Transcript Liver, Biliary Tract and Pancreas Problems.

Liver, Biliary Tract and
Pancreas Problems
Liver
Today’s Class: Chapter 39 & 40
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Function of liver, pancreas, biliary system
Jaundice
Cirrhosis & hepatitis
Portal circulation
Esophageal varices
Sengstaken-Blakemore & LeVeen-Peritoneovenous Shunt
Acute pancreatitis
Cholelithiais
Cholecystitis
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Class Objectives:
Identify basic functions of hepatobiliary system and
pancreas
Define jaundice, describe signs and symptoms,
nursing/medical management
Explain the etiology, pathophysiology, manifestations,
complications & collaborative care of the client with liver
cirrhosis
Describe the nursing care of the clients with cirrhosis
and hepatitis
Describe the types of viral hepatitis, including etiology,
pathophysiology, manifestations & collaborative care
Discuss risk factors and preventative measures for
Hepatitis
Describe the pathophysiology, manifestations,
collaborative & nursing care of the client with
pancreatitis and gallbladder disease.
Describe the medical and surgical treatment of
cholelithiasis and cholecystitis and nursing care.
http://www.youtube.com/watch?v=tat0QYxlCbo&feat
ure=related
(Black, Hawkes & Keene 2001)
Functions of the liver:
• Glucose metabolism: glucose is converted to glycogen,
stored in hepatocytes, & released to maintain normal
blood glucose.
• Ammonia conversation: ammonia (a potential toxin) is
a byproduct of glucogenesis and is converted to urea
(In liver) which can be excreted in the urine. Ammonia
produced by intestinal bacteria is also removed from
portal blood for urea synthesis/excretion
• Protein metabolism: including almost all plasma
proteins including:
• Blood clotting factors are synthesized in the liver. (Vitamin K
is required by the liver for synthesis of clotting factors.)
• Albumin, alpha & beta globulins
• Transport proteins
Liver function Con’t
• Fat metabolism: fatty acids can be broken
down to for production of energy and
ketones. Also produces cholesterol and
other complex lipids.
• Vitamin & iron storage: A, B, D, B-complex,
iron & copper are stored in large amts.
• Drug and toxin metabolism: alcohol,
barbituuates, opioids, sedative agents,,
anesthetics,etc.
Function Con”t
• Bile formation: stored in gallbladder and
emptied into intestine as needed
• Bilirubin excretion: bilirubin is derived
from the breakdown of hemoglobin,
removed from the liver, modified to make
it more water soluble, and then excreted
in the bile.
Prevention of Liver Disease
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No more than two alcoholic drinks a day.
Be cautious about mixing drinks,
combining with drugs OTC & prescription
Avoid exposure to chemicals whenever
possible.
Maintain a healthful, balanced diet.
Vaccinate against hepatitis
No sharing of needles, razors,
toothbrushes
Practicing safer sex will minimize the risk
of transmission of hepatitis B.
When things go wrong:
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The problem relates to one of the following
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portal & hepatic circulatory disturbance
hepatobiliary tract disturbance
hepatocellular disturbance
TESTS
Liver Function tests: see text
Consider: AST, ALT, Alk Phosp, Serum Ammonia &
Albumin, Prothrombin time, Cholesterol, Bilirubin
Liver Blood tests
Liver Blood tests
Liver Blood tests
Other Liver tests
Jaundice
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Defined as: ” the yellow pigmentation of
sclera, skin, and deeper tissues caused by
excessive accumulation of bile pigments in
the blood” (Black, Hawkes & Keene 2001)
It is a symptom rather than a disease, and
results from problems 1) outside the liver
or 2) inside the liver.
Is a result of excessive bilirubin
Three types of Jaundice
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Hemolytic jaundice: results in increased
breakdown of RBCs (blood transfusion reaction)
Hepatocellular jaundice: livers altered ability to
take up bilirubin from blood, conjugate, or
excrete it. (hepatitis, cirrhosis)
Obstructive jaundice; impeded outflow of bile
through liver & duct system (cholelithiasis,
cancer).
Jaundice
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Cirrhosis
http://www.youtube.com/watch?v=u6777Ig
xSYY
A chronic disease of the liver marked by
pathological formation of widespread fibrosis
(scarring) and degenerative changes.
Symptoms result from loss of liver cell function,
increased resistance to blood flow through
liver, leading to ammonia toxicity
Types include: Laennec’s (alcoholic),
postnecrotic (toxic), biliary
(obstruction/infection), cardiac (severe ® sided
heart failure)
Cirrhosis
Healthy liver
Cirrhosis
Progression
of alcoholic liver
disease
in heavy drinkers.
Signs and symptoms of Alcohol-related
Liver disease
Damage to liver tissue results in:
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scarring of the liver (fibrosis; nodular
formation )
progressive decrease in liver function,
excessive fluid in the abdomen (ascites)
bleeding disorders (coagulopathy)
increased pressure in the blood vessels (portal
hypertension)
and brain function disorders (hepatic
encephalopathy).
Coagulopathy
Bleeding Disorder
Scarring
Ascites
Cirrhosis:
Signs & Symptoms
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Weakness, fatigue
Weight loss, anorexia,
nausea, diarrhea
Abdominal pain, sterility,
loss of libido, impotence
Hematemesis
Urine may be dark
( urobilinogen)
Stools may be pale or
grey (lack of bilirubin)
Physical Assessment
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Jaundice
Hepatomegaly
Ascites
Pleural effusion
Spider angiomas,
spider nevi
Asterixis (advanced)
Personality or
behavioral changes
Spider Nevi
Vascular abnormalities,
spider naevus (or spider
telangiectasia) are
common, and occur in
more than half of the
clients. In this picture,
another feature of the
cirrhosis is also seen, the
skin is icteric (jaundiced).
Cirrhosis
Diagnostic tests
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CBC, electrolytes, BUN, Bilirubin levels
LFTs (AST, SGOT, SGPT, ALT)
Albumin levels, Ammonia levels
Coagulation tests
Urinalysis
Liver biopsy
Barium swallow
CT scan, liver scan
EEG
Collaborative Management
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Monitor for complications: esophageal
varices, hepatic encephalopathy, renal
failure, infection
Maximize liver function with diet
Treat underlying cause
Prevent infection
Nursing Diagnosis
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Imbalanced nutrition: less than body
requirements
Impaired skin integrity
Ineffective breathing pattern
Risk for injury
Risk for infection
PC: hepatic encephalopathy
PC: hemorrhage
Portal Circulation
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Portal Circulation: Blood from the gut (GI Tract) and spleen
flow to and through the liver through portal vein before
returning to the right side of the heart.
After passing through the liver, blood flows into the
hepatic vein, which leads into the inferior vena cava to the
right side of the heart.
The liver also receives some blood
directly from the heart via the hepatic artery.
In the esophagus, stomach, small intestine and rectum, the
portal circulation and veins of the systemic circulation are
connected. Under normal conditions, there is little to no
back flow from the portal circulation into the systemic
circulation. So what do nurses assess for?
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Decreased blood flow to the liver and blood back up in
the portal vein and portal circulation leads to some of
the serious complications of cirrhosis. Blood can back
up causing an enlarged spleen and sequester
(increase breakdown) blood cells. Most often, the
platelet count falls because of splenic sequestration
leading to abnormal bleeding.
If the pressure in the portal circulation increases
(because of cirrhosis and blood back up) blood can
flow backwards from the portal circulation to the
systemic circulation where they are connected.
Portal hypertension can lead to:
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Varicose veins in the stomach and esophagus
(gastric and esophageal varices) and rectum
(hemorrhoids).
Gastric and esophageal varices can rupture,
bleed massively and even cause death.
Portal hypertension along with other
hormonal, metabolic and kidney abnormalities
in cirrhosis, can also lead to fluid
accumulation in the abdomen (ascites) and
the peripheral tissue (peripheral edema).
Ascites:
Ascites results from several
factors:
 Increased capillary pressure and
the obstruction of venous flow
through the liver.
 The liver cannot metabolize
aldosterone so there is an
increase in sodium and water
retention by the kidneys
 Decreased synthesis of albumin
by the liver.
Figure 47-6 : LeVeen Peritoneovenous Shunt
:
Provides
continuous
reinfususion
of ascitic fuid
into the
venous
system
Black, Hawkes &
Keene 2001)
Paracentesis
Esophageal Varices
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Esophageal varices are
a common - and
dangerous –
complication of alcoholic
cirrhosis, and bleeding
from the varices is a
medical emergency.
Figure 47-3: Sengstaken-Blakemore Tube Used
to Control Ruptured Esophageal Varices
Balloon
tamponade
of varices
(Black, Hawkes & Keene 2001)
Sengstaken-Blakemore Tube Used to
Control Ruptured Esophageal Varices
Hepatic Encephalopathy
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Hepatic Coma : impaired CNS function
resulting from liver disease.
The liver is unable to de-toxify the blood
resulting in increased ammonia (CNS
toxin) accumulation.
Any process that leads to increased
protein in the intestine causes elevated
ammonia
Read text for medical and nursing
management
Hepatic Encephalopathy
Liver Cirrhosis
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Know what cirrhosis is & what causes it
Note common assessment findings
Consider ways that nurses can help clients
through support, comfort measures, & teaching
How can a nurse help a person who is itchy?
What is a Sengstaken Blackemore tube for?
What are the risks?
How would you explain what jaundice is?
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What is portal hypertension?
What causes ascites and what are the
complications?
What is the medical management of ascites?
What are esophageal varices?
What is a Le Veen peritoneovenous shunt for?
What dietary modifications are made for persons
with liver disease? & Why?
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Daily weight - same what?
Fluid & electrolyte comparisons
Assess dependent edema- Where?
Assess stool & urine & vomit for what?
Assess for internal bleeding - How?
Dependent areas exercised - Why & how?
How can pruritis associated skin breakdown be
averted?
Why no constipation, sneezing, hard toothbrushes and
straight razor
Why check on OTC meds?
Why no alcohol?
What drugs will likely be used?
References
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Black, J.M., Hawks, J.H., Keene, A .M. (2001). Medical surgical nursing: Clinical
managementfor positive outcomes. W.B. Saunders Company: Philadelphia (or
current alternative).
Karach, A.M.. (2003) Lippincott’s Nursing Drug Guide. Philadelphia, Lippincott, Willims
& Wilkins.
Malarkey, L.M., McMorrow, M.E. (2000). Nurse’s manual of laboratory tests and
diagnostic procedures, (2 ed.). Philadelphia: W.B. Saunders.
Smeltzer, S.C., Bare, B.G. (2004) Brunner & Suddarth’s textbook of medical surgical
nursing. Philadelphia: Lippincott.
www. gastromd.com/lft.html Liver Function Studies
www.hepnet.com/liver/fig6html The Liver in health
www.liver.ca/Home.aspx The Canadian Liver Foundation
Hepatitis
See text re:
 What are the most common types
 Why are health care professionals at risk?
 What can be done to reduce incidence?
 How may nurses protect themselves &
their clients?
 Know assessment data & rationale
Hepatitis
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Is an inflammation of the
liver and may be caused by
viruses, bacteria, toxins,
chemicals (including drugs).
Most common types are:
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Hepatitis
Hepatitis
Hepatitis
Hepatitis
Hepatitis
Hepatitis
A
B
C
D
E
G
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Hepatitis A virus (HAV) lives in feces in the
intestinal tract. Transmission is through fecal
oral route.
Hepatitis B virus (HBV) lives in blood and other
body fluids. HBV is transmitted from person to
person through unprotected sexual contact, the
sharing of infected needles or other sharp
instruments that break the skin (such as
tattooing & body piercing).
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High risk populations include morticians,
homosexual males, IV drug users, hemodialysis
clients, people undergoing body tattooing & body
piercing.
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The hepatitis C virus (HCV),
called the ‘silent epidemic’
Risk factors same as for HBV
(illicit IV drug use,
occupational exposure to
blood, perinatal exposure,
blood transfusion or organ
transplant, exposure to
contaminated equipment
(including toothbrushes and
razors), unprotected sexual
contact.
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Hepatitis D is always found with
HBV since it is a virus of HBV.
(same risk factors as HBV)
Hepatitis E is a water borne
virus (transmission trough oralfecal route) that is endemic in
many parts of the world.
Epidemics occur in countries
such as India, Mexico, Africa
Nepal.
Hepatitis G (HGV) is not well
understood but is spread
through contaminated blood,
body fluids, needles.
Pathophysiology
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Hepatocytes undergo pathological changes as a
result of the body's immune response to the
virus.
There is generalized inflammation with areas of
necrosis
This leads to functional impairment of the liver
cells.
There is Kuppfer cell hyperplasia (increase in
number of phagocytes)
Disruption of structure and function leads to
obstruction of portal & hepatic blood flow.
Viral Illness That May Result in Hepatitis
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Cytomegalovirus
Epstein Barr virus
Herpes simplex
Varicella zoster causes multi system
disease & liver disease in
immunosuppressed people
Measles, Yellow fever (mosquito) Marbug
& Ebola viruses
Manifestations
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Preicteric stage (before jaundice): malaise,
fever, nausea, vomiting, diarrhea,
anorexia, enlarged liver and lymph nodes,
electrolyte imbalance, abdominal
tenderness, painful joints, fever.
Icteric stage (jaundice): Jaundice,
pruritus, light-colored stools, brown urine,
malaise.
Post-icteric phase: decrease in fatigue,
appetite returns to normal, lab work
normalizes, pain subsides
Diagnostic Tests
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LFTs – elevated
Electrolytes – abnormal
Virus/antibodies – serum
Bilirubin – elevated
Urinalysis - bilirubinuria
Nursing Management
Medications include: Vit K if prolonged PT,
antihistamines for relief of pruritis,
antiemetics.
 Bile acid sequestrants (Clestid, Questran) bind
with bile acids in the GI tract and is excreted in
feces, relieving pruritis.
 Skin care: emollients and lipid cream (Eucerin)
 Reduce fatique
 Diet of low fat, high carb is better tolerated. Na
restriction may be necessary.
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Prevention
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Immune globulin (IG): prophylaxis for
family and friends exposed to HAV
Hepatitis B immune globulin (HBIG);
individuals exposed to B virus
contaminated material.
Vaccines: available for HAV & HBV –
recommended for people with potential
for exposure (HCPs and people who
travel to endemic areas)
Prevention Cont’d
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HAV & HAE : Good hand washing &
personal hygiene.
HBV, HCV, HDV: careful handling of
needles/sharps, proper sterilization of nondisposable instruments, use of
condoms/refrain from multiple partners,
needle exchange programs.
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FYI: According to the
Children's Hunger
Relief Fund, A child
dies every eight
seconds from drinking
contaminated water.
Disorders of the Pancreas and
Biliary Tract
What is the Pancreas?
The pancreas is a 6” organ located in the upper
abdomen, and connected to the small intestine.
It is posterior in the body, against the spine,
and it is this deep location that at times makes
diagnosis of the disease difficult. The pancreas
is essential:
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Pancreatic enzymes that help digest protein, fat and
carbohydrates before they can be absorbed through
the intestine
Pancreatic endocrine cells produce insulin which
regulate the use and storage of the body's main
energy source, glucose or sugar.
Acute Pancreatitis
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It is thought that enzymes
normally secreted by the
pancreas leak into the
pancreatic tissue and initiate
autodigestion the pancreatic
tissue.
This process results in edema,
vascular damage,
hemorrhage, necrosis, and
finally, fibrous changes.
An acute attack may last for
48 hours.
PANCREATITIS: COMMON CAUSES
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Biliary disease (Gallstones, obstruction of
pancreatic duct)
Alcohol use
Viral infection (mumps), pneumonia
Injury
Pancreatic or common bile duct surgical
procedures
Certain medications (especially estrogens,
corticosteroids, thiazide, diuretics,
acetaminophen, tetracycline)
Signs and Symptoms
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Abdominal pain
nausea./vomiting
Fatty stools
Anxiety, chills, fever
Weakness
Weight loss
Jaundice
Plural effusion
Multi system failure
Coagulation defects
Shock
Elevated: serum amylase, lipase, glucose & urine amylase,
bilirubin, WBC
Endoscopic Retrograde
Cholangiopancreatography (ERCP)
Pain & Drugs: Biliary Tract
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Morphine used to be contraindicated. It is now
known that all opiates create spasm of the
Sphincter of Oddi
Since the metabolite of Demerol has such
negative side effects (CNS stimulant, seizures) it
is no longer the drug of choice.
Antacids: reduce gastric acid & associated pain.
Histamine blockers: reduce gastric acid
secretion, which stimulates pancreatic enzymes.
Anticholenergics: reduce spasm of sphincter of
ODDI
Gardner, A (2002) Meperidine: Time for a change. The Disatllate, 27 (4)
NURSING CARE & PANCREATIC
DISEASE
•Keen Assessment
•Strategies to deal with S/S especially
pain, itch, body image, anxiety,
behavioral changes if alcohol related
•Education
Pancreatic Cancer
Pancreatic cancer is the fifth
leading cause of cancer death
around the world. Its incidence
cuts across all racial and socioeconomic barriers and is nearly
always fatal.
90% die within the 1st yr of
diagnosis
SYMPTOMS DEPEND ON THE LOCATION
AND SIZE OF THE Pancreatic TUMOR
• Severe abdominal pain
• Pressure in the abdomen
• If the tumor blocks the common bile duct so that bile
cannot pass into the intestines,
• the skin and whites of the eyes may become
jaundiced,
• urine may become dark
• pain often develops in the upper abdomen and back
• nausea
• loss of appetite
• loss and weakness may occur
• Cullen’s sign (bruising around umbilicus)
Gall Bladder Disease
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Manifestations
Common Tests
Medical Treatment
Nursing Management
Impact on Pancreas
RESEARCH NEWS!! PHYSICAL ACTIVITY AND
GALLSTONES
Gallstones affect 10-15% of adults in Canada. The
majority of cases produce no symptoms, but there are
still a half million operations to remove gallbladders
each year because of gallstones. Three of four stones
are made of cholesterol, which have many contributing
factors including over secretion of cholesterol by the
liver, obesity, high fat diet, and rapid weight loss. A
recent prospective study of over 60,000 women found
that physical inactivity is related to higher incidence of
gallstones.
Common Symptoms of Gallbladder
Disease
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Severe and intermittent pain in the right
upper abdomen. This pain can also
spread to the chest, shoulders or back.
Sometimes this pain may be mistaken
for a heart attack.
Chronic indigestion and nausea.
STONES
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Block
Traumatize
Cause Pain
May be symptomatic
Usually made of
cholesterol (80%)
or Calcium (20%)
RISK FACTORS
The three most important risk factors for
developing gallstone disease are
 Body weight (recent loss)
 Increasing age
 Being female
Medical Management
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An oral medication such as ursodiol,
dissolves cholesterol gallstones
Surgery 1) Open & 2) Lap
Shock wave lithotripsy
Cholecystectomy
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Gallbladder is removed through an abdominal
incision
Performed for acute and chronic cholecystitis
Bile duct injury is a serious complication of this
procedure
Once one of the most common surgical
procedures in Canada, this procedure has largely
been replaced by laparoscopic cholecystectomy.
OPEN CHOLECYSTECTOMY
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Performed when:
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Patient's condition prevents more extensive surgery or when an
acute inflammatory reaction is severe
Gallbladder is surgically opened, the stones and the bile
or the purulent drainage are removed, and a drainage
tube is secured with a purse-string suture
Location of incision / breathing
Wound care & care of “T” tube if used
Pre & post op teaching
Dietary management
OPEN CHOLECYSTECTOMY
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Location of incision / breathing
Wound care & care of “T” tube if used
Pre & post op teaching
Dietary management
What is a “T” Tube?
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Comes right out of bile duct
Sutured in place on skin
1st 24-48 hours
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200-500 ml of drainage
Potential Complications:
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Dislodgement
Infection
Nursing Implications???
Figure 46-4a: Standard Sites of Laparoscopic
Cholecystectomy
B
Menu
F
Figure 46-4b: Laparoscopic Cholecystectomy:
Preparing the Gallbladder for Removal
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Lap Cholecystectomy
Watch for
indications of:
 Infection
 Hemorrhage
 Damage to
adjacent organs
Lap Cholecystectomy
Figure 46-2: Cholendoscopic Removal of
Gallstones
B
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