2 - routes of administration Flashcards

1
Q

how much do genetic factors account for in the risk for addiction

A

50%

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2
Q

do monozygotic or dizygotic twins have a more similar rate of addiction

A

monozygotic

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3
Q

do kids have addiction habits more like birth family or adopted family

A

birth family

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4
Q

what is epigenetics

A

change in expression or regulation in genes

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5
Q

how do epigenetics play a role in addiction

A

long term neuroplasticity, they can be passed on

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6
Q

what did they find with the “candidate” genes (DAT, DRD2, OPRM1)

A

contradicting results, not just 1 gene has a role in addiction

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7
Q

what do genome wide associates studied (GWAS) do

A

compare as many genes as possible between dependent and non dependent subjects

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8
Q

do you need to know about certain candidate genes before doing a GWAS

A

no, because results of GWAS will show differences at any genetic location present

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9
Q

what do GWAS tell us about addiction (3)

A
  • many different genes are involved (polygenic)
  • unexpected genes emerged
  • genes overlap with different drugs
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10
Q

what are some of the unexpected types of genes found in GWAS

A

genes that are involved in neuronal adhesion

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11
Q

what do neuronal adhesion genes do

A

help with learning and plasticity

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12
Q

what does the link between the drug-GWAS and the neuronal adhesion genes mean

A

that drug dependence may be a learning problem

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13
Q

do certain genes only cause addiction susceptibility to only 1 drug

A

no, gene changes make you susceptible to many different addictions in general, not just 1 drug

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14
Q

why is it hard to reproduce studies that link addiction to genetics

A

it is hard to define if someone is truly dependent and there is a large spectrum of dependence (people need different amounts of drug to getting to the point they want to achieve)

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15
Q

why are GWAS for drugs critizied

A

lots of stats involved, easy to make a mistake there

also people argue whether there are any truly significant variations in genes that lead to abuse/dependence

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16
Q

what are the 4 major routes of administration

A

mouth
injection
inhalation
insufflation(snorting)

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17
Q

what route of administration has the fastest route to brain

A

inhalation

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18
Q

what route of administration has the second fastest route to brain

A

injection

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19
Q

what route of administration has the third fastest route to brain

A

snorting

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20
Q

what route of administration has the slowest route to brain

A

ingestion

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21
Q

what route of administration has the highest peak of concentration in the brain

A

inhalation slightly higher than IV

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22
Q

do slower administration methods have a high concentration peak

A

no

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23
Q

do faster administration methods have a high concentration peak

A

yes

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24
Q

do slower administration methods have an intense high

A

no

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25
do faster administration methods have an intense high
yes
26
do slower administration methods last a long time in brain
yes
27
do faster administration methods last a long time in brain
no
28
what is bioavailability
the fraction of drug that ends up in circulation
29
what is the bioavailability for IV drug intake
100%
30
what are the 2 main properties of drugs that make them easily absorbed in the gut
lipid soluble | uncharged
31
what is first pass metabolism
when drugs are metabolized by enzymes in the liver or gut before entering general circulation
32
why do we eventually sober up from drugs but why isnt it immediate
many drugs arent 100% metabolized by the liver the first time through, so thats why it takes time
33
what are the main enzymes in the liver that provide the majority of metabolism
cytochrome P450 enzymes | -CYP
34
does intravenous, intramuscular or subcutaneous injections have 100% bioavailability
only IV
35
why does injection have high bioavailability
avoids first pass metabolism
36
how does rate of injection affect peak height
pushing the drug faster makes the peak higher
37
where is a good place to inject if there are drugs with contaminants and why
blood vessels because they are insensitive in irritants
38
what are the downsides to injecting into veins (2)
veins collapse due to inflammation and risk of disease/infection
39
is intramuscular or subcutaneous quicker at absorbing
intramuscular because of better blood supply to the muscle
40
rate thigh, glutes and deltoid in terms of fastest absorption rate
fastest is deltoid, then thigh, then glutes
41
can IM or subQ inject more volume
IM
42
does IM or subQ have a higher chance of irritation
subQ
43
why does inhalation occur faster than IV (for drugs to get in brain)
inhale - lungs to brain | IV - vein to heart to lung to brain
44
what is a difficulty in inhalation
hard to control doses
45
how can snorting and chewing avoid first pass metabolism
if you use the mucous membranes in the mouth or nose (cocaine or chewing tobacco)
46
what kind of drugs have the lowest abuse potential
hallucinogens
47
what kind of drugs have the highest abuse potential
IV or smoked things
48
what are the 4 main things in pharmacokinetics
ADME | absorption, distribution, metabolism and excretion
49
are drugs free or bound to plasma protein
both
50
what 3 factors determines how much drug is in the plasma
rate of absorption, excretion and metabolism
51
how are drug removed from the body
excretion and/or metabolism (some drugs are excreted unchanged/unmetabolized)
52
what is a drug half-life?
the time it takes for the concentration of drug in plasma to fall 50%
53
what does the dose response curve describe
amount of drug in system and the response it produces /or %of a population in affects
54
why is there overlap in the curves in the dose response curve
because some people are affected quicker than others
55
what is TD50
the concentration of drug that is toxic in 50% of subjects
56
what is ED50
the concentration that produces the desired effect in 50% of users
57
what is theraputic index formula
LD50/ED50 | the ratio
58
what does theraputic index measure
how different a dose must be for the effective dose and the lethal/toxic dose measures safety of a drug
59
what does a low therapeutic index mean
not a big different in dosage from ED to TD (easier to overdose)
60
what does a high therapeutic index mean
big different in dosage from ED to TD (harder to overdose)
61
how can TI change when other drugs are present
they can drop dramatically