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Supporting life block > Recreational drugs in the A&E > Flashcards

Recreational drugs in the A&E Flashcards

1
Q

Describe and explain the FRAMES approach

A

-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.

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2
Q

How can we recognize alcohol withdrawal?

A
  • 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
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3
Q

What is the CIWA?

A

‘Gold standard’ alcohol withdrawal scale

-It is subjective & has its limitations

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4
Q

What makes up the CIWA.

A
  • Nausea
  • agitation
  • sweating
  • perceptual disturbances
  • anxiety
  • headache
  • orientation
  • Tremor
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5
Q

What cut offs does the CIWA use

A

10= give benzos

20=admit

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6
Q

How can tolerance and withdrawal of alcohol be understood in terms of GABA and glutamate?

A
  • 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
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7
Q

What is the relationship between alcohol and NMDA receptors

A
  • 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
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8
Q

What does alcohol withdrawal symptoms result from

A
  • 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
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9
Q

What kind of pneumonia are people with alcohol dependance at risk to

A

Aspiration pneumonia

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10
Q

What are the differentials for alcohol withdrawal sypmtoms

A
  • Wernicke’s-Korsakoff syndrome
  • Central Pontine myelinolysis
  • Agitated delirium secondary to sepsis(aspiration pneumonia)
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11
Q

What is Wernicke’s-Korsakoff syndrome?

A

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
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12
Q

What is central pontine myelinolysis?

A
  • Caused by an area of demyelination in the pons.

- Confusion, nausea, gait changes, hyperreflexia

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13
Q

How can you predict who will suffer DTs & seizures?

A

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

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14
Q

What is GGT and what is it useful for?

A
  • Gamma-glutamyl transferase
  • Marker of oxidative stress
  • The higher it is the more likely you are to suffer complications
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15
Q

How can we take care of a patient in alcohol withdrawal?

A
  • 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
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16
Q

What is GHB/GBL?

A
  • 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
17
Q

What are the acute effects of G?

A
  • euphoria
  • Increased sexual arousal, stamina &pleasure
  • altered perception of time
  • impaired memory
  • salivation
  • unsteadiness
  • loss of deep consciousness
  • bradycardia
  • hypotension
  • respiratory depression
  • death
18
Q

Why is G taken as soy fishies or with an eye dropper?

A
  • 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
19
Q

How else can you overdose on G?

A

-By false timing( if you take some more before you should)

20
Q

What is pabrinex

A
  • used for care of the alcohol patient in withdrawal

- an injection that contains vitamins B(including thiamine) and C

21
Q

What is the relationship between GHB and GABA?

A
  • 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
22
Q

What are the symptoms of GHB/GBL withdrawal?

A
  • Like alcohol withdrawal but quicker onset with fewer seizures and more DTs
  • Anxiety
  • Agitation
  • sweating
  • shaking
  • increased HR
  • increased BP
  • visual& auditory hallucinations
  • confusion
23
Q

How do you perform an emergency GHB/GBL detox?

A
  • 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
24
Q

Explain how opioids suppress respiration.

A
  • 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
25
Q

Why is opiod overdose not always an actual overdose?

A
  • 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
26
Q

How can opioid toxicity be reversed?

A
  • 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
27
Q

What is the endocannabinoid system?

A
  • 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
28
Q

Outline a distrinction between SCs and THCs

A

-SCs (synthetic cannabinoid) are more toxic then THC(tetrahydrocannabinol) because their pharmacology differs

29
Q

What are some clinical features of SCRA(spice) intoxication?

A
  • 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
30
Q

How can we take care of the SCRA(synthetic cannabinoid receptor antagonist) intoxicated patient?

A
  • 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
31
Q

How does SCRA intoxication differ from THC intoxication

A

-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)

Supporting life block (28 decks)

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