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Patho Miscellaneous > Test 2 Drugs of abuse > Flashcards

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
Q

What is the most commonly abused drug?

A

Alcohol

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26
Q

How much of alcohol is metabolized in the liver?

A

over 90%

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27
Q

What type of kinetics does alcohol have?

A

Zero order kinetics, a constant amount of drug is eliminated per unit of time

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28
Q

What is ethanol metabolised into?

A

Acetaldehyde, the toxic intermediate

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29
Q

What does the genetic variability ADH1B*2 cause?

A

Trouble converting ethanol to acetyladehyde

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30
Q

What does ALDH2*2 cause?

A

Lack of ALDH ability, so unable to covert acetaldehyde to acetate

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31
Q

What will ALDH2*2 heterozygotes do to alcohol? Homozygotes?

A

Will flush

Severe reactions

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32
Q

Why can men consume more alcohol safely?

A

More ADH in men

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33
Q

Explain the process of alcohol metabolism

A

Ethanol metabolized by ADH (alcohol dehydrogenase) to acetaldehyde, then broken down by acetaldehyde dehydrogenase (ALDH) to acetate

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34
Q

What is the abuse MOA of ethanol?

A

Increased DA release in the nucleus accumbens

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35
Q

What can chronic alcohol consumption result in? Hint, its a syndrome

A

Wernicke-Korsakoff syndrome

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36
Q

How does acetaldehyde affect dopamine?

A

It increases it

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37
Q

What are the characteristics of withdrawal syndrome of alcohol?

A

Hyperexcitability including seizures, psychosis, and delirium tremens

38
Q

What is the normal MOA of benzos/barbituates?

A

Allosteric GABA a agonist

39
Q

What should benzos not be combined with?

40
Q

What are the drugs listed for benzos?

A

Alprazolam, diazepam, clonazepam, clorazepate

41
Q

What is the abuse MOA of benzos/barbituates?

A

Inhibit GABA a1 neurons in the VTA, leading to disinhibition of dopamine neurons

42
Q

What is the antagonist to benzos?

A

Flumazenil

43
Q

What are the withdrawal symptoms of benzos?

A

Anxiety, agitation, phonophobia, photophobia, muscle cramps, sleep disturbance, dizziness
At high doses, even seizures and delirium

44
Q

What are treatment considerations for benzos?

A

No long term deterrent med, can give buspirone to treat anxiety

45
Q

What is the one common use of barbituates?

A

Epileptics

46
Q

What is one of the most common uses of barbituates? Not in the clinical setting necessarily

A

Euthanasia in animals, lethal injection, physician assisted deaths

47
Q

What is the metabolism for barbituates?

A

CYP inducer

48
Q

What are some concerns with barbituates, given its metabolistic pathway?

A

Its a CYP inducer, so many DDI, including oral contraceptives

49
Q

What can be given for barbituates OD? Flumazenil?

A

Nothing, not even flumazenil

50
Q

What is the salt form of gamma hydrocybutyric acid available for treating narcolepsy?

A

Sodium oxybate

51
Q

What is GHB’s MOA?

A

GHB binds to GHB

52
Q

How long after administration of GHB can it be detected in blood?

A

6 hours, but not found on routine toxicology screens

53
Q

How are catecholamines (epi/NE) related to drugs of abuse?

A

Drugs of abuse increase dopamine, which is a precursor to NE

54
Q

What is cocaines MOA?

A

Inhibits DAT-dopamine transporter, which causes more DA to be available (Also inhibits NE and 5-HT reuptake)

55
Q

What is the metabolite used for testing? Why don’t they use cocaine itself?

A

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
Q

What is the antagonist for cocaine?

A

None available, just behavioral support, as well as supportive care for OD

57
Q

How severe is cocaines withdrawal?

58
Q

What is commonly used to make amphetamines?

A

Pseudophedrine

59
Q

What is meth’s MOA?

A

Stimulate release of presynaptic NT’s via inhibitory action on vesicular monamine transporter

60
Q

What is the pneumonic for memorizing cocaines and meths MOA?

A

ABC, Amphetamines before cocaine

Meth causes release of NT’s, cocaine causes decreased reuptake of DA via DAT inhibition

61
Q

What are the side effects of meth?

A

Paranoia, hallucinations, dry mouth, increased energy, anxiety, aggression common

Also euphoria, irritability, chest pain, confusion, dental carries, and bugs on face feeling

62
Q

What are the withdrawal syndrome symptoms of meth?

A

Dysphoria, irritability, anhedonia (inability to feel pleasure), insomnia, psychomotor agitation

63
Q

How long does meth withdrawal last?

A

1-2 weeks, common among IV users

64
Q

What is nicotine’s MOA?

A

Selective agonist of the nicotinic acetylcholine receptor

65
Q

What is the abuse MOA of nicotine?

A

a4B2 agonism in the VTA, leading to increased DA release

66
Q

What happens in withdrawal of nicotine?

A

Irritability, anxiety, depression, restlessness, increase appetite/weight gain, decreased HR

67
Q

What are two options for nicotine treatment?

A 
Buproprion
Varenicline (chantix)- a4B2 receptor agonist
68
Q

E Cigs has been known to cause _____

A

E cig, vape, product use associated ling injury (EVALI)

69
Q

What is a cannaboid medication used for appetite stimulation in cancer pts?

A

Dronabinol

70
Q

What DEA class in dronabinol?

71
Q

What is chronic cannabinoid associated with?

A

Schizophrenia, amotivational syndrome, and cannabis hyperemesis syndrome

72
Q

What is cannaboids MOA?

A

Binds to CB receptors in CNS (CB1 is psychoactive)

73
Q

What are some beneficial effects of cannabinoids?

A

Anti-emetic, Decreased IOP, anticonvulsant, appetite stimulant

74
Q

What is the hallucinagenic compound in cannabinoids?

75
Q

What is cannabinoids abuse MOA?

A

Increased rate of DA neuron firing in VTA by distinhibition of GABA neurons (same as most others)

76
Q

Which component of cannabinoids is the non psychoactive component?

77
Q

What condition in kids can CBD treat?

78
Q

What are the hallucinogenic compounds that for sure have VTA activity?

A

MDA and MDMA (Esctasy)

79
Q

What is the receptor for LSD and MDA and MDMA?

80
Q

What are the functions of 5HT-2A receptors?

A

Psychosis, depression, anxiety, appetite, memory

81
Q

What does activation of 5HT-2A led to a release of?

A

NE release in locus ceruleus, glutamate release in PFC

82
Q

What is the main effect of ecstacy and molly? Minor effect?

A

Affinity for the serotonin transporter, SERT, causing decreased reuptake of serotonin

But can also affect DAT

83
Q

What are the “positive effects” of ecstasy and molly?

A

Energy, altered sense of time

84
Q

What are the negative effects of ectasy and molly?

A

Tachycardia, dry mouth, muscle aches, jaw clenching

85
Q

What group is ecstasy and mollys a part of?

A

Phenethylamines

86
Q

What group is LSD a part of?

A

Indoleamines

87
Q

What disorder can LSD cause?

A

Hallucinogen persisting perception disorder, aka LSD flashbacks

88
Q

Is there an underlying physical dependence with LSD?

89
Q

What are the dissociative anesthetics?

A

Ketamine and PCP

Phenycyclidine and special K

90
Q

How does PCP and ketamine work?

A

Blocks NMDA type receptors

91
Q 
What is the MOA for
Cocaine
Meth
Opiods
Nicotine
Cannabinoids
A

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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