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Symptoms of varying BAC levels. Additional symptoms may occur. The short-term effects of alcohol consumption range from a decrease in anxiety and motor skills and euphoria at lower doses to intoxication (drunkenness), to stupor, unconsciousness, anterograde amnesia (memory "blackouts"), and central nervous system depression at higher doses.
Alcohol depresses the central nervous system, slowing cerebral messaging and altering the way signals are sent and received. Progressively larger amounts of alcohol are needed to achieve the same physical and emotional results. The drinker eventually must consume alcohol just to avoid the physical cravings and withdrawal symptoms.
Alcohol flush reaction is a condition in which an individual's face or body experiences flushes (appears red) or blotches as a result of an accumulation of acetaldehyde, a metabolic byproduct of the catabolic metabolism of alcohol. It is best known as a condition that is experienced by people of Asian descent.
Alcohol-related brain damage [1] [2] alters both the structure and function of the brain as a result of the direct neurotoxic effects of alcohol intoxication or acute alcohol withdrawal. Increased alcohol intake is associated with damage to brain regions including the frontal lobe , [ 3 ] limbic system , and cerebellum , [ 4 ] with widespread ...
In 2019, a 25-year-old man presented with symptoms consistent with alcohol intoxication, including dizziness, slurred speech and nausea. He had no prior alcoholic drinks but had a blood alcohol level of 0.3 g/dL. The patient was given 100 mg of the antifungal fluconazole daily for 3 weeks, and his symptoms were resolved. [8]
Many cases of alcohol-induced respiratory reactions, which involve rhinitis and worsening of asthma, develop within 1–60 minutes of drinking alcohol and are due to the same causes as flush reactions. [11] Disulfiram, a drug sometimes given as treatment for alcoholism, induces effects similar to alcohol flush or hangover causing the disulfiram ...
Alcohol is also converted into phosphatidylethanol (PEth, an unnatural lipid metabolite) by phospholipase D2. This metabolite competes with PIP 2 agonist sites on lipid-gated ion channels. [28] [29] The result of these direct effects is a wave of further indirect effects involving a variety of other neurotransmitter and neuropeptide systems. [25]
Alcoholic ketoacidosis is caused by complex physiology that is the result of prolonged and heavy alcohol intake, usually in the setting of poor nutrition. Chronic alcohol use can cause depleted hepatic glycogen stores and ethanol metabolism further impairs gluconeogenesis.