Heavy Metals Flashcards

(182 cards)

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
What are the uses of organic arsenicals?
Feed additives to improve weight gain and feed efficiency | control enteric infections in swine and poultry
26
What organic arsenical is used in swine?
Arsanilic acid
27
What organic arsenical is used in poultry?
Roxarsone
28
What are the common sources of organic arsenicals toxicosis?
Overdosage or prolonged use | Recommended concentrations in debilitated dehydrated or sick animals
29
What are the properties of organic arsenicals?
phenylarsonic acid derivatives | Pentavalent oxidation state
30
What is important about the toxicity of organic arsenicals?
Organic pentavalent arsenicals are less toxic than inorganic arsenic
31
What enhances toxicity of organic arsenicals?
dehydration water deprivation renal insufficiency
32
Where are organic arsenicals absorbed from?
GI tract
33
How are organic arsenicals excreted?
Urine
34
What is the mechanism of action for organic arsenicals?
Peripheral nerve demyelination and axonal damage
35
What is the mechanism of action for organic arsenicals similar to?
Vitamin B deficiency
36
What are the clinical signs of organic arsenicals toxicosis in swine?
``` incoordination ataxia partial paralysis blindness erythema in white pigs, sensitivity to light ```
37
How long for onset of clinical signs of organic arsenicals toxicosis?
3-5 days
38
What are the clinical signs of organic arsenicals toxicosis in poultry?
``` Incoordination Ataxia Anorexia Depression Coma Death ```
39
What are lesions associated with organic arsenicals toxicosis in swine?
erythemia in light skinned pigs muscle atrophy in chronic cases peripheral nerve and optic nerve demyelination and degeneration gliosis
40
What is the treatment for organic arsenicals toxicosis?
Withdrawal of organic arsenicals | Supportive therapy: water, fluid therapy, multiple vitamins, antibiotics for bacterial infection
41
How long can recovery from organic arsenicals take?
2-4 weeks
42
What is the source of acute copper toxicosis?
Ingestion of high concentrations of copper
43
What are the clinical signs of acute copper toxicosis?
``` severe GI signs vomiting colic hemorrhagic diarrhea dehydration shock ```
44
What is the treatment for acute copper toxicosis?
Supportive and symptomatic therapy
45
What is the source of acute copper toxicosis?
Coins
46
What is the source of chronic copper toxicosis in sheep?
Feed additives Natural copper in soil and plants fertilizer Molybdenum deficiency
47
How does Molybdenum deficiency cause chronic copper toxicosis in sheep?
Copper levels increase causing a decrease in the ratio of Copper to Molybdenum
48
What is the normal ratio of Copper to Molybdenum?
6:1
49
What can cause a sudden loss of copper from the liver to the blood?
Stress
50
How long does accumulation of copper take in sheep?
2-10 weeks
51
What is the mechanism of action of chronic copper toxicosis in sheep?
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
52
What does chronic copper toxicosis in sheep cause?
methemoglobin
53
What are the clinical signs of chronic copper toxicosis in sheep?
``` weakness anorexia pale mucous membranes icterus hemoglobinuria fever dyspnea shock ```
54
What are the lesions associated with chronic copper toxicosis in sheep?
Icterus hemolysis methemoglobinemia Enlarged yellow friable liver enlarged hemorrhagic bluish dark friable kidneys "gunmetal kidneys" enlarged dark brown spleen "blackberry jam spleen"
55
What are the clinical pathology findings for chronic copper toxicosis in sheep?
Elevated serum and whole blood Cu Elevated liver and kidney Cu Elevated Liver enzymes (AST, LDH)
56
What is the treatment for chronic copper toxicosis in sheep?
Ammonium tetrahiomolybate D-penicillamine Molybdenized copper phosphate sprayed on pastures
57
What is the mechanism of action of chronic copper toxicosis in sheep?
Excess free copper causes chronic active hepatitis and liver necrosis due to lipid peroxidation of mitochondrial membranes
58
What is the source of Molybdenum toxicosis?
Excess Molybdenum | Copper deficiency
59
What are the properties of Molybdenum toxicosis?
component of xanthine oxidase | elevated molybdenum interferes with copper absorption
60
Which species is most susceptible to Molybdenum toxicosis?
Cattle
61
What increased toxicity of Molybdenum?
Dietary sulfate
62
What decreased toxicity of Molybdenum?
Dietary copper
63
Where is molybdenum absorbed from?
GI Tract
64
What is the mechanism of action of Molybdenum toxicosis?
Copper deficiency | Copper is an essential component of enzymes
65
What are the clinical signs of Molybdenum toxicosis?
``` 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 ```
66
What is the laboratory findings found with Molybdenum toxicosis?
Elevated Molybdenum Decreased Copper Decreased cytochrome oxidase
67
What is the treatment for Molybdenum toxicosis?
Copper glycinate SC | Copper sulfate added to the diet
68
What does selenium deficiency cause in lambs, calves, and foals?
White muscle disease
69
What does selenium deficiency cause in young pigs?
Hepatosis dietetica
70
What does selenium deficiency cause in chicks?
Exudative diathesis
71
What does selenium deficiency cause in chickens?
Nutritional pancreatic atrophy
72
What does selenium deficiency cause in pigs?
Porcine stress syndrome
73
Which areas have selenium defiecient soil?
NW NE SE Great lakes
74
What is selenium used in?
Feed supplements Injectable selenium-vitamin E Antioxidant supplements Medicated shampoos for dermatitis
75
What are the different types of seleniferous plants?
Obligate accumulators Facultative accumulators Passive accumulators
76
What are the obligate selenium accumulators?
Locoweed Prince's Plume Golden Wood Woody aster
77
Obligate accumulators
accumulate up to 15,000ppm Se | Require Se for growth
78
Facultative accumulators
Accumulate up to 25-100ppm | Do not require Se, but they can accumulate it
79
Passive Accumulators
Accumulate up to 1-25ppm | Accumulate Se passively in Se-rich soil
80
What plants are passive accumulators?
Crop plants: Corn, wheat, oats, barley, grass, hay
81
What are the three oxidation states of selenium?
Selenate Selenite Selenide
82
What are some properties of Selenium?
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
What does selenium and vitamin E do for cells?
prevents cell degeneration and cell membrane damage in animals and poultry
84
How selenium related to thyroid?
Se is found in 5-deiodinase (conversion of T4 to T3)
85
What is the order of selenium toxicity in plants?
Organic selenium is greater than selenate = selenite which is greater than selenide which is greater than synthetic organoselenium compounds
86
What promotes the formation of selenate?
Alkaline soil of the Great Plains
87
What form of selenium is relatively non toxic?
Elemental Selenium
88
What reduces toxicity of selenium?
high protein diet | ingestion of other elements that bind Se such as Cu
89
Where is selenium absorbed from?
Small intestine
90
What form of selenium is more rapidly absorbed?
Organic selenium
91
What form of selenium is not readily absorbed?
Elemental selenium
92
Where would you find high concentrations of selenium after chronic exposure?
Hair and Hoof
93
What increases the biliary excretion of selenium?
Arsenic
94
What is the mechanism of Action for selenium toxicosis?
Depletion of tissue glutathione Selenium replaces sulfur in AAs causing abnormal proteins Decrease ATP in chronic toxicosis Decreased tissue ascorbic acid
95
What is the cause of death with acute and subacute selenium toxicosis?
respiratory insufficiency resulting from pulmonary edema hemorrhage
96
What is the cause of death with chronic selenium toxicosis?
starvation and thirst resulting from weakness, lameness, and blindness
97
What are the clinical signs of oral acute selenium toxicosis?
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
What are the clinical signs of parenteral selenium toxicosis?
Neurologic signs Mydriasis incoordination
99
What are the clinical signs of subacute selenium toxicosis in cattle?
"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
What are the clinical signs of selenium toxicosis in swine?
``` "porcine focal symmetrical poliomyelomalacia" Incoordination lameness paralysis alopecia hoof abnormalities separation of the hoof ```
101
What are the clinical signs of chronic selenium toxicosis?
``` 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
What are the Acute lesions associated with selenium toxicosis?
``` Hemorrhagic gastroenteritis congestion of organs hemorrhages pulmonary edema hydrothorax gut contents may smell like rotten garlic or horseradish ```
103
What are the lesions associated with subacute selenium toxicosis in swine?
Focal symmetrical poliomyelomalacia
104
What lesions are associated with chronic selenium toxicosis?
Abnormal hooves Cardiac damage hepatic necrosis
105
What are the laboratory findings associated with selenium toxicosis?
Elevated selenium
106
What is the treatment for acute selenium toxicosis?
Saline cathartics Symptomatic therapy: Oxygen, treatment of pulmonary edema and circulatory shock and gastroenteritis Acetylcysteine
107
What is the prevention for selenium toxicosis?
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
What is the prognosis for acute selenium toxicosis?
Poor
109
What are the highly toxic Heavy Metals?
Pb - Lead Hg - Mercury Cd - Cadmium
110
What are the properties of lead?
Not readily degraded in the environment | Not easily absorbed or metabolized
111
What happens to lead in the GI tract?
forms insoluble compounds in the GI tract
112
What type of lead is more readily absorbed?
Organic lead
113
What conditions favor dissolution an absorption of lead?
Acid conditions
114
What is the most common source of lead toxicosis in animals?
Lead-based paints
115
What are the sources of exposure to lead toxicosis?
``` Paint Old batteries Plumbing Galvanized wire Lead shot lead weight fishing sinkers ```
116
What animals are most vulnerable to lead toxicosis from lead shot?
Waterfowl
117
What absorption of lead is poor?
Dermal
118
How is lead absorbed?
active transport using the same carrier proteins as calcium
119
What increased lead toxicity?
Increased GI tract acidity
120
What important element does Lead displace?
Calcium
121
What deficiencies increased the absorption of lead?
Calcium deficiency Vitamine D deficiency Zinc deficiency Iron deficiency
122
Where does lead bind for transport?
RBCs membrane
123
What is the main route of absorption for lead toxicosis?
GI Tract
124
What is a liver protein that is involved in cellular detoxification of inorganics and sequesters metal ions present in elevated concentrations?
Metallothionein
125
Where does lead accumulate?
Active bone matrix
126
What activates lead stored in the active bone matrix?
Pregnancy Lactation Chelating agents
127
How is lead excreted?
Urine
128
What ions does lead substitute for?
Calcium Zinc Magnesium Iron
129
What is the mechanism of action for lead toxicosis?
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
What are the target tissues for lead toxicosis?
GI tract Blood CNS
131
What neurotransmitters does lead interfere with?
GABA acetylcholine dopamine
132
What does chronic exposure to lead lead to?
anemia from inhibited heme synthesis and delayed erythrocyte maturation and fragility
133
What effect does lead toxicosis have on the brain?
Breakdown of the blood brain barrier and alteration of microvascular systems causing brain edema
134
What are the GI tract clinical signs of lead toxicosis?
``` Anorexia salivation vomiting "lead colic" diarrhea constipation rumen atony ```
135
What signs do you seen on the erythrocytes with lead toxicosis?
Basophilic stippling
136
What should we test antemortem for lead toxicosis?
Whole Blood concentration
137
What should we test post mortem for lead toxicosis?
Kidney and liver
138
What are the CNS clinical signs seen with lead toxicosis?
``` Anxiety hyperexcitability vocalization head pressing circling running maniacal behavior tremors blindness ```
139
What Clinical signs can you see in a horse with acute lead toxicosis?
Pharyngeal paralysis "Roaring" seizure like activity
140
What are the clinical pathology findings associated with lead toxicosis?
Increased nucleated RBCs Non-regenerative anemia Basophilic stippling Fluorescence of porphyrins in plasma or urine
141
What do you find on urinanalysis with lead toxicosis?
Increased delta-animolevulinic acid dehydrase levels
142
What is the treatment for lead toxicosis?
Stabilize the patient: Fluids/electrolytes Eliminate the Lead if possible NO ACTIVATED CHARCOAL! Chelating agent
143
Which chelating agents is used to treat lead toxicosis?
Calcium disodium EDTA Dimercaptosuccinic acid Dimercaprol D-penicillamine
144
What do you use to treat the neurologic signs of lead toxicosis?
Mannitol | Diazepam
145
What are some adjunct therapies that can be used to treat lead toxicosis?
Taurine Thiamine Zinc supplementation
146
What is the prognosis for lead toxicosis?
Good with mild to moderate clinical signs and treated prompty Guarded to poor in animals showing severe CNS signs
147
Ingesting some forms of Zinc can cause the creation of what?
toxic zinc salts
148
What is zinc important for?
``` 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
Where is zinc widely found in the environment?
``` EVERYWHERE! Air Water Foodstuffs Living organisms ```
150
How are animals exposed to zinc toxicosis
``` Ingestion of pennies Galvanized metals batteries jewelry skin ointments lotions shampoos wound healing agents overdose of zinc dietary supplement ```
151
What increases zinc release and absorption?
Acid environment
152
What decreased zinc absorption?
Dietary fiber Phytate Phosphorus Calcium
153
Where is the most rapid accumulation of zinc?
``` Pancreas Liver Kidneys Spleen Male reproductive organs ```
154
What is the mechanism of action of zinc toxicosis?
Unknown | Intravascular hemolysis
155
What are the two ways zinc toxicosis affects the body?
Intravascular hemolysis | Renal injury
156
How does zinc affect the RBCs?
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
What are the GI tract clinical signs of zinc toxicosis?
``` vomiting anorexia lethargy abdominal pain diarrhea pica ```
158
What are the Hematologic clinical signs of zinc toxicosis?
Hemolytic anemia icterus hemoglobinuria
159
What are the renal clinical signs of zinc toxicosis?
Azotemia | hyperphosphatemia
160
What are the lesions associated with zinc toxicosis?
``` Gastritis Gastric ulcers renal tubular casts liver damage pancreatitis ```
161
What are the laboratory findings associated with zinc toxicosis?
``` Hemolytic anemia icterus hemoglobinuria azotemia hyperphosphatemia pancreatitis? ```
162
What is the treatment for zinc toxicosis?
Decontamination: remove the object, Cathartics | Supportive care: Blood transfusion, oxygen, fluids, treatment of renal failure or pancreatitis
163
What is wrong with using chelating agents with zinc toxicosis?
May increase zinc absorption and cause further damage to the kidneys
164
What is the prognosis for zinc toxicosis?
Good with early diagnosis | Guarded to poor with severe hemolytic crisis
165
What is ferric stored as?
Hemosiderin Ferritin Transferrin
166
Which form of iron is used in enzymes?
Ferric
167
What is the source of exposure to iron toxicosis?
``` Oral supplements fertilizers slug/snail bait Hand warming pads Iron products parenteral iron preparations ```
168
What are the forms of injectable iron used?
Iron dextran Iron dextrin iron sorbitol ferric ammonium citrate
169
What are the forms of iron?
Elemental divalent trivalent
170
What inreases the risk of iron toxicity in piglets?
Selenium and Vitamin E deficiency in sows
171
Which form of iron is less irritant?
Organic iron | Ferrous
172
What is different about iron excretion?
Animals lack a mechanism to excrete iron
173
How does acute iron toxicosis cause free iron?
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
What is the mechanism of Action for iron toxicosis?
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
What can excessive free iron cause?
fatty necrosis of myocardium post arteriolar dilation increased capillary permeability reduced cardiac output
176
What are the acute clinical signs of iron toxicosis?
Severe depression shock acidosis death within hours
177
What are the stages of acute iron toxicosis?
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
What are the lesions associated with iron toxicosis?
``` Yellowish brown discoloration at injection sites and lymph nodes GIT ulceration hemorrhagic enteritis Congestion of liver and kidney liver necrosis icterus hemoglobinuria ```
179
What are the laboratory findings associated with iron toxicosis?
Elevated serum iron Increased saturation of the serum Total Iron-Binding capacity Acidosis Hemoglobinuria
180
What is the treatment for iron toxicosis?
GI tract decontamination: Emesis, gastric lavage, Milk of Magnesia to precipitate iron Supportive treatment: IV fluids, GI protectants, treatment of anaphylactoid reactions
181
What are the chelating agents used for iron toxicosis?
Deferoxamine
182
What is the prognosis for iron toxicosis?
Good if treated early | Guarded to poor in animals with severe clinical signs