326 Liver

Disorders of synthesis and storage functions: Bile salts

---> impaired fat absorption--> fatty stools and deficiency of fat soluble vitamins

Disorders of synthesis and storage functions: lipoprotein cholesterol

--->decreased cholesterol

Disorders of synthesis and storage functions: proteins

--->hypoalbuminemia-->edema and ascites

Disorders of synthesis and storage functions: glucose

--->hypoglycemic events

Disorders of metabolic and excretory functions: Drugs

--> drug interactions and toxicities

Disorders of metabolic and excretory functions: amino acids

--> impaired conversion of ammonia to urea-->encephalopathy

Disorders of metabolic and excretory functions: steroid hormones

--> increased aldosterone (leads to increased aldosterone) and increased androgens and estrogens (leads to menstrual irregularities in women and gynecomastia and testicular atrophy in men)

Disorders of metabolic and excretory functions: Bilirubin

-->hyperbilirubinemia-->jaundice

Clinical therapies of liver disease: Increased pressure in portal venous system with collateral vessel development

-Beta-blocker nadolol with isosorbide mononitrate -For bleeding esophageal varices, central line insertion; monitoring of central venous and pulmonary artery pressures -Upper endoscopy with gastric lavage -Balloon tamponade -TIPS

Clinical therapies of liver disease: Engorged veins in the gastrointestinal system Alcohol ingestion Impaired bile synthesis and fat absorption

-Cessation of alcohol intake -Nutrition therapy -Supportive therapy

Consequences of impaired hepatic function

-Decreased detoxification of toxins, chemicals and hormones -decreased metabolism of carbs, fats and proteins -decreased metabolism of medications -decreased bile secretions -decreased clotting--> increased bleeding -Decreased storage of vitamins/iron

Clinical therapies of liver disease: -Decreased clotting factor synthesis, Increased platelet destruction by enlarged spleen and Impaired vitamin K absorption and storage

-Ferrous sulfate, folic acid to treat anemia -Vitamin K to reduce risk of bleeding -For acute bleeding, possible administration of packed RBCs, fresh frozen plasma, or platelets to promote hemostasis -Institution of bleeding precautions

Impaired function of the liver

-Impaired protein metabolism with decreased production of albumin and clotting factors. Low albumin levels contribute to edema in peripheral tissues and ascites (accumulation of fluid in the abdomen) as plasma oncotic pressure is reduced (when oncotic pressure is low, fluid leaks out of the blood stream into peripheral tissues). Impaired clotting-factor production increases the risk for bleeding. -Disrupted glucose metabolism and storage with resulting alterations in blood glucose levels (either hyperglycemia or hypoglycemia). -Reduced bile production that impairs the absorption of lipids and fat-soluble vitamins. Inadequate vitamin K, a fat-soluble vitamin, affects the production of clotting factors, leading to a bleeding tendency. -Impaired metabolism of steroid hormones (including estrogen and testosterone) that leads to feminization in men and irregular menses in women.

Clinical therapies of liver disease: Accumulated metabolic toxins Impaired ammonia metabolism and excretion

-Medications to reduce nitrogenous load and lower serum ammonia levels -Protein restrictions in acute encephalopathy -Parenteral nutrition as needed

Nursing assessment

-Observation and patient interview. Observe for current manifestations, including abdominal distention, bleeding, bruising, and jaundice. -Physical examination. The physical examination for this patient includes monitoring vital signs; conducting a mental status exam; inspecting the color and condition of skin and mucous membranes; and palpating peripheral pulses for the presence of peripheral edema. Conduct a focused abdominal assessment, including appearance, shape and contour, bowel sounds, abdominal girth, percussion for liver borders, and palpation for tenderness and liver size.

Prevention of cirrhosis

-See the healthcare provider on a regular basis. This is especially important for those diagnosed with hepatitis. -Maintain a healthy weight -Avoid alcoholic beverages and illegal drugs -Take all medications as prescribed; this is especially important for those diagnosed with autoimmune hepatitis

Pharmacologic therapy

-diuretics: reduce fluid retention and ascietes -lactulose and neomycin: reduce nitrogenous waste load and lower serum ammonia levels (clinical manifestations of hepatic encephalopathy) -beta blocker (given with isosorbide): prevents rebleeding of esophageal varisces -ferrous sulfate and folic acid: given as needed to treat anemia. vitamin k ordered to reduce risk of bleeding -Oxazepam (serax) a benzo antianxiety drug tp treat acute agitation. it is not metabolized by the liver

Consequences of impaired hepatic function: Hepatic encephalopathy

-liver cannot detoxify ammonia, ammonia crosses BBB. -ammonia can no longer be converted to urea, and it accumulates in the blood. Other nervous system depressants, such as narcotics and tranquilizers, also may contribute to hepatic encephalopathy. Accumulation of other metabolic toxins is thought to contribute as well. Additional factors are constipation, blood transfusions, gastrointestinal bleeding, hypoxia, high-protein diet, severe infection, and surgery. -hepatic encephalopathy results from cerebral edema and the accumulation of neurotoxins in the blood.

Essential functions of the liver

1.the metabolism of proteins, carbohydrates, and fats. 2.Detoxification(breakdown) of toxins, chemicals and hormones. 3. Drug metabolism 4. production of clotting factors 5. bile secretion (bile is necessary for digestion and absorption of fats, can eliminate waste products via the bile). The liver is responsible for the metabolism of steroid hormones and most drugs; it detoxifies alcohol and other substances. It synthesizes essential blood proteins—albumin and clotting factors, in particular. Ammonia, a toxic by-product of protein metabolism, is converted to urea in the liver for elimination by the kidneys. The liver produces bile, an essential substance for absorbing fats and eliminating bilirubin from the body. Minerals and fat-soluble vitamins are stored in the liver, as is glycogen (stored carbohydrate for energy reserves).

Posthepatic cirrhosis

Advanced progressive liver disease resulting from chronic hepatitis B or C or from an unknown cause is called post hepatic or post necrotic cirrhosis. With this type of cirrhosis, the liver is shrunken and nodular, with fibrosis and extensive loss of liver cells.

Clinical therapies of liver disease: Impaired nutrient metabolism Impaired fat absorption Impaired hormone metabolism

Arranging for consultation with a dietitian for meal planning

Consequences of impaired hepatic function: Ascites

Ascites is the accumulation of plasma-rich fluid in the abdominal cavity. Although portal hypertension is the primary cause of ascites, decreased serum proteins and increased aldosterone also contribute to the fluid accumulation. Hypoalbuminemia (low serum albumin) decreases the colloidal osmotic pressure of plasma. -This pressure normally holds fluid in the intravascular compartment, but when the plasma colloidal osmotic pressure decreases, fluid escapes into extravascular compartments. Hyperaldosteronism (an increase in aldosterone) causes sodium and water retention, contributing to ascites and generalized edema.

Clinical manifestations of liver disease: Accumulated metabolic toxins Impaired ammonia metabolism and excretion

Asterixis, encephalopathy

Implementation

Balance fluid volume, promote mental status, minimize bleeding, promote skin integrity, promote balanced nutrition and manage complications

Common diagnostic tests:

Biopsies, imaging/radiologic tests, direct observation tests (jaundice-look at sclera of eyes), ascites, colonoscopy, endoscopy.

Leading cause of death of hepatic encephalopathy

Cerebral edema that leads to increased intracranial pressure and cerebral hypoxia is the leading cause of death in individuals with portal systemic encephalopathy and liver failure.

Cirrhosis may result from

Chronic hepatits C (most common);chronic hepatitis B, prolonged obstruction of the bilary (bile drainage) system; long term, severe right heart failure and other liver diseases.

increased ammonia effects

Elevated ammonia (from liver's inability to convert ammonia to urea) crosses the BBB and causes impairment in neurological function.

Consequences of impaired hepatic function: Esophageal varisces

Esophageal varices are enlarged, thin-walled veins that form in the submucosa of the esophagus. These collateral vessels form when blood is shunted from the portal system because of portal hypertension. The thin-walled varices may rupture and cause massive hemorrhage; even eating high-roughage foods can precipitate bleeding in these patients. Thrombocytopenia, platelet deficiency, and impaired production of clotting factors by the liver contribute to the risk for hemorrhage.

Clinical manifestations of liver disease: Engorged veins in the gastrointestinal system Alcohol ingestion Impaired bile synthesis and fat absorption

Gastritis, anorexia, diarrhea

ALT/AST

Liver enzymes. Increased liver enzymes mean that the liver is overworked and irritated. Could also be increased from meds and alcohol

Diagnostic tests for cirrhosis

Liver function studies, CBC w/ platelets, coagulation studies, serum electrolytes, bilirubin, serum albumin, serum ammonia, serum glucose and cholesterol, abdominal ultrasound, esophagoscopy and liver biopsy

Clinical manifestations of liver disease: Impaired nutrient metabolism Impaired fat absorption Impaired hormone metabolism

Malnutrition, muscle wasting

Nursing evaluation

Monitoring laboratory data such as liver function tests. Elevated liver enzymes indicate hepatocellular destruction. Liver function tests should remain stable during the treatment phase of the disease. Monitoring other lab tests including CBC, hematocrit (Hct) and hemoglobin (Hgb), coagulation studies, serum electrolytes, serum albumin, serum ammonia levels, and urine specific gravity tests. These values are expected to improve if therapy is successful. Assessing vital signs and level of consciousness for improvement.

Consequences of impaired hepatic function: portal hypertension

Portal hypertension causes blood to be rerouted to adjoining, lower pressure vessels. This shunting of blood involves collateral vessels. Affected veins, which become engorged and congested, are located in the esophagus, rectum, and abdomen. Portal hypertension increases the hydrostatic pressure in vessels of the portal system. Increased hydrostatic pressure in the capillaries pushes fluid out, contributing to ascites formation.

liver function

The liver synthesizes serum albumin and clotting factors, stores glycogen, and detoxifies metabolic waste.

Early clinical manifestations of cirrhosis:

The liver usually is enlarged and may be tender. A dull, aching pain in the right upper abdominal quadrant may be present. Other early signs include weight loss, weakness, and anorexia. Bowel function is disrupted with diarrhea or constipation

Alcohol causes metabolic changes in the liver:

Triglyceride and fatty acid synthesis increases, and a decrease in the formation and release of lipoproteins leads to fatty infiltration of hepatocytes (fatty liver).

bilary cirrhosis

When bile flow is obstructed within the liver or in the biliary system, the retained bile damages and destroys liver cells close to the interlobular bile ducts. This activity leads to inflammation, fibrosis, and formation of regenerative nodules.

Paracentesis

aspiration of fluid from the peritoneal cavity. may be a diagnostic or a therapeutic procedure (to relieve severe ascites that does not respond to diuretic therapy). The goal of paracentesis is to relieve respiratory distress caused by excess fluid in the abdomen.

Consequences of impaired hepatic function: Splenomegaly

backup towards spleen from portal hypertension causes englarged spleen. Because portal hypertension causes blood to be shunted into the splenic vein, the spleen enlarges (splenomegaly). Splenomegaly increases the rate at which red blood cells (RBCs), WBCs, and platelets are removed from circulation and destroyed. This increased destruction of blood cells leads to anemia (low RBC count), leukopenia (low WBC count), and thrombocytopenia (low platelet count)

Clinical manifestations of liver disease: Decreased clotting factor synthesis, Increased platelet destruction by enlarged spleen and Impaired vitamin K absorption and storage

bleeding brusing

signs of hepatic encephalopathy

changes in personality and mentation. Agitation, restlessness, impaired judgment, and slurred speech are early manifestations; as the condition progresses, confusion, disorientation, and incoherence develop.

Consequences of impaired hepatic function: nutritional deficiencies

decreased albumin

many different disorders can disrupt liver function, their manifestations relate to three primary effects:

disrupted liver cell function, impaired bilirubin conversion and excretion leading to jaundice, and disrupted blood flow through the liver, with resulting portal hypertension.

cirrhosis

end stage of chronic liver disease. It is a progressive, irreversible disorder, eventually leading to liver failure.

Clinical manifestations of liver disease: Increased pressure in portal venous system with collateral vessel development

esophageal varisces

Risk factors for cirrhosis

excess alcohol use, injection drug use-->increased risk of contracting bloodborne hepatitis B, C, or D.

pathophysiology of cirrhosis

functional liver tissue is gradually destroyed and replaced by fibrous scar tissue. As hepatocytes and liver lobules are destroyed, the metabolic functions of the liver are lost. Structurally abnormal nodules encircled by connective tissue form. This fibrous connective tissue forms constrictive bands that disrupt blood and bile flow within liver lobules. Blood no longer flows freely through the liver to the inferior vena cava. This restricted blood flow leads to portal hypertension (increased pressure in the portal venous system).

low blood glucose d/t liver failure has what effects on brain

hypoglycemia reactions that can lead to coma are caused in liver failure by the liver's decreased ability to store glycogen for glucose production.

How to test for asterixis

instructing the patient to extend the arms and dorsiflex the wrists; if present, asterixis causes a downward flapping of the hands.

Clinical manifestations of liver disease: Impaired bilirubin metabolism and excretion

jaundice

Kupffer cells

line the sinusoids phagocytize foreign cells and damaged blood cells.

In what organ is angiotensinogen produced?

liver

Asterixis (also known as liver flap)

muscle tremor that interferes with the ability to maintain a fixed position of the extremities and causes involuntary jerking movements. It also is an early sign of portal systemic encephalopathy. Asterixis primarily affects the upper extremities, but it may affect the tongue and feet.

Clinical therapies of liver disease: Impaired bilirubin metabolism and excretion

supportive therapy

with continued alcohol abuse...

the disease continues to progress. Inflammatory cells infiltrate the liver (alcoholic hepatitis), causing necrosis, fibrosis, and destruction of functional liver tissue. In the final stage of alcoholic cirrhosis, regenerative nodules form, and the liver shrinks and develops a nodular appearance. Malnutrition commonly accompanies alcoholic cirrhosis.

A transjugular intrahepatic portosystemic shunt (TIPS)

used to relieve portal hypertension and its complications of esophageal varices and ascites. A channel is created through the liver tissue with a needle inserted transcutaneously. An expandable metal stent is inserted into this channel to allow blood to flow directly from the portal vein into the hepatic vein, bypassing the cirrhotic liver. The shunt relieves pressure in esophageal varices and allows better control of fluid retention with diuretic therapy.