We and alcohol

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We and alcohol

Post  counselor on Mon Oct 15, 2012 11:38 am


Alcoholic beverages in Western societies are freely marketed and publicized.
This can be misleading, because:
• Alcohol is a drug with marked effects on the central nervous system effects;
• Alcohol is a major cause of death in Western societies.
• The abusodi alcohol is associated with serious toxic effects on


In the past it depressant effects of alcohol have been attributed to non-specific interaction with membrane lipids

Recent evidence documenting interaction of ethanol with various membrane receptors:
• improves the function of the GABAA receptor,
• inbisce the function of NMDA and kainate
• interaction with nicotinic receptors
• enhances the function of 5-HT3 receptors
• enhances the function of the potassium channel
• increased synthesis of pro-opiomelanocortin and opioid peptides, which may mediate the rewarding effects
• stimulates the mesolimbic dopamine system.

Central nervous system
Alcohol has a marked CNS depressant.
Consequently causes:
• thought-chaotic and messy,
•-weakening of concentration and memory,
• self-criticism and self-reduction,
•-altered control of motor processes.
• full-confidence, expansive personality.
•-At high doses, there is intense and widespread depression, extended activity reflected istaura spinal and general anesthesia.
•-L'alcol also depressed the response of the respiratory center to carbon dioxide.

Dilates cutaneous vessels for central vasomotor depression and direct action on blood vessels.
In laboratory animals, but not humans, there is dilation of the coronary arteries.
Alcohol can give vasoconstriction of cerebral arteries.

Little effect for moderate amounts of alcohol.
A moderate doses increases HDL and lowers LDL. It seems that moderate amounts of alcohol reduce the incidence of coronary heart disease.
Excessive use of alcohol causes heart disease and chronic lesions (intracellular).

Gastro-intestinal tract
Alcohol stimulates gastric secretions and saliva by:
• Stimulation of psychic origin
• Stimulation of alcohol reflected due to contact with the oral mucosa and gastric ulcers.
• Direct action on the stomach (mediated by release of gastrin and histamine)

The gastric secretion stimulated by alcohol are rich in acid and has normal content of pepsin.

A concentration of 20%, gastric secretion tends to be depressed.
The spirits (40%) are irritating and can cause erosive gastritis. Alcohol potentiates the harmful action of aspirin.
It is often observed alcoholic chronic diarrhea.
Alcohol contributes to damage the esophagus and duodenum.

• Long-term use of alcohol causes accumulation of fat (increased synthesis) and protein (reduced secretion) in hepatocytes. These processes can become irreversible.
• The risk of cirrhosis is also due to malnutrition and vitamin deficiency.
• The alcohol generates problems of storage of vitamins in the plasma level of the liver.

Alcohol produces a diuretic effect because it inhibits the release of ADH.
Alcohol abuse can cause nephropathy.

Anemia (sideroblastic and megablastiche) are due to interference with the metabolism of alcohol and transport of folate.
Alcohol depresses the bone marrow (thrombocytopenia). Depresses leukocyte migration into inflamed areas.

Sexual Functions
Alcohol, in moderate doses, acts as an aphrodisiac as it results in loss of inhibition and self-control.
Chronic alcohol abuse causes infertility and testicular atrophy (the hepatic lesion reduces the production of testosterone, enzyme induction accelerates the inactivation of testosterone).

Body temperature
Alcohol produces reduction of body temperature because:
1) gives cutaneous vasodilation
2) can produce sweating
3) at high doses depress temperature control centers

Skeletal muscle
High doses of alcohol produce direct muscle damage (alcoholic skeletal myopathy)

Teratogenic effect
Alcohol inhibits the proliferation of embryonic cells of the first period of pregnancy and can lead to fetal alcohol syndrome (low IQ, slow growth, facial abnormalities, increased susceptibility to infectious diseases).
Alcohol also increases the incidence of abortions and births of dead fetuses.

Local actions
Antiseptic. Alcohol is active on bacteria, has low activity of fungi and viruses, is inactive on spores.
Astringent action of subcutaneously administered gives intense pain followed by anesthesia.


Rapid absorption through the stomach, small intestine, colon and, if vaporized, through the lungs. In the stomach, but not in the intestine, the absorption is hindered by the presence of food.
High concentrations of alcohol (after an initial rapid absorption) they slow the absorption and also for producing pirolospasmo.

Is uniformly distributed in the organism. Well through the placental barrier and the blood-brain barrier.

• About 2% of alcohol is eliminated via urine production by the kidney and the lung.
• Elimination of metabolic oxidation of the remaining 98%. Takes place mainly in the liver.
• Alcohol is oxidized to acetaldehyde by alcooldeidrogenasi and microsominali oxidase.
• Alcohol is firstly decrease and then increase the activity of liver enzymes microsominali.
• The oxidation of alcohol in case of intoxication follows a zero-order kinetics (about 30 ml in 3 hours).

Alcohol causes already at moderate doses
• sleepiness
• mental confusion
• impaired balance
and may cause
• Problems guide
• Attitude violent

Acute intoxication
A strong acute intoxication is manifested to about 150 mg of alcohol per dl of blood. At 400 mg / dl has generally lethal intoxication.
Attention to diagnosis: possibility of diagnostic errors (such as diabetes, drug intoxication depressing the CNS, cardiovascular and chronic fractures).

Chronic intoxication
Both are due to nutritional deficiencies than to direct harmful effects of alcohol: peripheral polyneuropathy, Wernicke's encephalopathy, pellagra, cirrhosis, myopathy, cardiomyopathy, cognitive deficits.

Drug addiction
Central effects that motivate alcohol intake
• induction of a certain degree of euphoria
• removal of anxiety and depression
• inhibition of self-criticism
• inhibition of the sense of self

Alcohol can lead to severe drug addiction:

We have tolerance and pharmacokinetics farmacodimamica. Alcohol tolerance is generally crusade with general anesthetics and benzodiazepines.

Physical dependence
The suspension of alcohol intake in addicts gives withdrawal syndrome within 17-72 hours after discontinuation of alcohol consumption.

Describes three stages of severe withdrawal:
• Syndrome trembling. Intense tremor, nausea, vomiting, "visions" to the alcoholic hallucination.
• seizure disorders
• Delirium tremens. Persecutory delusions that appear on the 3rd day and terrorize the subject.

In subjects with moderate physical dependence withdrawal syndrome is manifested by insomnia, anxiety, restlessness, weakness and slight tremor.

Trattamentodella intoxication
Measures of life support, such as intubation and mechanical ventilation, gastric lavage, hemodialysis

DellaSindrome treatment withdrawal
- A long-acting benzodiazepines (chlordiazepoxide, diazepam), or intermediate (oxazepam and lorazepam).
- Anticonvulsants (gabapentin, vigabatrin, carbamazepine)
-  adrenergic blockers or  2 adrenergic agonists such as clonidine to control the vegetative symptoms
- Thiamine, to treat or prevent the Wernicke, as well as administration of fluids and electrolytes.

Pharmacological treatments for weaning
Inhibitor of aldehyde dehydrogenase. Causes accumulation of acetaldehyde and discomfort when the subject takes alcohol.

Opioid receptor antagonist, reduces the rewarding effects and motivation for alcohol intake

Selective inhibitor of serotonin reuptake

Calcium salt of N-acetilomotaurina. Inhibits influence of Ca + + ions mediated by NMDA receptors; interacts with presynaptic GABAB receptors by increasing GABA release

-acid-hydroxybutyric acid (GHB).
Replaces the effect of ethanol, has been defined as the "methadone alcohol."

5-HT3 receptor antagonist

a) Sedatives, hypnotics, anticonvulsants, antidepressants, anxiolytics, analgesics potentiate the depressant effects of alcohol.
b) Oral hypoglycaemic agents and cephalosporins + alcohol damage unpleasant symptoms such as disulfiram.
c) Alcohol potentiates the hypoglycaemic effect of insulin and oral hypoglycemic agents.
d) Pharmacokinetic interactions with many drugs metabolized by hepatic microsomal oxidase.

This is the intake of 20-30 g per day,
in other words, a glass of wine per meal.
This quantity does not evoke effects of central importance.

Small amounts of alcohol:
• stimulate the gastrointestinal secretions
• stimulate the 'appetite
• have a preventive effect against coronary artery disease (especially red wine).

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