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BB2 > DRUG DEPENDENCE: Neurobiology of addiction > Flashcards

DRUG DEPENDENCE: Neurobiology of addiction Flashcards

1
Q

What are the two main molecular targets for ethanol? [2]

A

GABAA and NMDA receptors

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2
Q

What are the three main molecular targets for cocaine? [3]

A

DA, NAd (nicotinamide adenine dinucleotide) and 5-HT uptake systems

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3
Q

What are the three main factors that determine the development of addiction? [3]

A

Environment
Drug-induced effects
Genes

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4
Q

Name 3 selected genes involved in the vulnerability to develop opiate or cocaine addiction [3]

A

OPRM: Mu opoid receptor
OPRK: kappa opoid receptor
OPRD: delta opoid receptor

Probably don’t need to know in loads of detail

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5
Q

Describe the results of of this experiment; where participants were given raclopride (a tracer) that binds to dopamine receptors.

When givien ampethamines what was the physioloigcal response for:

  • those who experienced pleasure? [1]
  • those who experienced unpleasantness? [1]
A

Pleasure: ligand was displaced more: greater release of endogenous dopamine

Unpleasant: ligand stay attached more: less release of endogenous dopamine

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6
Q

Describe the mesolimbic pathway that controls reward circuits in the brain [2]

Which NT controls this pathway? [1]

A

dopaminergic projection from the ventral tegmental area
to the nucleus accumbens is essential in reward and drug dependence

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7
Q

Describe the neurobiological mechansim underlying withdrawal [3]

A

If take drug (e.g. morphine) causes a release of dopamine from dopaminergic neuron from the VTA

Synapses onto nucleus accumbens

But nucleus accumbens has inhibitory synapses back onto VTA through release of GABA and dynorphin on kappa opoid receptors

Causes feelings of dysphoria due to reduced dopamine release

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8
Q

What are the three stages of addiction? [3]

A

Binge / intoxication
Withdrawal / negative affect
Pre-occupation

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9
Q

Describe the neuroplasticity of the brain during drug-seeking behaviour [6]

A

Brain connectivity changes occur during the development of
addiction; there is gradual involvement of many CNS structures
and several neurotransmitter systems:

  • ventral tegmental area
  • nucleus accumbens
  • amygdala
  • insula
  • prefrontal cortex
  • hippocampus
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10
Q

Other than dopamine, which NTs become implicated in drug addiction / drug tking behaviour? [2]

A

gaba; glutamate

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11
Q

State two changes to brain metabolism in cocaine addicts [2]

A

Reduced availability of dopamine D2 receptors

Reduced cortical metabolism in cocaine abusers

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12
Q

If an addict had an impaired ability to perform the following, which part of their brain is most likely to be affected? [1]

Attention and flexibility
Working memory
Decision making
Awareness and insight
Learning and memory
Salience attribution

A

prefrontal cortex

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13
Q

What is iRISA syndrome [1]?

Which 4 symptoms is addiction underpinned by? [4]

A

There is impaired response inhibition and salience attribution (iRISA)

Addiction is underpinned by
* intoxication
* bingeing
* withdrawal
* craving

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14
Q

Explain an example of how chronic drug abuse can alter gene expression and therefore change brain structure [1

A

Chronic drug use causes an increase in the expression of expression of ΔFosB gene

Fos family of transcription factors, accumulates within a subset of neurons of the nucleus accumbens and dorsal striatum

FosB functions as a type of sustained “molecular switch” that gradually converts acute drug responses into relatively stable adaptations that contribute to the long-term neural and behavioral plasticity that underlies addiction.

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15
Q

State the impact of spine density and dendrite branching due to cocaine [1] and morphine [1] abuse

A

Cocaine: increases spine density and dendrite branching

Morphine: Decreases spine density and dendrite branching

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16
Q

What is alchohol abuse for:

  • men [1]
  • women [1]
A

over 5 units a day for men
over 3 units a day for women

17
Q

Describe the effects of acute [2] and chronic [1] alcohol abuse on the brain [1]

A

Acute alcohol ingestion:
* leads to depressed excitatory transmission
* potentiated inhibitory transmission

Chronic:
* Shrinkage of brain grey matter in alcoholic patients

18
Q

Release of which molecule drives the physchomotor effect of MDMA use? [1]

A

5-HT release

Behavioural effects co-incide with time course of 5-HT release

19
Q

Describe the physiological consequence of long term MDMA use [1]

Describe three effects of brain function from long term MDMA use [3]

A

MDMA:

  • glucose metabolism reduces
  • Causes decreased learning perfomance, recall, recall consistency
20
Q

Describe 6 effects that occur from acute MDMA toxicity [6]

A

Temperature elevation

Disseminated intravascular coagulation

Rhabdomyolysis (blocked by dantrolene)

Increased renal reabsorbtion of water

Hyponatraemia

Cerebral oedema

21
Q

Describe impact of long term MDMA use on axons in brain [1]

A

Loss of serotonin axons after long term MDMA use

22
Q

Cannabinoids bind to [] and [] receptors

Main agonist present in cannabis preparations: []

A

Cannabinoids bind to CB1 and CB2 receptors

Main agonist present in cannabis preparations: THC

23
Q

CB1 receptors are concentrated in the []

CB2 receptors are present in [] and are associated
with the [] system

A

CB1 receptors are concentrated in the central nervous system

CB2 receptors are present in peripheral organs and are associated
with the immune system

24
Q

Describe the mode of action of cannabinids [1]

A

CB1 receptors are pre-synaptic & control how much glutamate / gaba is released

Cannabinoids, as neuromodulators, exert mainly inhibitory effects

25
Q

Long term use of cannibis increases the liklihood of developing which psyciatric disorders? [2]

A

schizophrenia and major depression

26
Q

What are the key steps in addiction managment? [5]

A
  • Detoxification (eliminate the drug from the body)
  • Psychological support - counseling
  • Medication (when available, e.g. for opioid, tobacco or alcohol addiction)
  • Evaluation and treatment for co-occurring mental health problems
  • Long-term follow-up
27
Q

Which aspect of cannabis has potential to treat treatment-resistance eplepsy? [1]

A

Cannabidiol (CBD)

28
Q

Which drug can be used for reduction of alcohol consumption? [1]

Describe MoA [1]

A

nalmefene: opiate antagonist

29
Q

Which drug can be used for reduction of nicotine addiction? [1]

Describe MoA [1]

What is major problem with this drug? [1]

A

Varenicline: α4β2 selective partial agonist
at nicotinic receptors

Adverse effects of varenicline: nausea, psychiatric disturbances

30
Q

Which of the following is ketamine’s target?

NMDA glutamate receptors
CB1 receptors
GABA-A receptors
5HT3 receptors

A

Which of the following is ketamine’s target?

NMDA glutamate receptors
CB1 receptors
GABA-A receptors
5HT3 receptors

31
Q

Which of the following are ethanol’s targets? [2]

NMDA glutamate receptors
CB1 receptors
GABA-A receptors
5HT3 receptors

A

Which of the following are ethanol’s targets? [2]

NMDA glutamate receptors
CB1 receptors
GABA-A receptors
5HT3 receptors

32
Q

A 32-year-old male with opioid use disorder presents to the emergency department with chest pain radiating to the left arm. Pain is rated at 5/10 and described as tightness. Currently, he is not in pain, and his vital signs are stable. For his addiction, he is currently receiving methadone prescriptions with occasional relapses for over a year. Given the chronicity of his addiction, where would changes in the patient’s brain be expected, and what neurotransmitter would be involved?

A. Occipital lobe and serotonin
B. Temporal lobe and norepinephrine

D. Wernicke’s area and dopamine

A

C. Prefrontal region and dopamine

33
Q

A 24-year-old male patient is seen in the emergency department with paranoid behavior and agitation. He attended a party an hour ago but refused to disclose any further information. His blood pressure is 160/100 mmHg, heart rate is 130 bpm, respiratory rate 20/minute, and the temperature is 38 degrees Celsius. ECG reveals wide QRS complexes suggestive of ventricular tachycardia. What drug was most likely ingested?
A. Heroin
B. Cocaine
C. Methylenedioxyamphetamine (MDMA, ecstasy)
D. Phencyclidine (PCP)

A

B. Cocaine

34
Q

Which of the following would be the most appropriate for the blank space?

The meso-limbic dopamine system that projects from the ventral tegmental area (VTA) to the [] has been implicated in the rewarding effects of drugs of abuse

Amygdala
Hypothalamus
Cingulate cortex
Pre-frontal cortex
Nucleus accumbens

A

Which of the following would be the most appropriate for the blank space?

The meso-limbic dopamine system that projects from the ventral tegmental area (VTA) to the [] has been implicated in the rewarding effects of drugs of abuse

Amygdala
Hypothalamus
Cingulate cortex
Pre-frontal cortex
Nucleus accumbens

35
Q

Which of the following would be the most appropriate for the blank space?

The meso-limbic dopamine system that projects from the ventral tegmental area (VTA) to the [] has been implicated in the rewarding effects of drugs of abuse

Amygdala
Hypothalamus
Cingulate cortex
Pre-frontal cortex
Nucleus accumbens

A

Which of the following would be the most appropriate for the blank space?

The meso-limbic dopamine system that projects from the ventral tegmental area (VTA) to the [] has been implicated in the rewarding effects of drugs of abuse

Amygdala
Hypothalamus
Cingulate cortex
Pre-frontal cortex
Nucleus accumbens

36
Q

Which of the following would be the most appropriate for the blank space?

The meso-limbic dopamine system that projects from the ventral tegmental area (VTA) to the [] has been implicated in the rewarding effects of drugs of abuse

Amygdala
Hypothalamus
Cingulate cortex
Pre-frontal cortex
Nucleus accumbens

A

Which of the following would be the most appropriate for the blank space?

The meso-limbic dopamine system that projects from the ventral tegmental area (VTA) to the [] has been implicated in the rewarding effects of drugs of abuse

Amygdala
Hypothalamus
Cingulate cortex
Pre-frontal cortex
Nucleus accumbens

37
Q

Activation of which receptor by dynorphins and GABA-A underlines the mechanism of withdrawal symptoms

NMDA receptors
Mu opoid receptors
Dopamine (D1) receptors
Kappa opoid receptors

A

Activation of which receptor by dynorphins and GABA-A underlines the mechanism of withdrawal symptoms

NMDA receptors
Mu opoid receptors
Dopamine (D1) receptors
Kappa opoid receptors

38
Q

CHECK DRUGS list released if any need to know from here

A

BB2 (65 decks)

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