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Clinical Chemistry 2 - CEUMLS > Toxicology > Flashcards

Toxicology Flashcards

1
Q

Study of poisons and xenobiotics

A

TOXICOLOGY

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2
Q

substances that can cause harmful effects upon exposure

A

Poisons

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3
Q

substances that are not normally found or produced by the body

A

Xenobiotics

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4
Q

4 MAJOR INTERRELATED DISCIPLINES OF TOXICOLOGY

A

Mechanistic Toxicology
Descriptive Toxicology
Forensic Toxicology
Clinical Toxicology

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5
Q

Dose-Response Mechanism

A

Mechanistic Toxicology

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6
Q

Dose of toxin that will result in harmful effects

A

Dose-Response Mechanism

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7
Q

Determines the dose of toxin that will result in harmful effects

A

Mechanistic Toxicology

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8
Q

Provides a basis for rational therapy design from the known harmful dose

A

Mechanistic Toxicology

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9
Q

Development of laboratory tests to assess the degree of exposure in individuals

A

Mechanistic Toxicology

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10
Q

involves risk assessment of toxins

A

Descriptive Toxicology

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11
Q

Performed by FDA and part of pre-clinical studies of novel drugs

A

Risk assessment

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12
Q

Assesses toxic, lethal, and effective dose

A

Risk assessment (Descriptive Toxicology)

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13
Q

Uses result from animal experiments to predict what level of exposure will cause harm in humans

A

Descriptive Toxicology

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14
Q

Medical & legal consequence of toxin exposure; performed in autopsy

A

Forensic Toxicology

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15
Q

Establishes & validates analytical performance of tests methods used to generate evidence in legal situations

A

Forensic Toxicology

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16
Q

Study of interrelationship between toxin exposure and disease states (toxic effect)

A

Clinical Toxicology

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17
Q

Emphasis on diagnostic testing and therapeutic intervention (antidote to toxins)

A

Clinical Toxicology

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18
Q

ROUTES OF TOXIN EXPOSURE

A

Ingestion – most often in clinical setting
Inhalation
Transdermal absorption

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19
Q

how is toxin absorbed in GI tract

A

Passive diffusion

*not requiring transport protein

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20
Q

substances readily diffusible across cell membranes along GI

A

Hydrophobic (non-polar) subs.

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21
Q

substances that cannot passively diffuse across cell membranes (require transporters)

A

Ionized subs.

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22
Q

absorbed in the stomach; proteinated by gastric juices → became non-ionized → readily absorbed by stomach

A

Weak acids

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23
Q

absorbed in the intestine (neutral to slightly alkaline pH)

A

Weak bases

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24
Q

some toxins that are not absorbed by GI produce these local effects given that they are toxic to that site

A

diarrhea
malabsorption
GI bleeding

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25
Q

Factors that influence toxin absorption

A

Rate of Dissolution
GI mobility
Resistance to degradation
Interaction with other substances in GI

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26
Q

Effect in absorption rate when there is imbalance in mobility such as low bowel movement, diarrhea

A

Less/decreased toxin absorption

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27
Q

T/F
Some toxins are resistant to degradation = remains intact in GI (may or may not be absorbed by the GI)

A

T

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28
Q

Effect in absorption rate when toxins interact with other GI substances

A

Decreased rate of absorption

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29
Q

single, short-term exposure to toxic substance

A

Acute toxicity

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30
Q

repeated exposure for extended period of time

A

Chronic toxicity

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31
Q

dose that would predict to produce a toxic response in 50% of the population

A

TD50 (toxic dose)

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32
Q

dose that would predict death in 50% of the population

A

LD50 (lethal dose)

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33
Q

dose predicted to be effective or have a therapeutic benefit in 50% of the population; used in therapeutic drugs that may cause adverse effects

A

ED50 (effective dose)

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34
Q

Rapid, simple, qualitative procedure intended to detect the presence of specific substance

A

Screening test

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35
Q

test that has good sensitivity, lack specificity

A

Screening test

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36
Q

Quantitative tests; specific for a single substance or class

A

Confirmatory test

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37
Q

Example of Confirmatory tests for toxic agent analysis

A

TLC (Thin Layer Chromatography), GC (Gas Chromatography)

ICP-MS/AA (Inductively Coupled Plasma – Mass Spectrometry/Atomic Absorption)

GC-MS (Gas Chromatography-Mass Spectrometry)

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38
Q

test used for inorganic substance

A

ICP-MS/AA (Inductively Coupled Plasma – Mass Spectrometry/Atomic Absorption)

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39
Q

test used for organic substance

A

GC-MS (Gas Chromatography-Mass Spectrometry)

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40
Q

reference method for toxic agents analysis

A

GC-MS (Gas Chromatography-Mass Spectrometry)

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41
Q

Common CNS depressant

A

Alcohol

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42
Q

effect of LOW dose exposure to alcohol

A

Confusion
Euphoria
Disorientation

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43
Q

effect of HIGH dose exposure to alcohol

A

Unconsciousness
Paralysis
Death

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44
Q

Sample used for alcohol det.

A

Whole Blood
Serum
Plasma

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45
Q

Methods used for alcohol det.

A

Enzymatic method
Gas Chromatography
Osmometry methods (Osmolal Gap)

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46
Q

test that uses alcohol dehydrogenase (ADH)

A

Enzymatic method

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47
Q

Reference method for ethanol det.; may quantitate methanol and isopropanol

A

Gas Chromatography

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48
Q

Computed method; NOT ethanol specific (may increase in other conditions)

A

Osmometry methods (Osmolal Gap)

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49
Q

formula of Osmometry methods (Osmolal Gap)

A

Osmolal Gap = MEASURED osmolality - CALCULATED osmolality

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50
Q

serum ethanol if there is ↑ 10 mOsm/Kg

A

60 mg/dL serum ethanol

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51
Q

Most common toxicant & substance of abuse (US)

A

Ethanol (Grain Alcohol)

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52
Q

aka ethanol

A

Grain Alcohol

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53
Q

Depresses CNS; ↑ heart rate and BP

A

Ethanol (Grain Alcohol)

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54
Q

a Vasopressin inhibitor (↑ urine output leading to diuresis)

A

Ethanol (Grain Alcohol)

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55
Q

Effects of ethanol intoxication

A

blurred vision
incoordination
slurred speech and coma
“hangover symptoms”

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56
Q

FATAL DOSE of ethanol

A

300-400 mL (pure alc.) in <1 hr

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57
Q

TOXIC BLOOD LVL of ethanol

A

> 400 mg/dL

> 500 mg/dL: requires hemodialysis to filter all alcohol

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58
Q

ANTIDOTE for ethanol intoxication

A

Diazepam

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59
Q

method for ethanol det.

A

Gas Chromatography
Enzymatic (ADH) method

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60
Q

T/F

Serum and plasma have lower ethanol conc. than whole blood

A

F

Serum and plasma have HIGHER ethanol conc. than whole blood (ethanol is uniformly distributed in body water such as serum or plasma)

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61
Q

conditions that causes false INCREASED ethanol

A

Use of alcohol antiseptic during venipuncture
Failure to use fluoride tubes

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62
Q

Tube necessary for blood collection during ethanol det.

A

Fluoride tubes (prevent glycolysis and bacterial fermentation as they produce alc. (byproduct)

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63
Q

aka methanol

A

Wood Alcohol

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64
Q

Most commonly used solvent

A

Methanol (Wood Alcohol)

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65
Q

Homemade liquor contaminant

A

Methanol (Wood Alcohol)

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66
Q

Methanol (Wood Alcohol) metabolites

A

formaldehyde
formic acid

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67
Q

Methanol (Wood Alcohol) metabolite that causes intoxication

A

Formic acid

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68
Q

T/F

Ethanol has more severe intoxication than methanol

A

F

METHANOL has more severe than ethanol

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69
Q

Effects of methanol intoxication

A

metabolic acidosis
pancreatic necrosis
ocular toxicity (frank blindness)

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70
Q

toxins that can cause ocular toxicity (frank blindness)

A

Methanol (Wood Alcohol)

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71
Q

FATAL DOSE of methanol

A

60-250 mL

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72
Q

TOXIC BLOOD LVL of methanol

A

> 50 mg/dL

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73
Q

ANTIDOTE for methanol intoxication

A

Sodium Bicarbonate

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74
Q

Commonly available alcohol

A

Isopropanol (Rubbing Alcohol)

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75
Q

aka Isopropanol

A

Rubbing Alcohol

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76
Q

Isopropanol (Rubbing Alcohol) metabolite

A

acetone

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77
Q

enzyme that converts isopropanol to its metabolite

A

hepatic ADH

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78
Q

has longer halflife in the body compared to ethanol metabolite

A

acetone

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79
Q

has similar to ethanol toxicity but has a longer intoxication due to its metabolite having a longer half life

A

Isopropanol (Rubbing Alcohol)

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80
Q

FATAL DOSE of Isopropanol

A

250 mL

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81
Q

ANTIDOTE for Isopropanol intoxication

A

Active charcoal

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82
Q

aka Ethylene Glycol

A

1,2-ethanediol

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83
Q

Component of hydraulic fluid and anti-freeze

A

Ethylene Glycol (1,2-ethanediol)

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84
Q

Accidentally ingested by children due to its sweet taste

A

Ethylene Glycol (1,2-ethanediol)

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85
Q

Ethylene Glycol (1,2-ethanediol) metabolites that can cause severe metabolic acidosis

A

oxalic acid
glycolic acid

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86
Q

Effects of Ethylene Glycol intoxication

A

severe metabolic acidosis

Ingestion (↑levels): Calcium oxalate crystals
deposition in renal tubules → kidney damage

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87
Q

Blood ethanol level if there is no obvious impairment

A

0.01-0.05%

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88
Q

Blood ethanol level if there is mild euphoria, decrease inhibitions, some impairment of motor skills

A

0.03-0.12%

89
Q

Blood ethanol level if there is decrease inhibitions, loss of critical judgment, memory impairment, diminished reaction time

A

0.09-0.25%

90
Q

Blood ethanol level if there is decrease inhibitions

A

0.03-0.25%

91
Q

Blood ethanol level if there is mental confusion, dizziness, strongly impaired motor skills (staggering, slurred speech)

A

0.18-0.30%

92
Q

Blood ethanol level if there is inability to stand or walk, vomiting, impaired consciousness

A

0.27-0.40%

93
Q

Blood ethanol level indicating coma and possible death

A

0.36-0.50%

94
Q

Produced by incomplete combustion of carbon-containing substances

A

Carbon monoxide (CO)

95
Q

Colorless, odorless and tasteless gas that is rapidly absorbed into the blood

A

Carbon monoxide (CO)

96
Q

Carbon monoxide (CO) has _____X more affinity to Hb than O2

A

200–225x

97
Q

caustic agents of carbon monoxide (CO)

A

household products
occupational settings

98
Q

formed when CO is bound to Hb

A

Carboxyhemoglobin

99
Q

Leads to hypoxia since O2 is not bound to Hb → affects heart and brain

A

Carboxyhemoglobin formation due to CO

100
Q

one of the indication is cherry-red colored blood

A

Carboxyhemoglobin formation

101
Q

routes of exposure to CO

A

Aspiration
Ingestion

102
Q

CO intoxication if exposed through aspiration

A

pulmonary edema and shock
can lead to death

103
Q

CO intoxication if exposed through ingestion

A

esophageal lesions and GIT lesions (perforation)

CAN LEAD TO:
hematemesis (vomiting of blood)
abdominal pain & shock (if there is chronic blood loss)
metabolic acidosis/alkalosis

104
Q

T/F

Carboxyhemoglobinemia Symptoms depends on the carboxyghemoglobin formed

A

T

105
Q

COHb (%) typical in nonsmoker

A

0.5

106
Q

COHb (%) seen in smokers

A

5-15

107
Q

COHb (%) having shortness of breath with vigorous exercise

A

10

108
Q

COHb (%) having shortness of breath with moderate exercise

A

20

109
Q

COHb (%) having severe headache, fatigue, impairment of judgment

A

30

110
Q

COHb (%) having confusion, fainting on exertion

A

40-50

111
Q

COHb (%) when there is unconsciousness, respiratory failure, death with continuous exposure

A

60-70

112
Q

COHb (%) that is immediately FATAL

A

80

113
Q

CoHb Tx

A

100% O2 therapy

114
Q

ANTIDOTE for CO

A

Dilution (of substance)

115
Q

METHODS for CO det.

A

Spot Plate Test
Differential Spectrophotometry
Gas Chromatography

116
Q

How is spot plate test for CO det. performed?

A

5mL aqueous whole blood (1/20) + 5mL of 40% NaOH

Aqueous whole blood: prepared by diluting blood with water (1 part of blood per 20 parts volume of solution)

Add 5mL of 40% NaOH

Pink color solution = >20% COHb

117
Q

Indication if there is >20% COHb in Spot Plate Test

A

Pink colored solution

118
Q

Principle: Different forms of Hgb present with different spectral absorbency curves (6 diff. wavelengths)

A

Differential Spectrophotometry

119
Q

Most commonly used method and basis of automated systems for CO det.

A

Differential Spectrophotometry

120
Q

Principle: utilizes thermal conductivity by releasing carbon monoxide using potassium
ferricyanide

A

Gas Chromatography

121
Q

an accurate and precise method (Ref. method) for CO

A

Gas Chromatography

122
Q

Supertoxic substance

A

Cyanide

123
Q

Cyanide may exist as

A

solid or gas

124
Q

odor of the gas form of cyanide

A

Bitter almond odor

125
Q

One of the most common suicidal agents (in the form of silver cleaners)

A

Cyanide

126
Q

Used in many industrial processes

A

Cyanide

127
Q

Insecticides and rodenticides component

A

Cyanide

128
Q

Produced by pyrolysis of some plastics

A

Cyanide

129
Q

Routes of exposure to cyanide

A

Inhalation
Ingestion
Transdermal absorption

130
Q

route of exposure when one may be exposed to both cyanide and CO

A

smoke inhalation

131
Q

blood component where cyanide may bind

A

heme iron
mitochondrial cytochrome oxidase

132
Q

intoxication if Cyanide + heme iron

A

Hb can no longer bind O2 leading to hypoxia and anemia

133
Q

intoxication if Cyanide + mitochondrial cytochrome oxidase

A

Inhibits mitochondrial cytochrome oxidase → increases cellular oxygen tension and venous partial O2 pressure

134
Q

METHODS for cyanide det.

A

Ion-selective electrode

Photometric assay (two-well microdiffusion separation)

Urinary thiocyanate concentration

135
Q

most commonly used methods for cyanide det.

A

Ion-selective electrode
Photometric assay (two-well microdiffusion separation)

136
Q

test used in exposure to very low levels of cyanide

A

Urinary thiocyanate concentration

137
Q

Some METALS AND METALLOIDS assessed in toxicology

A

Arsenic
Cadmium
Lead
Mercury
Pesticides

138
Q

A metalloid that exists as a bound to or as a primary constituent of many organic or inorganic compounds

A

Arsenic

139
Q

Binds to thiol groups in protein due to high affinity

A

Arsenic

140
Q

Common homicidal & suicidal agent

A

Arsenic

141
Q

Can cross the placenta

A

Arsenic

142
Q

Arsenic intoxication

A

IV hemolysis
Hemoglobinemia
Nephrotoxicity
Multi-organ involvement

143
Q

Indications of Arsenic intoxication

A

Garlic breath odor

Metallic taste

144
Q

SPECIMENS used if there is short-term Arsenic exposure

A

Blood
Urine

145
Q

SPECIMENS used if there is long-term Arsenic exposure

A

Hairs
Nail

*As loves to bind to keratinized tissues

146
Q

METHODS for As det.

A

Atomic Absorption Spectrophotometry (AAS)
Reinsch test

147
Q

Utilized in electroplating and galvanizing

A

Cadmium

148
Q

Found in paints and plastics

A

Cadmium

149
Q

Binds to proteins and cellular constituents

A

Cadmium

150
Q

Cadmium Intoxication

A

Nephrotoxic
o Tubular proteinuria
o Glucosuria
o Aminoaciduria

151
Q

Spx for Cadmium det.

A

Urine
Whole blood

152
Q

merhod for Cadmium det.

A

AAS

153
Q

Paints & make-ups color enhancer

A

Lead

154
Q

Found in gasoline & pipe plumbing

A

Lead

155
Q

Common water contaminant

A

Lead

156
Q

Potent enzyme inhibitors

A

Lead
Mercury

157
Q

Enzymes inhibited by lead

A

Delta-aminolevulinic acid (D-ALA) synthetase

Pyrimidine-5’-nucleotidase (P5’N)

Na-K ATPase

158
Q

responsible for excess DNA removal in RBC nucleus

A

Pyrimidine-5’-nucleotidase (P5’N)

159
Q

What will happen if Pyrimidine-5’-nucleotidase (P5’N) is inhibited by LEAD?

A

DNA accumulates inside the RBC causing basophilic stippling

160
Q

Has high affinity to many macromolecular structures and distributed throughout the body; Present in all biologic system but has NO physiologic nor biochemical function

A

LEAD

161
Q

has SLOW elimination through renal filtration

A

lead

162
Q

reasons why lead has SLOW elimination through renal filtration

A

LOW Pb conc. in the blood

Pb combines with the bone matrix (hence, largest Pb conc. is in skeletal system): may persists up to 20 years

163
Q

toxic dose of lead

A

> 0.5 mg/day

164
Q

fatal dose of lead

A

0.5 g

165
Q

toxic blood lvl of lead

A

> 70 ug/dL

166
Q

Lead Intoxication

A

Anemia – Pb inhibits heme synthesis
Decreased RBC membrane integrity
Encephalopathy
Nephrosis
Anorexia
Peripheral neuropathy
Birth defects
Low IQ
Carcinogenesis
Renal damage

167
Q

Indications of Lead intoxication

A

Basophilic stippling/ blueberry muffin-like RBC
Increased Urinary ALA
Free RBC protoporphyrin

168
Q

sensitive indicator of Pb poisoning; due to inhibited P5’N

A

Basophilic stippling

169
Q

this presence is due to Pb inhibiting multiple steps of heme synthesis

A

Free RBC protoporphyrin

170
Q

Tx for lead intoxication

A

chelators

171
Q

examples of chelators used for lead intoxication tx

A

EDTA
Dimercaptosuccinic acid (DMSA)

172
Q

SPECIMENS used for Lead det.

A

Whole blood
Urine (recent Pb exposure)
Hair

173
Q

spx used if there is RECENT lead exposure

A

urine

174
Q

Methods for lead det.

A
  1. Screening
    a. Zinc Protoporphyrin test (Fluorometric test)
    b. Aminolevulinic acid dehydratase (ALAD) test
  2. In-vivo X-ray Fluorescence of Bone
  3. AAS
  4. ICP-MS
  5. Anodic stippling voltammetry
175
Q

sensitive method for Lead screening

A

Aminolevulinic acid dehydratase (ALAD) test

176
Q

enzyme inhibited by mercury

A

Catecholamine-0-methyltransferase

177
Q

Catecholamine metabolic enzyme (metabolizes epinephrine or norepinephrine)

A

Catecholamine-0-methyltransferase

178
Q

unmetabolized catecholamines due to MERCURY presence may lead to

A

pheochromocytoma - tumor that autonomously produces catecholamines

179
Q

reference value of mercury

A

<10 ug/dL

180
Q

3 forms of mercury with different toxicity levels

A

elemental mercury
inorganic salts
component of organic compounds

181
Q

value if there is significant exposure to Hg

A

> 50 ug/dL (whole blood)

182
Q

Hg intoxication mimics these disorders

A

adrenal gland disorders (due to inhibited catecholamine metabolism)

183
Q

Indicators of Hg intoxication

A

Hypertension
Tachycardia
Sweating

*these are pheochromocytoma symptoms

184
Q

spx for Hg det.

A

Whole Blood
24h Urine

185
Q

methods for Hg det.

A

Reinsch test
AAS
Anodic Stippling Voltammetry

186
Q

Hg liquid at RT

A

Elemental mercury

187
Q

Ingested but may not show significant effects (not absorbed)

A

Elemental mercury

188
Q

Inhalation is very rare and insignificant (due to low vapor pressure

A

Elemental mercury

189
Q

Elemental mercury intoxication

A

Pink disease (acrodynia)
Erethism

190
Q

continuous skin exfoliation upon exposure until skin turns pink caused by elemental mercury

A

Pink disease (acrodynia)

191
Q

moderately toxic form of Hg

A

inorganic salts

192
Q

Hg form that is partially absorbed by the GI tract

A

inorganic salts

193
Q

this form of Hg not absorbed shows GI tract toxicity

A

Inorganic salts

194
Q

Inorganic salts (Hg) intoxication

A

Nephrotoxic (glomerular proteinuria)

195
Q

Alkyl mercury intoxication

A

congenital Minimata disease

196
Q

a neurologic disorder resembling cerebral palsy

A

congenital Minimata disease

197
Q

Most toxic form of Hg; rapidly absorbed

A

component of organic compounds

198
Q

ex. of Hg component of organic compounds

A

methylmercury

199
Q

Substances intentionally added to the environment to kill/harm undesirable life forms

A

Pesticides

200
Q

Pesticides can be classified as either

A

insecticides or herbicides

201
Q

Forms of insecticides

A

Organophosphate
Carbamates
Halogenated Hydrocarbons

202
Q

most common form of insecticide

A

Organophosphate

203
Q

responsible for 1/3 of all pesticide poisoning

A

Organophosphate

204
Q

forms of insecticides that inhibits ACETYLCHOLINESTERASE

A

Organophosphate
Carbamates

205
Q

Muscle cell stimulant; stimulant of some endocrine and exocrine glands

A

Acetylcholine

206
Q

Metabolized by acetylcholinesterase

A

Acetylcholine

207
Q

what is the effect of Organophosphate and Carbamates in inhibiting acetylcholine metabolism?

A

cause systemic effects (since acetylcholine stimulates several parts of the body)

208
Q

Effects of low level exposure to pesticides

A

Salivation
Lacrimation
Involuntary urination & defecation

209
Q

Effects of high level exposure to pesticides

A
  • Bradycardia
  • Muscular twitching
  • Cramps
  • Apathy
  • Slurred speech
  • Behavioral changes
  • Death (due to respiratory failure)
210
Q

spx used for pesticides det.

A

RBC for AIA

211
Q

Used for INDIRECT measurement of organophosphate poisoning

A

Acetylcholinesterase Inhibition Assay (AIA)

212
Q

T/F

direct organophosphate poisoning measurement is highly possible

A

F

Direct organophosphate poisoning measurement is highly IMPOSSIBLE because of its high affinity to proteins

213
Q

Alternative & Screening test for pesticides

A

Serum Pseudocholinesterase Activity

214
Q

a method used for pesticide det. that lacks sensitivity and specificity

A

Serum Pseudocholinesterase Activity

215
Q

methods for pesticide det.

A

Acetylcholinesterase Inhibition Assay (AIA)
Serum Pseudocholinesterase Activity

216
Q

other conditions where Serum Pseudocholinesterase Activity may be decreased?

A

acute infection, pulmonary embolism, hepatitis, cirrhosis

217
Q

alcohols that can cause metabolic acidosis

A

methanol
ethylene glycol

218
Q

nephrotoxic metals and metalloids

A

arsenic
cadmium
inorganic Hg

Clinical Chemistry 2 - CEUMLS (9 decks)

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