Recreational drugs in the A&E Flashcards
Describe and explain the FRAMES approach
-approach to tackle harmful drug use or dependence with a patient
FEEDBACK: discuss the risks associated with that person’s drug use& listen to responses
RESPONSIBILITY: up to them to change
ADVICE: harm minimization advice, advice how to change
MENU: give people opinions
EMPATHY: non judgemental & warm clinical approach
SELF-EFFICACY: project optimism that they have the ability to make a positive change.
How can we recognize alcohol withdrawal?
- Increased pulse and BP
- Sweating
- Shaking
- Agitation
- May be confused
- May be hallucinating (tactile,auditory,visual)
- seizures
- Does not have to be BAC 0.00mg/l
- use the CIWA-Ar to assess
What is the CIWA?
‘Gold standard’ alcohol withdrawal scale
-It is subjective & has its limitations
What makes up the CIWA.
- Nausea
- agitation
- sweating
- perceptual disturbances
- anxiety
- headache
- orientation
- Tremor
What cut offs does the CIWA use
10= give benzos
20=admit
How can tolerance and withdrawal of alcohol be understood in terms of GABA and glutamate?
- GABA= the main inhibitory neurotransmitter in the brain
- GABA-A receptors- chloride channel
- alcohol potentiates GABA as well as directly opening channel at high dose
- Chronic drinking causes adaptations-fewer and less responsive GABA-A receptors( this causes withdrawal symptoms cos it leads to less inhibition i.e symptoms of hyperexcitation due to down regulation if GABA-A
What is the relationship between alcohol and NMDA receptors
- NMDA receptors are ionotropic and a sub type of glutamate receptors
- Alcohol is an NMDA antagonist
- Chronic alcohol leads to receptor up-regulation which is associated with impaired memory
What does alcohol withdrawal symptoms result from
- The sudden removal of alcohol in the presence of the glutamate/GABA imbalance
- Theres increased excitation due to the increased no. if glutamate NMDA receptors without alcohol being present, leading to an increase in calcium influx
- There’s decreased inhibition due to the down regulation of GABA-A receptors whilst there’s no alcohol present.
- The increased excitation and decreased inhibition results in neuronal hyperexcitatbility, seizures and cell death
- Think of it as cos the body is expecting alcohol to counteract an increase in things like HR&BP, in the absence of alcohol the addict doesnt feel normal cos the alcohol isnt there to make the feel right. the body has adapted to normally receiving alcohol
What kind of pneumonia are people with alcohol dependance at risk to
Aspiration pneumonia
What are the differentials for alcohol withdrawal sypmtoms
- Wernicke’s-Korsakoff syndrome
- Central Pontine myelinolysis
- Agitated delirium secondary to sepsis(aspiration pneumonia)
What is Wernicke’s-Korsakoff syndrome?
Wernicke’s encephalopathyy is Secondary to thiamine deficiency(B1); an acute severe deficiency of vitamin B1
- Classically a triad of opthalmoplegia, ataxia &confusion
- But this is rare, they just look drunk
- Korsakoff syndrome is a chronic result of the acute deficiency of thiamine
What is central pontine myelinolysis?
- Caused by an area of demyelination in the pons.
- Confusion, nausea, gait changes, hyperreflexia
How can you predict who will suffer DTs & seizures?
DTs(delirium tremens): Number of previous detoxifications; history of DTs, history of seizures, acute medical illness, low chloride, sodium, potassium; high ALT& GGT
-Tends to happen in days 4-7 of alcohol withdrawal
Seizures: History of seizures, GGT
-Tends to happen in the 1st 72hours
What is GGT and what is it useful for?
- Gamma-glutamyl transferase
- Marker of oxidative stress
- The higher it is the more likely you are to suffer complications
How can we take care of a patient in alcohol withdrawal?
- Well lit side room
- 1:1 nursing
- Orientation to time and place
- Reassurance
- Generous decreasing regime of benzos which potentiate action of GABA
- Generous helpings of pabrinex
- Correct electrolyte abnormalities slowly
- assess motivation to maitain abstinence
- link in with alcohol services
- Consider relapse prevention medication
What is GHB/GBL?
- aka G,Gina, Charisma, liquid ectasy
- taken as a sushi soy sauce container(fish) or eyedropper
- Take 1-2ml as dose
- A drug almost exclusively used by men who have sex with men, used in sex parties
What are the acute effects of G?
- euphoria
- Increased sexual arousal, stamina &pleasure
- altered perception of time
- impaired memory
- salivation
- unsteadiness
- loss of deep consciousness
- bradycardia
- hypotension
- respiratory depression
- death
Why is G taken as soy fishies or with an eye dropper?
- 1-2ml doses need to be taken to ensure the acute effects
- The difference between the dose that produces the desirable effect and the dose that causes death is very small i.e GHB & GBL have a narrow therapeutic index
How else can you overdose on G?
-By false timing( if you take some more before you should)
What is pabrinex
- used for care of the alcohol patient in withdrawal
- an injection that contains vitamins B(including thiamine) and C
What is the relationship between GHB and GABA?
- GHB is a GABA analogue
- GHB binds to pre-synaptic GHB receptors and this decreases GABA release
- GHB also binds to presynaptic GHB receptors and this decreases GABA release
- GHB in high concentrations binds to post-synaptic GABA-B receptors and this inhibits post-synaptic neuron(so is a weak GABA-B receptor agonist)
- GHB is metabolised to GABA
What are the symptoms of GHB/GBL withdrawal?
- Like alcohol withdrawal but quicker onset with fewer seizures and more DTs
- Anxiety
- Agitation
- sweating
- shaking
- increased HR
- increased BP
- visual& auditory hallucinations
- confusion
How do you perform an emergency GHB/GBL detox?
- use CIWA to evaluate withdrawal severity
- Once in withdrawal,add benzos (diazepam or librium) may need large doses
- Initially 20mg diazepam the reasess every couple of hours
- may need 80mg diazepam in the 1st 24 hours
- If not controlled, add baclofen 20mg tds
- If not controlled, get anaesthetists involved -may need to be sedated using propofol
- Treatment is prolonged- about 10-14days
Explain how opioids suppress respiration.
- Via action on regions in the medulla and pons which control ventilation
- There are mu receptors in both the respiratory centres in the brainstem and medulla and in the chemoreceptors
- Stimulation of these receptors slows respiration
- Makes your brainstem less responsive to changes in oxygenation and co2
Why is opiod overdose not always an actual overdose?
- Hypoxia and hypercapnia can occur at usual dose
- Medical comorbidity e.g chest infection or COPD; hence increased risk of overdose on usual opiod substitution over age of 50
- prescribed/recreationally consumed sedatives can increase risk- alcohol, benzos, pregabalin
- Illicit opiates can change in potency without patients being aware e.g contamination with fentanyl
How can opioid toxicity be reversed?
- Using nalaxone.
- High potency opiod anatagonist
- Short acting drug, so you may need to keep repeating the dose
- It binds to a receptor and has no action at the receptor
- When it reaches the brain, it competes with the opiods for binding sites, blocking their action
- Nalaxone had a high affinity for the mu opioid receptor
- But it is rapidly redistributed from the brain
- Half life is 60-90mins, so may need to observe and dose again
- High affinity opiods e.g fentanyl may need high&repeated doses
What is the endocannabinoid system?
- Plays an important regulatory role in the secretion of hormones related to reproductive functions and response to stress.
- G protein coupled receptors- CB1( brain) & CB2( immune system)
- widely distributed in the brain
- endocannabinoids- anandamide and 2-AG
- reward; learning& memory; emotional regulation; sleep; appetite & pain
Outline a distrinction between SCs and THCs
-SCs (synthetic cannabinoid) are more toxic then THC(tetrahydrocannabinol) because their pharmacology differs
What are some clinical features of SCRA(spice) intoxication?
- Tachycardia/ Bradycardia
- Hypertension/ Hypotension
- Chest pain
- cardiac arrest
- nausea
- hepatoxicity
- acute renal injury
- agitation
- anxiety
- coma
- seizures
- psychotic symptoms
- Catatonia with posturing
- rhabdomyolysis
- conjunctival injection
How can we take care of the SCRA(synthetic cannabinoid receptor antagonist) intoxicated patient?
- cardiac monitoring
- U&Es, LFTs,CK
- fluids
- benzos
- anti-emetics
- antipsychotics
- involvement of liason psychiatry
- severe behavioural disturbance
- need higher doses of antipsychotics than cannabis (THT) induced psychosis
How does SCRA intoxication differ from THC intoxication
-Similar demographics – men, mid-30s
-Usually in context of polysubstance use
-More likely to be associated with agitation (OR
3.8)
-More likely to be associated with cardiac
arrhythmia (OR 9.2)
