Central nervous system ethanol causing

Procarbazine causes myelosuppression, hypnotic and other effects on the central nervous system, e.g., vivid nightmares. Also, procarbazine causes a disulfiram like syndrome on ingestion of ethanol. 

Attempts to diminish the overall metabolism of trichloroethylene might be useful (e.g., hypothermia, mixed-function oxidase inhibitors, competitive inhibitors of trichloroethylene metabolism [i.e., P-450 substrates]), if instituted soon enough after trichloroethylene exposure. Catecholamines (especially beta agonists) act in concert with trichloroethylene, increasing the risk of cardiac arrhythmias. Hence, catecholamines should be administered to patients only in the lowest efficacious doses and for certain limited presentations of trichloroethylene poisoning. Ethanol should also be avoided because concurrent exposure to trichloroethylene and ethanol can cause vasodilation and malaise and may potentiate central nervous system depression at high dosage levels of either compound. 

Ingestion of ethanol acts on the central nervous system. In moderate amounts, it affects Judgment and lowers inhibitions. Higher concentrations cause nausea and loss of consciousness. Even at higher concentrations, it interferes with spontaneous respiration and can be fatal. 

Ethanol can increase the levels of many enzymes involved in metabolism of xenobiotics. Prolonged ethanol intake causes irreversible damage in the central nervous system and in the liver, resulting in marked decreased capacity for detoxification of xenobiotics and thereby increased sensitivity to a number of chemicals (KEMI 2003). 

Buspirone causes less psychomotor impairment than diazepam and does not affect driving skills. The drug does not potentiate the central nervous system depressant effects of conventional sedative-hypnotic drugs, ethanol, or tricyclic antidepressants, and elderly patients do not appear to be more sensitive to its actions. Tachycardia, palpitations, nervousness, gastrointestinal distress, and paresthesias may occur more frequently than with benzodiazepines. Buspirone also causes a dose-dependent pupillary constriction. Blood pressure may be elevated in patients receiving MAO inhibitors. A number of buspirone analogs have been developed (eg, ipsapirone, gepirone, tandospirone) and are under study. 

Ethanol is a vasodilator, probably as a result of both central nervous system effects (depression of the vasomotor center) and direct smooth muscle relaxation caused by its metabolite, acetaldehyde. In cases of severe overdose, hypothermia—caused by vasodilation—may be marked in cold environments. Ethanol also relaxes the uterus and—before the introduction of more effective and safer uterine relaxants (eg, calcium blockers, magnesium ion, NSAIDs, and -adrenoceptor stimulants)—was used intravenously for the suppression of premature labor. 

Ethanol is a central nervous system depressant and ingestion of low to moderate quantities can lead to symptoms of intoxication including muscle incoordination, visual impairment, slurred speech, etc. Ingestion of higher concentrations may cause depression of medullary action, lethargy, amnesia, hypothermia, hypoglycemia, stupor, coma, respiratory depression, and cardiovascular collapse. The lethal human blood-alcohol concentration is generally estimated to be 400-500 mg/ 100 mL. 

Ethanol is a central nervous system (CNS) depressant that initially and selectively depresses some of the most active portions of the brain (reticular activity system and cortex). The mechanism of action most likely involves interference with ion transport at the axonal cell membrane rather than at the synapse, similar to the action of other anesthetic agents. Ethanol can bind directly to the gamma-aminobutyric acid (GABA) receptor in the CNS and cause... 

Major toxic effects are caused by formaldehyde and formic acid. The former is responsible for damage to retinal cells that may cause blindness, while the latter produces severe acidosis that may eventually lead to death. A minor effect of methanol is depression of the central nervous system (CNS). Retardation of the first step in the oxidation of methanol is accomplished by administration of ethanol, the oxidation products of which are not as toxic as those of methanol. Other therapeutic modalities include removal of methanol by gastric lavage (to prevent further absorption), hemodialysis (to remove absorbed methanol), and administration of exogenous bicarbonate (for treatment of severe acidosis). 

Ethanol is a teratogen partly because it inhibits embryonic cellular proliferation. Maternal alcoholism causes fetal alcohol syndrome, which is characterized by abnormal function of the central nervous system, microcephaly, cleft palate, and micrognathia. 

Methanol, which has caused many fatalities when ingested accidentally or consumed as a substitute for beverage ethanol, is metabolically oxidized to formaldehyde and formic acid. In addition to causing acidosis, these products affect the central nervous system and the optic nerve. Acute exposure to a lethal dose causes an initially mild inebriation, followed in about 10-20 hours by unconsciousness, cardiac depression, and death, Subletal exposures can cause blindness from deterioration of the optic nerve and retinal ganglion cells. Inhalation of methanol fumes may result in chronic, low level exposure. 

Most, if not all, of the tissues and organs in the body are adversely affected by chronic ingestion of excessive amounts of alcohol, including the liver, pancreas, heart, reproductive organs, central nervous system, and the fetus. Some of the effects of alcohol ingestion, such as the psychotropic effects on the brain or inhibition of vitamin transport, are direct effects caused by ethanol itself. However, many of the acute and chronic pathophysiologic effects of alcohol relate to the pathways of ethanol metabolism (see Chapter 25). 

Al Martini is suffering from both short-term and long-term effects of ethanol on his central nervous system. Data support the theory that the shortterm effects of ethanol on the brain partially arise from an increase in membrane fluidity caused when ethanol intercalates between the membrane lipids. The changes in membrane fluidity may affect proteins that span the membrane (integral proteins), such as ion channels and receptors for neurotransmitters involved in conducting the nerve impulse. 

Ethanol is a central nervous system depressant-it slows the rate at which nerve impulses travel. One or two alcoholic drinks lead to mild sedation. Four or more drinks can cause a loss of coordination and even unconsciousness. Overly excessive drinking—20 shots of a 90-proof spirit in a short time—is lethal. 

Frequency and Duration of Exposure. The frequency and duration of exposure to toxic chemicals play an important role in toxicity. For many toxic chemicals, the adverse health effects associated with a single exposure are different from those associated with repeated exposures. A single exposure to benzene may cause central nervous system depression, while repeated exposures may cause leukemia. Infrequent exposure to ethanol affects the central nervous system while frequent exposure includes the liver as a target organ. 

Ethanol acts on the central nervous system, causing euphoria at the beginning, but severe poisoning can lead to death. Ethanol is an addictive poison that causes alcoholism (ethyhsm). Ethylene glycol is a sweet toxic compound that can damage the kidneys, nervous system, heart and lungs. 

Central nervous system depressants. Affect voluntary motor functions, causing loss of fine motor coordination, unconsciousness. Examples methanol, ethanol, ether. 

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