1.There is a disease in the liver called cirrhosis that might cause loss of the liver cells and irreversible scarring of the liver. Nathan is a chain smoker and also consumes two glasses of beer every day. He also used to take drugs and was diagnosed with hepatitis C. These are the main facts behind the Nathan’s liver problem because the main cause of liver cirrhosis disease is the consumption of alcohol and viral hepatitis B and C. It refers to the replacement of normal liver tissue with non-living scar tissues and it is related to another disease of the liver (Gine?s, Kamath & Arroyo, 2011). Liver cirrhosis is the third most common cause of death after heart and cancer. It is considered to be the end stage of liver. There are few symptoms liver diseases such as, easy bleeding or bruising, intense itching, nausea, loss of appetite, swelling due to fluid buildup in your abdomen and legs, Persistent or recurring yellowing of your skin and eyes and Problems with concentration and memory.
Alcohol is the main cause of Nathan’s liver disease as it is poison for all living cells and might become a reason for inflamed and death of cells. The death of living cells can lead Nathan’s body to form scar tissue around the veins of the body. Hepatitis is considered to be a viral infection of the liver and it is the second most common cause of this illness, however, poisonous substances might also become the reason for it (Carnevale, 2012). Biliary cirrhosis is also from one of the causes of this disease. In this case, the small tubes that help in digesting food become blocked and our body turns on automatically and starts reacting against these bile tubes. C
Liver Cirrhosis has increased Nathan’s blood pressure in the vessels of the blood of the liver. This problem can be found in 60% of people. It is the most common cause of portal hypertension. Hepatic encephalopathy is the condition when toxins start building in our bloodstream as the liver is not able to get them away from our body (Yadav & Vargas, 2015). These toxins may cause Nathan with bizarrely behavior and make him confuse. The other risk factors are as follow:
The cirrhosis disease effects directly to the liver in some cases. The liver stops making enough platelets that is the reason behind Nathan’s bleeding gums, nosebleed and brushing. This may also cause brain fog to Nathan and other serious mental changes related to haptic encephalopathy. If the liver gets injured it cannot clear the toxin ammonia from the blood and that could be a serious issue with Nathan. The families of Nathan also face problems as it might affect their daily life. They have to take care of him and this might prevent them from managing their day to day work. Nathan is the only working person in the family and has two children. His health condition is affecting the entire family and he must think about leaving smoking and drinking habit.
2.Cirrhosis has no sign until the liver is damaged extensively. The symptoms of cirrhosis are easily bleeding and bruising, Confusion, drowsiness and slurred speech (hepatic encephalopathy) and Jaundice. A bruise is a traumatic injury to the skin or underlying tissues. The blood vessels lying underneath the skin rupture and leak blood, the blood collects under the skin. There are 28 possible conditions of bruises they are low platelet count, leukemia, factor X deficiency, disseminated intravascular coagulation, factor II deficiency, idiopathic thrombocytopenic purpura, factor V deficiency, factor VII deficiency, haemophilia A, hemophilia B, acute lymphocytic leukemia, chronic myeloid leukemia, acquired platelet function disorder, kidney failure etc. The pathophysiology of the symptons are compensated and decompensated (Kaplowitz & DeLeve, 2013). Compensated means the liver is scarred but can carry out most of its functionsby coping with the damages. In case of compensated liver cirrhosis no symptons are witnessed. In decompensated liver cirrhosis the liver is unable to function properly. In this stage the liver develops a number of symptons and complications. Cytokines, many cells and miRNAs are included in the progression of fibrosis and liver cirrhosis. A pivotal event in fibrosis is the activation of the hepatic stellate cells (HSCs). The cirrhosis is caused by chronic hepatitis C virus infection, alcoholism, chronic hepatitis B, hemochromatosis, primary biliary cirrhosis, Wilson’s diseases, primary sclerosing cholangitis, and autoimmune hepatitis cirrhosis (Klavan & Fortune, 2016)s. The causes of liver cirrhosis are multifactorial. The treatment for liver cirrhosis is lacking because of the poor understanding of the molecular mechanism leading to liver cirrhosis. Most effective treatment can only be developed with the proper understanding of the pathogenesis of liver. Liver cirrhosis is the pathological result of liver diseases.
3.The treatment of liver cirrhosis is caused by a drug known as ursodiol which slow down the process of liver damage. The potential treatment option of biliary cirrhosis is Budesonide. The effect of liver cirrhosis on pharmacokinetics and pharmacodynamics varied on the basis of the situation. Four different theories on liver cirrhosis are the sick cell theory the impaired drug uptake theory, the oxygen limitation theory and intact hepatocyte theory. In cirrhosis, other conjunctive pathways may also get impaired. In cirrhosis, the biliary drug excretion is impaired. Both creatinine clearance and serum creatinine levels are not useful for the renal dysfunction connected with cirrhosis and may overestimate the renal function in patients with cirrhosis (Lazenby & Corwin, 2011). Some drugs have shown altered receptor sensitivity with cirrhosis. Some other drugs have no change in pharmacodynamics. In order to determine the drug dosage in the cirrhosis information is needed regarding changes in plasma protein binding and pharmacodynamics. Information is also required regarded changes in the elimination of drugs. In many Pharmacokinetic examinations without cirrhosis suggests that in the lack of cirrhosis mutilation of the drug elimination is not enough to guarantee a reduction of drug. In the case of liver cirrhosis decrease of drug, the dose is the only way regardless of the route of elimination of metabolite. The most commonly used drugs in liver cirrhosis are memantine , galantamine, donepezil and rivastigmine. Galantamine, Donepezil, and rivastigmine are of different pharmacodynamic and pharmacokinetic profiles. Galantamine is a selective acetylcholinesterase inhibitor. cytochrome P450 (CYP) 2D6 and CYP3A4 is responsible for metabolizing Donepezil and galantamine in the liver (Macheras, 2018).
4.
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Nursing care plan goals |
Interventions |
Rationales |
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The main goal of a nursing care plan is to provide adequate care to the patient within first 8 hours post ward admission. |
· Comparing the changes in the fluid status, measurement of skinfold and recent history of weight. · The patient should be provided frequent meals but in small quantity. |
· It can be difficult for using the weight as the indicator for the nutritional status in ascites or edema view. · The patient cannot eat in a larger quantity because of increased ascites and intra-abdominal pressure. · The patient can eat in small quantity because of the loss of interest or generalized weakness, nausea, and malaise. · Glucose can reduce due to the impaired gluconeogenesis, inadequate intake or depleted glycogen stores. Protein can be low due to impaired metabolism, loss in the peritoneal cavity and reduced hepatic synthesis (Srivastava & Siddiqui, 2017). |
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The aim is to develop a nursing care planning with liver cirrhosis which consists of promoting test, skin care and decreasing the risk for injury. |
· Monitoring the laboratory studies which consists of serum glucose, total protein, albumin, prealbumin, and ammonia. · Salt substitute can be provided but ammonium should be avoided contained in it. |
· The patient can face problem due to bad mouth taste and bleeding gums that can lead to anorexia. · The conservation of energy can help to encourage cellular regeneration and decreasing metabolic demands on the liver. · The measurements of skinfold are useful to assess the changes in fat reserves and muscle mass. |
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The aim is to provide appropriate nutrition and managing complications. |
· Encouraging patient for eating food in an appropriate manner. The patient needs to be assisted to consume his diet. Appropriate meal planning should consider food choices that are preferred by the patient (Carpenito, 2009). · The consumption of caffeine, cold or hot foods and spicy or gas-producing foods should be restricted. · Soft foods should be directed to consume and avoid roughage. · Encouraging the patient to take care of his mouth before taking meals. |
· Improved diet and nutrition is an important recovery. The patient can eat in a better manner if preferred foods are provided and family members are also involved (Adams & Towle, 2009). · The salt substitute improves the food flavor and helps to increase appetite but ammonia increases the risk of encephalopathy. · It will help to decrease gastric irritation and abdominal discomforts that can impair the oral intake. · The high-calorie food needs to be taken by the protein. The supply of carbohydrates increases the energy level. The fats are not absorbed appropriately due to the dysfunction of the liver. Protein improves the level of serum protein for decreasing edema and promoting liver cell regeneration. |
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The aim is to provide significant information to the patient |
· The patient should be suggested to take rests in an appropriate manner. · The patient should be provided with information about the negative impact of smoking and drinking alcohol (Michelli, 2011). |
· The consumption of alcohol and smoking damages the liver adversely. · The patient should be suggested to consume high calories, low fat, moderate and high protein, simple carbohydrates, limit fluid and sodium. |
References
Adams, E., & Towle, M. (2009). Pediatric nursing care (8th ed.). Upper Saddle River, N.J.: Pearson/Prentice Hall.
Carnevale, A. (2012). Healthcare (3rd ed.). Washington, D.C.: Georgetown University, Georgetown Public Poicy Institute, Center on Education and the Workforce.
Carpenito, L. (2009). Nursing care plans & documentation (7th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
Gine?s, P., Kamath, P., & Arroyo, V. (2011). Chronic liver failure (4th ed.). New York: Humana Press.
Iacobuzio-Donahue, C., & Montgomery, E. (2012). Gastrointestinal and liver pathology (6th ed.). Philadelphia: Elsevier/Saunders.
Kaplowitz, N., & DeLeve, L. (2013). Drug-induced liver disease (5th ed.). Oxford: Academic.
Klavan, H., & Fortune, B. (2016). Elevated creatinine in a patient with cirrhosis. Clinical Liver Disease, 7(3), 48-52. doi: 10.1002/cld.534
Lazenby, R., & Corwin, E. (2011). Handbook of pathophysiology (3rd ed.). Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health.
Macheras, P. (2018). Modeling In Biopharmaceutics, Pharmacokinetics And Pharmacodynamics (5th Ed.). Sydney: Springer.
Michelli, M. (2011). Liver cirrhosis (3rd ed.). New York: Nova Science Publishers.
Srivastava, V., & Siddiqui, A. (2017). Cryptococcal Peritonitis in A Patient with Liver Cirrhosis: Case Report. International Journal Of Life-Sciences Scientific Research, 3(3), 55-115. doi: 10.21276/ijlssr.2017.3.3.1
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