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LCRS Pharma > Drugs of Abuse: Drugs and Cannabis > Flashcards

Drugs of Abuse: Drugs and Cannabis Flashcards

1
Q

what system in the brain enables euphoria?

A

dopaminergic neurones from the VTA stimulate the release of dopamine into the NAcc in the reward system

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2
Q

what are the methods of drug administration?

A

o Intranasal (via mucous membranes in nasal sinuses) – slow absorption.
o Oral – very slow absorption.
o Inhalational – rapid absorption.
o Intravenous – rapid absorption.

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3
Q

what is the fastest route of administration to the brain?

A

inhalation- pulmonary circuit is very short

IV has to do the systemic circuit before reaching the brain

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4
Q

what are the main classification of drugs?

A
  • narcotics (painkillers)
  • depressants
  • stimulants
  • miscellaneous
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5
Q

examples of narcotics

A

opiate-like drugs e..g heroin

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6
Q

examples of depressants

A

alcohol

benzodiazepines (valium)

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7
Q

examples of stimulants

A 
cocaine
amphetamines
caffeine
methamphetamines
nicotine
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8
Q

example of miscellaneous drugs

A

cannabis
ecstasy

these drugs have effects from multiple classes

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9
Q

what is the order of onset of euphoria in ascending order based on administration

A

oral< intranasal < IV, inhalation

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10
Q

what are the components of cannabis?

A
  • cannabis sativa is the plant
  • hashish/resin is the trichomes (glandular hairs that contain the highest concentration of THC)
  • hash oil is the solvent extract
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11
Q

how many compounds in cannabis?

A

over 400, >60 of them being cannibinoids

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12
Q

what is the most potent cannabinoid?

A

delta 9-THC

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13
Q

what produces the positive effects of cannabis smoking?

A

the inclusion of cannabidiol may regulate the negative effects of delta 9 THC

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14
Q

how has dosage of THC changed over time?

A

Doses in 60’s and 70’s was ~10mg THC

Now it is 150-300mg of THC.

Potency has increased over the years; delta9-THC has increased, so has cannabidiol. Here, the negative effects are more pronounced

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15
Q

what are the route of administration of cannabis?

A

o Oral – 5-15% THC delivered.

o Inhalation – 25-25% THC delivered. Must be breathed in deeply

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16
Q

why is THC delivery lower when cannabis is taken orally?

A

delayed onset due to slow absorption with first pass metabolism

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17
Q

how does cannabis accumulate and leave?

A
  • slowly accumulates in the body as it is very lipid soluble
  • builds up fatty acid conjugates.
  • Accumulation in poorly perfused fatty tissue with chronic use
    takes 30 days for effects to cease
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18
Q

how is cannabis metabolised?

A

THC converted to a more potent molecule: 11-OH THC, a phase 1 metabolite

11-OH THC is more potent than delta 9 THC

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19
Q

how is cannabis excreted?

A
  • GIT 65%:enters bile and is enterohepatically recycled due to its lipid solubility
  • urine 25%
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20
Q

what is the difference in concentration of THC in the brain and the blood?

what is the effect of this?

A

THC is more concentrated in the brain (which is very fatty) compared to the blood due to the lipid soluble property of cannabis

therefore there is a poor correlation between plasma cannabinoid and degree of toxicity

21
Q

what receptors do cannabinoids bind to ? where are they located?

A
  • CB1 receptors in the brain: Hippocampus, cerebellum, cortex and basal ganglia
  • CB2 receptors in the periphery: immune cells
22
Q

what type of receptor is CBr?

A

inhibitory GPLR linked to adenylate cyclase

depresses cell activity

23
Q

what is the endogenous version THC that normally binds to the CBr?

A

anandamide

result of fatty acid amide hydrolase inhibition

24
Q

how does binding to CBr lead to euphoria?

A

binding of Cb1 receptors on GABA neurones inhibits the release of GABA. This has a disinhibition effect on the VTA neurone releasing dopamine. The inhibition on dopamine release is reduced so more dopamine is released

25
Q

what effect does cannabis have on the anterior cingulate cortex (ACC)? what is the ACC?

A

ACC is involved in performance monitoring with behavioural adjustment.

Cannabis causes the hypoactivity of ACC

26
Q

how does cannabis increase the need for food?

A

increase in orexin production:

  • cannabis has effects on the lateral hypothalamus in two places:
  • presynaptic inhibition of GABA increases MCH (Melanin Concentrating Hormone) neuronal activity.
  • this increases food seeking behaviour
27
Q

what are the major impacts of cannabis?

A
  • euphoria
  • CNS: psychosis, schizophrenia
  • food intake/hunger/munchies
  • memory loss
  • tachycardia
  • immunosuppressant
28
Q

how does cannabis act on the immune system?

A 
agonise CB2r on immune cells: 
o	Macrophage.
o	Mast cell.
o	B-cell.
o	T-cell.
o	Natural Killer cell.
29
Q

what are the central effects of cannabis?

A

o Psychosis, schizophrenia.
o Food intake – lateral hypothalamus.
o Memory loss – Limbic regions (Amnestic effects/decreased BDNF (Brain Derived Neurotrophic Factor)).
o Psychomotor performance – affects cerebral cortex.

30
Q

what are the peripheral effects of cannabis?

A 
o Immunosuppressant (CB2 binding on immune cells) 
o Tachycardia/vasodilation – via TRPV1 receptors (NOT CBr) leads to red eyes as conjunctiva vasodilate.
31
Q

why is cannabis sometimes considered safer than alcohol?

A

cannabis does not effect the cardio-respiratory centre as much as alcohol (which surpasses the medulla) so its near impossible to overdose on cannabis and cause cardio-respiratory failure

32
Q

why does cannabis not affect the cardio-respiratory centre much?

A

there is a low concentration of CB1r on the medulla

33
Q

when can CBr be unregulated?

A

o MS/pain/stroke patients – to regulate pain.

o Fertility/obesity – this is pathologic and may contribute to obesity and infertility.

34
Q

what are the autoprotective cannabis based drugs?

A

Dronabinol, Nabilone, Sativex

35
Q

what is the use of dronabinol, nabilone?

A

anti-emetic in cancer

stimulate appetite in AIDS and chemo patients

36
Q

what is the use of savitex?

A

used as analgesic for neuropathic pain in MS

37
Q

what are the autoimpairment cannabis based drugs?

A

rimonabant

38
Q

what is the use of rimonabant?

A

anti-obesity drug by blocking feeling of hunger (lateral hypothalamus)
decreases weight

off the market now due to depression side effect leading to suicide.

39
Q

what is the active ingredient in cannabis?

A

delta 9 tetrahydrocannabinol

40
Q

which receptors does cannabis bind to and where are these receptors?

A

CB1 receptors : found on GABA neurones (central)

CB2 receptors: found on immune cells (peripheral )

41
Q

why does cannabis cause psychosis, schizophrenia?

A
  • targeting the anterior cingulate cortex
  • causes hypoactivity
  • this increases agitation and fright
42
Q

why does cannabis cause increased hunger?

A
  • increases orexin activity
  • orexinogenic activity stimulates the lateral hypothalamus
  • lateral hypothalamus increases hunger
43
Q

why does cannabis cause memory loss/amnesia?

A
  • decrease in brain derived neurotrophic factor

- this is needed for memory formation in the hippocampus

44
Q

why does cannabis cause tachycardia?

A
  • binds to TRPV 1 (Ca2+) channels
  • increases calcium influx

binding to TRPV also causes the red eyes

45
Q

why does cannabis lead to a immunosuppressive effect?

A
  • decreases B and T cell numbers
  • NK cell activity decreases

binding to CB2

46
Q

what is dronabinol?

what are its uses?

A

THC type used as anti-emetic in cancer patients and treating appetite loss in AIDS patients

47
Q

what is sativex?

what are its uses?

A

THC/cannabidiol mixture

used to treat MS as it binds to CBr in the brain to depress activity (neuropathic pain is pain that originates from the CNS)

48
Q

what is rimonabant?

what are its uses?

A

CB1 receptor antagonist
- blocks CB receptors in adipocytes (which cause obesity) there causes weight loss

however no longer in use due it increased depression and suicidal thoughts

LCRS Pharma (32 decks)

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