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401 - Toxicology, Drug Abuse, Pharmacology > 5+6: Intro to Toxicology + ADRs > Flashcards

5+6: Intro to Toxicology + ADRs Flashcards

1
Q

list 3 possible classifications for toxic agents

A

physical state
chemical stability/ reactivity
chemical structure
poisoning potential
biochemical MOA
target organ
use
source

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2
Q

T or F: most toxic agents can be classified by a single classification system

A

F- No single classification that is applicable to entire spectrum, combination of classification systems generally needed

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3
Q

to have a toxic exposure, 3 things are required

A

sufficient concentration
of active form
for enough time

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4
Q

describe the 3 characteristics of acute effects

A

<24hrs or immediately
usually relatively high dose
short duration/ reversible

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5
Q

describe the 3 characteristics of subacute effects

A

<1mth
from repeated doses
reversible/ irreversible

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6
Q

describe the 3 characteristics of subchronic effects

A

1-3mths
repeated doses
rev/ irrev

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7
Q

describe the 3 characteristics of chronic effects

A

> 3mths after exposure
due to lower repeated doses over months/ years
usually irreversible

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8
Q

defattening of the skin is a
1. local effect
2. systemic effect
3. allergic reaction
4. idiosyncratic reaction

A

1

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9
Q

combined effect of 2 substances equal to sum of the individual effects (2+2=4)

A

additive

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10
Q

toxic eff of each substance is unaffected by simultaneous exposure (2+2 = 2 and 2)

A

independent

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11
Q

combined effect is greater than the sum of the individual effects

A

synergistic

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12
Q

enhancement of one agent by another so that the combined effect is greater than the sum of the effects of each alone (0+2=7)- one drug does not elicit a response on its own

A

potentiation

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13
Q

when 2 chemicals administered together interfere with each other’s actions, or one with the other (4+6=8, 4+0=1)

A

antagonism

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14
Q

what are the 4 types of antagonism

A

receptor (blocker)
chemical
dispositional
functional

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15
Q

describe receptor antagonism

A

prevention of chemical receptor interaction or activation

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16
Q

describe chemical antagonism

A

direct interaction of 2 chemicals preventing receptor interaction/ activation

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17
Q

describe disposition antagonism

A

altered metabolism or CL of chemical prevents receptor interaction or activation

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18
Q

activated charcoal preventing absorption of toxin is an example of
1. receptor antagonism
2. chemical antagonism
3. functional antagonism
4. dispositional antagonism

A

4

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19
Q

describe functioning antagonism

A

opposing effects on the same physiologic system

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20
Q

Fall in BP caused by barbiturate (GABA4 receptor) antagonized by vasopressor norepinephrine (a-adrenergic receptor) is an example of
1. receptor antagonism
2. chemical antagonism
3. functional antagonism
4. dispositional antagonism

A

3

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21
Q

NOAEL is

A

no observable AE level

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22
Q

LOAEL

A

lowest observable AE level

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23
Q

the slope on a dose response relationship indicates

A

the change in % of the population responding as the dose increases (Steep vs shallow)

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24
Q

a steep curve on a dose response relationship indicates

A

some beneficial effect will be offset by toxicity, small ↑ dose = large ↑ in response

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25
Q

a shallow curve on a dose response relationship indicates

A

safer, low dose may be effective without producing toxicity

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26
Q

what is ED50

A

effective dose 50% of the population (normally ref to beneficial eff but can be used for harmful eff)

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27
Q

what is TD50

A

toxic dose 50% of the population (AEs)

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28
Q

what is LD50

A

lethal dose for 50% of pop (common for acute toxicity- not really used)

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29
Q

what is the threshold dose on dose response relationships

A

point where toxicity first occurs

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30
Q

therapeutic index =

A

TD50/ED50

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31
Q

Therapeutic index is used to

A

compare therapeutically effective dose to toxic dose of drug

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32
Q

a ______ TI = better safety

A

larger

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33
Q

MOS =

A

TD10/ED90

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34
Q

SI =

A

TD10/ED90

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35
Q

efficacy is

A

the extent a chemical can elicit a response
max on Y axis

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36
Q

potency is

A

the range of doses where the chemical produces a response
x axis (lower = more potent)

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37
Q

what is the difference between an ADE vs and ADR

A

ADE = does not necessarily have a causal relationship

ADR = a response to a drug that is unintended

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38
Q

medical occurrence that may present during tx with a pharmaceutical product but which does not necessarily have a causal relationship with this tx describes AD_

A

ADE

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39
Q

Occurs while taking the drug but not always attributable to it describes AD_

A

ADE

40
Q

May be associated with inappropriate use of the drug or other confounders that occur during drug therapy- but are not necessarily caused by the pharmacology of the drug itself describes AD___

A

ADE

41
Q

Attributed to some action of the drug and Occur despite appropriate prescribing and dosing describes AD__

A

ADR

42
Q

a response to a drug that is noxious and unintended and occurs at doses normally used in humans for prophylaxis, diagnosis, therapy, or modification of physiologic function describes AD___

A

ADR

43
Q

any unintended effect of a drug occuring at doses normally used in humans which is related to the pharmacological properties of the medicine

A

side effect

44
Q

what is the difference between an ADR vs a SE

A

ADRs are always noxious and usually worse than SEs
SEs are only unintended effects- may not always be undesired

45
Q

an AD__ is a type of AD___ is a type of _________

A

ADR is a type of ADE is a type of adverse event

46
Q

what is a medication error

A

any preventable even that may cause or lead to inappropriate medication use or patient harm while the medication is in the control of the HCP, pt, or consumer

47
Q

type A reactions are dose _______ and _________

A

dependent and predictable

48
Q

type A reactions are (more/less) common than type B

A

more

49
Q

type A reactions primarily result from ___________ and represent ______________

A

drug pharmacology + represent augmentation or exaggerated effect

50
Q

type A reactions are problematic when there is a

A

narrow therapeutic window

51
Q

warfarin causing bleeds is a type ____ reaction

A

A

52
Q

malignant hyperthermia in response to anesthetics is a type ___ reaction

A

B

53
Q

type B reactions are _____ of dose, _______ to known pharm actions

A

independent of dose
unrelated to known pharm actions

54
Q

type B reactions are often caused by

A

immunological responses and pharmacogenic mechanisms

55
Q

type B reactions are often _______ and affects _____ populations

A

idioxyncratic
small populations

56
Q

type C reactions are _____ reactions that _____________________________

A

continuing reactions that persist for relatively long periods of time with cumulative doses

57
Q

how to treat type C reaction

A

reduce dose or withhold meds

58
Q

type A reactions are reversible by

A

reducing dose/ withdrawal

59
Q

osteonecrosis of the jaw from chronic use of BPs is a type ___ reaction

A

C

60
Q

what type of reaction emerges after the patient has started treatment

A

type D- delayed

61
Q

doxorubicin used to treat cancer resulting in later cardiomyopathies is an example of type ___ reactions

A

d

62
Q

describe a type E reaction

A

Occurs after pt stops tx, uncommon

63
Q

how to avoid/ stop type E reaction

A

reintroduce then slowly withdrawal causative agent

64
Q

stopping BZDs suddenly results in anxiety, insomnia, and psychosis is an example of ______

A

type E reaction

65
Q

what is a type F reaction

A

unexpected failure of efficacy, common

66
Q

type F may be ____ or _____

A

dose related or drug intx

67
Q

which of the following is common
1. type B
2. type D
3. type E
4. type F

A

4

68
Q

what is an example of a type F reaction

A

resistance to antibiotics

69
Q

what is type 1 hypersensitivity

A

antibody mediated hypersensitivity due to IgE release

70
Q

reexposure after sensitization triggers response in type __ hypersensitivity

A

1

71
Q

type ___ hypersensitivity is antibody based and primarily involving IgG or IgM response

A

2

72
Q

type 2 hypersense rxn primarily involves

A

IgG or IgM antibody mediated response

73
Q

type 2 hypersense rxns emerge in ____ days and sx in _____

A

5-21 days
sx in 24-48 hrs

74
Q

_____ and _____ are often targets in type 2 hypersens rxn

A

blood cells and platelets

75
Q

type 3 hypersensitivity is

A

nonimmediate immune complex mediated hypersensitivity

76
Q

type 3 hypersens reactions are ____ reactions involving ___

A

antibody reactions
IgG

77
Q

what type of hypersens rxns are due to elevated levels of antigen- antibody complexes

A

type 3

78
Q

what type of hypersensitivity rxn causes serum sickness

A

type 3

79
Q

which type of hypersensitivity takes the longest to develop sx

A

type 4

80
Q

type 4 hypersens is also known as

A

T cell mediated hypersensitivity

81
Q

type 4 hypersense is a reaction involving ___________________________

A

drug sensitizing T cells

82
Q

which hypersensitivity type doesn’t depend on antibodies
1. type 1
2. type 2
3. type 3
4. type 4

A

4

83
Q

SJS is an example of type ___ hypersens rxn

A

type 4 hypersens

84
Q

therapeutic agent used to counteract toxic action of a drug or toxin

A

antidotes

85
Q

which of the following is true
1. less than 2% toxins have a known antidote
2. you should treat the patient’s specific toxin, not the sx which will go away with adequate toxin control
3. antidotes typically have low potential SEs and toxicity or a large TI
4. all of the above are true

A

1

86
Q

activated charcoal is commonly given as a (single/ multiple), (large/ small) dose

A

single large dose

87
Q

activated charcoal characteristics

A

large SA
small particle size
very porous

88
Q

activated charcoal is not useful with

A

alcohols
cyanide
iron
lithium
arsenic

89
Q

activated charcoal is CI with

A

caustics

90
Q

4 ways antidotes can work

A

direct action on toxin
action on the toxin binding site
decreasing toxic metabolites
counteracting the effects

91
Q

activated charcoal works by
1. direct action on toxin
2. action on the toxin binding site
3. decreasing toxic metabolites
4. counteracting the effects

A

direct action on toxin

92
Q

NAC works by
1. direct action on toxin
2. action on the toxin binding site
3. decreasing toxic metabolites
4. counteracting the effects

A

3

93
Q

naloxone and flumazenil work by
1. direct action on toxin
2. action on the toxin binding site
3. decreasing toxic metabolites
4. counteracting the effects

A

2

94
Q

atropine works by
1. direct action on toxin
2. action on the toxin binding site
3. decreasing toxic metabolites
4. counteracting the effects

A

4

95
Q

when actvated charcoal is given in multiple smaller doses, the intent is to

A

enhance elimination like dialysis

96
Q

when activated charcoal is given as a large single dose, the intent is

A

to bind poison and avoid systemic absorption

401 - Toxicology, Drug Abuse, Pharmacology (32 decks)

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