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Year 2 Pharma > Drugs of Abuse > Flashcards

Drugs of Abuse Flashcards

1
Q

What is the fastest route of drugs going to the brain? Why?

A

Inhalation because pulmonary circuit is very short and IV must do the systematic circuit before entering the brain

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2
Q

What are different classifications of drugs?

A
  • narcotics
  • depressants
  • stimulants
  • miscellaneous (have effects from multiple classes)
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3
Q

What is the order of onset of euphoria of a drug according to their administration method?

A
  1. inhalation
  2. IV
  3. intranasal
  4. oral
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4
Q

What is the difference between cannabis, hashish/resin and hash oil?

A

Cannabis is the plant, hashish/resin is the trichomes, hash oil is the solvent extract

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5
Q

What is the most potent cannabinoid?

A

Delta9 THC

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6
Q

What are the positive aspects of smoking weed from?

A

Cannabidiol

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7
Q

What is the difference between doses of THC between now and the 60/70s?

A

In the 60/70s it was ~10mg THC but now it’s 150-300mg

Cannabidiol potency would also have increased proportionally

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8
Q

What are routes of administration of cannabis? How much THC is delivered by this route?

A

Oral - 5-15% THC

Inhalation - 25% THC

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9
Q

Why and how does cannabis accumulate in the body?

A

It is very lipid soluble so builds up as fatty acid conjugates

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10
Q

How is cannabis metabolised in the body?

A

Liver converts THC to 11 OH THC which is more potent, then GIT excretes 65% of it - much of THC undergoes enterohepatic recycling due to lipid solubility and urine excretes 25%

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11
Q

What is the correlation between plasma concentration of cannabis and the degree of intoxication and why?

A

THC is more concentrated in brain matter than in blood as the blood is very lipid soluble, leading to a poor correlation

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12
Q

What receptors in the brain respond to cannabis and where in the brain are they

A

CB1R in:

Hippocampus, cerebellum, cortex, and basal ganglia

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13
Q

What receptors in the peripheral respond to cannabis and where are htey

A

CB2R in

Immune cells

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14
Q

What causes the euphoric affects of cannabis?

A

Stimulation of the Gi CB1 receptor inhibits the release of DABA - disinhibition leading to an increase in the release of dopamine by inhibiting DA release

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15
Q

What is CBR?

A

An inhibitory gpCr linked to Adenylate Cyclase

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16
Q

What is the body’s natural version of THC

A

endogenous anadamide

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17
Q

What is the anterior cingulate cortex in the brain involved in?

A

Performance monitoring with behavioural adjustment eg driving a car whilst talking to a friend then it starts raining so you stop talking to focus on the road

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18
Q

What is cannabis’ affect on the anterior cingulate cortex?

A

hypoactivity which can lead to psychosis and schizophrenia

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19
Q

How does cannabis affect food intake?

A
  • presynaptic inhibition of GABA leading to an increase in MCH (melanin concentrating hormone) neuronal activity
  • increase orexin production

which increases hunger

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20
Q

What is cannabis’ affect on the immune system and how does it do this?

A

Immunosuppressant bu agonising CB2Rs on:

mast cells, macrophages, b cells, t cells and natural killer cells

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21
Q

What are central affects of cannabis?

A 
Psychosis, 
schizoprenia, 
food intake - lateral hypothalamus, 
memory loss, 
decreased psychomotor performance
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22
Q

What are peripheral effects of cannabis?

A

Immunosuppressant

Tachycardia/vasodilation

23
Q

How does cannabis cause memory loss

A

By having amnestic effects by decreasing BDNF (brain derived neurotrophic factor)

24
Q

How does cannabis cause tachycardia/vasodilation

A

via TRPV1 receptors

25
Q

Why is it impossible to overdose on cannabis?

A

Medulla has low CB1R expression so the cardio-respiratory centre is not affected much

26
Q

What effect do CBRs have on the eyes

A

Red eyes due to conjunctiva vasodilate

27
Q

What patients would cannabis cause an upregulation of CBRs in?

A

MS/pain/stroke patients - to regulate pain

Fertility/obesity patients - pathological and may contribute to obesity and infertility

28
Q

What are effects of cannabis in drugs? What are examples of drugs that use it?

A

Autoprotection:
- dronabinol, nabilone - anti-emetics in cancer
- sativex - treat MS pain
Autoimpairment:
- rimonabant - anti obesity drug (off market) that blocks the feeling of hunger

29
Q

What are the different ways you can administer cocaine?

A

Oral, IV, intranasal, inhalation

30
Q

What are the different forms of cocaine?

A

Paste - 80% cocaine (organic solvent)
Cocaine HCL - dissolved in acidic solution
Crack - precipitated with alkaline solution eg baking soda
Freebase - dissolved in a non polar solvent (eg ammonia + ether)

31
Q

How is cocaine administrated?

A

Oral, IV, intranasal - paste/cocaine HCL

Inhalation - crack/freebase

32
Q

What method of administration of cocaine is the fastest acting and which has a short lasting high

A

IV fasted onset and short lasting high

33
Q

Where is cocaine ionised? Why?

A

GIT because the pKa is 8.7

34
Q

Where is cocaine metabolised and how? What’s the half life?

A

75-90% is metabolised very fast into ecogonine methyl ester and benzoylecgonine. The half life is 20-90 minutes and it’s broken down by plasma and liver cholinesterase

35
Q

How do the pharmacokinetics of cocaine lead to addictive capabilities?

A
  • fast onset of action and short half life

- lots of methods to take the drug

36
Q

How does cocaine work as a local anaesthetic?

A

High dose cocaine can block the sodium channels to cause a local anaesthetic effects - inhibits conduction of AP

37
Q

How does cocaine cause reuptake inhibition?

A

MAO-A re-uptake inhibition (uptake 1), which can affect re-uptake of NA, DA and 5HT which does not change the affinity or efficacy of dopamine, only the DA in the synaptic cleft

38
Q

How does cocaine cause euphoria?

A

Reduces re-uptake of DA into pre-synaptic neurone so more DA in the NAcc (from the VTA)

39
Q

What are affects of cocaine after acute use?

A

initially positively reinforcing effects such as mood amplification and heightened energy

40
Q

What are affects of cocaine after chronic use?

A

Severe effects eg insomnia and decreased libido

41
Q

What are effects of cocaine on the cardiovascular system?

A

Increased catecholamines and increased sympathetic drive on the heart increasing oxygen demand on the heart. Vasoconstriction decreases delivery of oxygen to the heart. Result is ischaemia of the heart muscle

42
Q

What are the effects of cocaine on the CNS?

A

Vasoconstriction and hyper-pyrexia (fever) that can lead to epilepsy

43
Q

What types of substances are produced from nicotine?

A

95% volatile substances eg N2, CO/CO2, Benzene, HCN
5% particulates eg alkaloids (nicotine), tar

Nicotine diffuses out of the tar droplets in the lungs when deposited

44
Q 
How much nicotine comes from the 
spray: 
gum:
cigarettes:
patch:
A

spray: 1mg 20-50% effective
gum: 2-4mg 50-70% effective
cigarettes: 9-17mg 20% effective
patch: 15-22mg/day 70%

45
Q

What combination of action and concentration of nicotine leads to addiction?

A

Short lasting action and a fast reduction in plasma concentration of nicotine leads to addiction

46
Q

What is the half life of nicotine?

A

1-4 hrs

47
Q

How is nicotine metabolised and cleared from the body?

A

Hepatic CYP-2A6 metabolises 70-80% -> cotinine and cotinine is not active and rapidly cleared

48
Q

What are the effects of nicotine on the cardiovascular system?

A

Stimulates the nAChRs leading to SNS activation (CNS adrenals)
- increases HR and SV
- vasoconstriction of skin arterioles
- vasodilation of coronary arterioles, skeletal muscle arterioles
Increased lipolysis, ffAs, VlDLs, decreased HDL
Increased TXA2, reduced NO
-> long term use leads to cardiovascular disease

49
Q

How does nicotine cause a euphoric effect?

A

nAChRs are found on the soma of the dopamine nuclei in the VTA and the stimulation of these receptors stimulates DA release in the NAcc

50
Q

What effect does nicotine have on the metabolic system in the body

A

Increases metabolic rate and decreasing appetite

51
Q

What effect does nicotine have on parkinson’s and alzheimers?

A

It is protective against both diseases

52
Q

What happens in parkinson’s disease in the brain?

A

Increases brain CYPs (neurotoxin enzymes) -> increased breakdown of neurotoxins

53
Q

What happens in alzheimer’s disease in the brain?

A

Decreased beta-amyloid toxicity and decreases amyloid precursor protein (APP)

Year 2 Pharma (34 decks)

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