Summery Info-DD Flashcards

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1
Q

Phase One Reactions

A

Oxidations
Hydrolysis
Reductions

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2
Q

Phase Two Reactions

A

Conjugations

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3
Q

Phase One Enzymes

A

CYP450
esterase-amidase
reductase

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4
Q

Phase Two Enzymes

A

Transferase

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5
Q

Gen Polymorph Phase 1 and 2

A

significant

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6
Q

Phase One Induce- Inhibit

A

Significant

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7
Q

Phase Two Induce-Inhibit

A

Possible- Less

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8
Q

FDA Regulates

A

Drugs to be sold to the public
Evaluate new drug safety
Prescription vs non

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9
Q

State regulates

A

who can prescribe drugs

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10
Q

Local regulates

A

drug use in their area

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11
Q

Schedule 1

A

no medical use
high abuse potential
high phys/psy dependance

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12
Q

Schedule 2

A

medical use
high abuse potential
high phy/psy dependence

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13
Q

Schedule 3`

A

Medical use
Moderate abuse potential
moderate/high dependence

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14
Q

Schedule 4

A

medical use
Low abuse
Low dependence

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15
Q

Schedule 5

A

medical use
limited abuse
lowest dependence

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16
Q

Phase One CT

A

is it safe?
Pharmacodynamics- metabolism, toxicity, response

~100 Healthy human

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17
Q

Phase Two CT

A

Does it work in patients?- compare placebo/existing treatment with new
Also safety and dose

200-300 Subjects

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18
Q

Phase Three CT

A

Does it work Double Blind-

a. Compare established therapies
b. Adverse rxn studies
c. FDA grants approval

1000-6000 people

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19
Q

Phase Four CT

A

Post market surveillance

a. Mortality/morbidity
b. Physicians must report adverse reactions

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20
Q

Animal Studies

A

Follows in vitro tests (synthesis and bio products)
Efficacy
Safety
Mechanism

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21
Q

Most rapid (sec to min) onse

A

Inhalational (volatile gas-aerosol), intravenous

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22
Q

Intermediate (5-15 min) onset

A

Sublingual, intramuscular, subcutaneous, buccal

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23
Q

Slower (15-30 min) onset

A

Oral - immediate release formulations

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24
Q

Slowest Onset (hours)

A

Transdermal, Oral - enteric-coated and sustained release formulations, IM and SC (depot forms)

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25
Q

Vd 3-5 compartment

A

Highly bound to plasma proteins

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26
Q

Vd 12-15 compartment

A

Highly water soluble. enters the cell poorly

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27
Q

Vd 42 L compartment

A

drugs that freely enter cells

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28
Q

Over 50 Vd

A

often highly lipid soluble

Sequesters at spesific site ex: CNS, Fate, Protein

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29
Q

pH>pKa

A

A- and B predominate

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30
Q

pH<pKa

A

HA and BH+ predominate

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31
Q

Inducer/Inhibitor definition

A

Inducer: Increase CL (7-10 days)

Inhibitor: Inhibit CL, inc drug levelsto possibly toxic

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32
Q

Cimetidine

A

Inhibitor

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33
Q

Phenytoin

A

Inducer

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34
Q

Erthromycin/clarithromycin

A

inhibitor

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35
Q

Azol Antifungal

A

Inhibitor

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36
Q

Carbamazepine

A

Inducer

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37
Q

Phase One saturablity

A

minimal

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38
Q

Phase Two saturablity

A

substantial

39
Q

Rifampin

A

Inducer

40
Q

Fluoxetine

A

Inhibitor

41
Q

Grapefruit Juice

A

Inhibitor

42
Q

Phenobarbital

A

Inducer

43
Q

Ethanol

A

Inducer

44
Q

St. Johns Wort

A

Inducer

45
Q

HIV protease inhibitor

A

inhibitor

46
Q

Tobacco Smoke

A

Inducer

47
Q

Omeprazole

A

Inhibitor

48
Q

Acetaminophen poison

A

N-acetylcysteine (Mucomyst)** antidote

49
Q

Methanol, ethylene glycol poison

A

Ethanol, 4-methylpyrazole (Antizol)** antidote

50
Q

Pregnancy risk A

A

no known risk to the fetus

51
Q

Pregnancy risk B

A

no evidence for risk in humans

52
Q

Pregnancy risk C

A

Risk cannot be ruled out (no studies or bad animal studies)

53
Q

Pregnancy risk D

A

Positive risk, life threatening situations only

when use outweighs harm

54
Q

Pregnancy risk X

A

DO NOT USE

risks outweigh any benefit

55
Q

Chemical Antagonist

A

No receptor involved

56
Q

Physiological Antagonist

A

Acts on a separate receptor

57
Q

Allosteric binding

A

noncompetitive

58
Q

Irreversible active site binding

A

non competitive

59
Q

Reversible active site binding

A

competitive

60
Q

bio-equivalent products are considered to be

A

therapeutic equivalent

61
Q

Cmax

A

measures rate of absorption

Measure of bioequivalence

62
Q

Tmax

A

measure rate of absorption

Measure of bioeq

63
Q

AUC

A

measures extent of absorption

64
Q

Controlled substance potentials

A

Medical usefulness
Abuse potential
Dependence risk

65
Q

Colorado Controlled Substance Prescription requirements

A

requires a prescription for schedule V

and 2-4

66
Q

Abbreviations to avoid

~timing

A

qd
qid
qod

67
Q

Abbreviations to avoid

~Routes

A
ad
as, al
au
od
os, ol
ou
68
Q

Tight cellular junction compartments

A

BBB
Gut
Kidney REABSORPTION

69
Q

Factors affecting membrane passage

A

Molecular size- plasma protein binding
lipid solubility- oil water partion
degree of ionization- affected by tissue pH
concentration gradient- at site of admin

70
Q

Passive diffusion through membrane

A

Lipid soluble drugs

71
Q

Passive diffusion of water soluable drugs

A

aq channels

72
Q

Routes affected by first pass metabolism

A

oral, rectal

73
Q

Routes for systemic effect

A
oral 
rectal 
sub lingual/buccal
intravenous
IM
sq
Volitle inhalation
Trandermal
74
Q

Drug bioavailability

A

fraction of dose reaching blood

75
Q

Rate of onset of drug effect

A

time to peak effect

76
Q

Duration of drug action

A

time above MEC

77
Q

Single dose equation

A

cp=DOSE/Vd

78
Q

Endogenous/Phase2

A

substrate combines with pre-existing or metabolically inserted functional group (via Phase I reaction) on the drug

79
Q

Time to see drug induction

A

7-10 days

80
Q

Inhibition time frame

A

hours, dependent on the inhibited drug’s half-life

81
Q

First order kinetics

A

Proportional clearance (fraction)
Most drugs follow this patter
Hepatic and renal

82
Q

Zero order kinetics

A

Constant clearance

83
Q

Time to eliminate a drug

A

4-5 half lives

84
Q

Time to reach steady state

A

4-5 half lives

85
Q

Inducers and inhibitors affect which metabolism?

A

Hepatic

86
Q

Potency

A

concentration (EC50) or dose (ED50) required to produce 50% of the individual drug’s Emax

87
Q

Emax

A

limit of dose-response relationship on response (y) axis

most important
determinant of clinical utility

88
Q

antagonist definition

A

binds to the drug receptor but is unable to bring about the characteristic response

rather, it blocks response

89
Q

Competitive Antagonist graphical changes

A

EC50 increases (potency decreases) - Emax unchanged (surmountable)

90
Q

non-Competitive Antagonist graphical changes

A

Minimal effect on EC50 - Emax is reduced (insurmountable)

91
Q

Toxic doses of acetaminophen

A

N-acetylcysteine antidote
Gastric lavage
helps to prevent hepatic cell death

92
Q

acetaminophen with ethenol

A

causes hepatic cell death

93
Q

Methanol Poisoning toxin

A

formaldehyde formic acid

treated with ethanol

94
Q

Ethylene gycol toxin

A

oxalic acid

treated with ethanol