Session 07 - Substance Abuse Flashcards
Define alcohol abuse.
The regular or binge consumption of alcohol which can lead to physical, neuropsychiatric or social damage.
Calculation of units (alcohol).
Units = Volume (L) * ABV (%)
Symptoms of acute intoxication.
- slurred speech
- impaired coordination
- hypoglycaemia
- coma
Can resemble other causes of acute confusion, especially head trauma.
Management of acute intoxication.
Effects usually wear off in 24 hours, provide supportive management.
Pathophysiology of alcoholic ketoacidosis.
When alcoholics miss meals or vomit, this can lead to episodes of starvation, increasing insulin:glucagon ratio.
Glucagon stimulates lipolysis, which generates ketone bodies. These accumulate in the blood and cause acidosis.
Symptoms of alcoholic ketoacidosis.
- nausea
- vomiting
- abdominal pain
In contrast to diabetic ketoacidosis, patients are usually alert and lucid.
Signs of alcoholic ketoacidosis.
- tachypnoea
- tachycardia
- hypotension
Diagnosis of alcoholic ketoacidosis.
ABG showing metabolic acidosis with a raised anion gap, and high ketones.
The glucose levels will be normal, showing it is not a diabetic ketoacidosis.
Management of alcoholic ketoacidosis.
- IV saline with dextrose and thiamine*
*thiamine to prevent Wernicke encephalopathy
What is alcohol dependence?
A strong compulsion to drink alcohol, despite awareness of the physical and psychological harms.
CAGE questionnaire for alcohol dependence screening.
Have you tried to Cut down drinking?
Have people Annoyed you by suggesting you do so?
Have you ever felt Guilty about drinking?
Have you needed an Eye-opener (early morning drink)?
Management of alcohol dependence.
Patients are referred to an alcohol dependence programme to help them quit. These use a mixture of behavioural interventions (e.g. CBT) and pharmacological treatment.
Give some medications that can be used to treat alcohol dependence.
Disulfiram: inhibits acetaldehyde dehydrogenase, so people feel hungover as soon as they drink alcohol.
Acamprosate: weak NMDA antagonist, which is used to reduce alcohol craving.
Pathophysiology of Wernicke’s encephalopathy.
Lack of Vitamin B1 causes a peripheral neuropathy, and leads to cerebellar degeneration giving ataxic signs.
Symptoms of Wernicke’s encephalopathy.
- ataxia
- nystagmus
- opthalmoplegia
- acute confusion
Investigations of Wernicke’s encephalopathy.
- MRI shows cerebellar degeneration
- decreased red cells transketolase*
*enzyme that catalyses transfer of alcohol group between sugars.
Management of Wernicke’s encephalopathy.
IV infusion of thiamine (Vitamin B1).
Pathophysiology of Korsakoff’s syndrome.
Untreated Wernicke’s encephalopathy leading to irreversible brain changes.
Symptoms of Korsakoff’s syndrome.
- ataxia
- nystagmus
- opthalmoplegia
- acute confusion
PLUS
anterograde / retrograde amensia.
What is confabulation?
A symptom of memory dysfunction where patients make up stories to fill in gaps in memory.
Pathophysiology of alcohol withdrawal.
Alcohol consumption enhances GABA-inhibition in the CNS, and inhibits NMDA glutamate receptors.
In withdrawal it is thought that the opposite occurs; less GABA and more NMDA transmission.
Symptoms of alcohol withdrawal.
Early on: increased anxiety, sweating, agitation, tremor.
After 24 hours: seizures with visual hallucinations.
After 48 hours: Course tremors, agitation, delusions, severe visual hallucinations (Delirium Tremens).
Bloods for alcohol dependence.
- U&Es
- FBCs
- LFTs
- INR (synthetic function of liver; indicates irreversible damage)
Management of alcohol withdrawal.
Benzodiazepine chlordiazepoxide.
MOA of stimulant drugs.
Block the reuptake of dopamine and noradrenaline, increasing transmission at synapses.
Examples of stimulant drugs.
- cocaine
- amphetamine
Main effect of stimulant drugs.
Clinically resemble a state of increased sympathetic activity.
Increased energy and concentration; euphoria; hyperactivity.
Cardiovascular side effects of stimulant drugs.
- tachycardia
- hypertension
- hyperthermia
- aortic dissection
ECG changes associated with stimulant drugs.
- QRS widening
- QT prolongation
Gastrointestinal side effects of stimulant drugs.
- reduced appetite
- ischaemic colitis
Psychological side effects of stimulant drugs.
- insomnia
- agitation
- hallucinations
- psychosis
Withdrawal effects from stimulant drugs.
- depression with irritability and agitation
- cravings and hyperphagia
- hypersomnia
Management of stimulant drug withdrawal.
- IV benzodiazepines
- treat complications
- antipsychotics if required
MOA of MDMA (ecstasy)?
Blocks the reuptake of monoamines, particularly serotonin and Na.
Commonly used to give people a high with a feeling of euphoria.
Main effect of MDMA.
- increased energy
- empathy
- pleasure
- mild hallucination
Cardiovascular side effects of MDMA.
- hyperthermia
- tachycardia
- hypertension
Psychological side effects of MDMA.
- insomnia
- increased psychomotor activity
- trismus
- impulsivity
How can MDMA lead to hyponatraemia?
MDMA causes dehydration and increases thirst drive.
Patients then drink lots of water, leading to a dilutional hyponatraemia, coma and potential death.
MOA of cannabinoids.
Tetrahydrocannabinol (THC) binds to CB1 receptors, causing a high.
The other component is CBD, which is known to dampen the THC effects.
Main effect of cannabinoids.
- euphoria
- relaxation
- distortion of sense of time and place
Respiratory side effects of cannabinoids.
- red eyes
- dry mouth
- coughing
Psychological side effects of cannabinoids.
- paranoid thinking
- anxiety
- depression
- schizophrenia
Gastrointestinal side effects of cannabinoids.
Increased appetite after the high (ie. the munchies).
In Leicester, which local service can be contacted with regards to substance abuse?
Turning Point - a local service where people can be referred to or self refer.
The team can identify a support worker, give employment support, therapy, detox help and online courses.
Why do we prescribe to drug users?
Harm minimisation.
Also gets people into and engaging with the services.
Legal - only for the person prescribed.
Risks of prescribing to drug users.
- diversion
- misuse
- overdose
- dependency
Early symptoms of opiate withdrawal (within 12 hours).
- sweating / clammy skin
- persistent yawning
- rhinorrhoea
- tachycardia
- restlessness
- dilated pupils
- lacrimation
- goosebumps
Late symptoms of opiate withdrawal (within 2-3 days).
- nausea and vomiting
- diarrhoea
- insomnia
- abdominal cramps
- muscle pains
Very rare to die of opiate withdrawal.
Methadone titration.
Initial dose 20mg.
If after 2 hours withdrawal symptoms persist, give further 10mg. Continue until no further withdrawal symptoms.
Give the total from the day before the next morning.
Max 60mg.
Buprenorphine titration.
Must be in withdrawal to start.
4mg initial dose.
4mg prn.
Max 32mg.
Pharmacokinetics of buprenorphine vs heroine.
Buprenorphine will displace heroine from opiate receptors.
Buprenorphine is only a partial agonist though, so can only be used effectively when a person is withdrawing - otherwise, you will induce withdrawal.
