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PHAR300 > L7 Nicotine > Flashcards

L7 Nicotine Flashcards

1
Q

What was nicotine originally used as?

A

insecticide

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2
Q

From which plant is nicotine extracted from?

A

tobacco plant

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3
Q

How is nicotine mainly used consumed?

A

Smoking

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4
Q

TF: the acute and long term effects of nicotine are the same.

A

False

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5
Q

Why do companies target their ads to children/teens/young adults?

A

They are more likely to become addicted

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6
Q

What is the main method of administration/drug delivery system for nicotine? Why do companies promote this method?

A

cigarette, increases probability of addiction due to its rapid effects

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7
Q

Why is nicotine absorption so rapid when smoking?

A

Gas exchange between the lungs and the capillaries is very high due to the surface area ratio which allows rapid absorption of any smoked substance.

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8
Q

TF: nicotine when smoking is metabolized by the liver first-pass

A

False (the blood from the lungs go to the heart where it is then pumped to other tissues e.g. brain)

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9
Q

Why is nicotine so addictive? (hint: cigarettes)

A

It reaches the brain very fast (7 seconds). This rapid effect is what makes it so addictive

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10
Q

What are Ciliotoxins

A

compounds that paralyze the cilia in our lungs momentarily. (cilia function by “beating up” any mucus or pathogens that get into the respiratory tract)

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11
Q

TF: smoking contributes to high blood pressure

A

True

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12
Q

What kinds of cancers can be linked to smoking?

A

breast, prostate, bladder (common), pancreatic, etc. (14 kinds)

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13
Q

What is the role of the mucociliary system in the lungs?

A

to beat and propel particles and mucus out of the lungs: its how the lungs clean themselves

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14
Q

What is the effect of smoking on the mucociliary system

A

the mucociliary clearance rate is compromised (reduced clearance rate)

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15
Q

What are some cardiovascular consequences of smoking?

A

increases coronary heart disease (CHD) and strokes (due to hypertension and damaged blood vessels)

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16
Q

What is peripheral vascular disease?

A

blood flow to legs is impaired making it harder for people to walk

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17
Q

List the kinds of coronary heart diseases

A

hypertension, cardiac output, endothelial injury, atherosclerosis, platelet aggregation

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18
Q

TF: Nicotine causes vasodilation

A

False, nicotine causes vasoconstriction

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19
Q

What is a symptom of vasoconstriction due to nicotine abuse?

A

wrinkles and cataracts (+other)

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20
Q

What are the consequences of vasoconstriction?

A

damage to fine vessels in the periphery, decreases blood flow, decrease cardiac output, etc.

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21
Q

TF: Nicotine abuse causes chronic lung diseases like bronchitis and emphysema

A

True

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22
Q

TF: Smokers have increases rates of influenza, diabetes, pneumonia tuberculosis, and COVID-19

A

True

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23
Q

What is the name used to refer to the smoke that is exhaled when smoking

A

mainstream smoke

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24
Q

What does sidestream smoke refer to?

A

the smoke that comes off the burning end of the cigarette

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25
Q

TF: smoke and second-hand smoke have the same chemical compositions

A

False

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26
Q

Name some features of nicotine that affect its pharmacokinetics

A

lipid-soluble, weak base (absorption depends on pH of surroundings)

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27
Q

What happens if a weak base is in a more basic environment?

A

it will become unionizes, making it more lipid-soluble and readily absorbed

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28
Q

What are other drug delivery systems for nicotine?

A

chewing tobacco leaves, oral - swallowing (pills), sublingual delivery, transdermal patches through the skin

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29
Q

TF: increases absorption increases the probability of addiction

A

True

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30
Q

TF: Absorption through the lungs is as fast as an IV injection

A

True

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31
Q

Why aren’t lower nicotine cigarettes safer?

A

Smokers will adjust the drug delivery in order to get the level of nicotine they are addicted to

Chronic smokers with lower-nicotine cigarettes will take more puffs and hold the smoke in their lungs for longer

Chronic smokers with higher-nicotine cigarettes will take just a few puffs

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32
Q

How do smokers control the bioavailability of nicotine?

A

They adjust how many puffs they’re taking, how deeply they inhale, and how long it stays in the lungs (frequency and depth)

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33
Q

TF: The rate of rise and delivery of nicotine to the blood is the same for chewing or smoking

A

False, smoking has a higher rate of absorption

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34
Q

Why does smoking make you vomit the first few times?

A

Nicotine is distributed everywhere, including Chemoreceptor Trigger Zone (CTZ) which is connected to the vomiting center

34
Q

TF: The level of nicotine delivered to the blood whether chewing or smoking is the same

A

True (except for nicotine gum)

35
Q

TF: In order for nicotine to reach the CTZ, it must cross the blood brain barrier

A

False

35
Q

Why don’t experience smokers vomit despite nicotine triggering the CTZ

A

They develop a tolerance, the CTZ will become resistant to nicotine and thus desensitized after chronic use

35
Q

What is the main system of metabolism for nicotine?

A

the P450 system in the liver, where CYP2A6 is the predominant P450 enzyme for nicotine metabolism

36
Q

What metabolite is created when nicotine is metabolizes by CYP2A6?

A

cotinine

37
Q

How many half-lives does it take for a drug to reach steady state in the blood?

A

4 half-lives (4 cigarettes for nicotine)

38
Q

Why do smokes take more puffs at the start of their day?

A

To get nicotine to the levels that they are used to (since nicotine levels decrease when they sleep)

39
Q

What happens if you have an underactive CYP2A6 enzyme and you smoke?

A

Underactive CYP2A6 metabolizes nicotine slower than the normal functioning enzyme. Thus, they don’t need to smoke as many cigarettes to maintain blood nicotine levels. Consequently, less smoking equals less exposure to the other toxic chemicals inside a cigarette. (also lower level of cotinine metabolite)

40
Q

Compared to someone with a normal function CYP2A6, someone with a defective CYP2A6 will have a higher or lower increase in nicotine blood plasma levels after one cigarette?

A

higher

41
Q

What does CYP2A6 activate?

A

it activates procarcinogens and makes some toxic metabolites

42
Q

TF: A defective CYP2A6 decreases the carcinogenicity of cigarettes.

A

True (since CYP2A6 activates procarcinogens and makes toxic metabolites)

43
Q

Where is nicotine, cotinine, and carcinogens mainly excreted?

A

kidneys

44
Q

How does alkaline urine affect excretion of nicotine?

A

It will decrease nicotine excretion since nicotine will be un-ionizes (weak base) a thus more lipid soluble causing reabsorption into the tubules of the kidney where it will go back into circulation

45
Q

What kind of receptor is the nicotinic receptor?

A

it is a ligand-gated ion channel (nicotinic cholinergic receptor)

46
Q

Which neurotransmitter interacts with nicotinic receptors?

A

acetylcholine (ACh)

47
Q

TF: Acetylcholine acts on muscarinic receptors

A

True, it acts on both muscarinic and nicotinic receptors

48
Q

TF: nicotinic receptors are only found on the postsynaptic side of synapsis

A

False, there are also receptors on the presynaptic side in order to modulate the amount of neurotransmitters released (alter the release of GABA and glutamate)

49
Q

List where nicotinic receptors can be found

A

1) in the ganglia of sympathetic and parasympathetic nervous systems
2) in the brain
3) at the innervation of skeletal muscles
4) in the adrenal gland

50
Q

TF: there are nicotinic receptors in the parasympathetic nerve terminals

A

False, although they are acetylcholine receptors, they are muscarinic not nicotinic

51
Q

What is the nicotinic cholinergic receptor

A

It is an ion channel selective to sodium and calcium (to varying degrees)

52
Q

TF: acetylcholine and nicotine act on the same receptors

A

False, ACh also acts on muscarinic receptors, but nicotine only acts on nicotinic receptors

53
Q

What can explain the change in a smoker’s reaction to cigarettes as the day progresses?

A

Nicotine starts by stimulating (agonist) (low concentrations of nicotine) the nicotinic receptor and then blocking (antagonist) it (high concentrations of nicotine + high affinity of nicotine for receptors).

54
Q

Describe the nicotinic cholinergic receptor (e.g. number of subunits)

A

1) 5 subunits with different combination of alpha and beta subunits
2) 9 variants for alpha subunits
3) 3 variants for the beta subunits
4) Can be homomeric (only alpha) or heteromeric (alpha and beta)

55
Q

what is the most common nicotinic receptor in the brain

A

alpha-4-beta-2 (heteromeric) alpha-4 (homomeric)

56
Q

TF: Nicotine binds at the same site as ACh

A

True

57
Q

How many molecules does it take to activate the nicotinic receptor?

A

2

58
Q

What are the differences in effects between ACh binding and nicotine binding to receptor?

A

Nicotine binding causes a longer desensitization phase and binds to the receptor longer than ACh. Nicotine also disrupt the regeneration of channels to their standby state.

This contributes to tolerance

59
Q

Why do smokes have increased nicotinic receptors in their brains than non-smokers?

A

Nicotine stimulate the recruitment and synthesis of receptors on the plasma membrane

This is because nicotine compromises nicotinic cholinergic receptor function (increases desensitization phase, increases binding time, decreases regeneration of standby state)

60
Q

How can nicotine affect the periphery? What are the consequences of this?

A

It can block and stimulate the autonomic nervous system (sympathetic and parasympathetic)

This can contribute to side effects

61
Q

What neurotransmitters does nicotine release that has effects on the heart? And from which organs?

A

Norepinephrine from sympathetic nerve endings
Epinephrine from medulla

62
Q

What effects does nicotine have on the heart and the vascular system?

A

increased HR
vasoconstriction
increased BP
vessel damage due to toxic compounds

63
Q

Does nicotine have sedative effects? If so, what kind?

A

the blocking of receptors causes sedation (which occurs after initial excitation)

decreased skin temperature
feeling less hungry
skeletal muscle relaxation
increased BMR (basic metabolic rate)

64
Q

What happens during nicotine poisoning

A

excitation followed by inhibition in the CNS causing tremors, convulsions, paralysis, death from respiratory failure

65
Q

Why does nicotine have effects on memory and cognition

A

because it modulates glutamate and gaba

66
Q

What pathways does nicotine modulate?

A

reward, memory, arousal, cognition, etc.

67
Q

Why does nicotine affect so many pathways?

A

nicotinic receptors are found on presynaptic nerve endings of many neurons throughout the brain - causing widespread effect on the CNS

68
Q

TF: nicotine can affect muscle tone and Parkinson’s disease

A

True

69
Q

What happens if you knockout the beta2 subunit of the nicotinic receptor in a mouse

A

the mouse will not get addicted to nicotine since there will not be an increase in dopamine when exposed to nicotine

70
Q

which subunits of the nicotinic receptor are essential for dopamine release

A

alpha-4 and beta-2

71
Q

Name a psychoactive compound found in cigarettes

A

MAO (monoamine oxidase) inhibitor - a common antidepressant

72
Q

What does MOA do? and MOA inhibitor?

A

MOA breaks down NE and dopamine at presynaptic terminals

MOA inhibitor would result in NE and dopamine not being broken down - these decreased levels of MOA activity in the brain and periphery affects transmission systems in the brain

73
Q

How does menthol modulate nicotine activity

A

modulates the cholinergic receptor which increases addiction rate

it decreases GABA inhibition of dopaminergic neurons (thus more dopamine is released than normal)

it lowers the concentration of CYP2A6 thus increasing bioavailability

74
Q

What is the ventral tegmental area (VTA)?

A

It is related to the reward pathway. It is a region located in the midbrain of the central nervous system. It is an important component of the brain’s reward system and is involved in the regulation of mood, pleasure, and motivation.

75
Q

There is a high or low concentration of alpha-4 and beta-2 nicotinic receptors in the ventral tegmental area (VTA)

A

high

76
Q

How does nicotine promote the rewards pathway?

A

nicotinic receptors are desensitized quite rapidly, thus less inhibition of the dopaminergic neurons by GABA causing more dopamine release than normal (less inhibition of dopamine neurons)

it also promotes glutamate releases which promotes dopamine release

77
Q

how does nicotine affect glutaminergic neurons

A

nicotine stimulates the alpha-7 nicotinic receptor on those neurons causing release of glutamate which stimulates dopamine release by dopaminergic neurons (underlying mechanism of addiction)

78
Q

what are some symptoms of nicotine withdrawal

A

depression, irritability, trouble concentrating, trouble sleeping, increased appetite, constipation

79
Q

how long does it take for receptors that are bound by nicotine to turn over and be replaced by normal receptors (+ get back to the normal number of receptors)

A

6 weeks

80
Q

What are 3 ways to treat nicotine addiction

A

1) replacement therapy (patch, spray) will help with withdrawal symptoms
- bupropion blocks nicotinic receptors on dopaminergic neurons in the VTA
- varenicline is a partial agonist of a4b2 nicotinic receptors in the VTA thus resulting in moderate dopamine release

2) block CYP2A6 in order to decrease nicotine metabolism
- fewer cigarettes smoked, decreased toxicity
- methoxsalen

3) Topiramate which decreases dopamine release
- blocks the ability of nicotine to give you a high
- vaccine being tested

81
Q

What are the short term effects of vaping?

A

acute toxicity causes lung injury, impaired respiratory immunity, respiratory inflammation and injury, epigenetic modification, infections, mucus overproduction

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