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PHAR300 > L10 Benzodiazepines and Cannabinoids > Flashcards

L10 Benzodiazepines and Cannabinoids Flashcards

1
Q

TF: there is conclusive evidence that cannabinoids have therapeutic effects for chronic pain in adults and chemotherapy-induced nausea/vomiting

A

true

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2
Q

what are the 2 major compounds in marijuana

A

THC (tetrahydrocannabinol)
CBD (cannabidiol)

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3
Q

What receptors do cannabinoids act on and where are they located

A

CB1 (GPCR): brain (psychotropic effects)
CB2: immune system/periphery

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4
Q

What is the action of cannabinoids on CNS? Which receptor is activated?

A

inhibition of GABA, glutamate, dopamine mainly presynaptically
CB1 receptors

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5
Q

what are the functions associated with the hippocampus?

A

stress, learning, memory

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6
Q

what functions are associated with the medulla

A

nausea/vomiting, CTZ

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7
Q

what functions are the basal ganglia and the cerebellum involved with

A

movement

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8
Q

TF: hypothalamus is associated with higher cognitive function

A

false

it is associated with appetite

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9
Q

what are the 3 families of compounds that act on cannabinoid receptors

A

1) endocannabinoids: made in the body
2) phytocannabinoids: plant-derived cannabinoids similar to endocannabinoids
3) synthetic cannabinoids: made in labs, mimics of THC and other plant-derived compounds

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10
Q

What are the major endocannabinoids? Which compound are they derived from and how are they produced?

A

anandamide, AEA (arachidonoylethanolamide)
2-AG (2-arachidonoylglycerol)

both are arachidonic acid derivatives (arachidonic acid is a constituent of the plasma membrane and a precursor of many compounds)

produced/synthesized by postsynaptic enzymes (thus in the postsynaptic neuron) so that they can act on presynaptic CB1 receptor to inhibit transmitter release (that is the role of CB1)

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11
Q

explain what the retrograde signaling system does in the context of cannabinoids

A

it involves the presynaptic inhibition of transmitter release

  1. AEA or 2-AG (endogenous cannabinoids) are synthesizes in the post-synaptic neuron and act pre-synaptically at the CB1 receptor
  2. activation of CB1 at pre-synaptic terminal decreases Ca2+ intake (blocks channels) into pre-synaptic neuron and increase K+ efflux into synaptic cleft (opens channels) - it also inhibits vesicle exocytosis
  3. decreased reuptake of calcium thus decreasing release of neurotransmitters (also cell hyperpolarization decreases excitability as well)
  4. less neurotransmitters = less stimulation
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12
Q

which compounds can act on CB1

A

endocannabinoids (AEA, 2-AG), THC, dronabinol, nabilone

*NOT CBD (low affinity)

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13
Q

activation of CB1 opens/blocks calcium channels and opens/blocks potassium channels

A

blocks calcium channels (decreasing synaptic transmission)
opens potassium channels (hyperpolarization

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14
Q

TF: cannabinoid receptors are on multiple types of cells

A

true

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15
Q

How can cannabinoids be absorbed?

A

smoking, ingesting/orally (readily absorbed by small intestine and colon), skin/topical (lipid soluble compounds)

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16
Q

how are cannabinoids distributed in the body

A

they are distributed to extracellular water since they are highly lipid soluble

they can also be stored in fat

some bind to serum proteins

rapidly cross the blood brain barrier

can also be passed to the fetus

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17
Q

where does cannabinoid metabolism occur? does it result in metabolites?

A

liver, yes

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18
Q

how are cannabinoids excreted

A

through saliva, sweat, urine (largely), feces, bile

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19
Q

where are the major sites of action for THC and CBD?

A

THC: CYP1A2 inducer
CBD: CYP3A4 inhibitor

both are involved in the metabolism of many other drugs

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20
Q

Why must you be cautious of THC and CBD use when consuming other drugs?

A

THC and CBD can modify the metabolism of other drugs

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21
Q

TF: Smoking weed isn’t harmful to lungs

A

false

there are carcinogens when smoking weed (similar to smoking cigarettes)

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22
Q

what are the main risks associated with smoking cannabis

A

cancer, heart attacks, strokes

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23
Q

TF: cannabinoids do not act on the reward pathway in the brain

A

false, they do act on the reward pathway

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24
Q

Can chronic use of cannabinoids change the properties of GABA and glutamate receptors?

A

yes (the details are still being researched)

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25
Q

what is the likely withdrawal reaction associated with chronic cannabinoid usage (CUD - cannabis use disorder)

A

withdrawal is likely excitatory since cannabinoids have inhibitory action

non-lethal (like nicotine)

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26
Q

TF: schizophrenia is more dependent on genetic factors rather than environmental factors

A

false, it is the opposite

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27
Q

how are dopamine levels in a schizophrenic patient?

A

dopamine levels are elevated

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28
Q

what is the name of the first effective neuroleptic (antipsychotic) drug

A

Chlorpromazine

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29
Q

TF: Amphetamines and cocaine (CNS stimulants) caused higher risks of schizophrenia

A

True, since these would block dopamine reuptake thus increasing dopamine levels

30
Q

Which receptor does chlorpromazine act on and in what way

A

D2 receptor, blocks it thus preventing activation by dopamine

BUT not selective and will block other things

31
Q

What is the effectiveness of antipsychotic drugs based on?

A

the blocking of D2 receptors

32
Q

which pathways do antipsychotic drugs act on

A

mesolimbic and mesocortical

33
Q

overactivation of the mesolimbic and mesocortical pathways due to incerased dopamine causes what effects respectively?

A

mesolimbic: delusion and hallucination
mesocorticol: impaired effect, intellectual impairment, defective cognitive abilities

34
Q

TF: dopamine receptors can excite or inhibit

A

true

35
Q

is D2 an excitatory or inhibitory dopamine receptor

A

inhibitory

Blocking D2 receptors can help reduce the overactivity of dopaminergic transmission, particularly in the mesolimbic pathway, which is thought to contribute to symptoms like hallucinations and delusions.

36
Q

What are the 4 major categories of antidepressants and what do they act on?

A

they mainly act on the metabolism and uptake of transmitters

1) MAOIs (monoamine oxidase inhibitors)
2) Tricyclic antidepressants
3) SSRIs (selective serotonin reuptake inhibitors)
4) Atypical NA + 5-HT reuptake inhibitors

37
Q

Where are MAOs found and what do they do

A

in the presynaptic terminal and in the synaptic cleft, they breakdown neurotransmitters (NA, DA, 5-HT)

38
Q

How do tricyclic antidepressants help with depression

A

they interfere with neurotransmitter reuptake by blocking 5-HT and NA transporter

though this has many side effects due to blocking other receptors (adrenergic, histamine, cholinergic)

39
Q

Why do tricyclic antidepressants cause so many side effects

A

NA blockage affects vascular system (sympathetic nervous system)
histamine receptor blockage causes sedation
ACh receptor blockage affects GI tract and vision

40
Q

What distinguishes SSRIs from other antidepressants

A

they are more specific as they only block 5-HT reuptake transporters without inhibiting reuptake of other neurotransmitters

41
Q

TF: 5-HT receptors are only found in the CNS

A

false,

found in smooth muscles, platelets, CNS, PNS, GIT, blood vessels, etc.

42
Q

TF: 5-HT3 is a GPCR 5-HT receptor

A

false, it is an ion-gated ion channel

though most 5-HT receptors are GPCRs

43
Q

what is commonly administered SSRI

A

fluoxetine (prozac)

most effective at inhibiting 5-HT reuptake with lower side affects due to being more selective

44
Q

which type of antidepressant is most used nowadays

A

SSRIs

45
Q

Why is the brain so difficult to study in terms of drug action and effect

A

neurons follow a diffused patterns making it difficult to pinpoint the order of transmission

46
Q

What are benzodiazepines used to treat

A

anxiety

47
Q

what are the major effects of benzodiazepines

A

antianxiety (hippocampus and amygdala)
sedative/hypnotic (cerebral cortex)
anticonvulsant (cerebellum, hippocampus)
muscle relaxant (spinal cord, cerebellum, brainstem)
amnesia (cerebral cortex, hippocampus)
antiepileptic (cerebellum, hippocampus)

48
Q

why do benzodiazepines have abuse potential

A

they can act on the midbrain which is involved in dopamine pathways

49
Q

what does it mean when the lethal to therapeutic dose is a small number

A

it means the lethal dose is very close to the therapeutic dose

50
Q

what is the first benzodiazepine drug to be widely used

A

diazepam (valium)

51
Q

TF: benzodiazepines act as antagonists to GABAA receptors

A

false, they act allosterically

52
Q

which was the first benzodiazepine

A

chlordiazepoxide (librium)

53
Q

describe the action of GABA receptors

A

2 neurotransmitters must bind, allowing Cl- influx into cell
this leads to hyperpolarization (inhibitory effect)
GABA thus has an inhibitory effect on many neurotransmitter systems
This results in antianxiety/sedative/anticonvulsant/etc. effects

54
Q

when benzodiazepine binds to the BDZ (benzodiazepine binding site), what happens?

A

the binding facilitates the 2 GABA neurotransmitters to bind thus increasing GABA activity and facilitates GABAergic inhibition

55
Q

TF: benzodiazepines and ethanol both act at the same location of the GABA receptor

A

false

benzodiazepines, ethanol, barbiturates, steroids, anesthetics all act on different locations of the same receptor

56
Q

what are the subsynaptic GABA_A receptors responsible for

A

phasic inhibition and major site of action of benzodiazepines

57
Q

what are the extrasynaptic GABA_A receptors responsible for

A

tonic inhibition

58
Q

TF: benzodiazepines will shift the dose-response curve to the right

A

false, it will shift to the LEFT

(increase chloride flow i.e. action of the GABA_A receptor)

59
Q

What is the difference between benzodiazepines and barbiturates

A

benzodiazepines affect frequency of opening (safer and more selective)

barbiturates increase the duration of channel opening and act directly to increase chloride passage through channel (affect many sites, not as safe)

60
Q

TF: it is easy to overdose on barbiturates

A

false

61
Q

why would one need to use a benzodiazepine antagonist? give an example of a benzodiazepine antagonist

A

to reverse the effects of benzodiazepines

flumazenil

62
Q

what is an inverse agonist of benzodiazepine? example and what it does

A

beta-carbolines

increase anxiety (opposite to benzodiazepines)

63
Q

inverse agonists of benzodiazepine shift the dose-response curve to the left/right

A

right

64
Q

TF: benzodiazepine inverse agonists bind to the same site as benzodiazepines

A

true

65
Q

What is Zolpidem

A

a nonbenzodiazepine that only binds to alpha 1 of GABAA receptor to treat insomnia without altering REM sleep (binds next to BDZ site)

66
Q

GABA + benzodiazepine agonist = ? (effect of GABA)

A

increased effect of GABA

67
Q

GABA + benzodiazepine inverse agonist = ? (effect of GABA)

A

decreased effect of GABA

68
Q

GABA + benzodiazepine antagonist = ? (effect of GABA)

A

no effect of GABA (GABA somewhat normal function depending on whether the antagonist is competitive or not, since BDZ is an allosterically binding molecule, i believe there would be no competition thus normal GABA function)

69
Q

what is Zolpidem

A

it is a newer drug that acts on GABAergic transmission, binds close (but not at) DBZ and has a range of side effects

70
Q

what effect do GABA_B agonists have?

A

they cause muscle relaxation

PHAR300 (13 decks)

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