Week 3 - F - Alcohol misuse - Dependance, Alcohol withdrawal, delirium tremens, prevention of relapse, , Wernicke's&Korsakoffs Flashcards
10% of the drinking population drink half of all the alcohol drunk. Age of first drink falling to 12 and 14. Highest rates of drinking in adolescence and early twenties How do you calculate the units of alcohol in a drink?
Look at the volume of alcohol - eg 750 ml bottle of wine
Look at the percentage of alcohol in the drink eg 12% bottle of wine
Units = Volume in litres x % alcohol = 0.75 x 12 = 9 units alcohol
For the concepts of the risks of drinking, it has been defined as high, increased and low risk drinking What is high risk drinking?
High risk drinking is where you regularly consume over 35 units of alcohol per week
What is increased risk drinking? What is low risk drinking?
Increased risk drinking - this is where you regularly consume between 15 and 35 units of alcohol per week
Low risk drinking is where you meet the guidelines for both men and women where less than 14 units of alcohol is consumed on a weekly basis - this should be spread out over three day s
What is harmful use of alcohol?
This is a pattern of psychoactive substance misuse that is cause damage to health - be it physical or mental health
What is alcohol dependence syndrome criteria? (this is the same as the ICD-10 criteria for dependence)
There is a strong desire or sense of compulsion to take the drug
There is difficulty in controlling substance use - onset, termination or level of use
There is a physiological withdrawal state
Evidence of tolerance
Persistence of neglect of other pleasures / interests/ others despite clear evidence of harmful consequences
There is a range of tools available for the screening of alcohol dependency syndrome What is the acronym that s used to diagnose abuse and dependence?
CAGE!
Cut down - have you ever considered drinking less
Annoyed - have you ever been annoyed at somebody bringing up the amount that you drink
Guilty - have you ever felt guilty at the amount that you dirnk
Eye opener - have you ever had an experience where you thought, wow i need to stop - eg drinking when you get out of bed
Laboratory tests are not useful in screening for alcohol related problems May have a role in monitoring response to treatment. What can be measured as an indication for liver injury? What i the carbhydrate deficient transferrin and when can this be measured?
As an indication of liver injury - an measure GGT - gamma glutamyl transferase
Carbohydrate deficient transferin- this identifies men who drink great than 5 units per day for two weeks
What happens to the mean cell volume (mean corpuscular volume MCV) in patients who have alcohol dependency?
Mean corpuscular volume- alcoholism is the most common cause of raised MCV.
Brief interventions target audience : adults who have been identified via screening as drinking a hazardous or harmful amount of alcohol. Attending NHS or NHS-commissioned services or services offered by other public institutes. How long should brief interventions work and what is the acronym used for these interventions?
These brief interventions last 5-15 minutes
The acronym used is FRAMES
What does FRAMES stand for?
F-feedback p review the problems experienced because of alcohol
R-responsibility - its the patients responsibility to change
A-advice - advise reduction or abstinence
Menu - provide options for changing behaviours
E - empathy - use an empathetic approach
S-self efficacy - encourage optimism about changing behaviour
When should you consider referral for specialist treatment in alcohol abuse?
Consider if they show moderate or severe levels of alcohol dependence Or
Have failed to benefit from structured, brief advice and
Only refer to a specialist if they wish to tackle the issue- this is important
Show signs of severe alcohol-related impairment or co-morbid condition
What is detoxification? What is relapse prevention?
Detoxification is the process by which the patient becomes alcohol free
Relapse prevention - a combination of pshycosocial and pharmacological interventions aimed at maintaining abstinence or problem free drinking without detoxification
What ion channels does alcohol effect in the body?
It effects the NDMA-glutamate ion controlled channels and it effects the GABA type A ion controlled channels
What effects does alcohol and its chronic effects have on the NMDA-glutamate controlled ion channels and the GABA type A controlled ion channels?
Alcohol inhibits the NMDA-glutamate controlled ion channels, chronic use leads to upregulatin of the receptors
Alcohol potentiates the effects of GABA-type A controlled ion channels - chronic use leads to deregulation of the GABA channels
After speaking of upregulation of NDMA glutamate controlled ion channels and deregualtion of GABAtype A controlled ion channels, what happens when there is alcohol withdrawal?
When a patients present with alcohol withdrawal, there is a massive increase in glutamate activity due to the upregulation of the receptors and There is a massive decrease in GABA activity due to the deregulation of the receptors
What effect does excess glutamate have on the nerve cells?
Excess glutamate activity is toxic to the nerve cells.
Withdrawal of alcohol too quickly leads to CNS excitability and neurotoxicity.
How does alcohol withdrawal syndrome present?
There is restlessness, tremor, anxiety, nausea, loss of appetite and insomnia, tachycardia and hypertension may be evident also
Generalised seizures can also occur usually within the first 24 hours of alcohol withdrawal
How long does it usually take for the symptoms of alcohol withdrawal to resolve? When are the symptoms at their worst?
usually start in the first few hours and resolve after 5-7 days.
Symptoms are at their worst at 48 hours.
How do you manage alcohol withdrawal?
Give the patient general support and advice
If necessary then treat the withdrawal by giving the patient benzodiazepines - preferably long acting benzos are given eg Diazepam or chlordiazepoxide
Which benzo cannot be given if there is evidence of liver damage? How long must the benzos be given for? What must be given as vitamin supplementation?
If there is evidence of liver damage, then do not give the patient chlordiazepoxide
Reduce the benzo dose gradually over 7 days
Give vitamin B1 - thiamine supplementation as prophylais against Wernicke’s encephalopathy
How is the thiamine supplementation given to prevent Wernicke’s encephalopathy? What is done if wernicke’s encaphlopathy is suspected?
It is given IV route to prevent the possible Wernicke’s
If Wernicke’s encephalopathy is suspected, then give the patient high dose thiamine
What is the syndrome that can occur which represents the most severe withdrawal from alcohol?
This is delirium tremens
How does delirium tremens present? When does it present also?
It often presents insidiously with nighttime confusion.
You get confusion, agitation, fever, visual and auditory hallucinations and paranoid ideation
Peak onset is 2 days after abstinence
How would you treat a patient with delirium tremens who was agitated and needed sedating?
Lorazepam - fast acting benzo
Majority of patients can be detoxified in the community. Inpatient treatment if * A history of Delirium Tremens or alcohol withdrawal seizures Severe dependence * A history of failed community detoxifications * Poor social support Cognitive impairment * Psychiatric co-morbidity Poor physical health * Delirium Tremens requires prompt transfer to general medical ward.
What psychosocial interventions can stop relapse?
* CBT for the patient
* Motivational enhancement therapy
* 12 step facilitation eg alcoholics anonymous
Also can try * Family and couple therapy * Behavioural self controlling therapy
Does benzodiazepines have a place for helping prevent relapses in alcohol dependency?
There is no place for benzodiazepines beyond the detoxification period
What pharmacological therapy can help stop relapse in alcohol addiction?
Disulifram (also known as antabuse)
Acamprosate
Naltrexone
What is the mode of action of disulifram? Why is disulfiram used?
Disulifram (antabuse) - inhibits the acetaldehyde dehydrogenase leading to the accumulation of acetaldehyde if alcohol is ingested there is a build up of acetaldehyde
When alcohol is suggested there is a build up of acetalhyde which causes different side effects
What does the build up of acetaldehyde if alcohol is ingested cause? What does the efficacy of disulfiram therefore depend upon?
Cause flushed skin, tachycardia, nausea+vomiting, arrhythmia and hypotentison depending on volume of alcohol consumed
The efficacy of this drugs therefore depends on the patients compliance
What were the other two drugs that can be given for relapse prevention?
Acamprosate and naltrexone
How does acamprosate work? When should it be started?
Acamprosate acts centrally on glutamate and GABA systems (believed to be an NMDA receptor antagonist - reduces glutamate) (increases effects of inhibitory neurotransmitter GABA)
Start this drug as soon as detoxification finishes if choosing this method
What are side effects of acamprosate? What is the first line drug for relapse prevention?
Acamprosate can cause headaches, diarrhoea, nausea and vomiting
Naltrexone is generally first line for preventing relapse - it is an opioid antagonist and reduced reward from alcohol as well as the cravings
State what the three options were again and how they work? What was first second and third line?
- Naltrexone - generally first line for relapse prevention - works on the opioid receptors specifically the MOP channel - reduces reward from alcohol and reduces cravings
- Acamprosate - NMDA-glutamate antagonist and GABA agaonist
- Disulifram - acetylaldehydre dehydrogenase inhibitor so leads to accumulation of acetyladehyde which reacts when alcohol is ingested - flushed skin, tachycardia
What is wernickes encephalopathy? What is the classic triad? What is the treatment for Wernicke’s encephalopathy?
Wenicke’s ecnaphalopthy is due to a vitamin B1 deficiency (thiamine) - chronic alcohol abuse interferes with the uptake of thiamine in the gut leading to this deficiency
The encephalopathy classically presents with the triad pf confusion, ataxia (wide based gait) and ophthalmoplegia - nystagmus, lateral rectus or conjugate gaze palsy
Treatment is to give high dose thiamine .
What is Korsakoff’s encephalopathy?
This is the progressed state from wernicke’s encephalopathy
What percentage of patients with Wernick’es encaphalopathy go on to develop Korsakoffs syndrome? What is korsakoffs characeterized by?
85% of patients go on to develop Korsakoff’s
In Korsakoffs, there is hypothalamic damage and cerebral atrophy due to thiamine deficiency
Patient presents with anterograde (inability to form new memories) and retrograde amnesia (forget all the old memories), there is also confabulation and a lack of insight and apathy
What is confabulation?
This is where the patient invents memories upon questioning to make up for the gaps in their memory due to the amnesia
What is the treatment of Korsakoff’s syndrome?
IV thiamine followed by oral thiamine - very poor prognosis
