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2nd Year 2nd Term > MT6314 HEAVY METALS AND CHELATORS > Flashcards

MT6314 HEAVY METALS AND CHELATORS Flashcards

1
Q

Heavy metals include?

A
  • Lead
  • Arsenic
  • Mercury
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2
Q

Chelators include?

A
  • Dimercaprol
  • Succimer
  • Edetate Calcium Disodium
  • Unithiol
  • Penicillamine
  • Deferoxamine
  • Deferasirox and Deferiprone
  • Prussian Blue
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3
Q

Oldest occupational and environmental disease in the world

A

Lead poisoning

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4
Q

Used in storage batteries, ammunition, metal alloys, solder, glass, plastics, pigments and ceramics

A

Lead

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5
Q

Presence of lead where led to exposure in children and adults?

A

Folk medicine and cosmetics

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6
Q

Low level of lead exposure may have subtle adverse clinical effects on what in children and adults?

A

Children - neurocognitive function
Adults - cardiovascular

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7
Q

Does lead have a purpose in the body?

A

No

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8
Q

Lead is absorbed slowly but consistently via?

A

respiratory and gastrointestinal tract

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9
Q

Respiratory or GI exposure in lead: industrial exposure

A

Respiratory

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10
Q

Respiratory or GI exposure in lead: nonindustrial
exposure

A

GI

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11
Q

Up to how much lead is absorbed in children and adults?

A
  • Up to 50% absorbed in children
  • Up to 10-15% in adults
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12
Q

What are the causes of worsening lead absorption?

A

Low dietary calcium, iron deficiency and ingestion on an empty stomach increases absorption

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13
Q

T or F: Lead is absorbed well into the skin

A

F, poor absorption on skin

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14
Q

Which heavy metal: Distributed predominantly in the soft tissues, avidly bound on skin, hair, and nails

A

Arsenic

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15
Q

What form of lead: Causes encephalopathy and is distributed into the soft tissues especially liver, CNS

A

Tetraethyl lead (organic lead)

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16
Q

Which heavy metal: Major route of absorption is the GI and respiratory tract

A

Arsenic and Lead

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17
Q

Which heavy metal: MOA inhibits enzymes, interferes with oxidative phosphorylation, alters cell signaling, gene expression

A

Arsenic

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18
Q

What form of lead: MOA inhibits enzymes, interferes with essential cations, alters membrane structure

A

Inorganic lead

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19
Q

Which heavy metal: MOA inhibits enzymes, alters membranes

A

Mercury

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20
Q

Which heavy metal: metabolism includes methylation, renal, and sweat and feces

A

Arsenic

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21
Q

Which form of mercury: Found only in respiratory tract

A

Elemental mercury

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22
Q

Which form of mercury: causes acute renal tubular necrosis and gastroenteritis

A

Inorganic mercury

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23
Q

Which heavy metal: Mechanism includes deacylation

A

Organic alkyl, aryl

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24
Q

99% bound to RBCs, 1% free in plasma

A

Lead

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25
Q

Where is lead distributed?

A

to bone marrow, brain, kidney, liver, muscle and gonads; then bones

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26
Q

Lead also crosses the?

Hint: potential harm to the fetus

A

Placenta

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27
Q

Half life of lead? How about in bones?

A

1-2 months
In bones: years to decades

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28
Q

How much lead is excreted in urine?

A

70%

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29
Q

The multi systemic toxic effects of lead are mediated by?

A

Inhibition of enzymatic function
Interference with action of essential cations (calcium, zinc, iron)
Oxidative stress generation
Gene expression changes
Cell signaling alteration
Disruption of membrane integrity

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30
Q

Whose CNS is the most sensitive taft organ for lead toxicity?

A

Fetus and young children

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31
Q

T or F: Adults are less sensitive to the CNS effects of lead

A

T

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32
Q

Occurs at blood lead concentrations of higher than 100 mcg/dL

A

Lead encephalopathy

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33
Q

Lead can cause normocyctic or hypo chromic _____.

A

anemia

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34
Q

May occur with high exposure to lead

A

Frank hemolysis

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35
Q

Effects off lead to the kidneys?

A

Renal interstitial fibrosis and nephrosclerosis
Lead neuropathy
Azotemia

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36
Q

Effects of lead on reproductive system?

A

Stillbirth or spontaneous abortion

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37
Q

Effects of lead on the GI?

A

Loss of appetite, constipation, diarrhea (less common)

Lead colic
Gingival lead lines

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38
Q

Effects of lead on cardiovascular system?

A

Elevated BP

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39
Q

Diagnosis of lead intoxication is best measured through?

A

Measuring lead in whole blood

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40
Q

Treatment for lead poisoning?

A

IV EDTA 30-50mg/kg/d by continuous infusion for up to 5 days only

Oral Succimer (DMSA) after 5 days

Retained lead objects require gastrointestinal
decontamination

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41
Q

Occurring element in the earth’s crust used in commercial and industrial products

A

Arsenic

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42
Q

Seen in semiconductors, wood preservatives, nonferrous alloys, glass and turf herbicide monosodium methane arsonate (MSMA)

A

Arsenic

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43
Q

Type of arsenic produced by the semiconductor industry

A

Arsine (arsenous hydride)

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44
Q

T or F: Groundwater may contain high amounts of arsenic

A

T

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45
Q

T or F: Arsenic used to be involved in pharmaceutical use

A

T

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46
Q

Contains 1% potassium arsenide and used for medicine in the 18th century

A

Fowler’s solution

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47
Q

Designed in the 20th century as warfare agents

A

Lewisite

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48
Q

T or F: Melarsoprol is a trivalent arsenical

A

T

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49
Q

Arsenic is well-absorbed via?

A

Respiratory and GI, percutaneous absorption is limited

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50
Q

Arsenic is metabolized by?

A

Liver via methylation

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51
Q

Arsenic excreted in?

A

Urine (major), sweat and feces

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52
Q

Inorganic arsenide or its metabolites may induce?

A

Oxidative stress, alter gene expression, and interfere with cell signal transduction

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53
Q

Multiple mechanism of actions of arsenic?

A
  • Inhibition of enzyme functions
  • Oxidative stress generation
  • Gene expression changes
  • Cell signaling alteration
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54
Q

Interferences with enzyme function in arsenic may lead to?

A

sulfhydryl groups binding by trivalent arsenic or by substitution for phosphate

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55
Q

Which is more toxic, trivalent form of methylated metabolites or inorganic parent compounds of arsenic?

A

Trivalent form of methylated metabolites

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56
Q

Major routes of arsenic intoxication?

A

GI, respiratory

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57
Q

Distribution of arsenic?

A

Predominantly soft tissues (highest in liver and
kidney). Tightly bound to skin, hair and nails

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58
Q

Major clinical findings of arsenic intoxication?

A

Cardiovascular: shock, arrythmias;
CNS: Encephalopathy, Peripheral Neuropathy;
Others: Gastroenteritis, Pancytopenias, Cancer

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59
Q

Metabolism and Elimination of arsenic?

A

Methylation; Excreted via Urine (major), Sweat and Feces (minor)

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60
Q

Chronic inorganic arsenic poisoning also causes?

A

“Raindrop pattern”: Hyperpigmentation and hyperkeratosis involving hands and feet

61
Q

Treatment of arsenic intoxication?

A

*Immediate termination of exposure, supportive care and chelation therapy
*Gut decontamination if appropriate
*Acute Poisoning: Chelation with Unithiol 3-5mg/kg every 4-6 hours or Dimercaprol every 4-6 hours

62
Q

T or F: Arsenic disappears quickly from the blood

63
Q

What treatment has also been effective in animal models and has a higher therapeutic index than dimercaprol?

64
Q

Quicksilver or liquid metal, mined predominantly as HgS in cinnabar ores

65
Q

Found in electrolytic production of chlorine and caustic soda; electrical equipment, thermometer, fluorescent lamps, dental amalgams and artisanal gold production

66
Q

An organomercurial now removed from almost all vaccines

A

Thimerosal

67
Q

Environmental release of mercury is from?

A

burning of fossil fuels contributed to bioaccumulation in fishes

68
Q

Absorption of mercury varies depending on?

A

Chemical form

69
Q

Mercury is absorbed in the?

A

lungs, GI tract, and percutaneous route

70
Q

Mercury is distributed well into?

A

Tissues, most concentrated in kidneys

71
Q

What form of mercury is quite volatile and can be absorbed in the lungs, but poorly absorbed in GI?

A

Elemental mercury

72
Q

What kind of mercury is well-absorbed into the skin?

A

Alkylmercury compounds

73
Q

Has a half-life of approximately 50 days, and undergoes biliary excretion and enterohepatic circulation

A

Methylmercury

74
Q

Mercury is absorbed in the?

A

lungs, GI tract, and percutaneous route

75
Q

What form of mercury: major route is respiratory

76
Q

What form of mercury: Major route is skin and GI

77
Q

What form of mercury: GI, skin, repiratory and distributed in soft tissues only

78
Q

Treatment of mercury intoxication?

A

Immediate removal from source, supportive care
and chelation therapy
Acute: Unithiol, dimercaprol or succimer
Dimecaprol should never be used for elemental or
organic mercury intoxication

79
Q

Acute or chronic mercury intoxication: erethism

80
Q

Acute or chronic mercury intoxication: chemical pneunomitis and noncardiogenic pulmonary edema

81
Q

Acute or chronic mercury intoxication: treatment is succorer, dimercaprol and unithiol

82
Q

Acute or chronic mercury intoxication: treatment is unithiol and succimer

83
Q

Drugs used to prevent or reverse toxic effects of heavy metals on an enzyme or cellular target to accelerate the elimination of metal from the body

84
Q

The metal-mobilizing effects of a therapeutic chelating agent may also?

A

redistribute some of the metal to vital organs

85
Q

Chelating agents contain one or more coordinating atoms such as?

A

oxygen, sulfur, or nitrogen that donates a pair of electrons to a catatonic metal ion to form one or more coordinate-covalent bonds

86
Q

Chelating agents may also enhance excretion of?

A

essential cations (Zinc, Copper)

87
Q

The longer the half-life of a metal in a particular organ, _____.

A

the less effectively they can be removed by chelation.

88
Q

Benefits of chelation

A

Effective against acute poisoning
Form non-toxic complexes
Remove metal from soft tissue
Oral therapy is available

89
Q

Drawbacks of chelation

A

Redistribution of toxic metal
Essential metal loss
No removal of metal from intracellular sites
Hepatotoxicity and nephrotoxicity
Poor clinical recovery
Pro-oxidant effects
Headache, nausea, increased BP

90
Q

Dimercaprol redistributes what to the brain while enhancing the excretion of what?

A

Redistributes mercury and arsenic
Excretes urinary mercury and arsenic

91
Q

When is the capacity of the chelating agents greatest?

A

When they are administered very soon after an acute metal exposure

92
Q

Antidote to a warfare agent

93
Q

Dimercaprol as a single agent treats?

A

acute poisoning by arsenic and inorganic mercury

94
Q

Oily, colorless liquid with strong mercaptan-like odor

A

Dimercaprol

95
Q

Other names for dimercaprol

A

2,3-Dimercaptopropanolol, BAL

96
Q

What form of administration of dimercaprol appears to be readily absorbed, metabolized, and excreted by the kidney within 4-8hrs?

A

IM administered BAL

97
Q

BAL prevents and reverses?

A

metal-induced inhibition of sulfhydryl-containing enzyme

98
Q

Succimer other names?

A

Dimercaptosuccinic Acid, DMSA

99
Q

Water-soluble analog of dimercaprol that prevents and reverses the metal-induces inhibition of sulfhydryl-containing enzyme to protect against lethal effects of arsenic

100
Q

Succimer is a treatment for?

A

children with blood lead concentration of >45mcg/dL

101
Q

DMSA increases the rate of excretion of ___ and decreases excretion of _______

A

Lead
Mercury

102
Q

DMSA has a protective agent against?

103
Q

How if DMSA given?

A

Oral or IV

104
Q

DMSA iso sed against the poisoning of?

A

Mercury and arsenic

105
Q

T or F: Succimer has an impact on the calcium, iron and magnesium stores of the body

A

F, negligible

106
Q

Succimer is been associated with increase in?

A

ALT, AST, mild neutropenia

107
Q

Other name for Edetate Calcium Disodium?

A

Ethylenediaminetetraacetic Acid, EDTA

108
Q

Where does EDTA come from?

A

Calcium disodium salt form of EDTA

109
Q

EDTA is indicated mainly for?

A

chelation of lead, zinc, manganese and certain heavy radionucleotide poisoning

110
Q

T or F: EDTA penetrates the cell membranes well

111
Q

What character of EDTA limits oral absorption?

A

highly polar ionic character

112
Q

How is EDTA usually administered?

A

IV infusion

113
Q

Other name for Unithiol?

A

Dimercaptopropanesulfonic Acid, DMPS

114
Q

Water-soluble analog of dimercaprol with no FDA-approved indications

115
Q

How is unithiol administered?

A

Orally and IV (slow infusion)

116
Q

Unithiol is a protective agent against?

A

mercury and arsenic

117
Q

Unithiol increases urinary excretion of?

A

mercury, arsenic and lead

118
Q

Elimination of the half life of unithiol takes about how long?

119
Q

IV unithiol offers advantages over?

A

IM dimercaprol and oral succimer in initial treatment of severe acute mercury or arsenic poisoning

120
Q

Unithiol can be a substitute to what in the treatment of lead intoxication?

121
Q

What syndrome has been reported to occur within treatment using unithiol?

A

Steven-Johnson syndrome

122
Q

White, crystalline, derivative of Penicillin to treat or prevent Copper poisoning

A

Penicillamine (D-Dimethylcysteine)

123
Q

used in Severe Rheumatoid Arthritis

A

Penicillamine (D-Dimethylcysteine)

124
Q

How is Penicillamine (D-Dimethylcysteine) absorbed?

125
Q

What is less toxic than the L-isomer form?

A

D-Penicillamine

126
Q

What replaced penicillamine due to having stronger metal-mobilizing capacity and lower-adverse effect profile?

127
Q

Deferoxamine is isolated from?

A

Streptomyces pilosus

128
Q

The parenteral chelator of choice for iron poisoning

A

Deferoxamine

129
Q

Useful in treatment of aluminum toxicity

A

Deferoxamine plus hemodialysis

130
Q

How is deferoxamine administered?

131
Q

Deferoxamine is poorly absorbed in this route and may increase iron absorption

132
Q

Rapid IV administration of Deferoxamine may result in?

A

hypotension

133
Q

Tridentate iron chelator

A

Deferasirox

134
Q

Oral treatment of iron overload due to blood transfusion (esp. seen in patients with thalassemia major and myelodysplastic syndrome

Relatively, more efficient in decreasing hepatic iron

A

Deferasirox

135
Q

Adverse Effects include hypotension, flushing, abdominal discomfort, rashes, pulmonary complications

A

Deferoxamine

136
Q

Given orally; Excreted in Bile

A

Deferasirox

137
Q

Adverse effects include mild to moderate GI disturbances and skin rashes; Liver profile abnormalities

A

Deferasirox

138
Q

Bidentate iron chelator

A

Deferiprone

139
Q

Second-line oral chelator for iron overload due to blood transfusion in thalassemia major
Relatively, more efficient in decreasing cardiac iron

A

Deferiprone

140
Q

Given orally; excreted via urine

A

Deferiprone

141
Q

Adverse effects include Neutropenia, agranulocytosis

A

Deferiprone

142
Q

Prussian Blue other name?

A

Ferric Hexacyanoferrate

143
Q

Prussian blue is an indicated treatment for?

A

contamination with radioactive Cesium and intoxication with thallium salts

144
Q

Ferric Hexacyanoferrate is a hydrated crystalline compound in which ____ are coordinated with _____

A

Fe2+ and Fe3+ with cyanide in a cubic lattice structure

145
Q

Prussian Blue is used for?

A

Ion exchange and mechanical trapping or adsorption

146
Q

How is Prussian Blue administered and excreted?

A

orally, minimal GI absorption (<1%), excreted via
feces

147
Q

Why does Prussian Blue have minimal GI absorption?

A

Its complexes form with cesium or thallium which are non absorbable

148
Q

Adverse effects of Prussian Blue?

A

Constipation

2nd Year 2nd Term (38 decks)

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