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Alcohol intoxication

 

Alcohol intoxication

Alcohol intoxication
Classification and external resources
The Drunkenness of Noah by Michelangelo
ICD-10 F10.0, T51
ICD-9 305.0, 980
MedlinePlus 002644
MeSH D000435

Alcohol intoxication (also known as drunkenness or inebriation) is a physiological state (that may also include psychological alterations of consciousness) induced by the ingestion of ethyl alcohol (ethanol).

Alcohol intoxication is the consequence of alcohol entering the bloodstream faster than it can be metabolized by the liver, which breaks down the ethanol into non-intoxicating byproducts. Some effects of alcohol intoxication (such as euphoria and lowered social inhibitions) are central to alcohol's desirability as a beverage and its history as one of the world's most widespread recreational drugs. Despite this widespread use and alcohol's legality in most countries, many medical sources tend to describe any level of alcohol intoxication as a form of poisoning due to ethanol's damaging effects on the body in large doses; and some religions consider alcohol intoxication to be a sin.

Symptoms of alcohol intoxication include euphoria, flushed skin and decreased social inhibition at lower doses, with larger doses producing progressively severe impairments of balance, muscle coordination (ataxia), and decision-making ability (potentially leading to violent or erratic behavior) as well as nausea or vomiting from alcohol's disruptive effect on the semicircular canals of the inner ear and chemical irritation of the gastric mucosa. Sufficiently high levels of blood-borne alcohol will cause coma and death from the depressive effects of alcohol upon the central nervous system.

"Acute alcohol poisoning" is a related medical term used to indicate a dangerously high concentration of alcohol in the blood, high enough to induce coma, respiratory depression, or even death. It is considered a medical emergency. The term is mostly used by healthcare providers. Toxicologists use the term "alcohol intoxication" to discriminate between alcohol and other toxins.

Contents

  • Pathophysiology 1
  • Name 2
    • Synonyms 2.1
  • References 3
  • Pharmacology 4
  • Pathophysiology 5
  • Pathophysiology 6
  • Pharmacology 7
  • Ethanol and GABAA Receptors 8
  • Name 9
    • Synonyms 9.1
  • References 10
  • Diagnosis 11
  • Acute alcohol poisoning 12
    • Signs and symptoms 12.1

Pathophysiology

Alcohol is metabolized by a normal liver at the rate of about 50 ml (1.7 US fl oz) of spirits (roughly a typical drink-size serving of beer, wine, or spirits) every 90 min== Taxonavigation == Species: Holoarctia cervini

Name

Holoarctia cervini (Fallou, 1864)

Synonyms

  • Nemeophila cervini Fallou, 1864
  • Arctia cervini var. hnateckii Frey, 1872
  • Phragmatobia cervina Hampson, 1901
  • Orodemnias cervini rougemonti O. Bang-Haas, 1927
  • Orodemnias cervini scriniensis Berthet, 1948
  • Orodemnias cervini steitei Röber, 1930
  • Orodemnias cervini teriolensis Burmann, 1975
  • Orodemnias cervini splendida Gerber, 1979

References

  • Bang-Haas, O., 1927: Horae Macrolepidopterologie regionis palaearcticae 1: I-XXVIII, 1-128 S., Taf. 1-10, Verlag O. Staudinger & A. Bang-Haas, Dresden-Blasewitz.
  • Berthet, H., 1948: Orodemnias cervini Fallou dans les Alpes françaises du Dauphiné ssp. (ou forme individuelle?) Dutch artist Jan Steen c. 1663]]

Ethanol's acute effects are due largely to its nature as a central nervous system depressant, and are dependent on blood alcohol concentrations:

  • 20–79 mg/dL – Impaired coordination and euphoria
  • 80–199 mg/dL – Binge drinking: Ataxia, poor judgement, labile mood. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines the term "binge drinking" as a pattern of drinking that brings a person’s blood alcohol concentration (BAC) to 0.08 g/dL or above.[1]
  • 200–299 mg/dL – Marked ataxia, slurred speech, poor judgement, labile mood, nausea and vomiting
  • 300–399 mg/dL – Stage 1 anaesthesia, memory lapse, labile mood
  • 400+ mg/dL – Respiratory failure, coma

As drinking increases, ed by respiratory failure. Patients may also present with hypothermia.

Pharmacology

In the past, alcohol was believed to be a non-specific pharmacological agent affecting many neurotransmitter systems in the brain.[2] However, molecular pharmacology studies have shown that alcohol has only a few primary targets. In some systems, these effects are facilitatory and in others inhibitory.

Among the neurotransmitter systems with enhanced functions are: GABAA,[4] It takes roughly 90 minutes for a healthy liver to metabolize a single ounce, approximately one hour per standard unit.

5-HT3 receptor agonism[7] (responsible for GABAergic (GABAA receptor PAM), glycinergic, and cholinergic effects), nicotinic acetylcholine receptors.[9] It takes roughly 90 minutes for a healthy liver to metabolize a single ounce, approximately one hour per standard unit.
Wine is a Mocker by Dutch artist Jan Steen c. 1663
Ethanol's acute effects are due largely to its nature as a central nervous system depressant, and are dependent on blood alcohol concentrations:
  • 20–79 mg/dL – Impaired coordination and euphoria
  • 80–199 mg/dL – Binge drinking: Ataxia, poor judgement, labile mood. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines the term "binge drinking" as a pattern of drinking that brings a person’s blood alcohol concentration (BAC) to 0.08 g/dL or above.[1]
  • 200–299 mg/dL – Marked ataxia, slurred speech, poor judgement, labile mood, nausea and vomiting
  • 300–399 mg/dL – Stage 1 anaesthesia, memory lapse, labile mood
  • 400+ mg/dL – Respiratory failure, coma
As drinking increases, people become sleepy, or fall into a stupor. After a very high level of consumption, the respiratory system becomes depressed and the person will stop breathing. Comatose patients may aspirate their vomit (resulting in vomitus in the lungs, which may cause "drowning" and later pneumonia if survived). CNS depression and impaired motor co-ordination along with poor judgement increases the likelihood of accidental injury occurring.[10] It is estimated that about one third of alcohol-related deaths are due to accidents (32%), and another 14% are from intentional injury.[11] In addition to respiratory failure and accidents caused by effects on the central nervous system, alcohol causes significant metabolic derangements. Hypoglycaemia occurs due to ethanol's inhibition of gluconeogenesis, especially in children, and may cause lactic acidosis, ketoacidosis, and acute renal failure. Metabolic acidosis is compound
Alcohol intoxication
Classification and external resources
The Drunkenness of Noah by Michelangelo
ICD-10 F10.0, T51
ICD-9 305.0, 980
MedlinePlus 002644
MeSH D000435
Alcohol intoxication (also known as drunkenness or inebriation) is a physiological state (that may also include psychological alterations of consciousness) induced by the ingestion of ethyl alcohol (ethanol). Alcohol intoxication is the consequence of alcohol entering the bloodstream faster than it can be metabolized by the liver, which breaks down the ethanol into non-intoxicating byproducts. Some effects of alcohol intoxication (such as euphoria and lowered social inhibitions) are central to alcohol's desirability as a beverage and its history as one of the world's most widespread recreational drugs. Despite this widespread use and alcohol's legality in most countries, many medical sources tend to describe any level of alcohol intoxication as a form of poisoning due to ethanol's damaging effects on the body in large doses; and some religions consider alcohol intoxication to be a sin. Symptoms of alcohol intoxication include euphoria, flushed skin and decreased social inhibition at lower doses, with larger doses producing progressively severe impairments of balance, muscle coordination (ataxia), and decision-making ability (potentially leading to violent or erratic behavior) as well as nausea or vomiting from alcohol's disruptive effect on the semicircular canals of the inner ear and chemical irritation of the gastric mucosa. Sufficiently high levels of blood-borne alcohol will cause coma and death from the depressive effects of alcohol upon the central nervous system. "Acute alcohol poisoning" is a related medical term used to indicate a dangerously high concentration of alcohol in the blood, high enough to induce coma, respiratory depression, or even death. It is considered a medical emergency. The term is mostly used by healthcare providers. Toxicologists use the term "alcohol intoxication" to discriminate between alcohol and other toxins.

Pathophysiology

Alcohol is metabolized by a normal liver at the rate of about 50 ml (1.7 US fl oz) of spirits (roughly a typical drink-size serving of beer, wine, or spirits) every 90 minutes. An "abnormal" liver with conditions such as hepatitis, cirrhosis, gall bladder disease, and cancer are likely to result in a slower rate of metabolism. Ethanol is metabolised to acetaldehyde by alcohol dehydrogenase (ADH), which is found in many tissues, including the gastric mucosa. Acetaldehyde is metabolised to acetate by acetaldehyde dehydrogenase (ALDH), which is found predominantly in liver mitochondria. Acetate is used by the muscle cells to produce acetyl-CoA using the enzyme acetyl-CoA synthetase, and the acetyl-CoA is then used in the citric acid cycle.[12] It takes roughly 90 minutes for a healthy liver to metabolize a single ounce, approximately one hour per standard unit.
Wine is a Mocker by Dutch artist Jan Steen c. 1663
Ethanol's acute effects are due largely to its nature as a central nervous system depressant, and are dependent on blood alcohol concentrations:
  • 20–79 mg/dL – Impaired coordination and euphoria
  • 80–199 mg/dL – Binge drinking: Ataxia, poor judgement, labile mood. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines the term "binge drinking" as a pattern of drinking that brings a person’s blood alcohol concentration (BAC) to 0.08 g/dL or above.[1]
  • 200–299 mg/dL – Marked ataxia, slurred speech, poor judgement, labile mood, nausea and vomiting
  • 300–399 mg/dL – Stage 1 anaesthesia, memory lapse, labile mood
  • 400+ mg/dL – Respiratory failure, coma

As drinking increases, people become sleepy, or fall into a stupor. After a very high level of consumption, the respiratory system becomes depressed and the person will stop breathing. Comatose patients may aspirate their vomit (resulting in vomitus in the lungs, which may cause "drowning" and later pneumonia if survived). CNS depression and impaired motor co-ordination along with poor judgement increases the likelihood of accidental injury occurring.[13] It is estimated that about one third of alcohol-related deaths are due to accidents (32%), and another 14% are from intentional injury.[14] In addition to respiratory failure and accidents caused by effects on the central nervous system, alcohol causes significant metabolic derangements. Hypoglycaemia occurs due to ethanol's inhibition of gluconeogenesis, especially in children, and may cause lactic acidosis, ketoacidosis, and acute renal failure. Metabolic acidosis is compounded by respiratory failure. Patients may also present with hypothermia.

Pharmacology

In the past, alcohol was believed to be a non-specific pharmacological agent affecting many neurotransmitter systems in the brain.[2] However, molecular pharmacology studies have shown that alcohol has only a few primary targets. In some systems, these effects are facilitatory and in others inhibitory. Among the neurotransmitter systems with enhanced functions are: GABAA,[4] 5-HT3 receptor agonism[7] (responsible for GABAergic (GABAA receptor PAM), glycinergic, and cholinergic effects), nicotinic acetylcholine receptors.[15] Among those that are inhibited are: NMDA,[7] dihydropyridine-sensitive L-type Ca2+ channels[16] and G-protein-activated inwardly rectifying K+ channels.[17] The result of these direct effects is a wave of further indirect effects involving a variety of other neurotransmitter and neuropeptide systems, leading finally to the behavioural or symptomatic effects of alcohol intoxication.[2]

Ethanol and GABAA Receptors

Ethanol binding to GABAA Receptor
Many of the effects of activating GABAA receptors have the same effects as that of ethanol consumption. Some of these effects include anxiolytic, anticonvulsant, sedative and hypnotic effects, cognitive impairing, and motor incoordination.[18] This correlation between activating GABAA receptors and the effects of ethanol consumption has led to the study of ethanol and its effects on GABAA receptors. It has been shown that ethanol does in fact exhibit positive allosteric binding properties to GABAA receptors. However, binding is only limited to pentamers containing the δ-subunit rather than the γ-subunit.[19] GABAA receptors containing the δ-subunit have been shown to be located exterior to the synapse and are involved with tonic inhibition rather than its γ-subunit counterpart, which is involved in phasic inhibition.[18] The δ-subunit has been shown to be able to form the allosteric binding site which makes GABAA receptors containing the δ-subunit more sensitive to ethanol concentrations, even to moderate social ethanol consumption levels (30mM).[20] While it has been shown by Santhakumar et al. that GABAA receptors containing the δ-subunit are sensitive to ethanol modulation, depending on subunit combinations receptors, could be more or less sensitive to ethanol.[21] It has been shown that GABAA receptors that contain both δ and β3-subunits display increased sensitivity to ethanol.[19] One such receptor that exhibits ethanol insensitivity is α3-β6-δ GABAA.[21] It has also been shown that subunit combination is not the only thing that contributes to ethanol sensitivity. Location of GABAA receptors within the synapse may also contribute to ethanol sensitivity[18]

Diagnosis

Definitive diagnosis relies on a blood test for alcohol, usually performed as part of a toxicology screen. Law enforcement officers often use breathalyzer units and field sobriety tests as more convenient and rapid alternatives to blood tests. There are also various models of breathalyzer units that are available for consumer use. Because these may have varying reliability and may produce different results than the tests used for law-enforcement purposes, the results from such devices should be conservatively interpreted. Many informal intoxication tests exist, which, in general, are unreliable and not recommended as deterrents to excessive intoxication or as indicators of the safety of activities such as motor vehicle driving, heavy equipment operation, machine tool use, etc. For determining whether someone is intoxicated by alcohol by some means other than a blood-alcohol test, it is necessary to rule out other conditions such as hypoglycemia, stroke, usage of other intoxicants, mental health issues, and so on. It is best if his/her behavior has been observed while the subject is sober to establish a baseline. Several well-known criteria can be used to establish a probable diagnosis. For a physician in the acute-treatment setting, acute alcohol intoxication can mimic other acute neurological disorders, or is frequently combined with other recreational drugs that complicate diagnosis and treatment.

Acute alcohol poisoning

Signs and symptoms

The signs and symptoms of acute alcohol poisoning include:
  • severe confusion, unpredictable behavior and stupor
  • sudden lapses into and out of unconsciousness or semi-consciousness (with later alcoholic amnesia)
  • vomiting while unconscious or semi-conscious[22]
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