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Disease and Defense class of 2019 > Pharmacology-Unit 1 > Flashcards

Pharmacology-Unit 1 Flashcards

1
Q

pharmacology

A

study of drug interactions (chemical substances) with biological systems

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2
Q

pharmacotherapy

A

selection of right drug/dose to interact with right target to produce a therapeutic effect

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3
Q

what are the therapeutic effects of pharmacotherapy?

A

prevention, diagnosis, treatment, cure of a disease

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4
Q

pharmacokinetic and pharmacodynamic principles allow what determination?

A

relationship btw. Dose of drug, plasma concentration (Cp) and clinical effect from that Cp

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5
Q

drug effects are directly correlated for what in clinical use?

A

Cp (plasma concentration)

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6
Q

graphs of what determine pharmacokinetics?

A

Cp vs. time

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7
Q

what is the MEC?

A

minimum effective concnentration

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8
Q

what can MEC be determined for?

A

for the therapeutic/desired response and adverse responses

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9
Q

onset of effect

A

time to reach MEC

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10
Q

duration of action

A

time above MEC

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11
Q

therapeutic window

A

difference in Cp btw. Desired and adverse response MEC

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12
Q

what is the goal of pharmacotherapy?

A

multiple doses are administered to maintain plasma concentrations at steady state in therapeutic window to produce responses with minimum toxicity

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13
Q

steady state

A

contition where rate in=rate out (elimination)

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14
Q

time to steady state

A

attained in 4-5 half lives when using maintenance doses at constant intervals

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15
Q

steady sate concentration

A

average Cp after SS is achieved

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16
Q

fluctuations in steady state Cp

A

the related number of half lives in dosing intervals (time btw. Doses)

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17
Q

dosage regimens are designed to ensure what?

A

steady state drug level is maintained in the therapeutic window

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18
Q

how do dosage regimens maintain a therapeutic window?

A

by balancing rate of elimination with prescribed rate of administration

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19
Q

how do you select drug and dose?

A

by looking at: pharmacodynamics–disease targets–drug regulation

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20
Q

how do you select a route of administration?

A

look at pharmacokinetics: absorbtion–distribution

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21
Q

how do you select drug duration?

A

base on disease pathophysiology

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22
Q

how do you select dosage frequency?

A

look at pharmacokinetics: metabolism–excretion

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23
Q

What should you see on a prescription?

A

drug, dosage, frequency, route, duration

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24
Q

pharmacodynamics is what?

A

what the drug does to the body, the mechanism of action

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25
Q

what does pharmocodynamics allow you to identify?

A

drug target and the therapeutic category of the specific drug

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26
Q

what are common drug targets?

A

intracellular receptors, enzymes, membrane transport proteins

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27
Q

do drugs have unique actions in the body?

A

NO! They enhance/blodk normal physiology of the organ systems

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28
Q

pharmacokinetics is what?

A

what the body does to the drug

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29
Q

what does pharmacokinetics provide a physician with?

A

information on absorption, distribution, elimination of drugs needed for dosing regimens

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30
Q

bioavailibilty (F)

A

how much of the dose of the drug reaches it’s target

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31
Q

time to peak effect (Tmax or Cmax)

A

how fast does the drug reach its target

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32
Q

volume of distribution (Vd)

A

what dose (mg) is needed to obtain desired Cp

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33
Q

absorption

A

passage of drug from administration site to blood

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34
Q

distribution

A

movement of drug from bloodstream to tissues

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35
Q

what must be considered when looking at distribution?

A

drug protein binding, passage across BBB/placenta, selecticve accumulation affecting efficacy/toxicity

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36
Q

route of administration

A

site of application of drug into/on the patient

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37
Q

what is a systemic effect?

A

absorbed into bloodstream for distribution ot sites of action in body

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38
Q

what is a topical effect?

A

remain at the site of application for local action

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39
Q

what is half life? (t1/2)

A

how long a drug stays at its target (duration of action)

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40
Q

what is elimination?

A

elimination of drug activity following administration. Can be done via metabolic or excratory paths

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41
Q

CL

A

clearance

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42
Q

describe a path of elimination/excretion

A

drug is absorbed into bloodstream, is distributed to site of action and organs of elimination (liver-metabolism, kidney-excretion)

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43
Q

what is the rate of elimination?

A

the length of time the drug remains in the bloodstream to exert clinical effects

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44
Q

therapeutic uses derive from?

A

mechanism of action–>Drug Target

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45
Q

how do drugs act?

A

via enhancement or blockade of physiological paths to alter an abnormal pahtophysiological disease state

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46
Q

are adverse reactions predictable from drug target mechanisms?

A

YES! Via mechanism of action

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47
Q

adverse reactions at a non-target system

A

side effects are seen at therapeutic doses, are dose-dependent and predictable

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48
Q

adverse reactions at target system

A

extension effects seen at higher than therapeutic doses (dose dependent and predictable)

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49
Q

adverse reactions not at drug target

A

idiosyncratic reactions (peculiar to individual). Less predictable/common

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50
Q

immunoligic reaction

A

allergic reaction

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51
Q

metabolic reaction

A

in origin (hepatotoxicity or blood dyscrasias)

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52
Q

what should you know about specific drugs/categories?

A

most common and severe effects

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53
Q

physiology of absorbtion

A

pharmacokinetic processes involving passage of drugs across membranes

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54
Q

what influences drug membrane passage?

A

molecular size, lipid solubility, degree ionization, concentration gradient

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55
Q

molecular size

A

can be affected by drug binding to plasma proteins

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56
Q

lipid solubility

A

estimated by oil:water partition coefficient

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57
Q

degree ionization

A

affected tissue pH, influences lipid solubility

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58
Q

concentration gradient

A

created at site of administration

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59
Q

list the mechanisms of membrane passage

A

passive diffusion, carrier mediated diffusion, endocytosis/exocytosis

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60
Q

passsive diffusion is driven by what?

A

driven by concentration gradient

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61
Q

aqueous diffusion/filtration

A

limited capacity, size varies, drugs

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62
Q

lipid diffusion

A

favored for drugs w/ high lipid:water partition coefficient, pH dependent, unionized moiety crsossed down conc. gradient. Drugs 500-800mw

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63
Q

carrier mediated diffusion

A

specialized transporters regulating entry/exit. Some transport foreign chemicals including drugs

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64
Q

endo and exo cytosis

A

vesicles that bring things in (vit B12 and iron) or release (neurotransmitters)

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65
Q

what does the effect of a drug on Cp depend on?

A

rate (time from peak to peak) and extent (bioavailability) of transfer of drug from administration site to blood

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66
Q

what is bioavailability (extend of absorption, F, f[%])?

A

the fraction of unchanged drug reaching systemic circulation after administration

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67
Q

how is bioavailability determined?

A

compare area under curve (AUC, from Cp vs. time) folloiwng a single dose of drug between IV and oral routes

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68
Q

what information is readily available for most drugs on extent of absorption?

A

bioavailability of oral route

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69
Q

what does knowledge of bioavailablity of a drug allow for?

A

dosage adjusmtents when giving the drug by a different route

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70
Q

IV administration

A

fraction of dose reading general circulation (F)=100%

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71
Q

oral administration

A

F varies from 100-0%

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72
Q

what does oral administration F depend on?

A

survival of GI environment, ability to cross GI membrane (lipid solubility, size, ionization state), efficiency of drug in gut wall/liver, variation btw. Patients

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73
Q

what is first pass effect?

A

a drug’s metabolic efficeincy in the gut wall/liver

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74
Q

what are some other routes of drug administration?

A

systemic drug action via IM, SC, inhalation, sublingual

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75
Q

what is the F for other routes of drug administration?

A

~100% (75-100%) since tissue is non-destructive to drugs

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76
Q

what is the rate of absorption estimated as?

A

the peak Cp or time to attain peak Cp plasma levels

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77
Q

what is the rate of absorption for oral route?

A

affected by preparation (liquid or rapid disentigration=faster; enteric coas or sustained release=slower), this changes time and Cp max

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78
Q

what is the rate of absorption for parenteral routes?

A

determined by the route rather than drug charachteristics. Intravenous=inhalation>intramuscular>subQ>oral

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79
Q

how is equivalency of drug products for the oral route determined?

A

FDA requires that formulations are bioequivalent. Rate and extent of active ingredient must be similar (within set limits) to brand name. if there is a 90% conficence interval in man AUC and mean Cmax is w/in 80-125% of brand name

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80
Q

what general factors affect drug absorption?

A

solubility in bilogic fluids (aq environment)=must be hydro and lipo phylic to cross membranes/distribute self; rate of solid dissoution; concentration of drug at site of administration; circulation at site of absorption; area of absorbing surface

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81
Q

what are the most important variable to consider about routes of drug administration?

A

bioavailability and rate of onset

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82
Q

what is the most common route for systemic effects?

A

oral. Slow onset of action, variable bioavailability

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83
Q

is absorption greater in the stomach or small intestine?

A

small intestine due to surface area

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84
Q

when is a drug favorable for absorption in GI tract?

A

when it is non-ionized and lipophilic

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85
Q

how does gastric emptying time effect absorption?

A

increased motility increases emptying speed and increases speed of absorption. Food delays gastric emptying and absorption

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86
Q

what do enteric coatings do?

A

prevent GI irritation, destruction from gastric secretions until they reach the basic intestines

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87
Q

slow release preparations do what?

A

slow rate of dissolution allowing for 8 hr or longer uniform absorption

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88
Q

what are the advantages to slow release preparations?

A

decreased frequency of administration, compliance, effect is maintained, eleiminates peaks/troughs

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89
Q

what are the disadvantages to slow release preparations?

A

greater independent variability, dose dumping, toxicity

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90
Q

describe rectal route charachteristics

A

not rapid onset, variable bioavailability (greater than oral route). Used when vomiting, unconscious, post GI surgery, GI irritation, uncooperative pt. 50% bypasses liver (less 1st pass than oral), faster onset of action. Useful for lipid soluble and potent drugs (

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91
Q

describe systemic IV route charachteristics

A

direct route, fastest (

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92
Q

describe systemic intramuscular route charachteristics

A

close to IV route (~90%), aqueous are absorbed quickly (5-10min), affected by blood flow/activity factors, depot/oil suspended vehicles are slower and sustained, can have erratic/incomplete absorption, can cause pain/necrosis/contamination

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93
Q

describe systemic subcutaneous route charachteristics

A

close to IV route (~100%), slower/constant rate of absorption, rate can be altered (eg: insulin), local anasthetics/contraceptives, non-irritating and volume limited

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94
Q

describe systemic inhalation route charachteristics

A

fast (

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95
Q

describe systemic transdermal route charachteristics

A

patch to skin allows for 1st pass avoidance, allows for prolonged drug levels, must be potent drug (

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96
Q

describe local inhalation route charachteristics

A

aerosol/microparticles molecules in suspension, increases local topical effects reducing systemic effects (asthma), depends on size (

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97
Q

describe local topical route charachteristics

A

treats local conditions, skin/mucosal membranes, minimal systemic absorption

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98
Q

how do tight junctions affect drug distribution?

A

tissues with tight junctions (GI mucosa, BBB, placenta, renal tubules) require drugs to pass through lipid membranes, and into/out of the blood. Drugs that can’t pass through membranes (large, protein bound, charged, hydrophilic) can’t move btw. compartments

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99
Q

GI mucosa absorption

A

oral-negligable absorption

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100
Q

bbb/placenta absorption

A

limited distribution

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101
Q

renal tubule absorption

A

filtration at glomerulus, then reduced reabsorption of drug into blood, excretion via urine

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102
Q

how does pH affect drug distribution?

A

affects lipid solubility. HH equation and tissue pH and pKa let you predict conditions favoring passage or preventing passage.

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103
Q

describe what dissociation of a proton does to a weak acid or base drug?

A

dissociation of proton from acid=ionized drug, dissociation of proton from base=unionized drug

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104
Q

what is the significance of ionization for drug absorption?

A

nonionized forms are more readily absorbed, ionized don’t cross lipid membrane

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105
Q

state the conditions that form nonionized acids and bases

A

acids become nonionized in acid medium, bases in alkaline medium

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106
Q

what does the HH equation allow you to predict with drugs?

A

the pH at which the majority of the drug will be non-ionized

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107
Q

what is the rule of thumb for qualitative preditions regarding drug absorption?

A

note whether the drug is weak acid/base, and pH of the fluid it’s in relative to pKa of the drug. pH is lower than pKA, more protons, protonated base/acid will dominate. When pH is higher than pKa of drug fewer protons, unprotonated form of weak acid/base, absorption favored.

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108
Q

state HH weak acid equation

A

HA H+ + A- [non-ionized in acidic solutions, ph

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109
Q

state HH weak base equation

A

BH+ H+ + B- [non-ionized in basic solutions, ph>pKa]

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110
Q

what is ion trapping?

A

lipid barriers separate 2 aqueous phases at different pHs, only non-ionized drugs can cross, equilibration is same on both sides of membrane, on each side of membrane separate equilibriums occur btw. Ionized and un-ionized forms of drug. At equilibrium, unionized conc. of drug is same, but total concentrationo of drug is greater on side where ionization is greater. drugs are trapped where they ionize

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111
Q

where are acidic drugs trapped

A

basic solutions

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112
Q

where are basic drugs trapped

A

acidic solutions

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113
Q

what is the clinical significance of ion trapping?

A

alters urine pH to trap weak acids/bases and hasten excretion, potential to concentrate basic drugs, weak bases are concentrated in acidic stomach contents

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114
Q

can ionized drug molecules cross capilary walls?

A

YES! Through pores.

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115
Q

can lipid solubility affect the rate of passage of non-ionized drugs?

A

YES! 2 drugs may have similar pKa, but will absorb differently

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116
Q

how does protein binding affect drug absorption?

A

will influence distribution if the free drug is diffusible. Acidic drugs bind albumin, basic to alpha-1-glycoprotein. Reduces concentration of active drug, hinders metabolic degredation/excretion, prolongs drug action, decreases volume o distribution, decreases ability to enter CNS across BBB

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117
Q

displacement drug interactions

A

displacement of a 1st drug from a protein binding site by a second drug, results in increased levels of unbound 1st drug. Total levels of drugs are unchanged b/c administration rate is the same

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118
Q

when does drug displacement have clinical consequences?

A

drug has narrow therapeutic index, started in high doses, Vd is small, response occurs more rapidly than distribution

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119
Q

why do most drugs act as if they display single compartment kinetics?

A

they are absorbed into/eliminated from a central compartment and are rapidly distributed. Some drugs may go from a second compartment (tissue) and are slower (2 compartment kinetics)

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120
Q

Vd

A

size of compartment necessary to account for total amount of drug in body if it were present throughout body at same concentration found in plasma. Gives indication of extent a drug passes from plasma to extravascular tissue. Partition coefficient btw plasma and body.

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121
Q

determination of Vd

A

single dose of drug is administered in IV (Ab), plasma concentration at time 0 (C0) is determined and Vd is calculated. Ab/C0

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122
Q

distribution compartments

A

distribution may not be homogenous. Sites are speculative w/o comparison

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123
Q

what are the volumes of body compartments?

A

plasma=3-5L, extracellular water=12-15L, total body water=42L, other compartments >50L

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124
Q

higher values of Vd indicate what?

A

drugs are located outside the plasma (lipid soluble, tissue binding)

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125
Q

lower values of Vd indicate what?

A

drugs located inside plasma or ECF (bind plasma proteins, large size, low lipid solubility)

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126
Q

what are the values of Vd?

A

L/kg

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127
Q

Vd allows you to determine what of a dose?

A

effect a dose will have on Cp. Dilution factor. Cp=D/Vd

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128
Q

necessary dose calculation

A

LD=Cp desired x Vd. The loading dose (LD) to fill the distribution volume to achieve steady state plasma

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129
Q

what is biotransformation/drug metabolism?

A

enzyme catalyzed chemical structure transformation

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130
Q

what are the general principles/charachteristics of drug metabolism?

A

enzymes have endogenous substrates and play role in metabolism, liver is the primary organ of metabolism (others can do it too), oxidation is the most frequent path (some by enzyme bound of smooth ER, some by cytosol enzymes), lipid soluble compounds are converted to water soluble then excreted

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131
Q

biotransformation phase 1

A

inserts/unmasks fundtional group into drug rendering it water soluble and able to be conjugated. Oxidation, reduction, hydrolysis

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132
Q

biotransformations phase 2

A

conjugation. Combine with pre-existing/metabolically inserted functional groups, forms polar conjugate excreted in urine.

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133
Q

what type of process is drug metabolism?

A

detoxifying. Forms readily excreted metabolytes (inactive). Drug metabolized to less active compound

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134
Q

what are other metabolic outcomes?

A

can become more active drug, inactive to active, toxic metabolyte

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135
Q

what are cytochrome p450-dependent oxidations?

A

part of oxidation system that includes NADPH, NADPH-cytochrome P450 reductase, molecular O2. Liver is richest source

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136
Q

list the charachteristics of CYP450

A

substrate must be lipid soluble, inducible, inhibitable, postnatal development variable, different isozymes

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137
Q

inducibility

A

increase in enzyme protein and drug metabolizing activity

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138
Q

postnatal development variable

A

early neonatal levels exist at 50-75% of adult, some are metabolized faster

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139
Q

isozymes of CYP450

A

CYP1-3

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140
Q

how are pateints classified regarding enzyme activity?

A

ultra rapid metabolizers (UM) or decreased/poor metabolizers (PM). Depends on ethnic groups.

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141
Q

amplichip cyp450 test

A

analyzes blood derived DNA and detects genetic polymorphisms in activity of CYP2 D6 and C19. these account for 25% of drug metabolism

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142
Q

what does clinical effect depend on?

A

whether metabolism is detoxifying or activating and whether polymorphism results in increase or decreased enzyme activity

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143
Q

PM CYP2D6 detoxifying

A

increased antipsychotic drug toxicity

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144
Q

UM CYP2D6 detoxifying

A

nonresponse to antidepressants

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145
Q

PM CYP2C19 activating

A

decreased PPI efficacy for peptic ulcer disease

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146
Q

PM CYP2D6 activating

A

insufficient analgesia with codine-dont metabolize to morphine

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147
Q

UM CYP2D6 activating

A

codeine intoxication-too rapid metabolism

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148
Q

differences in warfarin response may be due to genetic variation in?

A

vitamin K reductase (what it targets), CYP2C9 (metabolizes)

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149
Q

cytochrome P450-independent oxidations

A

several types, dehydroginases, oxidases

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150
Q

amine oxidases

A

located in outer membrane of mitochondria (monoamine oxidase), important for neurotransmitter metabolism

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151
Q

dehydrogenations

A

alcohol dehydrogenase, hepatic soluble fraction, several types, reached at 5 yr, aldehyde dehydrogenase

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152
Q

list the reductions of Phase 1

A

azo reduction (activates slfonamides), nitro reduction (diff. enzymes; toxic intermediate), carbonyl reduction

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153
Q

list hydrolysis of phase 1

A

esterases, amidases

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154
Q

esterases

A

adult values in 1st few months (used for pro-drugs). Hydrolyze exters to alcohol and acid, very reactive. Present plasma, liver, tissue.

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155
Q

amidases

A

liver and gut, amides to acids and amines

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156
Q

conjugations of phase 2

A

synthetic transformations. Drug or drug metabolite is condjugated to endogenous biochemical unit by a coenzyme. Done by transferases. Product is often water soluble and excreted.

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157
Q

glucuronidation

A

create conjugates that are excreted in urine, some in bile, some in feces. Groups that conjugate: aliphatic OH, aromatic OH, COOH, NH, SH. When doen by beta glucuronidase results in free drug

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158
Q

gucuronyl transferases

A

microsomal enzymes in liver, kidney, GI. Inducible.

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159
Q

enterohepatic recirculation

A

drug secreted by liver into bile as conjugate then absorbed by GI as free drug. Source of drug interactions?

160
Q

n acetylation

A

amide bond formation via n-acetyltransferase. Donated by acetyl CoA. Catalyzed in hepatic soluble fraction. Products can be less water soluble

161
Q

glutathione conjugation

A

glutathione s-transferases have limited role in drug metabolism. Detoxify carcinogens, pollutants, toxic metabolites

162
Q

sulfate conjugation

A

forms strong acids (pKa ~1). Sulfotransferases occur in soluble cell fraction. Ionized and water soluble conjugates. PAPS is coenzyme. Acceptors: aromatic OH, N-OH

163
Q

what is induction?

A

stimulation of CYP450 system resluting in increase drug metabolizing activity. Observed in >300 compounds

164
Q

what is the mechanism of induction?

A

increased synthesis of enzyme protein. Accompanied (sometimes) by morphological/biological changes (liver weight increase, proliferation SER, NADPH and CYP-450 increase). Requires 48-72 hrs for effect

165
Q

list mechanisms of inhibition

A

inhibit enzyme synthesis, compete with substrate, inhibit without being a substrate, metabolite formation (suicide inhibition or tight complex)

166
Q

how do most interactions occur on Cytochrome P450 system?

A

effects are obvious through oral routes: pass through liver, inducers increase metabolic rate, decreasers decrease amount of drug available for interaction

167
Q

what are therapeutic consequences of induction?

A

maximal effects of enzyme induction, production of pharmacokinetic tolerance, induction (increase other drug clearance, implications=reduced therapeutic effect/increased toxicity), induce metabolism of another drug to toxic metabolites

168
Q

what are therapeutic consequences of inhibition?

A

can occur when sufficient hepatic concentration is reached, inhibition by one agent can result in decreased clearnce of inhibited drug (higher Cp/toxicity)

169
Q

what are some biological factors that influence drug metabolism?

A

diet and nutrition (high protein stimulates mixed function oxidase), malnutrition (changes drug metabolism), sex differences, age (perinatal vs neonatal vs old age)

170
Q

what are some genetic factors that influence drug metabolism?

A

metabolism mediated by enzymes is genetically controlled. See notes for more depth

171
Q

What are some disease states consequences that influence drug metabolism?

A

require dosage adjustment/avoidance. Hepatic diseases (effect depends on severity, drug, biotransformation), alcohol consumption (inhibits transformations, chronic exposure-induction microsomal biotransformations, cirrhosis), blood flow to liver issues reduce rate of elimination, non-hepatic diseases reduce drug metabolism.

172
Q

transportors on membranes of intestinal, renal, hepatic epithelial cells play a role in eliminating what?

A

xenobiotics (including drugs). Most important is P-glycoproteins (MDR1 gene) (ABC=Atp Binding Cassette, pumps fueled by ATP)

173
Q

where are ABC transporters located?

A

renal brush border membranes, bile canaliculi, astrycyte foot processes (brain), GI tract

174
Q

what do ABC transporters do?

A

move molecules out of cell at sites of entry into body. Also decrease absorption at sites of exit (enhance elimination)

175
Q

how many genes code for polymorphic variations and transporters that contribute to individual genetic variation in drug response?

A

over 300

176
Q

inhibitors of p-glycoproteins will ______ plasma levels of drug substrates

A

increase

177
Q

inducers of p-glycoproteins will ______ plasma levels of drug substrates

A

decrease

178
Q

what organ is the most important for drug excretion?

A

kidney. For water soluble/non-volatile compounds

179
Q

glomerular filtration clears at a rate of ? mL/min

A

120

180
Q

drugs smaller than _____ are filtered by kidney

A

albumin (MW 69,000)

181
Q

is protein bound drug filtered?

A

NO! only free drug

182
Q

what 2 thing affect renal excretion?

A

renal blood flow and renal function

183
Q

what is the half life of drugs cleared by the kidney?

A

t1/2~1-4 hrs (lots of protein is a longer t1/2)

184
Q

active tubular secretions are drugs transported from ____ to ______

A

blood to urine

185
Q

how quickly can actively secreted drugs be cleared?

A

120-600 mL/min

186
Q

where does active tubular secretion occur and with what types of drugs?

A

proximal tubule with stronger acids and bases

187
Q

what are some acid and base substrates for tubular secretion?

A

acids (penicillins, diuretics), bases (morphine, catecholamines, histamine, tolazoline)

188
Q

does plasma protein binding affect rate of secretion?

A

not appreciably (T1/2~1-2 hrs)

189
Q

how quickly are drugs that are lipid soluble and uncharged cleared?

A

at the rate of urine formation- 1mL/min

190
Q

a primary function of drug metabolism is to produce _____ that is less likely to be reabsorbed.

A

water soluble metabolite

191
Q

where does passive diffusion occur in the kidney?

A

in proximal and distal tubules with lipid soluble molecules

192
Q

diffusion of weak acids/bases in distal/proximal tubules depends on ______.

A

urine pH. Non-ionized form will diffuse across membrane

193
Q

what changes urinary pH to acidify or alkalize it?

A

NH4Cl/ascorbic acid acidifies, NaHCO3 alkalinizes

194
Q

active reabsorption is important for ______ compounds

A

endogenous (glucose, AA). Drugs act to reduce this active transport

195
Q

many drugs (high molecular weight) are excreted into _______, then _______ by small intestine where they can be ______ in the urine

A

the bile, resorbed, eliminated

196
Q

drug metabolites (as conjugates) are ____ into the bile where they are ______ by bacterial enzymes back to ______ (more lipid soluble) and are _____ by the gut (enterohepatic recycling)

A

secreted, hydrolized, parent, resorbed

197
Q

enterohepatic cycle

A

drugs and metabolites w/ molecular weights >300 are excreted via bile, stored in gallbladder, delivered to intestines, resorbed to circulation where can go to liver. Reduces drug elimination, prolongs half life/duration

198
Q

how much of a reservoir can a recirculating drug have in the body?

A

20% of the total drug present

199
Q

antibiotics decrease _______ recycling and _______drug levels

A

enterohepatic, plasma. They are a potential mechanism for drug-drug interactions

200
Q

do drugs cross into breast milk?

A

yes, but at low levels. Infant plasma level is below therapeutic level. Can work to reduce possible reactions. Breast milk is more acidic than plasma-can ion trap.

201
Q

what drugs can affect milk synthesis?

A

dopanimne receptor agonists/antagonists and ethanol

202
Q

drug assays can be performed on samples from what 3 things?

A

sweat, saliva, hair

203
Q

first order kinetics

A

principle that governs rate of drug elimination. How almost all drugs are eliminated

204
Q

rate of elimination (mg/hr) is ______ to concentration of drug in _______.

A

proportionsl, plasma (mg/L)

205
Q

how is the relationsip of the rate of elimination complicated?

A

as drug is eliminated, concentration changes, so rate of elimination changes constantly

206
Q

when are most drugs eliminated by first order kinetics?

A

when they are given in does w/in the therapeutic dosage range

207
Q

what major biologic processes are first order processes responsible for drug elimination?

A

hepatic metabolism and renal excretion

208
Q

Cp vs. time graph

A

slope represents rate of elimination (mg/ml per time). Steep when Cp is high, slows as drug is eliminated

209
Q

lof of Cp vs time graph

A

follows a straightl ine

210
Q

the ________ rate of elimination changes constantly along with amount of drug eliminated in first order kinetics

A

absolute

211
Q

a ______ fraction of drug is eliminated per unit time in first order kinetic elimination.

A

constant (independent of total amount of drug present)

212
Q

half life (t1/2, units of hours/minutes) in 1st order kinetics

A

the time required to eliminate 1/2 of the drug present

213
Q

how long would it take a drug with a t1/2 of 3 hours to decline from 1000 to 500 mg/mL?

A

3 hours. Duh.

214
Q

how long does it take plasma concentration to decline from 500 to 250 mL?

A

3 hours

215
Q

rules of thumbs for estimating t1/2 calculations

A

time for elimination from plasma=4-5 half-lives; time to reach steady state plasma drug levels after multiple doses=4-5 half lives; fluctuations in plasma levels between doses=number of half lives in dosing interval

216
Q

when t=t1/2 then C2=????

A

1/2 C1

217
Q

what is ke?

A

the fraction of drug leaving body per unit time via all elimination processes

218
Q

ke is best thought of as a _______ or _______ allowing us to calculate the amount of remaining drug at any time in the elimination process

A

number or constant

219
Q

what is clearance?

A

the Vd which is cleared of a drug in a given period of time by combined processes of tissues (kidney, liver) with some contribution from other tissues (lung, muscle, etc.)

220
Q

what formula gives us the value of clearance?

A

CL= Vd x Ke. This volume remins constant through course of elimination

221
Q

the actual amount of drug eliminated depends on its _____ in the cleared volume at any particular time

A

concentration

222
Q

how is clearance BEST thought of?

A

proportionality constant that makes Cp at steady state = to the rate of administration

223
Q

clearances from each organ of elimination are ______

A

additive

224
Q

which 2 organs are most important for clearing most drugs?

A

kidney, liver

225
Q

clearance ranges from just above _____ to a _______ determined by blood flow to organs of elimination

A

zero, maximum

226
Q

CL (total body) = ???

A

CL (renal) + CL (hepatic) + CL (all other routes)

227
Q

hepatic clearance is subject to.?

A

co-administration of inducers and inhibitors. Varies with blood flow to liver, protein binding, intrinsic metabolic activity

228
Q

if metabolism is unefficient, are changes in hepatic blood flow clearance influenced?

A

not significantly

229
Q

if metabolism is efficient are changes in hepatic blood flow clearance influenced?

A

major influence on total body clearance

230
Q

what 2 things are used to measure kidney function?

A

CrCL (creatinine clearance) or serum creatinine clearance (SCr)

231
Q

changes in renal function will _________ clearance of renally eliminated drugs and ______ dose changes to prevent accumulation

A

alter, necessitate

232
Q

a graph of ln concnetration vs. time is composed of ________ portion representing _________ phase of drug equilibrating btw blood and tissue

A

initial curvilinear, distribution

233
Q

linear portion of graph represents the ______ phase of drug elimination

A

elimination

234
Q

when discussing pharmacokinetics, it is assumed the route of administration is ____ and bioavailablity is ___%

A

IV, 100%

235
Q

for a drug with oral bioavailability of 50% (F=0.5), IV dose would need to be divided by _____ to calculate necessary oral dose

A

0.5

236
Q

if IV dose is 100 mg, what is oral dose?

A

100/0.5=200 mg

237
Q

what happens when a drug is administered by infusion at a constant rate?

A

Intially, Cp rises with time, but as it rises, rate of elimination rises. The rise continues until increasing drug concentration produces rate of elimination equal to constant rate of infusion—Steady State Exists!

238
Q

when is infusion stopped?

A

when plasma concentrations (reflecting elimination) after constant infusion reach steady state and are turned off.

239
Q

after a drug is discontinued, how long does it take to be eliminated?

A

it is assumed it is eliminated after 4-5 half lives (ie: only 3.12-6.25% steady state remains, no effect)

240
Q

time to reach steady state AND plateau is related to what?

A

half life of drug ONLY. This is independent of dosage.

241
Q

will increasing a maintenance dose allow the steady state to be reached sooner?

A

No. It will cause the steady state plasma level to be higher when it is reached

242
Q

How do you reach a desired steady state plasma level sooner?

A

administer a loading does with a normal dose schedule after

243
Q

when is a loading dose given?

A

in clinical situations where you can’t wait for the 4-5 half lives for therapeutic levels to be reached.

244
Q

what is a loading dose?

A

loading doses are higher than maintenance doses to help you approach steady state plasma levels more quickly

245
Q

how do you calculate loading doses?

A

estimate using the Vd for the drug and desired Cp. LD (mg)= Cp0 (mg/L) x Vd (L)

246
Q

can the calculated loading dose cause toxicity?

A

YES! Due to transiently high lpasma levels in the alpha-distribution phase. Can be lessened if you give the LD over a longer interval that still gets you faster than 4-5 half lives

247
Q

________ lead to fluctuations in plasma drug levels (as opposed to continuous infusion).

A

repeated administrations (of a dose of drug)

248
Q

What is useful to know when shooting for a therapeutic endpoint (Cp average at steady state)?

A

the amount of fluctuation btw max and min Cpss in a dosing schedule

249
Q

average steady state concentration is the ______ for intermittent and continuous infusion

A

same

250
Q

what fluctuates between doses of intermittent drug infusion?

A

plasma concentration. Size increases with dosage interval increase.

251
Q

what is the magnitude of fluctuation equation?

A

1/fraction of drug remaining at end of dosing interval [Cp2/Cp1]

252
Q

T1/2 is useful in _____ estimating an appropriate dosing interval (tau) for maintenance therapy.

A

qualitatively

253
Q

if tau is

A

less thatn 50% in the dosing interval

254
Q

if tau is larger than t1/2, how much of the drug is eliminated before the next dose?

A

all of the drug (effectively), fluctuation is maximal

255
Q

if tau is shorter than t/12 how much fluctuation is there?

A

little

256
Q

the more t1/2’s in a dosage interval the _________the fluctuation.

A

greater

257
Q

how can fluctuations in plasma levels be blunted?

A

slow absorbtion via controlled/extened release preparations

258
Q

zero order kinetics describe the rate of what from the body?

A

rate of elimination that is independent of the drug in the body

259
Q

are zero order kinetics first order?

A

NO! the amount of drug removed per unit time is constant (independent of concentration)

260
Q

how do zero order kinetics occur?

A

saturation of hepatic metabolic enzyme systems via drug administration

261
Q

do drugs eliminated by zero order kinetics have half lives?

A

NO! This presents dosage challenges, at upper end-large changes in Cp

262
Q

a drug is a.?

A

neurotransmitter-hormone

263
Q

recognition and binding occurs at the?

A

receptor

264
Q

signal transduction occurs via?

A

g-proteins or other effectors

265
Q

amplification occurs via.?

A

transport of ions/molecules, transcription factors, enzyme activation/deactivation, protein synthesis, release of neuroactive agents

266
Q

what occurs after amplification?

A

physiological response

267
Q

list the generalized scheme of drug action.

A

binding of drug to receptor, transduction, transduction and amplification, physiological response

268
Q

drug receptor

A

component of system that drug binds to and causes a change in the system function. Specificity is important

269
Q

transduction

A

alters celular function via effector molecules. Components of system that create biologic effect after activation (translate the interaction of drug and receptor into cellular activity)

270
Q

major mechanisms of transduction and amplification

A

ligand gated ion channels, g protein coupled receptors, kinase linked receptors, hormone receptors

271
Q

physiological response examples

A

muscle contract/relax, neurotransmitter release, changes transcription/protein synthesis

272
Q

specialized receptors

A

designed to detect chemical signals and initiat response through signal transduction paths

273
Q

generalized receptors

A

molecules with any function (eg: enzymes, lipids, NA)

274
Q

list some types of receptor molecules

A

proteins, nucleic acids, membrane lipids

275
Q

are protein receptor molecules specific?

A

yes. Most specific

276
Q

are receptor nucleic acids and mebrane lipids specific?

A

no. lower specificity

277
Q

receptors are responsible for _________ of drug action

A

selectivity. Size, shape, charge determine binding affinity. Changes in chemical structure affect affenity

278
Q

some drugs can bind and regulate the function of receptor macromolecules as ______.

A

agonists, they act in the same way as endogenous ligands-promote receptor function

279
Q

drugs as pharmcologic agonists

A

bind receptors, cannot generate charachteristic response. Prevent binding of endogenous agonist molecules to receptor to block action

280
Q

receptor theory and does-response curves

A

this theory allows determination of quantitative relationships btw. Dose/concentration of drug and it’s effects via the response curve.

281
Q

what is necessary to know about a therapeutic drug option when choosing between different types?

A

potency and efficacy

282
Q

explain what drug receptor theory assumes

A

interactions folllow mass action relationships, binding is reversible, response is proportional to receptors occupied by drug. RD is proportional to response

283
Q

what shape do you want to see in a dose vs. response curve?

A

hyperbola. This confirms the mathematical relationship btw. Dose and response.

284
Q

what does a hyperbolic shape of a dose-response curve indicate?

A

curve is linear at low doses, curve levels off at high drug doses (limit to the increase of response achieveable)

285
Q

what does a log dose-response curve allow you to do?

A

It allows you to plot a wide range of doses for comparison, dose response relationship is nearly a straight line over many dose ranges. No special biologic or pharmacologic significance

286
Q

potency

A

concentration or dose required to produce 50% of drug’s individual maximal effect

287
Q

what does potency depend upon?

A

affinity of Kd of receptors for binding, and efficiency of the drug receptor comples to generate a response

288
Q

the potency of a drug provides info on _____ drug is required to produce an effect

A

how much (dose)

289
Q

maximal effect or efficacy

A

the limit of dose-response relationship on response (y axis). Relationship btw binding to the receptor nd ability to create a response at molecular, cellular, tissue, system

290
Q

what is the most important determinat of a drug’s clinical utility?

A

it’s efficacy

291
Q

potency determines what______ is needed to achieve a desired level of _______

A

dose, response

292
Q

agonists

A

drug that activates receptor and brings about a tissue response

293
Q

full agonists

A

drugs that occupy receptors to create MAXIMAL responses

294
Q

partial agonists

A

drugs that occupy same receptor as full agonist but create a less than maximal response at even full dosage levels

295
Q

are partial agonists more or less efficacious?

A

less

296
Q

potency and efficacy vary ________.

A

independently. For example, partial agonists may be more, less, or equally potent than full agonists

297
Q

when 2 drugs don’t produce maximal response charachteristics of the tissue, the observed maximal response is a function of their _______.

A

relative intrinsic efficacies.

298
Q

the vast majority of agonist drugs in clinical practice are _______agonists.

A

full

299
Q

pharmacologic potency

A

determines the dose needed to be administered to the patient

300
Q

clinical effectiveness of a drug depens on its __________ and ability to reach the relevant receptors.

A

maximal efficacy

301
Q

in therapeutics, efficacy refers to the extent a given ________ can be achieved in a patient.

A

clinical effect

302
Q

antagonists

A

drugs that inhibit actions of agonists with no effect in absence of an agonist. Receptor and non-receptor.

303
Q

receptor antagonists

A

bind the same receptor as agonist

304
Q

nonreceptor antagonists

A

physiological antagonists that bind different receptor and chemical antagonists that bind agonist molecule directly

305
Q

competitive reversible antagonist

A

antagonist binds reversibly to active site but doesn’t stabilize it to confirmation required for activation. Blocks agonist binding

306
Q

Emax is _______ with competitive reversible antagonists

A

unchanged. Potency decreased. Curve shifts right. Maximal efficacy of agonist is unchanged because agonist concentration can be increased to outcompete antagonist

307
Q

noncompetitive antagonists

A

binds irriversibly or pseudoirreversibly to active site or allosteric site of receptor

308
Q

Emax is ______ with noncompetitive antagonists

A

decreased. Potency unchanged. Curve shifts downward, maximal efficacy is reduced.

309
Q

what are the 2 nonreceptor agtagonists?

A

physiologic and chemical antagonists

310
Q

physiological antagonist

A

activates or blocks a receptor that mediates physiologic response oppposite of activation of receptor for agonist

311
Q

chemical antagonist

A

doesn’t bind receptor. Occurs via inactivation of agonist itself (modifies or sequesters it).

312
Q

quantal dose response (effect) curves charachterize.?

A

pharmacologic respones in all or nothing events in a population. Generated by arbitrarily defining some specific therapeutic effect and determining minimum dose to produce the response in the population

313
Q

all or nothing

A

brings about the response or it doesnt

314
Q

benefit-risk ratio

A

provides a measur of how safe a drug is clinically.

315
Q

therapeutic effect

A

benefits. All or nothing response. Intiate till response achieved

316
Q

ED50

A

the dose that initiates effect in 50% of test population

317
Q

how can the degree of risk be evaluated?

A

by comparing quantal dose-response curves for desirable and toxic effects

318
Q

LD50

A

lethal dose that causes death in 50% of subjects

319
Q

TD50

A

dose that produces undesirable effect in 50% of subjects

320
Q

therapeutic index

A

LD50/ED50=TI. Factor by which dose is therapeutically effective in 50% of population must be increased to cause death in 50% of the population.

321
Q

the _____the therapeutic index, the safer the drug

A

higher

322
Q

what is the therapeutic index of most drugs?

A

greater than 10-20

323
Q

standard safety margin

A

percent by which dose effective in 99% of the population must be increased to cause death in 1% of the population.

324
Q

is the standard safety margin more or less conservative than the therapeutic index?

A

more. Takes into account the population extremes (rather than midrange)

325
Q

therapeutic window

A

concept used to provide indication of safety of a drug. Thought of as the safe “opening” btw. The minimum therapeutic concentrationand minimum toxic concentration of drug in plasma and dosage regimens.

326
Q

adverse reactions

A

response to a drug that is not desired/harmful/occurs at usual doses.

327
Q

extension effects

A

dose related and predictable. Arise from extension of therapeutic effect

328
Q

side effects

A

predictable, dose dependent reactions unrelated to the therapeutic goal. Produced by same receptor responsible for the therapeutic effect at a different organ/system

329
Q

idiosyncratic reactions

A

genetically determined abnormal response to a drug, unpredictable.

330
Q

drug allergy

A

adverse response of immunologic origin, unpredictable, severity is dose dependent

331
Q

what are the 5 categories for classifying risk to a fetus with a drug?

A

safe (A) to teratogenicity (X). Most drugs are in B/C/D categories. See notes for full description of each

332
Q

drug drug interactions

A

categories of patients and specific drug/drug classifications are associated with increased risk for interations. Must be aware of these!

333
Q

pharmakokinetic drug interactions can result in ______ drug concentrations leading to toxicity OR they may cause _____ in plasma concentrations leading to levels below therapeutic effectiveness.

A

elevated, decreases

334
Q

what patient categories are at high risk for drug-drug interactions?

A

elterly, high risk, renal/hepatic disease, multiple prescribing physicians

335
Q

single most important determinant of poisoning outcomes is the provision of __________ (3 words).

A

good, supportive care

336
Q

list the supportive measures needed in poisoning cases:

A

cardiopulmonary, electrolyte/acid-base balance/fluids, CNS precautions, renal function

337
Q

toxicokinetics

A

study of absorption, distribution, eliminaton of toxic parent compounds and metabolic producs that aids in prediction of amount of toxin that reaches site of injury and damage

338
Q

volume of distribution can be useful in predicting which drugs would be removed by ______.

A

dialysis/exchange transfusion

339
Q

pharmacokinetic treatment strategies for toxic poisoning

A

prevent/decrease absorption (decrease rate in), inibition of toxication, enhancement of metabolism, increase toxin elimination

340
Q

pharmacodynamic treatment strategies for toxic poisoning

A

antidotes

341
Q

emesis

A

empties stomach contents rapidly. Ipecac, amorphine. Be careful of contraindications (comatose, corrosive poisons, seizure risk, pregnancy)

342
Q

things to do to prevent absorption of poisons

A

emesis, gastric lavage, chemical adsorption/activated charcoal, osmotic cathartics

343
Q

lavage+emesis removes ____% of poisons

A

30%

344
Q

when is lavage best timing wise?

A

within 60 minutes of ingestion

345
Q

what do osmotic cathartics do?

A

decrease time of toxin in GI tract. Sorbital is recommended (70%).

346
Q

symptoms of toxicity (poison)

A

appearance is delayed by 8-36 hrs. severe is 4-12 hrs. methanol=visual disturbances (formic acid on optic disc). Etylene glycol=damage to kidneys due to calcium deposits

347
Q

mechanism of toxicity

A

alcohols are well absorbed orally and metabolized to organic acids. Methanol/ethylne glycol-minimal toxicity till metabolized (formic acid). Rate limiting enzyme is alcohol dehydrogenase-inhibit with fomepizole

348
Q

severe poisoning treatment

A

suppression of toxic metabolites, hemodialysis, correction metabolic acidosis.

349
Q

acetominophen toxicity symptoms

A

4 stages: initial 24 hrs=nausea vomiting abdomen pain (symptoms don’t show the severity), 24-48hrs=hepatic damage apparent (plasma aminotransferases elevated and prolonged prothrombin), 72-96hrs=peak hepatotoxicity (severere hepatic necrosis), 7-8 days=recovery if timely treatment (if not timely, severe damage in 10%, 10-20% death of liver failure)

350
Q

phases of acetomenophen

A

conjugated with glucoronic acit/sulphate (phase 2 rxn)–>phase 1 cytochrome P450 oxidation–> metabolite is detoxified by phase 2 GSH-transfease–> mercapturate excreted

351
Q

hepatocellular injury involves ______ of phase 2 sulfate and glucuronide conjugation paths by toxic doses.

A

saturation. Results in excessive formation of Ac* by unsateruated IP450 path, depletion of cellular gluthatione, binding of NAPQI to critical protein or cellular constituents

352
Q

how do you treat acetomeniphin poisoning?

A

gastric lavage in 4 hrs, supportive therapy, N-acetylcysteine in 12-36 hours of ingestion ( precoursor glutathione syntesis)

353
Q

entracorporeal removal of toxins from blood

A

potential complications and expense are high. Hemodialysis/peritoneal dialysis (blood pumped through filter, effective for small Vd toxins), hemoperfusion (blood pumped through column of adsorbent material)

354
Q

enhanced metabolism removal of toxins from blood

A

since cytochrome P450 metabolism takes 1-3 days it’s not realistic. Instead, enhance detoxification paths with N-acetylcysteine. Inhibit metabolism to block metabolites that are toxic.

355
Q

is enhanced renal excretion of proved value for removing toxins from blood?

A

no. done with forced diuresis or blocking reabsorption from kidney

356
Q

chelation of heavy metals for removing toxins from blood

A

combines aspects of enhancing the elimination of toxin and inactivating it.

357
Q

how does normal chemistry work with heavy metal ions?

A

heavy metal ions form coordinate covalent bonds with protein side chain nucleophiles

358
Q

how do toxic mechanisms work with heavy metal ions?

A

they interact with macromolecule essential to normal function, and form tight covalent bonds. Toxic manifestations are due to enzyme inhibition and alteration of membrane structure

359
Q

how do you treat heavy metal toxicity?

A

administer chelating agents that complex with free metal ions in body fluids.

360
Q

federal government controls what in relation to drugs?

A

what drugs can be sold to the public via the FDA

361
Q

FDA regulates what in relation to drugs?

A

evaluation process for safety and efficacy, removal of dietary supplements deemed unsafe, equivalency to brand names, placmetn of drugs into prescription/non-prescription categories

362
Q

can local governments pass laws about drug use in their jurisdiction?

A

Yes.

363
Q

what are the distinguishing factors of the drug categories of prescription or controlled substances?

A

whether they are evaluated for efficacy and safety, availability by prescription for direct purchase, potential for abuse for pysiologic/psychologic dependence

364
Q

drug

A

molecular entity as a therapeutic agent intended to diagnose, treat, cure or prevent a disease

365
Q

what does the FDA require of new drugs released since 1938?

A

that they demonstrate proof of efficacy and safety before marketing to public

366
Q

dietary supplement

A

defined as product intended to supplement the diet, contains vitamin, mineral, amino acid, herb/botanica. Not food. Can be sold without prior evidence safety/efficacy.

367
Q

evaluation of drugs steps (list):

A

animal studies, clinical trials in humans, phase 2, phase 3, post marketing surveilance

368
Q

phase 2 clinical trial

A

2 year clinical investigation. Does it work in patients? 200-300 pts

369
Q

phase 3 clinical trial

A

fulll scale clinical trial, 3 years. Does it work double blind? 1-6000pts

370
Q

abbreviated new drug application (ANDA)

A

submitted for generic drugs allowing manufacturer to bypass clinical trials. Bioequivalence standards must be met

371
Q

phase 4 clinical trial (post marketing surveilance)

A

submit reports to FDA of adverse effects. FDA can revoke approval/restrict drug use.

372
Q

are most generic brands bioequivalent?

A

yes. Bioavailability variation is less than 4%

373
Q

what are the 2 drug categories where 1 formulation consistently is advised ( or use of name brand is recommended)?

A

levothyroxine and anti-epileptic drugs

374
Q

pharmaceutical equivalents

A

drugs with same active ingredient in same dosage formulation, same administration route, inentical strength/concentration

375
Q

pharmeceutical alternatives

A

products w/ same therapeutic moiety, with different salts, esters, complexes, dosage forms, strengths

376
Q

extent of absorption

A

area under the plasma concentration time curve (AUC) and rate of absorption. Estimated by maximum of peak drug concentration Cmax

377
Q

therapeutic equivalents

A

equivalents that when administered to the same individual in the same regimen, provide same efficacy and safety.

378
Q

dietary supplement definition

A

supplement diet, taken by mouth, one or more dietary ingredients of vitamins/mineral/aa/botanicals or herbs

379
Q

regulation of dietary supplements

A

classification is based on intended use

380
Q

do supplement manufacturers have to provide evidence to FDA that their products are save and effective?

A

NO. not permitted to market unsafe/ineffective products. Minimal regulatory control of restricton/removal by FDA once marketed

381
Q

do health claims require FDA evaluation?

A

YES! They must be authorized too.

382
Q

structure/function claim

A

describes role of substance intended to maintain structure/function of body. Don’t require pre-approval. Must have disclaimer that not evaluated by FDA

383
Q

do all ingredients have to be listed on the label?

A

yes

384
Q

medical foods

A

food formulated to be consumed/administered enterally under the supervision of a physician, intended for specific dietary management of disease or condition

385
Q

OTC status requirements

A

is the condition self-diagnosible/treatable?, what is product toxicity/habit forming/high dose safety?, do the benefits outweigh the risks?, do methods preclude OTC availability?, can directions be written and understood?

386
Q

prescription

A

written or verbal order from prescriber to pharmacist concerning medical substances for patient

387
Q

what is required on a prescription?

A

construction of drug product, date, identity of prescriber (preprinted), patient info, Rx symbol, drug strength, directions to patient (amount, time, frequency, route administration, duration), chart info (name, strength, dose, route, frequency, date, signature), refill info, childproof container, signature, DEA number

388
Q

controlled substances act of 1970 provides for control of manufacture/distribution of drugs and divides into _____ schedules.

A
  1. based on potential for usefulness, abuse potential, degeree of which they may lead to physical/psychological dependence
389
Q

schedule 1 drugs

A

high abuse potential, no current medical use: opioids, haluciongens, depressants

390
Q

schedule 2 drugs

A

high abuse potential, high abuse potential: opioid analgesics, stimulants , barbituates

391
Q

schedule 3 drugs

A

accepted medical use, moderate abuse: opioids, stimulants, depressants, anabolic steroids, cannabinoids

392
Q

schedule 4 drugs

A

accepted medical use, low potential abuse: opioids, depressants,stimulants, benzodiazepines, hypnotic agents

393
Q

schedule 5 drugs

A

accepted medical use, lowest abuse potential: opioids in low amounts

394
Q

what drugs can be/require a prescription?

A

schedule 2-4 drugs (colorado is 2-5)

395
Q

which prescriptions can be phoned in?

A

3-4. Schedule 2 drugs must be handwritten

396
Q

should you use abbreviations in prescriptions?

A

NEVER!

Disease and Defense class of 2019 (9 decks)

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