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RUSVM Toxicology 2016 > Heavy Metals > Flashcards

Heavy Metals Flashcards

1
Q

Heavy Metals

A

Metals having an atomic weight greater than sodium (23) and specific gravity (density) greater than 5gm/cm^3

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2
Q

What are the clinical signs of an inorganic heavy metal?

A

GI signs

Paralysis

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3
Q

What does toxicity depend on with Heavy metals?

A

Valency
metal to metal interaction
metal to diet interaction

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4
Q

What are the sources of inorganic arsenic toxicosis?

A 
Ant and roach baits
Wood preservatives
insecticides
herbicides
fungicides
rodenticides
milk from poisoned cows are toxic to calves
Pastures near smelters
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5
Q

What are the three oxidative states that inorganic arsenic exists in?

A

Elemental
Trivalent (arsenite)
Pentavalent (arsenate)

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6
Q

What are properties of inorganic arsenic?

A

Reacts with -SH group

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7
Q

What species is most susceptible to inorganic arsenic toxicosis?

A

Cattle

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8
Q

Which form is most toxic of inorganic arsenic?

A

Inorganic trivalent

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9
Q

What is the list of toxicities of inorganic arsenic?

A

Trivalent is greater than pentavalent is greater than organic arsenic

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10
Q

How are animals exposed to inorganic arsenic?

A

Absorbed from the GI tract
Intact skin
inhalation

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11
Q

What is the mechanism of action with inorganic arsenic toxicosis?

A

The trivalent binds to 2-SH groups of lipoic acid which is an essential cofactor for enzymatic decarboxylation of keto acids this slows glycolysis and citric acid cycle
Pentavalent uncouples oxidative phosphorylation and may interfere with vitamins B1 and B6 metabolism

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12
Q

What cells are the most sensitive to inorganic arsenic toxicosis?

A

Capillary endothelial cells

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13
Q

What tissues are most affected?

A

Tissues rich in oxidative enzymes: Intestines, liver, kidneys

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14
Q

What are the peracute clinical signs of inorganic arsenic toxicosis?

A

Sudden death
severe colic
collapse
death

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15
Q

What are the acute clinical signs of inorganic arsenic toxicosis?

A

severe colic
vomiting
diarrhea - maybe hemorrhagic

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16
Q

What are the subacute clinical signs of inorganic arsenic toxicosis?

A

diarrhea with blood or mucosal shreds
partial paralysis of hind limbs
detachment of the mucosa causing hypovolemic shock

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17
Q

What are the lesions associated with inorganic arsenic toxicosis?

A

GI mucosal edema and hemorrhage with sloughing and perforation
capillary degeneration
skin lesions and blistering with skin exposure

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18
Q

What are the best specimens for inorganic arsenic toxicosis?

A

Liver

Kidney

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19
Q

What is the best antemortem specimen?

A

urine

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20
Q

What clinical pathology findings are associated with inorganic arsenic toxicosis?

A

Increased PCV
Increased BUN
High levels in the liver or kidney

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21
Q

What is the symptomatic treatment of inorganic arsenic toxicosis?

A 
Fluids 
Electrolytes
Blood transfusion 
Treatment of acidosis 
Vitamins 
Antibiotics
analgesics
dopamine 
acetylcysteine
Decontamination: Gastric Lavage, Mineral oil, Activated charcoal, Emetics 
Demulcents to coat the GI mucosa
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22
Q

What is the chelator of choice for inorganic arsenic toxicosis?

A

Chelation therapy: Dimercaprol

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23
Q

What are the chelators used for inorganic arsenic toxicosis?

A

Dimercaprol

Dimercaptosuccinic acid

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24
Q

What is the prognosis for inorganic arsenic toxicosis?

A

Grave if not treated early

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25
Q

What are the uses of organic arsenicals?

A

Feed additives to improve weight gain and feed efficiency

control enteric infections in swine and poultry

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26
Q

What organic arsenical is used in swine?

A

Arsanilic acid

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27
Q

What organic arsenical is used in poultry?

A

Roxarsone

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28
Q

What are the common sources of organic arsenicals toxicosis?

A

Overdosage or prolonged use

Recommended concentrations in debilitated dehydrated or sick animals

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29
Q

What are the properties of organic arsenicals?

A

phenylarsonic acid derivatives

Pentavalent oxidation state

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30
Q

What is important about the toxicity of organic arsenicals?

A

Organic pentavalent arsenicals are less toxic than inorganic arsenic

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31
Q

What enhances toxicity of organic arsenicals?

A

dehydration
water deprivation
renal insufficiency

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32
Q

Where are organic arsenicals absorbed from?

A

GI tract

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33
Q

How are organic arsenicals excreted?

A

Urine

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34
Q

What is the mechanism of action for organic arsenicals?

A

Peripheral nerve demyelination and axonal damage

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35
Q

What is the mechanism of action for organic arsenicals similar to?

A

Vitamin B deficiency

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36
Q

What are the clinical signs of organic arsenicals toxicosis in swine?

A 
incoordination 
ataxia 
partial paralysis 
blindness
erythema in white pigs, sensitivity to light
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37
Q

How long for onset of clinical signs of organic arsenicals toxicosis?

A

3-5 days

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38
Q

What are the clinical signs of organic arsenicals toxicosis in poultry?

A 
Incoordination 
Ataxia
Anorexia 
Depression 
Coma 
Death
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39
Q

What are lesions associated with organic arsenicals toxicosis in swine?

A

erythemia in light skinned pigs
muscle atrophy in chronic cases
peripheral nerve and optic nerve demyelination and degeneration
gliosis

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40
Q

What is the treatment for organic arsenicals toxicosis?

A

Withdrawal of organic arsenicals

Supportive therapy: water, fluid therapy, multiple vitamins, antibiotics for bacterial infection

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41
Q

How long can recovery from organic arsenicals take?

A

2-4 weeks

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42
Q

What is the source of acute copper toxicosis?

A

Ingestion of high concentrations of copper

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43
Q

What are the clinical signs of acute copper toxicosis?

A 
severe GI signs 
vomiting 
colic 
hemorrhagic diarrhea
dehydration 
shock
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44
Q

What is the treatment for acute copper toxicosis?

A

Supportive and symptomatic therapy

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45
Q

What is the source of acute copper toxicosis?

A

Coins

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46
Q

What is the source of chronic copper toxicosis in sheep?

A

Feed additives
Natural copper in soil and plants
fertilizer
Molybdenum deficiency

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47
Q

How does Molybdenum deficiency cause chronic copper toxicosis in sheep?

A

Copper levels increase causing a decrease in the ratio of Copper to Molybdenum

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48
Q

What is the normal ratio of Copper to Molybdenum?

A

6:1

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49
Q

What can cause a sudden loss of copper from the liver to the blood?

A

Stress

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50
Q

How long does accumulation of copper take in sheep?

A

2-10 weeks

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51
Q

What is the mechanism of action of chronic copper toxicosis in sheep?

A

copper accumulation in the liver causes liver degeneration and necrosis
Release of copper from the liver and excess copper in the blood causes oxidation of erythrocyte membranes increasing their fragility resulting in a hemolytic crisis

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52
Q

What does chronic copper toxicosis in sheep cause?

A

methemoglobin

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53
Q

What are the clinical signs of chronic copper toxicosis in sheep?

A 
weakness 
anorexia 
pale mucous membranes 
icterus 
hemoglobinuria 
fever 
dyspnea
shock
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54
Q

What are the lesions associated with chronic copper toxicosis in sheep?

A

Icterus
hemolysis
methemoglobinemia
Enlarged yellow friable liver
enlarged hemorrhagic bluish dark friable kidneys “gunmetal kidneys”
enlarged dark brown spleen “blackberry jam spleen”

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55
Q

What are the clinical pathology findings for chronic copper toxicosis in sheep?

A

Elevated serum and whole blood Cu
Elevated liver and kidney Cu
Elevated Liver enzymes (AST, LDH)

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56
Q

What is the treatment for chronic copper toxicosis in sheep?

A

Ammonium tetrahiomolybate
D-penicillamine
Molybdenized copper phosphate sprayed on pastures

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57
Q

What is the mechanism of action of chronic copper toxicosis in sheep?

A

Excess free copper causes chronic active hepatitis and liver necrosis due to lipid peroxidation of mitochondrial membranes

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58
Q

What is the source of Molybdenum toxicosis?

A

Excess Molybdenum

Copper deficiency

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59
Q

What are the properties of Molybdenum toxicosis?

A

component of xanthine oxidase

elevated molybdenum interferes with copper absorption

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60
Q

Which species is most susceptible to Molybdenum toxicosis?

A

Cattle

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61
Q

What increased toxicity of Molybdenum?

A

Dietary sulfate

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62
Q

What decreased toxicity of Molybdenum?

A

Dietary copper

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63
Q

Where is molybdenum absorbed from?

A

GI Tract

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64
Q

What is the mechanism of action of Molybdenum toxicosis?

A

Copper deficiency

Copper is an essential component of enzymes

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65
Q

What are the clinical signs of Molybdenum toxicosis?

A 
Severe diarrhea (greenish with fluids and gas bubbles) 
Rough hair coat 
depigmentation of hair especially around the eyes 
Weight loss 
anemia 
osteoporosis 
exostosis 
lameness
pica
Decreased libido and infertility
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66
Q

What is the laboratory findings found with Molybdenum toxicosis?

A

Elevated Molybdenum
Decreased Copper
Decreased cytochrome oxidase

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67
Q

What is the treatment for Molybdenum toxicosis?

A

Copper glycinate SC

Copper sulfate added to the diet

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68
Q

What does selenium deficiency cause in lambs, calves, and foals?

A

White muscle disease

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69
Q

What does selenium deficiency cause in young pigs?

A

Hepatosis dietetica

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70
Q

What does selenium deficiency cause in chicks?

A

Exudative diathesis

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71
Q

What does selenium deficiency cause in chickens?

A

Nutritional pancreatic atrophy

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72
Q

What does selenium deficiency cause in pigs?

A

Porcine stress syndrome

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73
Q

Which areas have selenium defiecient soil?

A

NW
NE
SE
Great lakes

74
Q

What is selenium used in?

A

Feed supplements
Injectable selenium-vitamin E
Antioxidant supplements
Medicated shampoos for dermatitis

75
Q

What are the different types of seleniferous plants?

A

Obligate accumulators
Facultative accumulators
Passive accumulators

76
Q

What are the obligate selenium accumulators?

A

Locoweed
Prince’s Plume
Golden Wood
Woody aster

77
Q

Obligate accumulators

A

accumulate up to 15,000ppm Se

Require Se for growth

78
Q

Facultative accumulators

A

Accumulate up to 25-100ppm

Do not require Se, but they can accumulate it

79
Q

Passive Accumulators

A

Accumulate up to 1-25ppm

Accumulate Se passively in Se-rich soil

80
Q

What plants are passive accumulators?

A

Crop plants: Corn, wheat, oats, barley, grass, hay

81
Q

What are the three oxidation states of selenium?

A

Selenate
Selenite
Selenide

82
Q

What are some properties of Selenium?

A

Se combines with -SH group of glutathione
Se is a component of glutathione peroxidase
acts as antioxidant by prevention of peroxide accumulation through reduction of glutathione
Irritant to mucous membranes

83
Q

What does selenium and vitamin E do for cells?

A

prevents cell degeneration and cell membrane damage in animals and poultry

84
Q

How selenium related to thyroid?

A

Se is found in 5-deiodinase (conversion of T4 to T3)

85
Q

What is the order of selenium toxicity in plants?

A

Organic selenium is greater than selenate = selenite which is greater than selenide which is greater than synthetic organoselenium compounds

86
Q

What promotes the formation of selenate?

A

Alkaline soil of the Great Plains

87
Q

What form of selenium is relatively non toxic?

A

Elemental Selenium

88
Q

What reduces toxicity of selenium?

A

high protein diet

ingestion of other elements that bind Se such as Cu

89
Q

Where is selenium absorbed from?

A

Small intestine

90
Q

What form of selenium is more rapidly absorbed?

A

Organic selenium

91
Q

What form of selenium is not readily absorbed?

A

Elemental selenium

92
Q

Where would you find high concentrations of selenium after chronic exposure?

A

Hair and Hoof

93
Q

What increases the biliary excretion of selenium?

A

Arsenic

94
Q

What is the mechanism of Action for selenium toxicosis?

A

Depletion of tissue glutathione
Selenium replaces sulfur in AAs causing abnormal proteins
Decrease ATP in chronic toxicosis
Decreased tissue ascorbic acid

95
Q

What is the cause of death with acute and subacute selenium toxicosis?

A

respiratory insufficiency resulting from pulmonary edema hemorrhage

96
Q

What is the cause of death with chronic selenium toxicosis?

A

starvation and thirst resulting from weakness, lameness, and blindness

97
Q

What are the clinical signs of oral acute selenium toxicosis?

A

GI signs: colic, bloat, dark watery diarrhea
Respiratory signs: fluid in the lungs, bloody froth from the nares, and cyanosis
fever
polyuria
mydriasis
uncertain gait
Death within hours

98
Q

What are the clinical signs of parenteral selenium toxicosis?

A

Neurologic signs
Mydriasis
incoordination

99
Q

What are the clinical signs of subacute selenium toxicosis in cattle?

A

“blind staggers”
Stage 1: Poor appetitie, aimless wandering, circling, walking through objects
Stage 2: depression, incoordination, foreleg weakness and walking on knees, complete anorexia
Stage 3: Colic, hypothermia,emaciation, clouded corneas near blindness, paresis, coma, and death within hours

100
Q

What are the clinical signs of selenium toxicosis in swine?

A 
"porcine focal symmetrical poliomyelomalacia"
Incoordination 
lameness
paralysis 
alopecia 
hoof abnormalities
separation of the hoof
101
Q

What are the clinical signs of chronic selenium toxicosis?

A 
Rough hair coat
loss of hair from mane and tail 
hoof abnormalities
sloughing of hooves
stiffness in joints
lameness
partial blindness
anemia
lethargy
emaciation
infertility 
birth defects
102
Q

What are the Acute lesions associated with selenium toxicosis?

A 
Hemorrhagic gastroenteritis 
congestion of organs 
hemorrhages
pulmonary edema 
hydrothorax 
gut contents may smell like rotten garlic or horseradish
103
Q

What are the lesions associated with subacute selenium toxicosis in swine?

A

Focal symmetrical poliomyelomalacia

104
Q

What lesions are associated with chronic selenium toxicosis?

A

Abnormal hooves
Cardiac damage
hepatic necrosis

105
Q

What are the laboratory findings associated with selenium toxicosis?

A

Elevated selenium

106
Q

What is the treatment for acute selenium toxicosis?

A

Saline cathartics
Symptomatic therapy: Oxygen, treatment of pulmonary edema and circulatory shock and gastroenteritis
Acetylcysteine

107
Q

What is the prevention for selenium toxicosis?

A

Test soil and forage regularly
Addition of copper to the diet
Increasing sulfur containing proteins in the diet
Addition of organic arsenicals to the diet to increase biliary excretion

108
Q

What is the prognosis for acute selenium toxicosis?

A

Poor

109
Q

What are the highly toxic Heavy Metals?

A

Pb - Lead
Hg - Mercury
Cd - Cadmium

110
Q

What are the properties of lead?

A

Not readily degraded in the environment

Not easily absorbed or metabolized

111
Q

What happens to lead in the GI tract?

A

forms insoluble compounds in the GI tract

112
Q

What type of lead is more readily absorbed?

A

Organic lead

113
Q

What conditions favor dissolution an absorption of lead?

A

Acid conditions

114
Q

What is the most common source of lead toxicosis in animals?

A

Lead-based paints

115
Q

What are the sources of exposure to lead toxicosis?

A 
Paint 
Old batteries
Plumbing
Galvanized wire 
Lead shot 
lead weight 
fishing sinkers
116
Q

What animals are most vulnerable to lead toxicosis from lead shot?

A

Waterfowl

117
Q

What absorption of lead is poor?

A

Dermal

118
Q

How is lead absorbed?

A

active transport using the same carrier proteins as calcium

119
Q

What increased lead toxicity?

A

Increased GI tract acidity

120
Q

What important element does Lead displace?

A

Calcium

121
Q

What deficiencies increased the absorption of lead?

A

Calcium deficiency
Vitamine D deficiency
Zinc deficiency
Iron deficiency

122
Q

Where does lead bind for transport?

A

RBCs membrane

123
Q

What is the main route of absorption for lead toxicosis?

A

GI Tract

124
Q

What is a liver protein that is involved in cellular detoxification of inorganics and sequesters metal ions present in elevated concentrations?

A

Metallothionein

125
Q

Where does lead accumulate?

A

Active bone matrix

126
Q

What activates lead stored in the active bone matrix?

A

Pregnancy
Lactation
Chelating agents

127
Q

How is lead excreted?

A

Urine

128
Q

What ions does lead substitute for?

A

Calcium
Zinc
Magnesium
Iron

129
Q

What is the mechanism of action for lead toxicosis?

A

interferes with biological structure and function
Forms complexes with nucleophilic functional groups
Competes with calcium in the bone and alters calcium movement across membranes

130
Q

What are the target tissues for lead toxicosis?

A

GI tract
Blood
CNS

131
Q

What neurotransmitters does lead interfere with?

A

GABA
acetylcholine
dopamine

132
Q

What does chronic exposure to lead lead to?

A

anemia from inhibited heme synthesis and delayed erythrocyte maturation and fragility

133
Q

What effect does lead toxicosis have on the brain?

A

Breakdown of the blood brain barrier and alteration of microvascular systems causing brain edema

134
Q

What are the GI tract clinical signs of lead toxicosis?

A 
Anorexia
salivation 
vomiting
"lead colic"
diarrhea
constipation 
rumen atony
135
Q

What signs do you seen on the erythrocytes with lead toxicosis?

A

Basophilic stippling

136
Q

What should we test antemortem for lead toxicosis?

A

Whole Blood concentration

137
Q

What should we test post mortem for lead toxicosis?

A

Kidney and liver

138
Q

What are the CNS clinical signs seen with lead toxicosis?

A 
Anxiety 
hyperexcitability 
vocalization 
head pressing
circling 
running
maniacal behavior 
tremors
blindness
139
Q

What Clinical signs can you see in a horse with acute lead toxicosis?

A

Pharyngeal paralysis
“Roaring”
seizure like activity

140
Q

What are the clinical pathology findings associated with lead toxicosis?

A

Increased nucleated RBCs
Non-regenerative anemia
Basophilic stippling
Fluorescence of porphyrins in plasma or urine

141
Q

What do you find on urinanalysis with lead toxicosis?

A

Increased delta-animolevulinic acid dehydrase levels

142
Q

What is the treatment for lead toxicosis?

A

Stabilize the patient: Fluids/electrolytes
Eliminate the Lead if possible
NO ACTIVATED CHARCOAL!
Chelating agent

143
Q

Which chelating agents is used to treat lead toxicosis?

A

Calcium disodium EDTA
Dimercaptosuccinic acid
Dimercaprol
D-penicillamine

144
Q

What do you use to treat the neurologic signs of lead toxicosis?

A

Mannitol

Diazepam

145
Q

What are some adjunct therapies that can be used to treat lead toxicosis?

A

Taurine
Thiamine
Zinc supplementation

146
Q

What is the prognosis for lead toxicosis?

A

Good with mild to moderate clinical signs and treated prompty
Guarded to poor in animals showing severe CNS signs

147
Q

Ingesting some forms of Zinc can cause the creation of what?

A

toxic zinc salts

148
Q

What is zinc important for?

A 
Growth 
cell proliferation 
skeletal development 
collagen formation 
skin 
feathering 
wound healing 
reproduction 
immune system function 
direct stabilizing effect on cellular membranes 
Function of taste and smell receptors 
Component of many enzymes
149
Q

Where is zinc widely found in the environment?

A 
EVERYWHERE!
Air
Water 
Foodstuffs
Living organisms
150
Q

How are animals exposed to zinc toxicosis

A 
Ingestion of pennies
Galvanized metals
batteries 
jewelry 
skin ointments 
lotions 
shampoos
wound healing agents
overdose of zinc dietary supplement
151
Q

What increases zinc release and absorption?

A

Acid environment

152
Q

What decreased zinc absorption?

A

Dietary fiber
Phytate
Phosphorus
Calcium

153
Q

Where is the most rapid accumulation of zinc?

A 
Pancreas
Liver 
Kidneys 
Spleen 
Male reproductive organs
154
Q

What is the mechanism of action of zinc toxicosis?

A

Unknown

Intravascular hemolysis

155
Q

What are the two ways zinc toxicosis affects the body?

A

Intravascular hemolysis

Renal injury

156
Q

How does zinc affect the RBCs?

A

Direct damage of the RBCs membrane
damage to red blood cell organelles
Immune mediated destruction from hapten formation
inhibition of specific red blood cell biochemical mechanisms

157
Q

What are the GI tract clinical signs of zinc toxicosis?

A 
vomiting 
anorexia lethargy 
abdominal pain 
diarrhea
pica
158
Q

What are the Hematologic clinical signs of zinc toxicosis?

A

Hemolytic anemia
icterus
hemoglobinuria

159
Q

What are the renal clinical signs of zinc toxicosis?

A

Azotemia

hyperphosphatemia

160
Q

What are the lesions associated with zinc toxicosis?

A 
Gastritis
Gastric ulcers
renal tubular casts
liver damage
pancreatitis
161
Q

What are the laboratory findings associated with zinc toxicosis?

A 
Hemolytic anemia
icterus 
hemoglobinuria
azotemia 
hyperphosphatemia 
pancreatitis?
162
Q

What is the treatment for zinc toxicosis?

A

Decontamination: remove the object, Cathartics

Supportive care: Blood transfusion, oxygen, fluids, treatment of renal failure or pancreatitis

163
Q

What is wrong with using chelating agents with zinc toxicosis?

A

May increase zinc absorption and cause further damage to the kidneys

164
Q

What is the prognosis for zinc toxicosis?

A

Good with early diagnosis

Guarded to poor with severe hemolytic crisis

165
Q

What is ferric stored as?

A

Hemosiderin
Ferritin
Transferrin

166
Q

Which form of iron is used in enzymes?

A

Ferric

167
Q

What is the source of exposure to iron toxicosis?

A 
Oral supplements
fertilizers 
slug/snail bait 
Hand warming pads
Iron products 
parenteral iron preparations
168
Q

What are the forms of injectable iron used?

A

Iron dextran
Iron dextrin
iron sorbitol
ferric ammonium citrate

169
Q

What are the forms of iron?

A

Elemental
divalent
trivalent

170
Q

What inreases the risk of iron toxicity in piglets?

A

Selenium and Vitamin E deficiency in sows

171
Q

Which form of iron is less irritant?

A

Organic iron

Ferrous

172
Q

What is different about iron excretion?

A

Animals lack a mechanism to excrete iron

173
Q

How does acute iron toxicosis cause free iron?

A

Acute iron toxicosis overwhelms the selective absorption mechanism and saturates ferritin in the GI mucosal cells leading to absorption of toxic concetrations of free iron

174
Q

What is the mechanism of Action for iron toxicosis?

A

Free iron ions are very reactive and cause free radical lipid peroxidation and direct damage to the membranes
Circulating iron accumulates int he liver causing mitochondrial damage and liver damage and systemic acidosis

175
Q

What can excessive free iron cause?

A

fatty necrosis of myocardium
post arteriolar dilation
increased capillary permeability
reduced cardiac output

176
Q

What are the acute clinical signs of iron toxicosis?

A

Severe depression
shock
acidosis
death within hours

177
Q

What are the stages of acute iron toxicosis?

A

Stage 1: Nausea, vomiting, diarrhea, GI hemorrhage
Stage 2: apparent recovery, GI signs resolve, animal becomes more alert
Stage 3: Vomiting, diarrhea, metabolic acidosis, coagulation disorders, heaptic failure, CV collapse
Stage 4: GIT obstruction secondary to fibrosisng of damaged GI tract

178
Q

What are the lesions associated with iron toxicosis?

A 
Yellowish brown discoloration at injection sites and lymph nodes
GIT ulceration 
hemorrhagic enteritis
Congestion of liver and kidney 
liver necrosis 
icterus 
hemoglobinuria
179
Q

What are the laboratory findings associated with iron toxicosis?

A

Elevated serum iron
Increased saturation of the serum Total Iron-Binding capacity
Acidosis
Hemoglobinuria

180
Q

What is the treatment for iron toxicosis?

A

GI tract decontamination: Emesis, gastric lavage, Milk of Magnesia to precipitate iron
Supportive treatment: IV fluids, GI protectants, treatment of anaphylactoid reactions

181
Q

What are the chelating agents used for iron toxicosis?

A

Deferoxamine

182
Q

What is the prognosis for iron toxicosis?

A

Good if treated early

Guarded to poor in animals with severe clinical signs

RUSVM Toxicology 2016 (32 decks)

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