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Alcoholism's Impact on Liver Function

   

Added on  2020-01-28

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INTRODUCTIONIncrease in alcohol consumption by chunk of population is considered be the majorconcern in present scenario. The medical science has proved from time-to-time that alcohol hasrange of negative impacts on human body. The report proposed herewith emphasizes onanalyzing various negative impacts of alcohol consumption. It throws light on manner in whichalcohol destroys organ’s capacity to control mechanism of human body. ALCOHOLIC CIRRHOSIS EVALUATIONUse of alcohol leads to progressive damage of the liver to a point where cirrhosis occurs.The liver has an innate ability to regenerate after an injury. However, continuous alcoholdrinking does not offer the liver an opportunity to heal.Liver cirrhosis develops in heavy drinkers who drink more than 230 g of alcohol per day(Galvani, 2012 p. 3). Apart from the drinking patterns, there seem to be other factors responsiblefor an individual developing liver disease since not all people who drink heavily are affected.Women require approximately half the alcohol percentage for susceptible men to develop thesame condition. Alcohol is readily absorbed beginning from the stomach to the small intestine. Ethanolcannot be stored in the body, and the degradation process begins in the gastric mucosa. Onreaching the liver, alcohol is acted upon by the liver enzymes, alcohol dehydrogenase (ADH) andthe cytochrome P-450 enzymes. The microsomal enzyme oxidation system (MEOS) also acts onthe substance in chronic alcoholism. ADH converts alcohol into acetaldehyde which is thenoxidized by acetaldehyde dehydrogenase (ALDH) to form acetate. In the process, hydrogen isformed, and it serves to convert nicotinamide adenine dinucleotide (NAD) to NADH hence
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increasing the liver’s redox potential. Fatty acid oxidation, as well as gluconeogenesis, isinhibited, and the result is fat accumulation in the hepatocytes. The export of fat to the rest of the body is hampered due to a reduction in the synthesis oflipoproteins and hepatic fatty oxidation. The decreased export of fat leads to an increase in theinflux of fat in the liver as a result of peripheral lipolysis and synthesis of triglycerides. Alcoholeffects in the gut include changes in permeability and increase in absorption of bacterialendotoxins. The Kupfer cells produce free radicals increasing the oxidative stress in the liver. The under nutrition related to alcoholism leads to a reduced antioxidant action of glutathione,vitamins A and E in the body. The body cells bind to acetaldehyde to form new antigens andinflammatory response ensues. The white cells release inflammatory cytokines and interleukinsto deal with the antigens. High blood pressure in the liver venous system is caused by cirrhosis (Runyon, 2013 p.1651). The normal blood flow through the liver parenchyma is slowed, and the pressure in theveins is increased. Portal hypertension causes fluid to accumulate in the extremities and theabdomen. The reason is that the liver cirrhosis leads to the inability of the liver to manufactureproteins that maintain the oncotic pressure such as albumin. Splenic damage due to cirrhosisleads to a reduced white blood cells, platelets, and red cells due to sequestration and the patientsbecome easily fatigued. Malnutrition due to cirrhosis also leads to the inability of the body toaccumulate nutrients and hence the easy fatigability. The liver is damaged leading tohepatomegaly with a firm, sharp edge. Portal hypertension leads to hypoxemia andintrapulmonary arteriovenous shunting, and the patient becomes tired on little exertion. Livercirrhosis leads to a raised blood pressure that may push a patient towards hypertension. Theendotoxic damage from the gut bacteria leads to the gastrointestinal symptoms of anorexia,
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indigestion, constipation, and diarrhea (Bajaj et al., 2014 p. 943). Liver cirrhosis also leads tobiliary malfunction and hence reduced digestive functions of the bile duct. This in turn leads toan increased transit time in the gut and constipation.The glucose levels are within range, and this is an indication that the patient’s status isnot progressing towards diabetes. However, more tests on glucose are required before aconclusion is made. Alcohol interferes with the production of leukocytes in the bone marrow.The leukocyte levels of Mr. Chris are within limits for his age group. The hematocrit level of 38% however, raises the alarm because it is slightly reduced. The patient is, therefore, anemic, afactor that is associated with alcoholism. The anemia results from both nutritional deficiency andinfections that an alcoholic is predisposed. The process of iron absorption is interfered with byalcohol, and resulting condition is iron deficiency anemia. The iron loss can also come from thebleeding in gut and esophageal varices. Folic and other vitamin deficiencies due to excessivealcohol consumption can also cause anemia in the alcoholics (Ballard, 1997 p. 43). The blood-clotting mechanisms of body are affected by excessive alcohol consumption(Trevejo-Nunez, 2015 p. 177). The platelets secrete clotting factors and proteins responsible forhemostasis. The effect of alcohol can be thrombocytopenia or low levels of platelets,thrombocytopathy (impaired function of platelets and inhibition of fibrinolysis hence formationof thrombi). The platelet levels are way below normal range for Mr. Chris. Some studies showthat alcohol may be leading cause of extremely low platelet count in individuals apart from thosewho are immune compromised. Patients who have low platelets are at risk of bleeding disordersthat are difficult to control. Thrombocytopenia is self-limiting, and it takes only a week to restorenormal platelet counts if the patient abstains from drinking alcohol.
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