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Year 4 - Psychiatry > Session 07 - Substance Abuse > Flashcards

Session 07 - Substance Abuse Flashcards

1
Q

Define alcohol abuse.

A

The regular or binge consumption of alcohol which can lead to physical, neuropsychiatric or social damage.

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2
Q

Calculation of units (alcohol).

A

Units = Volume (L) * ABV (%)

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3
Q

Symptoms of acute intoxication.

A
  • slurred speech
  • impaired coordination
  • hypoglycaemia
  • coma

Can resemble other causes of acute confusion, especially head trauma.

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4
Q

Management of acute intoxication.

A

Effects usually wear off in 24 hours, provide supportive management.

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5
Q

Pathophysiology of alcoholic ketoacidosis.

A

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.

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6
Q

Symptoms of alcoholic ketoacidosis.

A
  • nausea
  • vomiting
  • abdominal pain

In contrast to diabetic ketoacidosis, patients are usually alert and lucid.

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7
Q

Signs of alcoholic ketoacidosis.

A
  • tachypnoea
  • tachycardia
  • hypotension
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8
Q

Diagnosis of alcoholic ketoacidosis.

A

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.

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9
Q

Management of alcoholic ketoacidosis.

A
  • IV saline with dextrose and thiamine*

*thiamine to prevent Wernicke encephalopathy

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10
Q

What is alcohol dependence?

A

A strong compulsion to drink alcohol, despite awareness of the physical and psychological harms.

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11
Q

CAGE questionnaire for alcohol dependence screening.

A

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)?

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12
Q

Management of alcohol dependence.

A

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.

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13
Q

Give some medications that can be used to treat alcohol dependence.

A

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.

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14
Q

Pathophysiology of Wernicke’s encephalopathy.

A

Lack of Vitamin B1 causes a peripheral neuropathy, and leads to cerebellar degeneration giving ataxic signs.

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15
Q

Symptoms of Wernicke’s encephalopathy.

A
  • ataxia
  • nystagmus
  • opthalmoplegia
  • acute confusion
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16
Q

Investigations of Wernicke’s encephalopathy.

A
  • MRI shows cerebellar degeneration
  • decreased red cells transketolase*

*enzyme that catalyses transfer of alcohol group between sugars.

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17
Q

Management of Wernicke’s encephalopathy.

A

IV infusion of thiamine (Vitamin B1).

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18
Q

Pathophysiology of Korsakoff’s syndrome.

A

Untreated Wernicke’s encephalopathy leading to irreversible brain changes.

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19
Q

Symptoms of Korsakoff’s syndrome.

A
  • ataxia
  • nystagmus
  • opthalmoplegia
  • acute confusion

PLUS

anterograde / retrograde amensia.

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20
Q

What is confabulation?

A

A symptom of memory dysfunction where patients make up stories to fill in gaps in memory.

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21
Q

Pathophysiology of alcohol withdrawal.

A

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.

22
Q

Symptoms of alcohol withdrawal.

A

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).

23
Q

Bloods for alcohol dependence.

A
  • U&Es
  • FBCs
  • LFTs
  • INR (synthetic function of liver; indicates irreversible damage)
24
Q

Management of alcohol withdrawal.

A

Benzodiazepine chlordiazepoxide.

25
Q

MOA of stimulant drugs.

A

Block the reuptake of dopamine and noradrenaline, increasing transmission at synapses.

26
Q

Examples of stimulant drugs.

A
  • cocaine
  • amphetamine
27
Q

Main effect of stimulant drugs.

A

Clinically resemble a state of increased sympathetic activity.

Increased energy and concentration; euphoria; hyperactivity.

28
Q

Cardiovascular side effects of stimulant drugs.

A
  • tachycardia
  • hypertension
  • hyperthermia
  • aortic dissection
29
Q

ECG changes associated with stimulant drugs.

A
  • QRS widening
  • QT prolongation
30
Q

Gastrointestinal side effects of stimulant drugs.

A
  • reduced appetite
  • ischaemic colitis
31
Q

Psychological side effects of stimulant drugs.

A
  • insomnia
  • agitation
  • hallucinations
  • psychosis
32
Q

Withdrawal effects from stimulant drugs.

A
  • depression with irritability and agitation
  • cravings and hyperphagia
  • hypersomnia
33
Q

Management of stimulant drug withdrawal.

A
  • IV benzodiazepines
  • treat complications
  • antipsychotics if required
34
Q

MOA of MDMA (ecstasy)?

A

Blocks the reuptake of monoamines, particularly serotonin and Na.

Commonly used to give people a high with a feeling of euphoria.

35
Q

Main effect of MDMA.

A
  • increased energy
  • empathy
  • pleasure
  • mild hallucination
36
Q

Cardiovascular side effects of MDMA.

A
  • hyperthermia
  • tachycardia
  • hypertension
37
Q

Psychological side effects of MDMA.

A
  • insomnia
  • increased psychomotor activity
  • trismus
  • impulsivity
38
Q

How can MDMA lead to hyponatraemia?

A

MDMA causes dehydration and increases thirst drive.

Patients then drink lots of water, leading to a dilutional hyponatraemia, coma and potential death.

39
Q

MOA of cannabinoids.

A

Tetrahydrocannabinol (THC) binds to CB1 receptors, causing a high.

The other component is CBD, which is known to dampen the THC effects.

40
Q

Main effect of cannabinoids.

A
  • euphoria
  • relaxation
  • distortion of sense of time and place
41
Q

Respiratory side effects of cannabinoids.

A
  • red eyes
  • dry mouth
  • coughing
42
Q

Psychological side effects of cannabinoids.

A
  • paranoid thinking
  • anxiety
  • depression
  • schizophrenia
43
Q

Gastrointestinal side effects of cannabinoids.

A

Increased appetite after the high (ie. the munchies).

44
Q

In Leicester, which local service can be contacted with regards to substance abuse?

A

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.

45
Q

Why do we prescribe to drug users?

A

Harm minimisation.

Also gets people into and engaging with the services.

Legal - only for the person prescribed.

46
Q

Risks of prescribing to drug users.

A
  • diversion
  • misuse
  • overdose
  • dependency
47
Q

Early symptoms of opiate withdrawal (within 12 hours).

A
  • sweating / clammy skin
  • persistent yawning
  • rhinorrhoea
  • tachycardia
  • restlessness
  • dilated pupils
  • lacrimation
  • goosebumps
48
Q

Late symptoms of opiate withdrawal (within 2-3 days).

A
  • nausea and vomiting
  • diarrhoea
  • insomnia
  • abdominal cramps
  • muscle pains

Very rare to die of opiate withdrawal.

49
Q

Methadone titration.

A

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.

50
Q

Buprenorphine titration.

A

Must be in withdrawal to start.

4mg initial dose.

4mg prn.

Max 32mg.

51
Q

Pharmacokinetics of buprenorphine vs heroine.

A

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.

Year 4 - Psychiatry (11 decks)

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