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Cannabanoid_Master Flashcards

1
Q

Where are CB1 receptors most abundantly found in the CNS?

A

Neocortex, hippocampus, basal ganglia, cerebellum, and brainstem.

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2
Q

Where are CB1 receptors found outside of the CNS?

A

Peripheral nerve terminals and extra-neural sites such as the testis, eye, vascular endothelium, and spleen.

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3
Q

What is the primary function of CB1 receptors?

A

Restricting their function to sites of synaptic activity.

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4
Q

What happens upon ligand binding to CB1 receptors?

A

Activation leads to a decrease in cAMP by inhibiting adenylate cyclase activity.

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5
Q

How do CB1 receptors affect G proteins?

A

They are coupled to PTX-sensitive Gi/o type G proteins.

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6
Q

Where are CB2 receptors primarily found?

A

In cells and tissues of the immune system.

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7
Q

What is the association of CB2 receptor expression in the CNS?

A

Linked with inflammation and primarily localized to microglia.

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8
Q

How do CB2 receptors affect microglia function?

A

They modulate microglial function which is relevant in Alzheimer’s disease.

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9
Q

What is the role of CB2 receptors in neurons?

A

Control synaptic function and are involved in drug abuse and synaptic plasticity.

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10
Q

How are cannabinoids (CBs) produced?

A

Produced on demand, typically triggered by increased intracellular calcium at postsynaptic sites.

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11
Q

What are the key regulatory functions of the ECS in the brain?

A

Controlling mood, pain perception, learning, and memory.

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12
Q

How do endocannabinoids (eCBs) function in the CNS?

A

Act as retrograde messengers, mediating feedback inhibition and modulating synaptic plasticity.

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13
Q

What results from prolonged exposure to CB1 receptor agonists?

A

Tolerance, attributed to desensitization and reduction in cell surface-expressed receptors.

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14
Q

What is Sativex and its effects on MS patients?

A

A cannabis extract spray improving symptoms in MS, reducing motor dysfunction and pain.

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15
Q

Why is Sativex not recommended by the UK’s National Institute for Health and Care Excellence for treating spasticity in MS?

A

It is not cost-effective.

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16
Q

What molecular effects are linked to the activation of CB receptors?

A

Anti-inflammatory and neuroprotective effects via up-regulation of prosurvival molecules and reduction of cytotoxic factors.

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17
Q

How is the expression of ECS components altered in AD patients?

A

Changes in MAGLs levels suggest altered eCB signaling.

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18
Q

How might CB receptors be beneficial in AD experimental models?

A

Activation may offer neuroprotection against amyloid-beta toxicity.

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19
Q

What additional neuroprotective mechanism does CBD provide?

A

Reduces Tau protein phosphorylation in PC12 cells.

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20
Q

What are the main differences in expression between CB1 and CB2 receptors?

A

CB1 receptors are abundant in CNS regions, while CB2 receptors are predominantly in immune system cells.

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21
Q

What are the histological hallmarks of active MS?

A

Infiltrations of T cells, macrophages, B cells, degradation of myelin, and reactive changes in astrocytes and microglia.

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22
Q

What effects do cannabinoids have in an animal model of MS?

A

Alleviate spasticity and tremors.

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23
Q

What was the primary aim of the Cannabinoids in Multiple Sclerosis (CAMS) study?

A

To assess the beneficial effects of cannabinoids on MS symptoms.

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24
Q

How many patients and centers were involved in the CAMS study?

A

630 patients at 33 UK centers.

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25
Q

What treatments were compared in the CAMS study?

A

Oral cannabis extract, Δ9-tetrahydrocannabinol (Δ9-THC), and placebo.

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26
Q

What was the primary outcome measure in the CAMS study?

A

The Ashworth assessment of muscle spasticity.

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27
Q

What significant results were reported in the CAMS study?

A

Improvement in patient-reported spasticity and pain.

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28
Q

Was there a change in Ashworth score in the CAMS study?

A

No significant change in Ashworth score from baseline.

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29
Q

What other benefits did patients report in the CAMS study?

A

Improvement in walking time, spasticity perception, muscle spasms, pain, and sleep.

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30
Q

What did a subsequent study of cannabinoids in MS assess?

A

Long-term safety and effectiveness of cannabinoids in MS.

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31
Q

What was the primary outcome in the follow-up study to CAMS?

A

Change in the Ashworth spasticity scale.

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32
Q

How long did the follow-up study to the CAMS study last?

A

Up to 12 months.

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33
Q

What was the finding of the follow-up study?

A

A small treatment effect on muscle spasticity as measured by the Ashworth score.

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34
Q

What is Sativex and how is it administered?

A

A combined cannabinoid medicine (THC and CBD in a 1:1 ratio) administered via an oromucosal pump spray.

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35
Q

What were the findings related to Sativex in the treatment of MS?

A

Effective with no evidence of tolerance in patients with central neuropathic pain and MS over approximately 2 years.

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36
Q

What concerns remain regarding the long-term use of cannabinoids in MS treatment?

A

Potential side effects and the need for long-term studies to establish roles beyond symptom amelioration.

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37
Q

What did the Vaney et al. 2003 study report about cannabinoids in MS?

A

Indicated trends in reduction of spasms and improved mobility in patients.

38
Q

What type of clinical trial was the CAMS study?

A

A randomized, placebo-controlled trial.

39
Q

What secondary outcomes were measured in the follow-up study to CAMS?

A

Rivermead Mobility Index, timed 10-m walk, UK Neurological Disability Score, among others.

40
Q

What was the trial duration of the CAMS study?

A

15 weeks.

41
Q

What often accompanies paraparesis in patients?

A

Paresis and spasticity.

42
Q

What does spasticity commonly produce?

A

Pain and functional disability.

43
Q

Characteristic of hands in patients with cerebral lesions?

A

Tightly fisted, dystonic hands or paralysis with little spasticity.

44
Q

What is a common characteristic in patients with hemiplegia?

A

Rigid muscles which are length-sensitive.

45
Q

What differentiates patients with spinal lesions from those with cerebral lesions?

A

Exaggerated cutaneous reflexes.

46
Q

What can a non-noxious light touch on the distal lower extremity cause in spinal spasticity?

A

Massive reflex contraction (triple flexion).

47
Q

What type of pain do tonically contracting, dystonic muscles produce?

A

Chronic pain.

48
Q

When does full-blown spasticity develop compared to paresis after CNS damage?

A

Spasticity develops over time, whereas paresis is maximal immediately.

49
Q

What increases in spasticity?

A

Muscle tone, phasic proprioceptive, cutaneous, and autonomic reflexes.

50
Q

What could cause spastic hyperreflexia?

A

Increased excitability of LMN or segmental reflex arcs.

51
Q

What effect does serotonin have on motor neuron excitability?

A

It prolongs depolarization when neuron is activated.

52
Q

How might CNS damage affect presynaptic inhibition?

A

Reduce presynaptic inhibition, increasing tendon jerks and stretch reflexes.

53
Q

Major neurotransmitters related to spasticity and their roles?

A

Glutamate (excitatory), GABA (inhibitory), Glycine (inhibitory).

54
Q

How does dantrolene affect muscle contraction?

A

Blocks calcium release, interfering with excitation-contraction coupling.

55
Q

How does botulinum toxin A affect muscle activity?

A

Cleaves SNAP-25, interfering with acetylcholine release.

56
Q

What are three drugs widely used to treat spasticity?

A

Baclofen, diazepam, and tizanidine.

57
Q

What is the primary therapeutic action of baclofen?

A

It is a GABA-B agonist reducing excitatory transmission.

58
Q

How does tizanidine work?

A

It enhances noradrenergically mediated presynaptic inhibition.

59
Q

What are common side effects of oral medications for spasticity?

A

Sedation, weakness, and hepatotoxicity.

60
Q

What exacerbates spastic hypertonia?

A

Environmental factors, position, fatigue.

61
Q

What clinical manifestations does spasticity include?

A

Increased resistance to passive movement, clonus, spasms.

62
Q

How is spasticity differentiated from rigidity?

A

Spasticity occurs during muscle stretch and is velocity-sensitive.

63
Q

How does the Ashworth scale assess spasticity?

A

Based on examiner’s assessment of resistance during muscle lengthening.

64
Q

What does the pendulum test correlate with?

A

The Ashworth scale.

65
Q

What is the H-reflex?

A

An electrically elicited tendon jerk.

66
Q

What does a higher H/M ratio indicate?

A

Hyperactive tendon jerks in spastic patients.

67
Q

How does the UMN syndrome impact motor control?

A

It includes weakness, pattern movements, lack of fine motor control.

68
Q

How does peripheral changes affect hypertonia?

A

Changes in muscle properties contribute to resistance to passive movement.

69
Q

What is contracture and how is it related to spasticity?

A

Permanent loss of joint motion due to severe spasticity.

70
Q

What interventions can help manage contractures?

A

Range-of-motion exercises, splinting, and using casts.

71
Q

What are THC and CBD?

A

Tetrahydrocannabinol (THC) and Cannabidiol (CBD) are phytocannabinoids found in cannabis.

72
Q

What are endocannabinoids derived from?

A

All endocannabinoids are derived from Arachidonic acid.

73
Q

How many known endocannabinoids are there?

A

There are five known endocannabinoids.

74
Q

Name the five known endocannabinoids.

A

N-Arachidonoyl Ethanolamide (Anandamide), 2-Arachidonoyl Glycerol, 2-Arachidonoyl Glyceryl Ether (Noladin ether), O-Arachidonoyl Ethanolamine (Virodhamine), and N-Arachidonoyl Dopamine (NADA).

75
Q

What is the function of CB1 receptors?

A

CB1 receptors inhibit the release of neurotransmitters.

76
Q

Where are CB1 receptors primarily present?

A

In nerve terminals.

77
Q

What is the function of CB2 receptors?

A

CB2 receptors regulate cytokine production and immune cell movement.

78
Q

Where are CB2 receptors primarily expressed?

A

Mainly by immune cells.

79
Q

What disorders are linked to changes in the ECB system?

A

Neuronal disorders including age-related neurodegeneration.

80
Q

What effects do cannabinoids signaling through CB1 receptors cause?

A

Synaptic plasticity, cell migration, and neuronal growth.

81
Q

What effects are associated with cannabinoids signaling through CB2 receptors?

A

Mechanisms that stop, slow down, and repair damage caused by inflammation.

82
Q

What neurotransmitters does cannabinoid signaling regulate the release of?

A

Cholinergic and dopaminergic neurotransmitters.

83
Q

Where are CB1 receptors found in the brain?

A

Primarily in the hippocampus among other regions.

84
Q

What impact does acute cannabinoid use have on cognition?

A

Negatively impacts cognition, affecting processing speed, attention, and executive functioning.

85
Q

What long-term effects does cannabinoid use have on young adults?

A

Affects cognitive abilities including learning, memory, and psychomotor speed.

86
Q

How does cannabinoid use affect MS patients according to one review?

A

Potential improvements in cognition with medicinal cannabinoids for MS patients.

87
Q

What is Sativex?

A

A commercial cannabinoid formulation used as supplemental therapy for MS with moderate to severe spasticity.

88
Q

What conventional medical uses are associated with cannabinoids?

A

Reducing pain and spasticity caused by MS and spinal cord injuries.

89
Q

What benefits have MS patients reported from cannabinoid use?

A

Relief from symptoms such as spasticity, muscle discomfort, and pain at night.

90
Q

What are the biodistribution characteristics of THC?

A

High volume of distribution due to its high lipophilicity.

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