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PMCOL 305 > 2 - routes of administration > Flashcards

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
Q

do faster administration methods have an intense high

A

yes

26
Q

do slower administration methods last a long time in brain

A

yes

27
Q

do faster administration methods last a long time in brain

A

no

28
Q

what is bioavailability

A

the fraction of drug that ends up in circulation

29
Q

what is the bioavailability for IV drug intake

A

100%

30
Q

what are the 2 main properties of drugs that make them easily absorbed in the gut

A

lipid soluble

uncharged

31
Q

what is first pass metabolism

A

when drugs are metabolized by enzymes in the liver or gut before entering general circulation

32
Q

why do we eventually sober up from drugs but why isnt it immediate

A

many drugs arent 100% metabolized by the liver the first time through, so thats why it takes time

33
Q

what are the main enzymes in the liver that provide the majority of metabolism

A

cytochrome P450 enzymes

-CYP

34
Q

does intravenous, intramuscular or subcutaneous injections have 100% bioavailability

A

only IV

35
Q

why does injection have high bioavailability

A

avoids first pass metabolism

36
Q

how does rate of injection affect peak height

A

pushing the drug faster makes the peak higher

37
Q

where is a good place to inject if there are drugs with contaminants and why

A

blood vessels because they are insensitive in irritants

38
Q

what are the downsides to injecting into veins (2)

A

veins collapse due to inflammation and risk of disease/infection

39
Q

is intramuscular or subcutaneous quicker at absorbing

A

intramuscular because of better blood supply to the muscle

40
Q

rate thigh, glutes and deltoid in terms of fastest absorption rate

A

fastest is deltoid, then thigh, then glutes

41
Q

can IM or subQ inject more volume

A

IM

42
Q

does IM or subQ have a higher chance of irritation

A

subQ

43
Q

why does inhalation occur faster than IV (for drugs to get in brain)

A

inhale - lungs to brain

IV - vein to heart to lung to brain

44
Q

what is a difficulty in inhalation

A

hard to control doses

45
Q

how can snorting and chewing avoid first pass metabolism

A

if you use the mucous membranes in the mouth or nose (cocaine or chewing tobacco)

46
Q

what kind of drugs have the lowest abuse potential

A

hallucinogens

47
Q

what kind of drugs have the highest abuse potential

A

IV or smoked things

48
Q

what are the 4 main things in pharmacokinetics

A

ADME

absorption, distribution, metabolism and excretion

49
Q

are drugs free or bound to plasma protein

A

both

50
Q

what 3 factors determines how much drug is in the plasma

A

rate of absorption, excretion and metabolism

51
Q

how are drug removed from the body

A

excretion and/or metabolism (some drugs are excreted unchanged/unmetabolized)

52
Q

what is a drug half-life?

A

the time it takes for the concentration of drug in plasma to fall 50%

53
Q

what does the dose response curve describe

A

amount of drug in system and the response it produces /or %of a population in affects

54
Q

why is there overlap in the curves in the dose response curve

A

because some people are affected quicker than others

55
Q

what is TD50

A

the concentration of drug that is toxic in 50% of subjects

56
Q

what is ED50

A

the concentration that produces the desired effect in 50% of users

57
Q

what is theraputic index formula

A

LD50/ED50

the ratio

58
Q

what does theraputic index measure

A

how different a dose must be for the effective dose and the lethal/toxic dose

measures safety of a drug

59
Q

what does a low therapeutic index mean

A

not a big different in dosage from ED to TD (easier to overdose)

60
Q

what does a high therapeutic index mean

A

big different in dosage from ED to TD (harder to overdose)

61
Q

how can TI change when other drugs are present

A

they can drop dramatically

PMCOL 305 (26 decks)

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