Forensic Toxicology & Drug Chemistry

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A comprehensive flashcard deck covering key concepts in forensic toxicology and drug chemistry, including drug scheduling, testing methods, specimen types, and legislative context.

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224 Terms

1
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Who collects toxicology specimens during an autopsy?

The forensic pathologist or medical examiner.

2
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What is the “chain of custody”?

The documented path of evidence from collection to courtroom ensuring no tampering occurred.

3
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What happens if the chain of custody is broken?

The evidence may be ruled inadmissible in court.

4
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What specimens are most useful in postmortem toxicology?

Blood, urine, liver, vitreous humour, bile, hair, gastric contents.

5
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Why are multiple specimens tested?

To confirm consistency and eliminate false negatives/positives from decomposition or contamination.

6
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Why might vitreous humour be used for alcohol testing?

It resists postmortem decomposition and shows BAC more reliably than blood.

7
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Why are pre-hospital admission blood samples important?

They show true antemortem concentrations before metabolism or treatment interference.

8
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What toxicology result is considered “screening only”?

A positive immunoassay result without GC-MS confirmation.

9
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Recommended specimens for Suicide / motor vehicle / industrial accident

Blood, urine, vitreous humour, liver

10
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Recommended specimens for Homicide / suspicious death

Blood, urine, vitreous humour, gastric contents, bile, liver, hair

11
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Recommended specimens for Drug-related death

Blood, urine, vitreous humour, gastric contents, bile, liver, hair

12
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Recommended specimens for Volatile substance abuse

Blood, urine, vitreous humour, lung fluid or tied-off lung, liver

13
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Recommended specimens for Heavy metal poisoning

Blood, urine, vitreous humour, liver, hair, kidney

14
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Why is hair useful for toxicology?

It provides a long-term exposure record (weeks to months).

15
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Why are stomach contents tested?

To identify undissolved pills or poisons in acute overdose cases.

16
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Why is the liver so valuable in toxicology?

It’s where most drug metabolism occurs, and drugs concentrate there.

17
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Why is urine often tested even though it doesn’t show intoxication?

It shows recent use via drug metabolites.

18
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What’s the purpose of presumptive testing?

To indicate a drug may be present (field or lab screening).

19
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What’s the purpose of confirmatory testing?

To definitively identify the drug using advanced instrumentation.

20
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Examples of presumptive tests?

Colorimetric, microcrystalline, UV spectroscopy, microscopic analysis.

21
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Examples of confirmatory tests?

GC-MS, LC-MS, IR spectroscopy, capillary electrophoresis.

22
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What is GC-MS used for?

Separating and identifying components by mass spectral fingerprint.

23
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What does LC-MS stand for?

Liquid Chromatography–Mass Spectrometry. Used for heat-sensitive drugs.

24
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What does IR spectroscopy detect?

Bond vibrations to determine functional groups and compound identity.

25
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What does capillary electrophoresis use to separate compounds?

An electric field.

26
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What’s the difference between qualitative and quantitative tests?

Qualitative = “what’s there”; Quantitative = “how much is there.”

27
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Why is immunoassay used as a first screen?

It’s fast, detects broad drug classes via antibodies, and cheap.

28
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What’s the most reliable confirmatory test used in forensic toxicology?

GC-MS (Gas Chromatography–Mass Spectrometry).

29
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Characteristics and examples of Schedule I drugs?

No accepted medical use, high abuse potential – Heroin, LSD, MDMA, Marijuana (federally).

30
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Characteristics and examples of Schedule II drugs?

Restricted medical use, high abuse potential – Cocaine, Methamphetamine, Oxycodone, Fentanyl.

31
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Characteristics and examples of Schedule III drugs?

Moderate abuse potential – Ketamine, Anabolic steroids, Barbiturates.

32
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Characteristics and examples of Schedule IV drugs?

Low abuse potential – Xanax®, Valium®, Ambien®.

33
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Characteristics and examples of Schedule V drugs?

Lowest abuse potential, limited narcotics – Robitussin® AC, Tylenol® with Codeine.

34
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Which act established drug schedules in the U.S.?

The Controlled Substances Act.

35
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Why are Schedule I drugs federally illegal?

They’re considered to have no accepted medical use.

36
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Who enforces drug scheduling?

The Drug Enforcement Administration (DEA).

37
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What determines drug scheduling?

Medical value, abuse potential, and physical/psychological dependence risk.

38
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Common effects and examples of Stimulants?

Increased alertness, energy, euphoria – Cocaine, Amphetamines, Methamphetamine.

39
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Common effects and examples of Depressants?

Relaxation, slowed CNS activity – Alcohol, Benzodiazepines, Barbiturates.

40
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Common effects and examples of Narcotics (Opiates)?

Pain relief, euphoria, drowsiness – Heroin, Morphine, Codeine, Oxycodone.

41
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Common effects and examples of Hallucinogens?

Altered perception, hallucinations – LSD, PCP, Psilocybin.

42
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Common effects and examples of Cannabinoids?

Euphoria, relaxation, impaired coordination – THC (Marijuana).

43
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Common effects and examples of Synthetic Drugs?

Unpredictable, psychotic effects – Synthetic cannabinoids (“Spice”), Bath Salts.

44
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Common effects and examples of Inhalants?

Euphoria, disorientation, slurred speech – Butane, Nitrous Oxide.

45
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Common effects and examples of Steroids?

Aggression, mood swings, muscle growth – Testosterone, HGH.

46
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What’s the first step once evidence reaches the lab?

Documentation, labeling, and storage under chain of custody.

47
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What test determines how much of a substance is present?

Quantitative test.

48
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What test determines what substance is present?

Qualitative test.

49
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What does the “Scientific Working Group for the Analysis of Seized Drugs” (SWGDRUG) do?

Publishes guidelines for drug analysis in forensic labs.

50
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What’s the role of a forensic chemist in court?

Provide expert testimony on testing methods and drug identity.

51
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What is a “true positive” in testing?

When the test correctly detects a drug that is present.

52
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What’s a “false negative”?

When the test fails to detect a drug that is actually present.

53
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What’s the main purpose of toxicology in a death investigation?

To determine whether toxic substances contributed to or caused death.

54
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Why can toxicology show positive results in non-drug deaths?

Some drugs indicate medical treatment or incidental use.

55
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What’s post-mortem redistribution?

The movement of drugs between tissues after death, affecting concentration levels.

56
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Why might alcohol and drugs appear in many traffic deaths?

Impaired driving and reaction times increase fatal crash likelihood.

57
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Why can a positive toxicology result not always mean cause of death?

The concentration may not be lethal or relevant to cause of death.

58
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Who certifies forensic toxicologists in the U.S.?

The American Board of Forensic Toxicology (ABFT).

59
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What organization regulates forensic lab accreditation?

ANAB / ASCLD-LAB.

60
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What’s the goal of “SWGTOX”?

To set national standards for forensic toxicology testing and reporting.

61
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What is EuroTox?

The European Register of Toxicologists certification program.

62
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What’s the role of a forensic chemist vs a toxicologist?

Chemist identifies drugs in seized materials; toxicologist identifies drugs in biological samples.

63
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Define pharmacodynamics.

What a drug does to the body (mechanism/receptor effects); contrasts with pharmacokinetics (what the body does to the drug).

64
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Define pharmacokinetics (ADME).

Absorption, Distribution, Metabolism, Excretion; determines onset, intensity, and duration.

65
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Potency vs efficacy?

Potency = dose needed for effect ( EC{50} ), efficacy = maximal effect ( E{max} ); high potency ≠ high efficacy.

66
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Agonist, partial agonist, antagonist?

Agonist activates fully, partial agonist activates partially, antagonist blocks receptor; partials can blunt full agonists.

67
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Inverse agonist vs antagonist?

Inverse agonist reduces basal activity; antagonist only blocks agonist without changing baseline.

68
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Competitive vs noncompetitive antagonism?

Competitive shifts dose–response right (surmountable); noncompetitive lowers E_{max} (insurmountable).

69
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Therapeutic index (TI)?

TI = TD{50}/ED{50} (or LD{50}/ED{50} ); wider TI = safer.

70
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First-pass metabolism—what is it?

Hepatic/intestinal metabolism before systemic circulation; reduces oral bioavailability.

71
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Bioavailability (F) definition.

Fraction of dose reaching systemic circulation unchanged; IV = 1, oral < 1.

72
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Volume of distribution (Vd) meaning.

Theoretical volume that accounts for drug distribution; high Vd suggests tissue binding.

73
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Clearance (Cl) concept.

Volume of plasma cleared of drug per unit time; determines maintenance dose rate.

74
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Half-life (t½) rules of thumb.

~5 half-lives to steady state or elimination; depends on Vd and Cl.

75
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Zero-order vs first-order elimination?

Zero-order = constant amount/time (capacity-limited), first-order = constant fraction/time.

76
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CYP450 most common hepatic phase I?

Oxidation via CYP3A4, 2D6, 2C9, etc.; polymorphisms matter.

77
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Phase II conjugation examples.

Glucuronidation, sulfation, acetylation; usually inactivating and increases polarity.

78
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Tolerance vs dependence vs addiction?

Tolerance = diminished effect; dependence = withdrawal on cessation; addiction = compulsive use despite harm.

79
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Upregulation vs downregulation of receptors?

Chronic antagonism → upregulation; chronic agonism → downregulation; informs withdrawal/tapering.

80
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Blood–brain barrier favors what?

Lipophilic, small, non-ionized drugs; ion trapping occurs with pH differences.

81
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Ionized vs non-ionized—who crosses membranes?

Non-ionized crosses; Henderson–Hasselbalch explains pH-dependent trapping.

82
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Pharmacodynamic drug–drug interaction example.

Benzos + alcohol → synergistic CNS depression; same direction on outcome.

83
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Pharmacokinetic drug–drug interaction example.

CYP3A4 inhibitors raise fentanyl levels; altered concentration drives effect.

84
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Chain of custody—why critical?

Documents evidence handling end-to-end; breaks can exclude evidence in court.

85
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Postmortem redistribution (PMR)—what is it?

Concentration shifts after death (central > peripheral); prefer femoral blood.

86
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Preferred blood site in autopsy toxicology?

Peripheral (femoral/subclavian) to minimize PMR effects.

87
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Urine utility in tox?

Great for detection window (metabolites), poor for impairment at time of event.

88
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Vitreous humour—why useful?

Stable matrix; good for ethanol (often ~20% higher than blood) and electrolytes.

89
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Liver in tox interpretation?

Metabolic “sink”; can detect drugs when blood negative but interpretation is complex.

90
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Hair testing window?

Weeks–months; shows chronic exposure but susceptible to external contamination.

91
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Nails vs hair?

Longer window than hair; interpretation less well-characterized.

92
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Stomach contents helpful when?

Acute ingestion/overdose—can see undissolved tablets and estimate unabsorbed load.

93
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Immunoassay screen vs confirmatory test?

Immunoassay = presumptive (sensitive, cross-reactivity), GC-MS/LC-MS = confirmatory (specific).

94
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Examples of presumptive lab tests.

Colorimetric kits, microscopic, microcrystalline, UV; indicate class not identity.

95
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Confirmatory instruments of choice.

GC-MS, LC-MS/MS, FTIR; provide molecular identity and often quantitation.

96
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SWGTOX/ABFT relevance.

Standards (SWGTOX) and certification (ABFT) assure validated methods and reliable interpretation.

97
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Routine postmortem tox panel commonly includes?

Alcohols, benzodiazepines/Z-drugs, antidepressants, antihistamines, antipsychotics, opioids, cocaine, THC, stimulants.

98
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“Special request” analytes often not in routine screen?

Barbiturates, digoxin, anticonvulsants (some), LSD, GHB, metals, pesticides, synthetic cannabinoids/cathinones.

99
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DEA Schedule I hallmark.

No accepted medical use, high abuse (e.g., heroin, LSD, MDMA at federal level).

100
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Schedule II examples.

Cocaine (medical), methamphetamine, oxycodone; high abuse, medical use.