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Pharm > Drugs of abuse 1 > Flashcards

Drugs of abuse 1 Flashcards

1
Q

Outline the reward pathway

A

MESOLIMBIC DOPAMINE SYSTEM:

Dopaminergic cell bodies in the VTA, projects to the Nucleus Accumbens, releases dopamine

=EUPHORIA

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2
Q

T/F VTA/Nucleus Accumbens pwathway is only activated by drugs

A

F.. natural pathway, activated by food etc.

Drugs hi-jack this system ,and produce powerful rewards

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3
Q

Routes of administration of drugs of abuse

A

‘Snort’ – Intra-nasal

Eat’ - Oral

‘Smoke’ - Inhalational

‘Inject’ – Intra-venous

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4
Q

Outline the speed of absorption depending on the route of administration

A

‘Snort’ – Mucous membranes of nasal sinuses. Slow absorption

‘Eat’ – Gastrointestinal tract. Stomach to small intestine to portal system to liver to heart to brai
Very slow absorption

‘Smoke’ – Small airways and alveoli. Close to the heart Rapid absorption

‘Inject’ – Veins
Rapid absorption

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5
Q

Which route of administration of drugs of abuse is the fastest and why

A

Inhalation

Because if it goes far into the lungs, the alveoli have such thin walls,they allow really fast passage from lungs to blood…

if injecting, it has to go through the right side of the heart, through pulmonary system, then back to the heart then out to the body

With inhalation comes straight into the left side of the heart from the pulmonary system, then straight around the body

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6
Q

Classify drugs of abuse

A

Narcotics/Painkillers
Depressants
Stimulants
Miscellaneous

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7
Q

Give examples of narcotics/painkillers

A

Narcotics/Painkillers – opiate like drugs e.g. heroin

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8
Q

Give examples of depressants

A

Depressants – ‘downers’

e.g. alcohol, benzodiazepines (valium), barbiturates

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9
Q

Give examples of stimulants

A

Stimulants – ‘uppers’
e.g. cocaine, amphetamine (‘speed’), caffeine
metamphetamine (‘crystal meth’)

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10
Q

Give examples of the miscellaneous drugs classification

A

Miscellaneous – e.g. Cannabis (although predom. depressant), Ecstasy (MDMA) (predom. stimulant)

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11
Q

Where is the cannabis found in the cannabis plant

A

Hashish/Resin – Trichomes (the glandular hairs)

Hash Oil – Solvent extraction (this concentrates the THC etc found in the trichomes)

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12
Q

T/f there is only 1 type of cannabis compound

A

F > 400 compounds;

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13
Q

What is a cannabinoid and how many are there

A

Cannabis compound with pharmacological effect. 60 of the 400 cannabis compounds are cannabinoids

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14
Q

Name the cannabanoid responsible for most of the psychactive effects of cannabis

A

Detla 9 tetrahydrocannabinol

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15
Q

Which compound is responsible for the bad effects of cannabis

A

Detla 9 tetrahydrocannabinol

THC

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16
Q

Which compound actually can mitigate the effects of the Detla 9 tetrahydrocannabinol

A

Cannabidiol

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17
Q

What has been happening to THC concentration is hash over the years

A

It has significantyl increased

60’s + 70’s: ‘Reefer’ – 10mg THC

21st Century: ‘Skunkweed/Netherweed’

	- 150mg THC
	- 300mg THC (+ hashish oil)
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18
Q

What can be found with increaseing THC

A

Increasing negative symptoms (e.g. suicidal thoughts, depression)

But much smaller difference in the positive experience (e.g. euphoria doesn’t increase much with THC concentration, compared to increase in negative effects)

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19
Q

Outline the two major routes of administration of cannabis, and how much of the drug that becomes bioavailable in each case

A

Oral – 5-15%
delayed onset/slow absorption
first pass metabolism

Inhalation – 25-35%

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20
Q

If inhalation is the fastest route of administration, why is only 25-35% becoming available

A
  • Inhalation: 25-35% of dose enters bloodstream
  • Anything inhaled suffers from about 50% loss automatically
  • This is because only about 50% gets far enough down into the lungs to diffuse into the bloodstream
  • Lots of it is breathed back out, much of it won’t be absorbed
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21
Q

Outline the solubility of cannabanoids. What are the implications of this

A

EXTREMELY lipid soluble (beaten only by GA)

Fatty acid conjugates build
up in fatty tissue

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22
Q

Why do drugs not usually accumulate in he fat

A

Most drugs not THAT lipid soluble, and very poor blood supply (only around 2% of CO)

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23
Q

What happens after drug is injected into the blood to the concentration of drug i the blood

A

It will decrease, as concentrations increase int he tissues as the drug diffuses out of the blood into the tissue

High perfursion tissues e.g. brain will have high THC concentration at first,

then just before 24hrs after administration, low perfusion tissue has higher concentration (as intensive accumulation occurs in less vascularised tissues and finally in body fat, the major long-term storage site, resulting in concentration ratios between fat and plasma of up to 104)

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24
Q

What can be the ration of drug in the plasma to drug in the fat in chronic cannabis users

A

104 : 1 fatty tissue vs plasma… then you get a slow leak back into the blood

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25
Q

T/f it is the active cannabanoid that stays in the fatty tissue

A

F… the metabolites

26
Q

What is the metabolite of cananbanoid

A

11-hydroxy-THC

27
Q

What is the problem with cannaboid metabolites

A

11-hydroxy-THC (metabolite) is actually more potent than the 9 delta THC! They are also very lipid soluble so they can accumulate in the fat

28
Q

What is the problem with THC excretion

A

65% is excretd by the bile, but there is a lot of enterohepatic cycling because the cannabanoid is lipid soluble so after it is excreted into the small intestine in the bile, it just gets reabsorbed back into the bloodstream

29
Q

Why is there poor correlation between plasma
cannabinoid concentration and degree
of intoxication

A

Due to the potent metaboite and the enterohepatic cycling, as well as that in chronic cannabis users a high amount builds up in the brain (as it is a fatty tissue).

When you measure the blood concentration of THC, the active metabolite and the inactive metabolite, it may be quite low. But if you look in the brain, there could be high levels of THC and 11OH-THC (active metabolite), because of accumulation in the brain, which is quite a fatty tissue, and this may be very intoxicating.

30
Q

What is the inactive metabolite of cannabanoid

A

THC-COOH (glucoronidated form).. then goes into the bile and is subject to enterohepatic cycling

31
Q

Other than fat, which other tissue is very fatty

A

The brain (there is an increase in cannabis concentraiton in the blood for the first few hours after taking the drug, and this does fall so effects most potent at the start)

32
Q

What is the problem with chronic users of cannabis in terms of the amount in the brain

A

There can be a huge times more in the brain than in the plasma

33
Q

How long does 1 cannabis cigarette effects persist in the body

A

30 days (accumulates in the fatty tissue over 5 days, and then remains and very slowly exits

34
Q

What is the mechanism of action of cannabanoids

A

There are GPCR….

CB1 and CB2….

depressant so the GPCR is Gi/o

35
Q

What is the effect of cannabis on cell activity and why

A

GPCR is Gi/o so cAMP is reduced

36
Q

Which endogenous compounds act on the cannabanoid receptors

A

Endogenous Anandamide

37
Q

What is the most prevalent GPCR in the brain

A

CB receptors

38
Q

Where are CB1

receptors located

A

Hippocampus/cerebellum/

cerebral cortex/basal ganglia

39
Q

Where are CB2 receptros located

A

Immune cells

40
Q

What is the usual inhibitor of the mesolimbic pathway to keep this system shut off until it needs to be activted due to a reward

A

GABA mediated inhibition

41
Q

How does cannabanoid receptor work in euphoria

A

As they are depressant, they reduce the GABA neuron which inhibits the dopaminerigc neurons coming from the VTA….

Act via CB1 rceptors on the GABA inhibitory neurons on the dopaminergic neurons.

Called dysinhibition

42
Q

What is the Anterior Cingulate

Cortex (ACC) involved in

A

error detection
performance monitoring with behaviour adjustment in order to avoid losses

e.g. if you driving on a big wide road, and you’re chatting, and then you go on a tight road, then you’re concentration will be refocused to the road… ACC responible for this to maintain perofmrance

43
Q

What is noticed about the ACC in cannabis (improve)

A

Hypoactivity in cannabis users

could lead to schizophrenia

44
Q

What is the effect of cannabis on food intake

A

Review the hypothalamic control of food

Ventromedial hypothalamus is catabolic and reduces feeding (MC4R)

Lateral hypothalamus is anabolic and increases feeding (Orexin and MCH)

  1. Presynaptic inhibition of GABA increases MCH neuronal activity
  2. Increased orexin production, which increases appetite
45
Q

What is the effect of cannabis on the immune system

A

Cannabis is IMMUNOSUPRESSANT.

CB2 receptors present on NK, macrophage, B cell, T cell and mast cells

Cannabanoid reduces all of these

46
Q

Review the function of immune cells on the diagram…

A

….

47
Q

Why do some people use cannabis in disease

A

To suppress inflammatory response due to the effect on immune cells

48
Q

What are the peripheral effects of cannabis and what is the effect mediated by

A

Immunosuppressant

AND

Tachycardia/vasodilation of (Conjunctivae!)-(not mediated by CB receptors… by TRPV1!)

Could lead to bloodshot eyes

49
Q

Effect of cannabis on memory

A

Memory loss – Limbic regions (Amnestic effects/↓ BDNF)

50
Q

Why is it difficult to overdose on cannabis to the point of death

A

They don’t have profound effects on the medulla, as there is low CB1 receptor expression

Because it shuts down the cardiorespiratory centre in the medulla

51
Q

What is the medical application of cannabis

A

CB receptors seem to go up in diseases like MS, pain and stroke….

this seems to be the body’s own response to pain etc to reduce these effects

Also in stroke, post-stroke iscahemia can be improved by reducing inflammation by the CB2 receptors

52
Q

What is the effect of cabbanoid receptors for obesity and/fertility

A

As adipose tissue increases etc. CB seems to increase which may be negative

Fertility has less evidence

53
Q

When would you want agonist of cannabanoid receptor

A

During MS/pain/stoke it’s regulatory so you’d want agonist

MS: neuropathic pain + spasticity

Stroke: post-stroke ischaemia can cause damage driven by inflammatory processes

54
Q

When would you want antagnist of cannabanoid receptor

A

To reduce pathalogical effect associated with obesity /fertility

55
Q

Give examples of antagonst drugs

A

Rimonabant…. obesity drug… suppresses appetite and reduced weight gain

but some committed suicide so not on market

56
Q

Give examples of agonist drugs and their use

A

You’’ want to use an agonist to increase cannabanoid receptor stimulation for things like post stroke ischaemia etc (where there is pain, this reduces pain)

57
Q

Explain the the nasal route of administration

A
  • Snort (intranasal) –> drug enters nasal sinus –> venous drainage –> lung –> heart –> brain

o Mucous membranes of the nasal sinuses will slow absorption

58
Q

What is the clinical use of Dronabinol

A

Used in AIDS patients and cachexia (appetite stimulate)

59
Q

What is nabilone used

A

Anti-nausea in cancer therapy

60
Q

When is sativex used

A

MS… control the pain and spasticity in this condition

61
Q

What other kind of drug could be used with cannabanoid like effect

A

Fatty acid amide hydrolase inhibitor… prevents breakdown of endogenous anandamide…. used in chronic pain

62
Q

What do the following drugs contain:

Dronabinol
Nabilone

Sativex

A

Dronabinol: delta 9 THC
Nabilone: delta 9 THC

Sativex: delta 9 THC + CBD

Autoprotection’ – Dronabinol, Sativex

‘Autoimpairment’ - Rimonabant

Pharm (33 decks)

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