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BB2 > Cannabis > Flashcards

Cannabis Flashcards

1
Q

How many people does MS affect in the UK? How many people worldwide? Is it more common in males or females?

A

120,000
2-3 million
Female ratio 2-3:1

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2
Q

Is MS inherited?

A

More than 100 genes identified, such as HLA-DR

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3
Q

List three risk factors for MS.

A

EBV infection
Vit D deficiency
Smoking

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4
Q

What are the four clinical courses of MS?

A

Relapsing-remitting
Secondary progressive
Primary progressive
Progressive-relapsing

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5
Q

What is MS?

A

MS is a chronic auto-immune-mediated demyelinating disease of the CNS. The onset is usually between 20-40 years of age.

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6
Q

What three major things does MS cause? What type of cells are lost?

A

Inflammation, demyelination and neurodegeneration

Oligodendrocyte loss

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7
Q

How does the normal ageing atrophy rate compare to the MS one?

A

0.1% p.a. compared to 0.5-1.35% p.a.

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8
Q

How does the treatment approach differ for…
Attacks
Relapses
Progressive disease?

A

Attacks treated with steroids
Relapses treated with disease modifying therapy
Progressive disease – currently nothing effective, just symptomatic treatments (baclofen, sativex).

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9
Q

What are the four main mechanisms of MS drugs? Give examples of drugs for each one.

A
  1. Pleiotrophic effects (e.g. beta inferons)
  2. Targeted cell lysis (e.g. alemtuzumab)
  3. Reduced proliferation (e.g. teriflunomide)
  4. Anti-migratory (fingolimod, natalizumab)
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10
Q

What do MS treatments mostly rely on?

A

Direct targeting of pro-inflammatory cells

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11
Q

Interferon beta 1a and 1b:

  • How is it administered?
  • How does it work?
  • What is its efficacy?
  • What is the major side effect?
A

Injection
Blocks viral replication (pleiotrophic effects)
Low efficacy
Can cause flu-like symptoms

Glatiramer acetate (copaxone). Injection.
TERIFLUNOMIDE - Blocks Immune activation & targets rapidly dividing cells and block NF-Κb.
FINGOLIMOD – oral. Sphingosine-1-phosphate receptor modulator Traps cells in the Lymph nodes.

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12
Q

Natalizumab:

  • How is it administered?
  • How does it work?
  • What is its efficacy?
A

Infusion
Blocks CD49d (blocks the migration of lymphocytes/monocytes into the CNS)
High efficacy

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13
Q

Alemtuzumab:

  • How does it work?
  • What is its efficacy?
A

CD52 T and B cell depletion

High efficacy

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14
Q

What are the main symptoms of MS? (9)

A 
Blindness and nystagmus
Fatigue
Pain
Tremor
Spasms and spasticity
Bladder problems and incontinence
Sexual problems
Cognitive deficits
Motor deficits
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15
Q

What neurotransmission problems are there in MS? (4)

A

Conduction block
Demyelination
Loss of axons and neurons
Loss of synaptic plasticity

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16
Q

What does “no evidence of disease activity” involve? (4)

A

No new lesions
No clinical relapses
No worsening of disability
No Brain Atrophy on MRI

17
Q

List some current anti-spastics.

A 
Baclofen
Gabapentin
Tizanidine
Benzodiazapines
Dantrolene 
Phenol and botulinum toxin
18
Q

How does baclofen work? What are the main side effects?

A

GABA B agonist,

Sedation and muscle weakness

19
Q

How does gabapentin work? What are the main side effects?

A

GABA analogue - ion channel modulator

Sedation, fatigue and dizziness

20
Q

How does tizanidine work? What are the main side effects?

A

Alpha 2 adrenergic agonist

Sedation, dry mouth, hypotension

21
Q

How does benzodiazepine work? What are the main side effects?

A

Allosteric GABA A modulation

Sedation and addiction

22
Q

How does dantrolene work? What are the main side effects?

A

Muscle relaxant

Sedation and liver damage

23
Q

How do phenol and botulinum work?

A

Nerve blocking agents

24
Q

Anandamide and 2-arachidonyl glycerol are both what?

What do they affect (what parts of the body) and via what receptor?

A

Endocannabinoids
Immune system - B cells, monocutes, spleen and tonsils
CB 2 receptor

25
Q

What is anandamide formed from?
What is 2-arachidonoyl glycerol formed from?
What are they BOTH formed by the action of (enzyme)?

A

NAPE
Arachidonic acid containing diacylglycerol
Phospholipases

26
Q

What is THC? What does it affect and via what receptor?

A

Plant cannabinoid
Nervous system (brain, adipose, muscle, liver, GI tract and pancreas)
CB 1 receptor

27
Q

Where are cannabis receptors located? (5)

A 
Cerebral cortex
Striatum
Amygdala
Hippocampus
Cerebellum
28
Q

What happens if you stimulate CB receptors?

A

INHIBIT TREMOR & SPASTICITY

29
Q

What happens if you block CB receptors?

A

WORSENS SPASTICITY

30
Q

What is Sativex/Nabiximols? How is it administered?

A

Mix of botanical cannabis, containing tetrahydrocannabinol and cannabidiol
Sublingual spray

31
Q

What is sativex used to treat? (2)

A

Neuropathic pain

MS

32
Q

Why might cannabis not be an ‘ideal’ treatment?

A

We can’t dissociate the therapeutic effects from the psychoactive side effects.

33
Q

What is Rimonabant/Acomplia used for? What is it?

A

Anti-obesity drug

CB1 Receptor Antagonist

34
Q

Explain how cannabinoids help with spasticity.

A

They act via cannabinoid receptors to cause hyper-polarisation, causing inhibition of spasticity. They limit the capacity to generate action potentials. They cause potassium ions to be expelled and an influx of chloride ions to do this.

(Spasticity is due to damage-induced over excitation/lack of neural inhibition.)

35
Q

What receptor does diazepam work on?

A

GABA A receptor

36
Q

What is spasticity due to?

A

Damage induced over-excitation/lack of neural inhibition

37
Q

What does the endocannabinoid system regulate?

A

Synaptic neurotransmission

BB2 (32 decks)

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