MARA SULIMAN
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blog 6
26 Apr 2021, 13:06
- Alcohol tolerance may result from ethanol-induced up-regulation of a pathway in response to the continuous presence of alcohol. Alcohol dependence may result from overactivity of that same pathway after ethanol effect dissipates and before the system has time to return to a normal ethanol-free state. Furthermore, GABA neurotransmission is believed to play a role in tolerance because there is evidence of down-regulation of GABA-A mediated responses with chronic alcohol exposure.
- Chronic alcohol consumption can cause metabolic repercussions of ethanol oxidation in the liver, liver injury caused by the toxicity of the metabolic byproducts of alcohol (acetaldehyde) as well as inflammation caused by these metabolic by products. Chronic alcohol consumption can also cause dysregulation of fatty acid-oxidation and synthesis as well as activation of the innate immune system.
- Wernicke-Korsakoff syndrome is a syndrome caused by a thiamine deficiency and is characterized by paralysis of external eye muscles, ataxia and a confused state that can lead to a coma and eventually death. This syndrome uncommon, but is rarely seen in the absence of alcoholism. The syndrome is treated with parenteral thiamine that is given to the patient.
- Fetal alcohol syndrome is a syndrome caused by chronic maternal alcohol abuse during pregnancy and is associated with teratogenic effects. Mental retardation and congenital malformations are seen commonly in infants with this syndrome. Other abnormalities often include: intrauterine growth retardation, microcephaly, underdevelopment of the midfacial region, congenital heart defects and well as minor joint abnormalities. This syndrome is caused because ethanol rapidly crosses the placenta and causes the fetal blood to reach the same concentration as that of the maternal blood. The fetal liver, however, does not have alcohol dehydrogenase activity and relies on the enzymes of the maternal blood to metabolize the alcohol. The ethanol in the fetal bloodstream then triggers apoptotic neurodegeneration and causes neuronal and glial migration in the developing nervous system.
- In acute alcohol consumption the most important enzymes at play are mostly alcohol dehydrogenase and MEOS can come into play when alcohol concentrations become too high. In chronic alcohol consumption the MEOS are the most active enzymes and their activity is induced by the chronic alcohol consumption and this increases the alcohol metabolism.
- Alcohol potentiates the effects of vasodilators, hypoglycemic drugs, sedatives and depressants (alcohol can increase their depressant response) as well as aspirin’s anti-platelet effects.