CHIKA

Most people in this generation has so many words to talk.Talks that can sometimes be unacceptable, pleasing and harassing which can either have evidences or not at all. When I say about "Chika" , it compasses the making of whole talks of something that caught you interested. Different people are usually involved in this area. It can either be your closest friends/ barkadas, classmates, seatmates, neighbors, parents, relatives or even people you've just met inside the train while waiting for arrival and it can mostly happen at any given time or place. Every words that goes out from your mouth counts and would mean a lot for someone who has a short emotional shield and if not controlled or accepted can lead to a disastrous/ long chaos. It is better that you think before you talk. Just like don't talk when your mouth is full. The food are the information and that you must finish grinding it into particles before releasing it through feces. Whatever comes in your mouth will never be eaten back in your existence.

LIVER CIRRHOSIS

LIVER CIRRHOSIS

- is a chronic disease of the liver characterized by alteration in structure, degenerative changes and widespread destruction of hepatic cells, impairing cellular function and impeding blood flow through the liver. Causes include malnutrition, inflammation (bacterial or viral), and poisons (e.g., alcohol, carbon tetrachloride, acetaminophen). Cirrhosis is the fourth leading cause of death in the United States among people ages 35 to 55 and represents a serious threat to long-term health.

- Is extensive scarring of the liver, usually caused by a chronic irreversible reaction to hepatic inflammation and necrosis. The disease typically develops insidiously and has a prolonged, destructive course.

- The most common causes of cirrhosis in the United States are alcoholic liver disease and hepatitis C... Worldwide, hepatitis B is the leading cause.

- Three types of cirrhosis:

· Alcohol cirrhosis, in which the scar tissue characteristically surrounds the portal areas. This is most frequently due to chronic alcoholism and is the most common type cirrhosis.

· Postnecrotic cirrhosis, in which there are broad bands of scar tissue as a late result of a previous bout of acute viral hepatitis.

· Biliary cirrhosis, in which scarring occurs in the liver around the bile ducts. This type usually is the result of chronic Biliary obstruction and infection (cholangitis); it is much less common than the other two types.

OBJECTIVES:

· To be able to describe the pathophysiology and complications associated with cirrhosis of the liver.

· To be able to interpret laboratory test findings commonly seen in clients with cirrhosis.

· To be able to analyze assessment data from clients with cirrhosis to determine priority nursing diagnosis and collaborative problems.

· To be able to formulate a collaborative plan of care for the client with severe late-stage cirrhosis.

· To be able to identify emergency intervention for the client with bleeding esophageal varices.

· To be able to evaluate care for client with liver cirrhosis.

· To be able to develop a community based teaching plan for the client with cirrhosis of the liver.

PREDISPOSING FACTORS/ETIOLOGY:

Cirrhosis can occur as a result of many factors and diseases such alcoholic liver disease, viral hepatitis, autoimmune hepatitis, steatohepatitis, drugs and toxins, biliary disease, metabolic/genetic causes, and cardiovascular disease.

ALCOHOL

Alcohol has a direct toxic effect on the hepatocytes and causes liver inflammation. The liver becomes enlarge with cellular degeneration and infiltration by fat, leukocytes and lymphocytes. Overtime the inflammatory process decreases and the destructive phase increases. Early scar formation is caused by fibroblast infiltration and collagen formation. Damage to liver tissue progresses as a result of malnutrition and repeated exposure to alcohol. If alcohol is withheld, the fatty infiltration and inflammation is reversible. If alcohol abuse continues, wide spread scar tissue formation and fibrosis infiltrate the liver as a result of cellular necrosis.

The amount of alcohol necessary to cause cirrhosis varies widely from person to person and there are gender differences. In women it may take as few as two to three drinks per day over a minimum of 10 years. In men, perhaps six drinks per day over the same time period may be needed to cause disease. However, there are other individuals, both male and female, who consume far more alcohol per day over a period of several years without ever developing cirrhosis.

VIRAL HEPATITIS

Hepatitis C is an infectious bloodborne illness that usually causes chronic diseases. Inflammation caused by infection over time leads to progressive scarring of the liver. It usually take decades for cirrhosis to develop, although alcohol use in combination with hepatitis C may accelerate the process.

Hepatitis B is the most common cause of cirrhosis worldwide. Hepatitis B also causes inflammation and low-grade damage over decades that can ultimately lead to cirrhosis. The role that concomitant use of alcohol plays in Hepatitis B cirrhosis is not a clear as that of hepatitis C cirrhosis.

Hepatitis D is another virus that reflects the liver, but only in people who already have hepatitis B.

AUTOIMMUNE HEPATITIS

Unlike viral hepatitis, this is not an infectious disease. For reasons not clearly understood, the host’s immune system produces high level of circulating autoantibodies, causing inflammation of liver. This chronic inflammation can lead to fibrosis and eventual cirrhosis.

STEATOHEPATITIS

Frequently referred to us “Fatty liver”, steatohepatitis occurs when fat and cholesterol deposits in the liver cause chronic inflammation. Overtime this inflammation may cause liver damage, or fibrosis and eventual cirrhosis. Obesity and elevated lipid profile are risk factors for steatohepatitis.

DRUGS AND TOXINS

Medication, herbal supplements, and environmental exposure to toxins may damage the liver so significantly that cirrhosis occurs. Sometimes the development of cirrhosis occurs decades after the initial exposure.

BILIARY DISEASE

Biliary cirrhosis develops as a result of chronic Biliary obstruction, bile stasis, inflammation, or diffuse hepatic fibrosis. The most common causes of Biliary cirrhosis are primary Biliary cirrhosis and primary sclerosing cholangitis. Both of these forms of Biliary cirrhosis may also present as secondary to either stone or strictures affecting the common bile duct.

Primary Biliary cirrhosis (PBC) is a disease, probably with an immunologic basis, that involves the slow progressive destruction of small intrahepatic duct, resulting in cholestasis. The disease usually affects middle-aged women. One of the most common presenting features is an asymptomatic elevation of the alkaline phosphatase.

Primary sclerosing cholangitis (PSC) is an illness that is characterize by diffuse inflammation and fibrosis that involves the Biliary system. It has the potential to cause chirrhosis because this process leads to a narrowing and eventual obliteration of the intrahepatic bile ducts. There is a strong association between PSC and inflammatory disease. This disease predominantly affects men.

METABOLIC/GENETIC CAUSES

There are many metabolic and genetic disorders that can cause cirrhosis of the liver:

A. Hemachromatosis, which is characterize by excessive iron storage.

B. Wilson’s disease, a disorder of copper metabolism.

C. Alpha 1, antitrypsin deficiency which may cause an abnormal accumulation of antitrypsin and produce inflammatory activity.

D. Cystic Fibrosis, which can cause cirrhosis from intrahepatic bile duct plugging.

CARDIOVASCULAR DISEASE

Vascular (cardiac) cirrhosis is associated with severe right sided heart failure. The liver becomes enlarge, is congested with venous blood, and appears edematous and dark in color. The liver serves as a reservoir for large amounts of venous blood that the failing part cannot pump back into the systemic circulation. The increase in hepatic volume and pressure causes severe venous congestion. The decrease in nourishing blood flow to the liver results in hepatic cell necrosis and fibrosis.

ANATOMY AND PHYSIOLOGY

The liver is located in the right upper quadrant of the abdomen in the peritoneal space just below the right side of the diaphragm and under the rib cage. It weighs approximately 1400 g in the adult and is covered by a fibrous capsule. It receives nearly 25% of the cardiac output, approximately 1500 mL of blood flow per minute, via two sources: venous flow from the portal vein, which is crucial to performance of the liver's roles in bodily functions, and arterial flow from the hepatic artery, which is important for liver oxygenation and which supplies the biliary system. These vessels converge within the liver, and the combined blood flow exits via the so-called central veins (also called terminal veins) that drain into the hepatic vein and ultimately the inferior vena cava.

The portal vein carries venous blood from the small intestine, rich in freshly absorbed nutrients—as well as drugs and poisons—directly to the liver. Also flowing into the portal vein before its entry into the liver is the pancreatic venous drainage, rich in pancreatic hormones (insulin, glucagon, somatostatin, and pancreatic polypeptide). The portal vein forms a specialized capillary bed that allows individual hepatocytes to be bathed directly in portal blood. In part because of this system of blood supply, the liver is a prime site for metastatic spread of cancer, especially from the GI tract, breast, and lung.

PHYSIOLOGY

There is considerable overlap between them, systematic consideration of each category is a useful way of approaching the patient with liver disease.

FUNCTIONS OF NORMAL LIVER

Energy metabolism and substrate interconversion

Glucose production through gluconeogenesis and glycogenolysis

Glucose consumption by pathways of glycogen synthesis, fatty acid synthesis, glycolysis, and the tricarboxylic acid cycle

Cholesterol synthesis from acetate, triglyceride synthesis from fatty acids, and secretion of both in VLDL particles

Cholesterol and triglyceride uptake by endocytosis of HDL and LDL particles with excretion of cholesterol in bile, beta-oxidation of fatty acids, and conversion of excess acetyl-CoA to ketones

Deamination of amino acids and conversion of ammonia to urea via the urea cycle

Transamination and de novo synthesis of nonessential amino acids

Protein synthetic functions

Synthesis of various plasma proteins, including albumin, clotting factors, binding proteins, apolipoproteins, angiotensinogen, and insulin-like growth factor I

Solubilization, transport, and storage functions

Drug and poison detoxification through phase I and phase II biotransformation reactions and excretion in bile

Solubilization of fats and fat-soluble vitamins in bile for uptake by enterocytes

Synthesis and secretion of VLDL and pre-HDL lipoprotein particles and clearance of HDL, LDL, and chylomicron remnants

Synthesis and secretion of various binding proteins, including transferrin, steroid hormone–binding globulin, thyroid hormone–binding globulin, ceruloplasmin, and metallothionein

Uptake and storage of vitamins A, D, and B₁₂ and folate

Protective and clearance functions

Detoxification of ammonia through the urea cycle

Detoxification of drugs through microsomal oxidases and conjugation systems

Synthesis and export of glutathione

Clearance of damaged cells and proteins, hormones, drugs, and activated clotting factors from the portal circulation

Clearance of bacteria and antigens from the portal circulation

MEDICAL DIAGNOSIS

Liver scans/biopsy: Detects fatty infiltrates, fibrosis, destruction of hepatic tissues, tumors (primary or metastatic), associated ascites.

Percutaneous transhepatic cholangiography (PTHC): May be done to rule out/differentiate causes of jaundice or to perform liver biopsy.

Esophagogastroduodenoscopy (EGD): May demonstrate presence of esophageal varices, stomach irritation or ulceration, duodenal ulceration or bleeding.

Percutaneous transhepatic portal angiography (PTPA): Visualizes portal venous system circulation.

Serum bilirubin: Elevated because of cellular disruption, inability of liver to conjugate, or biliary obstruction.

Liver enzymes:

AST/ALT, LDH, and isoenzymes (LDH₅): Increased because of cellular damage and release of enzymes.

Alkaline phosphatase (ALP) and isoenzyme (LAP1): Elevated because of reduced excretion.

Gamma glutamyl transpeptidase (GTT): Elevated.

Serum albumin: Decreased because of depressed synthesis.

Globulins (IgA and IgG): Increased synthesis.

CBC: Hb/Hct and RBCs may be decreased because of bleeding. RBC destruction and anemia is seen with hypersplenism and iron deficiency. Leukopenia may be present as a result of hypersplenism.

PT/activated partial thromboplastin time (aPTT): Prolonged (decreased synthesis of prothrombin)

Fibrinogen: Decreased.

BUN: Elevation indicates breakdown of blood/protein.

Serum ammonia: Elevated because of inability to convert ammonia to urea.

Serum glucose: Hypoglycemia suggests impaired glycogenesis.

Electrolytes: Hypokalemia may reflect increased aldosterone, although various imbalances may occur. Hypocalcemia may occur because of impaired absorption of vitamin D.

Nutrient studies: Deficiency of vitamins A, B₁₂, C, K; folic acid, and iron may be noted.

Urine urobilinogen: May/may not be present. Serves as guide for differentiating liver disease, hemolytic disease, and biliary obstruction.

Fecal urobilinogen: Decreased.

MEDICAL INTERVENTION

The management of the patients with cirrhosis is usually based on the presenting symptoms. For example, antacids are prescribed to decrease gastric distress and minimize the possibility of GI bleeding. Vitamins and nutritional supplements promote healing of damage liver cell and improve the general nutritional status. Potassium-sparing diuretics (spironolatone), triamterene (dyrenium) may be indicated to decrease ascites, if present; these diuretics are preferable to other diuretic agents because they minimize the fluid and electrolytes changes common with other agents. An adequate diet and avoidance of alcohol are essential. Although the fibrosis of cirrhotic liver cannot be reversed, its progression may be halted or slowed by such measures.

Preliminary studies indicate that colchicine, an anti-inflammatory agent used to treat the symptoms of gout, may increase the length of survival in patients with mild to moderate cirrhosis. Improved survival has been obserbed in patients with alcoholic cirrhosis. Colchicine is believed to reverse the fibrotic processes in cirrhosis, and this has improved survival.

NURSING MANAGEMENT

- Promoting rest

o The patient with active liver disease requires rest and other supportive measures to permit the liver to reestablish its functional ability. If hospitalized, weight and fluid I/O is measured and recorded daily. The nurse adjusts patient’s position in bed for maximal respiratory efficiency. O2 therapy may be required in order to oxygenate the damaged liver cells and prevent further cell destruction.

- Improving nutritional status

o The patient with cirrhosis who has no ascites or edema and exhibits no signs of impending hepatic coma should receive a nutritious, high protein diet if tolerated, supplemented by B-complex vitamins and others as indicated (incl. vitamins A, C, K, and Folic acid). The nurse must encourage the patient to eat because of the importance of nutrition. Often small, frequent meals are tolerated better than three large meals because of abdominal pressure due to ascites. Patient’s with prolonged or severe anorexia , or those who are vomiting and eating poorly may receive nutrients enterally or parenteral nutrition. Patients with steatorrhea should receive water soluble forms of fat soluble vitamins such as A, D, and E. Folic acid and iron are to prevent anemia.

- Providing skin care

o Providing careful skin care is important because of subcutaneous edema, the patient’s immobility, jaundice, and increased susceptibility to skin breakdown and infection. Frequent position changes are necessary to prevent pressure ulcers.

- Reducing risk of injury

o The nurse protects the patient from any form of injury. Prevention should be made such as use of side rails, assisting in activities e.g . Going to bathroom, ambulation etc.. the nurse should orient the patient about the time and place, explain procedures to prevent agitation.

- Monitoring and managing potential complications

o Bleeding and hemorrhage

§ The patient is at increased risk for bleeding and hemorrhage because of decreased production of prothrombin and decreased ability of the liver to synthesize the substances necessary for blood coagulation. The nurse should observe signs for possible internal bleeding. V/S should be monitored regularly. In case of hemorrhage, the nurse should assist the physician in initiating measures to halt bleeding.

o Hepatic encephalopathy

§ Hepatic encephalopathy and coma may present as deteriorating mental status and dementia as well as physical signs such as abnormal voluntary and involuntary movements. Treatment may include the use of lactulose and nonabsorbable intestinal tract antibiotics to decrease ammonia levels.

§ Monitoring is essential to identify early deterioration in mental status. The nurse monitors serum electrolyte levels. Also fever or abdominal pain, which may signal the onset of infection.

- Fuid Volume Excess

Patients with advanced chronic liver disease develop cardiovascular abnormalities. These occur due to an increased cardiac output and decreased peripheral vascular resistance, possibly resulting from the release of vasodilators. A hyperdynamic circulatory state develops in patients with cirrhosis, and plasma volume increases. These increase in circulating plasma volume may be due in past to splanchnic venous congestion. The greater the degree of hepatic decompensation, the more severe the hyperdynamic state.

References:

• Banasik, J. (2001). Diagnosing alpha 1 antitrypsin defieciency. The Nurse Practitioner, 26(1), 58-67.

• Bockhold, K.M. (2000). Who’s afraid of hepatitis C? American Journal for Nursing. 100(5), 26-31.

• DeCarlis, L., et al. (2003). Surgical treatment of hepatocellular cancer in the erz of hepatic transplatation. Journal of American College of Surgeons, 196(6), 887-897.

• Smeltzer, Suzanne and Brenda Bare. Medical-Surgical Nursing. 10^th Edition. Philadelphia: Lippincott Williams & Wilkins. 2004.

• Workman, M.L. Medical surgical nursing critical thinking for: Interventions for client with liver problems. 5^th Ed. USA: Elsevier INC. 2006.

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