Mechanisms of addiction development
The development of the disease is accompanied by a profound restructuring of the body's reactions to ethanol. The patient's willpower is suppressed, and once physical dependence is established, the substance is used exclusively to alleviate the symptoms of withdrawal syndrome (WS).
A critical marker of addiction is the change in tolerance. This process occurs in two stages:
- Increased tolerance. Significant doses cease to cause deep sleep, and the protective vomiting reflex disappears. Increasing amounts of alcohol are required to achieve euphoria. Cross-tolerance to all GABAergic drugs (benzodiazepines, barbiturates) develops.
- Decreased tolerance. The outcome of the disease. It arises due to organic damage to internal organs and the brain. The patient becomes intoxicated from minimal doses but tends to drink heavily, which creates a colossal risk of fatal poisoning.
ICD-10 diagnostic criteria
Alcoholism is coded under F10. The diagnosis of dependence syndrome is established if at least three of the following features have been periodically observed over the preceding year:
- An overpowering desire to drink.
- Loss of control over the dose and duration of intake.
- Development of a withdrawal syndrome upon cessation of drinking.
- Use of alcohol (or substitutes) to relieve withdrawal.
- Increase in tolerance (larger doses are needed for the same effect).
- Progressive neglect of all other interests: time is spent solely on acquiring the psychoactive substance, consuming it, and recovering.
- Continued use despite clear awareness of the harm.
Consequences of alcoholism
Chronic intoxication and the action of alcohol metabolites (particularly acetaldehyde) lead to fatal changes:
Organic brain damage. Toxic encephalopathy develops. Clinically, this manifests as Korsakoff's amnestic syndrome, dementia (intellectual decline), and personality degradation. Epileptic seizures are possible.
Social maladaptation. The need for alcohol completely displaces family and work. To avoid feelings of guilt, the psyche uses defense mechanisms: rationalization ("doctors recommend it for blood vessels"), projection ("anyone would start drinking with you"), or dissociation ("I don't know what came over me"). The patient suffers from anosognosia—a complete lack of insight into the severity of their condition.
Somatic pathologies and mortality. Alcohol damages the liver, pancreas, and heart. Nutrient deficiencies due to replacing a normal diet with "empty calories" lead to hypovitaminosis. Mortality in this group is high due to injuries, road traffic accidents, poisonings, and suicides (individuals with alcoholism account for up to 30–60% of all suicide attempts).
Types of alcohol intoxication
The effect of ethyl alcohol on the central nervous system is due to its action on chloride ion channels, which leads to the inhibition of nerve cell activity. In forensic psychiatric practice, it is essential to distinguish between two types of intoxication:
- Simple (and its modified forms). Depends on the dose. Manifests from euphoria to coma. Modified forms are common in alcoholics: dysphoric (aggressiveness), paranoid (jealousy, suspiciousness), or hysterical (theatrical despair). A person in simple or modified intoxication bears criminal responsibility for their actions.
- Pathological intoxication. This is an acute psychosis that occurs not due to a high dose, but due to individual intolerance against the background of exhaustion or brain trauma. It manifests as twilight state of consciousness, sudden aggression, and the absence of typical signs of intoxication (speech and coordination remain intact). It ends with deep sleep and complete amnesia. Such a state is recognized as insanity, excluding criminal responsibility.
Briefly: answers to topical questions
What stages of alcoholism are distinguished in clinical psychiatry?
Clinical psychiatry distinguishes three stages of alcoholism with progressively increasing severity of disorders.
- Stage I — loss of quantitative control over alcohol intake, exacerbation of chronic somatic diseases, possible amnestic forms of intoxication (palimpsests, blackouts)
- Stage II (subcompensated according to I.V. Strelchuk, addictological according to A.A. Portnov) — appearance of pseudo-dipsomania (pseudosprees), development of physical dependence, severe withdrawal syndrome, compulsive craving, tolerance plateau
- Stage III (terminal) stage — decreased tolerance, "true dipsomania (sprees)", alcoholic personality degradation, polyneuropathy, encephalopathy, irreversible somatic disorders
Which liver enzymes are involved in the breakdown of ethyl alcohol?
The breakdown of ethyl alcohol in the liver involves several enzyme systems.
- Alcohol dehydrogenase (ADH) — oxidizes ethanol to acetaldehyde using NAD+.
- Acetaldehyde dehydrogenase — oxidizes acetaldehyde to acetic acid.
- Microsomal ethanol-oxidizing system (MEOS) — involves cytochrome P450; with prolonged chronic alcohol use, metabolism proceeds primarily via this inducible system.
- Peroxisomal catalase system — one of the parallel pathways of ethanol oxidation.
Which medications are used to manage alcohol withdrawal syndrome?
Alcohol withdrawal syndrome is managed with agents aimed at reducing withdrawal symptoms and preventing complications.
- Benzodiazepine tranquilizers — are a mandatory prescription for alcohol withdrawal syndrome.
- Vitamin B1 (thiamine) — is administered routinely to prevent encephalopathy.
- Parenteral administration of fluids and vitamins — the basis of detoxification.
- In severe alcohol withdrawal syndrome and delirium tremens, GABAergic agents are used: benzodiazepine tranquilizers, barbiturates, zopiclone, zolpidem, sodium oxybate; available injectable drugs include diazepam, phenazepam, sodium thiopental, and hexobarbital.
What specific somatic diseases develop in chronic alcoholism?
Chronic alcoholism can lead to specific somatic and neurological disorders:
- alcoholic liver disease: fatty liver disease/steatosis, alcoholic hepatitis, fibrosis, liver cirrhosis, hepatic failure;
- pancreatic damage: pancreatitis, chronic inflammation with impaired exocrine and endocrine functions;
- cardiovascular system damage: arterial hypertension, tachycardia, arrhythmia attacks, alcoholic cardiomyopathy;
- peripheral nervous system damage: alcoholic polyneuropathy;
- brain damage: toxic encephalopathy, Korsakoff's amnestic syndrome, dementia;
- digestive system damage: gastritis, malabsorption;
- sialadenosis / "hamster face".
For the diagnosis of dependence according to ICD-10, use the "three out of seven in one year" rule: at least 3 characteristic criteria (craving, loss of control, withdrawal, etc.) must be present over the past 12 months.
Class and exam questions
What is cross-tolerance in alcoholism?
This is an increase in resistance to other substances with a similar mechanism of action. In patients with alcoholism, tolerance to all GABAergic agents increases: benzodiazepines, barbiturates, and general anesthetics.
Why do people get drunk from a single glass in later stages?
This is a manifestation of the second phase — decreased tolerance. Due to profound organic brain and liver damage, the body loses its ability to resist intoxication.
Does alcohol intoxication exempt from criminal liability?
Simple and altered (dysphoric, paranoid) intoxication does not exempt from liability. The only exception is pathological intoxication, which is regarded as an acute psychosis (a state of insanity/incompetence).
What else to study on this topic
- Dynamic approach to the classification of alcoholism in the Russian Federation (disease stages)
- Severity degrees of simple alcohol intoxication and blood alcohol concentration calculation in per mille
- Risk factors and protective factors for the development of substance use disorders
- Principles of primary, secondary, and tertiary prevention
- Fourth character in ICD-10 coding (from F10.0 to F10.9)
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Other topics in «Chapter 21. Disorders due to use of alcohol and other psychoactive substances»
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