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Year 2 - Pharm Lectures 11+ > DOA 1 - General/Cannabis > Flashcards

DOA 1 - General/Cannabis Flashcards

1
Q

Using general pharmacodynamics, explain why drugs are normally abused?

A

Dopaminergic neurones from the
• VTA (ventral tegmental area)

are STIMULATED to release DA (reward) into the
• NAcc (nucleus accumbens [ventral striatum])

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2
Q

General methods of administration of drugs and the speed of absorption?

A

• Intranasal
- mucous membranes of nasal sinuses = SLOW absorption

• Oral
- GI tract = VERY SLOW absorption

• Inhalation
- small airways & alveoli = RAPID absorption

• Intravenous
- veins = RAPID absorption

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3
Q

Which is the fastest route of administration to the BRAIN and why?

A

INHALATION

As pulmonary circuit is VERY SHORT
whereas
via. IV must do the systemic circuit before accessing the brain

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4
Q

Explain the 4 broad classifications of drugs

A

• Narcotics/painkillers

  • opiate-like drugs
  • e.g. heroin

• Depressants
- e.g. alcohol, benzodiazepines (valine), barbiturates

• Stimulants
- e.g. cocaine, amphetamine, caffeine, metamphetamine, nicotine

• Miscellaneous

  • have effects from MULTIPLE classes of drugs
  • e.g. cannabis, ecstasy (MDMA)
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5
Q

In regards to routes of administation for drugs, what is the order for onset of euphoria?

A

Oral < Intranasal < IV < Inhalation

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6
Q

Explain the different parts of cannabis and what is used for?

A

Cannabis/marijuana = the PLANT

Hashish (the resin) = is the TRICHOMES
• glandular hairs that contain the HIGHEST [THC]

Hash oil = SOLVENT EXTRACT

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7
Q

Cannabis contains over 400 compounds - what makes up for >60 of it?

A

CANNABINOIDS

• Delta9-THC is the MOST POTENT type
• Positive aspects from smoking weed are from cannabidiol
- believe balance between these two (cannabidiol vs. delta9-THC is needed)

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8
Q

Explain the dosing issues seen with cannabis in recent years

A

Doses in 60’s & 70s was
• ~10mg THC

Now the doses are
• ~150-300mg THC

Potency has increased over the years SO if delta9-THC has increased do has cannabidiol
• the -ve effects are therefore MORE pronounced than +ve effects (as more delta9-THC)

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9
Q

Explain the pharmacokinetics associated with the ROA of cannabis, oral and inhalation

A

ORAL - 5-15% THC delivered
• DELAYED onset (as slow absorption)
• First pass metabolism

INHALATION - 25-35% THC delivered
• fastest route to brain as pulmonary circuit is very short

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10
Q

General pharmacokinetics associated with cannabis?

A

Cannabis SLOWLY accumulates in the body as it is VERY LIPID SOLUBLE
• builds up as FA CONJUGATES in fatty tissue
• takes 30 days for the effects to cease on the body

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11
Q

Explain the pharmacokinetics associated with cannabis in terms of metabolism?

A

Liver CONVERTS THC
• to 11-OH-THC (more potent - PHASE 1 METABOLITE)

GIT excretes 65% of it
• much of the THC undergoes ENTEROHEPATIC RECYCLING due to lipid solubility (as part of BILE)

Urine excretes 25% of it

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12
Q

Explain the relationship between [plasma] of cannabis and degree of intoxication

A

POOR correlation between plasma [cannabinoid] & degree of intoxication
• THC is MORE [ ] in the brain matter than blood as it is very lipid soluble
• This leads to the poor correlation seen

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13
Q

Explain the receptors associated with cannabis usage

A

Brain
• CB1R - hippocampus, cerebellum, cortex & basal ganglia

Peripheral
• CB2R - immune cells

The CB Receptor is an INHIBITORY GPCR
• linked to adenylate cyclase

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14
Q

What is the body’s version of THC?

A

Endogenous Anandamide

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15
Q

Receptors associated with cannabis?

A

CBR = cannabinoid receptors
• depressants

2 main classes
• CB1
• CB2

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16
Q

Using pharmacodynamics, explain how people feel sense of euphoria when using cannabis?

A

Stimulation of CB1 receptor INHIBITS the release of GABA
• DISINHIBITON

This increases the release of dopamine by INHIBITING the inhibition of release of DA (via. VTA) to the NAcc

17
Q

Using pharmacodynamics, explain why some people that use cannabis can lead to psychosis & schizophrenia?

A

One target of cannabis is ACC
• Anterior Cingulate Cortex

ACC is invovled in performance monitoring with behavioural adjustment
i.e. driving & talking with friend BUT starts to rain so stop talking to focus on road

Cannabis causes HYPOACTIVITY in the ACC

18
Q

Using pharmacodynamics, explain the relationship of cannabis with food intake

A

Cannabis tends to affect the OUTPUT SYSTEMS (rather than the neurones that receive the signals)
[ONENOTE!!]

Has 2 primary actions on the LATERAL HYPOTHALAMUS
• Pre-synaptic inhibition of GABA = increases MCH (melanin concentrating hormone) neuronal activity
• Increases OREXIN production

BOTH of these act to INCREASE HUNGER

MCH - has a stimulatory effect on hunger
Orexin - has a stimulatory effect on hunger

19
Q

Using pharmacodynamics, explain the relationship between cannabis and immunosuppresant?

A

Outside the brain, cannabis main effect is on the IS (as peripherally affects the immune cells)

Cannabis acts to DEPRESS the IS by AGONISING CB2 receptors on the following:
 • macrophages
 • mast cell
 • B-cell
 • T-cell
 • NK cells
20
Q

Generally, explain the main CENTRAL effect of cannabis use?

A
  • Psychosis, schizophrenia
  • Food intake - Hypothalamus

• Memory loss

  • Limbic regions (amnestic effects, decreased BDNF [brain derived neurotrophic factor)
  • BDNF is the main thing in the hippocampus that drives memory formation

• Psychomotor performance - cerebral cortex

21
Q

Generally explain the main PERIPHERAL effect of cannabis use

A
  • Immunosuppresant
  • Tachycardia/vasodilation
  • via. TRPV1 receptors (NOT CBRs)
  • leads to RED EYES as conjunctiva vasoDILATE
22
Q

Why is it impossible to OD on cannabis?

A

Medulla has LOW CB1 receptor expression

• SO means the cardio-respiratory centre is NOT affected much

23
Q

In regards to health & disease, explain how upregulation of CBRs can affect the body

A

In

MS/pain/stroke patients
• HELPS as regulates pain (remember it is a depressant!)

Fertility/obesity
• it is PATHOLOGICAL and may contribute to obesity (as present on adipose tissue) & infertility (inhibits the gonadotrophins for e.g.)

24
Q

Drugs that be used for autoprotection purposes in term sof cannabis use as medical applications?

A

Delta9-THC drugs:
• Dronabinol
• Nabilone
(anti-emetics in cancer)

Delta9-THC + CBD drugs:
• Sativex
(treats MS pain)

ALL THESE ARE AGONISTS (stimulate the CBR)

25
Q

Drugs that can be used for autoimpairment purposes in terms of cannabis use as medical applicaitons?

A

Rimonabant
• anti-obesity drugs (off-market)
• blocks feeling of hunger
• become off-marker as was linked to suicide (feeding pathway heavily linked to reward pathway)

This is an ANTAGONIST (inhibits the CBR)

26
Q

Fatty acid amide hydrolase?

A

What produces the ENDOGENOUS ANANDAMIDE

So along with blocking the receptors can also block this
• Fatty acid amide hydrolase inhibitor

Year 2 - Pharm Lectures 11+ (23 decks)

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