Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology CAM202 & 304 > Treatment of Addiction > Flashcards

Treatment of Addiction Flashcards

1
Q

What do drugs do to the CNS?

A

Alter synaptic plasticity by changingg the synaptic plasticity in circuits involved in motivation & psychomotor activation -
> LTP and LTD

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

Explain the ADDICTION CIRCUITRY

- what system do addictive drugs target?

A
  • drug evoked synaptic plasticity outlasts the presence of drug in the brian and contributes to the reorginisation of a neural circuit.
  • Addictive drugs target the MESOCORTICOLIMBIC DOPAMINE (DA) system.
  • This area exists mainly in the ventral tegmental area (VTA) and projects mainly to the nucleus accumbens (Nac) and Prefrontal Cortex (PFC)
  • All addictive drugs increase dopamine (DA) concentrations in the VTA itself and in its projection areas
  • Drugs of abuse potentiate the effect of electrical brain stimulation.
  • Alcohol abuse can occur in the absence of dopamine activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some psychoactive drugs?

A

Cocaine and Amphetamine

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

How does cocaine/amphetamines work?

A

increase the amount of dopamine at synapses of the nucleus accumbens by blocking the dopamine transporter and reuptake from the synaptic cleft =>

  • cocaine directly inhibits the DA transporter
  • amphetamines are taken up in the cell to enhance the release of DA

Causes midbrain dopamine neurons (VTA) to also release DA from their dendrites
inhibition of DA transporters increases DA in the VTA, Nucleus accumbens and PFC

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

How does nicotine work?

A

Increases the firing of DA neurons through NICOTINIC receptors expressed on DA neurons
+ stimulates presynaptic cholinergic receptors = increases the amount of DA released at synapses in the nucleus accumbens

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

How to opioids and canaboids work?

A

MUI OPIOID RECEPTOR AGONISTS

  • target GABAergic interneurons in the VTA and decrease their activity
  • hence take off the effect the INHIBITIOn which is on the DA neurons in the VTA.
  • :. get reward because they inhibit the GABA neurons which usually act to inhibit DA release in the nucleus accumbens
  • why the GABAergic neurons are targeted may be due to mu opioid receptors expression on gaba but not on DA neurons or GABAergic neurons may be more SENSITISED than DA neurons.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are Benzodiazapines used for?

A
  • Anxiety and sleeping disorders
  • can be used in epilepsy
    CHRONIC DRUG USE CAN LEAD TO ADDICTION
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do Benzodiazapines work?

A

Bind to GABAa receptors, potentiating the inhibitory effect of GABA
Interneurons normally INHIBIT the activity of DA neurons in the VTA
Hence potentiation of GABA causes silencing of interneurons- ie. disinhibition.
Indirectly increases activity.
Lead to addiction - addiction takes a long time to “unwind”

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

What is Zolpidem (stillnox) & how does it work?

A

Zolpidem (Stillnox) is used in insomnia and other brain disorders
It is a SHORT ACTING non-benzodiazapine hypnotic that potentiates GABA by binding GABAa receptors at the same location as benzodiazapines.
- TGA 2008: warning- used for sleep.
- Zolppidem may be associated with potentially complex sleep related behaviours which may include sleep walking, sleep driving and other bizarre behaviours.
- Reccomended doses be reduced by 2-% in 2013 because of next morning alertness impairment

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

Explain some of the changes psychostimulants such as COCAINE and AMPHETAMINES have to the CNS.

A

Psychostimulants induce neuroplasticity:- cocaine and amphetamines increase spine density & dendritic branches
: on medium spiny GABAergic neurons within the shell & core of th Nucleus Accumbens
: Glutamatergic pyramidal neurons within the PFC
-> some changes evident within 24 hours after drug administration. & persist for 3-4 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does repeated exposure to METHAMPHETAMINES CAUSE?

A
  • Drug craving and relapse
  • Long term persistent synaptic changes that persist long after drug withdrawal.
    : Normalised after drug re-administration
  • Methamphetamine causes a DA release
    : 10 day administration –> long lasting depression at corticostriatal terminals
    : relieved by drug readministration
    : both processes are due to alteration in dopamine and cholinergic receptor systems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Overview:
How do you treat alcohol addiction?
Short term?
Long term- drug names

A

Short term: Diazepam & VB12
Acamprosate: + psychological, physical support
Naltrexone - high compliant, no chronic pain
Disulfiram - can kill

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

ACAMPROSATE: indications

A
  • maintenance of abstinence in patients with alcohol dependence. Must have additional psychological and physical support.
  • should be commenced 1 week after drinking stops
  • May prove to be effective for treating other psychomotor stimulant and opiate activity
  • Long term benefits are unclear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ACAMPROSATE: Pharmacodynamics

A

Mixed antagonist of NMDA and mGLuR5 glutamate receptors

  • decreases glutamatergic transmission and modulates neuronal hyperexcitability during withdrawal from alcohol.
  • Reduces neuronal hyperexcitability characteristic of alcohol withdrawal
  • Reduces alcoholic craving in some people
  • Some of these people remain abstinent, others drink less alcohol.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ACAMPROSATE: pharmacokinetics

A

Contraindicated in significant hepatic or renal impairment (decrease dose)
= diarrhoea, rashes, abdo pain, nausea and vomitting.

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

NALTREXONE:

indications

A

Used for alcohol and opiate withdrawal/ use disorder.
Most effective in:
- patients with a hx of binge drinking
- patients who have been drinking heavily for less than 20 yrs
- those who have a stable social support

  • TO PREVENT RELAPSE: some evidence it may be more efficacious to combine with acamprosate.
17
Q

NALTREXONE -alcohol

Pharmacodynamics

A

Naltrexone blocks the effects of endogenous opioids (enkephalins and endorphins are released following alcohol administration)
- Competitively inhibits all opioid receptors
:: pure opioid antagonist!
- If you drink whilst on Naltrexone, you will feel less pleasurable effects, but alcohol induced impairment remains
- Reduced cravings, reduced consumption and reduced relapse rates (for some, not all)

18
Q

NALTREXONE- alcohol

Pharmacokinetics

A

Long acting

  • because naltrexone blocks the effect of opioid analgesics, it is contraindicated in acute/chronic pain
  • IT will take them into withdrawal
19
Q

DISULFIRAM:

Indications

A
  • Use in highly motivated, compliant patients
  • Should not be commenced unless patient fully understands the risks and has not consumed alcohol in the previous 24 hours. Doses should be dispensed under the supervision of a clinic or trusted person.
20
Q

DISULFIRAM:

Pharmacodynamics

A
  • Blocks alcohol METABOLISM by blocking ACETALDEHYDE breakdown
    Unpleasant, potentially serious side effects if alcohol is consumed.
21
Q

DISULFIRAM:

Pharmacokinetics

A
  • Accumulation of acetaldehyde leads to:
    : intense flushing, sweating, palpitations
    : associated steep rise in BP followed by Hypotension
    : Severe reactions may have an affect on the heart, or be associated with convulsions and loss of consciousness.
    : Occasionally death from cardio respiratory failure
  • Metabolism varies a lot- individual variation
    : Patients cannot drink alcohol on it
    : Some will react to very small amounts of alcohol, others have little reaction despite consuing large amounts of alcohol.
    : Patients should be warned about the dangers of consuming alcohol whilst taking this, and to remain abstinent 1 week after stopping treatment
22
Q

How do we currently treat OPIOID ADDICTION?

A

Naltrexone
Methadone
Buprenorphine

*there are some clinical issues WRT opioid addiction.The biopsychosocial model of pain is based on the premise that chronic pain and the experience of pain is grounded in & influenced by biological, psychological and social factors. Childhood experiences are risk factors for a range of other problems- personality disorder, depression, PTSD, and substance use disorders- that are likely to interfere with the treatment of chronic pain

23
Q

NALTREXONE

Opioid Addiction indications

A

Opiate abuse- if administered to someone physically dependent on opioids it precipitates a severe withdrawal reaction
: dependent users must go through a gradual withdrawal program first
> perform a naxolone challenge to confirm that the person is absitinent from opioids: withdrawal signs- pilorection, rhinorrhoea, sweating, restlessness, vomiting
> wait a further 24 hours before drug administration

: Implants are being considered for treatment in opioid dependence



24
Q

NALTREXONE: opioid abuse

Pharmacodynamics

A

Naltrexone blocks the effects of endogenous opiioids (enkephalins and endorphins are released following alcohol admin) -> pure opioid antagonist.

  • Naltrexone may accelerate the loss of tolerance that occurs with abstinence from opioids
  • Use of opioid agonists after naltrexone cessation may place the person at high risk of overdose
25
Q

METHADONE

indications

A

SHORT TERM treatment of opioid withdrawal
LONG TERM substitution for heroin and other opioids:
- it has the advantages of high acceptability, particularly in comparison to withdrawal and abstinence based approaches, and proven effectiveness in reducing illicit opioid use.
- thought to be easier to wean an addict off methadone in comparison to heroin or morphine

26
Q

METHADONE

Pharmacodynamics

A
  • Orally active opioid (synthetic opioid, longer half life compared to morphine)
  • Removing the need for IV administration- administration within the clinic settings
27
Q

METHADONE

Pharmacokinetics

A

Schedule 8 drug - can be as dangerous as heroin.
Half life: varies 15-60 hours
- Duration of action: 4-6 hours, although with repeated oral dosing it may extend to 72 hours (takes several days to reach steady state)
: : Widely distributed in the plasma. Protein binding 60-90%.
:: autoinduction of metabolism- shorter half & tolerance

ADVERSE REACTION PROFILE:: no different to the other opioids
: euphoria, CNS and respiratory depression, GI, CV disturbances, spasm of biliary and renal tract smooth muscle
: tolerance meanst hat most people can usually resume a normal lifestyle and work patterns within a few weaks
: men: decrease in fertility and gynecomastia may develop
: additional effects with other CNS depressants

28
Q

BRUPRENORPHINE

Indications

A
  • Opioid withdrawal
    :: compared to methadone - lower risk of overdose, less dependence
  • Can also be used in pain
29
Q

BRUPRENORPHINE

Pharmacodynamics

A

PARTIAL opioid agonist- effective in reducing illicit opioid use- Dose determined demending on recent opioid usage of individual : may precipitate withdrawal syndrome if they have had a recent large dose of opioids.
: can be reversed with high doses of NALTREXONE
: will block the effects of OPIOID analgesics***

30
Q

NICOTINE addiction- what do we use

A

Nicotine replacement reduces the severity of tobacco withdrawal symptoms and increases the likelihood of smoking cessation
BUPROPION
VARENICLINE

31
Q

BUPROPRION:

info

A

Possible action due to its inhibition of neuronal reuptake of dopamine and NA,
*can worsen psychiatric conditions

32
Q

VARENICLINE:

info

A

Blocks nicotine binding to neuronal nicotine acetylcholine receptors, preventing the pleasurable effects of smoking, partial agonist activity reduces symptoms of withdrawal- post marketing reports of worsening psychiatric conditions

33
Q

Describe the APPROACH TO ADDICTION

A

• Precontemplation
: : No thoughts about changing behaviour
• Contemplation
: : Thoughts about the need to change but no action yet taken
• Preparation
: : Ready to take action
• Action
: : Attempts made to change behaviour & avoid environmental triggers
• Maintenance
: : Behaviour has been changed & the person is adjusting to these changes & working to prevent relapse

Pharmacology CAM202 & 304 (5 decks)

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