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PCOL2 > Nicotine and Tobacco > Flashcards

Nicotine and Tobacco Flashcards

1
Q

Nicotine is an X, derived from Y.

A

Plant alkaloid, nicotinic acid.

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2
Q

What is nicotine in pharmacological terms?

A

Nicotinic acetylcholine receptor agonist.

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3
Q

What is 70-80% of nicotine metabolised into in the liver?

A

Cotinine.

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4
Q

How does cotinine compare to nicotine pharmocologically? (i.e. potency and half life)

A

Lower potency, longer half life.

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5
Q

Nicotine affects brain nAChRs, but not ganglial or neuromuscular ones. What is the particular pentameric construction of brain nAChRs?

A

(alpha4)2(beta4)3

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6
Q

What particular nicotinic AChR is made of (alpha4)2(beta4)3?

A

Brain ones. These are the ones targeted by nicotine.

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7
Q

Think ‘prolonged nAChR stimulation’; think…

A

…desensitisation and resultant increase in expression.

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8
Q

The overall balance between activation and desensitisation leads to (two points):
PROMT: Aaaaah. Now I’m in a better mood to pay attention to how you’re gonna arouse me. Teach me daddy yeah!!

A

1- a. increased arousal b. attention c. mood, d. relaxation.
2- increased learning, particularly under stress.

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9
Q

The overall balance between activation and desensitisation leads to (two points):

A

1- a. increased arousal b. attention c. mood, d. relaxation.
2- increased learning, particularly under stress.

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10
Q

Increased activity in the X pathway is seen in drug addiction.

A

mesolimbic

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11
Q

Increased A activity in the B is seen in drug addiction.

A

dopamine, nucleus accumbens

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12
Q

What two neurological structures are involved in drug addiction and similar in nicotine addiction?

A

Mesolimbic pathway (increased activity) and nucleus accumbens (increased DA).

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13
Q

What is the significance of brain nAChR desensitisation in this lecture?

A

That’s the main basis of addiction.

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14
Q

Why is dopamine involved in the CNS effects?

A

DA release is triggered by nAChR stimulation.

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15
Q

What is the brain nAChR antagonist that demonstrated the mechanism of action of nicotine?
Cruel miller on a pilgrimage.

A

Mecamylamine

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16
Q

What is the brain nAChR antagonist that demonstrated the mechanism of action of nicotine?
No prompt.

A

Mecamylamine

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17
Q

What are the CV effects of nicotine?

A

Increased heart rate, CO, BP

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18
Q

What molecules does nicotine promote?

A

Ad, NAd (think sympathetic) and ADH

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19
Q

What is the effect of ADH output promoted by nicotine?

A

Decreased urination.

20
Q

Why did I get nauseous the first time I smoked?

A

Stimulation of stomach sensory receptors.

21
Q

Tolerance develops rapidly to the X effects, but the Y effects remain.

A

Peripheral; CNS.

22
Q

Smoking promotes pathological angiogenesis but is overall antivascular. What?

A

It’s good for angiogenesis, but bad for endothelial cells. So more vessels, and in poorer shape. More vessels is good for tumours. Bad shape is good for plaque formation and CV events.

23
Q

How much nicotine is in the average cigarette?

A

9-17mg

24
Q

How much nicotine is ABSORBED from the average cigarette?

A

1.5mg

25
Q

What is a normal blood level of nicotine to see after a ciggie?

A

15-30ng

26
Q

How fast is the phase phase of decay and why is it there? (The slow phase is over 1-2 hours and due to metabolism into cotinine).

A

10 minutes, due to rapid redistribution.

27
Q

Death between 35 and 65 yoa was X% in smokers but only Y percent in non-smokers.

A

40%; 15%.

28
Q

20-per-day increases the changes of lung cancer Y much.

A

10 times as much.

29
Q

D percent of lung cancers are due to the Es introduced by smoking.

A

90%; CARCINOGENIC TARS.

30
Q

Because of H and G, old dudes with a 20-a-day habit are at D greater risk of coronary thrombosis.

A

nicotine; carbon monoxide; 60%

31
Q

What are three respiratory problems associated with smoking?

A

COPD, chronic bronchitis, pneumonia, emphysema

32
Q

What is the basis for respiratory problems? It’s not burning holes like in the ad. There are two bases.

A

TARS again, as well as nicotine screwing up the CLEANSING FUNCTION OF CILIA.

33
Q

How long supposedly to smokers have to wait after quitting before they regain their normal life span?

A

Ten years.

34
Q

What is a possible long-term benefit of smoking?

A

NEUROPROTECTIVE esp. Parkinson’s. Via dopamine release and some other stuff.
Alzheimers too maybe.

35
Q

What are the five symptoms of nicotine withdrawal?

Hayley, awake eating chips, not studying and one more

A

Grumpy Hayley syndrome, insomnia, weight gain, lower HR, poor concentration.

36
Q

What are the five symptoms of nicotine withdrawal?

A

Grumpy Hayley syndrome, insomnia, weight gain, lower HR, poor concentration.

37
Q

How long do withdrawal symptoms last compared to cravings?

A

Much more short lived than cravings; 2-3 weeks.

38
Q

What is the most effective means of NRT?

A

There are none - they are equieffective.

39
Q

Xmg doses are better than Ymg doses for NRT.

A

4; 2.

40
Q

Can I take more than one form of NRT? Is it worth it?

A

Yes. People have had more success.

41
Q

Can I use NRT patches if I’m pregnant?

A

Only if you can’t manage without it, in which case we’d prefer you used short-acting oral forms rather than long-acting patches.

42
Q

I’ve got CV problems - can I use patches?

A

Yes, it’s recommended to you for that reason.

43
Q

NRT is no better than a placebo unless combined with other therapies (i.e. counselling or varenicline). T or F?

A

True.

44
Q

What is varenicline?

A

nAChR partial agonist with a strong affinity for the brain subtype of nAChR.
Is gr8. Shits on bupropion.

45
Q

What is bupropion?

A

Originally an antidepressant. DA and NAd reuptake inhibitor, may increase DA in the nucleus accumbens.
Is shat on by varenicline.

46
Q

What is a side effect of bupropion?

A

Lowers seizure threshold. Obvs can’t be used in bipolar patients (antidepressant).

PCOL2 (24 decks)

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