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Drugs and Toxicology > Lecture 18: Major Drugs and Forensic Toxicologist > Flashcards

Lecture 18: Major Drugs and Forensic Toxicologist Flashcards

1
Q

When was marijuana was introduced to the Caribbean and by who?

A

In 1838 by workers of India.

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2
Q

Why was the habit was taken on by the working class?

A

The habit was taken on by the working class as it was stated that marijuana increased morale and production.

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3
Q

Marijuana contain numerous compounds called

A

Marijuana contain numerous compounds called cannabinoids.

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4
Q

Cannabis contains over ______ chemical compounds and how many are classified as cannabinoids

A

Cannabis contains over 400 different chemical compounds and 85 are currently classified as cannabinoids

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5
Q

The group that contains the compound of interest,

A

tetrahydrocannabinol, commonly called THC.

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6
Q

Cannabinoids are a class of diverse chemical compounds that act on

A

the cannabinoid receptors in cells that repress neurotransmitter release in
the brain.

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7
Q

Ligands for these cannabinoid receptor proteins include:

A
  1. Endocannabinoids
  2. Phytocannabinoids
  3. Synthetic cannabinoids
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8
Q

WHat are Endocannabinoids ligands?

A

Endocannabinoids - produced naturally in the body by humans and
animals

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9
Q

What are phytocannabinoids?

A

Phytocannabinoids - found in cannabis and some other plants

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10
Q

What are Synthetic cannabinoids?

A

Synthetic cannabinoids are manufactured artificially.

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11
Q

The most notable cannabinoid is

A

The most notable cannabinoid is the phytocannabinoid tetrahydrocannabinol (THC),

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12
Q

The primary psychoactive compound of cannabis

A

Cannabidiol (CBD) is another major constituent of the plant.

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13
Q

What is the most psychoactive compound in marijuana?

A

THC the most psychoactive compound inmarijuana

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14
Q

How much percentage THC makes up the cannabinoid family.

A

THC constitutes 30% of the cannabinoid family.

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15
Q

THC is also known as

A

It is also known as delta-9-tetrahydrocannabinol (Δ9-THC).

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16
Q

THC was extracted by a team headed

A

by Dr. Raphael Mechoulam in 1964

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17
Q

What is the mechanism of THC?

A

Its mechanism involves its binding to the CB1 and CB2, which are cannabinoid receptors.

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18
Q

Is THC an agonist, antagonist or partial agonist

A

THC acts a partial agonist.

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19
Q

Cannabinoid receptors in the brain involved in a variety of physiological processes including

A
  • Appetite,
  • Pain-sensation
  • Mood
  • Memory.
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20
Q

When can THC be administered intravenously?

A

THC can be administered intravenously , however that is usually done under psychological clinical trial.

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21
Q

What is THC metabolised to in the human body

A

THC is metabolized mainly to 11-OH-THC (11-hydroxy-THC) by the human body.

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22
Q

11-OH-THC (11-hydroxy-THC) metabolite is oxidized to?

A

This metabolite (byproduct of metabolism) is still psychoactive and is further oxidized to 11-Nor-9-carboxy-THC (THC-COOH

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23
Q

How much of THC is excreted in the faeces and in the urine.

A

More than 55% of THC is excreted in the faeces and ~20% in the urine.

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24
Q

The main metabolite in urine is

A

The ester of glucuronic acid and THC-COOH and free THC- COOH.

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25
Q

Psychological effects of THC

A

Effect on mood - decreased anxiety, alertness, depression, tension and increased sociability
* Effects on perception – Vivid colours, clear music, meaningful emotions
* Effects on cognition and psychomotor performance – slow reaction time
* Driving and piloting skills – impaired driving similar to alcohol

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26
Q

What are the tolerance, dependence, withdrawal effects

A

restive, anxiety, aggression, insomnia

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27
Q

Systemic effects of THC

A
  • Cardiovascular effects – Dose related tachycardia – heart rate that exceeds the normal range
  • Effects on the respiratory system – 1/3 more tar than cigarette, linked to bronchitis
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28
Q

What is Hash oil?

A

Hash oil is cannabis concentrate containing many of its resins and terpenes – in particular, tetrahydrocannabinol, cannabidiol, and other cannabinoids.

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29
Q

What is Hashish?

A

Hashish is the potent form of cannabis produced by collecting and compressing
trichomes, the most potent material from cannabis plants.

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30
Q

Medicinal Effects of Marijuana?

A
  • Control of nausea
  • Appetite stimulant
  • Reduction in ocular pressure (treatment of glaucoma)
  • Anti-asthma
  • Pain relief
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31
Q

Marijuana related drugs on-the-market:

A

Canasol (glaucoma) & Asmasol (anti asthma)

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32
Q

Drug testing cutoff levels -

A

minimum concentrations of drugs or metabolites that must be present in specimens, before labs will report the drug testing results as positive

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33
Q

Urine Preliminary Immunoassay Cut off

A

50ng/mL…this level equates to a daily user remaining positive for approx. 7-30 days post cessation.

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34
Q

Urine Preliminary GCMS Cut off

A

15ng/mL…this level equates to the frequent user being positive for e.g. 15 weeks

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35
Q

Oral fluid cut off level

A
  • 4 µg/L
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36
Q

Sweat cutoff level

A
  • 4 ng/patch
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37
Q

What is drug dependence?

A

Drug dependence refers to the action of an individual becoming strongly attached to a drug.

38
Q

Dependency is subdivided into two categories

A
  • Physiological dependence
  • Psychological dependence
39
Q

Physiological dependence occurs when

A

Physiological dependence occurs when there is a need by the body to have the drug present. In this case person may experience sickness if they stop taking the drug.

40
Q

Psychological dependence occurs when

A

Psychological dependence occurs when a person develops an uncontrollable “craving” (mental or emotional need) for a drug. Craving is a desperate need to continue.

41
Q

Stimulants are

A

Stimulants are drugs that stimulate the brain and central nervous system, speeding up communication between the two.

42
Q

Common stimulants include:

A

Common stimulants include:
o Crack
o Cocaine
o Amphetamines
o Metamphetamines

43
Q

How does stimulants work?

A

They increase alertness and physical activity and increase the amount of dopamine which is a neurotransmitter responsible for feelings of pleasure resulting in euphoria.

44
Q

Depressants are

A

Depressants are drugs that slow down the activity of the brain and nervous system, slowing down the communication between the two.

45
Q

user of depressant drug may experience:

A

Slowed heartbeat , reduction in anxiety, and in some cases the
promotion of sleep

46
Q

Examples of depressant?

A

This drug class includes:
o Barbiturates
o tranquilizers
o sleep acids
o ethanol

47
Q

Hallucinogens interfere with the

A

brain and central nervous system in a way that results in radical distortions of a user’s perception of reality

48
Q

Two classes of Hallucinogens

A

o Phenethylamine - Methamphetamine and ecstasy
o Tryptamine – Psiclobin

49
Q

Common Hallucinogens include:

A

o Marijuna
o Psilocybin
o Ketamine
o Mescaline

50
Q

Common Alcohols of Interest

A

Methyl Alcohol (Methanol)
Ethyl Alcohol (Ethanol)
Isopropyl Alcohol (Isopropanol)
Ethylene Glycol (Antifreeze)

51
Q

Methyl Alcohol (Methanol) (Wood Alcohol) use

A

Primarily for commercial and industrial purposes and
also as a solvent in paints, paint remover, varnishes.

52
Q

Ethyl Alcohol (Ethanol) (Grain Alcohol) use

A

BEVERAGE SOLVENT; MEDICINAL VEHICLE

53
Q

Isopropyl Alcohol (Isopropanol) (Rubbing Alcohol) use

A

DENATURANT; ANTISEPTIC

54
Q

Ethylene Glycol (Antifreeze) use

A

COOLANT; SOLVENT

55
Q

What is Methanol?

A

Methanol, sometimes called wood alcohol or wood spirits, has no therapeutic properties

56
Q

Methanol in Consumer Products

A

Gas-line antifreezes (99-100% v/v)
Windshield washer fluids (17-95%
Duplicating fluids (60-90%)
Paint removers (3-50%)
Model airplane fuels (43-77%)
Carburator fluids (1-38%)
Ethanol denaturants (2-5%)
Solid can fuels (<4%)
Glass cleaners (1-40%)

57
Q

Metabolic acidosis

A

A condition that occurs when the body produces too much acid or when the kidneys do not remove enough acid from the body.

58
Q

If unchecked, metabolic acidosis leads to

A

academia.

59
Q

Metabolic acidosis causes are diverse, and its consequences can be

A

It causes are diverse, and its consequences can be serious, including coma and death.

60
Q

Methanol poisoning causes

A

nausea, abdominal pain, lethargy, confusion

61
Q

Severe methanol poisoning progresses to

A

anion-gap metabolic acidosis, coma, seizure, and respiratory/circulatory failure

62
Q

Lactic acid accumulation has been observed in methanol poisoned patients as a result of

A

methanol-induced hypotension.

63
Q

In methanol poisoning, metabolic acidosis may necessitate

A

the administration of bicarbonate and assisted ventilation.

64
Q

Bicarbonate potentially may

A

reverse visual deficits and help to decrease the amount of active formic acid.

65
Q

Antidote therapy, which frequently involves the use of ethanol or 4-methyl pyrazole (fomepizole), is aimed at

A

delaying methanol metabolism until the methanol is eliminated from the patient’s system, either naturally or through dialysis.

66
Q

Like methanol, ethanol is metabolized

A

by ADH, but the enzyme’s affinity for ethanol is 10-20 times higher than it is for methanol.

67
Q

Fomepizole is also metabolized

A

by ADH; however, its use is limited because of high cost and lack of availability

68
Q

Isopropanol is used in

A

some rubbing alcohol (70-90 %v/v), ethanol denaturants (5%), deicers (70-80%), glass cleaners (1-14%), liquid detergents (5-12%), cements (5-20%), paint strippers (2-11%), paint thinners (5-10%)

69
Q

Isopropanol is metabolized to

A

Metabolized to acetone (CNS depressant)

70
Q

How long is isopropanol half life compared to ethanol?

A

Longer t1/2 than ethanol

71
Q

Ethylene Glycol half life

A

t½ = 3 h

72
Q

Ethylene Glycol Sources

A
  • Automotive products (antifreeze, windshield de-icers, coolants)
  • Detergents
  • Paints
  • Polishes
  • Cosmetics
  • Improperly added preservatives to juices and wines
72
Q

Ethylene Glycol Sources

A
  • Automotive products (antifreeze, windshield de-icers, coolants)
  • Detergents
  • Paints
  • Polishes
  • Cosmetics
  • Improperly added preservatives to juices and wines
73
Q

Ethanol lethal dose

A

adults 5-8 g/Kg & children 3 g/Kg

74
Q

Alcohol Content of 12oz Beer and Malt Beverages

A

3.5-8% ethanol*

75
Q

Alcohol Content of 6oz Wine

A

8-14% ethanol

76
Q

Alcohol Content of 1.5 oz Hard Liquor

A

35 to 55% ethanol (70 to 110 proof)

77
Q

Calculate Ethanol Content of Beverage

A

Grams of Ethanol = F x V x 0.79 (g/mL)
F = fraction of ethanol (%v/v)
V = volume in mL (1 oz. = approx. 30 mL)
0.79 = ethanol specific gravity (gm/mL at 20ºC)

78
Q

Absorption of Alcohol

A
  • Simple Diffusion
  • Concentration gradient dependent
  • Non-linear process
  • Uses aqueous channels
  • Distributes in proportion to water content
79
Q

Factors Affecting Absorption

A
  • Gastric emptying
  • GI mobility and blood flow
  • Beverage alcohol conc.
  • Concentration gradient
80
Q

What is cocaine

A
81
Q

Coca is widely cultivated

A

in Bolivia, Peru and Ecuado

82
Q

The lead producer of cocaine is

A

Colombia, currently the source of about 80% of the world’s cocaine.

83
Q

CHEMICAL NAMES for Cocaine

A
  • Benzoylmethylecgonine
  • (1R,2R,3S,5S)-2-Methoxycarbonyltropan-3-yl benzoate
  • 2ß-carbomethoxy-3ß-benzoxytropane
  • 1aH, 5aH-tropane-2ß-carboxylic acid 3ß-hydroxy-methyl ester benzoate
  • 3-tropanylbenzoate-2-carboxylic acid methyl ester
  • 3-(benzoyloxy)-8-methyl-8-azabicyclo-(3.2.1.) octane-2-carboxylic acid methyl ester
84
Q

Street Names of Cocaine

A

Bernice; Bernies; Blow; Burese; C; Cadillac of drugs; Carrie; Cecil; Champagne of drugs; Charlie; Cholly; Coke; Corine; Crack; Dama blanca; Eritroxilina; Flake; Girl; Gold dust; Green gold; Happy dust; Happy trails; Her; Jam; Lady; Leaf; Nose candy; Pimp’s drug; Rock; She; Snow; Star dust; Star-spangled powder; Toot; White girl; White lady; Liquid lady (alcohol + cocaine); Speed ball (heroine + cocaine)

85
Q

Acute Cocaine progresses through three phases

A
  1. Early stimulation
  2. Advanced stimulation
  3. Depression
86
Q

Early stimulation phase of acute cocaine

A
  • Excitement, enlarged pupils, euphoria, agitation, irritability, bruxism, twitching, psychosis, elevated temperature, elevated pulse
87
Q

Advanced stimulation phase of acute cocaine

A

Convulsions, seizures, hyper-reflexia, diminished consciousness, increased blood pressure, hyperthermia

88
Q

Depression phase of acute cocaine

A

Paralysis, loss of reflexes, respiratory depression, coma, cardiovascular/circulatory collapse, cardiac arrest, death

89
Q

Medicinal Use of Cocaine

A

Nasal Surgery

90
Q

Cocaine and Driving

A
  • Increased risk taking behavior
  • Sensory abilities
  • Visual impairment
  • Motor coordination
  • Attentional abilities
  • Cognitive abilities
  • Post high “crash”

Drugs and Toxicology (14 decks)

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