Drugs Of Abuse Flashcards

1
Q

What are the four core behaviors that define substance use disorder (SUD) according to DSM-5?

A
  1. Impaired control over drug use
  2. Compulsive use
  3. Continued use despite harm
  4. Craving
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2
Q

Which brain system is central to the drug-induced reward response and addiction cycle?

A

The mesocorticolimbic dopamine pathway, which includes the ventral tegmental area (VTA), nucleus accumbens, and prefrontal cortex.

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3
Q

What are the primary functions of the mesocorticolimbic dopamine pathway in addiction?

A

It mediates reward, motivation, salience of stimuli, and reinforcement, contributing to the craving and relapse cycle.

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4
Q

What is the Controlled Substances Act (CSA), and what does it regulate?

A

Enacted in 1970, it is U.S. federal policy for classifying substances with abuse potential into Schedules I–V, regulating their manufacture, distribution, and possession.

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5
Q

What defines a Schedule I drug under the CSA?

A

No accepted medical use in the U.S. and high potential for abuse. Examples: heroin, LSD, marijuana, MDMA, DMT, mescaline, psilocybin.

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6
Q

What is cocaine’s mechanism of action that contributes to its addictive potential?

A

Cocaine inhibits reuptake of dopamine, serotonin, and norepinephrine by binding to their transporters (especially DAT), increasing synaptic levels.

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7
Q

What are key CNS and cardiovascular toxicities of cocaine?

A

• CNS: seizures, psychosis, depression, hemorrhage
• CV: tachycardia, vasoconstriction, MI, arrhythmias, sudden death from cardiac arrest

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8
Q

What is the “crash” phase in cocaine withdrawal and when does it occur?

A

Occurs within 1–4 days after cessation. Characterized by anxiety, anhedonia, hyperphagia, and hypersomnolence.

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9
Q

What is the pharmacologic action of amphetamines that makes them addictive?

A

Amphetamines release dopamine and norepinephrine from presynaptic vesicles, and reverse the dopamine transporter (DAT), flooding the synapse with DA.

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10
Q

What are subjective and peripheral effects of amphetamines?

A

• CNS: euphoria, alertness, exhilaration
• Peripheral: increased BP, respiration, tachycardia, mydriasis, and sweating

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11
Q

What are common chronic effects of amphetamine or methamphetamine abuse?

A

Tachyphylaxis, psychosis (paranoia, hallucinations), aggression, anorexia, insomnia, poor dentition (“meth mouth”), and memory impairment.

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12
Q

What dental risks are associated with chronic methamphetamine use?

A

Xerostomia, bruxism, tooth decay, gum disease, and poor hygiene—together called meth mouth due to acidic drug, dry mouth, and high sugar intake.

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13
Q

What is MDMA (ecstasy), and how does it act in the brain?

A

A synthetic amphetamine analog that releases serotonin, dopamine, and norepinephrine, especially 5-HT, producing stimulant and empathogenic effects.

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14
Q

What are short-term effects of MDMA (ecstasy)?

A

Increased empathy, sociability, sensory enhancement, euphoria, mild hallucinations, jaw clenching, hyperthermia, and hyponatremia due to excess water intake.

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15
Q

What are long-term effects or risks of MDMA use?

A

Serotonin depletion, depression, memory loss, and risk of serotonin syndrome—especially when combined with SSRIs or MAOIs.

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16
Q

What is the pharmacologic action of nicotine?

A

Agonist at nicotinic acetylcholine receptors (nAChRs) in the CNS and peripheral ganglia, stimulating dopamine release and autonomic responses.

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17
Q

Why is nicotine highly addictive?

A

It causes rapid dopamine release in the nucleus accumbens, reinforcing behavior. Its short half-life and frequent dosing maintain addiction.

18
Q

What is the mechanism of action of varenicline (Chantix) for smoking cessation?

A

Partial agonist at α4β2 nAChRs—reduces nicotine cravings and blocks its reinforcing effects.

19
Q

What is bupropion’s role in smoking cessation?

A

An atypical antidepressant that inhibits norepinephrine and dopamine reuptake, helping reduce withdrawal symptoms and cravings.

20
Q

What is the difference between classical hallucinogens and dissociative anesthetics?

A

Classical hallucinogens (e.g., LSD, psilocybin) act via 5-HT2A receptor agonism; dissociative anesthetics (e.g., PCP, ketamine) act via NMDA antagonism.

21
Q

What is the mechanism of action of LSD?

A

Partial agonist at 5-HT2A receptors, especially in the cortex, altering perception, time sense, and cognition.

22
Q

What are acute effects of LSD and other classic hallucinogens?

A

Sensory distortion, visual hallucinations, synesthesia, altered time perception, mydriasis, and possible panic or paranoia.

23
Q

What are “flashbacks” and how are they related to LSD?

A

Recurrent perceptual symptoms (hallucinations or distortions) that occur after the drug has worn off—called hallucinogen persisting perception disorder (HPPD).

24
Q

What is phencyclidine (PCP), and what is its mechanism of action?

A

A dissociative anesthetic and NMDA receptor antagonist causing hallucinations, agitation, aggression, and analgesia.

25
What is a key distinguishing feature of PCP intoxication?
Nystagmus (especially rotary), violent behavior, analgesia, and high pain tolerance with possible psychosis or seizures.
26
What is ketamine and how does it act in the brain?
A dissociative anesthetic that acts as a noncompetitive NMDA receptor antagonist, producing out-of-body experiences, hallucinations, and analgesia.
27
What are medical uses of ketamine?
Used for anesthesia, treatment-resistant depression, and acute pain. Known for maintaining airway reflexes and BP, unlike most anesthetics.
28
What are the psychoactive and non-psychoactive components of cannabis?
THC (tetrahydrocannabinol): psychoactive, binds CB1 receptors; CBD (cannabidiol): non-psychoactive, modulates THC effects.
29
What receptors does THC bind to, and where are they located?
THC binds CB1 receptors (CNS: basal ganglia, cerebellum, hippocampus) and CB2 receptors (immune system, periphery).
30
What are short-term effects of cannabis use?
Euphoria, relaxation, altered time perception, impaired memory, increased appetite, tachycardia, dry mouth, conjunctival injection (red eyes).
31
What are the long-term effects of heavy cannabis use?
Cognitive impairment, amotivational syndrome, dependence, bronchitis, and possible increased risk of psychosis in vulnerable individuals.
32
What are inhalants, and how do they exert their effects?
Volatile solvents (e.g., glue, paint thinner) that are inhaled and enhance GABAergic transmission or antagonize NMDA receptors, leading to euphoria and CNS depression.
33
What are risks and signs of inhalant abuse?
Sudden sniffing death syndrome, arrhythmias, brain damage, dermatitis, chemical odor on breath/clothes, and perioral rash.
34
What is gamma-hydroxybutyrate (GHB), and what are its effects?
A CNS depressant and GABA-B receptor agonist used illicitly as a “date rape” drug; causes euphoria, sedation, anterograde amnesia, and respiratory depression.
35
Why is GHB considered dangerous despite being naturally occurring?
It has a narrow therapeutic window, causes profound CNS depression at high doses, and is involved in sexual assault cases due to amnestic effects.
36
Which drug of abuse is most associated with reinforcing effects via dopamine release in the nucleus accumbens?
Virtually all drugs of abuse, but cocaine, amphetamines, nicotine, and opioids are strongest in this regard.
37
What is the general role of dopamine in addiction?
Dopamine mediates reward prediction, reinforcement, and motivation, driving drug-seeking behavior via the mesolimbic pathway.
38
What is drug tolerance, and how does it develop?
A decrease in drug response after repeated use, due to receptor downregulation, enzyme induction, or neuroadaptation.
39
What is drug sensitization and how does it differ from tolerance?
Increased response to a drug after repeated use, often seen in psychostimulants—opposite of tolerance.
40
What are common signs of substance use in the dental setting?
Poor oral hygiene, bruxism, xerostomia, rampant caries, meth mouth, delayed healing, erratic behavior, and missed appointments.