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Pharmacology Test #6 > Substance Abuse > Flashcards

Substance Abuse Flashcards

1
Q

Physical dependence

A

withdrawal signs occur upon discontinuation; can be physically dependent but not addicted

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2
Q

Psychological dependence

A

Addiction; compulsive drug use; drug seeking, craving, despite negative consequences

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3
Q

Tolerance

A

higher doses are required to elicit the same effect, functional changes in receptors or drug metabolism; reflects adaptive changes the body has made to compensate for the drug’s presence

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4
Q

Withdrawal

A

signs of symptoms occurring as a result of drug discontinuation

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5
Q

All abused drugs active which dopamine pathway?

A

all abused drugs activate the mesolimbic DA pathway, causing release of DA in forebrain structures such as the NAc and PFC

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6
Q

How is dopamine usually used in the brain?

A

dopamine is normally used as a learning signal in the brain (signaling the difference between expected and actual reward)

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7
Q

Addiction to drugs is what type of learning?

A

maladaptive learning, often stronger than “natural rewards”

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8
Q

Precipitated withdrawal

A

pharmacologically-induced onset of withdrawal; often worse than normal withdrawal because some or all the receptors are blocked at once

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9
Q

Example of precipitated withdrawal

A

buprenorphine can induced precipitated withdrawal to opioids such as heroin

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10
Q

Conditioned withdrawal

A

withdrawal (and possible drug seeking) brought on or exacerbated by environmental cues

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11
Q

What did the controlled substance ace of 1970 establish?

A

established schedules for controlled substances

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12
Q

Alcohol used recreationally for

A

anxiolytic and euphoria

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13
Q

Other uses of alcohol besides recreationally

A

disinfectant, analgesic, organic solvents

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14
Q

How do you define alcoholism?

A

If it interferes with daily life, if you continue to do it even though it negatively impacts your life

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15
Q

Differences in distribution of alcohol between men and women

A

Men have 58% body water whereas women have 48% , so men can dilute it more and therefore drink more

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16
Q

What type of kinetics is alcohol eliminated by?

A

eliminated with zero order kinetics (constant rate)

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17
Q

Acute tolerance of alcohol

A

intoxication greater when BAC is ascending versus descending

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18
Q

Chronic tolerance of alcohol

A

greater concentrations needed to achieve desired effect

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19
Q

Fomepizol inhibits

A

Alcohol dehydrogenase (ADH)

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20
Q

Disulfiram inhibits

A

Aldehyde dehydrogenase (ALDH)

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21
Q

Fomepizol is used to treat

A

methanol, ethylene glycol poisoning

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22
Q

Disulfiram is used for

A

used for motivated drinkers; sensitizes a person to ethanol; disuades ethanol use during abstinence

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23
Q

Describe alcohol metabolism

A
  1. Ethanol is metabolized to acetaldehyde by alcohol dehydrogenase
  2. Acetaldehyde is metabolized to acetate by aldehyde dehydrogenase
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24
Q

CNS targets of alcohol

A
  1. GABA(A) receptor potentiator (hyperpolarizes neuronal membrane, inhibits firing)
  2. NMDA receptor antagonist (inhibits excitatory aa receptor)
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25
What contributes to the CNS depression, cognitive deficits and memory impairment seen with alcohol?
NMDA receptor antagonism
26
Effects of the CNS targets of alcohol
1. Mild CNS stimulation (disinhibition) 2. CNS depression 3. Cognitive impairment 4. Motor impairment 5. Coma, death
27
Acute organ toxicity from alcohol
1. CNS: sedation, ataxia, intoxication | 2. Cardiovascular: vasodilation, CV depression
28
Chronic organ toxicity from alcohol
1. CNS: tolerance, physical dependence, nerve injury 2. CV: prevent coronary disease, cardiomyopathy, arrhythmias, hypertension 3. Liver/GI: liver disease (cirrhosis) 4. Cancer: mouth, pharynx, larynx, esophagus, liver
29
Drug interactions with alcohol
1. Synergy with CNS depressants 2. Inhibits metabolism of phenothiazines, TCAs, sedative-hypnotics 3. Disulfiram 4. Acetaminophen (promotes liver damage by NAPQI)
30
Contraindications for alcohol use
1. Liver disease 2. Peptic ulcers: ethanol is a secretagogue 3. Epilepsy: ethanol changes neuronal excitability
31
Treatment of ethanol intoxication
support respiration, prevent aspiration when at 300-500 mg/dl
32
Treatment of Methanol and ethylene glycol toxicity
fomepizole or ethanol, hemodialysis
33
General treatment of alcoholism
1. Detoxification (ethanol abstinence syndrome) | 2. Psycho-social and drug therapy
34
Treatment of ethanol abstinence syndrome
1. prevent seizures, delirium, arrhythmias 2. maintain potassium, magnesium, phosphate balance 3. Thiamine to prevent Wernicke-Korsakoff syndrome 4. Substitute benzodiazepine for alcohol initially, then taper 5. Antidepressants for mood
35
Naltrexone
mu, kappa opioid antagonist; attenuates alcohol's action
36
Acamprosate
GABA system activator; NMDA antagonist; substitutes for some of alcohol's actions
37
Ondansetron
5HT3 antagonism for emesis
38
Topiramate
anticonvulsant
39
Vaclofen
GABA(b) antagonism
40
Varenicline
nAChR partial agonist
41
Endogenous cannabinoids
2-arachidonyl glycerol (2-AG) and anandamide
42
Endogenous cannabinoids involved with which processes in the body?
memory, appetite, synaptic transmission
43
How does marijuana cause euphoria?
perhaps via disinhibition of the DA system and other NT systems
44
MOA of THC
Activates CB1 receptors on VTA GABA neurons; these receptors are coupled to K+ channels, and activation of CB1 receptors increases potassium conductance in these VTA GABA neurons (inhibits GABAergic neurons)
45
What does THC inhibition of GABAergic neurons do?
because these cells normally provide tonic inhibition to neighboring DA cells, reducing their activity causes activation of DA neurons via a disinhibition mechanism
46
Nabilone
THC analog for chronic pain
47
Rimonabant
CB1 inverse agonist, appetite suppressant (withdrawn)
48
Dronabinol
synthetic THC analog, chemotherapy nausea/vomiting, weight control in AIDS
49
Perceptual hallucinations
shape, color
50
Psychotic episodes
depersonalization, hallucinations, distorted time perception
51
Somatic symptoms of hallucinogens
dizziness, nausea, paresthesias, blurred vision
52
What are hallucinogens?
a group of drugs that produce perceptual disturbances that can span the range from slightly odd to highly dangerous (psychotic)
53
Are hallucinogens addictive?
No; tolerance develops but they are typically not addictive
54
Paresthesias
tickling, tingling, burning, prickling, or numbness of a person's skin with no apparent long term physical effect
55
Lysergic acid diethylamide
LSD; 5HT2a partial agonist; psychosis possible, enhanced Glu transmission
56
MDMA
ectasy; 5HT, NE, DA releaser, 5HT syndrome possible
57
Mescaline
5HT2A partial agonist
58
Psilocybin mushrooms
5HT2A agonist; mimics 5HT
59
Phencylidine
PCP; NMDA, nAChR antagonist, D2 partial agonist
60
Ketamine
dissociative anesthetic (separation of mind and body); NMDA antagonist
61
Hallucinogen pharmacology centers on the effects of which system?
serotonin system - with a few having actions at glutamate systems as well
62
Which hallucinogens target the glutamate system
PCP and ketamine
63
MOA for opioid dependence
1. MOR activation inhibits VGCCs, reducing GABA release onto DA neurons 2. MOR activation activates GIRK channels, hyperpolarizing GABa neurons, reducing AP firing 3. disinhibition of DA transmission
64
Opioids
1. Heroin 2. Morphine 3. Oxycodone 4. Methadone 5. Buprenorphine 6. Naltrexone
65
Methadone
MOR full agonist; NMDA antagonist; chronic pain, opiate cessation
66
Buprenorphine
potent MOR partial agonist; KOR/DOR antagonist; chronic pain, opiate cessation
67
Naltrexone
MOR, KOR antagonist, alcohol and opiate cessation
68
Morphine
MOR agonist, analgesia
69
Oxycodone
MOR and KOR agent, analgesia, chronic pain
70
Heroin
schedule I illicit drug
71
Physical symptoms of opioid withdrawal
tremors, chills, perspiration, tachycardia, flu-like symptoms, vomiting, diarrhea
72
Psychological symptoms of opioid withdrawal
dysphoria, anxiety, insomnia, depression, cravings
73
Treatment of opioid withdrawal
1. Substitute long-acting, high-affinity/potency often partial agonist (buprenorphine) 2. Detoxification

Pharmacology Test #6 (12 decks)

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