Alcohol and the brain Flashcards
DIRECT EFFECTS OF ALCOHOL
i) what net effect does it have on the brain?
ii) how does it affect glutamate? what does this cause?
iii) how does it affect mu opioid receptors? what sensation does this produce?
iv) how does it affect GABA receptors?
v) what is the main NT ETOH works on?
i) net inhibitory effect in the brain
ii) inhibits Glu > stops excite > net inhib
iii) stimulates mu opioid > pleasure from ETOH
iv) stimulates GABA receptors (inhibitory)
v) mainly works on GABA
GABA AND THE BRAIN
i) what effect does ETOH have on GABA receptors?
ii) what short term effect does GABA have?
iii) how does it affect the frontal lobe? name three things this lead to
iv) how can it affect gait?
v) name two other effects of GABA
i) activates GABA receptors > receptors bound by alcohol therefore less around to bind GABA > overall decreased inhibitory effect of GABA
ii) anxiolytic
iii) frontal lobe disinhibition > disinhib behaviour, poor planning, impulsivity
iv) causes ataxia > difficulty walking (cerebellar impact)
v) sedating and amnesia
CHRONIC ETOH MISUSE AND GABA
i) what happens to GABA receptors over time when alcohol is chronically misused?
ii) what does this ultimately lead to?
iii) what happens when there is sudden cessation of alcohol? why?
iv) how is glutamate implicated in withdrawal after sudden alcohol cessation?
i) chronic admin > excess inhibition > downregulation of GABA receptors
ii) drink more without the GABA effects > tolerance
iii) chronic use has already causes GABA receptors to be downregulated > enodog GABA cant activate many receptors > net excite effect
iv) net excite effect (more glu than GABA) > withdrawal symptoms occur due to reduced GABA levels
ALCOHOL CESSATION AFTER CHRONIC USE
i) how much GABA is around?
ii) nmae four symptoms of minor withdrawal
iii) between which days after last drink may seizures occir? what do they happen?
iv) name four signs of delirium tremens
i) low levels > unchecked balance with glu therefore net excite
ii) tremor, anxiety, N+V, sweating, palpitations, insomnia, anorexia
iii) seizures day 2-4
- uncontrolled electrical acitivyt due to GABA and Glu misbalance
iv) delirium tremens > agitation, global confusion, disorientation, hallucination, fever, autonomic hyperactive
seizures and DT are dangerous
SEIZURES
i) which type of seizures are classically seen in alcohol withdrawal?
ii) what is status epilepticus? can it be seen in alcohol misuse?
iii) name two things that should be checked to make sure its not causing the seizure
i) tonic clonic > full loss of conciousness
ii) SE = seizures that dont self resolve > can cause hypoxia > fatal
- up to 25% cases can be alcohol related
iii) check not due to hypogly or occult brain injury (image in first alcohol related seizure)
DELIRIUM TREMENS
i) what three things is it a combination of?
ii) do you see hallucinations?
iii) name three other symptoms
iv) what are 50% of cases associated with? what is the mortality rate?
v) how should it be treated? (2)
i) tremor, motor restlessness and autonomic overactivity
ii) get hallucinations > visual or tacile (animals/insects)
iii) sweating, dehydration, tachycardia
iv) 50% assoc with comorbid infection or trauma
- 5% mortality rate usually secondary to CV collapse or infection
v) treat with supportive care and tx of co morbidities
PHARMA MANAGEMENT OF WITHDRAWAL IN HOSPITAL
i) what is the primary aim of this?
ii) name three secondary aims
iii) which two drugs are the medicines of choice?
iv) what is needed alongside the detox to maintain abstinence?
v) what is given for minor withdrawal? generalised tonic clonic withdraw seizure? delirium tremens?
i) primarily want to prevent seizures
ii) reduce unpleasant withdraw effects, restore sleep, increase chance of complete detox
iii) chlordiazepoxide and diazepam
iv) need prep work and support groups alongside pharma treatment
v) minor withdraw/seizure prevent > reducing regimen of benzo
- generalised withdraw seizure > diazepam PR
- DT - lorazepam and treat underlying cause of there are comirbds
ALCOHOL RELATED BRAIN DAMAGE
i) what is a milder presentation of werenickes/korsakoffs?
ii) name two things that people who abuse alcohol are more at risk of?
iii) is ETOH related brain change common post mortem?
i) frontal lobe dysfunction
ii) head injury and secondary microvasc stroke/related disorders
iii) yes - seen in 0.5-1.5% general pop
WERENICKES ENCEPHALOPATHY
i) name three main symptoms? does it normally present with all three
ii) what is the mortality if left untreated
iii) how is thiamine implicated? why does it cause werenickes?
iv) name four areas affected by thiamine depletion? what does each of these cause?
v) what treatment route is needed for werenickes? what should be given?
vi) what does treating the werenickes prevent?
i) confusion, ataxia, and oculomotor abnormalities (nystagmus and 6th nerve palsy)
- doesnt usually present with all three
ii) 20% mortality if left untreated
iii) reduction in thiamine > co factor in the Krebs cucle so insufficiency causes cell death in that particular area
iv) cerebellum > balance and co ord probs (ataxia and nystagmus)
hypothal/thal/mam body > memory problems
frontal lobe > personality and executive function (disinhibition behaviours and behav change)
v) werenickes is reversible > need parenteral treatment (IV or IM))
- gastric abs is poor
- give pabrinex (thiamine and other B vitamins) tds for 3 days then 3-5 further days
vi) prevents progression to korsakoffs
THIAMINE
i) when should it be given in the form of pabrinex? why?
ii) what is the main reason for thiamine deficiency in alcohol dependence?
iii) give another reason?
iv) how many months worth of thiamine does the body store?
i) make sure its given before food or IV dextrose
- otherwise residual thyamines tores will preferentially be used on carb metabolism and pulls it away from the brain > ppt werenickes
ii) inadequate nutritional intake (alcohol is prioritised over food, alcohol can be filling and high calorie)
iii) changes to gastric villi and impaired absorption
iv) 3 months store
KORSAKOFFS AMNESIC SYNDROME
i) does all werenickes progress to korsakoffs?
ii) name four features that may be seen? what is a defining feature?
iii) what % have complete recovery? what is prognosis better with?
iv) name three things that can be seen in coarsening of personality in chronic alcoholism
i) no
ii) persistence of werenicke symptoms eg ataxia, anterograde amnesia, retrograde amnesia
- confabulation is defining (brain fills the gaps > speech sounds logical but isnt)
iii) 25% - prognosis is better with abstinence
iv) loss of social/sexual inhibitions, tendency to be irritable, abusive
ALCOHOL DEPENDENCE AND RISK OF HEAD INJURY
i) name four reasons why they are more likely to fall?
ii) name three reasons why they are at increased risk of bleeding?
i) seizure, intoxication, cerebellar dysfunction (ataxia), peripheral neuropathy (direct neurotox effects from alcohol offsets proprioception)
ii) increased risk of bleeding due to more friable vessels, increased INR and platelet changes (decreased levels) > clotting imapred therefore injuries can be more significant
