Example Of Alcoholic Liver Disease: Understanding Risk Factors, Signs, Symptoms, And Prevalence Case Study
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While it is universally evident that alcoholic liver diseases—suggestive by the name as well—are caused by alcohol, risk factors for it are still being argued and disputed. Some studies claim that ultimate risk factors for alcoholic liver diseases are still unknown or largely undiscovered while others have determined only excessive alcohol intake as the only risk factor that actually substantially causes alcoholic liver diseases (Huang, Yang, and Kao, 2011:1; Jackson and Gleeson, 2010:66). While it is true that excessive alcohol intake is the major risk factor for alcoholic liver disease, one study has also enumerated other various factors that increase the likelihood of developing alcoholic liver diseases and those factors include (1) genetic predisposition, (2) gender, (3) ethnic differences, (4) nutritional factors, (5) energy metabolism abnormalities, (6) oxidative stress, (7) immunological mechanisms, and (8) hepatic co-morbidities (Gramenzi, Caputo, Biselli, Kuria, Loggi, Andreone, and Bernardi, 2006:1151).
Excessive and progressive alcohol intake causes abnormal alterations to the normal structure of liver which in return give rise to various complications that affect the quality of life of the patient. Generally, alcoholic liver disease has three subtypes: (1) steatosis or fatty liver, (2) alcoholic hepatitis, and (3) cirrhosis (Jackson and Gleeson, 2010:66; Marsano et al., 2003:247). Steatosis, also called fatty liver, is characterized by excessive buildup of fat inside the liver cells (Marsano et al., 2003:247). Alcoholic hepatitis, on the other hand, can be characterized by the inflammation of the liver accompanied by injury caused by the response of the body’s immune system, resulting to the greater damage of the organ (Marsano et al., 2003:247). Different to both steatosis and hepatitis, cirrhosis occurs when the normal liver cells are replaced by scar tissues, a condition known as fibrosis (Marsano et al., 2003:247).
The three subtypes of alcoholic liver diseases—which also categorize the main abnormal alterations that happen to the liver resulting from the disease—cause further complications that negatively affect liver function. Steatosis, occurring in 90-100% of heavy drinkers, usually clears out after a few months following cessation of alcohol intake (Jackson and Gleeson, 2010:66). Hepatitis, on the other hand, affects 10-35% of heavy drinkers and is usually accompanied with signs of systemic inflammatory response syndrome and multiple organ failure (Jackson and Gleeson, 2010:66). Cirrhosis, the worst subtype of alcoholic liver disease, results in hepatic function failure and portal hypertension caused by increased resistance to portal blood flow (Jackson and Gleeson, 2010:66).
Cirrhosis often presents no symptoms during its early stage (Marsano et al., 2003:248). However, as it develops, symptoms such as hepatosplenomegaly or the enlargement of liver and spleen, muscle wasting, ascites or the accumulation of fluid in the abdominal cavity, venous collateral circulation or the development of smaller blood vessels in response to increased blood flow, malnutrition, parotid enlargement, vascular spiders, palmar erythema, portal hypertension, fluid and electrolyte redistribution, feminization, neuropathy, and encephalopathy may be observed (Marsano et al., 2003:248; Huang et al., 2011:2). Such symptoms all cause hepatic function failure accompanied by severe alterations in the physical architecture of the liver (Huang et al., 2011:2; Marsano et al., 2003:247).
Ascitis, edema, and jaundice are three of the most common symptoms associated with alcoholic liver disease. Both ascitis and edema occurs due to the fluid accumulation that happens at the end stage of liver diseases, particularly liver cirrhosis (Kashani, Landaverde, Medici, and Rossaro, 2008:71). In addition, both ascitis and edema are caused by the derangement in mechanisms that regulate extracellular fluid volume (Kashani et al., 2008:71). Jaundice or the yellowing of the skin, on the other hand, is caused by the elevated levels bilirubin in the blood, a condition referred to as hyperbilirubinemia (Huang et al., 2011:2).
Haematemesis or the vomiting of fresh blood is another symptom common among patients affected with alcoholic liver diseases. In the case of those affected with liver cirrhosis, development of esophageal varices or the small network of collateral veins forming in the esophagus can be observed during the terminal stages of the disease (Marsano et al., 2003:254). Such small veins that developed in order to accommodate abnormally increased blood flow characteristic of liver diseases inevitably grow larger, leading to spontaneous rupture (Marsano et al., 2003:254). Referring to the case presented, the patient may have had experienced an episode of such spontaneous rupture also referred to as spontaneous variceal bleeding originating in the esophagus.
Dark-colored stools may signal gastrointestinal bleeding—a symptom commonly observed in patients affected with alcoholic cirrhosis that have also developed spontaneous bacterial peritonitis (Kashani et al., 2008:75; Biecker, 2011:1242).
In order to know the extent of liver damage of the patient presented, it is important to subject him to laboratory test such as ultrasound, CT scan, and MRI to ultimately diagnose the presence or absence of cirrhosis (Huang et al., 2011:2). Furthermore, the patient may also be subjected to liver biopsy in order to determine the presence or absence of hepatitis since he presented jaundice or yellowing of the skin. Liver biopsy may also be helpful to evaluate the severity of hepatitis once proven present (Huang et al., 2011:2).
Prothrombin time is elevated because coagulation and haemostasis in patients with liver diseases are impaired (Amarapurkar and Amarapurkar, 2011:2). Prothrombin refers to the length of time of during which coagulation occurs (Amarapurkar and Amarapurkar, 2011:1). The liver is responsible for the production of the majority of plasma clotting factors as well as the fibrinolytic proteins and the proteins of anticoagulants (Amarapurkar and Amarapurkar, 2011:2). Once the liver becomes affected by alcoholic liver diseases, especially cirrhosis, the blood clotting mechanism becomes impaired and will show abnormal results in bleeding tests such as the prothrombin time (Amarapurkar and Amarapurkar, 2011:1).
Amarapurkar P.D. and Amarapurkar D.N. 2011. “Management of Coagulopathy in Patients with Decompensated Liver Cirrhosis”, International Journal of Hepatology. 2011:1-5. Available online at http://www.hindawi.com/journals/ijh/2011/695470/ (Accessed on 26 January 2015)
Biecker E. 2011. “Diagnosis and therapy of ascites in liver cirrhosis”, World Journal of Gastroenterology. 17(10):1237-1248. Available online at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068258/ (Accessed on 26 January 2015)
Gramenzi A., Caputo F., Biselli M., Kuria F., Loggi E., Andreone P. and Bernardi M. 2006. “Review article: alcoholic liver disease – pathophysiological aspects and risk factors”, Alimentary Pharmacology & Therapeutics. 24:1151-1161. Available online at https://www.med.upenn.edu/gastro/documents/AlimentaryPharmacolTherapAlcoholicLiverDz.pdf (Accessed on 26 January 2015)
Huang Y.W., Yang S.S. and Kao J.H. 2011. “Pathogenesis and management of alcoholic liver cirrhosis: a review”, Hepatic Medicine Evidence and Research. 2011(3):1-11. Available online at http://www.dovepress.com/pathogenesis-and-management-of-alcoholic-liver-cirrhosis-a-review-peer-reviewed-article-HMER (Accessed on 26 January 2015)
Jackson P. and Gleeson D. 2010. “Alcoholic liver disease”, Continuing Education in Anaesthesia, Critical Care & Pain. 10(3):66-71. Available online at http://ceaccp.oxfordjournals.org/content/10/3/66.extract (Accessed on 26 January 2015)
Kashani A., Landaverde C., Medici V. and Rossaro L. 2008. “Fluid retention in cirrhosis: pathophysiology and management”, Quarterly Journal of Medicine. 101:71-85. Available online at http://qjmed.oxfordjournals.org/content/101/2/71 (Accessed on 26 January 2015)
Marsano L.S., Mendez C., Hill D., Barve S. and McClain C.J. 2003. “Diagnosis and Treatment of Alcoholic Liver Disease and Its Complications”, Alcohol Research and Health. 27(3):247-256. Available online at http://pubs.niaaa.nih.gov/publications/arh27-3/247-256.pdf (Accessed 26 January 2015)
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