Mechanism of Action of Alcohol

Mechanism of Action of Alcohol

Alcohol both lipid and water soluble can cross the blood brain barrier

Acts as a CNS depressor by affecting three different membrane receptors:

Receptor / Normal Mechanism / Effects of alcohol / Symptoms
GABA a / Increase flow of Cl- across membrane Prevents depolarisation / Indirect agonist Increases GABA activity / Loss of Coordination
NMDA / Allows Ca2+ to enter the cell Causes Depolarisation / Indirect antagonist
Inhibits Ca2+ transport / Drowsiness Reduction in clear thought
Dopamine / Excites neurones responsible for memory and pleasure / Increases dopamine release Inhibits dopamine reuptake / Reduced memory

Blood levels and ‘THE OVERDOSE’

The amount of alcohol in your blood = Blood Alcohol Level (BAL)

Measured milligrams per 100 millilitres of blood

Effects of blood alcohol levels:

BAL

/ Effects
.02 / Mellow feeling, slight body warmth, lower inhibitions (“Merry”)
.05 / Noticeable relaxation, less alert, less self-focused, motor impairment begins
.08 / Drunk driving limit. Definite impairment in coordination and judgement
.10 / Noisy and possibly embarrassing behaviour. Reduction in reaction time
.15 / Impaired balance and movement. Clearly drunk
.30 / Many lose consciousness
.40 / Most lose consciousness, some die
.50 / Breathing stops

Overdose - when alcohol is consumed faster than the liver can metabolise it, leading to excess alcohol building up in the bloodstream.

Liver damage

Break down of alcohol occurs via two reactions

Both require NAD as a hydrogen acceptor

During an overdose body cannot regenerate NAD quickly enough

Alcohol cannot be metabolised

Damage to the liver occurs
May also act to compete with other metabolites so other toxic substances build up

Absorption of alcohol

After you finish drinking it can take from 30 to 90mins before your peak BAL is reached.

The actual time depends on factors such as:

The amount of food in the stomach
The rate of drinking
The concentration of alcohol consumed
The carbonation of drinks consumed

Your natural defence is too pass out to prevent more drinking, however alcohol can still be potentially absorbed for a further 90mins. This could suppress the CNS to the point of respiratory failure for example.

What is a coma?

A coma is a state of deep and prolonged unconsciousness, resulting from damage to the medulla, thalamus and brain stem (Reticular activating system), or the cerebral cortex itself
A coma can occur a result of a haemorrhage within the cranial vault
Heavy impacts or fractured bone fragments may cause haemorrhage

There are four types of haemorrhage:

Intracerebral haemorrhage / Rupture of blood vessels deep within the brain
Subdural / Near brain surface
Extradural/ Epidural / Between skull and dura
Subarachnoid / Escape of blood into subarachnoid space

Effects of Haemorrhage

A haemorrhage acts to increase intracranial pressure (ICP). The compression of the brain produced results in the damage that causes a coma. In the long term, this can lead to displacement of brain tissue and possible necrosis.

Alcohol causing hypoglycaemia affecting the brain - another cause of a coma

Metabolism of ethanol increases the NADH/NAD+ ratio. This inhibits gluconeogenesis (which requires NAD+ to produce glucose). Glucose is the only energy source that can be utilised by the brain. Hypoglycaemia can therefore reduce the ability of the brain to function.

Structures that support the cervical spine

Dislocation of a cervical vertebra

Chances of recovery – depend upon exact injuries sustained

Extradural haematoma – usually full recovery from coma, if haematoma is evacuated by Burr holes

Subdural haematoma – progressive severe brain damage, full recovery unlikely even with treatment

Unilateral dislocation of vertebra paraplegia

Bilateral dislocation of vertebra – likely transection of spinal cord  quadriplegia