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[LECT] CC 2 - Finals > [M8] Part 1: Toxicology > Flashcards

[M8] Part 1: Toxicology Flashcards

1
Q

Study of poisons

A

TOXICOLOGY

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2
Q

substances that cause harmful effect upon exposure

A

Poisons

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3
Q

According to bishop, toxicology is the study of ____

A

xenobiotics

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4
Q

substances that are not normally found or produced by the body

A

Xenobiotics

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5
Q

WHAT ARE THE 4 MAJOR DISCIPLINES OF TOXICOLOGY

A

Mechanistic Toxicology

Descriptive Toxicology

Forensic Toxicology

Clinical Toxicology

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6
Q

Studies the dose-response mechanism of toxins

A

Mechanistic Toxicology

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7
Q

dose of toxin
that will cause in harmful effects

A

Dose-response mechanism

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8
Q

Mechanistic toxicology elucidates the ___, ____, and ____ effects of toxins based on a given dose

A

cellular

molecular

biochemical

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9
Q

Provides a basis for rational therapy design

A

Mechanistic Toxicology

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10
Q

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

A

Mechanistic Toxicology

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11
Q

Risk assessment of toxins and/or therapeutic drugs that may elicit toxic effects

A

Descriptive Toxicology

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12
Q

a part of pre-clinical studies
for novel drugs (new drugs, therapeutic
methods, vaccines)

A

Risk assessment

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13
Q

It assesses the effective, toxic, and lethal dose

A

Risk assessment (descriptive toxicology)

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14
Q

Risk assessment is performed by the ____

A

food and
drug administration

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15
Q

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

A

Descriptive Toxicology

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16
Q

T/F: Dose harmful to animals may sometimes be
harmful to humans as well

A

T

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17
Q

Medical and legal consequences of exposure to toxins

A

Forensic Toxicology

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18
Q

Give an Example of Forensic Toxicology

A

autopsy

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19
Q

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

A

Forensic Toxicology

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20
Q

Study of interrelationship between toxin exposure and disease states

A

Clinical Toxicology

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21
Q

Emphasis on diagnostic testing and therapeutic intervention (antidote for specific toxins)

A

Clinical Toxicology

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22
Q

What are the ROUTES OF EXPOSURE in toxicology

A
  1. Ingestion
  2. Inhalation
  3. Transdermal absorption
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23
Q

most often observed route of exposure in clinical setting

A

inhalation

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24
Q

ABSORPTION in toxicology

A

Gastrointestinal tract

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25
Q

T/F: Gastrointestinal tract utilizes ACTIVE diffusion

A

F; passive diffusion

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26
Q

readily diffusible across cell membranes

A

Hydrophobic substance

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27
Q

Hydrophobic substance: polar or non-polar?

A

non-polar

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28
Q

cannot passively diffuse across cell membranes

A

Ionized substance

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29
Q

Ionized substance requires ___

A

transporters

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30
Q

Weak acids – absorbed in the___

A

stomach

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31
Q

Weak bases – absorbed in the___

A

intestine

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32
Q

T/F: There are toxins that are not absorbed by the GI tract

A

T

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33
Q

There are toxins that are not absorbed by the GI tract. These toxins produce ___

A

local effects

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34
Q

What are the 4 factors under absorption

A
  1. Rate of dissolution
  2. Gastrointestinal mobility
  3. Resistance to degradation
  4. Interaction with other substances
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35
Q

The rate of diffusion is dependent on the ___ of ___ in the ___

A

dissolution

toxins

GI tract

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36
Q

In Gastrointestinal mobility,

Low bowel movement, diarrhea = ___ (more/less) absorption

A

less

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37
Q

Toxins that are resistant to degradation may or may not be ___ by the ___

A

absorbed

GI tract

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38
Q

Interaction of toxins with other substances present in the GI tract may cause ____ (inc/dec) in the ___ of ___

A

decrease

rate

absorption

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39
Q

single, short-term exposure to a substance

A

Acute toxicity

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40
Q

repeated exposure for extended period of time

A

Chronic toxicity

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41
Q

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

A

TD50

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42
Q

dose that would predict death in 50% of the population

A

LD50

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43
Q

dose that would be predicted to be effective or have a therapeutic benefit in 50% of the population

A

ED50

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44
Q

Toxic agents are analyzed through:

A

screening test
confirmatory test

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45
Q

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

A

Screening Test

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46
Q

Screening test:

Good ___, lack ___

A

sensitivity

specificity

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47
Q

Quantitative analysis of toxic agents

A

Confirmatory test

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48
Q

Confirmatory Test is Specific for a ___ or ___

A

single substance

class

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49
Q

What are the methods used in the analysis of toxic agents

A

● Three-layer chromatography (TLC)
● Gas chromatography (GC)
● ICP-MS/AA
● GC-MS

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50
Q

ICP-MS/AA standa for:

A

Inductively coupled plasma-mass spectrometry/atomic absorption

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51
Q

Used for inorganic substances

A

ICP-MS/AA

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52
Q

GC-MS stands for:

A

Gas chromatography-mass spectrometry

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53
Q

Reference method

A

GC-MS

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54
Q

Used for organic substances

A

GC-MS

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55
Q

Common CNS depressant

A

Alcohol

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56
Q

Low dose exposure to alcohol will cause:

A

disorientation, confusion,
euphoria

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57
Q

High dose exposure to alcohol will cause:

A

unconsciousness, paralysis,
death

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58
Q

What are the 4 types of alcohol

A

ethanol
methanol
isopropanol
ethylene glycol

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59
Q

Ethanol is aka __

A

grain alcohol

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60
Q

Most common toxicant and substance of abuse (US)

A

ethanol

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61
Q

Depresses CNS and increases heart rate and blood pressure

A

ethanol

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62
Q

ethanol Depresses ___ and ____ heart rate and ___

A

CNS

increases

blood pressure

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63
Q

Vasopressin inhibitor

A

Ethanol

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64
Q

ethanol is a vasopressin inhibitor. It may cause ___ (dec/inc) urine output causing ___

A

increased

diuresis

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65
Q

Intoxication with alcohol will cause

A

blurred vision, incoordination, slurred speech, and coma, “hangover symptoms”

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66
Q

What is the antidote used in case of intoxication with ethanol

A

diazepam

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67
Q

what is the Fatal dose: of ethanol

A

300 – 400 mL (pure alcohol) ingested in < 1 hour

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68
Q

fatal dose of ethanol:

___-___ (pure ___) ingested in ____

A

300 – 400 mL

alcohol

< 1 hour

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69
Q

Toxic blood level of ethanol

A

> 400 mg/dL

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70
Q

The toxic blood level or ethanol is 400 mg/dL. If it reaches ___, patient is required to
undergo ___ to filter out the ___
and prevent ___

A

> 500 mg/dL

hemodialysis

alcohol

intoxication

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71
Q

Method of analysis in ethanol

A

enzymatic (alcohol
dehydrogenase)

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72
Q

STAGES OF IMPAIRMENT BY ALCOHOL:

What is the blood ethanol level if there is No obvious impairment

A

0.01 – 0.05 %, w/v

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73
Q

STAGES OF IMPAIRMENT BY ALCOHOL:

What is the blood ethanol level if there are Mild euphoria, decrease inhibitions, some impairment of motor skills

A

0.03 – 0.12 %, w/v

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74
Q

STAGES OF IMPAIRMENT BY ALCOHOL:

What is the blood ethanol level if there are Decrease inhibitions, loss of critical judgment, memory impairment, diminished reaction time

A

0.09 – 0.25 %, w/v

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75
Q

STAGES OF IMPAIRMENT BY ALCOHOL:

What is the blood ethanol level if there are Mental confusion, dizziness, strongly impaired motor skills (staggering, slurred speech)

A

0.18 – 0.30 %, w/v

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76
Q

STAGES OF IMPAIRMENT BY ALCOHOL:

What is the blood ethanol level if there are Inability to stand or walk, vomiting, impaired consciousness

A

0.27 – 0.40 %, w/v

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77
Q

STAGES OF IMPAIRMENT BY ALCOHOL:

Sign and symptoms: Coma and possible death
Blood Ethanol Level?

A

0.36 – 0.50 %, w/v

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78
Q

Methanol is aka

A

wood alcohol

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79
Q

aka wood alcohol

A

methanol

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80
Q

Most commonly used solvent

A

methanol

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81
Q

Contaminant of homemade liquors

A

methanol

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82
Q

Methanol is Metabolized to ___ and then to ___
in the ___

A

formaldehyde

formic acid

liver

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83
Q

causes intoxication

A

Formic acid

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84
Q

T/F: Ethanol intoxication is more severe than methanol intoxication

A

F; Methanol intoxication is more severe than ethanol intoxication

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85
Q

Methanol Intoxication will result in:

A

metabolic acidosis, pancreatic
necrosis, and ocular toxicity

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86
Q

ocular toxicity is aka

A

frank blindness

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87
Q

Antidote for methanol intoxication

A

sodium bicarbonate

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88
Q

Methanol fatal dose

A

60 – 250 mL

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89
Q

Methanol Toxic blood level:

A

> 50 mg/dL

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90
Q

Isopropanol is aka

A

rubbing alcohol

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91
Q

aka rubbing alcohol

A

Isopropanol

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92
Q

Commonly available form of alcohol

A

Isopropanol

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93
Q

Isopropanol is Metabolized to ____ by ___

A

acetone

hepatic ADH

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94
Q

Isopropanol is CNS ___

A

depressant

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95
Q

Toxicity is similar to ethanol toxicity

A

Isopropanol

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96
Q

Intoxication lasts longer than ethanol because of acetone

A

Isopropanol

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97
Q

Isopropanol Intoxication lasts longer than ethanol because of ___

A

acetone

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98
Q

has a longer half-life in the body compared to the metabolites of ethanol

A

acetone

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99
Q

Antidote for isopropanol Intoxication

A

activated charcoal

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100
Q

Isopropanol Fatal dose:

A

250 mL

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101
Q

Ethylene Glycol is aka

A

1,2-ethanediol

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102
Q

aka 1,2-ethanediol

A

Ethylene Glycol

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103
Q

Component of hydraulic fluid and anti-freeze

A

Ethylene Glycol

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104
Q

If Accidentally ingested by children, has a naturally sweet taste

A

Ethylene Glycol

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105
Q

Ethylene Glycol is Metabolized to ___ and ___
→ May cause ______

A

oxalic acid

glycolic acid

severe metabolic acidosis

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106
Q

Ingestion of high levels of Ethylene Glycol will cause deposition of ___ crystals in ___ causing ___

A

calcium oxalate

renal tubules

kidney damage

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107
Q

What are the sample used for the determination of alcohol

A

whole blood, serum, plasma

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108
Q

In Ethanol determination:

Capped at all times to prevent ___

A

alcohol evaporation

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109
Q

In Ethanol determination:

Use of _____ antiseptic

A

alcohol-free

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110
Q

Why is alcohol-free antiseptic used in ethanol determination?

A

because Alcohol-based antiseptics may
contaminate the sample and cause false increase

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111
Q

Alcohol-based antiseptics may
___ the sample and cause false ___ (inc/dec)

A

contaminate

increase

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112
Q

Ethanol determination:

Uses ___, which Prevent___ and ____
contamination. It may also produce alcohol as their ___ and cause false ___

A

fluoride tubes

glycolysis

bacterial

byproduct

increase

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113
Q

In ethanol determination:

Serum and/or plasma has ___ (higher/lower) ethanol concentration than ___

A

higher

whole blood

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114
Q

T/F: Ethanol is NOT uniformly distributed in body water such as serum and plasma

A

F; Ethanol is uniformly distributed in body water
such as serum and plasma

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115
Q

What are the methods used for the determination of alcohol

A

Enzymatic method
Gas Chromatography
Osmometry methods

116
Q

Utilizes alcohol dehydrogenase
for ethanol determination

A

enzymatic method

117
Q

Enzymatic method Utilizes ____ for ethanol determination

A

alcohol dehydrogenase

118
Q

Reference method for ethanol determination

A

Gas Chromatography

119
Q

may also be used to quantitate methanol and isopropanol

A

Gas Chromatography

120
Q

Computed method

A

Osmometry methods

121
Q

Osmometry methods or

A

osmolal gap

122
Q

what is the formula for osmometry method (osmolal gap)

A

● 𝑜𝑠𝑚𝑜𝑙𝑎𝑙 𝑔𝑎𝑝 = 𝑚𝑒𝑎𝑠𝑢𝑟𝑒𝑑 𝑜𝑠𝑚𝑜𝑙𝑎𝑙𝑖𝑡𝑦 − 𝑐𝑎𝑙𝑐𝑢𝑙𝑎𝑡𝑒𝑑 𝑜𝑠𝑚𝑜𝑙𝑎𝑙𝑖𝑡𝑦

123
Q

In Osmometry methods (osmolal gap),

___ mOsm/Kg = ___serum ___

A

↑ 10

60 mg/dL

ethanol

124
Q

T/F Osmometry methods (osmolal gap) is specific to ethanol

A

F; NOT specific to ethanol

125
Q

T/F: Osmometry methods (osmolal gap) is NOT specific to ethanol as it May also increase in other conditions

A

T

126
Q

Produced by incomplete combustion of carbon containing substances

A

CARBON MONOXIDE (CO)

127
Q

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

A

CARBON MONOXIDE (CO)

128
Q

CARBON MONOXIDE (CO) Has ___ more affinity to ___ than ___

A

200x – 225x

hemoglobin

oxygen

129
Q

Carbon monoxide has 200x – 225x more affinity to hemoglobin than oxygen, resulting to ____ formation giving a ___ blood

A

carboxyhemoglobin

cherry red-colored

130
Q

carboxyhemoglobin formation may: (2)

✓ May result to ___
✓ Affects ___ and ___

A

hypoxia

heart

brain

131
Q

Treatment for carbon monoxide

A

100% oxygen therapy

132
Q

Symptoms of ____ depends on the concentration of ___ in the blood

A

Carboxyhemoglobinemia

carboxyhemoglobin

133
Q

CARBON MONOXIDE (CO):

Signs and Symptoms: Typical in non-smoker
Carboxyhemoglobin (%): ___

A

0.5

134
Q

CARBON MONOXIDE (CO):

Signs and Symptoms: Range of values seen in smokers
Carboxyhemoglobin (%): ___

A

5 – 15

135
Q

CARBON MONOXIDE (CO):

Signs and Symptoms: Shortness of breath with vigorous exercise
Carboxyhemoglobin (%): ___

A

10

136
Q

CARBON MONOXIDE (CO):

Signs and Symptoms: Shortness of breath with moderate exercise
Carboxyhemoglobin (%): ___

A

20

137
Q

CARBON MONOXIDE (CO):

Signs and Symptoms: Severe headache, fatigue, impairment of judgment
Carboxyhemoglobin (%): ___

A

30

138
Q

CARBON MONOXIDE (CO):

Signs and Symptoms: Confusion, fainting on exertion
Carboxyhemoglobin (%): ___

A

40-50

139
Q

CARBON MONOXIDE (CO):

Signs and Symptoms: Unconsciousness, respiratory failure, death with continuous exposure
Carboxyhemoglobin (%): ___

A

60-70

140
Q

CARBON MONOXIDE (CO):

Signs and Symptoms: Immediately fatal
Carboxyhemoglobin (%): ___

A

80

141
Q

What are the Methods for Determining Carboxyhemoglobin in the Blood

A

Spot Plate Test

Differential Spectrophotometry

Gas Chromatography

142
Q

In Spot Plate Test
● Dilute ___ with ___
→ ___ part of blood per ___ parts volume of solution

A

blood

water

1

20

143
Q

In spot plate test

5mL of 40% ___ + 5mL aqueous ___ (1/20)

A

NaOH

whole blood

144
Q

In Spot Plate Test:

Observe formation of ___ color in solution

A

pink

145
Q

In Spot Plate Test:

Pink color = ___

A

> 20% COHb

146
Q

what method has this principle?

different forms of hemoglobin present with different spectral absorbency curves

A

Differential Spectrophotometry

147
Q

how many wavelengths are used in Differential Spectrophotometry

A

6 different wavelengths

148
Q

Most commonly used method and basis of automated systems

A

Differential Spectrophotometry

149
Q

An accurate and precise method for Determining Carboxyhemoglobin in the Blood

A

Gas Chromatography

150
Q

Reference method for Determining Carboxyhemoglobin in the Blood

A

Gas Chromatography

151
Q

What method has this principle?

utilizes thermal conductivity by releasing
carbon monoxide using potassium ferricyanide

A

Gas Chromatography

152
Q

Gas Chromatography utilizes ___ by releasing
carbon monoxide using ___

A

thermal conductivity

potassium ferricyanide

153
Q

Found in many household products and occupational settings

A

CAUSTIC AGENTS

154
Q

Caustic agents:

Exposure: ___ or ___

A

aspiration or ingestion

155
Q

causes pulmonary edema and
shock. Can lead to death

A

Aspiration

156
Q

cause lesions to the esophagus
and GIT (perforation)

A

Ingestion

157
Q

May lead to hematemesis, abdominal pain
and shock, and metabolic acidosis or
alkalosis

A

Ingestion of CAUSTIC AGENTS

158
Q

Ingestion of CAUSTIC AGENTS May lead to ___, ___
and ___, and___ or ___

A

hematemesis

abdominal pain

shock

metabolic acidosis

alkalosis

159
Q

Antidote for CAUSTIC AGENTS

A

dilution

160
Q

Super toxic substance

A

CYANIDE

161
Q

CYANIDE may exist as ___ or ___

A

solid or gas

162
Q

form of cyanide that has a bitter almond odor

A

gas form

163
Q

Used in many industrial processes

A

CYANIDE

164
Q

Component of insecticides and rodenticides

A

CYANIDE

165
Q

CYANIDE is Produced by ____ of some ___

A

pyrolysis

plastics

166
Q

decomposition or degradation at high temperature

A

Pyrolysis

167
Q

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

A

CYANIDE

168
Q

route of exposure for cyanide

A

inhalation, ingestion, transdermal absorption

169
Q

exposure to both cyanide and carbon monoxide

A

Smoke inhalation

170
Q

CYANIDE:

Toxicity: binds to ____ and ______

A

heme iron;

mitochondrial cytochrome oxidase

171
Q

If cyanide binds to ____, hemoglobin will not be able to bind with ___ and may cause ___ and ___

A

heme iron

oxygen

hypoxia

anemia

172
Q

CYANIDE:

If Mitochondrial cytochrome oxidase is ___, it may ___ (inc/dec) ____ and ___

A

inhibited

increase

cellular oxygen tension

venous partial oxygen pressure

173
Q

What are the methods in cyanide

A

Ion-selective electrode

Photometric assay

Urinary thiocyanate concentration

174
Q

most commonly used cyanide methods

A

Ion-selective electrode & Photometric assay

175
Q

Photometric assay is aka

A

two-well microdiffusion separation

176
Q

this method is only used when exposed to very low levels of cyanide

A

Urinary thiocyanate concentration

177
Q

what are the different metals and metalloids

A

Arsenic
Cadmium
Lead
Mercury
Pesticides

178
Q

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

A

Arsenic

179
Q

Arsenic Has ___ and binds to ___ groups in ___

A

high affinity

thiol

protein

180
Q

Common homicidal and suicidal agent

A

Arsenic

181
Q

Has the capacity to cross the placenta

A

arsenic

182
Q

Arsenic Intoxication will result to:

A

intravascular hemolysis, hemoglobinemia, nephrotoxicity, and multi-organ involvement

183
Q

what is the Indication of arsenic intoxication

A

garlic odor breath and
metallic taste

184
Q

Specimen used for SHORT TERM exposure to arsenic

A

Blood, urine

185
Q

Specimen used for LONG TERM exposure to arsenic

A

Hairs, nail

186
Q

Arsenic loves to bind to ___

A

keratinized tissues

187
Q

Methods in arsenic

A

AAS, Reinsch test

188
Q

Utilized in electroplating and galvanizing

A

Cadmium

189
Q

Found in paints and plastics

A

Cadmium

190
Q

Binds to proteins and cellular constituents

A

Cadmium

191
Q

Cadmium Binds to ___ and ___ constituents

A

proteins

cellular

192
Q

Cadmium Toxicity is ___

A

nephrotoxic

193
Q

Cadmium toxicity is nephrotoxic Such as ____, ___, and ___

A

tubular proteinuria

glucosuria

aminoaciduria

194
Q

Cadmium:

Specimen: ___

A

urine, whole blood

195
Q

Cadmium:

Method: ___

A

AAS

196
Q

Color enhancer in paints and make-ups

A

Lead

197
Q

Also found in gasoline and pipe plumbing

A

Lead

198
Q

Common water contamination

A

Lead

199
Q

A potent enzyme inhibitor
→ ____, ____, ____

A

LEAD

D-ALA synthetase

pyrimidine-5’-nucleotidase

Na-K ATPase

200
Q

Has high affinity to many macromolecular structures and distributed throughout the body

A

Lead

201
Q

___ is present in all biologic systems,
however, it has no ___ or ___
function

A

Lead

physiologic

biochemical

202
Q

Elimination of LEAD is through ____

A

renal filtration

203
Q

Elimination through renal filtration

A

LEAD

204
Q

Elimination is very slow dahil mababa ang concentration in the blood

A

LEAD

205
Q

It combines with the bone matrix

A

LEAD

206
Q

Largest pool of lead in the body is in the ____

A

skeletal system

207
Q

May persist for a long period of time (up to ____)

A

LEAD

20 years

208
Q

Lead Toxicity:

Toxic dose: ___

A

> 0.5 mg/day

209
Q

Lead Toxicity:

Fatal dose: ___

A

0.5g

210
Q

Lead Toxicity:

Toxic blood levels: ____

A

> 70 ug/dL

211
Q

Indications of LEAD TOXICITY

A

Basophilic stippling of RBC

Increased urinary ALA

Free RBC protoporphyrin

212
Q

Lead inhibits ____

A

pyrimidine-5’-nucleotidase

213
Q

Responsible for removing excess DNA in RBC nucleus

A

pyrimidine-5’-nucleotidase

214
Q

Indications of Lead toxicity:

In Basophilic stippling of RBC, ___ accumulates inside the ___ causing the ____ (____)

A

DNA

RBC

blueberry muffin-like RBC

basophilic stippling

215
Q

Presence of basophilic stippling is a sensitive indicator of ____

A

lead poisoning

216
Q

Presence of ___ is a sensitive indicator of lead poisoning

A

basophilic stippling

217
Q

What is the Treatment for lead toxicity

A

chelators

218
Q

give the 2 examples of chelators used as a treatment for lead toxicity

A

EDTA, dimercaptosuccinic acid

219
Q

What are the Toxic effects of lead toxicity (3)

A

→ Anemia
→ Decreased RBC membrane integrity
→ Encephalopathy, nephrosis, anorexia, peripheral neuropathy, birth defects, low IQ,
carcinogenesis, birth defects, renal damage

220
Q

Among the toxic effects of lead toxicity, what Inhibits heme synthesis?

A

Anemia

221
Q

LEAD:

Specimen: ____

A

whole blood, urine, hair

222
Q

specimen used in analysis of lead that is used to quantitate lead (it is bound to RBC)

A

Whole blood

223
Q

specimen used in the analysis of lead that is used when there is recent lead
exposure

A

urine

224
Q

What are the SCREENING METHODS used in the analysis of LEAD

A

Zinc Protoporphyrin test

ALA dehydratase (ALAD test)

225
Q

Zinc Protoporphyrin test is aka

A

Fluorometric test

226
Q

sensitive SCREENING method used in the analysis of LEAD

A

ALA dehydratase (ALAD test)

227
Q

Lead inhibits delta-ALA synthetase = ___ (inc/dec) in ALA activity = suggestive of ____

A

decrease

lead poisoning

228
Q

What are the OTHER METHODS used in the analysis of LEAD

A

→ In-vivo X-ray fluorescence of bone
→ AAS
→ ICP-MS
→ Anodic stippling voltammetry

229
Q

Exists in three forms which has different levels of toxicity

A

Mercury

230
Q

What are the 3 forms of MERCURY

A

Elemental mercury

Inorganic salts

Component of organic compounds

231
Q

form of mercury that is Liquid at room temperature

A

Elemental mercury

232
Q

form of mercury that Can be ingested and show no significant effects

A

Elemental mercury

233
Q

form of mercury that Cannot be absorbed

A

Elemental mercury

234
Q

in this form of mercury, Inhalation is very rare and insignificant

A

Elemental mercury

235
Q

Moderately toxic form of mercury

A

Inorganic salts

236
Q

form of mercury that is Partially absorbed by the GIT

A

Inorganic salts

237
Q

T/F Yung mga hindi naabsorb na Inorganic salt (form of mercury) may show GIT toxicity

A

T

238
Q

Most toxic form of mercury

A

Component of organic compounds

239
Q

form of mercury that is Rapidly absorbed

A

Component of organic compounds

240
Q

Mercury is a potent enzyme __.

For example: ____

A

inhibitor

Catecholamine-0-methyltransferase

241
Q

What enzyme Metabolizes catecholamines

A

Catecholamine-metabolic enzyme

242
Q

example of catecholamines

A

epinephrine and norepinephrine

243
Q

If the catecholamines are not ___, it may lead to ___

A

metabolized

toxicity

244
Q

The toxicity of this metal/metalloids Mimics adrenal gland disorders

A

mercury

245
Q

what are the indicators of mercury toxicity

A

hypertension, tachycardia, sweating

246
Q

the indicators of mercury toxicity is the Symptoms of ___

A

pheochromocytoma

247
Q

tumor
that autonomously produces catecholamines

A

Pheochromocytoma

248
Q

what are the three mercury Intoxication

A

Elemental mercury

Alkyl mercury

Inorganic form

249
Q

mercury intoxication:

pink disease (acrodynia), erethism

A

Elemental mercury

250
Q

pink disease is aka

A

acrodynia

251
Q

Upon exposure, it may cause continuous
skin exfoliation until the skin turns pink
(acrodynia)

A

Elemental mercury

252
Q

congenital minimata disease

A

Alkyl mercury

253
Q

neurologic disorder that resembles cerebral palsy

A

Congenital minimata disease

254
Q

Congenital minimata disease is a neurologic disorder that resembles ___

A

cerebral palsy

255
Q

nephrotoxic (glomerular proteinuria)

A

Inorganic form

256
Q

What are the specimen used in the analysis of mercury

A

whole blood, 24-hour urine

257
Q

What are the methods used in the analysis of mercury

A

→ Reinsch test
→ AAS
→ Anodic stippling voltammetry

258
Q

MERCURY:

Reference Value: ___

A

<10 ug/dL

259
Q

Mercury:

Significant exposure: ___ (____)

A

> 50 ug/dL

whole blood

260
Q

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

A

Pesticides

261
Q

Pesticides is Classified as ___ or ___

A

insecticides

herbicides

262
Q

What are the 3 Forms of insecticides:

A

Organophosphate

Carbamates

Halogenated Hydrocarbons

263
Q

most common form of insecticides

A

Organophosphate

264
Q

Responsible for about 1⁄3 of all pesticide poisoning

A

Organophosphate

265
Q

Organophosphate is Responsible for about ___ of all ___

A

1⁄3

pesticide poisoning

266
Q

Organophosphate Inhibits the enzyme ____

A

acetylcholinesterase

267
Q

Acetylcholine is Metabolized by ____

A

acetylcholinesterase

268
Q

Muscle cell stimulant

A

Acetylcholine

269
Q

Also the stimulant of some
exocrine and endocrine glands

A

Acetylcholine

270
Q

T/F When acetylcholinesterase is inhibited, acetylcholine is metabolized

A

F; When acetylcholinesterase is inhibited, acetylcholine is NOT metabolized

271
Q

When acetylcholinesterase is inhibited, acetylcholine is NOT
metabolized which may cause ____.

A

systemic effects

272
Q

Carbamates Inhibits the enzyme ___

A

acetylcholinesterase

273
Q

what are the 2 forms of insecticides that inhibit acetylcholinesterase

A

Organophosphate

Carbamates

274
Q

Toxicity (Pesticides)

Low-level exposure: (4)

A

Salivation, Lacrimation, Involuntary urination and defecation

275
Q

Toxicity (Pesticides)

High-level exposure: (7)

A

Bradycardia, muscular twitching, cramps, apathy, slurred speech, behavioral changes, death

276
Q

high level exposure pesticides may cause death which happens due to___

A

respiratory failure

277
Q

Direct measurement of organophosphates is ____

A

highly impossible

278
Q

Direct measurement of organophosphates is highly impossible because Organophosphate has ____ to ___

A

high affinity

proteins

279
Q

Pesticides:

Method of analysis: ____

A

indirect measurement.

280
Q

what are the 2 methods used in the analysis of pesticides

A

Acetylcholinesterase Inhibition Assay

Serum Pseudocholinesterase Activity

281
Q

Indirect measurement of organophosphate poisoning

A

Acetylcholinesterase Inhibition Assay

282
Q

Specimen used in Acetylcholinesterase Inhibition Assay

A

RBC

283
Q

Alternative and Screening test for pesticides

A

Serum Pseudocholinesterase Activity

284
Q

T/F: Serum Pseudocholinesterase Activity lacks sensitivity and specificity.

A

T

285
Q

Serum Pseudocholinesterase Activity is decreased in ___, ____, ____, ____

A

acute infection, pulmonary embolism, hepatitis, cirrhosis

286
Q

Decreased also in acute infection, pulmonary embolism, hepatitis, cirrhosis

A

Serum Pseudocholinesterase Activity

[LECT] CC 2 - Finals (9 decks)

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