Principles of Drug Toxicology Flashcards

1
Q

How do you study adverse effects of chemicals on living systems?

A
Mechanisms of action
Understanding physiology + pharmacology
Recognition + quantification of hazards
Discovery of new drugs
Development of standards + regulations
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2
Q

What are the different types of adverse drug reactions?

A
Type A (augmented)
Type B 
Type C (chemical)
Type D (delayed)
Type E (end of treatment)
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3
Q

What is the difference between Type A + B?

A

A can be predicted from pharmacology of drug B cannot
A typically dose-dependent
B can effect almost any organ system

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4
Q

What is Type A induced by?

A

Same pharmacological mechanism as therapeutic effect

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5
Q

How can Type A arise?

A

Changes in drug pharmacokinetics = pathology or aging

Changes in pharmacodynamics = concomitant pathology or non-compliance

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6
Q

Which is the most frequent of all adverse reactions?

A

Type A

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7
Q

Which is relatively less dangerous + why?

A

Type A = lower mortality rate

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8
Q

What is the intervention for Type A?

A

Dose reduction

Use of antagonist

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9
Q

What is the prevention for Type A?

A

Dose titration
Monitoring
Pharmacotherapy monitoring (PK/PD)

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10
Q

What is Type B?

A

Allergy to the drug

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11
Q

What is Type B caused by?

A

Genetic predisposition

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12
Q

Does Type B have an relation to dose of drug?

A

NO

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13
Q

Why does Type B have a higher serious clinical outcome?

A

Higher mortality rate

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14
Q

What is the intervention for Type B?

A

Instant drug withdrawal

Symptomatic treatment

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15
Q

What can be used for Type B since it is an allergy?

A

Antihistamines

Adrenaline

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16
Q

What is the prevention for Type B?

A

Avoiding certain drugs with known risks

17
Q

What does Type B (allergic reactions) require?

A

Previous exposition before manifestation

18
Q

What are the two different Type B?

A
Allergic reactions
Idiosyncratic reactions (genetics)
19
Q

How can immunogenicity be acquired in Type B (allergic reactions)?

A

Binding of drug on macromolecular carrier
Covalent bond
Carrier = protein

20
Q

What does idiosyncratic not require?

A

Prior exposure

21
Q

What is idiosyncratic primarily determined by?

A

Genetic deviations

22
Q

Are the effects of idiosyncratic related to pharmacological properties of drug?

A

NO

23
Q

Is Type C as frequent as B?

A

NO

24
Q

What is Type C associated with?

A

Cumulative-long term exposure inducing toxic response

25
Q

What is most accumulation in Type C?

A

Functional NOT immune

26
Q

What does Type C have a direct relationship with?

A

Cumulative dose

27
Q

What is Type C treatment?

A

Troublesome, largely irreversible in higher cumulative dose

28
Q

What is Type C prevention?

A

Cumulative dose reduction
Limitation of time exposure
Monitoring
Prevention of non-compliance + drug abuse

29
Q

What is part of Type D?

A

Teratogenesis

Mutagenicity + carcinogenicity

30
Q

What is teratogenesis?

A

Embryo/foetus death, morphologic malformations, functional defects
= penetration of placenta barrier

31
Q

Describe teratogenesis

A

Homogenous distribution between mother + foetus

32
Q

What is mutagenicity + carcinogenicity?

A

Mutation

33
Q

Describe mutagenicity + carcinogenicity

A

Impair regulation of cellular proliferation + differentiation = tumour formation

34
Q

What % of carcinogenic events are induced by chemical compounds?

A

60-70%

35
Q

What is Type E (end of use)?

A

Drug withdrawal syndromes

36
Q

What is Type E due to?

A

Up-regulation of receptors during chronic treatment

Withdrawal of long-term systemic treatment with glucocorticoids

37
Q

What is Type E prevention?

A

Avoid abrupt withdrawals
Slow decrease in dose
Avoid long treatment