Liver Dysfunction and
Pancreatitis
Nursing 210
Liver Anatomy and Physiology

Largest internal organ

Weighs about 1500 grams

Located right upper quadrant

Figure 39-1 p.1075
Anatomy and Physiology

Approximately 75% of the blood supply comes from the
portal vein
–

Remainder of blood supply enters by hepatic artery
–

Drains the GI tract and is rich in nutrients
Rich in oxygen
All blood leaves the liver through hepatic vein to the
inferior vena cava
Liver Functions

Glucose metabolism
– Important role in metabolism of glucose and
regulation of blood glucose
– Converts glucose to glycogen (storage)
– Breaks down glycogen into glucose (energy)
– Additional glucose is synthesized through
gluconeogenesis (amino acids or lactate)
Liver Functions

Ammonia Conversion
– Ammonia (potential toxin) is byproduct of
gluconeogenesis
– Liver converts ammonia into urea
– Also removes ammonia produced by
intestinal bacteria from portal blood
– Urea is excreted in urine
Liver Functions

Protein Metabolism
– Synthesizes all plasma proteins except
gamma globulin
 Albumin (osmotic pressure)
 Alpha and beta globulins
 Blood clotting factors
 Specific transport proteins
 Prothrombin: liver needs vitamin K
Liver Functions

Fat Metabolism
– Fatty acids broken down into ketones
– Provide source of energy for muscles and
other tissues
– Occurs when glucose is limited as in
starvation or uncontrolled diabetes
– Fatty acids also used for synthesis of
cholesterol, lipoproteins and other complex
lipids
Liver Functions

Vitamin and Iron Storage
–
Vitamins A, B12, D and several B-complex
vitamins stored in liver
–
Iron and copper
Liver Functions

Drug Metabolism
– Liver metabolism generally results in loss of
activity of the medication
–
Certain oral meds absorbed by GI tract may
be metabolized by liver to such a great
extent (first-pass effect) that bioavailability is
decreased
Liver Functions

Bile Formation
– Mainly water and electrolytes (potassium,
calcium, bicarbonate, chloride)
– Continuously made by hepatocytes and
stored in gallbladder
– Emptied into intestine when needed for
digestion
Liver Functions




Bilirubin Excretion
Pigment derived from breakdown of
hemoglobin
Modified by hepatocytes through conjugation to
be more soluble in aqueous solutions
Conjugated bilirubin is carried by bile into
duodenum for excretion
Liver Function and Lab Tests

Blood Studies (review Brunner p. 1079)
– Serum Aminotransferase
 AST
 ALT
–
–
Elevated levels usually indicate cellular
damage to the liver
> 70% of liver cells may be damaged before
LFT’s become elevated
Blood Studies, cont.

Pigment studies
–
–
–


Serum bilirubin, direct
Serum bilirubin, total
Urine bilirubin
These studies measure ability of liver to
conjugate and excrete bilirubin
Abnormal results are seen in liver and biliary
tract disease
Blood Studies, cont.



Serum Ammonia
– Liver converts ammonia to urea. Ammonia
rises in liver failure
Protein Studies
– Serum albumin
 Low levels seen with liver disease
Serum globulin
 Elevated levels with advanced cirrhosis
and chronic active hepatitis
Blood Studies, cont.


Tumor Marker
– Alpha-fetoprotein (AFP)
– Increased levels are seen with hepatic
carcinoma
Prothrombin Time (PT)
– Time required for a firm fibrin dot to form
– In liver dysfunction, increase clotting time
with increased risk of bleeding
Liver Biopsy



Used to obtain a specimen of liver tissue
Done under local anesthesia
Complications:
– Pneumothorax
– Peritonitis
– Hemorrhage
Manifestations of Liver Dysfunction






Jaundice
Ascites
Portal Hypertension
Esophageal Varices
Hepatic Encephalopathy
Nutritional Deficiencies
Jaundice




Also known as icterus, a yellow discoloration of
the skin, sclerae and mucous membranes
Caused by elevated bilirubin levels in the blood
Jaundice becomes clinically evident when the
serum bilirubin level exceeds 2.5mg/dL
Several types of Jaundice: Hemolytic,
Hepatocellular, Obstructive, and Hereditary
Hyperbilirubinemia
Jaundice, cont.

Symptoms
– Yellow discoloration of the skin, sclerae and
mucous membranes
– Itching (pruritus) due to deposits of bile salts
on the skin
– Stool becomes light in color
– Urine becomes deep orange and foamy
Portal Hypertension


Elevated pressure in the portal venous blood
– Blood flow through the liver is obstructed
– Vessels enlarge, collateral circulation
develops to take blood back to the systemic
circulation
Two major sequelae result
–
–
Ascites
Varices
Ascites

This is the accumulation of fluid in the
peritoneal cavity
–
Decrease albumin levels cause decreased oncotic
pressure
 Fluid leaves the plasma and leaks in to the
peritoneal cavity and interstitial spaces
 Decrease volume causes activation of the ReninAngiotensin system – Na & H2O retained in
attempt to return intravascular volume to normal–
more edema and ascites
Portal Hypertension and Ascites

Symptoms
– Portal HTN not evident unless bleeding from
collateral blood vessels or ascites occurs
– Ascites – increase abdominal girth,
unexplained rapid weight gain
– Striae and distended veins over abdomen
– Fluid and electrolyte imbalances
– Respiratory difficulty may occur due to
pressure on the diaphragm
Portal Hypertension and Ascites

Treatment
– Portal HTN – treat underlying cause
– Ascites
 Na and fluid restrictions
 Diuretic agents (Aldactone, Lasix)
 Albumin therapy
 Paracentesis
Varices

Esophageal, gastric, hemorrhoidal
– Due to elevated pressures in veins that drain
into portal system
– Often source of massive hemorrhage
– Potential for bleeding increased by blood
clotting abnormalities seen in patients with
liver disease
Hepatic Encephalopathy




Impaired neurological function that occurs with
profound liver failure
Accumulation of ammonia and other toxic metabolites
GI bleeding, high protein diet, bacterial infections
Other factors unrelated to increased ammonia levels
– Dehydration
– Surgery
– Medications - sedatives, tranquilizers,
analgesics,non sparing potassium diuretics
Hepatic Encephalopathy

Symptoms
–
Stage one





Normal level of consciousness w/periods of lethargy and
euphoria
Slowed thought process
Slight confusion
Reversal of day – night sleep pattern
Clinical signs
– Asterixis (flapping tremor of hand), impaired writing,
normal EEG
Hepatic Encephalopathy
–
Stage two




Disorientation
Sleeps most of time, but easily aroused
Agitation, mood swings
Clinical signs
–
–
Stage three



Deep sleep, difficult to arouse
Incoherent speech
Clinical signs
–
–
Asterixis, fetor hepaticus (musty odor to breath), abnormal EEG
Increased deep tendon reflexes, rigidity of extremities, markedly
abnormal EEG
Stage four

comatose
Hepatic Encephalopathy



Treatment
Restrict protein intake in early stages
Lactulose
 reduce
serum ammonia through bowel
evacuation
 Fecal flora are changed to organisms that do not
produce ammonia from urea

D/C sedatives, tranquilizers, analgesics
Viral Hepatitis




Inflammation and necrosis of hepatic cells
Bile flow is impaired
Necrosis occurs in a spotty pattern
Liver cells may regenerate during recovery
period
Viral Hepatitis

Types
– Hepatitis A (HAV)
– Hepatitis B (HBV)
– Hepatitis C (HCV)
– Hepatitis D (HDV)
– Hepatitis E (HEV)
HAV




Also known as “infectious hepatitis”
Mode of transmission is fecal – oral route; poor
sanitation
Incubation period 15-50 days
May occur with or without symptoms, flu like
–
–
Preicteric phase – headache, anorexia, fever
Icteric phase – dark urine, jaundice of skin, sclera
HAV



1995 FDA approved vaccine
Recommend for travelers to locations of poor
sanitation, high risk groups (homosexual
men,IV drug users, day care workers)
Nursing management includes
–
–
Stressing good hygiene
Environmental sanitation
HAV




Outcome – usually mild with recovery
Fatality rate less than 1%
No carrier state
No increased risk of chronic hepatitis, cirrhosis
or hepatic cancer
HBV






Also known as “serum hepatitis”
Transmission – blood and body fluids, through
mucous membranes and breaks in skin
Health care workers at great risk
IV drug users and homosexual activity
Very long incubation period: 1-6 months
May occur without symptoms, may develop
arthralgias, rash
HBV




Vaccine used to provide active immunity
Recommended for all health care workers
Passive immunity is provided through hepatitis
B immune globulin (HBIG)
Recommended for people exposed to HBV
who have not received vaccine or have never
had HBV
HBV




Nursing management includes: teaching
patient proper nutrition, rest, prevention of
spread (blood, body fluids)
Fatality 1-10%
Carrier state possible
Increase risk for cirrhosis, chronic hepatitis and
hepatic cancer
HCV






Also known as Non-A, Non-B hepatitis
Transmission through blood transfusion, exposure to
blood contaminated equipment or drug
paraphernalia,sexual contact
Incubation 15-160 days
Clinical course similar to HBV
Chronic carrier state occurs frequently
Increase risk for chronic liver disease and cancer
HCV

Treatment with interferon and ribavirin

HCV accounts for 30% of liver transplants in
US
HDV




Only individuals with HBV are at risk
Sexual contact, IV drug use
Symptoms similar to HBV, more likely to
progress to chronic active hepatitis and
cirrhosis
Investigation into interferon as treatment
HEV





Transmitted through fecal – oral route
Similar to HAV
Incubation variable 15-65 days
Jaundice usually always present
No chronic state
Toxic and Drug Induced Hepatitis

Toxic hepatitis
–
Inflammatory condition caused by ingestion or
inhalation of certain substances
 Dry cleaning fluid
 Glue
 Insecticides – pesticides
 Poisonous mushrooms
 Rat poison
Toxic and Drug Induced Hepatitis

Drug Induced Hepatitis
– Tylenol
– Aspirin
– Thorazine
– INH
– Valium
Toxic and Drug Induced Hepatitis

Symptoms
–
–
Similar to those of viral hepatitis
 GI and flu type symptoms
 Jaundice
 Hepatomegaly
Depending of substance, may take days to months
for symptoms to appear
Fulminant Hepatic Failure




Sudden and severely impaired liver function in
previously healthy person
Liver failure within 8 weeks of first clinical sign
Viral hepatitis is most common cause
Other causes
–
–
–
Acetaminophen
Chemicals
Wilson’s disease (copper build up in liver)
Cirrhosis



Chronic, degenerative process, replacement of normal
tissue with scar tissue
Three types
– Alcoholic (most common, chronic alcoholism)
– Postnecrotic (acute viral hepatitis)
– Biliary (chronic biliary obstruction and infection)
Other causes:
– Toxic drug or chemical reaction
– Unknown cause
Cirrhosis

Clinical manifestations
–
–
–
–
–
–
–
Liver enlargement
Ascites
Infection and Peritonitis
Varices
Edema
Vitamin deficiency
Mental deterioration
Cirrhosis

Treatment
–
–
–
No alcohol
Well balanced diet, unless:
 Hepatic Encephalopathy – restrict protein
 Ascites – restrict sodium
Vitamin supplements
 B-Complex
 Folic acid
 A,C,and K
Cirrhosis

Complications
–
–
–
–

Portal hypertension
Ascites
Hepatic Encephalopathy
Esophageal varices (dilated vein)
Read Nursing Process, Brunner, p.1103-1105
Esophageal Varices




Dilated veins usually found in submucosa of
lower esophagus
Occurs in 1/3 of patients with cirrhosis
Mortality 45-50%
Hemorrhage occurs from muscular exertion,
coughing, sneezing, vomiting, reflux of
stomach content (especially alcohol)
Esophageal Varices: Medical
Management
–
–
–
Non surgical management is preferable due to high
rate of mortality with emergency surgery
Pharmacologic therapy (Vasopressin) may be initial
mode
 Constriction of arterial bed and decrease in portal
pressure
 Nitroglycerin used to decrease side effect of
angina
Balloon Tamponade
 Pressure exerted against bleeding varices
Esophageal Varices

Medical management
–
–
–
Endoscopic Sclerotherapy
 Sclerosing agent is injected through endoscope
into varices to promote thrombosis
Esophageal Banding Therapy
 Provides thrombosis and mucosal necrosis of
bleeding sites by band ligation
Surgical management
 Surgical bypass procedures
 Devascularization and Transection
Esophageal Varices

Nursing Management
– Vital signs
– TPN
– Prevention of vomiting and straining
– NG tube for gastric suction
– Quiet environment, help reduce anxiety