Disease process
Alcoholic cirrhosis is a permanent liver damage resulting from prolonged inflammatory and noxious effects of alcohol (Hauser, 2005). In this condition, normal liver cells are substituted with scar tissues hence fibrosis and subsequent nodulation. Occurrence of fibrous tissues in the liver may lead to portal hypertension and consequent liver failure. The onset of alcoholic cirrhosis is proportional to the amount and period of ethanol intake (Fairbanks, 2010). Other risk factors may include an individual’s genetic constitution, environmental factors such as availability of alcohol and an individual’s gender (females are more vulnerable than males). Furthermore, the disease affects ten to fifteen percent of individuals who abuse alcohol for a period of about ten years and above. Alcoholic cirrhosis is viewed as a terminal phase of alcohol liver destruction.
Alcohol breakdown in the body occurs in the liver and partly in the alimentary canal. In the liver, there are 2 mechanisms of ethanol biosynthesis and they include “alcohol dehydrogenase and cytochrome P-450 (CYP) 2E1” pathways (Fairbanks, 2010). Alcohol dehydrogenase pathway involves ‘hepatocyte cytosolic enzyme’ which participates in transformation of ethanol to acetaldehyde. Acetaldehyde is then synthesized to acetate by ‘acetaldehyde dehydrogenase enzyme’ found in the mitochondria (Fairbanks, 2010). In addition, cytochrome P-450 2E1pathway participates in synthesis of ethanol to acetaldehyde.
Liver destruction is attributed to a combination of various pathways. Two enzymes are involved in reduction of Nicotinamide Adenine Dinucleotide (NAD) to form NADH (Lueckenotte, 2006). As such, the equilibrium between NAD and NADH is interrupted and this restricts gluconeogenesis process and also stops the oxidation of fatty acids. Cytochrome P-450 2E1 gets up-regulated in prolonged ethanol intake and it promotes the production of gratis hydrogen radicals via oxidation of hydrogenated ‘Nicotinamide Adenine Dinucleotide Phosphate’ (NADPH) to NADP (Fairbanks, 2010). Moreover, persistent intake of ethanol excites ‘hepatic macrophages’ which lead to formation of “tumor necrosis factor α (TNF-α)” (Fairbanks, 2010). This factor causes the mitochondria to generate more unstable oxygen radicals which enhance oxidative tension. Oxygen tension created leads to apoptosis and formation of fibrous tissues. This condition is severe in individuals who lack enough antioxidants like vitamin E. Gratis radicals start peroxidation of lipids and this as well leads to irritation and fibrosis. In addition, irritation is induced by acetaldehyde linked to cell proteins leading to creation of adducts that act as antigens (Fairbanks, 2010).
The clinical manifestation of alcoholic cirrhosis includes nausea and vomiting, exhaustion, weight loss and loss of appetite (Filbin, 2004). Besides, the disease may have symptoms like jaundice and pruritus as well as unusual diagnostic findings such as “thrombocytopenia, hypoalbuminemia, coagulopathy” (Fairbanks, 2010). In addition, the condition may be manifested by development of portal hypertension indicated by “variceal bleeding, ascites, edema and hepatic encephalopathy” (Fairbank, 2010). Furthermore, the condition may result to malnutrition and intestinal bleeding.
Pharmacologic management of the disease process
The condition is irreversible and treatment is aimed at checking further disease progression and also to control complications (Lehne, 2010). Stopping to take alcohol is an important step in treatment of alcoholic cirrhosis. However, disease victims may fail to recover completely and medical assistance and hospitalization is of great importance. Hospitalization is aimed at helping individuals with signs such as jaundice, encephalopathy and bleeding in the stomach (Wolf, 2010). Moreover, individuals who present to the clinic with renal failure, signs of dehydration as well as decreased liver activity may require hospitalization.
Blood pressure drugs such as beta-blockers assist in reduction of portal hypertension (Lippincott & Wilkins, 2005). Beta-blockers are drugs like nadolol and propranol. Propranol can also be used to control bleeding of the esophagus. The drug has generic names such as AstraZeneca, propranol hydrochloride and Wyeth. It has various trade names and some of them include Inderal, Deralin, Bedranol and Inderal LA among others (Wolf, 2010). The drug is readily absorbed in the body and its co-administration with meals seems to enhance its bioavailability. Propranol works by blocking the activity of neropinephrine as well as epinephrine at beta sites one and two of adrenergic receptors. Appropriate plasma concentrations of the drug are between 10-100ng/ml. Concentrations of above 200ng/ml may be toxic. The drug may have adverse effects in individuals suffering from shortness of breath, high blood pressure and distress as well as bradycardia. In addition, it should be used sparingly in patients having diabetes mellitus, phaeochromocytoma and in individuals taking other medications which can cause bradycardic effects.
Hemorrhage in the alimentary canal, vomiting and agony as well as nausea may be treated with drugs like sandostatin (Wolf, 2010). It is preferred as a first line drug and it is initially administered three times a day with a dosage of 100-500 µg. The drug has no known contraindications and it is appropriate to take it with meals rich in protein. It works by controlling the activities of “endocrine and exocrine glands” (Wolf, 2010). Diuretics, also known as water pills, are used to check the levels of fluid in legs and stomach (abdomen). These drugs include Spironolactone, also known as Aldactone, and Lasix, also known as Furosemide. These drugs are considered as second line chemotherapeutics. According to Wolf (2010), aldactone works by “blocking aldosterone receptors at the distal tubule”. Three hundred two five hundred milligrams should be administered on daily basis. The drug may lead to complications like “hyperkalemia, gynecomastia, and lactation” (Wolf, 2010). In such conditions, drugs like ‘amiloride and triamterene’ can act as alternative in individuals experiencing gynecomastia. The other drug, Furosemide, is either administered individually or together with spironolactone. The drug dosage is 40 to 240 mg/day and it is partitioned into one or two doses. The drug works by barring the re-absorption of sodium ions in the ‘loop of henle’. When the two drugs are used at the same time, patients rarely require potassium repletion (Fairbanks, 2010).
In addition, a patient may be treated with Lactulose, a drug that manages “hepatic encephalopathy, brain and nervous system” as a result of ammonia accumulation in blood (Wolf, 2010). This drug is a synthetic sugar (disaccharide) that enhances absorption of ammonia from tissues to the alimentary canal and prohibits the intestines from producing ammonia since the liver function on its elimination is compromised. At first, a patient is treated with 30ml two times a day and the amount is increased until the disease victim gets wet stool. However, increment of dosage may lead to “diarrhea, abdominal cramping, or bloating” (Wolf, 2010). As such, high dosage may be given using cathartics techniques. Besides, ammonia bacteria in the alimentary canal can be checked by use of antibiotic such as neomycin, metronidazole, oral vancomycin and quinolones as well as paromomycin (Rosdahl & Kowalski, 2007). However, neomycin may lead to problems of “nephrotoxicity and ototoxicity” (Wolf, 2010). An alternative to this drug may be Rifaximin, also known as Xifaxan. Other antibiotics, such as norfloxacin may be used to manage bacterial infection in case of gastrointestinal bleeding.
Proper nutrition should be given to individuals who mainly complain of anorexia and those with ascites (Wolf, 2010). They should be given sufficient amounts of proteins as well as calories. In addition, nutritional supplements and liquids may be given. Excessive fear of proteins may lead to exaggerated muscle wasting. Zinc sulphate (220mg) on daily basis may be used to increase appetite in addition to its effects on muscle cramps and hepatic encephalopathy (Wolf, 2010). Additionally, a physician may recommend upper endoscopy if the patient is experiencing internal bleeding like in the esophagus and verices. In a situation where the liver is highly damaged, transplant may be the only remedy. This is a risky operation and it requires administration of drugs that suppress the immune system so that it does not reject the new organ. The complications of this remedy are usually fatal.
Nursing implications in the use of these medications
The medication for alcoholic cirrhosis requires nurses to continually assess the patient’s fluid volume (Lueckenotte, 2006). One major function of the liver is generation of proteins that bar water leakage from blood vessels. However, in alcoholic cirrhosis, this function is compromised and water is allowed to accumulate in body cavities (Wolf, 2010). This leads to conditions like edema and ascites as well as unnecessary weight gain. Thus, appropriate fluid intake is necessary to avoid excessive water in body cavities. Individuals suffering from alcoholic cirrhosis should be limited to taking between 500ml to 1000ml per day (Wolf, 2010). Furthermore, individuals should be given a balanced diet rich in calories and containing sufficient proteins. Patients suffering from alcoholic cirrhosis may have signs of malnutrition (less than body requirement) as a result of disease process. Appropriate diet helps to control muscle wasting and provides the body with necessary energy. In addition, the patient may be put on constant vitamin K injection so as to enhance blood clotting and therefore minimize bleeding (Lueckenotte, 2006). Besides, the nurse may advise the patient to cease drinking since it leads to aggravation of the condition.
Furthermore, nurses should assess the patient’s rate of gaseous exchange. Normally, individuals suffering from alcoholic cirrhosis may have difficulties in breathing due to excessive pressure exerted on the diaphragm by ascites fluid (Wolf, 2010). Therefore, the patient should be given appropriate amounts of water and allowed to rest between activities. This helps to eliminate the problem of excessive fluids and increased demand for oxygen respectively.
Alcoholic cirrhosis is a condition affecting a big percentage of individuals who drink. It leads to fibrosis and nodulation as well as liver failure if not treated early enough. The main way of dealing with the condition is stopping to consume alcohol. This may be complimented with various drugs which are aimed at treating the disease process and its complications. Such medications require appropriate nursing interventions so as to work well.
References
Fairbanks, K. D. (2010). Alcoholic Liver Disease. Web.
Filbin, M. R. (2004).Blueprints Notes & Cases – Pathophysiology: Pulmonary, Gastrointestinal and Rheumatology. Massachusetts: Blackwell Publishing.
Hauser, C. (2005). Mayo Clinic Gastroenterology and Hepatology Board Review. United States: CRC Press.
Lehne, R. A. (2010). Pharmacology for Nursing Care (7th Ed.). St. Louis, MO: Saunders Elsevier.
Lippincott, W., & Wilkins. (2005). Pathophysiology: a 2-in-1 reference for nurses. United States of America: Library of Congress.
Lueckenotte, Annette G. (2006). Gerontologic nursing. Philadelphia: Elsevier Health Sciences.
Rosdahl, B. C., & Kowalski, M. T. (2007). Textbook of basic nursing. United States of America: Lippincott Williams & Wilkins.
Wolf, D. C. (2010). Cirrhosis. Web.