Pharmacology Substance Abuse I-X

Front 1

What drug is used for the treatment of nicotine dependence?

Back 1

Bupropion

Front 2

Bupropion

Back 2

-Antidepressant with weak inhibition of NE and serotonin reuptake
-Produces dose-related stimulant effects
-Seizure risk -- avoid in patients with previous seizures and with eating disorders

Front 3

Describe the absorption of cocaine in the GI tract

Back 3

-Bioavailability: 20-30%
-Tmax: 45-60min
-First pass hepatic metabolism of 70-80% of dose
-Low rate of addiction due to slowly rising blood levels

Front 4

Describe the absorption of cocaine intranasally

Back 4

-Low bioavailability (20-30%)
-Tmax=10-30min
-Effects fade by 45-60min

Front 5

Describe the anesthetic applications of cocaine

Back 5

Cocain is a local anesthetic. It can block conduction of the nerve impulse by decreasing the Na current

Front 6

Describe the mechanism of the CV effects of cocaine

Back 6

Acts on peripheral autonomic nerves to prevent reuptake of NE and dopamine and can potentiate the response of peripheral autonomic effectors to sympathetic activation.

Front 7

Describe the mechanism of the main effect of cocaine

Back 7

Domapine is released into synapses and then is taken back up into the nerve terminal by the dopamine transporter as a means of terminating the dopamine effect. Cocaine binds to the dopamine transporter to prevent reuptake and increases the amount of dopamine at the postsynaptic site. An important site of action is in the nucleus accumbens (dopaminergic neurons) which is associated with mood elevation and arousal, and reward (cocaine self-administration)

Front 8

Describe the mechanism of developing cocaine tolerance.

Back 8

The same are SRIs. There is downregulation of the receptor.

Front 9

What are the toxic effects of cocaine?

Back 9

-MI and arrhythmias
-CNS toxicity
-lung damage and pneumonia from smoking
-pregnancy complications, premature
-perforated nasal septum
-sexual dysfunction

Front 10

What agent is showing promising effect in the treatment of cocaine abuse?

Back 10

Disulfiram (beta-hydroxylase inhibitor)

Front 11

Disulfiram

Back 11

Beta-hydroxylase inhibitor
For treatment of cocaine abuse

Front 12

What is the mechanism of action for amphetamines?

Back 12

Blocks dopamine reuptake and enhances dopamine release into the synapse. It enhances the synaptic activity of serotonin and NE.

Front 13

Compare the toxicity of cocaine and amphetamine

Back 13

The enhanced dopamine release of amphetamines renders them,. especially methamphetamine, more neurotoxic than cocaine

Front 14

Describe the reinforcing effect of amphetamines

Back 14

These depend on dopaminergic neurons in the mesencephalic VTA

Front 15

Describe the administration, pharmacokinetics, and tolerance of amphetamines

Back 15

-Available as pills, liquid, or powder. Most commonly oral or IV. Smokable "ice" available
-Produce longer lasting effects than cocaine: 6-24 hours.
-Tolerance to euphoric effect, no tolerance to psychomimetic effect

Front 16

Describe the mechanism of heroin

Back 16

-Heroin quickly crosses the BBB
-Converts to monoacetyl morphine
-Morphine binds the mu, kappa, and delta receptors

Front 17

What are benzodiazepines for in opioid withdrawal?

Back 17

-Insomnia
-Anxiety
-Muscle spasm (clonazepam, oxazepam more commonly used)

Front 18

What are NSAIDs for in opioid withdrawal?

Back 18

Muscle and bone pain (ketrolac, oral NSAIDs)

Front 19

What are alpha-2 agonists for in opiod withdrawl?

Back 19

-Reduce sympathetic hyperactivity by feedback inhibition of presynapic neurons
-Clonidine

Front 20

Clonidine

Back 20

An alpha 2 agonist useful for opioid withdrawal

Front 21

What are the agonists available for maintenance in opioid substance abuse treatment?

Back 21

-Methadone
-LAAM

Front 22

What mixed agonist-antagonists are available for opioid treatment?

Back 22

Buprenophine

Front 23

Buprenophine

Back 23

A mixed agonist-antagonist for opioid addiction treatment
-Partial agonist at mu receptor and kappa receptor antagonist
-Gives less adverse effects
-High affinity for mu receptors - displaces morphine and methadone
-Difficult for naloxone to displace buprenorpine and precipitate withdrawl
-Can be given every other day
-Metabolized by CYP3A4

Front 24

What are CYP3A4 inhibitors

Back 24

-SSRIs
-Anti-infectious agents
-Ca channel blockers
-Retrovirals
-Grapefruit juice

Front 25

What are CYP3A4 inducers

Back 25

-Antiepileptics
-Anti-Tb agents

Front 26

What is the ORL-1 receptor

Back 26

-Opiate like receptor
-May account for much of buprenorphines unique features

Front 27

Describe the abuse potential of buprenorphine in non-dependent opioid users

Back 27

-Produced euphoria IV, not blocked by naloxone
-Less euphoria sublingual because of slower onset

Front 28

Describe the abuse potential of buprenorphine in dependent opioid users

Back 28

Effect depends on:
-Level of physical dependence
-Time interval between agonist and buprenorphrine
-Amount of acute buprenorphine dose

Front 29

Naltrexone

Back 29

Antagonist maintainance drug for opioid abuse treatment
-Mu antagonists - blockes effects of opiates and in physically dependent individuals will precipitate withdrawals. Need to be off short acting opiates at least 5-7 days
-Oral tablet, depot lasts 1 month
-High dropout rate
-Works best for those with extended pressure

Front 30

What are the nonpharmacological treatments for opioid addiction

Back 30

Therapeutic commuinity
-24 h/d
-9,18,24 months
--Remedy social, economic, educational deficits
-Long lasting improvements in functioning
-High drop out rate