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A. MLA Map Others > Alcohol and other Psychoactive Substance Use > Flashcards

Alcohol and other Psychoactive Substance Use Flashcards

1
Q

Drugs are classified according to how dangerous they are. Opioids are drugs that patients can become addicted to. Which class are opioids categorised in?

1 - class A
2 - class B
3 - class C

A

1 - class A

  • includes codeine and heroin
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2
Q

Drugs are classified according to how dangerous they are. Opioids are drugs that patients can become addicted to. What is the primary action of opioids?

1 - act on GABA receptors
2 - act on opioid receptors
3 - increase noradrenaline/adrenaline
4 - serotonin and acetylcholine

A

2 - act on opioid receptors

  • mainly used as analgesics
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3
Q

Drugs are classified according to how dangerous they are. Stimulants, such as cocaine and speed are drugs that patients can become addicted to. Which class are opioids categorised in?

1 - class A
2 - class B
3 - class C

A

1 - class A

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4
Q

Drugs are classified according to how dangerous they are. Stimulants, such as cocaine and speed are drugs that patients can become addicted to. What is the primary action of stimulants?

1 - act on GABA receptors
2 - act on opioid receptors
3 - increase noradrenaline/adrenaline and dopamine
4 - serotonin and acetylcholine

A

3 - increase noradrenaline/adrenaline and dopamine

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5
Q

Drugs are classified according to how dangerous they are. Sedatives, such as benzodiazepines, alcohol and pregabalin are drugs that patients can become addicted to. Which class are these sedatives categorised in?

1 - class A
2 - class B
3 - class C

A

3 - class C

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6
Q

Drugs are classified according to how dangerous they are. Sedatives, such as benzodiazepines, alcohol and pregabalin are drugs that patients can become addicted to. What is the primary action of sedatives?

1 - act on GABA A and B receptors
2 - act on opioid receptors
3 - increase noradrenaline/adrenaline and dopamine
4 - serotonin and acetylcholine

A

1 - act on GABA A and B receptors

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7
Q

Drugs are classified according to how dangerous they are. Hallucinogens, such as LSD/psilocybin and mushrooms are drugs that patients can become addicted to. Which class are these hallucinogens categorised in?

1 - class A
2 - class B
3 - class C

A

1 - class A

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8
Q

Drugs are classified according to how dangerous they are. Hallucinogens, such as LSD/psilocybin and mushrooms are drugs that patients can become addicted to. What is the primary action of hallucinogens?

1 - act on GABA A and B receptors
2 - act on opioid receptors
3 - increase noradrenaline/adrenaline and dopamine
4 - serotonin and acetylcholine

A

4 - serotonin and acetylcholine

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9
Q

Drugs are classified according to how dangerous they are. Cannabis is a drug that patients can become addicted to. Which class are these hallucinogens categorised in?

1 - class A
2 - class B
3 - class C

A

2 - class B

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10
Q

Drugs are classified according to how dangerous they are. Cannabis is a drug that patients can become addicted to. What is the primary action of cannabis?

1 - act on CB1 and CB2
2 - act on opioid receptors
3 - increase noradrenaline/adrenaline and dopamine
4 - serotonin and acetylcholine

A

1 - act on CB1 and CB2

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11
Q

Which group of patients is most at risk of using drugs?

1 - those earning >£100,000
2 - those earning >£50,000
3 - those earning <£50,000
4 - those earning <£10,000

A

4 - those earning <£10,000

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12
Q

Which of the following are dangerous effects of substance use?

1 - accidents
2 - overdose
3 - violence
4 - suicide
5 - breakdown of relationships
6 - unplanned pregnancy
7 - all of the above

A

7 - all of the above

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13
Q

Which of the following is NOT a common risk factor for substance use?

1 - stress
2 - gender
3 - poverty
4 - trauma
5 - mental illness
6 - genetics

A

2 - gender

  • drugs are often described as self medicating
  • typically this is a cumulative effect of multiple risk factors
  • protective factors can mitigate risk factors
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14
Q

Which of the following is NOT a common risk factor that patients with mental health and substance users typically have?

1 - trauma/abuse
2 - age
3 - stress
4 - genetics

A

2 - age

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15
Q

In acute alcohol use what would we expect to see in GABA-A and NMDA receptors?

1 - GABA and NMDA agonist
2 - GABA and NMDA antagonist
3 - GABA agonist and NMDA antagonist
4 - GABA antagonist and NMDA agonist

A

3 - GABA agonist and NMDA antagonist
- NMDA is glutamate

  • GABA A
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16
Q

Patients who associate alcohol with a positive valence (which increases dopamine release) and associate with a feeling of reward when consumed will have increased dopamine release from the ventral tegmental area (VTA). What effect does alcohol then have on the VTA?

1 - NMDA (glutamate, an excitatory neurotransmitter) antagonist of cortical input disinhibits VTA and increases dopamine
2 - GABA receptor antagonist of cortical input disinhibits VTA and decreases dopamine
3 - NMDA (glutamate) agonist of cortical input disinhibits VTA and decreases dopamine

A

1 - NMDA (glutamate, an excitatory neurotransmitter) antagonist of cortical input disinhibits VTA and increases dopamine

  • causes an increase in dopamine release to the nucleus accumbens
  • means we continue to want alcohol to get the same reward effects
  • nucleus accumbens = main dopamine nucleus)
  • located in the midbrain
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17
Q

Which of the following drugs is used to treat alcohol dependence?

1 - adenosine
2 - haloperidol
3 - disulfiram
4 - lithium

A

3 - disulfiram

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18
Q

Disulfiram is used to treat alcohol dependence. What is the mechanism of action of this drug?

1 - agonist of NMDA receptors and increases glutamate
2 - inhibits GABA A receptors
3 - inhibits aldehyde dehydrogenase
4 - all of the above

A

3 - inhibits aldehyde dehydrogenase

Disulfiram creates unpleasant side effects when alcohol is consumed, so acts as a deterrent

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19
Q

In chronic alcohol we can see dependency, which is where the patient cannot function normally without alcohol. What would we expect to see in GABA and NMDA receptors?

1 - GABA and NMDA receptors upregulated
2 - GABA and NMDA receptors downregulated
3 - GABA receptors downregulated and NMDA receptors upregulated
4 - GABA receptors upregulated and NMDA receptors downregulated

A

3 - GABA receptors downregulated and NMDA receptors upregulated

  • down regulation of GABA-A receptors because alcohol acts as an agonist so less receptors are needed
  • up-regulation of NMDA (glutamate) receptors as alcohol is an antagonist, so more receptors needed to increase sensitivity
  • the increased number of NMDA receptors means the firing rate of the NMDA receptors returns to a normal level as a compensatory mechanism
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20
Q

What scoring tool is used to assess a patients alcohol withdrawal?

1 - CWAR score
2 - Wells score
3 - Chad-vasc score
4 - AUDIT-C

A

1 - CWAR score

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21
Q

Typically, how long is it before a patient begins to have withdrawal symptoms following cessation of alcohol?

1 - <6hours
2 - <12 hours
3 - <24 hours
4 - <48 hours

A

2 - <12 hours
- can be variable though

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22
Q

Which of the following medications is typically used in alcohol withdrawal?

1 - chlordiazepoxide
2 - haloperidol
3 - disulfiram
4 - lithium

A

1 - chlordiazepoxide
- essentially benzodiazepines

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23
Q

During withdrawal from alcohol, patients can experiencer tonic (muscle stiffening) /clonic (twitching or jerking) seizures that resemble epilepsy. Which of the following is also common?

1 - Tremor
2 - Sweating
3 - Anxiety
4 - Tachycardia
5 - Insomnia
6 - Nausea/vomiting
7 - All of the above

A

7 - All of the above

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24
Q

Delirium tremens can occur in a patient in alcohol withdrawal, typically after 3 days. Which of the following are features of delirium tremens?

1 - rapid onset of confusion
2 - severe tremor
3 - clouding of consciousness
4 - paranoia
5 - agitation
6 - autonomic instability
7 - all of the above

A

7 - all of the above

  • high mortality rate if not treated
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25
Q

Delirium tremens can occur in a patient in alcohol withdrawal, typically after 3 days and carries a high mortality. Which 2 of the following is typically used to treat this?

1 - chlordiazepoxide
2 - haloperidol
3 - disulfiram
4 - thiamines

A

1 - chlordiazepoxide
4 - thiamines (B1)

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26
Q

Wernicke’s encephalopathy is a degenerative brain disorder caused by the lack of vitamin B1 (thiamine) and can occur in alcohol withdrawal. Which of the following is NOT part of the typical triad of Wernicke’s?

1 - Confusion
2 - Ataxia
3 - Ophthalmoplegia (paralysis/weakness of the eyes)
4 - Tremor

A

4 - Tremor

  • important to treat Wernicke’s asap as this can lead to permanent neurological damage
  • Nystagmus can also occur
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27
Q

What is the locus coeruleus, which in Latin means “blue spot”?

1 - nucleus in the pons of the brainstem responsible for dopamine synthesis
2 - nucleus in the pons of the brainstem responsible for the synthesis of norepinephrine
3 - nucleus in the pons of the brainstem responsible for the synthesis of corticol
4 - nucleus in the pons of the brainstem responsible for the synthesis of serotonin

A

2 - nucleus in the pons of the brainstem responsible for the synthesis of norepinephrine

  • principal site for brain synthesis of norepinephrine
  • involved in stress and panic (fight or flight response)
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28
Q

Opioid receptors are present throughout the mesocorticolimbic pathway, of which the locus coeruleus (LC), which in Latin means “blue spot” is part of. The LC is the principal site for brain synthesis of norepinephrine, a nucleus in the pons of the brainstem that is involved in stress and panic (fight or flight response). Opioids are able to reduce intracellular Ca2+ in the pre-synapse and increase K+ leaving the post-synapse, both of which cause hyperpolarisation. Do opioids inhibit or excite the LC?

A
  • inhibit their firing
  • acute opioids = acute inhibition of LC
  • chronic opioids = LC neuronal activity returns to normal levels. But if opioids are stopped then this causes an influx of norepinephrine causing physical symptoms and is linked with withdrawal from opioids
29
Q

Opioid receptors are present throughout the mesocorticolimbic pathway, of which the locus coeruleus (LC), which in Latin means “blue spot” is part of. The LC is the principal site for brain synthesis of norepinephrine, a nucleus in the pons of the brainstem that is involved in stress and panic (fight or flight response) and pain. Acute opioid use causes acute inhibition of the LC, but chronic activation of the opioid receptors leads to compensatory functional changes, this can lead to tolerance, why?

  • tolerance = desensitisation to a drug, meaning we need more of the drug for the same effects
A
  • LC develops tolerance to the inhibitory effect of opioids
  • LC begins firing but at an increased rate in an attempt to return to normal
  • larger doses of opioids are required to inhibit this additional firing from the LC causing tolerance
30
Q

Opioid receptors are present throughout the mesocorticolimbic pathway, of which the locus coeruleus (LC), which in Latin means “blue spot” is part of. The LC is the principal site for brain synthesis of norepinephrine, a nucleus in the pons of the brainstem that is involved in stress and panic (fight or flight response) and pain. Acutely opioids inhibit the LC, but during chronic activation of the opioid receptors on the LC mean the LC goes into overdrive just to get back to normal levels. This can leads to compensatory functional changes and then dependance, why?

1 - cessation of opioids does not stop over activation of locus coeruleus (LC)
2 - no inhibition of LC by opioids leads to increased firing of LC and release of large amounts of norepinephrine
3 - patients who stop taking opioids after becoming dependent will experience excessive fight or flight response, which is what withdrawal symptoms are.
4 - this can lead to a disturbance in physical homeostatic when the drug is removed
5 - all of the above

A

5 - all of the above

31
Q

If a patient is addicted to opioids, the aim is for complete absence. However, this is generally not possible and a treatment pathway should be used. What should be the first aim of a treatment plan?

1 - stop the drug and monitor the patient
2 - motivate the patient towards change and involve them in treatment plan
3 - start on a lower dose of opioids and slowly withdraw the drug

A

2 - motivate the patient towards change and involve them in treatment plan
- important to consider the stages of change model

32
Q

If a patient is addicted to opioids, the aim is for complete absence. However, this is generally not possible and a treatment pathway should be used. The first step is to try and motivate the patient towards change and involve them in treatment plan. What should be the next phase?

1 - stop the drug and monitor the patient
2 - motivate the patient towards change and involve them in treatment plan
3 - start on a lower dose of opioids and slowly withdraw the drug
4 - minimise harm related to taking substances, improve mental and physical health, reduce criminal activity and blood born infections

A

4 - minimise harm related to taking substances, improve mental and physical health, reduce criminal activity and blood born infections

33
Q

If a patient is addicted to opioids, the aim is for complete absence. However, this is generally not possible and a treatment pathway should be used. What should be the final phase of any treatment plan?

1 - stop the drug and use naloxone (opiod antagonist) and monitor the patient
2 - motivate the patient towards change and involve them in treatment plan
3 - start on a lower dose of opioids and slowly withdraw the drug
4 - minimise harm related to taking substances, improve mental and physical health, reduce criminal activity and blood born infections

A

1 - stop the drug and use naloxone (opiod antagonist) and monitor the patient

  • if the opiod cannot be stopped then it should be substited to a safer drug
34
Q

Which mediation is used to reverse opioids?

1 - naloxone
2 - flumazenil
3 - neostigmine
4 - protamine sulfate

A

1 - naloxone

  • flumazenil = benzodiazepines
  • neostigmine = ACh
  • protamine sulfate = heparin
35
Q

Which of the following is NOT a common acute cardiac effect of opioids?

1 - Tachycardia
2 - Prolonged QTc
3 - Peripheral vasodilation
4 - Hypotension

A

1 - Tachycardia
- typically causes bradycardia

36
Q

Which of the following is NOT a common acute respiratory effect of opioids?

1 - Respiratory depression
2 - Hypoxia (in OD)
3 - Hypoventilation
4 - Barrel chested

A

4 - Barrel chested
- common in COPD

37
Q

Which of the following is NOT a common acute gastrointestinal effect of opioids?

1 - Nausea
2 - Vomiting
3 - Diarrhoea
4 - Dry mouth

A

3 - Diarrhoea
- typically causes constipation

38
Q

Which of the following is NOT a common acute neurological effect of opioids?

1 - Disorientation/confusion
2 - Enlarged pupils
3 - Sedation
4 - Reduced GCS
5 - Analgesic
6 - Dizziness

A

2 - Enlarged pupils
- typically causes pin point pupils because it is inhibiting the fight or flight response

39
Q

Which of the following is NOT a common acute effect of opioids?

1 - Euphoria
2 - Itching
3 - Urinary retention
4 - Overdose
5 - Depression

A

5 - Depression

40
Q

Benzodiazepines are drugs that act on GABA-A receptors, increasing Cl- and causing repolarisation. Which of the following is NOT a typical use of benzodiazepines?

1 - ataxia
2 - slurred speech
3 - euphoria
4 - hypnotic
5 - anti-epileptic
6 - anterograde amnesia
7 - anxiolytic (anxiety)

A

3 - euphoria
- typically used for confusion

  • ataxia =disorganised speech and balance
41
Q

In overdose, what is the most dangerous affect of benzodiazepines?

1 - heart failure
2 - respiratory depression
3 - liver failure
4 - renal failure

A

2 - respiratory depression
- also increased risk in overdose

42
Q

In overdose, although rare, an adverse event of benzodiazepines overdose is paradoxical disinhibition. What is this?

1 - depression
2 - generalised anxity
3 - mania following by severe depression
4 - excitement, agitation and altered mental state

A

4 - excitement, agitation and altered mental state

43
Q

Which mediation is used to reverse benzodiazepines in the event of an overdose?

1 - naloxone
2 - flumazenil
3 - neostigmine
4 - protamine sulfate

A

2 - flumazenil

44
Q

Although benzodiazepines can initially help with sleep, do these help with sleep in the long term?

A
  • no
  • reduce total sleep and rapid eye movement (REM) sleep
45
Q

In women taking benzodiazepines that have given birth, what can happen to their babies?

1 - low foetal weight
2 - genetic deformities
3 - floppy baby syndrome
4 - all of the above

A

3 - floppy baby syndrome
- mums can also develop a withdrawal syndrome

46
Q

Does cannabis cause a physiological dependence syndrome?

A
  • no
  • can lead to psychoactive dependence though
47
Q

Cocaine is a stimulant drug. Which of the following does cocaine typically NOT stimulate?

1 - adrenaline
2 - serotonin
3 - noradrenaline
4 - dopamine

A

2 - serotonin

48
Q

Which of the following is NOT a typical chronic effect of cannabis use?

1 - Possible reduction in memory/attention/cognitive
2 - Psychosis
3 - Depression/Anxiety
4 - Psychological Dependence
5 - Hyperemesis
6 - A motivational Syndrome
7 - Increased total sleep

A

7 - Increased total sleep
- leads to impaired sleep

49
Q

Dopamine D1 receptors are involved in long term potentiation through the modification of glutamatergic transmission, which then allows long term potentiation (essentially more glutaminergic receptors are located on the cells membrane). What does this do to the synapses on dendrite spines and branches?

1 - nothing
2 - dendrite number and length increases
3 - synaptic remodelling causing increased number of dendritic spines
4 - synaptic remodelling causing a decreased number of dendritic spines

A

3 - synaptic remodelling causing increased number of dendritic spines
- more dendritic spines increase the surface area to receive information)

50
Q

Dopamine D1 receptors are involved in long term potentiation in cocaine addiction through the modification of glutamatergic transmission, which then allows long term potentiation. This causes synaptic remodelling (essentially means more dendritic spines that increase surface area to receive information). Even in abstinence do these changes just disappear?

A
  • no
  • dendritic spines can remain for months following abstinence
  • memories in these pathways can trigger relapse, hence why its so difficult to remain abstinent
51
Q

In cocaine addiction are there more D1 or D2 dopaminergic receptors?

A
  • D1 receptors
  • cocaine activates the reward pathway of mesolimbic system
52
Q

In cocaine addiction there are less D2 dopaminergic receptors. What can this then cause in patients for natural rewards?

1 - previous non-psychoaddcitve rewards no longer provide same reward stimulus
2 - patient more likley to seek cocaine to enhance reward pathways
3 - impact adversely on classic conditioning (memory/learning) and motivational states
4 - all of the above

A

4 - all of the above

53
Q

Which of the following is NOT a typical acute effect of cocaine?

1 - depression
2 - arrhythmias
3 - increased energy
4 - aggression
5 - increased sociability
6 - psychiatric effects
7 - reduced appetite

A

1 - depression
- typically causes euphoria

54
Q

Does cocaine cause a physical dependency effect?

A
  • no
  • does cause a psychological dependency
55
Q

Which of the following is NOT a typical chronic effect of cocaine use?

1 - Psychological dependence
2 - Paranoia/Psychosis
3 - Panic attacks
4 - Calmness/Tranquility

A

4 - Calmness/Tranquility
- typically causes irritability
- effects depend on the route of administration

56
Q

Does speed/amphetamine have any tolerance or dependency issues?

A
  • typically no
57
Q

Which of the following is NOT an affect of speed/amphetamines?

1 - increased sociability
2 - hypotension/bradycardia
3 - weight loss
4 - insomnia

A

2 - hypotension/bradycardia
- causes hypertension and tachycardia

58
Q

Does MNDA have any tolerance or dependency issues?

A
  • no
59
Q

MNDA has some hallucination properties. Which of the following is NOT a common risk of MNDA?

1 - failure of temperature regulation
2 - arrhythmias
3 - seizures
4 - dehydration
5 - rhabdomyolysis
6 - drowsiness

A

6 - drowsiness

60
Q

If a patient has taken an overdose, which of the following is most commonly used if you think you can reduce absorption?

1 - activated charcoal
2- induce vomiting
3 - endoscopy
4 - gastric lavage

A

1 - activated charcoal

The others are not recommended

61
Q

Which drug class accounts for 50% of all non-accidental (overdose) deaths due to poisoning?

1 - Alcohol
2 - Tricyclic antidepressants
3 - Benzodiazepines
4 - Opioids
5 - Paracetamol

A

5 - Paracetamol

62
Q

In children >6 y/o, above what dosage if consumed in a single ingestion is toxic?

1 - >50mg/kg
2 - >75mg/kg
3 - >100mg/kg
4 - >150mg/kg

A

2 - >75mg/kg

63
Q

Activated charcoal is the treatment of choice if a child has taken an overdose of paracetamol. This is really only effective if the paracetamol has been taken in what time frame?

1 <10 minutes
2 - <30 minutes
3 - <60 minutes
4 - <4 hours

A

3 - <60 minutes

64
Q

What is the antidote to paracetamol?

1 - digibind
2 - glucagon
3 - N-Acetyl cysteine
4 - naloxone

A

3 - N-Acetyl cysteine
- precursor for glutathione

65
Q

Acetaminophen (paracetamol) is typically metabolised by glucuronidation and sulfation to non-toxic metabolites. However, cytochrome P450 also metabolises acetaminophen into a toxic substance. What is this substance called?

1 - acetaldehyde
2 - azithromycin
3 - N-acetyl-p-benzoquinone imine (NAPQI)
4 - methanol

A

3 - N-acetyl-p-benzoquinone imine (NAPQI)

This is essentially acetylcysteine

Only given if the paracetamol levels are >100mg/litre

66
Q

Some paracetamol is metabolise by cytochrome P450 into N-acetyl-p-benzoquinone imine (NAPQI). Although this is toxic and can damage the liver, the liver is able to produce what that inactivates NAPQI?

1 - beta-carotene
2 - glutathione
3 - carotenoids
4 - coenzyme Q10

A

2 - glutathione
- in a paracetamol overdoes means lots of NAPQI and there is insufficient glutathione causing liver damage and cell death
- in extreme cases it can cause liver failure and death

67
Q

Patients who take an excess of paracetamol need a blood test to identify the concentration of paracetamol in the blood. When do paracetamol levels peak in the blood?

1 - 30 mins
2 - 60 mins
3 - 2 hours
4 - 4 hours

A

4 - 4 hours

  • need to identify when the 4 hours is as this is when treatment needs to be started
  • antidote is 3 - N-Acetyl cysteine a precursor for glutathione
68
Q

In addition to measuring paracetamol levels within 4hours of ingestion, which of the following also need to be checked?

1 - LFTs
2 - INR
3 - ABG or VBG
4 - all of the above

A

4 - all of the above

All linked with liver failure

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