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Alcohol consumption long-term effects

The terms acute and chronic are also used to characterize the time delay between exposure and the onset of symptoms. Acute effects are those noticed directly following exposure and are usually easily related to the agent. The chronic or long-term effects of an agent may occur years later and are often very difficult to attribute to a particular cause. The acute effects of alcohol consumption or exposure to the solvent in glue are obvious in the drunkenness produced. The effects of chronic exposure to these compounds, as seen by an alcoholic, are very different specifically, cirrhosis of the liver. The chronic effect of childhood lead exposure... [Pg.27]

Ethanol has been used widely as a beverage, a medicinal, and a solvent in numerous pharmaceutical preparations. Such common usage often overshadows the fact that ethanol is a toxic substance. Ethanol consumption is associated with a variety of long-term effects, including cirrhosis of the Uver, death of brain cells, and alcoholism. Alcohol consumed by the mother can even affect the normal development of her unborn child and result in fetal alcohol syndrome. For these reasons, over-the-counter cough and cold medications that were once prepared in ethanol are now manufactured in alcohol-free form. [Pg.379]

Feid LP, Moore RD, Pearson TA. Long-term effect of cigarette smoking and moderate alcohol consumption on coronary artery diameter. Mechanisms of coronary artery disease independent of atherosclerosis or thromboses Am 7 Med 1986 80 37 4. [Pg.51]

Alcohol has a range of effects for some, desirable acute effects unwanted effects on the developing fetus and with long-term consumption, effects on the liver and other organs. In the US, over 2 million people experience alcohol related liver disease. Effects on the liver are dose related the more you consume the greater the effects. Early on there is an accumulation of fat in the liver as a result of the metabolism of alcohol. Some heavy drinkers develop an inflammation (alcoholic hepatitis) of the liver. Metabolites of alcohol, produced by the liver, are toxic to the liver cells. [Pg.40]

Recall from our discussion of cocaine and amphetamines that the body responds to the long-term abuse of these stimulants by creating more depressant receptor sites. Likewise, the body recognizes the excessive inhibitory actions produced by alcohol and tries to recover by increasing the number of synaptic receptor sites that lead to nerve excitation. A tolerance for alcohol therefore develops. To receive the same inhibitory effect, the drinker is forced to drink more, which induces the body to create even more excitable synaptic receptor sites. Eventually, an excess of these excitatory receptor sites leads to perpetual body tremors, which can be subdued either by more drinking or, with greater difficulty, by a long-term cessation of alcohol consumption. [Pg.506]

Consumption of alcohol during early adolescence has been linked to delays in the onset of female puberty. The response appears to be related to alcohol s effect on the function of IGF-1, which is synthesized in the liver and which is active in the brain to coordinate overall physical growth. Long-term consumption of alcohol inhibits the production of IGF-1, and short-term consumption of alcohol may alter IGF-1 function within the brain (Dees et al., 1998). [Pg.84]

There is no question that alcohol abuse contributes significantly to liver-related morbidity and mortality in the United States. Long-term alcohol use is the leading cause of illness and death from liver disease. There are three phases of alcohol-induced liver damage, alcoholic fatty liver, which is usually reversible with abstinence alcoholic hepatitis or inflammation and alcoholic cirrhosis or scarring of the liver. Patients with both alcoholic cirrhosis and hepatitis have a death rate of more than 60% over a 4-year period. The prognosis is bleaker than the outlook for many types of cancers. As many as 900 000 people in the United States suffer from cirrhosis and some 26 000 of these die each year. The risk for liver disease is related to how much a person drinks the risk is low at levels of alcohol consumption but steeply increases with higher levels of consumption. Because effects of alcohol are dose-related and because of the steepness at which the adverse effects are... [Pg.63]

Bone marrow toxicity that leads to leukopenia, anemia, and thrombocytopenia has been shown to be induced by methotrexate. A serious long-term adverse effect is hepatotoxicity. Consequently, methotrexate should typically be avoided in patients with liver disease. Risk factors for hepatotoxicity include a history of excessive alcohol consumption, hepatitis, persistent elevated liver function tests, and family history of inheritable liver disease. ... [Pg.1778]

Despite the widespread belief that alcohol can enhance sexual activities, the opposite effect is noted more often. Many drugs of abuse, including alcohol, have disinhibiting effects that may lead initially to increased libido. With excessive, long-term use, however, alcohol often leads to a deterioration of sexual function. While alcohol cessation may reverse many sexual problems, patients with significant gonadal atrophy are less likely to respond to discontinuation of alcohol consumption. [Pg.379]

A study in 12 patients receiving chlorpromazine 600 mg to 1.2 g daily long-term, found that chlorpromazine had no apparent effect on alcohol metabolism. However, about half of the patients had a statistically significant decrease (up to 33%) in urinary excretion of chlorpromazine and its metabolites during the 24-hour period following the consumption of 50 to 75 mL of alcohol. ... [Pg.50]


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See also in sourсe #XX -- [ Pg.603 , Pg.604 ]




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