransferase: present in all cell
membranes, inj or disease = elevates in cell lysis, (8 – 55).
increases when bile ducts are blocked & hepatitis.
Elevated until function returns.
Diagnostic tests
– Alkaline phosphatase – present in liver & bone cells.
Elevated in hepatitis.(44-147 IU/L)
– CBC – low RBC, Hct, Hgb related to anemia, RBC
destruction, bleeding, folic acid and vitamin deficiencies.
– Low WBC and Platelets
 Increased blood flow to spleen – cells destroyed faster
than needed
–
AFP- alpha fetoprotein– liver cancer marker
– Lactic dehydrogenase LDH5 specific for liver damage
Diagnostic tests
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Coagulation – prolonged prothrombin time due to
poor production of prothombin by liver and
decreased Vitamin K absorption (Normal PT 12-15
seconds, INR 0.8 to 1.2)
Hyponatremia –hemodilution
Hypokalemia, hypophosphatemia,
hypomagnesemia –malnutrition & renal loss
Bilirubin – Total (2-14 umol/L)
Bilurubin – direct/conjugated (0-4
umol/L)
Diagnostic tests
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Serum albumin – low due to impaired liver
production (3.3 – 5)
Serum ammonia – high (0 – 150)(10 to 80 ug/l)
Glucose and cholesterol –abnormal due to
impaired liver function
Abd. Ultrasound – liver size, ascites, or
nodules
Esophagascopy – look for varices
Liver biopsy
CT, MRI
Rx Impacting Liver
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A host of medications can cause abnormal liver
enzymes levels. Examples include:
Pain relief medications such as aspirin,
acetaminophen (Tylenol), ibuprofen (Advil, Motrin),
naproxen (Narosyn), diclofenac (Voltaren), and
phenylbutazone (Butazolidine)
Anti-seizure medications such as phenytoin
(Dilantin), valproic acid, carbamazepine (Tegretol),
and phenobarbital
Antibiotics such as the tetracyclines, sulfonamides,
isoniazid (INH), sulfamethoxazole, trimethoprim,
nitrofurantoin, etc.
Rx Impacting Liver
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Cholesterol lowering drugs such as the
"statins" (Mevacor, Pravachol, Lipitor, etc.)
and niacin
Cardiovascular drugs such as amiodarone
(Cordarone), hydralazine, quinidine, etc.
Anti-depressant drugs of the tricyclic type
(ie elavil)
With drug-induced liver enzyme
abnormalities, the enzymes usually
normalize weeks to months after stopping
the medications.
Liver Biopsy
Needle biopsy
Most common in past
Laparoscopic biopsy:
Used to remove tissue from specific parts of the liver.
Liver Biopsy (Cont’d)
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Transvenous biopsy
Catheter into a vein in the neck and
guiding it to the liver.
A biopsy needle is placed into the
catheter and advanced into the liver.
Used for patients with blood-clotting
problems or excess fluid
Liver Biopsy
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Adequacy of clotting- PT/ INR, Platelets
(Vit. K?)
Type and cross match for blood
Usually hold aspirin, ibuprofen, and
anticoagulants
Chest x-ray
Consent form & NPO 4 to 8 hr.
Liver Biopsy (Cont’d)
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Consent form & NPO 4 to 8 hr.
Vital signs & Empty bladder
Supine position, R arm above head
Hold breath after expiration when
needle inserted
Be very still during procedure – 20
minutes
Liver Biopsy Video
Complications are:
Puncture of lung or gallbladder, infection, bleeding, and pain.
After Needle Liver Biopsy
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Pressure to site, place pt on Rt side to maintain site
pressure minimum of 2 hrs. & flat 12-14 hrs.
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Vital signs & check for bleeding
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NPO X 2H after
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Assess for peritonitis, shock, & pneumothorax
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Rt. shoulder pain common
– caused by irritation of the diaphragm muscle
– usually radiates to the shoulder for a few hours or days.
After Needle Biopsy
(Cont’d)
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Soreness at the incision site
Avoid aspirin or ibuprofen for pain control
for the first week because they decrease
blood clotting, which is crucial for healing.
CONSULT HEALTHCARE PROVIDER!
Avoid coughing, straining, lifting x 1-2
weeks
Hepatitis Care
 Rest
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is a priority!
Diet –High calorie & protein, Low fat
– Vitamin supplement – B complex & K
– Avoid alcohol & drugs detoxed in liver
Life style changes
Meds for Chronic
Hepatitis
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Chronic HBV
Pegylated a-interferon (Pegasys, PEG-Intron)
 Lamivudine (Epivir)
 Adefovir (Hepsera)
 Entecavir (Baraclude)
 Telbivudine (Tyzeka)
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Chronic HCV
Pegylated a-interferon (Pegasys, PEG-Intron)
 Ribavirin (Rebetol, Copegus)
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Hepatitis
Nursing Management
Nursing assessment
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Past health history
– Hemophilia
– Exposure to infected persons
– Ingestion of contaminated food or water
– Past blood transfusion (before 1992)
Hepatitis
Nursing Management
Nursing assessment
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Medications (use and misuse)
– Acetaminophen
– Phenytoin
– Halothane
– Methyldopa
Hepatitis
Nursing Management
Nursing assessment
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IV drug and alcohol abuse
Weight loss
Dark urine
Fatigue
Right upper quadrant pain
Pruritus
Hepatitis
Nursing Management
Nursing assessment
 Low-grade
fever
 Jaundice
 Abnormal
laboratory values
Hepatitis
Nursing Management
Nursing diagnoses
Imbalanced nutrition: Less than
body requirements
 Activity intolerance
 Ineffective therapeutic regimen
management

Hepatitis
Nursing Management
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Overall goals: Planning
–Relief of discomfort
–Resumption of normal activities
–Return to normal liver function
without complications
Hepatitis
Nursing Management
Nursing implementation
 Health
promotion
–Hepatitis A
Education
Vaccination
Good hygiene practices
Hepatitis
Nursing Management
Nursing implementation
Health Promotion
–Hepatitis B
Vaccination
 Education
 Workplace safety

Hepatitis
Nursing Management
Nursing implementation
 Health
promotion
–Hepatitis C
Education
 Infection control precautions
 Modification of high-risk behavior

Hepatitis
Nursing Management
Nursing implementation
 Acute
intervention
–Rest
–Jaundice
Assess degree of jaundice
Small, frequent meals
Hepatitis
Nursing Management
Nursing implementation
 Ambulatory
and home care
–Dietary teaching
–Assessment for complications
–Regular follow-up for at least
1 year after diagnosis
Hepatitis
Nursing Management
Nursing implementation

Ambulatory and home care
–Avoid alcohol
Hepatitis
Nursing Management
Evaluation

Expected outcomes
–Adequate nutritional intake
–Increased tolerance for activity
–Verbalization of understanding
of follow-up care
Hepatitis
Nursing Management
Evaluation
 Expected
outcomes
–Able to explain methods of
transmission and methods of
preventing transmission to
others
Hepatitis Reporting
Break!
Cirrhosis
Cirrhosis Pathophysiology
Cirrhosis is the end stage of
chronic liver disease
 Progressive, leads to liver failure
 Insidious, prolonged course
 Ninth leading cause of death in
United States
 Twice as common in men

Cirrhosis Pathophysiology

Hepatocytes are destroyed and portal
hypertension develops
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Liver cells attempt to regenerate
Regenerative process is disorganized
Functional liver tissue is destroyed and
scarring of liver occurs
New fibrous connective tissue distorts
liver’s normal structure, with impeded
blood flow
Four Types of Cirrhosis
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Alcoholic Cirrhosis – formerly called
Laennec’s
Post necrotic Cirrhosis
Biliary/obstructive - bile flow
obstructed causing damage to liver
Cardiac- from right side heart failure
Alcoholic or Nutritional Cirrhosis
(formerly called Laennec’s)

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Usually associated with alcohol abuse
Most common cause of cirrhosis
Causes metabolic changes in liver; fat
accumulates in liver (fatty liver)
Fatty liver potentially reversible if
alcohol consumption ceases
Post Necrotic Cirrhosis
Results from complication of viral
infections, Hepatitis, or exposure to
toxins
 Liver shrinks because lobules
destroyed, broad bands of scar
tissue form within the liver

Biliary Cirrhosis


Associated with chronic biliary
obstruction and infection
Retained bile damages and
destroys liver cells, causing fibrosis
of liver
Cardiac Cirrhosis


Results from long-standing severe
right sided heart failure
Elevated central venous pressures
cause stasis of blood in veins of
liver, which leads to fibrosis
Early Signs of Cirrhosis
Complications
and Common Manifestations
1. Hepatomegaly and RUQ pain
2. Weight loss
3. Weakness
4. Anorexia
5. Diarrhea and constipation
Cirrhosis Interventions-
Drugs
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Diuretics– Aldactone (spironolactone): decreases aldosterone levels, K+
sparing
– Lasix (furosemide)
Salt-poor albumin
Neomycin – decrease ammonia forming organisms. Typically only
recommended when unable to tolerate lactulose

Lactulose – decreases ammonia forming organisms and inc. acidity
of bowel. Goal is 2-3 loose stools per day.

Ferrous sulfate and folic acid – to treat anemia/ vitamin deficiency
Cirrhosis InterventionsDrugs (Cont’d)
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Beta blocker: propranolol (Inderal),
nadolol- to prevent bleeding of E varices in
conjunction with isosorbide mononitrate
(Imdur) lowers hepatic venous pressure
Proton Pump Inhibitors, H2 Receptor
Blockers– decrease irritation of varices
Serax (oxazepam) – benzodiazepine for
alcohol withdrawal, sedation, sleep. Is
metabolized in the liver – use cautiously.
Nursing Diagnoses Cirrhosis
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Fluid Volume deficit
Ineffective protection: bleeding
Disturbed thought process
Ineffective breathing pattern
Impaired skin integrity
Imbalanced nutrition: less than body
requirements
Cirrhosis Interventions- Diet
and fluids
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Low protein (sometimes), high carbohydrate, high
calorie-if signs of acute hepatic encephalopathy
With cirrhosis and no hepatic encephalopathy, high
carbohydrate, high protein, low salt
Low sodium-500 mg-2gms
At first sign of encephalopathy or ammonia level
increasing- decrease protein intake (sometimes)
Early stage for liver regeneration- need high
protein-(75-100gms)
Later Manifestations of
Cirrhosis Jaundice

Jaundice occurs as a result of the
decreased ability to conjugate and
excrete bilirubin
 In
the late stages of cirrhosis,
patient is usually jaundiced
JAUNDICE
 Hepatocellular
 Obstructive
 Hemolytic
CirrhosisHepatocellular or intrahepatic
jaundice
 Diseased
liver cells can’t clear
normal amounts of bilirubin
from the blood.
Obstructive or Extrahepatic
Jaundice
 Due
to the interference with
the flow of bile in the hepatic
duct.
 Liver is conjugating bilirubin
but it cannot reach small
intestines so is released into
blood stream
Hemolytic Jaundice

Due to excessive destruction of
RBC’s.
– transfusion reaction
– Faulty hemoglobin – sickle cell
– Autoimmune destruction of RBC’s
Major Complications of Cirrhosis
Portal hypertension
Variceal bleeding
Ascites
Spontaneous bacterial peritonitis
Hepatorenal syndrome
Hepatic encephalopathy
Break!
Portal Hypertension
• The portal vein carries about 1500 ml/min of blood
from the small and large bowel, spleen, and stomach
to the liver.
• Any obstruction or increased resistance to flow or,
rarely, pathological increases in portal blood flow may
lead to portal hypertension with portal pressures over
12 mm Hg.
• alcoholic and viral cirrhosis are the leading causes of
portal hypertension in Western countries.
Portal Hypertention (Cont’d)
– Increases in portal pressure cause development of a
portosystemic collateral circulation with resultant
compensatory portosystemic shunting and disturbed
intrahepatic circulation.
– These factors are partly responsible for the important
complications of chronic liver disease, including variceal
bleeding, hepatic encephalopathy, ascites, hepatorenal
syndrome, recurrent infection, and abnormalities in
coagulation.
– Variceal bleeding is the most serious complication
and is an important cause of death in patients with
cirrhotic liver disease.
PORTAL HYPERTENSION
normal 3 mmHg
12 mmHg = esophageal rupture

Resistance to blood flow = Increase in
pressure in portal venous system.
– Swelling, inflammation, fibrosis, scarring of liver
– Thrombus
– Resistance in Inferior vena cava: Rt.CHF,
myopathy


Blood takes collateral channels - esophagus,
stomach, spleen etc, veins, hemorrhoids
May need shunts or TIPS Transjugular Intrahepatic
Portosystemic Shunt to decrease pressure, beta
blockers also help
Portal Hypertension
Esophageal
Varices
Arteriovenous shunting
Hypersplenism
Caput
medusae
Moderate anemia
(dilated abd.
veins)
Thrombocytopenia
Hemorrhoids
Neutropenia
Marked ascites
Ascites &Caput medusae
Spider angiomas
Treatment of esophageal
varices
Active bleeding
 Central line & pulmonary artery pressures
 Blood transfusions & fresh frozen plasma for clotting factors
 Somatostatin or Vasopressin – constrict gut vessels
 Nitroglycerin- to counter negative affects of vasopressin
 Airway/trach
Later prevention of re-bleeding
 Beta-blockers
 Long-acting nitrates
 Soft food, chew well, avoid intra-abdominal pressure
 Protonix (pantoprazole)
Rapid Endoscopy!
Sclerotherapy:
• A sclerosant solution
(ethanolamine oleate or
sodium tetradecyl
sulphate) is injected into
the bleeding varix or the
overlying submucosa
• Complications can
include fever, dysphagia
and chest pain,
ulceration, stricture, and
(rarely) perforation.
Band ligation:
• Band ligation is
achieved by a banding
device attached to the
tip of the endoscope
Band Ligation
Balloon Tube Tamponade:
• The balloon tube tamponade may be life
saving in patients with active variceal
bleeding if emergency sclerotherapy or
banding is unavailable
• The main complications are gastric
and esophageal ulceration,
aspiration pneumonia, and
esophageal perforation.
Minnesota TubeFour lumens:
• one for gastric aspiration
• two to inflate the gastric
and esophageal balloons
• one above the esophageal
balloon for suction of
secretions to prevent
aspiration
Sengstaken-Blakemore Tube
Three Lumens:



Esophageal balloon
inflation
Gastric balloon
inflation
Gastric aspiration
Long term Management of
Esophageal Varices
Repeated endoscopic treatment
Repeated endoscopic treatment eradicates esophageal varices in most
patients, recurrent variceal bleeding is uncommon.
Because portal hypertension persists, patients at risk for recurrent
varices
Long term drug treatment
The use of beta-blockers after variceal bleeding has been shown to
reduce portal blood pressures and lower the risk of further
variceal bleeding.
Prophylactic management
Most patients with portal hypertension never bleed, and it is difficult to
predict who will. Beta blockers have been shown to reduce the risk
of bleeding.
Transjugular Intrahepatic
Portosystemic Shunt


Special procedures – fistula created with
portal vein and hepatic vein and then stents
placed to keep it open.
Bypasses the liver by returning blood to
hepatic vein to inferior vena cava
TIPS
Transjugular intrahepatic
portosystemic shunt
TIPS POST
TIPS:
• Shunted blood contains
high ammonia
• Can lead to:
hepatic encephalopathy
Splenomegaly due to
Portal hypertension




The spleen enlarges as blood is
shunted to splenic vein
This increases rate of destruction of
RBCs, WBCs, and platelets
Decreases storage capacity of spleen
Causes anemia, leukopenia and
thrombocytopenia
Ascites – Complication of
Cirrhosis





Blood flow diverted to mesenteric vessels
– Increased capillary pressure leads to fluid
leaving vessels out into peritoneal cavity
High pressure in liver causes fluid to leave liver into
peritoneal cavity
This fluid is plasma filtrate with high concentration
of albumin
Minerals- Ca++ is attached to albumin decreases so
phosphorus increases.
K+ is low due to aldosterone
Four Factors Lead to Ascites
Hypoproteinemia
Increased Na+
&
Increased
capillary
permeability
H2O retention
Portal Hypertension
Responses to third
spacing



Loss of albumin to ascites leads to
hypoproteinemia, depletion of plasma proteins
Loss of blood volume = lowered BP
Reflexes aimed at returning blood pressure to
normal include release of aldosterone
– Increases reabsorption of NA+ back into blood
and H2O follows, thus increasing blood volume
ASCITES
accumulation of high protein fluid in
the abdomen - 3rd spacing
Nursing Management ASCITES



Assess for
Respiratory
Distress- Fowler’s
position helps ease
work of breathing
in ascites
Measure Abdominal
Girth
Accurate I&O
MEDICAL TREATMENT

Na+ restriction500 mg –2 gms

Fluids-1500 ml/day

Diuretics-Aldactone

Albumin - NaCl poor

Paracentesis





To treat respiratory
distress
Pt will loose 10-30 grams
of protein
Pt in sitting position
Empty bladder first
Post--watch for
hypotension, bleeding,
shock & infection
Additional
Complications
Liver Failure
Liver Failure
Complex syndrome characterized
by impairment of many organs
and body functions
Two conditions:
 Hepatic Encephalopathy
 Hepatorenal Syndrome
Hepatic encephalopathy:
Alteration in neuro status
due to accumulation of
ammonia
Build-up of other substances
such as hormones,
GI toxins, drugs also
contribute
Where does ammonia
come from?



A by-product of protein metabolism
Protein and amino acids are broken
down by bacteria in GI tract,
producing ammonia.
Liver converts this to urea which is
eliminated in the urine
Precipitating Factors – all place
demands on liver








Bleeding esophageal varices
Ingestion of narcotics or barbiturates,
anesthetics
Excessive protein intake
Electrolyte imbalance
Hemodynamic alterations
Diuretics
Severe infection
Blood transfusions
Stages of Hepatic
Encephalopathy
Hepatic Encephalopathy - Onset Phase

Personality
changes,
disturbances of
awareness,
forgetfulness,
irritability, &
confusion
Hepatic Encephalopathy - Second Phase


Hyperreflexia
Asterixis or flapping
– Altered hand writing

Violent, abusive
behavior
Hepatic Encephalopathy


+ Babinski
hyperactive reflexes
obtained with reflex
hammer
- Coma
Babinski Video
Medical Management
Hepatic Encephalopathy
Neomycin
Lactulose
Protein reduction
Hepatorenal syndrome
Complication of Hepatic
Failure
Hepatorenal syndrome
Complication of Hepatic Failure




kidneys may appear normal physically but
functioning impaired.
Usually sudden decrease Urine production,
increase BUN & Creatinine, jaundice and
signs of liver failure
Poor prognosis- most die within 3 wks
without transplant
Think due to decreased perfusion &/or
toxins from failure of liver
Liver Dialysis


Bridge to transplant
Dialyze 6 hours at a time
Donors:




Live donor liver transplants are an excellent option.
Liver regenerates to appropriate size for their
individual bodies.
Survival rates increase / shorter wait time
The donor - a blood relative, spouse, or friend, will
have extensive medical and psychological
evaluations to ensure the lowest possible risk.


Blood type and body size are critical factors in
determining who is an appropriate donor.
Potential donors evaluated for:
–
–
–
–

liver disease, alcohol or drug abuse, cancer, or infection.
hepatitis, AIDS, and other infections.
matched according to blood type and body size.
Age, race, and sex are not considered.
Cadaver donor have to wait
Liver Transplant Video
Liver transplant
complications





Rejection. About 70% of all liver-transplant
patients have some degree of organ rejection prior
to discharge.
Anti-rejection medications are given to ward off the
immune attack.
Infection
Most infections can be treated successfully as they
occur.
Cancer
Review
1. Pathophysiology
1. Cirrhosis
2. Portal hypertension
3. Liver failure
1. Encephalopathy
2. Hepato-renal syndrome
2. Signs & Symptoms
3. Treatment
4. Nsg. Care
5. Complications
The End