[Exam 1] Chapter 49: Assessment and Management of Patients with Hepatic Disorders Flashcards
(340 cards)
1
Q
Anatomy: Liver receives rich-blood from where?
A
Portal vein, which drains the GI tract and is rich in nutrients but lacks oxygen
2
Q
Anatomy: Liver is essentially important in regulation of what
A
glucose and protein metabolism
3
Q
Anatomy: What does the liver do?
A
Manufacture and secrete bile
4
Q
Anatomy: What does bile do?
A
Has a major role in digestion and absorption o ffats in GI tract.
5
Q
Anatomy: The liver removes what
A
waste products from the bloodstream and secretes them into bile
6
Q
Anatomy: Bile is stored where?
A
In the gallbladder until it is needed for digestion.
7
Q
Anatomy: what are lobules?
A
Small functional units of the liver
8
Q
Anatomy: What are Kupffer Cells?
A
Phagocytic cells of liver. Most common phagocyte in human body and main function are to engulf particulate matter that enters the liver through the portal blood
9
Q
Anatomy: What are canaliculli?
A
The smallest bile ducts, and are located between the lobules of the liver. Receive secretions from the hepatoctytes and carry them to larger bile ducts
10
Q
Function of Liver - Glucose Metabolism: What happens to glucose after a meal?
A
It is taken up from the portal venous blood by the liver and converted into glycogen, and stored in the hepatocytes.
11
Q
Function of Liver - Glucose Metabolism: Glycogen is converted back to glucose why?
A
Released into bloodstream to maintain normal levels of blood glucose.
12
Q
Function of Liver - Glucose Metabolism: What is gluconeogenesis?
A
A process where additional glucose can be synthesized by the liver . Uses amino acids from protein breakdown or lactate produced bye exercising muscles. Occurs because of hypoglycemia
13
Q
Function of Liver - Ammonia Conversion: Why is this formed?
A
When amino acids from protein are used for gluconeogenesis.
14
Q
Function of Liver - Ammonia Conversion: What does liver convert this to?
A
Urea, that is excreted in the urine
15
Q
Function of Liver - Protein Metabolism: What does liver to for protein metabolism?
A
Synthesizes almost all of the plasma proteins (albumin, alpha globulins, beta globulins, blood clotting factors)
16
Q
Function of Liver - Protein Metabolism: Why is Vit K required?
A
For synthesis of prothrombin and some other clotting factors.
17
Q
Function of Liver - Protein Metabolism: What is used for protein synthesis?
A
Amino acids
18
Q
Function of Liver - Fat Metabolism: Fatty acids can be broken down for what
A
production of energy and ketone bodies (small compounds that can enter bloodstream and provide source of energy for muscles)
19
Q
Function of Liver - Fat Metabolism: When does breakdown of fatty acids into ketone bodies occur?
A
When the availability of glucose for metabolism is limited, like starvation or uncontrolled diabetes.
20
Q
Function of Liver - Vit/Iron Storage: What is stored in large amounts in liver?
A
Vit A, B, D, and B-Complex Vitamins. Iron and Copper too.
21
Q
Function of Liver - Bile Formation: What specifically forms bile?
A
Hepatocytes
22
Q
Function of Liver - Bile Formation: What is bile composed of?
A
Mainly water and electrolytes such as sodium, potassium, calcium, chloride, and bicarbonate. Also contains lecithin, fatty acids, cholesterol, bilirubin, and bile salts.
23
Q
Function of Liver - Bile Formation: Bile serves as an aid to digestion how
A
through emulsification of fats by bile salts
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Q
Function of Liver - Bile Formation: Bile salts are synthesized how
A
by the hepatocytes from cholesterol. After binding with amino acids, bile salts are excreted into the bile.
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Function of Liver - Bile Formation: Bile salts with cholesterol are required for what?
Emulsification of fats in the intestine, which are necessary for efficient digestion and absorption.
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Function of Liver - Bile Formation: What happens when bile salts are reabsorbed?
Primarily done in distal ileum, into portal blood for return to liver and again excreted into the bile.
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Function of Liver - Bile Formation: What is enterohepatic circulation?
The pathway from hepatocytes to bile to intestine and back to the hepatocytes. Only fraction of bile salts that enter intestine are excreted in feces
28
Function of Liver - Bilirubin Excretion: What is bilirubin?
Pigment derived from breakdown of hemoglobin by cells of the reticuloendothelial system, including the kupffer cells of the liver.
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Function of Liver - Bilirubin Excretion: What do HEpatocytes do to bilirubin?
Remove it from blood and chemically modify it through conjugation to glucuronic acid, which makes the bilirubin more osluble in aqueous solutions.
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Function of Liver - Bilirubin Excretion: COnjugated bilirubin secreted by hepatocytes into what
adjacent bili canaliculi and is eventually carrired in the bile into the duodenum
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Function of Liver - Bilirubin Excretion: What happens to bilirubin in small intestine?
Converte dinto urobilinogen, which is partically excreted in the feces and partially absorbed through the intestinal mucosa into the portal blood. Some enters systemic circulation and excreted by kidneys in the urine
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Function of Liver - Drug Metabolism: One of the important pathways for medication metabolism involves what?
Conjugation (binding) of the meds with a variety of compounds, such as glucuronic acid.
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Function of Liver - Drug Metabolism: What is bioavailability?
The fraction of the given medication that actually reaches systemic circulation.
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Function of Liver - Drug Metabolism: How can bioavailability of an oral medication be decreased?
if the medication is metabolized to a great extent by the liver before it reaches the systemic circulation
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Liver Assess, Health Hx: Alcohol intake of how much is considered high risk for cirrhosis?
Men: 60-80 g/ day (4 glasses of beer)
Women: 40-60 g/day
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Liver Assess, Health Hx: What is cirrhosis?
Chronic liver disorder characterized by fibrotic changes, the formation of dense connective tissue within the liver, and loss of functional liver tissue.
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Liver Assess, Health Hx: Symptoms that may have their origin in liver disease include what?
Jaundice, malaise, weakness, fatigue, pruritus, abdominal pain, fever, anorexia, weight gain, edema., easy bruising, and personality changes.
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Liver Assess, Physical Assess: What physical signs may occur with liver dysfunction?
Pallor often seen with chronic illness and jaunice
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Liver Assess, Physical Assess: Extremities are assessed foro what?
Muscle atrophy, edema, and skin excoriation secondary to scratching.
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Liver Assess, Physical Assess: Skin is observed for what?
petechiae or ecchymotic areas (bruises) spider angiomas, and palmar erythema.
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Liver Assess, Physical Assess: What specific things are males assessed for?
Unilateral or bilateral gynecomastia and testicular atrophy due to hromonal changes.
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Liver Assess, Physical Assess: What neurologic parts are assessed?
General tremor, astreixis, weakness, and slurred speech
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Liver Assess, Physical Assess: Abdomen is palpaed to assess what?
Liver size and to detect any tenderness over the liver. May be palpable in the right upper quadrant.
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Liver Assess, Physical Assess: How does a palpable liver present?
As a firm, sharp ridge with a smooth surface.
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Liver Assess, Physical Assess: If the liver is not palpable but tenderness is suspected, tapping the lower right thorax may elicit what
tenderness.
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Liver Assess, Physical Assess: What does nurse do if liver is palpable and enlarged?
Record its size, consistency and tenderness. If enlarged, the degree to which it descends below the right costal margin.
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Liver Assess, Physical Assess: Tenderness of the liver indicates what?
recent acute enlargement with nonsequent stretching of the liver capsule.
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Diagnostic Eval - Liver Function Tests: How much of the parenchyma of the liver need to be damaged before tests are abnormal?
More than 70%.
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Diagnostic Eval - Liver Function Tests: Function is generally measures in terms of what
enzyme zctivity (serum amniotransferases, alkaline phosphate) and serum concentration of proteins (albumin, bilirubin, ammonia, clotting factors, lipids).
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Diagnostic Eval - Liver Function Tests: What are serum aminotrasnferases?
Sensitive indicators of injury to the liver cells and are useful in deteting acute liver disease like hepatitis
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Diagnostic Eval - Liver Function Tests: What are the most frequently used tests of liver damage?
ALT, AST, and GGT
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Diagnostic Eval - Liver Function Tests: What to know for ALT levels?
Increase primarily in liver disorders, and can be used to monitor course of hepatitis or cirrhosis or effects of treatments that may be toxic
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Diagnostic Eval - Liver Function Tests: What to know for AST?
AST is present in tissues that have high metabolic activity, therefore level may be increased if there is damage to or death of tissues of organs.
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Diagnostic Eval - Liver Function Tests: AST may be increased in what?
Cirrhosis, hepatitis, and liver cancer.
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Diagnostic Eval - Liver Function Tests: Increased GGT levels are assocaiated with what
cholestasis but can also be due to alcoholic liver disease.
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Diagnostic Eval - Liver Biopsy: What is liver biopsy?
Removal of a small amount of liver tissue, usually through needle aspiration.
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Diagnostic Eval - Liver Biopsy: Most common indication for this is to diffuse disorders of what?
Parenchyma and to diagnose space-occupying lesions.
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Diagnostic Eval - Liver Biopsy: Most common complication after this?
Peritonitis caused by blood or bile after liver biopsy
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Diagnostic Eval - Liver Biopsy: Other techniques for liver biopsy are preferred if why?
AScites (accumulation of alabumin-rich fluid in the peritoneal cavity) or coagulation abnormalites exist.
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Diagnostic Eval - Liver Biopsy: How can a liver biopsy be performed?
Percutaneously with ultrasound guidance or transvenously through the right internal jugular vein .
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Diagnostic Eval - Other Diagnostic Tests: What can be used to idetnify normal structures and abnormalities?
Ultrasonography, CT, and MRI
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Diagnostic Eval - Other Diagnostic Tests: Radioisotope liver scan may be performed to assess what?
Liver size, blood flow, and obstruction
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Diagnostic Eval - Other Diagnostic Tests: Noninvasive liver stiffness measures are used why
to identify liver fibrosis and determine its extent.
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Diagnostic Eval - Other Diagnostic Tests: Why may laparoscopy be used?
To examine liver and other pelvic strucutres. Also used to perform guided liver biopsy, determine cause of ascites, and diagnose and stage tumors.
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Manifestations of Hepatic Dysfunction: Hepatic dysfunction results from what?
Damage to the livers parenchymal cells, directly from primary liver diseases, or indirectly from either obstruction of bile flow
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Manifestations of Hepatic Dysfunction: What are pigment studies?
Studies measure the ability of the liver to conjugate and excrete bilirubin. Results are abnormal in liver and biliary tract disease associated with jaundice
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Manifestations of Hepatic Dysfunction: Albumin is affected in what?
Cirrhosis, chronic hepatitis, edema, and ascites
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Manifestations of Hepatic Dysfunction: Globulins are affected in what?
Cirrhosis, liver disease, chronic obstructive jaundice , and viral hepatitis.
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Manifestations of Hepatic Dysfunction: A/G ratio is reserved where?
In chronic liver disease (decreased albumin and increased globulin)
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Manifestations of Hepatic Dysfunction: What may affect prothrombin time?
May be prolonged in liver disease. It will not return to normal with Vitamin K in severe liver cell damage.
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Manifestations of Hepatic Dysfunction: Serum alkaline phosphatase is a sensitive emeasure of what?
biliary tract obstruction
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Manifestations of Hepatic Dysfunction: When are AST and ALT elevated?
Are elevated in liver cell damage.
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Manifestations of Hepatic Dysfunction: When is GGT and GGTP elevated?
In alcohol abuse and markers for biliary cholestasis
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Manifestations of Hepatic Dysfunction: When would ammonia levels rise?
In liver failure
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Manifestations of Hepatic Dysfunction: How are cholesterol levels in liver disease?
Elevated in biliary obstruction and decreased in parenchymal liver disease
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Manifestations of Hepatic Dysfunction: Disease processes that lead to hepatocellular dysfunction may be caused by what?
infectious agents such as bacteria and viruses and by anoxia, meabolic disorders, toxins and medications.
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Manifestations of Hepatic Dysfunction: Most common cause of parenchymal damage?
Malnutrition, especially that related to alcoholism
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Manifestations of Hepatic Dysfunction: Parenchymal cells respond to most noxious agents how?
By replacing glycogen with lipids, producing fatty infiltration with or without cell death or necrosis. Commonly associated with inflammatory cell infiltration and growth of fibrous tissue.
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Manifestations of Hepatic Dysfunction: What can cause fatty liver disease?
When lipids accumulate in the hepatocytes
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Manifestations of Hepatic Dysfunction: What is nonalcoholic fatty liver disease?
When lipids accumulate and is unrelated to alcohol
81
Manifestations of Hepatic Dysfunction: Most common signs of liver disease include?
Jaundice, portal hypertension, ascites, and varcies, nutritional deficiencies, and hepatic encephalopathy or coma
82
Jaundice: Bilirubin concentraiton in blood may be increased when?
In presence of liver disease, if flow of bile is impended (by gallstones) or is there is excessive destruction of red bloodo cells
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Jaundice: What happens when bilirubin does not enter the intestine?
Urobilinogen is absent from the urine and decreased in the stool
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Jaundice: What happens when bilirubin concentration is abnormally elevated?
All of the body tissues, including the sclera and skin and become tinged yellow or greenish-yellow
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Jaundice: What bilirubin level is needed to become seen?
When levels go above 2.0
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Jaundice: Increased serum bilirubin levels and jaundice may result from what?
Impairment of hepatic uptake, conjugfation of bilirubin, or excretion of bilirubin into the biliary system
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Jaundice: What types of jaundice are associated with liver disease?
Hepatocellular and obstructive
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Jaundice - Hemolytic Jaundice: What is this a result of?
Increased destruction of red blood cells, and plasma is rapidly floodly with bilirubin so liver cannot excrete the bilirubin as quicklky as its formed
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Jaundice - Hemolytic Jaundice: This type of jaundice is encountered with which patient?
With hemolytic transfusion reactions and other hemolytic disorders. Here, bilirubin is predominately unconjugated or free.
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Jaundice - Hemolytic Jaundice: What is increased in fecal and urine?
Urobilinogen levels are increased, but urine is free of bilirubn.
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Jaundice - Hemolytic Jaundice: What symptoms do they expereince?
Do not experience symptoms or complications as a result of jaundice
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Jaundice - Hemolytic Jaundice: What happens if its prolonged?
Even if mild, predisposes to the formation of pigment stones in the gallbladder . Extremly severe jaundice poses a risk for CNS effects.
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Jaundice - Hepatocellular Jaundice: What is this caused by?
Inability of damaged liver cells to clear normal amounts of bilirubin from blood.
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Jaundice - Hepatocellular Jaundice: Cellular damage may be caused by what
hepatitis viruses, other viruses that affect the liver, chemical toxins or alcohol.
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Jaundice - Hepatocellular Jaundice: How is cirrhosis related to this?
This is a form of hepatocellular disease that may promote jaundice.
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Jaundice - Hepatocellular Jaundice: This is usually caused by what?
Excessive alcohol intake, but may also be a result of liver cell necrosis caused by viral infection.
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Jaundice - Hepatocellular Jaundice: What happens in prolonged obstructive jaundice?
Cell damage eventually develops and both types of jaundice appear together
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Jaundice - Hepatocellular Jaundice: Patients with this may have what signs?
Lack of appetite, nausea, malaise, fatigue, weakness, and possible weight loss.
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Jaundice - Hepatocellular Jaundice: How may serum bilirubin concentration and urine urobilinogen be?
May be elevated.
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Jaundice - Hepatocellular Jaundice: How may AST and ALT levels be?
May be increased, indicating cellular necrosis. Patient may report headache, chills, and fever.
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Jaundice - Obstructive Jaundice: This resulting from extrahepatic obstruction may be caused by?
occlusion of the bile ducct from a gallstone, an inflammatory process, a tumor, or pressure from enlarged organ. Or also involve small bile ducts within liver.
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Jaundice - Obstructive Jaundice: What may cause obstruction with small bile ducts?
Inflammatory swelling of the liver or by an inflammatory exudate within the ducts themselves.
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Jaundice - Obstructive Jaundice: When may intrahepatic obstruction resulting from stasis and inspissation (thickening) of bile within the canaliculi may occur when
after ingestion of certain meds, which are referred to as cholestatic agents.
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Jaundice - Obstructive Jaundice: What happens since bile cannot flow normally into the intestine and becomes backed up into the liver?
It is then reabsorbed into the blood and carried throughout the entire body, staining the skin, mucous membranes and sclerae.
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Jaundice - Obstructive Jaundice: What color does urine change into when obstructed?
deep orange and foamy
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Jaundice - Obstructive Jaundice: What happens because there are decreased amount of bile in intestinal tract?
Stools become light or clay colored.
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Jaundice - Obstructive Jaundice: How may their diet change?
May have dyspepsia and intolerance to fatty foods
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Jaundice - Hereditary Hyperbilirubinemia: increase serum bilirubin levels can produce what
jaundice
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Jaundice - Hereditary Hyperbilirubinemia: What is Gilbert Syndrome?
Familial disorder characterized by an increased level of unconjugated bilirubin that causes jaundice.
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Jaundice - Hereditary Hyperbilirubinemia: How does the rest of the liver act even though bilirubin levels increased?
Liver histology and liver function test results are normal and there is no hemolysis.
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Jaundice - Hereditary Hyperbilirubinemia: Other conditions that are probably caused by inborn errors of biliary metabolism include what
Dubin-Johnson syndrome, Rotor syndrome, the benign cholestatic jaundice of pregnancy.
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Portal Hypertension: What is this?
Increased pressure throughout the portal venous system that results from obstruction of blood flow into and through the damaged liver.
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Portal Hypertension: Common manifestations of portal hypertension?
ascites and varices
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Ascites - Patho: What are some contributing factors to this?
Portal hypertensiona nd the resulting increase in capillary pressure and obstruction of vneous blood flow through damaged liver.
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Ascites - Patho: What can cause there to be an increase in sodium and water retention by kidney?
Failrue of the liver to metabolize aldosterone
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Ascites - Patho: What can contirbuute to the movement of fluid from the vascular system into the peritoneal space?
Sodium and water retention, increased intravascular fluid volume, increased lymphatic flow, and decreased synthesis of albumin by the damaged liver
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Ascites - Patho: The loss of fluid into the peritoneal space causes further what?
Sodium and water retention by the kidney in an effort to maintain the vascular fluid volume
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Ascites - Patho: As a result of liver damanage, large amount of albumin-rich fluid accumulate in peritoneal cavity as what
ascites
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Ascites - Patho: With the movement of albumin from the serum to the peritoneal cavity, the osmotic pressure of serum decreases. This results in what
movement of fluid into the peritoneal cavity.
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Ascites - CMs: Common presenting symptoms of ascites?
Increased abdominal girth and rapid weight gain. May be SOB and uncomfortable from the enlarged abdomen and striae and distended veins may be visible over abdominal wall.
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Ascites - Assess/Diagnostic: Presence and extent of ascites are assessed how
by percussion of the abdomen
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Ascites - Assess/Diagnostic: What happens when fluid accumulated in peritoneal cavity?
Flanks bulge when the patient assumes a supine position
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Ascites - Assess/Diagnostic: Presence of fluid can be confirmed how?
either by percussing for shifting dullness, by detecting a fluid wave or by performing ballottement technique
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Ascites - Assess/Diagnostic: What is a ballottement technique?
Palpation technique performed to identify a mass or enlarged organ within an abdomen with ascites.
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Ascites - Medical Mx: This includes what?
Dietary modification, pharmacologic therapy, bed rest, paracentesis and use of shunts.
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Ascites - Nutritional Therapy: Goal of treatment for this patient?
Negative sodium balance to reduce fluid retention.
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Ascites - Nutritional Therapy: How long for patients taste buds to adjust for unsalted foods?
2-3 months
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Ascites - Nutritional Therapy: Foods that contain ammonia could cause what in patient?
Hepatic encephalopathy and coma
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Ascites - Nutritional Therapy: What happens if fluid accumulation is not controlled?
Daily sodium allowance may be further lowered and diuretic agents may be given.
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Ascites - Nutritional Therapy: What can increase the chances of the patient following this diet?
If the patient and partner preparing the meals understand the rationale for the diet
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Ascites - Pharmacologic therapy: First line of therapy for this patients?
Spironolactone , an aldosterone-blocking agent, is used first. Prevents potassium loss.
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Ascites - Pharmacologic therapy: Daily weight los should not exceed what?
1 kg in patients with ascites and peripheral edema and 0.5-0.75 for those without edema.
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Ascites - Pharmacologic therapy: Possible complications of diuretic therapy?
Fluid and electrolyte disturbances (hypovolemia, hypokalemia, hyponatremia, and hypochloremia alkalosis) and encephalopathy
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Ascites - Pharmacologic therapy: What happens in the body when potassium stores are depleted?
Amount of amonia in systemic circulation increases.
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Ascites - Bed Rest: An upright posture activates what?
RAAS and Sympathetic Nervous System. Causes reduced glomerular filtration and sodium excretion and decreased response to loop diuretics.
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Ascites - Paracentesis: What is this?
Removal of fluid (ascites) from the peritoneal cavity through a puncture or a small surgical incision throught he abdominal wall under sterile conditions.
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Ascites - Paracentesis: When would ultrasound guidance be indicated?
For patients who are at high rsik for bleeding because of an abnormal coagulation profile and in those with previous abdominal surgery and may have adhesions.
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Ascites - Paracentesis: When is this performed?
As a diagnostic exam, in treatment for massive ascites that is resistant to nutritional/diuretic therapy, and prelude to diagnostic imaging.
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Ascites - Paracentesis: This is often paired with what for immediate effect?
IV infusion of salt-poor albumin or other colloid.
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Ascites - Paracentesis: What can refractive, massive ascites be unresponsive to?
Multiple diuretic agents and sodium restriction for 2 week or more can result in respiratory distress.
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Ascites - Paracentesis: Albumin infusions help with what?
To correct decreases in effective arterial blood volume that lead to sodium retention. Reduces incidence of postparacentesis circulatory dysfunction with renal dysfunction.
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Ascites - Transjugular Intrahepatic Portosystemic Shunt: What is this?
Method of treating ascites in which a cannula is threaded into the portal vein by the transjugular route. Expandable shunt inserted to serve as intrahepaptic shunt. Decreases sodium retention and improves renal response to diuretic therapy.
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Ascites - Other Methods of Tx: How does the insertion of a peritoneovenous shunt help?
Redirects ascitis fluid from the peritoneal cavity into the systemic circulation via an abdominal and thoracic catheter that drain into the superior vena cava.
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Ascites - Nursing MX: What should be assessed and measured by nurse?
Assessment and documentation of intake/output, abdominal girth, and daily weight to assess fluid status.
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Ascites - Nursing MX: Why do we monitor respiratory status?
Large volume of ascites can compress the thoracic cavity and inhibit adequate lung expansion.
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Ascites - Nursing MX: What levels in body does the nurse monitor?
Serum ammonia, creatinine and electrolyte levels.
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Ascites - Nursing MX: Nurse should instruct the patient about what when discharged?
Avoid alcohol, low sodium-diet, take meds.
148
Esophageal Varices: What is this?
Varicosities that develop from elevated pressure in the veins that drain into the portal system. Prone to rupture and source of massive hemorrhages from upper GI tract and rectum
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Esophageal Varices: What happens once esophageal varices form?
They increase in size over time and may eventually bleed.
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Esophageal Varices: How are varices related to cirrhosis?
Most significant source of bleeding.
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Esophageal Varices - Patho: Description of this?
Dilated, tortous veins that are usually found in submucosa of lower esophagus. Always caused by portal hypertension, which results from obstruction of portal venous circulation.
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Esophageal Varices - Patho: What happens because of increased obstruction of portal vein?
Venous blood from the intestinal tract and spleen seeks an outlet through collateral circulation. These collateral vessels are not elastic.
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Esophageal Varices - Patho: How serious are esophageal varices
Life threatening and can result in hemorrhagic shock that produces decreased cerebral, hepatic, and renal perfusion.
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Esophageal Varices - Patho: What is increased in body due to bleeding?
Increase dnitrogen load from bleeding, with increases serum ammonia level, and increasing risk of encephalopathy.
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Esophageal Varices - Patho: Factors that contribute to hemorrhage are what
muscular exertion from lifting heavy objects, straining at stool, sneezing, coughing, or vomiting.
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Esophageal Varices - CMs: Patient with bleeding esophageal varices may present with what?
Hematemesis, melena, or general deterioration in mental or physical status and have sicks of shock as well.
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Esophageal Varices - Assessment: What is used to identify the bleeding site?
Endoscopy, along with ultrasonography, CT scanning, and angiogaphy.
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Esophageal Varices - Assess/Diagnostic, Endoscopy: Why is immediate endoscopy indicated?
To identify the cause nd site of bleeding.
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Esophageal Varices - Assess/Diagnostic, Endoscopy: Careful monitoring can detect early signs of what?
Cardiac dysrhythmias, perforation, and hemorrhage.
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Esophageal Varices - Assess/Diagnostic, Endoscopy: After exam, fluids are not given until when?
Until their gag reflex returns.
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Esophageal Varices - Assess/Diagnostic, Portal Hypertension Measurements: This may be suspected when?
If dilated abdominal veins and hemorrhoids are detected. Palpable enlarged spleen and ascites may also be present.
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Esophageal Varices - Assess/Diagnostic, Portal Hypertension Measurements: How is an indirect mesurement of the hepatic vein performed?
Insertion of catheter with a balloon into the antecubital or femoral vein. Advanced under fluroscopy to hepatic vein. Fluid infused once catheter in position to inflate the balloon. "Wedged" pressure obtained by occluding blood flow.
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Esophageal Varices - Assess/Diagnostic, Portal Hypertension Measurements: Hepatic venous pressure gradient (HVPG) of what is clinically significant of portal hypertension?
10 mmHg
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Esophageal Varices - Assess/Diagnostic, Portal Hypertension Measurements: How can direct measure of portal vein pressure be obtained?
Insertion of a catheter into the portal vein or one of the branches.
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Esophageal Varices - Lab Tests: What liver function tests will be performed?
Serum aminotransferases, bilirubin, alkaline phosphatase and serum proteins.
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Esophageal Varices - Lab Tests: What diagnostics will be performed?
Splenoportography (serial or segmental x-rays)
Hepatoportography and celiac angiography
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Esophageal Varices - Medical Mx: What is given to the patient since they are subject to volume depletion?
IV fluids, electrolytes, and volume expanders are provided to restore fluid volume.
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Esophageal Varices - Pharmacologic therapy: What drugs are given ASAP?
Vasoactive drugs. Octreotide is effetive in decreasing bleeding from esophageal varcies, and lacks the vasoconstrive effects of vasopressin
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Esophageal Varices - Pharmacologic therapy: Why is Vasopressin not initially given??
Because it produces constriction of the splanchnic arterial bed and decreases portal pressure. This compromises arterial blood supply.
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Esophageal Varices - Pharmacologic therapy: What may be a contraindication in the use of vasopressin?
Coronary artery disease, because vasoconstriction is a side effect that may cause myocardiac infarction.
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Esophageal Varices - Pharmacologic therapy: Vasopressin has been paired with nitroglycerin why?
To reduce or prevent the side effects caused by vasopressin alone.
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Esophageal Varices - Pharmacologic therapy: What drugs are the most common to prevent a first bleeding episode in patients with known varices and to prevent rebleeding
Beta-blocking agents ike propranolol.
173
Esophageal Varices - Balloon Tamponade: This may be used why?
Infrequently used, but can temporarily control hemorrhage and to stabilize a patient with massive bleeding
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Esophageal Varices - Balloon Tamponade: Risks with this?
Displacement of tube and balloon into orophrarynx can obstruct airway. Gastric contents can also go into the lungs.
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Esophageal Varices - Balloon Tamponade: Performing endotracheal intubation before insertion helps with what?
Protects the airway and minimizes the risk of aspiration.
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Esophageal Varices - Balloon Tamponade: What may occur if tube is left in place for too long or at too high of a pressure?
Ulceration and necrosis of the nose, mucosa of stomach, or esophagus may occur.
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Esophageal Varices - Balloon Tamponade: Nursing measures for this?
Frequent mouth and nasal care.
178
Esophageal Varices - Endoscopic Sclerotherapy: What is this
A sclerosing agent is injected through the fiberoptic endoscope into or adjacent to the bleeding esophageal varices to promote thrombosis and eventual sclerosis.
179
Esophageal Varices - Endoscopic Sclerotherapy: How does this process ocur in the body?
Inflammation occurs with the involved vein with eventual thrombosis and loss of lumen of the vesel. Not reccomended for prevention.
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Esophageal Varices - Endoscopic Sclerotherapy: What must they be observed for after this?
Bleeding, perforation of esophagus, aspiration pneumonia, and esophageal stricture.
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Esophageal Varices - Endoscopic Sclerotherapy: What meds may be given after procedure?
Actacids H2 Antagonists or PPI to counteract chemical affects of sclerosing agent
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Esophageal Varices - Endoscopic Variceal Ligation (Banding Therapy): How is this performed?
endoscope loaded with elastic rubber band is passed through an overtube directly onto varix to be banded. After bleeding varix is suctioned into tip, rubber band is slipped over the tissue, causing necrosis, ulceration, and sloughing.
183
Esophageal Varices - Endoscopic Variceal Ligation (Banding Therapy): This helps reduce what?
Rebleeding rate, mortality, procedure-related complications, and number of sessions needed to eradicate varices.
184
Esophageal Varices - Endoscopic Variceal Ligation (Banding Therapy): Complications of this?
Superficial ulceration a nd dysphagia, transient chest discomfort, and esophageal strictures.
185
Esophageal Varices - Endoscopic Variceal Ligation (Banding Therapy): This is recommended for which patient stype?
REceiving beta-blocker therapy and for those who cannot tolerate beta-blocking agents
186
Esophageal Varices - Transjugular Intrahepatic Portosystemic Shunt: This treatment recommended for who?
Uncontrolled variceal bleeding refractory to pharmacologic or endoscopic therapy.
187
Esophageal Varices - Transjugular Intrahepatic Portosystemic Shunt: This can help control what?
Acute variceal hemorrhage by rapidly lowering portal pressure.
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Esophageal Varices - Transjugular Intrahepatic Portosystemic Shunt: Potential complications of this?
Bleeding, sepsis, heart failure, organ perforation, shunt thrombosis, and progressive liver failure.
189
Esophageal Varices - Additional Therapies: What is an alternative way tot reat it?
Using tissue adhesives and fibrin glue
190
Esophageal Varices - Surgical Mx, Surgical Bypass Procedure: Surgical decompression (shunt surgery) not used often?
Effective in eradicating bleeding, but survival statistics are worse than other preventive measures.
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Esophageal Varices - Surgical Mx, Surgical Bypass Procedure: What is a dital splenorenal shunt?
Made between the splenic vein and left renal vein. Mesocaval shunt is created by anastomosing the superior mesenteric vein to proximal end of vena cav.
192
Esophageal Varices - Surgical Mx, Surgical Bypass Procedure: Goal os distal splenorenal and mesocaval shunts?/
To decrease protal pressure by draining only a portion of venous blood from the portal bed.
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Esophageal Varices - Surgical Mx, Surgical Bypass Procedure: Portacaval shunts are considered nonselective shunts why?
Because they divert all portal flow to the vena cava via end-to-side or side-to-side approaches
194
Esophageal Varices - Surgical Mx, Surgical Bypass Procedure: Why are these procedures not always successful?
Because of secondary thrombosis in veins used for shunts and complciations
195
Esophageal Varices - Surgical Mx, Devascularization and Transection: How does this work??
Lower end of the esophagus is reached through small gastrostomy incision, and a staple gun permits anastomosis of transected ends of the esophagus.
196
Esophageal Varices - Nursing Mx: what may be indicated because of blood loss?
Vitamin K therapy and multipe blood transfusions
197
Hepatic Encephalopathy and Coma: What is this?
Life threatening complication of liver disease that occurs with profound liver failure. Is the neuropsychiatric manifestation of hepatic failure associated with portal hypertension and shunting of blood from the portal venous sytem into systemic circulation
198
Hepatic Encephalopathy and Coma - Patho: What two major alterations underlie its development?
1. Hepatic insufficiency may result in encephallopathy because of instability of liver to detoxify toxic by products
2. Portosystemic shunting, where collateral vessels develop as result of portal hypertension, allows elements of portal blood to enter systemic circulation
199
Hepatic Encephalopathy and Coma - Patho: How does ammonia affect brain?
Enters brain and excites peripheral benzodiazepine type recetprs. Stimulates GABA which causes depression of CNS that inbhibits neurotransmission and synaptic regulation.
200
Hepatic Encephalopathy and Coma - Patho: Where is the largest source of ammonia?
Enzymatic and bacterial digestion of dietary and blood proteins in the GI tract. Increases as a r result of GI bleeding, high protein diet, or infection.
201
Hepatic Encephalopathy and Coma - Patho: Serum ammonia is decreased how
by elimination of protein from teh diet and by administration of antibiotics such as neomycin sulfate.
202
Hepatic Encephalopathy and Coma - Patho: What other factors can result in excess ammonia?
Excessive diuresis, dehydration, infections, surgery, fever, and some meds.
203
Hepatic Encephalopathy and Coma - CMs: Earliest signs of this?
Mental status changes and motor disturbances. Patient appears ocnfused and unkempt and has alterations in mood and sleep patterns. Sleep during day and restless at night.
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Hepatic Encephalopathy and Coma - CMs: What happens as this progresses?
Difficult to awaken and are completely disoriented with respect to time and place.
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Hepatic Encephalopathy and Coma - CMs: What may be seen in stage II?
Asterixis, an involuntary flapping of hands. Simple tasks like handwriting become difficult.
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Hepatic Encephalopathy and Coma - CMs: What is done daily to track asterixis?
Handingwriting or drawing sample taken daily.
207
Hepatic Encephalopathy and Coma - CMs: what is constructional apraxia?
Inability to reproduce a simple figure in two or three dimensions
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Hepatic Encephalopathy and Coma - CMs: How are deep tendon reflexes here?
In early stages, are hyperactive. Later on, reflexes disappear and extremities may become flaccid.
209
Hepatic Encephalopathy and Coma - CMs: What is fetor hepaticus?
Sweight, slightly fecal odor to breath. Will be noticed as well
210
Hepatic Encephalopathy and Coma - Assess/Diagnostic: What does the electroencephalogrm show?
Generalized slowing, an increase in amplitude of brain waves, and characteristic triphasic waves.
211
Hepatic Encephalopathy and Coma - Medical Mx: This focuses on what?
Idetnifying and eliminating the precipitating cause, if possible, initiating ammonia lowering therapy, minimizing potental medical complications of cirrhosis and depressed consciousness.
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Hepatic Encephalopathy and Coma - Medical Mx: What med can be given to reduce serum ammonia levels?
Lactulose. Acts by trapping and expelling the ammonia in the feces. 2-3 stools per day are desirable
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Hepatic Encephalopathy and Coma - Medical Mx: Possible side effects of lactulose?
Intestinal bloating and cramps. Can also have a sweet taste.
214
Hepatic Encephalopathy and Coma - Medical Mx: what may indicate lactulose medication overdose?
Development of watery diarrhea stools.
215
Hepatic Encephalopathy and Coma - Medical Mx: Why may IV glucose be given?
To minimize protein breakdown, admin of vitamins to correct deficneinces, adn correction of electrolyte imbalances.
216
Hepatic Encephalopathy and Coma - Medical Mx: What can the nurse monitor here?
```
Neurologic status
Mental Status
I/O
Vital Signs
Potential sites of infection
```
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Hepatic Encephalopathy and Coma - Nursing Mx: What is a great risk given the patients depressed neurologic status?
The potential for respiratory compromise.
218
Hepatic Encephalopathy and Coma - Nursing Mx: What does deep breathing encouragement help with?
Prevents formation of atelectasis, pneumonia, and other respiratory complications.
219
Other Manifestations of Hepatic Dysfunction - Edema and Bleeding: Why is edema developed?
Because of hypopalbuminemia due to decreased hepatic production of albumin. `
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Other Manifestations of Hepatic Dysfunction - Edema and Bleeding: Decause production of blood clotting factors by liver leads to what
increased incidence of bruising, epistaxis, bleeding from wounds, and gi bleeding.
221
Other Manifestations of Hepatic Dysfunction - Vitamin DEficiency: DEcreased production of several clotting factors may be partially due to what?
Deficient absorption of vit K from GI tract.
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Other Manifestations of Hepatic Dysfunction - Vitamin DEficiency: Vit A defiency leads to what
night blindness and eye and skin changes
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Other Manifestations of Hepatic Dysfunction - Vitamin DEficiency: Thiamine deficiency leads to what
beriberi, polyneuritis, and wernicke-korsakoff psychosis
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Other Manifestations of Hepatic Dysfunction - Vitamin DEficiency: riboflavin deficiency leads to what
skin and mucous membrane lesions
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Other Manifestations of Hepatic Dysfunction - Vitamin DEficiency: folic acid deficiency leads to what?
Macrocytic anemia
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Other Manifestations of Hepatic Dysfunction - Metabolic Abnormalities: Why may hypoglycemia occur?
Because of decreased hepatic glycogen resesrves and decreased gluconeogenesis. Meds must be used cautiously.
227
Other Manifestations of Hepatic Dysfunction - Metabolic Abnormalities: Failure of damaged liver to inactivate estrogens can cause what?
Gynecomastia, amenorrhea, testicular atrophy, loss of pubic hair in male, menstrual irregularities in female.
228
Other Manifestations of Hepatic Dysfunction - Pruritus and other Skin Changes: Pruritus may develop why?
Due to retention of bile salts.
229
Viral Hepatitis: What is this?
systemic viral infection in which necrosis and inflamaation of liver cells produce cluster of changes.
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Hepatitis A Virus: What isi this caused by
RNA virus of the enterovirus family.
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Hepatitis A Virus: TRansmitted how?
Fecal-oral route, along with Hep E.
Also ingestion of foods or liquids.
232
Hepatitis A Virus: Typically a child or young adult acquires it how
due to poor hygiene, hand-to-mouth contact, or other close ocntact.
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Hepatitis A Virus: Incubation period?
Can be 2-6 weeks and illness can last 4-8 weeks.
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Hepatitis A Virus: This rarely progresses to what
acute liver necrosis or fulminant hepatic failure.
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Hepatitis A Virus - CMs: Many patients show what signs
Anicteric (without jaundice) and symptomless.
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Hepatitis A Virus - CMs: When symptoms appear, they resemble what?
Those of a mild, flu like upper respiratory tract infection with low-grade fever. Anorexia is an early symptom.
237
Hepatitis A Virus - CMs: What causes anorexia?
Release of a toxin by the damaged liver or from failure of damaged cells to detoxify an abnromal product.
238
Hepatitis A Virus - CMs: What happens later on?
jaundice an dark urine become apparent.
239
Hepatitis A Virus - CMs: Patients develop a strong aversion to the taste of what?
cigarettes or prescence of cigarette smoke. Tend to clear as soon as jaundice reaches its peak.
240
Hepatitis A Virus - Assess/Diagnostic: How does this appear on assessment?
Liver/spleen enlarged moderately for a few days after onset.
241
Hepatitis A Virus - Assess/Diagnostic: What may be found in stool?
HAV antigen may be found in stool 7-10 days before illness, and 2-3 weeks after symptoms appear.
242
Hepatitis A Virus - Prevention: Bests way to prevent?
Proper sewage disposal, hand hygiene. Also effective and save HAV vaccines. Recommended that two-dose vaccine be given after 18. Younger than 18 recieve 3 doses.
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Hepatitis A Virus - Medical Mx: What should patient recieve during anorexia phase?
Frequent small feedings, supplemented by IV fludis with glucose.
244
Hepatitis A Virus - Medical Mx: What are important aspects of treatment?
Bed rest during the acute stage and a nutritious diet.
245
Hepatitis A Virus - Nursing Mx: Nurse assits the patient and family with what?
Coping with temporary disability and fatigue, and educates them to seek additional health care if symptoms worsen.
246
Hepatitis A Virus - Nursing Mx: Specific education about reducing risk of contracting HAV i nclude?
Good, personal hygiene, stressing careful hand hygiene, and environemtnal sanitation
247
Hep B: Transmited how
through blood, saliva, semen, and vaginal secretions. Can be transmited through breaks in skin.
248
Hep B: Incubation period?
Long. Replicates in liver and remains in serum for long periods.
249
Hep B: Those who do not recover from this within 6 months develop what
chronic hepatitis with persistent HBV infection and hepatocellular injury and inflammation.
250
Hep B: In older adults, there is an increased risk of what?
Severe liver cell necrosis or fulminant hepatic failure. Particularly if other illnesses are present.
251
Hep B - CMs: What are some signs that patients have?
Fever/Respiratory problems. Arthralgias and rashes. Loss of appetite, dyspepsia, abdominal pain, generalized aching, malaise, and weakness.
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Hep B - CMs: What accompanies jaundice?
light-colored stools and dark urine accompany it.
253
Hep B - Assess/Diagnostic: What appears in circulation in 80-90% of infected patients 1-10 weeks after exposure?
HBsAg.
254
How can HepC be gotten?
From circulation, like transmission, blood and semen. No vaccine
255
How can HepB be gotten?
CO infection wiht HBV and transmision by blood. No vaccine
256
Signs and Symptoms of all types of hepatitis?
```
REQ Discomfort
GI: N/Vm Anorexia, Weight Loss
Fever
Chills
Jaundice
Dark Urine
```
257
Treatment for all types of hepatitis?
Rest, Activity, Nutrition, Hydration
258
Diagnossi for all types of Hepatitis?
Presence of specific antbody/antigen in serum
259
HepA (HAV): Incubation period?
15-50 days
260
HepA (HAV): Illness lasts how long
4-8 weeks
261
HepA (HAV): Manifestations of symptoms?
Mild flu-like symtpoms, lowgrade fever, anorexia, later jaundice and dark urine, and enlargement of liver and spleen
262
HepA (HAV): Antibodies in body?
Anti-HAV antibody in serum after symptoms appear.
263
HepA (HAV): How is this spread?
Fecal Oral Transmission
Poor hygiene, hand-to-mouth contact, and close contact.
264
HepA (HAV) - Prevention: How?
Good handwashing, safe water, proper sewage disposal.
Immunoglobulin for contacts to provide passive immunity
265
HepA (HAV) - Management: What shiuld be done?
Bed rest during acute stage with nutritional support
266
Hep B (HBV): Tranmitted how?
Blood, saliva, semen, vaginal secretions, sexually transmitted, transmitted to infant at birth
267
Hep B (HBV): This is a major cause of what liver problems
cirrhosis and liver cancer, with 10% not recovering.
268
Hep B (HBV): Incubation period?
1-6 months
269
Hep B (HBV): Manifestations of this?
Insidious and variable, seimilar to hep A
270
Hep B (HBV): What to know for antibody markers?
Has antigenic particles that elicit specific antibody markers during different stages of diseases
271
Hep B (HBV): Prevention?
Vaccine: For those high risk
Passive immunization
Standard precuations
Screening of blood products
272
Hep B (HBV): Nursing Management?
Bed Rest until symptoms subside and liver decreases in size.
Nuritional Support - restrict protein because liver damaged.
273
Hep B (HBV): Medications include?
Alpha Interferon and Antiviral Agents like Lamivudine and Adefovir
May take 3-4 months for patients to recover.
274
Hep C: Transmitted how?
Blood and sexual contact, including needle sticks and sharing of needle
275
Hep C: This is the most common what?
Blodborne infection
276
Hep C: How does this affect livere?
Cause of 1/3 of cases of liver cancer and most common reason for liver transplant
277
Hep C: Incubation period?
Variable, 15-160 days
278
Hep C: How are the symptoms?
Usually mild
279
Hep C: What happens if they do not heal?
Chronic carrier state frequently occurs.
280
Hep C - Management: What is the best way to prevent this?
Education. Screening for blood, preventing sharing needles, and measures to reduce spread of infection
281
Hep C - Management: How does alcohol affect this?
Encouragees the progression of the disease, so alcohol and meds that affect liver should be avoided
282
Hep C - Management: What meds are given?
Antiviral agents, such as interferon and ribavirin to reduce risk of becoming chronic carriers of hepatitis C
283
Hep D: Only people with what are at risk for this?
Hep B
284
Hep D: Transmission?
Through blood and sexual contact
285
Hep D: Symptoms and treatment?
Are similar to Hep B
286
Hep D: Patients with this are most likely to develop what?
Fulminant liver failure (rapid onset of liver failure and need new liver ASAP) and chronic active hepatitis and cirrhosis
287
Hep E: TRansmitted how?
By the fecal-oralroute
288
Hep E: Incubation period?
15-65 days
289
Hep E: How are the symptoms here?
Resembles hep A and is self-limited with abrupt onset. No chronic form
290
Hep E: How to prevent this?
Hand-washing measures
291
Nonviral Hepatitis: Toxic is caused by what?
Chemicals that cn harm the liver that causes necrosis like botanical agents.
292
Nonviral HEpatitis: Way to fix toxic hepatitis?
Through a liver transplant but there may not be many treatment options for thus
293
Nonviral HEpatitis: What is drug-inducecd hepatitis?
Drugs like Tylenol. Can be very damaging to liver like 4000 mg per day.
294
Nonviral HEpatitis: How to treat drug-inducced hepatitis?
Take away the medication that is causing the issue, such as discontinuing Tylenol. Also give higher dose of cortocosteroids.
295
Fulminant Hepatic Failure: What is this?
The rapid onset of liver failure where you need a liver transplalnt to treat.
296
Canceer of the Liver: Why are benign tumors more common now?
Due to the use of oral contraceptives
297
Canceer of the Liver: Cancers are usually associated with what?
Hep B and C, Cirrhosis.
298
Hepatic Cirrhosis: Types?
Alcoholic (Scar tissue around portal area)
Postnecrotic (Broad band of scar tissues caused by hepatitis)
Biliary (Scarring over, around bile ducts)
299
Hepatic Cirrhosis - Patho: What is this?
This is when the liver cells become so severely damaged, they get replaced with fibrous tissue that leads to scarring.
300
Hepatic Cirrhosis - Patho: Why does this happen?
Some people are more susceptible than other. Others use alcohol which causes fatty liver disease leads to cirrhosis.
301
Hepatic Cirrhosis - Patho: What other reasons are there for this being caused?
Hepatitis or Hep C, Increased fat in liver, obesity and diabetes are linked to liver disease because of increased fat in liver.
302
Hepatic Cirrhosis - Patho: What happens if theres a blockage in bile duct?
Bile duct gets blocked and causes backflow to liver and so that could cause lvier damage as well.
303
Hepatic Cirrhosis - Manifestations: What are some manifestations of this?
Liver enlargement, portal obstruction and ascites, GI Varices, Edema, Vitamin Deficiency, and Anemia, Mental Deterioration
304
Hepatic Cirrhosis - Manifestations: How does the liver appear?
Becomes firm, palpable and can be seen.
305
Hepatic Cirrhosis - Manifestations: What are some late clinical manifestations of this?
Jaundice, spleen enlarged, hemorrhoids, edema, changes in memory, spideer angiomas,
306
Hepatic Cirrhosis - Manifestations: What changes occur in hematologic system since liver cannot produce them anymore?
Anemia, Leukopenia, Thrombocytopenia, Coagulation Disorders
307
Hepatic Cirrhosis - Assessment: What will we do
Health Hx, and focus assessment on skin, GI, mental status. Good head-to-toe assessment.
308
Hepatic Cirrhosis - Diagnosis: This includes what?
Fluid volume excess, perfussion, ineffective breathing pattern, fatigued, RF infection, RF bleeding
309
Hepatic Cirrhosis - Potential Complications: This includes?
Esophageal Varicies, Varices Rupture,
310
Hepatic Cirrhosis - Interventions: We want to promote what?
Rest
311
Hepatic Cirrhosis - Interventions: What do we want to improve?
Nutritional status, reduce risk for bleeding. Managing the symptoms.
312
Hepatic Cirrhosis - Interventions: What manifestations may we see if left untreated?
Jaundice
Portal hypertension, ascites, and varices
Hepatic encephalopathy or coma
Nutritional deficiencies
313
Cancer of the Liver: What is the name given when this is caused by smoking?
Hepatocellular Carcinoma (HCC)
314
Cancer of the Liver: Liver is a frequent site of metastatic cancer, why?
Because theres the portal lymphatic system and all the cancer cells are directed back toward the liver
315
Cancer of the Liver: Pain will be felt where?
Pain will be dull and continuous. Ache in the RUQ, epigastrium, or back.
316
Cancer of the Liver: What changes may a person go through?
Weight loss, loss of strength, anorexia, and anemia may occur.
317
Cancer of the Liver: What would cause Jaundice?
If the bile ducts are occluded
318
Cancer of the Liver: What would cause ascites?
If the portal veins were obstructed
319
Cancer of the Liver -- Diagnosis: What can be analyzed here?
LFTs, ASTs, ALTs.
320
Cancer of the Liver -- Diagnosis: What diagnostic studies can be performed?
Imaging, CT or Ultrasound of Liver, BIopsies, and Draw Specific Tumor Markers.
321
Nonsurgical Management of Liver Cancer: Why must we know if they have cirrhosis?
It is prevalent in patients with liveer cancer, and increases the risks of surgery because at greater risk for bleeding and don't feel well.
322
Nonsurgical Management of Liver Cancer: Major effect of nonsurigcal therapy may be what?
Palliative
323
Nonsurgical Management of Liver Cancer: What are some thing that may try?
Radiation Therapy
| Chemotherapy into hepatic artery and put in percutaneous biliary drainage.
324
Nonsurgical Management of Liver Cancer: What is Laser Hypothermia?
Heat up the canceer cells in the liveer
325
Nonsurgical Management of Liver Cancer: Immunotherapy would help why
Gives them more help and support for their immune system.
326
Nonsurgical Management of Liver Cancer: What is arterial embolization?
Embolize the blood flow to the tumor on the liver so it won't be fed anymore
327
Nonsurgical Management of Liver Cancer: What is a ultrasound guided injection of alcohol?
Injected into tumor to promote dehydration of the tumor to try to kill it off that way.
328
Surgical Management of Liver Cancer: When would this be the treatment of choice?
For HCC if confined to one lobe and liver. function in adequate. They go in and remove the tumor on there.
329
Surgical Management of Liver Cancer: What is the liver able to do if it has not gone through cirrhosis yet?
It has a regenerative capcity.
330
Surgical Management of Liver Cancer: What types of surgery are there?
Lobectomy (Remove one lobe)
Cryosurgery (Liquid nitrogen to destroy cancer cells)
Liver Transplant (end-stage liver disease.)
331
Surgical Management of Liver Cancer - Liver Transplant: If the donor is living, what side do they take this from?
Usually their right side because it will regenerate.
332
Surgical Management of Liver Cancer - Liver Transplant: How do they decide about a liver transplant?
There will be a Milan criteria , and it looks to determine who is the most urgent to get new liver. Look at creatine, bilirubin, and what has caused thisneed for liver. This is how they pick who needs one.
333
Surgical Management of Liver Cancer - Liver Transplant: Liver transplant is dependent on what?
Successful immunosuppression. Immune system has to be suppressed so that the new organ does not object it
334
Nursing Care of Patient Undergoing a Liver Transplant - PreOp: What psychosocial needs does the patient need addressed?
The fact that someone has to die in order to receive a new liver. Educatio n about that and managing their current signs and symptoms of current liver failure.
335
Nursing Care of Patient Undergoing a Liver Transplant - PostOp: What will need to be done?
Monitor VS, Monitor Drains, Teach about liver labs, and how they will need to have labs drawn frequently, and signs of rejection and infection.
336
Nursing Care of Patient Undergoing a Liver Transplant - PostOp: Most important thing they need to be taught of?
That they need to take their medication, their immunosuppressants , their anti-rejection meds as scheduled .
337
Nursing Care of Patient Undergoing a Liver Transplant - Complications: What can happen
Bleeding, tissue rejection.
338
Nursing Care of Patient Undergoing a Liver Transplant - Live Donor Liver TRansplant: What part will be donated?
The right lobe.
339
Nursing Care of Patient Undergoing a Liver Transplant - Live Donor Liver TRansplant: What needs to be done teaching wise?
Teaching, and helping the person is the personn were to die when donating.
340
Nursing Care of Patient Undergoing a Liver Transplant - Live Donor Liver TRansplant: If you have a liver transplant patient, what can they not have?
Cannot give NSAIDS because they can interfere with rejection meds. No ibuprofen. Need to give Tylenol instead.
