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Pharm > Drugs of abuse II > Flashcards

Drugs of abuse II Flashcards

1
Q

What are the clinical uses for benzos?

A

Anxiety, sleeping disorders, convulsions etc

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2
Q

What is the MOA of benzos?

A

Positive modulators of GABA-(A) receptors (increased Cl influx)

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3
Q

How do benzos cause the euphoric effect in the brain?

A

Inhibit the inhibitory interneurons that connect to dopaminergic neurons

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4
Q

Why don’t benzos also affect the dopaminergic neurons in the VTA of the brain, since these neurons also have GABA-(A) receptors?

A

These receptors lack the alpha subunit, and are thus less responsive.

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5
Q

What are the two most commonly abused benzos?

A

Diazepam

Alprazolam

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6
Q

What is the “date rape” drug?

A

Flunitrazepam

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7
Q

What is Flunitrazepam?

A

Roofies

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8
Q

What is the antidote to benzos? MOA?

A

Flumazenil–GABA-(A) receptor antagonist

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9
Q

Why aren’t barbiturates usually abused? Which one is usually abused?

A

Low margin of safety

Pentobarbital

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10
Q

What is the MOA of barbiturates? How do these produce the increased dopamine in the VTA?

A

GABA-(A) receptor agonist

Inhibit inhibitory interneurons

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11
Q

What is the street use for gamma-hydroxybutyric acid (GHB)?

A

Date rape drug

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12
Q

What is the MOA of GHB?

A

GABA-(B) receptor agonist on inhibitory interneurons

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13
Q

What is the relative risk of addiction for CNS stimulants?

A

5

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14
Q

What is the MOA of cocaine in the CNS?

A

Inhibits the dopamine transporter (DAT) on synaptic terminals of dopaminergic neurons, causing increased synaptic dopamine and epi levels

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15
Q

What is the MOA of cocaine in the PNS?

A

In the peripheral nervous system cocaine inhibits voltage-gated sodium
channels resulting in blocked initiation and conduction of action potentials  used as local
anesthetic.

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16
Q

What is the street name for methylene dioxy-methyl amphetamine (MDMA)?

A

Ecstasy

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17
Q

Amphetamine-like CNS stimulants are structurally similar to what endogenous molecule?

A

Epinepherine

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18
Q

What is the metabolite that the liver turns EtOH and cocaine into?

A

Cocaethylene

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19
Q

What has a longer half-life: cocaine or meth?

A

Meth, by a lot: 12 hours compared to 1 hour

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20
Q

What is the MOA of amphetamines?

A

decreased re-uptake via DAT and inhibits VMAT, causing instant release of dopamine

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21
Q

What are the major adverse effects of CNS stimulant abuse?

A

MI

Cerebrovascular hemorrhage

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22
Q

What is the generic name for ritalin? MOA?

A

Methylphenidate

Amphetamine

23
Q

What is the MOA of MDMA?

A

Causes the release of 5HT vira the serotonin transporter (SERT)

24
Q

What are the side effects of MDMA?

A

Hyperthermia
Dehydration secondary to all night dance party

Hyponatremia if too much water

25
Q

What are the long term effects of MDMA use?

A

Neurological problems d/t permanent serotonin depletion

26
Q

What are the long term effects of psychostimulant use?

A

Paranoid schizophrenia

27
Q

What is the relative risk of addiction with psychedelics (hallucinogens)?

A

1

28
Q

What is lysergic acid diethylamide (LSD)?

A

Ergot alkaloid

29
Q

What are the eye findings of LSD use?

A

Dilation

30
Q

What is psilocybin? MOA?

A

Hallucinogenic found in mushrooms. Converted into psilocin.

31
Q

What is the MOA of hallucinogens?

A

Increased glutamate release in the cortex, via thalamic excitation, and targeting of 5HT-2 receptors.

32
Q

What is the major risk with hallucinogenic use?

A

Risk to self and others

33
Q

What are the 5HT-2 receptor G protein?

A

Gq

34
Q

What are the flashbacks with hallucinogens?

A

Reproduction of visual effects of prior LSD trips years after use

35
Q

Why do hallucinogens pose such a low addictive rate?

A

Not much effect on dopamine release in the VTA

36
Q

What are the four hallucinogenic drugs?

A

LSD
Psilocybin
Ketamine
PCP

37
Q

What is the MOA of ketamine?

A

Block the NMDA type glutamate receptors in the cortex and limbic system, causing a decrease of excitation in these areas

38
Q

What is the MOA of PCP?

A

Block the NMDA type glutamate receptors in the cortex and limbic system, causing a decrease of excitation in these areas

39
Q

What is the clinical use for ketamine?

A

Anesthetic

40
Q

What is the relative risk of addiction for opioids?

A

4

41
Q

What are the four most commonly abused opioids?

A

Codeine
Heroin
Morphine
Oxycodone

42
Q

What is the MOA of opioids? (2)

A

Inhibition of GABAergic neurons via activation of mu-opioid receptors in the VTA, causing euphoria

Inhibit kappa-opioid receptors, causing dysphoria

43
Q

What is the emergency antidote for opioid use? MOA?

A

Naloxone

mu-opioid receptor competitive antagonist

44
Q

What is the NON-emergency antidote for opioid use? MOA?

A

Naltrexone

mu-opioid receptor competitive antagonist

45
Q

What is methadone, and what is it used for?

A

Long acting opioid agonist (not as powerful) to reduce withdrawal symptoms

46
Q

What is opioid abstinence syndrome?

A

Opioid withdrawal

47
Q

What is codeine metabolized to?

A

Morphine

48
Q

What is the MOA of THC?

A

Inhibition of GABAergic

interneurons on dopaminergic neurons

49
Q

What is dronabinol?

A

medicinal cannabinoid approved for medical use

50
Q

What are the two synthetic cannabinoids that are approved for medical use?

A

Dronabinol

Nabilone

51
Q

What is the relative risk for addiction of the cannabinoids?

A

2

52
Q

What is the MOA of nicotine on the VTA?

A

Activates nicotinic receptors on dopaminergic neurons

53
Q

What are the two drugs used to treat nicotine addiction?

A

Bupropion

Varenicline

54
Q

What is the MOA of varenicline?

A

High-affinity nAChRs agonists

that compete for binding with nicotine

Pharm (73 decks)

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