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Test 2 Drugs of abuse Flashcards

1
Q

GABA and NMDA, which is inhibitory/excitatory?

A

GABA-inhibitory

NMDA-excitatory

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2
Q

What is the definition of dependece?

A

A state that develops as a result of tolerance produced by resetting of homeostatic mechanisms in response to repeated drug use

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3
Q

What is the definition of tolerance?

A

Reduction in response to the substance after repeat administrations

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4
Q

What is the definition of withdrawl?

A

Syndrome occurring when the drug administration in a physically dependent person is terminated

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5
Q

What is the definition of addiction?

A

Compulsive, relapsing drug use despite negative consequences; triggered cravings

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6
Q

When can dependence develop?

A

Anytime, even to those who are taking meds as prescribed

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7
Q

What are the two types and definitions of tolerance mechanisms?

A

Pharmacokinetics-a given dose produces lower than initial dose
Pharmacodynamics- Adaptive changes to reduce the response (Down regulation of receptors)

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8
Q

Which drugs are stimulant/hallucinaginic?

A

Cocaine, nicotine, amphetamines, cannabinooids, hallucagenics, dissociative anesthetics

CHANDa C

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9
Q

Which drugs are depressants?

A

Opiods, cannabinoids, ethanol, Benzos, barbituates, Gamma-hydroxybuteric acid

OCEBBG
BEG COB

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10
Q

Where does the VTA project to?

A

DA receptors

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11
Q

What do ALL drugs of abuse result in an increase of?

A

Net increase of dopamine in the mesolimbic pathway

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12
Q

What does the nucleus accumbans do?

A

Works with motor functioning. Allows the person to seek out the drug

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13
Q

What two drugs are considered the most addictive?

A

Amphetamines and cocaine

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14
Q

When we refer to depressant drugs, we are actually _____ the ______ pathway

A

Activating, inhibitory

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15
Q

How do Mu receptors lead to inhibition?

A

Pre synaptically- leads to inhibition of ca influx, not allowing exocytosis
Post synaptically- Causes outflux of K, causing repolarization, preventing AP

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16
Q

Abuse MOA is

A

Inhibit GABA neurons in the VTA leading to disinhibition of dopamine neurons

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17
Q

Is opiod withdraw life threatening?

A

Nah

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18
Q

What are withdraw symptoms?

A

Dysphoria, N/V, muscle aches, anxiety, sweating, diarrhea

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19
Q

How long can prolonged withdrawal syndrome last?

A

Up to 6 months

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20
Q

What is the full agonist to treat withdrawal?

A

Methadone

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21
Q

What is the partial agonist/antagonist to treat withdrawal?

A

Buprenorphine

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22
Q

What is the antagonist to overdose?

A

Narcan

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23
Q

What receptor does ethanol bind to?

A

GABA a

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24
Q

What does agonism of GABA receptor lead to?

A

increased Cl release and hyperpolarization

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25
What is the most commonly abused drug?
Alcohol
26
How much of alcohol is metabolized in the liver?
over 90%
27
What type of kinetics does alcohol have?
Zero order kinetics, a constant amount of drug is eliminated per unit of time
28
What is ethanol metabolised into?
Acetaldehyde, the toxic intermediate
29
What does the genetic variability ADH1B*2 cause?
Trouble converting ethanol to acetyladehyde
30
What does ALDH2*2 cause?
Lack of ALDH ability, so unable to covert acetaldehyde to acetate
31
What will ALDH2*2 heterozygotes do to alcohol? Homozygotes?
Will flush | Severe reactions
32
Why can men consume more alcohol safely?
More ADH in men
33
Explain the process of alcohol metabolism
Ethanol metabolized by ADH (alcohol dehydrogenase) to acetaldehyde, then broken down by acetaldehyde dehydrogenase (ALDH) to acetate
34
What is the abuse MOA of ethanol?
Increased DA release in the nucleus accumbens
35
What can chronic alcohol consumption result in? Hint, its a syndrome
Wernicke-Korsakoff syndrome
36
How does acetaldehyde affect dopamine?
It increases it
37
What are the characteristics of withdrawal syndrome of alcohol?
Hyperexcitability including seizures, psychosis, and delirium tremens
38
What is the normal MOA of benzos/barbituates?
Allosteric GABA a agonist
39
What should benzos not be combined with?
Alcohol
40
What are the drugs listed for benzos?
Alprazolam, diazepam, clonazepam, clorazepate
41
What is the abuse MOA of benzos/barbituates?
Inhibit GABA a1 neurons in the VTA, leading to disinhibition of dopamine neurons
42
What is the antagonist to benzos?
Flumazenil
43
What are the withdrawal symptoms of benzos?
Anxiety, agitation, phonophobia, photophobia, muscle cramps, sleep disturbance, dizziness At high doses, even seizures and delirium
44
What are treatment considerations for benzos?
No long term deterrent med, can give buspirone to treat anxiety
45
What is the one common use of barbituates?
Epileptics
46
What is one of the most common uses of barbituates? Not in the clinical setting necessarily
Euthanasia in animals, lethal injection, physician assisted deaths
47
What is the metabolism for barbituates?
CYP inducer
48
What are some concerns with barbituates, given its metabolistic pathway?
Its a CYP inducer, so many DDI, including oral contraceptives
49
What can be given for barbituates OD? Flumazenil?
Nothing, not even flumazenil
50
What is the salt form of gamma hydrocybutyric acid available for treating narcolepsy?
Sodium oxybate
51
What is GHB's MOA?
GHB binds to GHB
52
How long after administration of GHB can it be detected in blood?
6 hours, but not found on routine toxicology screens
53
How are catecholamines (epi/NE) related to drugs of abuse?
Drugs of abuse increase dopamine, which is a precursor to NE
54
What is cocaines MOA?
Inhibits DAT-dopamine transporter, which causes more DA to be available (Also inhibits NE and 5-HT reuptake)
55
What is the metabolite used for testing? Why don't they use cocaine itself?
Cocaine is metabolized by tissue esterases/hydrolysis, causing its half life to be 1 hour. In order to detect its presence, you have to test for bezoylecgonin, which is a metabolite of cocaine
56
What is the antagonist for cocaine?
None available, just behavioral support, as well as supportive care for OD
57
How severe is cocaines withdrawal?
Not bad
58
What is commonly used to make amphetamines?
Pseudophedrine
59
What is meth's MOA?
Stimulate release of presynaptic NT's via inhibitory action on vesicular monamine transporter
60
What is the pneumonic for memorizing cocaines and meths MOA?
ABC, Amphetamines before cocaine Meth causes release of NT's, cocaine causes decreased reuptake of DA via DAT inhibition
61
What are the side effects of meth?
Paranoia, hallucinations, dry mouth, increased energy, anxiety, aggression common Also euphoria, irritability, chest pain, confusion, dental carries, and bugs on face feeling
62
What are the withdrawal syndrome symptoms of meth?
Dysphoria, irritability, anhedonia (inability to feel pleasure), insomnia, psychomotor agitation
63
How long does meth withdrawal last?
1-2 weeks, common among IV users
64
What is nicotine's MOA?
Selective agonist of the nicotinic acetylcholine receptor
65
What is the abuse MOA of nicotine?
a4B2 agonism in the VTA, leading to increased DA release
66
What happens in withdrawal of nicotine?
Irritability, anxiety, depression, restlessness, increase appetite/weight gain, decreased HR
67
What are two options for nicotine treatment?
``` Buproprion Varenicline (chantix)- a4B2 receptor agonist ```
68
E Cigs has been known to cause _____
E cig, vape, product use associated ling injury (EVALI)
69
What is a cannaboid medication used for appetite stimulation in cancer pts?
Dronabinol
70
What DEA class in dronabinol?
3
71
What is chronic cannabinoid associated with?
Schizophrenia, amotivational syndrome, and cannabis hyperemesis syndrome
72
What is cannaboids MOA?
Binds to CB receptors in CNS (CB1 is psychoactive)
73
What are some beneficial effects of cannabinoids?
Anti-emetic, Decreased IOP, anticonvulsant, appetite stimulant
74
What is the hallucinagenic compound in cannabinoids?
THC
75
What is cannabinoids abuse MOA?
Increased rate of DA neuron firing in VTA by distinhibition of GABA neurons (same as most others)
76
Which component of cannabinoids is the non psychoactive component?
CBD
77
What condition in kids can CBD treat?
Epilepsy
78
What are the hallucinogenic compounds that for sure have VTA activity?
MDA and MDMA (Esctasy)
79
What is the receptor for LSD and MDA and MDMA?
5HT-2A
80
What are the functions of 5HT-2A receptors?
Psychosis, depression, anxiety, appetite, memory
81
What does activation of 5HT-2A led to a release of?
NE release in locus ceruleus, glutamate release in PFC
82
What is the main effect of ecstacy and molly? Minor effect?
Affinity for the serotonin transporter, SERT, causing decreased reuptake of serotonin But can also affect DAT
83
What are the "positive effects" of ecstasy and molly?
Energy, altered sense of time
84
What are the negative effects of ectasy and molly?
Tachycardia, dry mouth, muscle aches, jaw clenching
85
What group is ecstasy and mollys a part of?
Phenethylamines
86
What group is LSD a part of?
Indoleamines
87
What disorder can LSD cause?
Hallucinogen persisting perception disorder, aka LSD flashbacks
88
Is there an underlying physical dependence with LSD?
Nope
89
What are the dissociative anesthetics?
Ketamine and PCP Phenycyclidine and special K
90
How does PCP and ketamine work?
Blocks NMDA type receptors
91
``` What is the MOA for Cocaine Meth Opiods Nicotine Cannabinoids ```
Cocaine- Blocks DAT Meth- Blocks VMAT Opioids- Disinhibits VTA by inhibiting GABA neurons Nicotine- Directly stimulates VTA DA neurons and indirectly stimulates it by activating glutamatergic terminals to the VTA Cannabinoids- Regulates DA signaling via CB1

Patho Miscellaneous (6 decks)

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