NURS4581 HEPATIC DYSFUNCTION
Your textbook does a good condensed version of reviewing the A&P and the functions of the liver; you may
want to review this to understand what complications these patient will experience. You should know these
functions of the liver: glucose metabolism, ammonia conversion, protein metabolism, fat metabolism, vitamin
and iron storage, bile formation, bilirubin excretion, & drug metabolism. When the patient experiences liver
failure then it impacts its ability to perform these functions. Liver disorders are common and may result from a
virus, obesity, and insulin resistance, or exposure to toxic substances, such as alcohol, or tumors.
The liver plays a major role in the metabolism of glucose and the regulation of blood glucose concentration.
After a meal, glucose is taken up from the portal venous blood by the liver and converted into glycogen, which
is stored in the hepatocytes. When glucose is needed glycogenolysis occurs releasing glucose into the
bloodstream to maintain normal levels of blood glucose. In hypoglycemia, additional glucose can also be
synthesized gluconeogenesis.
The use of amino acids from protein for gluconeogenesis results in the formation of ammonia as a by-product.
The liver converts this metabolically generated ammonia into urea. Ammonia produced by bacteria in the
intestines is also removed from portal blood for urea synthesis. In this way, the liver converts ammonia, a
potential toxin, into urea, a compound that is excreted in the urine. The liver synthesizes almost all of the
plasma proteins. Vitamin K is required by the liver for synthesis of prothrombin and some of the other clotting
factors. The liver is also active in fat metabolism. Fatty acids can be broken down for the production of energy
and ketone bodies. Breakdown of fatty acids into ketone bodies occurs primarily when the availability of
glucose for metabolism is limited, as in starvation or in uncontrolled diabetes. Fatty acids and their metabolic
products are also used for the synthesis of cholesterol, lecithin, lipoproteins, and other complex lipids. Vitamins
A, B, and D and several of the B-complex vitamins are stored in large amounts in the liver. Certain substances,
such as iron and copper, are also stored in the liver.
Bile is continuously formed by the hepatocytes and collected in the canaliculi and bile ducts. The functions of
bile are excretory, as in the excretion of bilirubin; bile also serves as an aid to digestion through the
emulsification of fats by bile salts. Bile is collected and stored in the gallbladder and is emptied into the
intestine as needed for digestion. Bile salts are synthesized by the hepatocytes from cholesterol and are excreted
into the bile. Bile salts are then reabsorbed, primarily in the distal ileum, into portal blood for return to the liver
and are again excreted into the bile. This pathway from hepatocytes to bile to intestine and back to the
hepatocytes is called the enterohepatic circulation. Because of the enterohepatic circulation, only a small
fraction of the bile salts that enter the intestine are excreted in the feces. Hepatocytes remove bilirubin from the
blood and chemically modify it through conjugation to glucuronic acid, which makes the bilirubin more soluble
in aqueous solutions. The conjugated bilirubin is secreted by the hepatocytes into the adjacent bile canaliculi
and is eventually carried in the bile into the duodenum. In the small intestine, bilirubin is converted into
urobilinogen, which is partially excreted in the feces and partially absorbed through the intestinal mucosa into
the portal blood. Some of the urobilinogen enters the systemic circulation and is excreted by the kidneys in the
urine. Elimination of bilirubin in the bile represents the major route of its excretion.
The liver metabolizes many medications, such as barbiturates, opioids, sedatives, anesthetics, and
amphetamines. Metabolism generally results in drug inactivation, although activation may also occur. One of
the important pathways for medication metabolism involves conjugation of the medication with a variety of
compounds, such as glucuronic acid or acetic acid, to form more soluble substances, excreted in the feces or
urine, similar to bilirubin excretion. Bioavailability is the fraction of the given medication that actually reaches
the systemic circulation. The bioavailability of an oral medication can be decreased if the medication is
metabolized to a great extent by the liver before it reaches the systemic circulation; this is known as first-pass
NURS4581 HEPATIC DYSFUNCTION: Comprehensive Overview and Key Concepts
, NURS4581 HEPATIC DYSFUNCTION
effect. Some medications have such a large first-pass effect that their use is essentially limited to the parenteral
route, or oral doses must be substantially larger than parenteral doses to achieve the same effect.
It is important to obtain a health history focusing on previous exposure of the patient to hepatotoxic substances
or infectious agents; occupational, recreational, and travel history may assist in identifying exposure to
hepatotoxins; history of alcohol and drug use; use of hepatotoxic medications. Many medications are
responsible for hepatic dysfunction and disease. A thorough medication history should address all current and
past prescription medications, over-the-counter medications, herbal remedies, and dietary supplements. The
history also addresses symptoms that suggest liver disease. Symptoms that may have their origin in liver disease
but are not specific to hepatic dysfunction include jaundice, malaise, weakness, fatigue, pruritus, abdominal
pain, fever, anorexia, weight gain, edema, increasing abdominal girth, hematemesis, melena, hematochezia,
easy bruising, changes in mental acuity, personality changes, sleep disturbances, and decreased libido in men
and secondary amenorrhea in women.
The history also addresses symptoms that suggest liver disease. Symptoms that may have their origin in liver
disease but are not specific to hepatic dysfunction include jaundice, malaise, weakness, fatigue, pruritus,
abdominal pain, fever, anorexia, weight gain, edema, increasing abdominal girth, hematemesis, melena,
hematochezia, easy bruising, changes in mental acuity, personality changes, sleep disturbances.
The nurse assesses the patient for physical signs that may occur with liver dysfunction, including the pallor
often seen with chronic illness and jaundice. The skin, mucosa, and sclera are inspected for jaundice, and the
extremities are assessed for muscle atrophy, edema, and skin excoriation secondary to scratching. The nurse
observes the skin for petechiae or ecchymotic areas, spider angiomas, and palmar erythema. The male patient is
assessed for unilateral or bilateral gynecomastia and testicular atrophy due to hormonal changes. The patient’s
cognitive status and neurologic status are assessed. The nurse observes for general tremor, asterixis, weakness,
and slurred speech.
When assessing the patient the nurse will look at the abd, listen, and then palpate for a fluid wave and palpate
the liver. If the liver is palpable, the nurse notes and records its size, its consistency, any tenderness, and
whether its outline is regular or irregular. Tenderness of the liver indicates recent acute enlargement while
absence of tenderness may imply that the enlargement is of long-standing duration. The liver of a patient with
viral hepatitis is tender, whereas that of a patient with alcoholic hepatitis is not.
There are a variety of diagnostic tests that can be done. The nurse should note trends in results because they
provide information about disease progression as well as the patient’s response to therapy. Over 70% of the
parenchymal must be damaged before there will be changes in the liver function test results. Serum
aminotransferases are sensitive indicators of injury to the liver cells and are useful in detecting acute liver
disease such as hepatitis. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-
glutamyl transferase (GGT) are the most frequently used tests of liver damage. ALT levels increase primarily in
liver disorders and are used to monitor the course of hepatitis, cirrhosis, the effects of treatments that may be
toxic to the liver. AST is not specific to liver diseases however levels of AST may be increased in cirrhosis,
hepatitis, and liver cancer; and Gamma-glutamyl transferase (GGT) levels are associated with cholestasis and
alcoholic liver disease. In end-stage liver disease, AST and ALT levels may be normal.
A liver biopsy may be needed. The most common indication is to evaluate diffuse disorders of the parenchyma
and to diagnose space-occupying lesions. Liver biopsy is especially useful when clinical findings and laboratory
tests are not diagnostic.
NURS4581 HEPATIC DYSFUNCTION: Comprehensive Overview and Key Concepts
, NURS4581 HEPATIC DYSFUNCTION
Ultrasonography, computed tomography (CT) scans, and magnetic resonance imaging (MRI) are used to
identify normal structures and abnormalities of the liver and biliary tree. A radioisotope liver scan may be
performed to assess liver size, blood flow, and obstruction. Noninvasive liver stiffness measurements or
elastography uses ultrasound-based vibration and scanning to identify liver fibrosis and determine its extent.
Magnetic resonance elastography uses mechanical shear waves to identify stiff tissue. Liver fibrosis and other
liver diseases can be identified, evaluated and monitored with a variety of other noninvasive studies. These
studies may reduce the need for liver biopsy.
Laparoscopy is used to examine the liver and other pelvic structures. It is also used to perform guided liver
biopsy, to determine the cause of ascites, and to diagnose and stage tumors of the liver and other abdominal
organs.
Hepatic dysfunction results from damage to the liver’s parenchymal cells, directly from primary liver diseases,
or indirectly from either obstruction of bile flow or derangements of hepatic circulation. Liver dysfunction may
be acute or chronic though chronic is far more common.
Chronic liver disease is the 12th leading cause of death in the United States among young and middle-aged
adults with at least 40% of those deaths associated with alcohol use. Approximately 80% of patients diagnosed
with cirrhosis compensate and remain asymptomatic for the next 10 years. Disease processes that lead to
hepatocellular dysfunction may be caused by infectious agents such as bacteria and viruses and by anoxia,
metabolic disorders, toxins and medications, nutritional deficiencies, and hypersensitivity states. The most
common cause of parenchymal damage is malnutrition, especially that related to alcoholism.
Nonalcoholic fatty liver disease and nonalcoholic steatohepatitis are two diseases within the spectrum of fatty
liver to fibrosis and cirrhosis that are strongly associated with obesity and alcohol consumption. In patients who
are overweight, obese, or have high alcohol intake, the nurse observes for signs of associated liver dysfunction.
In some conditions, lipids may accumulate in the hepatocytes, resulting in the abnormal condition called fatty
liver disease. If unrelated to alcohol, this disease is referred to as nonalcoholic fatty liver disease (NAFLD). A
condition known as nonalcoholic steatohepatitis (NASH) represents a more serious condition within the broad
spectrum of NAFLDs and may result in damage, fibrotic changes in the liver, and cirrhosis. These two are
strongly associated with obesity.
The parenchymal cells respond to most noxious agents by replacing glycogen with lipids, producing fatty
infiltration with or without cell death or necrosis. This is commonly associated with inflammatory cell
infiltration and growth of fibrous tissue. Cell regeneration can occur if the disease process is not too toxic to the
cells. The result of chronic parenchymal disease is the shrunken, fibrotic liver seen in cirrhosis. The
consequences of liver disease are often incapacitating or life-threatening, and their presence is ominous. Among
the most common and significant manifestations of liver disease are jaundice, portal hypertension, ascites and
varices, nutritional deficiencies, and hepatic encephalopathy or coma. We will review each of these starting
with jaundice.
The bilirubin concentration in the blood may be increased in the presence of liver disease, if the flow of bile is
impeded, or if there is excessive destruction of red blood cells. With bile duct obstruction, bilirubin does not
enter the intestine; as a consequence, urobilinogen is absent from the urine and decreased in the stool. When the
bilirubin concentration in the blood is abnormally elevated, all of the body tissues, including the sclerae and the
skin, become tinged yellow or greenish-yellow, a condition known as jaundice. Jaundice becomes clinically
NURS4581 HEPATIC DYSFUNCTION: Comprehensive Overview and Key Concepts
Your textbook does a good condensed version of reviewing the A&P and the functions of the liver; you may
want to review this to understand what complications these patient will experience. You should know these
functions of the liver: glucose metabolism, ammonia conversion, protein metabolism, fat metabolism, vitamin
and iron storage, bile formation, bilirubin excretion, & drug metabolism. When the patient experiences liver
failure then it impacts its ability to perform these functions. Liver disorders are common and may result from a
virus, obesity, and insulin resistance, or exposure to toxic substances, such as alcohol, or tumors.
The liver plays a major role in the metabolism of glucose and the regulation of blood glucose concentration.
After a meal, glucose is taken up from the portal venous blood by the liver and converted into glycogen, which
is stored in the hepatocytes. When glucose is needed glycogenolysis occurs releasing glucose into the
bloodstream to maintain normal levels of blood glucose. In hypoglycemia, additional glucose can also be
synthesized gluconeogenesis.
The use of amino acids from protein for gluconeogenesis results in the formation of ammonia as a by-product.
The liver converts this metabolically generated ammonia into urea. Ammonia produced by bacteria in the
intestines is also removed from portal blood for urea synthesis. In this way, the liver converts ammonia, a
potential toxin, into urea, a compound that is excreted in the urine. The liver synthesizes almost all of the
plasma proteins. Vitamin K is required by the liver for synthesis of prothrombin and some of the other clotting
factors. The liver is also active in fat metabolism. Fatty acids can be broken down for the production of energy
and ketone bodies. Breakdown of fatty acids into ketone bodies occurs primarily when the availability of
glucose for metabolism is limited, as in starvation or in uncontrolled diabetes. Fatty acids and their metabolic
products are also used for the synthesis of cholesterol, lecithin, lipoproteins, and other complex lipids. Vitamins
A, B, and D and several of the B-complex vitamins are stored in large amounts in the liver. Certain substances,
such as iron and copper, are also stored in the liver.
Bile is continuously formed by the hepatocytes and collected in the canaliculi and bile ducts. The functions of
bile are excretory, as in the excretion of bilirubin; bile also serves as an aid to digestion through the
emulsification of fats by bile salts. Bile is collected and stored in the gallbladder and is emptied into the
intestine as needed for digestion. Bile salts are synthesized by the hepatocytes from cholesterol and are excreted
into the bile. Bile salts are then reabsorbed, primarily in the distal ileum, into portal blood for return to the liver
and are again excreted into the bile. This pathway from hepatocytes to bile to intestine and back to the
hepatocytes is called the enterohepatic circulation. Because of the enterohepatic circulation, only a small
fraction of the bile salts that enter the intestine are excreted in the feces. Hepatocytes remove bilirubin from the
blood and chemically modify it through conjugation to glucuronic acid, which makes the bilirubin more soluble
in aqueous solutions. The conjugated bilirubin is secreted by the hepatocytes into the adjacent bile canaliculi
and is eventually carried in the bile into the duodenum. In the small intestine, bilirubin is converted into
urobilinogen, which is partially excreted in the feces and partially absorbed through the intestinal mucosa into
the portal blood. Some of the urobilinogen enters the systemic circulation and is excreted by the kidneys in the
urine. Elimination of bilirubin in the bile represents the major route of its excretion.
The liver metabolizes many medications, such as barbiturates, opioids, sedatives, anesthetics, and
amphetamines. Metabolism generally results in drug inactivation, although activation may also occur. One of
the important pathways for medication metabolism involves conjugation of the medication with a variety of
compounds, such as glucuronic acid or acetic acid, to form more soluble substances, excreted in the feces or
urine, similar to bilirubin excretion. Bioavailability is the fraction of the given medication that actually reaches
the systemic circulation. The bioavailability of an oral medication can be decreased if the medication is
metabolized to a great extent by the liver before it reaches the systemic circulation; this is known as first-pass
NURS4581 HEPATIC DYSFUNCTION: Comprehensive Overview and Key Concepts
, NURS4581 HEPATIC DYSFUNCTION
effect. Some medications have such a large first-pass effect that their use is essentially limited to the parenteral
route, or oral doses must be substantially larger than parenteral doses to achieve the same effect.
It is important to obtain a health history focusing on previous exposure of the patient to hepatotoxic substances
or infectious agents; occupational, recreational, and travel history may assist in identifying exposure to
hepatotoxins; history of alcohol and drug use; use of hepatotoxic medications. Many medications are
responsible for hepatic dysfunction and disease. A thorough medication history should address all current and
past prescription medications, over-the-counter medications, herbal remedies, and dietary supplements. The
history also addresses symptoms that suggest liver disease. Symptoms that may have their origin in liver disease
but are not specific to hepatic dysfunction include jaundice, malaise, weakness, fatigue, pruritus, abdominal
pain, fever, anorexia, weight gain, edema, increasing abdominal girth, hematemesis, melena, hematochezia,
easy bruising, changes in mental acuity, personality changes, sleep disturbances, and decreased libido in men
and secondary amenorrhea in women.
The history also addresses symptoms that suggest liver disease. Symptoms that may have their origin in liver
disease but are not specific to hepatic dysfunction include jaundice, malaise, weakness, fatigue, pruritus,
abdominal pain, fever, anorexia, weight gain, edema, increasing abdominal girth, hematemesis, melena,
hematochezia, easy bruising, changes in mental acuity, personality changes, sleep disturbances.
The nurse assesses the patient for physical signs that may occur with liver dysfunction, including the pallor
often seen with chronic illness and jaundice. The skin, mucosa, and sclera are inspected for jaundice, and the
extremities are assessed for muscle atrophy, edema, and skin excoriation secondary to scratching. The nurse
observes the skin for petechiae or ecchymotic areas, spider angiomas, and palmar erythema. The male patient is
assessed for unilateral or bilateral gynecomastia and testicular atrophy due to hormonal changes. The patient’s
cognitive status and neurologic status are assessed. The nurse observes for general tremor, asterixis, weakness,
and slurred speech.
When assessing the patient the nurse will look at the abd, listen, and then palpate for a fluid wave and palpate
the liver. If the liver is palpable, the nurse notes and records its size, its consistency, any tenderness, and
whether its outline is regular or irregular. Tenderness of the liver indicates recent acute enlargement while
absence of tenderness may imply that the enlargement is of long-standing duration. The liver of a patient with
viral hepatitis is tender, whereas that of a patient with alcoholic hepatitis is not.
There are a variety of diagnostic tests that can be done. The nurse should note trends in results because they
provide information about disease progression as well as the patient’s response to therapy. Over 70% of the
parenchymal must be damaged before there will be changes in the liver function test results. Serum
aminotransferases are sensitive indicators of injury to the liver cells and are useful in detecting acute liver
disease such as hepatitis. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-
glutamyl transferase (GGT) are the most frequently used tests of liver damage. ALT levels increase primarily in
liver disorders and are used to monitor the course of hepatitis, cirrhosis, the effects of treatments that may be
toxic to the liver. AST is not specific to liver diseases however levels of AST may be increased in cirrhosis,
hepatitis, and liver cancer; and Gamma-glutamyl transferase (GGT) levels are associated with cholestasis and
alcoholic liver disease. In end-stage liver disease, AST and ALT levels may be normal.
A liver biopsy may be needed. The most common indication is to evaluate diffuse disorders of the parenchyma
and to diagnose space-occupying lesions. Liver biopsy is especially useful when clinical findings and laboratory
tests are not diagnostic.
NURS4581 HEPATIC DYSFUNCTION: Comprehensive Overview and Key Concepts
, NURS4581 HEPATIC DYSFUNCTION
Ultrasonography, computed tomography (CT) scans, and magnetic resonance imaging (MRI) are used to
identify normal structures and abnormalities of the liver and biliary tree. A radioisotope liver scan may be
performed to assess liver size, blood flow, and obstruction. Noninvasive liver stiffness measurements or
elastography uses ultrasound-based vibration and scanning to identify liver fibrosis and determine its extent.
Magnetic resonance elastography uses mechanical shear waves to identify stiff tissue. Liver fibrosis and other
liver diseases can be identified, evaluated and monitored with a variety of other noninvasive studies. These
studies may reduce the need for liver biopsy.
Laparoscopy is used to examine the liver and other pelvic structures. It is also used to perform guided liver
biopsy, to determine the cause of ascites, and to diagnose and stage tumors of the liver and other abdominal
organs.
Hepatic dysfunction results from damage to the liver’s parenchymal cells, directly from primary liver diseases,
or indirectly from either obstruction of bile flow or derangements of hepatic circulation. Liver dysfunction may
be acute or chronic though chronic is far more common.
Chronic liver disease is the 12th leading cause of death in the United States among young and middle-aged
adults with at least 40% of those deaths associated with alcohol use. Approximately 80% of patients diagnosed
with cirrhosis compensate and remain asymptomatic for the next 10 years. Disease processes that lead to
hepatocellular dysfunction may be caused by infectious agents such as bacteria and viruses and by anoxia,
metabolic disorders, toxins and medications, nutritional deficiencies, and hypersensitivity states. The most
common cause of parenchymal damage is malnutrition, especially that related to alcoholism.
Nonalcoholic fatty liver disease and nonalcoholic steatohepatitis are two diseases within the spectrum of fatty
liver to fibrosis and cirrhosis that are strongly associated with obesity and alcohol consumption. In patients who
are overweight, obese, or have high alcohol intake, the nurse observes for signs of associated liver dysfunction.
In some conditions, lipids may accumulate in the hepatocytes, resulting in the abnormal condition called fatty
liver disease. If unrelated to alcohol, this disease is referred to as nonalcoholic fatty liver disease (NAFLD). A
condition known as nonalcoholic steatohepatitis (NASH) represents a more serious condition within the broad
spectrum of NAFLDs and may result in damage, fibrotic changes in the liver, and cirrhosis. These two are
strongly associated with obesity.
The parenchymal cells respond to most noxious agents by replacing glycogen with lipids, producing fatty
infiltration with or without cell death or necrosis. This is commonly associated with inflammatory cell
infiltration and growth of fibrous tissue. Cell regeneration can occur if the disease process is not too toxic to the
cells. The result of chronic parenchymal disease is the shrunken, fibrotic liver seen in cirrhosis. The
consequences of liver disease are often incapacitating or life-threatening, and their presence is ominous. Among
the most common and significant manifestations of liver disease are jaundice, portal hypertension, ascites and
varices, nutritional deficiencies, and hepatic encephalopathy or coma. We will review each of these starting
with jaundice.
The bilirubin concentration in the blood may be increased in the presence of liver disease, if the flow of bile is
impeded, or if there is excessive destruction of red blood cells. With bile duct obstruction, bilirubin does not
enter the intestine; as a consequence, urobilinogen is absent from the urine and decreased in the stool. When the
bilirubin concentration in the blood is abnormally elevated, all of the body tissues, including the sclerae and the
skin, become tinged yellow or greenish-yellow, a condition known as jaundice. Jaundice becomes clinically
NURS4581 HEPATIC DYSFUNCTION: Comprehensive Overview and Key Concepts
