Alcohol, primarily in the form of ethyl alcohol (ethanol), the most commonly abused drug in the world, consumed. Like other sedative-hypnotic drugs, alcohol in low to moderate amounts relieves anxiety and fosters a feeling of well-being or even euphoria.
Pharmacokinetics Ethanol is a small water-soluble molecule that is absorbed rapidly from the gastrointestinal tract. After ingestion of alcohol in the fasting state, peak blood alcohol concentrations are reached within 30 minutes.
For an equivalent oral dose of alcohol, women have a higher peak concentration than men, in part because women have a lower total body water content. Over 90% of alcohol consumed is oxidized in the liver; much of the remainder is excreted through the lungs and in the urine.
At levels of ethanol usually achieved in blood, the rate of oxidation follows zero-order kinetics, i.e., it is independent of time and concentration of the drug. The typical adult can metabolize 7–10 g (150–220 mmol) of alcohol per hour.Two major pathways of alcohol metabolism to acetaldehyde have been identified. Acetaldehyde is then oxidized by a third metabolic process.
The primary pathway for alcohol metabolism involves alcohol dehydrogenase (ADH), a cytosolic enzyme that catalyzes the conversion of alcohol to acetaldehyde This enzyme is located mainly in the liver, but it is also found in other organs such as brain and stomach.
A significant amount of ethanol metabolism by gastric ADH occurs in the stomach in men, but a smaller amount occurs in women, who appear to have lower levels of the gastric enzyme. This difference in gastric metabolism of alcohol in women probably contributes to the sex-related differences in blood alcohol concentrations noted above.
This enzyme system uses NADPH as a cofactor in the metabolism of ethanol. At blood concentrations below 100 mg/dL (22 mmol/L), the MEOS system contributes little to the metabolism of ethanol.
However, when large amounts of ethanol are consumed, the alcohol dehydrogenase system becomes saturated owing to depletion of the required cofactor, NAD+. As the concentration of ethanol increases above 100 mg/dL, there is increased contribution from the MEOS system, which does not rely upon NAD+ as a cofactor.
Much of the acetaldehyde formed from alcohol appears to be oxidized in the liver in a reaction catalyzed by mitochondrial NAD-dependent aldehyde dehydrogenase. The product of this reaction is acetate which can be further metabolized to CO2 and water.
Some people, primarily of Asian descent, have a genetic deficiency in the activity of the mitochondrial form of aldehyde dehydrogenase. When these individuals drink alcohol, they develop high blood acetaldehyde concentrations and experience a flushing reaction similar to that seen with the combination of disulfiram and ethanol.
Much attention has focused on alcohol's effects upon neurotransmission by glutamate and GABA. Acute ethanol exposure enhances the action of GABA at GABAA receptors. Ethanol also inhibits the ability of glutamate to open the cation channel associated with the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors.
Mechanisms implicated in tissue damage include: 1.increased oxidative stress 2.depletion of glutathione, 3.damage to mitochondria, 4.growth factor dysregulation, 5.potentiation of cytokine induced injury.
The test result is usually more reliable than with breath, but the requirements are considerably more substantial. Most blood is drawn after the client has refused to offer a breath sample BAC Kit: A sealed kit containing the equipment and documentation necessary for the collection of a blood sample for forensic purposes
1. The blood should be timely taken 2. from a particular identified body 3. by an authorized licensed physician medical technologist, or registered nurse designated by a licensed physician
4. the instruments used were sterile, 5. the blood taken was properly preserved or kept 6. and labeled. 7. if transported or sent, the method and procedures used therein 8. the method and procedures used in conducting the test
9.the identity of the person or persons under whose supervision the tests were conducted is established 10.The type of swab used to disinfect the draw site is also an important issue. A non-alcohol swab must be used
The authority lab uses a process known as gas chromatography. Gas chromatography is essentially a function of time and temperature.
The sample is first mixed with one of two internal standards, either 1-propanol or t-butanol. Each sample is then tested separately by two different chromatograms, and the lab reports the lower of the two results. Once the sample is diluted, it is then heated to produce a vapor. The vapor is then passed through a glass column. The vapor is then timed and measured as it passes out of (elutes out) the other end of the column. .
The peak measurement or curve on the chromatograph is then compared with a calibration curve, and the amount of blood alcohol is determined by reading where this sample peak passes over or meets the calibration curve
Non tolerant individuals who consume alcohol in large quantities develop typical effects of acute sedative-hypnotic drug overdose along with the cardiovascular effects (vasodilatation, tachycardia )and gastrointestinal irritation. Since tolerance is not absolute, even chronic alcoholics may become severely intoxicated. The average blood alcohol concentration in fatal cases is above 400 mg/dL; however, the lethal dose of alcohol varies because of varying degrees of tolerance.
The degree of intoxication depends upon three factors: 1.the blood ethanol concentration, 2.the rapidity of the rise of the alcohol level, 3.the time during which the blood level is maintained. The most important goals in the treatment of acute alcohol intoxication are to prevent severe respiratory depression and aspiration of vomitus.
Metabolic alterations may require treatment of hypoglycemia and ketosis by administration of glucose. Thiamine is given to protect against the Wernicke-Korsakoff syndrome. Alcoholic patients who are dehydrated and vomiting should also receive electrolyte solutions. If vomiting is severe, large amounts of potassium may be required as long as renal function is normal. Especially important is recognition of decreased serum concentrations of phosphate, which may be aggravated by glucose administration.
The major objective of drug therapy in the alcohol withdrawal period is prevention of seizures, delirium, and arrhythmias. Potassium, magnesium, and phosphate balance should be restored as rapidly as is consistent with renal function. Thiamine therapy is initiated in all cases.
Specific drug treatment for detoxification in severe cases involves two basic principles: substituting a long-acting sedative-hypnotic drug for alcohol and then gradually reducing ("tapering") the dose of the long-acting drug.
Because of their wide margin of safety, benzodiazepines are preferred for treatment of alcohol withdrawal syndrome. After the alcohol withdrawal syndrome has been treated acutely, sedative-hypnotic medications must be tapered slowly over several weeks.