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Pharm > Drugs of abuse I > Flashcards

Drugs of abuse I Flashcards

1
Q

What are the two qualities of dependence?

A
  1. Development of tolerance

2. Withdrawal symptoms

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2
Q

How does tolerance come about?

A
  1. Decrease in amount of available drug

2. Changes of drug receptor action

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3
Q

What is addiction?

A

Relapsing drug use despite negative consequences

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4
Q

What is the dopamine hypothesis of addiction?

A

All addictive drugs target the mesolimbic dopamine system in the VTA

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5
Q

What is the role of the ventral tegmental area in addiction?

A

Dopamine neurons in this area project to several brain receptors involved in reward processing

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6
Q

What are the two parts to drug abuse?

A
  1. get euphoria/reward

2. Detrimental to health

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7
Q

What is the hallmark of drug addiction?

A

Compulsive drug use

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8
Q

What is pharmacokinetic tolerance?

A

Increased drug metabolism or amount of drug availability

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9
Q

What is pharmacodynamic tolerance?

A

Desensitization and/or downregulation of receptors

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10
Q

What are the areas in the brain that the VTA projects neurons to in the reward pathway? (4)

A

Nucleus accumbens
Amygdala
Hippocampus
Prefrontal cortex

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11
Q

What is the general principle with withdrawal ssx?

A

Opposite of the drugs taken

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12
Q

What is “psychological dependence”? “Physiological dependence”?

A 
Psychological = Addiction
Physiological = dependence
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13
Q

What is the scale used for the relative risk of addiction?

A

1 through 5, with 1 being non-addictive and 5 being highly addictive

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14
Q

What are the three MOAs of increased dopamine release in the reward pathway via addictive drugs?

A
  1. Activation of Gi
  2. Activation of ionotropic receptors
  3. Targeting dopamine transporter
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15
Q

What does activation of Gi do in the dopaminergic neurons of the reward pathway do, and how does this lead to increased reward?

A

Inhibits the firing of the inhibitory interneurons on Dopaminergic neurons

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16
Q

What does activation of ionotropic receptors do in the dopaminergic neurons of the reward pathway do, and how does this lead to increased reward?

A

Enhances release of dopamine in activation of GABAergic neurons

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17
Q

What does targeting of dopamine transporter do in the dopaminergic neurons of the reward pathway do, and how does this lead to increased reward?

A

Blocks dopamine reuptake, leading to increased dopamine in the synapse

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18
Q

What is the MOA of opioids in generating reward pathway stimulation?

A

Activate Gi/GABA on inhibitory interneurons

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19
Q

What is the MOA of THC in generating reward pathway stimulation?

A

Activate Gi/GABA on inhibitory interneurons

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20
Q

What is the MOA of cocaine in generating reward pathway stimulation?

A

Block dopamine reuptake

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21
Q

What is the MOA of amphetamine in generating reward pathway stimulation?

A

Block dopamine reuptake and cause release of dopamine from vesicles

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22
Q

What is the MOA of nicotine in generating reward pathway stimulation?

A

Activates ion receptors to increase release of dopamine

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23
Q

What is the MOA of benzodiazepines in generating reward pathway stimulation?

A

Activates ion receptors to increase release of dopamine

24
Q

What is the MOA of EtOH in generating reward pathway stimulation?

A

Activates ion receptors to increase release of dopamine

25
Q

True or false: the area of the brain that is involved in addiction is usually different from its site of action

26
Q

What is the relative risk of addiction for CNS depressants?

27
Q

What are the three CNS depressants?

A

EtOH
Benzos
Barbiturates
Gamma-hydroxybutyric acid

28
Q

When does EtOH reach its peak concentration in the blood?

A

30 minutes

29
Q

True or false: EtOH is soluble in fat and water, and thus diffuses easily across all biological membranes

30
Q

How does the EtOH concentration of a mother’s blood compare to that of the fetus?

31
Q

What percent of EtOH is metabolized by the liver? What is the metabolic process occurring here?

A

90%

oxidation

32
Q

Why do women have a higher EtOH levels than men for the same dose?

A

Decreased first pass effect

Lower total body water

33
Q

What are the three MOA of EtOH metabolism?

A
  1. Alcohol dehydrogenase
  2. MEOS
  3. Aldehyde dehydrogenase
34
Q

Is EtOH zero or first order elimination? What does this mean?

A

Zero order–constant amount eliminated regardless of serum concentration

35
Q

What other organs metabolize EtOH besides the liver? What percent?

A

Kidney and lungs–10%

36
Q

Alcohol dehydrogenase catalyzes alcohol into what chemical?

A

acetaldehyde

37
Q

What is the cause of fatty liver of alcoholism?

A

Overproduction of NADPH and lower amount of NAD+ shunts energy down the FA synthesis pathway

38
Q

What is the drug that treats methanol and ethylene glycol poisoning? MOA?

A

Fomepizole

Inhibits ADH, which is involved in the conversion of these two substances into toxic metabolites

39
Q

What is the MEOS system?

A

Microsomal ethanol oxidizing system–complex of p450s

40
Q

After alcohol dehydrogenase turns alcohol into acetaldehyde, what is the next enzyme in the pathway? What does this produce?

A

Aldehyde dehydrogenase

Acetate

41
Q

What happens if Aldehyde dehydrogenase is not functioning properly? Symtoms?

A

Build up of acetaldehyde, causing hangover feeling + flushing

42
Q

What is the cofactor needed for Aldehyde dehydrogenase?

43
Q

What is the drug that is used to treat alcoholism? MOA?

A

Disulfiram

Inhibits ALDH, causing a buildup of acetaldehyde, and sickness

44
Q

How many drinks does it take most adults to reach the legal limit of 0.08% BAC?

45
Q

What is the ABV of beer? Wine? Liquor?

A 
Beer = 3.5-10%
Wine = 12%
Liquor = 40-50%
46
Q

What is one drink (in oz) for beer, wine, and liquor?

A 
Beer = 12 oz
Wine = 5 oz
Liquor = 1.5 oz
47
Q

What is the MOA of EtOH?

A

Potentiates GABA-(A- receptors, causing a Cl influx and inhibition of neurons.

Also inhibits glutamate excitatory neurons (NMDA receptors)

48
Q

What are the effects of CNS depressants with EtOH?

A

Additive effects

49
Q

What is Wernicke-Korsakoff syndrome?

A

Thiamine (vit B1) deficiency characterized by paralysis of the external eye muscles,
ataxia and a confused state that can progress to coma and death.

Also, confabulations.

50
Q

What are the three classic characteristics of fetal alcohol syndrome?

A

MR
Hyperactivity
Antisocial behavior

51
Q

What are the cells that are primarily affected in the pancreas with EtOH?

A

Acinar cells

52
Q

What are the 4 stages of liver changes with EtOH use?

A

Alcoholic fatty liver
Alcoholic hepatitis
Liver cirrhosis
Liver failure

53
Q

What is the effect of EtOH use and cocaine?

A

Liver combines the two to form cocaethylene, that potentiates the effects of cocaine

54
Q

Why is thiamine given to drunks in the ER?

A

Prevent Wernicke-Korsakoff syndrome

55
Q

What is the drug type of choice for treating acute EtOH withdrawal?

A

Benzodiazepines

56
Q

What is the MOA of naltrexone in treating chronic alcoholism?

A

Opioid antagonist that blocks the reinforcing properties of EtOH

57
Q

What is the MOA of disulfiram in treating chronic alcoholism?

A

Inhibits ALDH and produce acute sensitivity to EtOH (“hangover” ssx).

Pharm (73 decks)

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