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PHAR300 > L9 CNS stimulants (cocaine, amphetamines, caffeine) > Flashcards

L9 CNS stimulants (cocaine, amphetamines, caffeine) Flashcards

1
Q

What are 3 CNS stimulants (other than nicotine)

A

Cocaine, Amphetamine, Caffeine

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2
Q

TF: all CNS stimulates activate the rewards pathway and cause psychological and sometimes physiological dependence

A

True

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3
Q

How is powder cocaine referred to? and the solid form?

A

powder = cocaine hydrochloride
solid = crack (free base cocaine)

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4
Q

TF: cocaine has very rapid onset

A

True

and this promotes addiction if smoked

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5
Q

How does cocaine act as a local anesthetic

A

is interferes with voltage gated ion channels located in the axons which decreases axon conduction

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6
Q

Where are the 2 main places that cocaine acts on

A

1) the synapse at the nerve ending at reuptake pumps
2) ion channels along the axons (signal transmission)

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7
Q

In what way does cocaine affect the reuptake pumps at the presynaptic terminal

A

it blocks the reuptake of multiple neurotransmitters (dopamine, NE, serotonin) which increases the levels of these neurotransmitters in the synapses (CNS) and in the periphery (NE)

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8
Q

What major neurotransmitters does cocaine affect?

A

dopamine (reward pathways)
serotonin (many pathways)
NE (ANS - autonomic nervous system)

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9
Q

What is consequence of increasing neurotransmitter levels in the synapse?

A

leads to increase postsynaptic response

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10
Q

TF: cocaine is an appetite-suppresant

A

true

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11
Q

Why did people postulate the cocaine could help with opium and alcohol addicts?

A

People thought that the use of a CNS stimulant would counteract the effects of CNS depressants

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12
Q

What are the pharmacodynamic effects of cocaine

A

it blocks voltage gated Na+ (sodium) channels on axons which makes it an effective local anesthetic

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13
Q

Does cocaine increase or decrease glucose utilization by the brain

A

decrease

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14
Q

When cocaine is smoked or sniffed or injected, the effects are systemic or localized? Why?

A

systemic since Na+ channels are present on all excitable tissue

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15
Q

Why are the initial effects of cocaine use in the CNS excitatory?

A

there is decreased dopamine, NE, and serotonin reuptake resulting in convulsions

then inhibition occurs at higher doses which can lead to respiratory arrest

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16
Q

Why is cocaine a risk factor for cardiac arrest

A

the SA node can be blocked due to cocaine’s effects on Na+ channels in the heart and the Purkinje system (no depolarization due to blockage of action potential)

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17
Q

TF: other local anesthetics can also block neurotransmitter reuptake like cocaine

A

false, cocaine is unique in this function

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18
Q

what is the pharmacodynamic explanation has to why cocaine users experience a high

A

cocaine blocks the reuptake of neurotransmitters causing high levels of dopamine, NE, or 5HT in the synapse

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19
Q

How are cocaine derivatives which are used as local anesthetics today different from cocaine

A

cocaine derivatives only act on blocking the Na+ ion channels without interfering with neurotransmitter reuptake

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20
Q

what family of receptors is involved in amine neurotransmitter reuptake?

A

neurotransmitter/sodium symporter (NSS)

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21
Q

TF: excess dopamine is neurotoxic

A

true

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22
Q

why does cocaine cause hyperactivity

A

because it blocks the reuptake of NE at autonomic nerve endings (sympathetic nervous system, part of the ANS - autonomic nervous system)

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23
Q

TF: cocaine activates the reward pathway and the sympathetic fight-or-flight response simultaneously

A

true

dopamine (and serotonin) for reward pathway
NE for fight-or-flight in ANS, sympathetic system

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24
Q

How was the role of cocaine in the mesolimbic reward pathway identified

A

destruction of dopaminergic neurons (involved in the mesolimbic reward pathway) resulted in disinterest in cocaine

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25
Q

What kind of receptors does dopamine act on

A

GPCRs, mainly D2 dopaminergic receptors is involved in the mesolimbic reward pathway

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26
Q

How many kinds of dopaminergic receptors are there

A

at least 5 kinds

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27
Q

TF: inhibiting dopamine reuptake stimulates dopamine rectors only in specific areas of the brain

A

false, the whole brain is affected

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28
Q

the method of drug delivery affects what two things?

A

the rate of absorption
the peak concentration of the drug in blood

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29
Q

Why is snorting cocaine dangerous for blood flow?

A

snorting causes intense vasoconstriction -vasospasm- that could lead to tissue death in the nose due to impaired blood flow - physical injury to the nose to the point of ischemia (insufficient blood supply to organs)

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30
Q

TF: cocaine can cross the blood brain barrier

A

True

because it is small and lipid soluble

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31
Q

Why do people tend to binge use cocaine?

A

cocaine levels quickly rise in the brain, followed by a decrease due to it being redistributed to the rest of the body. In other words, the effects wear off quite quickly causing people to binge use cocaine

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32
Q

Which enzyme metabolizes cocaine

A

Human carboxylesterase 1 (hCE1)

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33
Q

Are cocaine metabolites biologically active?

A

yes, some but not all

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34
Q

TF: Consuming alcohol with cocaine does not change the pharmacokinetics of cocaine metabolism

A

False,

consuming alcohol with cocaine results in a different and toxic metabolite called cocaethylene

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35
Q

What makes cocaethylene a toxic metabolite?

A

it has a longer half-life (3-5x longer, 1-2 hours) resulting in a much lower LD (lethal dose)

it has similar but worse toxicity as cocaine - higher risks of cardiac arrest, chronic use can lead to severe liver damage and cerebral infarct (an area of the brain that has suffered from a lack of blood supply, resulting in tissue damage or cell death due to insufficient oxygen and nutrients)

36
Q

TF: you can tell whether an individual has been exposed to cocaine by examining their hair

A

true, cocaine metabolites are deposited in hair

37
Q

What are some cardiovascular toxicities that cocaine can cause

A

arrythmias
myocardial infract (heart attack) (largely due to Na+ channel blocking affecting the heart’s conduction system)
vasoconstriction

38
Q

what is vasospam

A

it is when the diameter of your blood vessel becomes so small it can affect blood flow, it is particularly dangerous if it occurs in the coronary artery because the heart muscle can die and it can cause arrythmias. It can also occur in the brain and affect breathing and cardiovascular function

39
Q

what is the difference between vasoconstriction and vasospasm

A

Vasospasm is a specific type of vasoconstriction, but it typically refers to an abnormal and sudden, often exaggerated, constriction of blood vessels. Vasospasms can be more intense and prolonged than regular vasoconstriction

40
Q

what causes hypertension (particularly in cocaine users)

A

increase in NE that stimulates the sympathetic system of the ANS resulting in vasoconstriction

41
Q

TF: chronic cocaine users then to get artherosclerosis

A

true

42
Q

TF: strokes can occur even after acute use of cocaine

A

True

due to vasospasm in the nose
chronic use results in damage to vasculature in the brain

43
Q

Why does cocaine abuse increase the likelihood of rupturing an aneurysm (bulging in the wall of a vessel)

A

it increases pressure in the vascular system in the brain, facilitating the rupture and thus causing a hemorrhagic stroke

44
Q

What are some consequences of constant activation of the sympathetic system (ANS fight or flight)

A

hypertension
vasoconstriction and vasospasm
arrythmias
sudden death

** not seizures since that is controlled by CNS

45
Q

what is agitated delirium and how much cocaine is needed to cause this

A

it is caused by a moderate dose meaning first time users can die from this - it is only in a subgroup of cocaine users

it is fatal

it results in respiratory arrest and hyperthermia (increase in body temperature incompatible with life) +delirium and agitation

it is unclear what causes it but some suggest its due to D2 variant receptors being linked to temperature control

46
Q

What is crack lung and what causes it

A

it is acute pulmonary injury due to altered blood flow which causes pulmonary embolism and tissue death

people can recover from this

47
Q

TF: cocaine can stimulate aggressive tendencies which can also cause death i.e. cocaine can indirectly cause death

A

true

48
Q

how are “crack babies” characterized

A

fetal hypoxia due to vasocontraction (less blood flow to placenta), premature labor, limb abnormalities, impaired brain development

49
Q

TF: the accumulated dopamine in the synaptic cleft isn’t broken down and remains there until reuptake is possible

A

false,

dopamine is broken down by enzymes eventually

50
Q

TF: the newly synthesized dopamine receptors are also more sensitized

A

true

51
Q

Why would the body create more dopamine receptors if they are already being activated at a higher extent?

A

Lack of dopamine in presynaptic terminals due to blocked reuptake signals the body to make new receptors

52
Q

how do glutamate receptors change with addiction?

A

there are fewer receptors (think of the rebound excitation effect) and new types of glutamate receptors (combination of different subunits)

53
Q

TF: the effects of substance abuse in ex-alcoholics last longer than ex-cocaine users

A

false

residual effects from cocaine use are longer lasting than those from alcohol use

54
Q

TF: chronic cocaine use results in increased cell density in the brain

A

false, cell density decreases

55
Q

why do cocaine users commonly use alcohol and heroin/fentanyl with cocaine

A

because cocaine makes people irritable, alcohol and heroin are used in hopes to counter this irritability

56
Q

Explain why cocaine users experience dysphoria (despair) when going through withdrawals

A

This is because during withdrawal, D2 receptors which were overstimulated during cocaine use have been downregulated, transporters have been upregulated resulting in dopamine deficiency

57
Q

which neurotransmitters do amphetamines act on and in what way?

A

amphetamines increase the release of dopamine and NE as well as block their reuptake

58
Q

what is the function of the noradrenaline pathway in the brain

A

involved in keeping you awake and alert

59
Q

TF: you gain resistance to the effects of amphetamines on motor activities after chronic use

A

false, you never get resistance to the effects of amphetamines on motor activity, though there is an increase in tolerance

60
Q

what are some derivatives of amphetamines

A

methamphetamine (meth) - “ice” refers to the smokable form
MDMA (ecstasy)

61
Q

How do amphetamines act on MOA (monoamine oxidase)

A

amphetamine derivatives block MAO, thus blocking the breakdown of dopamine and noradrenaline

62
Q

how does amphetamine act on the dopamine transporter at the synaptic terminal?

A

i causes reverse translocation of dopamine - the transporter pushes out dopamine into the synaptic cleft instead to recycling the dopamine back into the neuron

63
Q

through which mechanisms does meth lead to apoptosis

A

oxidative stress, excitotoxicity and neuroinflammation

64
Q

why does chronic use of meth result in neuronal loss?

A

the dopaminergic neurons are damaged due to increased calcium in the cell (which is cytotoxic)

65
Q

How is meth abuse related to Parkinson’s disease?

A

meth can destroy dopaminergic neurons, which is a predisposition to PD

66
Q

Are there more or less dopamine receptors in the brain of a meth user? Why?

A

Less, because meth and amphetamines upregulate dopamine levels in the synaptic cleft and to adapt to these elevated dopamine levels, neurons express less receptors

67
Q

TF: cognitive function recovers in meth users

A

false

although dopamine transporters can recover, there is permanent loss of function due to neuronal loss

68
Q

ecstasy (MDMA) acts on what kinds of neurons? are they different from the neurons meth acts on?

A

serotonergic, dopaminergic, and noradrenergic neurons

(same as meth)

69
Q

TF: ecstasy has hallucinogenic effects

A

true

70
Q

ecstasy blocks or activates serotonin transporter 5-HT transporter? how does this affect the level of serotonin in the synaptic cleft

A

it blocks 5-HT transporters, thus increasing the level of serotonin in the synaptic cleft

71
Q

TF: serotonin only affects the reward pathways

A

false, serotonin is important in many regions of the brain thus many pathways

72
Q

what unpleasant symptoms can MDMA (ecstasy) cause? what are the short-term and long term effects?

A

bruxism (jaw-clenching), hyperthermia, clouded thinking, arrythmia, renal failure

short term: irritability, depression, heightened perceptions, stimulation, reduced appetite, elevated moods

long term: neurotoxicity, change in brain chemistry (less serotonin and metabolites), change in brain structure & transporters in the cerebral cortex

73
Q

TF: An individual that abuses meth can recover back to normal within 5 years

A

false,

neurons and transporters are still damaged after 7 years, research shows

74
Q

what is herbal ecstasy? is it safer than normal ecstasy

A

it is a plant derived amphetamine that is safer than MDMA but still not safe

75
Q

When using ecstasy, what happens to serotonin and serotonin transporters/terminal

A

serotonin and its metabolites are reduced, serotonin transporters are reduced and serotonin terminals degenerate

76
Q

which family is caffeine part of

A

xanthine

77
Q

explain the pharmacokinetics of caffeine

A

rapid absorption & distribution to all tissues and through the BBB
rapidly metabolized by liver

78
Q

why is the half-life of caffeine lesser in smokers?

A

drug metabolizing enzymes are induced in smokers (metabolizes faster in smokers)

79
Q

How does the half-life of caffeine change with age

A

newborns have long caffeine half-lives since they do not possess the right enzyme for caffeine metabolism

80
Q

TF: caffeine is a competitive agonist of adenosine receptors

A

False, it is a competitive antagonist of adenosine receptors

81
Q

what kind of receptors are adenosine receptors? what is the effect of adenosine on neurotransmitters such as glutamate, ACh, DA, NA, GABA?

A

GPCRs, it is a neuromodulator that inhibits the release of various neurotransmitters

82
Q

Adenosine lowers/enhances activity in cholinergic stimulatory networks

A

lowers

83
Q

knowing that adenosine acts on cholinergic networks, how does caffeine act as a CNS?

A

it blocks adenosine receptors (competitive antagonist) resulting in lowered inhibition of neurotransmitter release (more excitation)

84
Q

which organs does caffeine affect

A

brain, heart, cerebral vessels, GIT (increase gastric acid), kidneys (diuresis)

85
Q

TF: tolerance to caffeine is slow

A

false, it is rapid

tolerance = more adenosine receptors are synthesized

86
Q

TF: individual prone to panic attacks can drink coffe

A

false

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