KYLA DU PLESSIS

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Blog #6, Kyla du Plessis, 31814425

8 Mar 2021, 15:18 Publicly Viewable
  1. Chronic alcohol intake causes a tolerance to alcohol. The occurrence of tolerance due to chronic alcohol intake can be due to induction of the MEOS (Microsomal Ethanol-Oxidizing System) and thus the up-regulation of this pathway (Katzung, 2018; Brand, 2021).
  2. Chronic alcohol use causes alcoholic fatty liver-condition. This condition is luckily reversible, however it can progress to alcoholic hepatitis, cirrhosis and eventually liver failure. All these conditions listed above decreases functioning of the liver. For this conditions to take place the following liver-metabolism problems can occur: the oxidation and synthesis of fatty acid is not correctly regulated, metabolic repercussions of the oxidation of ethanol in the liver (Katzung, 2018). Liver microsomal enzyme’s activity is increased due to the liver-conditions (Brand, 2021).
  3. Wernicke-Korsakoff syndrome is a syndrome caused by a thiamine deficiency, usually due to alcoholism, with ataxia, paralysis of the external eye muscles and a confused state that can develop to a coma, is the common characteristics of this syndrome. This syndrome is treated with thiamine-therapy (Katzung, 2018).
  4. Fetal alcohol syndrome is a syndrome with which a baby is born, due to chronic alcohol abuse of a mother during pregnancy (especially the first trimester) (Brand, 2021; Katzung, 2018). This causes teratogenic effects. This syndrome has behavioral and cognitive abnormalities for the fetus and later human and also a wide range of abnormalities with development of the fetus and child (Brand, 2021). Characteristic abnormalities include: the underdevelopment of the midfacial area, microcephaly, minor joint abnormalities, the retardation of intra-uterine growth and poor coordination. When the case is more severe the baby can also have mental retardation and congenital heart defects. The mechanism of action of alcohol causing teratogenic effects is however unknown. What is known, is that the liver at fetal-stage has no or just minor alcohol dehydrogenase activity, thus causing the fetus to be dependent on the placental- and maternal enzymes to eliminate the alcohol (Katzung, 2018).
  5. With acute alcohol intake the liver blood flow decrease and/or the enzyme activities of the liver decrease this can thus inhibit the metabolism of drugs take that are dependent on the enzymes, for example. With the chronic intake of alcohol can cause higher than normal levels (even toxic levels) of drugs in the body which is dependent on cytochrome P450 for conversion to active metabolites. Due to the increased activity of cytochrome P450 this can lead to hepatotoxicity (Katzung, 2018).
  6. Tricyclic antidepressants, sedative-hypnotic drugs,  phenothiazines and acetaminophen (Katzung, 2018).

Reference list

Brand, L. 2021. Alcohols. Study unit 3 [pdf]. Unpublished lecture notes on eFundi, FKLG 312. Potchefstroom: NWU.

Katzung, B.G. 2018. Basic & Clinical Pharmacology. 14th ed. International: Mc Graw Hill Education.