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Drug Action III > Drugs of Substance Abuse (Pharm) - Block 3 > Flashcards

Drugs of Substance Abuse (Pharm) - Block 3 Flashcards

1
Q

What drug is the costliest of all SUDs?

A

Alcohol

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2
Q

SUDs with the highest mortality rate?

A

Smoking (Nicotine)

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3
Q

SUDs where its dependency is rapidly growing?

A

Opioid

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4
Q

What are the psychoactive drugs that change conscious awareness and perception?

A

Depression: slow down the NS
Stimulants: speed up the NS
Narcotics: relieve pain
Hallucinogens: alter sensory perception

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5
Q

What is drug abuse?

A

Maladaptive pattern where there are repeated adverse consequences related to continual ue of the substance

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6
Q

What is addication?

A

Primary, chronic, neurobiological dx (substance use disorder)

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7
Q

What is tolerance?

A

When the body’s exposure to a drug causes changes (lessening of effect over time)

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8
Q

What is the diference between dependence and SUD?

A

Dependence: physical, will occur with chronic exposure
SUD: psychological, occurs in small percentage of population

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9
Q

What is tolerance?

A

With repetitive exposure dose has to be increased to maintian reward or analgesic

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10
Q

Drugs of abuse induce strong feelings of ____?

A

Euphoria and reward

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11
Q

What is metabolic tolerance?

A

Induction of enzymes that metabolizes the drug -> increased rate and lower AUC (barbiturates and ethanol)

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12
Q

What is functional tolerance?

A

Adaptive changes in brain and neurons to offset chronic effects of drug administration (altered levels of neurotransmitters, altered receptors, or regulation of expression of various genes)

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13
Q

What is cross-tolerance?

A

Two drugs produce similar pharm effects by similar mechanisms, tolerace developed to one can be conferred to the other (even if the subject has not been exposed to the second drug)

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14
Q

What is withdrawal?

A

When abused drug is no longer available: Sx of dependence is relieved by another dose of the drug (pattern of negative reinforcemnt)

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15
Q

Because of SUD, even after withdrawal and prolonged drug-free periods, pateints are at ___?

A

High risk of relapse

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16
Q

How does SUD develop?

A

Triggered by re-exposure to drug -> when paired with drug use (may undergo switch and motivate SUD-related behavior) -> Pharm stimulation of mesolimbic dopamine system -> strong larning signal

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17
Q

How does environment and genetics trigger SUD?

A
  1. Impulsivity or excessive anxiety
  2. Childhood trauma and early drug use
  3. Neurobiological basis of SUD can be inheritied
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18
Q

What are the SUD behaviors?

A

Includes ≥ 1 of the 5 Cs:
1. Chronicity
2. Imparied control over substance use
3. Compulsive use
4. Continued use despite harm
5. Craving

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19
Q

What is the DSM-5 diagnostic criteria for SUD?

A

≥2 of the following, within a 1-year period:
1. Substance taken in large amounts
2. Persistant desire and lack of control
3. Cravings
4. Significant time spent from substance use
5. Recurrent use leads to failure in obligations
6. Social problems fro use
7. Decreased involvement in important activites
8. Continued use leads to physical harm
9. Use continued despite having recurrent/persistent physical/psychological problem due to substance

Tolerance and withdrawal

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20
Q

What is the clinical course of SUD?

A
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21
Q

What is the mechanism of drug abue?

A

Mesolimbic dopamine system = main target of all addictive drugs (reward circuit: motivational system that regulats responses to natural reinorces)

Originates in ventral tegmental area (VTA): dapamine producing neurons fire bursts -> release large quantities of dopamine in nucleus accumbens (NAc) and prefrontal cortex

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22
Q

Phasic dopamine release may be what?

A

Prediction error of reward

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23
Q

Dopamine neurons in VTA are most efficiently activated by?

A

Non-anticipated reward

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24
Q

People with drug abuse develop?

A

A strong but inappropriate learning signal that hijack the reward system and lead to pathologic reinforcement -> increase dopamine even when reward is exected -> overridingof prediction error signal may be responsible for usuring of memory processes

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25
Types of drug abuse are based on what binding mechanisms?
1. Gio protein-coupled receptors: nhibit neurons through postsynaptic hyperpolarization and presynaptic regulation of transmitter release 2. Ionotropic receptors or ion channels 3. Dopamine transporter
26
What are the cellular mechanisms that increase dopamine?
1. Direct stimulation of dopamine neurons 2. Interferene with reuptake of dopamine or promotion of nonvesicular release 3. Inhibit GABA neurons that act as local inhibitory interneurons (indirect method)
27
Neuroadaptation/Neuroplasticity mechanism?
28
What is neuroplasticity?
Induction of transcription factor **ΔFosB**: 1. Alters gene expression to strengthen pathways that link memories of drug taking with reward -> **heightened memories of past drug experiences** 2. Induces increased dendritic spines -> increases connections and amplifies signals between cells 3. During protracted abstinence to drugs, contributes to **sensitized response to drug re-exposure**
29
What contributes to drug sensititvity and memory of drug use?
Nucleus accumbens neurons increases the risk of relapse due to ΔFosB
30
What is Synaptic Plasticity?
Long-term potentiation (LTP) and long-term depression (LTD) = forms of experience-dependent synaptic plasticity: 1. Induced by activating glutamate receptors (NMDA type) 2. Enhances synaptic efficacy and triggers formation of new connections 3. If presynaptic and postsynaptic not correlated well -> LTD 4. Modulated by dopamine
31
What is the difference between D1R and D2R expressing cells?
**D1R-expressing cells** – dopamine presence favors LTP **D2R-expressing cells** – dopamine presence -> inhibits LTP
32
What causes drug-evoked synaptic plasticity?
Drugs of abuse interfere with LTP and LTD at sites of convergence of dopamine and glutamate projections
33
What imaging studies reveals substance abuse?
**MRI:** structural abnormalities **fMRI, PET, SPECT:** functional abnormalities
34
What drugs cause disinhibition of dopamine neurons?
Drugs That Activate Gio-Coupled Receptors
35
MOA of µ opioids?
inhibition of GABAergic inhibitory interneurons in VTA -> disinhibition of dopamine neurons
36
Characteristics of opiods?
1. Strong tolerance and dependence 2. Severe withdrawal syndrome
37
What is the reversal agent for opiods?
Naloxone but can also provoke withdrawal syndrome in dependent patients
38
In order tx SUD, opiods are substituted for what agents?
Longer acting opioid (i.e. methadone, buprenorphine, Morphine ER) substitute shorter and more rewarding opioids
39
Drawbacks of using short acting opioids?
**Methadone:** abrupt terminal -> wthdrawal syndrome **Buprenorphine:** partial agonist -> inhibition of GABAergic inhibitory interneurons in VTA -> disinhibition of dopamine neurons **Lecomethodone:** only active enantiomer with lower ADRs
40
What is the major constituent of MJ? Characterisitcs?
Δ9-THC 1. Tolerace develops 2. Acts on CB-1 (brain) and 2 (periphery): disinhibition of dopamine neurons form inhibition of GABA neurons
41
Effects of cannabinoids?
Eupharia, relaxation, altered perception of passage of time, dysphoria state at high doses, memory and learning impairments
42
Chronic cannabinoids exposure leads to?
Dependence: mild and short lived withdrawal syndrome (Restlessness, irritability, mild agitation, insomnia, nausea, cramping)
43
What are hallucinogens?
Single doses changes in thoughts, mood, and perception that is nonaddicting
44
Why is are hallucinogens nonaddicting?
Doesn't cause reward and euphoria because it does not stimulate dopamine release (still produces tolerance)
45
What are the types of effects of LSD?
**Perceptual:** heightened hearing, visuals) **Psychic:** alterations in mood, depersonalization, visual hallucinations, altered sense of time) **Somatic:** N, blurred vision, DZ, parasthesias)
46
Main target of LSD?
5-HT2A receptor: very potent hence iven on blotter paper
47
Drugs that activate Gio coupled receptors?
1. Opioids 2. Cannabinoids 3. Hallucinogens 4. LSD
48
Drugs that act through inotropic receptors?
1. Nicotine 2. Alcohol 3. PCP 4. Inhalants
49
What is the most prevalant form of SUD?
Nicotine
50
Nicotine MOA?
Selective agonist of nAChR: releases dopamine in nucleus accumbens and prefrontal cortex
51
Nicotine withdraw sx?
Mild: irritability, insomnia, HA
52
What is the tx for nicotine abuse?
Slowly absorbed nicotine forms (chewed, inhaled, TD): 1. Varenicline (paritial agonist of nAChR): impair driving and cause suicidal ideation 2. Bupropion
53
Alcohol MOA?
Including GABAA receptors, Kir3/GIRK channels, adenosine reuptake (through ENT1), glycine receptor, NMDA receptor and 5-HT3 receptor: Increase dopamine release from mesolimbic reward system
54
Sx of alcohol withdrawls?
Hand tremos, N/V, sweating, agitation and ax (12-24 hr) Alcohol withdrawal delirium (delirium tremens) in 48-72 hr
55
Supportative tx for alcohol?
BZD
56
What is korsakoff syndrome?
Long term alcohol can kill brain cells -> loss of gray matter from temporal lobes and memory problems
57
Alcohol abuse is often part of ___?
Polydrug abuse
58
Medications used for alcohol dependence?
1. Disulfiram 2. Acamprosate 3. Naltexone
59
Disulfiram | MOA
**MOA:** Irreversible inhibition of aldehyde dehydrogenase (higher aceraldehyde concentrations) - reacts with sulfhydryl groups on proteins
60
Acanprosate | MOA
**MOA:** can take with alcohol and reduce cravings (less DDI than disulfiram) * Can also use gabapentic
61
Naltrexone | MOA
Opioid antagonist that can be taken with alcohol: Opioids modulate rewarding effects – antagonism reduces dopamine release when alcohol is consumed **DDI:** opioids
62
PCP | MOA
**MOA:** Noncompetitive NMDA antagonist like ketamine * Psychotomimetic – produces schizophrenic-like effects (ultimately can be long-lasting): effects on dopaminergic systems **Tolerance can develop but not halucinogenic**
63
Types of inhalants?
Nitrates, ketones, hydrocarbons
64
Inhalents | ADR
Huffing, sniffing, bagging **ADR:** euphoric, toxic effects from chronic exposure
65
How do you manage OD of inhalents?
Supportive
66
Drugs that bind to biogenic amine transporters?
1. Cocaine 2. Amphetamines 3. Ecstasy
67
Cocaine | MOA
**MOA:** Active via every route of administration that Blocks reuptake of DA through DA transporter. Increases dopamine concentrations in nucleus accumbens **DOsing:** insufflation, IV, smoking (freebase) **Characterisitcs:** Highly addictive (strong cravings) - dependence, tolerance, withdrawal sx (reverse tolerance) * Shorter acting and more intense
68
Management for cocaine intoxication?
Supportive
69
Amphetamines | MOA, ADR
**MOA:** Indirect-acting dopaminergic and noradrenergic agonist that can increase in DA and NE synaptic concetrations **ADR:** amphetamine psychosis from dopamine, neurotoxucm, tolerance and withdrawal **Form:** IV and SUD
70
Describe the potency of amphetamines?
Adding almost anything to amphetamine structure reduces potency - except methyl group on amine (meth)
71
Amphetamine withdrawal sx?
Dysphoria, drowsiness, irritability
72
What SAR of amphetamine?
Methamphetamine is more potent than amphetamine: if methylate MDA should be more potent and lowe hallucinogens like effects
73
Term for nonamphetamine like?
Empthogen
74
Ecstacy? | MOA, ADR, Withdrawal
**MOA:** Causes release of biogenic amines by reversing actions of transporters (especially seratonin) **ADR:** hyperthermia with dehydration can be fatal, seratonin syndrome, sz **Withdrawal:** mood offset, depression, aggression
75
What is the tx for SUD?
No pharm tx efficiently eliminates SUD however can alleviate withdrawal syndrome
76
What is a normal part of SUD recovery?
Relapses
77
What is used of pharm antagonism?
Naltrexone
78
What is used to reduce cravings?
Acamprosate
79
What is used for drug sub (legal and less reinforced drugs)?
1. Methadone 2. Buprenorphine 3. Morphine ER
80
What is used as an aversive compounds?
Disulfiram

Drug Action III (23 decks)

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