Transcript Unit_7

Unit 7
Hepatic & Pancreatic Conditions
Gordons Functional Health Pattern
Activity and Exercise
Part 1
 OBJECTIVES:

Identify the metabolic functions of the liver and the alterations in these functions that
occur with liver disease.

Explain liver function tests and the clinical manifestations of liver dysfunction in
relation to pathophysiologic alterations of the liver.

Relate jaundice, portal hypertension, ascites, varices, nutritional deficiencies, and
hepatic coma to pathophysiologic alterations of the liver.

Describe the medical, surgical, and nursing management of patients with esophageal
varices.

Compare the various types of hepatitis and their causes, prevention, clinical
manifestations, management, prognosis, and home health care needs.
Use the nursing process as a framework for care of the patient with cirrhosis of the
liver.


Compare the nonsurgical and surgical management of patients with cancer of the liver.
Hepatic & Pancreatic Conditions
• Review of A & P
• Functions:
Liver
– CHO metabolism• Glycogenesis = the formation of glycogen from glucose
• Glycogenolysis = conversion of glycogen into glucose in
the liver & muscles
• Storage of glycogen
• Converts galactose & fructose to glucose
• Converts ammonia into urea by deamination of AA
Hepatic & Pancreatic Conditions
– Protein metabolism
• Synthesizes plasma proteins
• Detoxifies & biotransforms hormones, drugs & other
chemicals
• Vitamin (ADEK) & iron, copper storage
– Lipid metabolism
• Oxidation of fatty acids  to ketones for energy sources
• Formation of most lipoprotein
• Synthesis of cholesterol & phospholipids
– Bile formation
Hepatic & Pancreatic Conditions
• Pancreas
• Functions:
– Endocrine
• Secretes insulin
• Secretes glucogon
• Secretes somatostatin = a peptide that regulates the
release of hormones of different neuroendocrine cells
found in brain, pancreas & GI tract; blocks the exocrine
& endocrine functions of the pancreas; used to treat
variceal hemorrhage in pts w cirrhosis & to treat
pancreatitis.
– Octreotide is synthetic version
Hepatic & Pancreatic Conditions
• Function
• Pancreas
– Exocrine:
• Amylase - carbohydrate
• Trypsin – protein
• Lipase – fat
• Effects of aging: increase fibrosis, decrease
secretions & enzyme  effects glucose
metabolism  potential for diabetes mellitus 
nursing implications – periodic blood glucose
test
Hepatic & Pancreatic Conditions
• Assessment of client
– General appearance
– Hx
– Assess all systems: head to toe
– Diagnostic tests:
• Liver Bx:
• Paracentesis – the puncture of the peritoneal cavity for
removal of fluid
– Nsg responsibility: consent, pre-procedure VS, amt of fluid
removed is recorded, specimens sent to lab; puncture site will
ooze for several days – change dsg frequently, documentation of
procedure & pt’s response; freq. post-procedure VS, may have
to start IV, may have to give plasma expander
QuickTime™ and a
TIFF (Uncompressed) decompressor
are needed to see this picture.
Hepatic & Pancreatic Conditions
• Jaundice = “yellow” skin, results of excessive
levels of bilirubin; total bilirubin > 3 mg/dl –
visible
The following is a review of the normal pathway
for bilirubin production and excretion and its
relationship to laboratory assessment of liver
function:
• Step 1: Red blood cells are broken down by the
reticuloendothelial system and unconjugated
bilirubin in the bloodstream is carried by
albumin to the liver. This is known as "prehepatic," "free," "unconjugated," or" indirect
bilirubin" (normal value = 0.1 - 1.0 mg/dl)
Hepatic & Pancreatic Conditions
• Step 2: The liver converts or conjugates bilirubin
and makes it water-soluble - an enzyme,
glucuronyl transferase, is necessary for the
conjugation of bilirubin (either a lack of this
enzyme, or the presence of drugs that interfere
with glucuronyl transferase, impairs the liver's
ability to conjugate bilirubin) - This is known as
"posthepatic", "conjugated" or "direct" bilirubin
(normal value = 0.0 - 0.4 mg/dl)
• Step 3: Conjugated bilirubin is excreted via bile
salts to intestine. Bacteria in the intestine break
down bilirubin to urobilinogen for excretion in the
feces (normal value for fecal urobilinogen = 40 280 mg/day)
Hepatic & Pancreatic Conditions
– Symptom of illness:
• Obstructive jaundice of biliary tracts [produces  conjugated bilirubin
due to bile regurgitation]
– gallstones, mass or tumor
• Alteration of bile metabolism at cellular level( hereditary ds)
• Hepatocellular jaundice results from injury or ds of the parenchymal
cells of liver
–
–
–
–
–
Liver cell toxic injury ( acetaminophen overdoses)
Viral infections
Cirrhosis
Infectious mononucleosis
Reactions of certain drugs ( chlorpromazine)
• Hemolytic jaundice: due to overproduction of bilirubin resulting from
hemolytic processes that produce  levels of unconjugated bilirubin
– Pernicious anemia, sickle cell anemia, after blood transfusions.
Transfusion reactions (abo or Rh incompatibility )
Hepatic & Pancreatic Conditions
• Bilirubin – lab values
– Adult total: 0.2 – 1.3mg/dl
• Panic value: > 12 mg/dl
–
conjugated [direct]: water soluble 0.0 – 0.2 mg/dl
• Elevated in conditions: cancer at head of pancreas,
choledocholithiasis
– unconjugated [indirect]: fat soluble
• hemolytic anemias due to large hematoma
• Trauma in presence of large hematoma
Hepatic & Pancreatic Conditions
• Hepatitis – widespread inflammation of the liver
resulting in degeneration & necrosis of liver
cells
– 50,000 - 70,000 cases / yr in USA
– Caused by viruses, toxins, chemicals (drugs)
– Often asymptomatic
– S&S: jaundice, pain upon palpation, subclinical –
anicteric (w/o jaundice), mild flu-like resp
symptoms, mild temp, anorexia
• Hepatitis A  G
– They differ in incubation, mode of transmission &
severity
Viral Hepatitis
• HAV --- Hepatitis A –aka infectious hepatitis;
– Occurrence: endemic in poor areas of world, poor
sanitation; common in fall & winter
– Transmission: infected feces, fecal – oral route; may be
airborne if copious secretions, Infected client contains the
virus before symptoms appear  infection spreads, day care
centers, prisons
• Infected water, milk & food, raw shellfish from c water
• No carrier state
– Caused by an RNA virus of the enterovirus family
– Incubation period (2-7weeks) often 4 weeks
– Severity: mortality low; rarely causes fulminating hepatic
failure.
– Diagnostic tests: Antibodies (anti-HAV) appear early in
course of illness [IgM,- positive in acute hepatitis; IgG –
positive after infection]
– Prophylaxis: hygiene; immune globuline [passive];
inactivated hepatitis A vaccine (active)
Viral Hepatitis
• HBV --- Hepatitis B;
– Occurrence: worldwide, even in remote areas; incidence  in
dense populations and poor hygiene; drug addicts,
homosexuals; HCW are at great risk, because of close
contact w blood of carriers; occurs all year
– Is a DNA virus w inner core & a surface envelope
• Body forms antibodies to viral antigens HBc Ag & HBsAg
• HBsAg presence in blood: a past / resolving infection; a continuous
chronic; or immunization w immunoglobin or Hep B vaccine
– Transmission: parenterally, sexually,  in HIV infections,
found in saliva, accounts for 5-10% of post transfusion
hepatitis
– Incubation: 2-5 months
– Severity: more serious, mortality rate – 10 -20%
– Diagnostic tests: HBsAg, HBc IgM
– Prophylaxis: hygiene, avoidance of risk factors; HBIG
[Hepatitis B immune globulin] – passive; Recombinant
hepatitis B vaccine (active) - (killed virus) x 3 doses,
Viral Hepatitis
• Hepatitis C – HCV
– Route of transmission: blood, blood products,
parenterally, IV drug users; possible fecal-oral
route; can be spread by carriers; occurs all year
– Transmission: contact w blood & body fluids, carrier
state
– Incubation period: 15 – 160 days
– Severity: can lead to chronic hepatitis, cancer of
liver
– Diagnostic tests: anti-HCV
– Prophylaxis: hygiene; no vaccine for active
immunization; interferon (Intron-A) & ribavirin
(Rebetol) helps improve clinical situation
Viral hepatitis
• HEV -- Hepatitis E
– Occurrence: parts of Asia, Africa, & Mexico where
there is poor sanitation.
– Transmission: fecal-oral route, food or water-borne,
no carrier state, resembles Hep A
– Incubation: 14 – 60 days
– Severity: illness self-limiting; jaundice is present,
mortality rate in pregnant women 10-20%
– Diagnostic: Anti-HEV
– Prophylaxis: hygiene, sanitation; no immunity
Viral hepatitis
• HDV -- Hepatitis D - delta hepatitis
– occurrence: virus causes hepatitis only in
association w hepatits B virus & only in presence
of HBsAg; endemic in Mediterranean.
– Transmission: co-infects w hepatitis, close
personal contact
– Incubation: 30 -180 day (same as Hep B)
– Severity: similar to Hep B; more severe if occurs w
chronic active hep B, may develop cirrhosis
– Diagnostic: HDAg- positive; RDA RNA in serum
– Prophylaxis: hygiene, Hep B vaccine (active)
Viral Hepatitis
• HGV -- Hepatits G
– Occurrence: associated w chronic viremia lasting
10 days
– Transmission: percutaneous, HCW in hemodialysis,
IV drug users, hemodialysis clients, chronic B or C
clients.
– Incubation period: -– Severity: does not appear to cause liver ds
– Diagnostic: Anti-HGV
– Prophylaxis: hygiene
Hepatitis Complications
• Recovery usually 3-16 weeks
• Fulminant hepatitis  acute liver necrosis,
jaundice, hepatic encephalopathy, and
ascites, labs: coagulation defects, elevated
BUN & Cr
– Mortality: 90-100% in > 60 yrs
• Tx: plasmapheresis, liver transplantation
Non viral hepatitis
• Toxic / drug induced hepatitis
– Chemicals when inhaled, ingested or injected 
acute liver cell necrosis
• Carbon tetrachloride, phosphorus, chloroform & gold,
benzene, Vit A (dose related)
• Medications: isoniazid, halothane, acetaminophen,
some antibiotics, antimetabolites
– Liver necrosis occurs w/I 2-3 days after acute
exposure to dose-related hepatoxin; minimal
exposure over time  chronic hepatitis or
cirrhosis
– Nsg interventions: detailed drug hx, remove
causative agent, rest, relieve SE –itching; diet:
restrict protien if impending hepatic
encephalopathy
Alcoholic hepatitis
• May be acute or chronic
• Caused by parenchymal necrosis r/t heavy
drinking; sometimes reversible  cirrhosis,
• S&S occur after heavy drinking bouts: anorexia,
nausea, abd pain, splenomegaly,
hepatomegaly, jaundice, ascites, &
encephalopathy
– Labs: anemia, leukocytosis, &  bilirubin
• Poor prognosis – if continues to drink
• Nsg interventions -  vitamin,  CHO diet, folic
acid, thiamine & IV fluids
Cirrhosis
A. Types of Cirrhosis
1. Biliary
2. Postnecrotic
3. Alcoholic (Laennec’s)
Clinical Manisfestations:
1.Early signs – weakness, fatigue, transient bouts of
jaundice, enlarged liver, RUQ tenderness, indigestions
2. Later Signs – liver decreases in size
Labs – increased SGOT,SGPT, serum bilirubin, PT, serum
globulin level. Decreased serum albumin, serum
cholinesterase. Leukopenia and thrombocytopenia.
Acities, portal hypertension, and varices
Cirrhosis
Management:
Baloon temponade – sengstaken-Blakemore tube
Endoscopic sclerotherapy
Esophageal Banding therapy
Surgery – direct ligation, portacavl shunt – decrease danger of
esophageal and gastric varices and decrease portal hypertension
Nursing Care:
•
Rest
•
Improve nutritious status – high protein diet if no ascities or
edema. Low protein diet if in hepatic coma. Moderate protein diet –
if no signs of hepatic encephalopathy. Maintain caloric intake
•
Skin care for puritus and jaundice
•
Reduce risk of injury/bleeding
•
Medication – lactulose
Complications:
Fluid retention, ascities, encephalopathy, esophageal varices
Pancreatitis
• Pancreatitis begins when the digestive enzymes
become active inside the pancreas and start
"digesting" it.
The pancreas secretes digestive enzymes into the
small intestine through a tube called the pancreatic
duct.
These enzymes help digest fats, proteins, and
carbohydrates in food.
The pancreas also releases the hormones insulin and
glucagon into the bloodstream. These hormones help
the body use the glucose it takes from food for energy.
Normally, digestive enzymes do not become active until
they reach the small intestine, where they begin
digesting food. But if these enzymes become active
inside the pancreas, they start "digesting" the
pancreas itself.
• Pancreatitis has two forms: acute and chronic
Pancreatitis
Pancreatitis
Acute pancreatitis occurs suddenly and lasts for
a short period of time and usually resolves.
Chronic pancreatitis does not resolve itself and
results in a slow destruction of the pancreas.
Either form can cause serious complications. In
severe cases, bleeding, tissue damage, and
infection may occur. Pseudocysts,
accumulations of fluid and tissue debris, may
also develop. And enzymes and toxins may
enter the bloodstream, injuring the heart,
lungs, and kidneys, or other organs.
Common causes of pancreatitis are gallstones or
alcohol abuse.
Sometimes no cause for pancreatitis can be
found.
Pancreatitis
Acute Pancreatitis Symptoms of acute pancreatitis include:
Upper abd or mid epigastic pain that may radiate to the
back. Pain may last a few days and can become
severe or get worse with eating, abdominal distention,
N/V, fever, tachycardia, in a severe case - respiratory
distress, hypotension, renal failure, shock.
DX: 3x more amylase and lipase (digestive enzymes
formed in the pancrease), change in blood glucose
levels, Ca, Mg, Na, K, and HCO3.
US abd (look for gallstones, CT (look for inflammation
or destruction of the pancrease, or pseudocyts)
Treatment for acute pancreatitis include:Depending on
severity, TPN, intravenous fluids, NPO, oxygen, pain
meds, antibiotics, or surgery.
Acute pancreatitis becomes chronic when pancreatic
tissue is destroyed and scarring develops.
Pancreatitis
Chronic Pancreatitis
Chronic pancreatitis occurs when digestive
enzymes attack and destroy the pancreas
and nearby tissues, causing scarring and
pain.
The usual cause of chronic pancreatitis is
many years of alcohol abuse, but the
chronic form may also be triggered by
only one acute attack, especially if the
pancreatic ducts are damaged.
The damaged ducts cause the pancreas to
become inflamed, tissue to be destroyed,
and scar tissue to develop.
Pancreatitis
Chronic Pancreatitis
While common, alcoholism is not the only cause of chronic
pancreatitis. The main causes of chronic pancreatitis are
• alcoholism
• blocked or narrowed pancreatic duct because of trauma
or pseudocysts have formed
• heredity
• unknown cause (idiopathic)
• Damage from alcohol abuse may not appear for many
years, and then a person may have a sudden attack of
pancreatitis. In up to 70 percent of adult patients, chronic
pancreatitis appears to be caused by alcoholism. This
form is more common in men than in women and often
develops between the ages of 30 and 40.
Pancreatitis
Chronic Pancreatitis
• Hereditary pancreatitis usually begins in childhood but
may not be diagnosed for several years. A person with
hereditary pancreatitis usually has the typical symptoms
that come and go over time.
• Episodes last from 2 days to 2 weeks.
• A determining factor in the diagnosis of hereditary
pancreatitis is two or more family members with
pancreatitis in more than one generation.
• Treatment for individual attacks is usually the same as it
is for acute pancreatitis.
• Any pain or nutrition problems are treated just as they
are for acute pancreatitis. Surgery can often ease pain
and help manage complications.
Pancreatitis
Chronic Pancreatitis
• Other causes of chronic pancreatitis are
• congenital conditions such as pancreas
divisum
• cystic fibrosis
• high levels of calcium in the blood
(hypercalcemia)
• high levels of blood fats (hyperlipidemia or
hypertriglyceridemia)
• some drugs
• certain autoimmune conditions
Chronic Pancreatitis - Symptoms
Most people with chronic pancreatitis have abdominal
pain, although some people have no pain at all.
The pain may get worse when eating or drinking, spread
to the back, or become constant and disabling.
In certain cases, abdominal pain goes away as the
condition advances, probably because the pancreas is no
longer making digestive enzymes.
Other symptoms include nausea, vomiting, weight loss,
and fatty stools.
People with chronic disease often lose weight, even
when their appetite and eating habits are normal.
The weight loss occurs because the body does not
secrete enough pancreatic enzymes to break down food,
so nutrients are not absorbed normally. Poor digestion
leads to excretion of fat, protein, and sugar into the stool.
If the insulin-producing cells of the pancreas (islet cells)
have been damaged, diabetes may also develop at this
Chronic Pancreatitis
Pancreatitis
Diagnosis
• Diagnosis may be difficult, but new techniques
can help. Pancreatic function tests help decide
whether the pancreas is still making enough
digestive enzymes.
• Ultrasonic imaging, endoscopic retrograde
cholangiopancreatography (ERCP), and CAT
scans, helps DX chronic pancreatitis (can
show calcification of the pancreas, in which
tissue hardens from deposits of insoluble
calcium salts).
Pancreatitis
Chronic Pancreatitis
Treatment
• Relieving pain is the first step in treating chronic pancreatitis.
The next step is to plan a diet that is high in carbohydrates
and low in fat.
• Patient may require pancreatic enzymes to take with meals if
the pancreas does not secrete enough of its own. The
enzymes should be taken with every meal to help the body
digest food and regain some weight.
• Sometimes insulin is needed to control blood glucose.
• In some cases, surgery is needed to relieve pain. The surgery
may involve draining an enlarged pancreatic duct or removing
part of the pancreas.
• For fewer and milder attacks, people with pancreatitis must
stop drinking alcohol, stick to their prescribed diet, and take
the proper medications.
Treatment for chronic pancreatitis includes easing the pain;
eating a high-carbohydrate, low-fat diet; and taking enzyme
supplements. Surgery is sometimes needed as well