Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BMSc - Neuropharmacology and Behaviour > Addiction Pharmacology > Flashcards

Addiction Pharmacology Flashcards

1
Q

What is a new psychoactive substance (NPS)?

A

New narcotic or psychotropic drug, in pure form or preparation that is not controlled by the UN drug conventions, but which may pose a public health threat comparable to that posed by substances listed in these conventions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe NPS opioids?

A

Structurally similar to fentanyl; highly potent and sold as heroin
Very dangerous; much stronger than heroin but sold as this potency - high rates of unintentional overdose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How has legislation modified to make NPS illegal?

A

Bans drugs based on their molecular structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the difference between class A, B and C drugs

A

A; no medicinal value but high misuse and abuse value
B and C; medicinal value
B; liked to be abused
C; unlikely to be abused

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When was the misuse of drugs act passed in UK?

A

2001; class A, B and C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the scheduling system of drug law in the UK

A

1-5
1, 2; no therapeutic or medicinal value; high abuse potential
3-5; medicinal value with varying levels of abuse potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What law was introduced in 2016 to mitigate NPS abuse?

A

Psychoactive Substances Act 2016
Makes it an offence to produce, supply or possess; import or export psychoactive substances
Excludes legitimate substances such as food, alcohol, tobacco, nicotine, caffeine and medical products
Exempts healthcare activities and approved scientific research

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the DSM5 criteria for substance use disorders

A 
Hazardous use
Social/ interpersonal problems
Neglected major roles to use
Withdrawal
Tolerance
Repeated attempts to quit 
Much time spent using 
Physical/ psychological problems related to use
Activities given up to use
Craving

2 or more required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the reward pathway

A

VTA
N. Acc
Prefrontal cortex
DOPAMINE RELEASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What nT receptors are involved in the reward pathway?

A 
Opioid
Cannabinoid
Nicotine
GABAA
Dopaminergic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the actions of alcohol, cannabis, opioids, cocaine, amphetamines and nicotine in the reward pathway

A

Alcohol/ opioids/ cannabis: suppress action of GABA in VTA (inhibit the inhibitory neuron)
Cocaine; blocks removal of DA from synapse
Amphetamines; directly stimulates transmission of DA
Nicotine ; stimulates DA neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is reward measured in rodent models?

A

Self administration paradigm
Lever is pressed to receive an injection of a rewarding substance

Conditioned place preference: side preference

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Are there genetic influences on addiction?

A

Yes; study that compared addictive behaviour between MZ and DZ twins showed a much higher rate in MZ twins; suggesting heritability
As high as 50-70% heritability
Implication of “addiction genes”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the derivative of cocaine?

A

Coca leaves; cocaine content of around 0.7%

Coca leaves when chewed can act as a very mild stimulant; suppress hunger, fight fatigue, altitude sickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the formulations of cocaine as an alkaloid?

A

Cocaine hydrochloride; soluble form (nasal or IV)

Crack (higher stability and when heated will vaporise; inhalation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the differing effects of cocaine in vivo when comparing crack to cocaine HCL?

A

Cocaine HCL; slower rate of rise of cocaine in blood and brain. Peaks within 1hr
Crack/ IV; rapid rise in cocaine levels, rapid rise in brain. Peaks within around 10 mins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the difference between inhaled/ IV cocaine in comparison to nasal ingenstion?

A

Due to the rapid peak and decay of crack/ IV when compared to nasal; there is much higher addictive and abusive potential
Important relationship between addictive potential and pharmacokinetics of drugs

18
Q

How does cocaine exert its action on the reward pathway?

A

Increases levels of extracellular dopamine in the striatum
Prevents reuptake of dopamine at the presynaptic terminal
Also increases levels of serotonin, adrenaline and noradrenaline (stimulatory effect on CVS; incr HR, incr BP)

19
Q

What other drug classes is cocaine structurally similar to?

A

Amphetamines - very similar behavioural properties to cocaine
Methamphetamines - crystal meth
Increase extracellular dopamine but in a different way to cocaine

20
Q

Describe the difference between the ways that cocaine and amphetamines increase DA?

A

Cocaine; blocks reuptake
Amphetamine; substrate for transporter, pumped into the presynaptic membrane to act on VMAT to enter vesicles. This elevates cytosolic DA which consequently increases DA in synaptic cleft by causing the dopamine transporter to work in reverse and pump DA out.

21
Q

Describe the pharmacokinetics of cocaine and methamphetamine

A

Cocaine; rapid uptake and rapid decay/ clearance (particularly crack/ IV)
Methamphetamine; slower to peak and a slow clearance; bound to DA transporters in the brain for many hours

Methamphetamine; less addictive than cocaine due to pharmacokinetic profile

22
Q

Describe the relationship between the route of administration and nicotine concentration

A

Cigarette; high peak and fast decay (highly addictive)
Oral snuff, chewing and Gum; slow increase and slow decay - stable pharmacokinetic profile
Patch; most stable formulation; very slow rise and very slow decay. Prevents nicotine withdrawal

23
Q

Compare nicotine absorption from e-cigs and cigarettes

A

Cigarettes; rapid peak
E-cigs; much slower rise and takes a lot longer to reach the same plasma concentration as tobacco cigarettes

E.cig; provides CV benefit compared to smoking. Less addictive

24
Q

Describe the CV effects of switching from tobacco to e.cigs

A

In those who smoke tobacco cigarettes; poor mean flow dilation (indicator of CV dysfunction)
E. cigs with nicotine/ without nicotine; significant in mean flow mediated dilation after quitting of tobacco cigarettes.

25
Q

How does nicotine stimulate DA release?

A

Stimulates nACHRs in reward pathway to directly depolarize dopaminergic neuron. If threshold is released, an action potential is triggered to activate voltage activated calcium channels at the post synaptic terminal

There are also nicotinic receptors post synaptically which can induce calcium release == dopamine release

26
Q

What are the behavioural effects of ethanol?

A

Sedative hypnotic - modulation of GABA receptor

27
Q

What are the absorption profiles of ethanol?

A

Rapid; slowed by food

Metabolised by gut; most distributes to all tissues (incl. placenta)

28
Q

What is the metabolism of ethanol?

A

ADH in liver and gut; zero order kinetics (7-10 g/h)

Microsomal ethanol oxidizing system (p450 enzymes); kicks in above 0.1% blood ethanol

29
Q

How is tolerance to ethanol established?

A

Primarily metabolic tolerance

30
Q

What are the different forms of tolerance?

A

Metabolic (pharmacokinetic)

Functional (pharmacodynamic)

31
Q

Describe metabolic (pharmacokinetic) tolerance

A

Drugs causes upregulation of enzymes responsible for metabolization
For example, alcohol consumption that leads to 0.1% ethanol concentration daily leads to upregulation of p450
This leads to lower blood alcohol levels with those who drink the same amount

32
Q

Describe functional tolerance

A

Change in the response of the brain to alcohol
Changes in composition of GABAA
Downregulation in GABA receptors to compensate for the sedative and hypnotic effects
Withdrawal; DTs (hallucinations, seizures)
LACK OF GABA

33
Q

Describe ethanol metabolism by ADH

A

Ethanol is metabolised to acetaldehyde by alcohol dehydrogenase (ADH)
This requires formation of NADH from NAH+
NAD+ is a free radical that can cause damage to liver membranes and leads to liver cirrhosis - the more alcohol, the more NADH produced
Acetaldehyde can be converted to acetic acid by acetaldehyde dehydrogenase

34
Q

What are the consequences of high levels of acetaldehyde?

A

Nausea
Vomiting
Headache
Hypotension

35
Q

What is the mode of action of disulfiram (Antabuse)?

A

Blocks acetaldehyde dehydrogenase leading to a build up of acetaldehyde

36
Q

Describe molecules that can modulate GABAA receptors

A 
BZD
Barbiturates
Neurosteroids
Volatile anaesthetics
Ethanol
IV anaesthetics; etomidate, Propofol
37
Q

What is the mode of naltrexone in alcohol substance use disorder?

A

Demonstrated using self administration paradigm to decrease alcohol use
Dose dependent reduction in self administration behaviour
Reduces relapse in recovering alcoholics

38
Q

Describe the the treatment of alcohol addiction

A

Psychosocial
Detoxification
Relapse prevention drugs; disulfiram, Acamprosate, naltrexone
Population level; screening and brief intervention, minimum pricing

39
Q

Describe the mode of action of nalmefene

A

Reduces craving by antagonising the effects of endogenous opioid peptides
Reduces rewarding effects of alcohol
Longer half life than naltrexone, greater bioavailability, reduction in liver toxicity

Universal antagonist with high affinity at mu receptors

40
Q

How can nicotine addiction be treated?

A

Nicotine patch
Varenicline; selective alpha4beta2 receptor agonist - acts as a sub for tobacco
Bupropion (antidepressant) - enhances NA and DA nT via reuptake inhibition of the NA and DA transporter

41
Q

Describe research that has formulated an anti-cocaine vaccine

A

Adenovirus capsid based anti-cocaine vaccine prevents cocaine from binding to the CNS dopamine transporter and therefore prevents access to the CNS
Antibodies bind to cocaine; sequestering it in the blood and preventing entrance into the CNS

BMSc - Neuropharmacology and Behaviour (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions