Sloshed - Pathophysiology

Pathophysiology

Alcohol is metabolized by a normal liver at the rate of about one ounce (one two-ounce shot of spirits, a normal beer, a regular sized glass of wine) every 90 minutes. An "abnormal" liver with conditions such as hepatitis, cirrhosis, gall bladder disease, and cancer will have 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 predominantly found 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. It takes roughly 90 minutes for a healthy liver to metabolize a single ounce, approximately one hour per standard unit.

Ethanol's acute effects are largely due 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) recently redefined the term "binge drinking" as any time one reaches a peak BAC of 0.08% or higher as opposed to some (arguably) arbitrary number of drinks in an evening.
  • 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. The most important thing for people who witness someone "passing out" from too much alcohol is to get them emergency medical treatment. 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. It is estimated that about one third of alcohol-related deaths are due to accidents (32%), and another 14% are from intentional injury.

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.

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