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eLCRS - 팜 > Pharm 14: Drugs of Abuse 2 (cocaine + nicotine) > Flashcards

Pharm 14: Drugs of Abuse 2 (cocaine + nicotine) Flashcards

1
Q

What are the different methods of dosing on cocaine?

A
  • paste (mushed up w org solvent)

–> cocaine Hcl (dissolved in acidic solution)

–> crack
(precipitate cocaine out of cocaine HCl using alkaline solution (e.g. baking soda) –> then heat precipitate + inhale vapour)

–> freebase
(purify crack + dissolve in non-polar solvent (e.g. ammonia + ether)

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2
Q

how do the different methods of administrating cocaine differ ?

A

Inhalation + IV have similar speed of onset –> rapid effects

o Inhalation poorest for bioavailability in blood

snorting / orally –> slow onset
o Cocaine pKa = 8.7 (gets ionised in acidic environment) –> very slow absorption/onset

o Slower absorption –> means prolonged action

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3
Q

describe the metabolism of cocaine

a) what is it converted to
b) what is its half life
c) what enzyme is involved in its breakdown?

A

75-90% converted to inactive metabolites = ecgonine methyl ester, benzoylecgonine

o T1/2 = 20-90min (how long metabolism takes)

o Breakdown uses cholinesterases either in plasma or liver

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4
Q

how does cocaine pharmacokinetics contribute to the addictive potential of the drug?

A

Cocaine = addictive because–>

a) it has fast onset of effect –> reinforcing
b) short-lasting effect,

–> people use it over + over (drives addiction)

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5
Q

how does cocaine action differ at high dose vs low dose?

A

HIGH DOSE = Action as a Local anesthetic by blocking Na+ channels –> reduce propagation of APs

o LA actions more prominent at higher doses

LOW DOSE = Reuptake inhibition of:

a. NA/Ad
b. 5-HT
c. DA

–> Enhances SNS activity (due to uptake blockade)

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6
Q

in what 3 ways can cocaine stimulate SNS ?

A
  • Cocaine stimulates SNS by:
    1. Inhibiting catecholamine reuptake (low dose effect) at sympathetic nerve terminals
    2. Stimulating central sympathetic outflow
    3. Increasing sensitivity of adrenergic nerve endings to NA
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7
Q

how does cocaine act like a class I antiarryhthmic?

A

Cocaine also acts like a class I antiarrhythmic (Local Anesthetic at high dose):

  • by blocking Na+ and K+ channels –> depresses cardiovascular function e.g. Left Ventricular function
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8
Q

how does cocaine stimulate vasoconstriction?

A

Cocaine also stimulates ET-1 from endothelial cells + inhibits NO production –> greater vasoconstriction (also due to greater a1 stimulation) + TPR –> decreased blood flow to heart

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9
Q

what effects does cocaine have on platelets?

A

activates platelets –> more aggregation + thrombosis

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10
Q

Cocaine Pharmacokinetics:

o Onset = Seconds

o Tissue t1/2 = <90min, short-lasting

o Elimination = ecgonine methyl ester, benzoylecgonine: Urine (75-90%)

Cocain Pharmacodynamics:

o Blockade of Na+ channels – LA at high dose

o Transport Inhibitor (low dose) –> euphoria (CNS), CVS problems

A

-

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11
Q

What is the tissue half life of cocaine?

A

t1/2 = <90min, short-lasting

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12
Q

What are the different methods of dosing on Nicotine?

A

Nicotine Dosing:

o Nicotine spray = 1mg
(20-50% bioavailability)

o Nicotine gum = 2-4 mg
(50-70% bioavailability)

o Cigarettes = 9-17 mg
(20% bioavailability)

o Nicotine patch = 15-22mg/day
(70% bioavailability - highest)

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13
Q

Cigarette smoke is acidic / basic

Absorption in alveoli independent / dependent of pH

A

Cigarette smoke is acidic
ie no buccal absorption.

Absorption in alveoli independent of pH
–> ionised nicotine will still cross alveoli

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14
Q

what is the aim of nicotine replacement method ?

A

aim of replacement method = maintain consistent nicotine level in blood to remove cravings;

–> as opposed to cigarette where you get rapid, large peak then quick fall

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15
Q

Describe the metabolism of nicotine

a) how is it broken down
b) what is its half life

A

Metabolism:

o Hepatic CYP2A6 breaks it down –> to cotinine (inactive metabolite)

o Half-life = 1-4 hours
= short-effect, yet fast onset –> addictive

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16
Q

How do you get feeling of euphoria with nicotine?

A

nicotine directly stimulates VTA at nAChR –> stimulates greater DA release onto NAcc

17
Q

What are the effects of nicotine on the cardiovascular system?

A

part a)

  • increased SNS output
  • increased catecholamines
  • increased HR
  • increased contractility
  • increased BP
  • -> increases oxygen demand of heart

part b)

  • increased platelet activation
  • -> decreases oxygen supply

part c)

  • increased coronary vasoconstriction
  • -> decreases oxygen supply
part d) 
- increased free fatty acids 
(VLDLD/LDL) 
--> increases risk of atherosclerosis 
--> decreases oxygen supply

–> can cause myocardial ischemia / MI

18
Q

How does nicotine affect the lipid profile?

A
  • increases lipolysis
    Free fatty acids, VLDL

–> But lowers HDLs

19
Q

Nicotine:

Increases/decreases metabolic rate

+ increases/ decreases appetite

A

Increases metabolic rate + decreased appetite

20
Q

What are the effects of nicotine on neurodegerative disorders:

a) Parkinsons’
b) Alzheimers’

Does smoking have therapeutic value in treating Parkinson’s or
Alzheimer’s?

A

chronic nicotine = protective for neurodegerative disorders:

a) Parkinsons’
- -> increase in brain’s capacity to metabolise neurotoxins (via increase in brain CYPs)

b) Alzheimers’
- -> decreases beta-amyloid toxicity
- -> decreases amyloid precursor protein (APP)

21
Q

What is the tissue half life of nicotine?

A

2-3 hours

22
Q

effects of caffeine

A

caffeine = adenosine receptor antagonist

normally:
- adenosine binds to its receptors on NAcc –> decrease DA release + decreases D1 receptor function –> -ve for euphoria

  • caffeine = antagonist
  • -> causes euphoria
23
Q

at high dose of Cocaine Hcl, it can act as a local anesthetic

explain how

A

cocaine hcl = local anesthetics
- cocaine –> sodium channel blocker

  • cocaine diffuses accrocs plasma membres –> into cytoplasm then:

a) accesses open channel (hydrophilic pathway)
b) diffuses into closed channel (hydrophobic pathway)

*cocaine has to be uncharged –> then only it can diffuse easily across the membrane

24
Q

How does cocaine induce euphoria?

A
  • cocain blocks dopamine transporter in NAcc
  • so lots of dopamine accumulates in the synapse
  • so there is increase in stimulation of dopamine receptors (D1R)

–> so more powerful euphoric effect

25
Q

note: at low dose –> effects tend to be positive / reinforcing
(euphoria)

at high dose –> effects tend to be negative/ stereotypic (chronic/tolerant cocaine use)
(irritability)

A

-

26
Q

how can cocaine cause myocardial infarction

in general

A

part a)

  • increased SNS output
  • increased catecholamines
  • increased HR
  • increased contractility
  • increased BP
  • -> increases oxygen demand of heart

part b)

  • increased platelet activation
  • -> decreases oxygen supply

part c)

  • increased coronary vasoconstriction
  • -> decreases oxygen supply

–> can cause myocardial ischemia / MI

27
Q

how can high dose cocaine cause arrhythmia ?

A
  • high dose cocaine = acts as local anesthetic
    a) decrease na+ transport in heart
    b) can also cause inflammation –> affecting endothelial cells + decreases function of left ventricles

–> which can cause arrhythmias / sudden death

28
Q

how does cocaine cause hyperthermic effects?

A
  • cocaine overdose causes:
  • -> increased agitation
  • -> increased locomotor activity
  • -> increased involuntary muscle contraction

= increase heat production

cocaine –> interferes with vasodilation + sweating
–> increases threshold for vasodilation + sweating
(change in set point)
–> can damage brain

29
Q

note: peak effect of cigarettes is much quicker than other methods of administration

A

-

30
Q

how does onset of euphoria effects differ between nicotine + cocaine?

A
  • nicotine increases activity of nerve itself

- cocaine increase DA survival in synapse

eLCRS - 팜 (36 decks)

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