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Toxicology > Exam two > Flashcards

Exam two Flashcards

1
Q

What is methaldehyde used for?

A

snail, slug and insect killer, fuel for camp stoves

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2
Q

What kind of pesticide is methaldehyde?

A

RUP

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3
Q

What are the properties of methaldehyde?

A

irritant, flammable powder, poorly soluble in H20, soluble in oil

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4
Q

How long can products release methaldehyde?

A

10-14 days under moderately moist conditions

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5
Q

What animals are susceptible to methaldehyde toxicity?

A

dogs, cats, livestock, horses

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6
Q

Which route makes methaldehyde most toxic?

A

inhalation

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7
Q

What happens to methaldehyde in the stomach?

A

some undergoes acid hydrolysis to acetaldehyde and both can be absorbed from GIT

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8
Q

Do methaldehyde and acetaldehyde cross the BBB?

A

YES

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9
Q

What is the elimination half life of metaldehyde?

A

~27 hours

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10
Q

What can decrease toxicity of methaldehyde?

A

enzyme inducers like phenobarbital

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11
Q

How is acetaldehyde metabolized?

A

by hepatic aldehyde dehydrogenase and converted to CO2 and exhaled

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12
Q

What is the MOA of methaldehyde?

A

metaldehyde > acetaldehyde, then concentration is higher than capability of liver to oxidize it, methaldehyde decreases brain GABA, NE and 5HT and increases MAO (breaks down more)

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13
Q

What contributes to toxicity of methaldehyde?

A

hyperthermia due to muscle tremors, metabolic acidosis

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14
Q

What is the cause of early death in methaldehyde toxicity?

A

respiratory failure within 4-24 hours

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15
Q

What is seen in dogs that survive acute phase of methaldehyde toxicity?

A

liver failure, damage, cirrhosis

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16
Q

When is the onset of action for methaldehyde toxicity?

A

w/i 3 hours

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17
Q

What are the clinical signs of methaldehyde toxicity?

A

salivation, vomiting, diarrhea, tachycardia, reversible blindness, convulsive seizures, CNS depression

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18
Q

If an animal recovers from methaldehyde toxicity, what is the time frame?

A

2-3 weeks

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19
Q

What lesions are found in methaldehyde toxicity?

A

formaldehyde odor in stomach contents, methaldehyde granules may be visible in GI, petechial and ecchymotic hemorrhages in GI

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20
Q

What lab work can be done to confirm methaldehyde toxicity?

A

look for methaldehyde/acetaldehyde in stomach contents

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21
Q

How do you diagnose methaldehyde toxicity?

A

history, clinical signs, odor, lab analysis

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22
Q

What is the antidote for methaldehyde toxicity?

A

none

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23
Q

How do you treat methaldehyde toxicity?

A

emetics, gastric lavage, activated charcoal, enemas, anticonvulsants, respiratory support, muscle relaxants, fluid therapy, monitor and manage temp

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24
Q

How is phenoxy2,4,D used?

A

herbicide, turf, agent orange

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25
Q

How does 2,4,D alter the metabolism of plants?

A

increases toxicity by increasing accumulation of nitrate or cyanide and improves palatability

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26
Q

How long does 2,4,D live in the environment?

A

not stable in environment

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27
Q

How is 2,4,D affected by the rumen?

A

not degraded by rumen microflora and don’t alter microflora, irritant to GI mucosa

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28
Q

What species are most susceptible to 2,4,D toxicity?

A

cattle and dogs

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29
Q

How is 2,4,D absorbed/distributed?

A

absorbed well from GI and poorly from skin - distributed all over body

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30
Q

What is the half life of 2,4,D?

A

a few hours (can be up to 4 days in dogs)

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31
Q

How is 2,4,D metabolized?

A

hydrolysis

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32
Q

How id 2,4,D excreted?

A

unchanged in urine, alkalization of urine enhances this

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33
Q

What is the MOA of 2,4,D toxicosis?

A

irritates GI mucosa, uncouples oxidative phosphorylation, affects skeletal muscle membranes in dogs

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34
Q

What clinical signs are seen w 2,4,D toxicosis?

A

GI and neuromuscular

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35
Q

What lesions are seen in 2,4,D toxicosis?

A

GI damage, degeneration of renal tubules, rumen stasis

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36
Q

What lab tests help with diagnosis?

A

elevated kidney levels, ALP, LDH, CK and checking forage, water, liver and stomach contents

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37
Q

How do you diagnose 2,4,D toxicity?

A

history of ingestion, chemical analysis, rule out other diseases

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38
Q

What is the antidote for 2,4,D?

A

none

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39
Q

How do you treat 2,4,D toxicity?

A

wash skin, activated charcoal, IV fluids, alkalinize urine

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40
Q

What are the dipyridyl herbicides?

A

paraquat (RUP) and diquat (GUP) broad spectrum herbicides

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41
Q

How well do dipyridyl herbicides live in the environment?

A

unstable, rapidly inactivated by light and soil, soluble in water but not alcohol, hydrocarbon solvents

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42
Q

What pH destroys dipyridyl herbicides?

A

alkaline

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43
Q

What species are susceptible to dipyridyl herbicide toxicity?

A

all esp dogs

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44
Q

What increases dipyridyl herbicide toxicity?

A

selenium vit D deficiency, depletion of tissue glutathione and oxygen therapy and preexisting renal failure

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45
Q

How is paraquat absorbed, distributed and excreted?

A

absorbed from GI and skin, distributed all over esp in lung, excreted unchanged in urine

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46
Q

How is diquat absorber?

A

poorly absorbed from GI

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47
Q

Where is paraquat selectively sequestered?

A

in alveolar cells - after 4hrs [ ] 10x other organs, 30-80x plasma after 4-10 days

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48
Q

What is the diphasix efflux?

A

initial rapid 1/2 life followed by slow phase as chemical is released from lung storage pool

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49
Q

What is the MOA of paraquat and diquat?

A

reduced by NADPH to produce singlet oxygen > reacts w lipids of membranes to form hydroperoxides > production of free radical and membrane damage and cellular degeneration and necrosis

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50
Q

What are the clinical signs of the first phase of acute herbicide toxicosis?

A

vomiting, anorexia, irritation of topical exposure, – ataxia, dyspnea and seizures at high doses

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51
Q

What are the clinical signs of the second phase of acute toxicosis in herbicide toxicity?

A

renal failure and hepatocellular necrosis, reversible renal injury

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52
Q

What are the clinical signs of the third phase of acute toxicosis in herbicide toxicity?

A

initially damage to the alveoli and consequent pulmonary edema, tachypnea, dyspnea, harsh respiratory sounds

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53
Q

What happens in subacute or chronic toxicosis of herbicides?

A

survive initial exposure > lungs undergo proliferative/fibrotic stage after 7 days and <30mmHg

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54
Q

What lesions are commonly seen with herbicide toxicosis?

A

respiratory tract and GIT lesions, pulmonary chanfes, lung may be shrunken and fibrotic if chronic, lingual ulcers

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55
Q

What lab work is done for herbicide toxicosis?

A

plant, stomach contents and urine sent to lab, mild changes in lungs on rads

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56
Q

How soon after herbicide toxicosis does the normal present negative?

A

48hours

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57
Q

How do you diagnose paraquat and diquat toxicity?

A

history, clinical signs, lesions, lab

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58
Q

What is the antidote for paraquat and diquat toxicity?

A

none

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59
Q

How do you treat paraquat and diquat toxicity?

A

emetics, oral adsorbants, saline cathartics, supportive treatment, hemodialysis

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60
Q

What is contraindicated in early treatment of paraquat and diquat toxicity?

A

oxygen! may increase lung damage

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61
Q

What are the biochemical antagonists for paraquat and diquat toxicity?

A

orgotein, acetylcysteine, ascorbic acid, niacin or riboflavin

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62
Q

How soon must treatments for herbicide toxicity begin to have much of an effect?

A

within 24 hours of exposure

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63
Q

What are fungicides used for?

A

prevent or treat fungal infections in plants

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64
Q

What are the fungicides?

A

chlorophenols and nitrophenols, pentachlorophenol (PCP)

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65
Q

What is the toxicity of fungicides like in animals?

A

usually low toxicity unless exposed in large amount

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66
Q

What is pentachlorophenol used for?

A

a wood preservative, protects from fugus and insects

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67
Q

What is the most toxic exposure of pentachlorophenol?

A

vapors penetrateing intact skin, dermal exposure

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68
Q

What ways can animals become poisoned by pentachlorophenol?

A

inhalation, licking wood, ingestion, vapors penetrating intact skin

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69
Q

How soluble is pentachlorophenol?

A

not in water, soluble in pils and organic solvents

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70
Q

What did older preparations of pentachlorophenol contain?

A

dioxins - carcinogenic and teratogenic

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71
Q

What factors increase toxicity of pentachlorophenol?

A

high temp, oily or organic solvent vehicles, previous exposure, poor condition, newborn, hyperthyroid

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72
Q

What factors decrease pentachlorophenol toxicity?

A

cold temp, antithyroid drugs, presence of body fat

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73
Q

How is pentachlorophenol absorbed?

A

GI, inhalation, intact skin

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74
Q

What is the half life of pentachlorophenol?

A

1.5-2 days

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75
Q

How is pentachlorophenol excreted?

A

as glucuronides or unchanged in urine

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76
Q

What is the MOA of pentachlorophenol?

A

uncouples oxidative phosphorylation and blocks or decreases ATP > overheating, metabolic acidosis and dehydration

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77
Q

What clinical signs are seen with pentachlorophenol toxicosis?

A

irritation of eye, respiratory or GI mucosa and intact skin, neurotoxic due to decreased cellular energy, CNS simulation and seizures

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78
Q

What signs of acute pentachlorophenol toxicity are seen in pigs?

A

hyperthermia, skin irritation and rapid death

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79
Q

What are the signs of chronic pentachlorophenol toxicity?

A

weight loss, decreased milk production, anemia, fever, respiratory distress

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80
Q

What lesions are seen in pentachlorophenol toxicosis?

A

rapid rigor mortis, local irritaiton, pulmonary congestion, dark blood

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81
Q

What lab diagnosis can be done in pentachlorophenol toxicosis?

A

chemical test of blood in urine (or kidney and skin if dead)

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82
Q

How do you diagnose pentachlorophenol toxicity?

A

history, signs, lesions, chemical analysis

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83
Q

What is the antidote for pentachlorophenol toxicity?

A

none

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84
Q

How do you treat pentachlorophenol toxicity?

A

removal of animal from site, emetics, activated charcoal, bath, oxygen therapy, lower temp, IV fluids, antibiotics

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85
Q

Where does non-protein nitrogen come from?

A

urea as feed additive, urea fertilizer, ammonium salts in feed products

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86
Q

What pH enhances hydrolysis of urea by urease?

A

alkaline – urea is basic

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87
Q

What species are most effected by non-protein nitrogen toxicity?

A

ruminants, horses

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88
Q

What compound is the most toxic of all NPN compounds?

A

urea

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89
Q

What age of animals are more sensitive to NPN toxicity?

A

<1year but 3-6weeks are tolerant

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90
Q

What increases toxicity of NPN?

A

fasting, dehydration or low water intake, between 6weeks-1yr, feeds rich in urease, hepatic insufficiency, diet low in energy and protein but high in fiber

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91
Q

What does too much urea and ammonia result in?

A

elevation of rumen pH in non-ionized form (BAD)

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92
Q

In NPN toxicity, what happens once non-ionized ammonia is absorbed?

A

converted by liver to urea > excreted in urine > too much = hyperammonemia

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93
Q

Why is non-ionized ammonia more toxic to animals?

A

crosses cell membranes, BBB, and placenta

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94
Q

What is the MOA of NPN toxicosis?

A

urea > ammonia, ammonia inhibits CAC > lack in energy > decreased cellular respiration and tissue damage

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95
Q

What is the cause of death in NPN toxicity?

A

cardiac failure or respiratory failure –> RAPID

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96
Q

What are the clinical signs of NPN toxicity?

A

RAPID onset of restlessness, muscle tremors, salivation, colic, bloat, sternal recumbency while standing on hind limbs, convulsions, death within 1-2hours

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97
Q

What are the lesions associated in NPN toxicity?

A

none- ammonia odor, vascular damage, dead animals are bloated

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98
Q

How do you diagnose NPN toxicity in the lab?

A

analysis of feed for urea content, ammonia in whole blood or rumen fluid, or frozen specimens

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99
Q

What is found in blood chemistry and rumen pH in NPN toxicity?

A

elevated rumen pH alkalotic, acidic blood

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100
Q

How do you diagnose NPN toxicity?

A

history, clinical signs, ammonia odor, lab

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101
Q

How do you treat NPN toxicity?

A

relieve bloat, acetic acid or vinegar to ruminants, sodium bicarb, normal saline

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102
Q

Which animals do you treat for NPN toxicity?

A

not showing signs yet - every 4-5hours for 48hours, ones showing signs die quickly, usually can’t treat in time

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103
Q

What are ionophores used for?

A

anti-coccidia, growth promotor, antibiotics, monensin for milk production efficiency

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104
Q

What is the solubility of ionophores like?

A

slightly soluble in water, soluble in organic solvents and oils - microphilic

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105
Q

What are sources of ionophores?

A

monensin, eating feed with high levels, malicious poisoning

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106
Q

What species are susceptible to ionophore toxicity?

A

all, equines most, then cattle, poultry least

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107
Q

Are cattle levels of ionophores toxic to horses?

A

NO

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108
Q

What increases ionophore toxicity?

A

tiamulin, chloramphenicol, erythromycin, sulfonamides, cardiac glycosides

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109
Q

What is the difference between ruminants and mongastrics absorption of ionophores?

A

monogastrics absorb all but ruminants absorb 50%

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110
Q

How are ionophores distributed?

A

throughout body, blood and tissue levels are small, doesn’t accumulate

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111
Q

How are ionophores metabolized and excreted?

A

metabolized by P-450 in liver, excreted in bile

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112
Q

What is the MOA of ionophores?

A

disrupt electrochemical gradients targeting mitochondria of highly energetic tissues, influx of sodium-ionophore complex increasing intracellular Na and Ca >decreased ATP, cell death, free radicals released

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113
Q

What organs/tissues are most affected by ionophore toxicity?

A

myocardium, kidneys

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114
Q

What is the onset of ionophore toxicity?

A

rapid

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115
Q

What are the clinical signs of ionophore toxicity?

A

GI, skeletal, cardiac –> anorexia, colic, hyperventilation, tachyarrythmias, diarrhea, ataxia, dyspnea, death, resting on knees with wings and legs outward in birds

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116
Q

What lesions are seen in ionophore toxicity?

A

cardiac and skeletal muscle lesions - pale white patchy areas on muscle

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117
Q

What is the lab diagnosis for ionophores?

A

feed and GI contents best for detection, look for ppb levels

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118
Q

What is seen on clinical pathology of ionophores?

A

increase enzymes, CPK, AST, LDH, ALP - decreased Ca, K, increased PCV – Na often normal

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119
Q

How do you diagnose ionophore toxicity?

A

history, clinical signs, lesions, lab

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120
Q

What poisonous plants are toxic to skeletal muscle?

A

coffee senna, coyotillo, white snakeroot

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121
Q

What are the cardiotoxic plants?

A

oleander, taxus, milkweed, vetch

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122
Q

What is the antidote for ionophores?

A

none

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123
Q

How do you treat ionophore toxicity?

A

remove medicated feed, activated charcoal, mineral oil, saline cathartics, symptomatic treatment, do NOT stress horses

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124
Q

How do animals get water deprivation?

A

feedining brine, whey or garbage, ingestion of salt licks, drinking water containing salt, overcrowding, frozen water, lack of water, medicated (unpalatable) water

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125
Q

What effect does salt have on animals?

A

taste is attractive, mild irritant to mucous membranes

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126
Q

How much salt can animals tolerate in feed?

A

> 10% salt in feed if they have free access to water

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127
Q

What species are susceptible to water deprivation?

A

pigs, cattle and poultry mostly, dogs less

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128
Q

How is salt absorbed?

A

by GI and distributed all over body - enters brain by passive diffusion and removed by active transport

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129
Q

How is excess sodium excreted?

A

in urine, as long as there is enough water

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130
Q

What is the MOA of water deprivation?

A

dehydration increases plasma sodium and cerebral spinal fluid - high sodium in brain inhibits anaerobic glycolysis resulting in lack of energy for active transport

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131
Q

What happens with sodium trapped in the brain?

A

attracts water because of osmotic gradient > cerebral edema and brain damage

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132
Q

What are the clinical signs of water deprivation?

A

early constipation and thirst, vomiting, PU, metabolic acidosis, seizures, circling, head pressing, blindness

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133
Q

What lesions are seen in water deprivation that are pathognomonic?

A

eosinophilic meningoencephalitis is pathognomonic in PIGS ONLY and only within 24 hours of exposure - disappears after

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134
Q

What other lesions could be seen with water deprivation?

A

fluid in body cavities, organ edema, cerebral edema

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135
Q

What is used for lab diagnosis of water deprivation?

A

serum and CSF concentrations, salt in feed

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136
Q

How do you diagnose water deprivation?

A

history, encephalitic signs, lesions and lab diagnosis

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137
Q

How do you treat water deprivation?

A

give small amounts of fresh water - large amount can kill them by causing more cerebral edema, IV fluids, furosemide, anticonvulsants

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138
Q

What is the prognosis of water deprivation?

A

poor, mortality 50%

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139
Q

What is the source of acute copper toxicosis?

A

ingestion of high concentrations of copper - feed additives, in soil

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140
Q

Why is acute heavy metal toxicity bad?

A

very small amount can cause toxicosis, irritants, poor penetrated of membranes, small amount that is absorbed can cause toxicosis because of potency

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141
Q

Which heavy metal crosses the BBB and causes CNS damage?

A

lead

142
Q

What are the clinical signs of acute copper toxicosis?

A

rapid onset of GI signs, dehydration, shock

143
Q

What species is chronic copper poisoning common in?

A

sheep > cattle, due to lower maliptinum in sheep that enhance copper toxicosis

144
Q

What is the treatment for acute copper toxicosis?

A

supportive and symptomatic therapy

145
Q

What enhances excess copper in the body?

A

molybdenum deficiency

146
Q

How do you get molybdenum deficiency?

A

unavailability of sulfate

147
Q

What is the normal ratio of copper to molybdenum

A

6:1

148
Q

Why does chronic copper toxicosis occur?

A

molybdenum deficiency makes copper accumulate in liver

149
Q

How long does chronic copper accumulation take in sheep?

A

2-10 weeks

150
Q

How is copper excreted?

A

bile

151
Q

What is the MOA of copper toxicosis?

A

accumulation in liver causes liver degeneration and necrosis, release > excess copper in blood, oxidation or RBC > hemolysis crisis, oxidizes hemoglobin to methemoglobin

152
Q

What are the clinical signs of chronic copper toxicity?

A

weakness, anorexia, icturus, hemoglobunuria, dyspnea, shock

153
Q

What lesions are seen with chronic copper toxicity?

A

liver is enlarged, friable, kidneys are enlarged, hemorrhagic, spleen enlarged and dark brown/black

154
Q

How do you diagnose chronic copper toxicosis?

A

history, sudden onset hemoglobinuria, jaundice

155
Q

What are the DDX for chronic copper toxicity?

A

hemolytic agents, poisonous plants, snake venom, infectious dz,

156
Q

How do you treat chronic copper toxicity?

A

add molybdate to sheep rations or pastures, ammonium tetrahiomolybate, D-penicillamine, supplemental zinc

157
Q

What dog breed is susceptible to chronic copper toxicosis?

A

bedlington terrier - recessive disorder at 2-6 years, also westie, skye terriers, dobermans

158
Q

How do animals get molybdenum toxicity?

A

excess molybdenum in soil, plants, industrial contamination, fertilizer OR copper deficiency

159
Q

What species are susceptible to molybdenum toxicity?

A

cattle most, seen in sheep, horses and pigs resistance

160
Q

What increases molybdenum toxicity?

A

high levels of dietary sulfate, low levels of copper

161
Q

How is molybdenum absorbed and excreted?

A

absorbed from GI, excreted in milk in toxic levels

162
Q

What is the MOA of molybdenum toxicosis?

A

copper deficiency > involved in hematopoesis, CT metabolism, myelin formation in newborn animals, pigmentation, bone formation

163
Q

How long does it take to see signs of molybdenum toxicity?

A

a few days after exposure, 8-10 days for diarrhea

164
Q

What are the clinical signs of molybdenum toxicity?

A

green/yellow non-hemorrhagic diarrhea, rough hair coat esp around eyes, decreased weight, anemia, decreased fertility

165
Q

What is seen in lab on molybdenum toxicity?

A

look for high molybdenum or low copper, OR decreased cytochrome oxidase (indicates low copper)

166
Q

How do you treat molybdenum toxicity?

A

copper glycinate SC, copper sulfate added to diet

167
Q

Where does inorganic arsenic come from?

A

ant/roach bait, wood preservative, insecticides, herbicides, fungicides, paint, pigments, detergents

168
Q

What is the oxidative state of inorganic arsenic?

A

3 oxidative states: elemental, trivalent arsenite, pentavalent arsenate

169
Q

Which form of inorganic arsenic is most toxic?

A

trivalent - arsenite

170
Q

How fast is inorganic arsenic toxicosis?

A

acute or per acute

171
Q

What species are susceptible to arsenic toxicosis?

A

most herbivores, dogs, rarely swine, chickens

172
Q

Is inorganic or organic arsenic more toxic?

A

inorganic more toxic

173
Q

Why is pentavalent dangerous when metabolized?

A

it is inverted to trivalent in vivo - more toxic

174
Q

How is inorganic arsenic absorbed?

A

GI, intact skin, inhalation - distributed all over body, higher in kidney and liver

175
Q

Does inorganic arsenic cross the BBB?

A

poorly

176
Q

How is inorganic arsenic excreted?

A

urine w/i 48 hours, feces, milk, saliva, sweat

177
Q

What is the MOA of inorganic arsenic?

A

trivalent binds to 2-SH groups of lipoic - inhibits glycolysis and CAC, locally corrosive, tissues rich in oxidative enzymes, capillary endothelial cells most sensitive

178
Q

What are the clinical signs of PERACUTE inorganic arsenic toxicity?

A

severe rapid colic, collapse, death,

179
Q

What are the clinical signs of ACUTE inorganic arsenic toxicity?

A

rapid onset, severe colic, staggering, vomiting, hemorhagic diarrhea, hematuria - corrosive effects, death in 1-3 days

180
Q

What are the clinical signs of SUBACUTE inorganic arsenic toxicity?

A

colic, anorexia, posterior paralysis

181
Q

What are the classical lesions of inorganic arsenic toxicity?

A

GI mucosal edema and hemorrhage, liver and kidney damage, capillary degeneration, skin lesions and blistering

182
Q

What is the best specimen for chemical analysis of inorganic arsenic?

A

urine for antemortem

liver and kidney in postmortem

183
Q

What on bloodwork can indicate inorganic arsenic toxicity?

A

increased PCV, increased BUN

184
Q

How do you treat inorganic arsenic toxicity?

A

emergency and supportive treatment (fluids, treat acidosis), fluids and electrolytes

185
Q

What ways can you decontaminate inorganic arsenic toxicity?

A

gastric lavage, mineral oil, activated charcoal, demulcents to coat mucosa - emetics CONTRAINDICATED because of corrosives if seeing clinical signs

186
Q

What compound is used in chelation therapy for inorganic arsenic toxicity?

A

dimercaprol (BAL) **treat and gets worse, metabolizes and gets in blood

187
Q

What are the side effects of dimercaprol used in inorganic arsenic toxicity?

A

vomiting, tremors, convulsions, shock, coma, death **can get at therapeutic doses

188
Q

What are organic arsenicals used for?

A

feed additives to improve weight gain

189
Q

What species is arsanilic acid used in?

A

swine

190
Q

What species is roxarsone used in?

A

poultry

191
Q

How do animals get organic arsenic toxicity?

A

overdose, prolonged use, contraindications in sick animals

192
Q

What is the classification of damage in organic arsenicals?

A

peripheral neural toxicity

193
Q

What enhances toxicity or organic arsenic?

A

dehydration, water deprivation, renal insufficiency

194
Q

How are organic arsenics absorbed?

A

through GI and distributed throughout body

195
Q

How is organic arsenic excreted?

A

unchanged in urine

196
Q

What is the MOA of organic arsenic?

A

unknown but beleve due to peripheral neuronal damage and demylination

197
Q

What are the clinical signs of organic arsenic (arsanilic acid) in swine?

A

3-5 days, incoordination, ataxia, partial paralysis but still GOOD appetite, NO GI SIGNS, erythema, blindness

198
Q

What are the clinical signs of organic arsenic toxicity (arsanilic acid) in poultry?

A

anorexia, depression, coma, death

199
Q

What are the clinical signs of roxarsone toxicity in swine?

A

sudden onset, hyperexcitability, tremors, collapse, coma, death, NO blindness

200
Q

What are the clinical signs of roxarsone toxicity in poultry?

A

incoordination and ataxia

201
Q

What lesions are seen with organic arsenic toxicity?

A

erythema in light skin pigs, muscle atrophy

202
Q

What is the best specimen to test for organic arsenic toxicity?

A

feed, GI - otherwise levels may be low because of absorption

203
Q

What is the antidote for organic arsenic?

A

none

204
Q

How do you treat organic arsenic toxicity?

A

withdrawal, supportive therapy –> if demylination will be permanent damage,

205
Q

How long does recovery of organic arsenic take?

A

2-4 weeks

206
Q

What does selenium deficiency cause?

A

white muscle dz, nutritional muscle dystrophy, hepatitis dietetic, exudative diathesis, nutritional pancreatic atrophy, porcine stress syndrome

207
Q

What areas get selenium deficient soil?

A

northwest, northeast, southeast, great lakes

208
Q

What is the requirement of selenium?

A

0.1mg/kg

209
Q

What is selenium used for?

A

feed supplement, injectable, supplements, medicated shampoos, seleniferous plants

210
Q

What is the palatability of selenium plants?

A

unpalatable, smell like rotting garlic

211
Q

What are the seleniferous plants?

A

astragalus, stanleya, oonopsis, xylorrhiza

212
Q

How does selenium effect mucous membranes?

A

irritant

213
Q

What type of soil enhances the formation of selenate?

A

arid alkaline soil of great planes

214
Q

How does diet effect toxicity of selenium?

A

reduced by high protein diet and ingestion of other things that bind Se like copper

215
Q

How is selenium absorbed?

A

SI, distributed throughout body esp. to liver, kidney, spleen

216
Q

Chronic exposure of selenium leads to high concentrations where?

A

hair and hoof

217
Q

Does selenium cross the placenta?

A

yes, also in milk

218
Q

What is the MOA of selenium?

A

oxidative damage, free radicals, irritant

219
Q

How is selenium excreted?

A

mostly urine, also bile

220
Q

What increases biliary excretion of selenium?

A

arsenic

221
Q

What causes death in acute and subacute toxicosis of selenium?

A

cardiogenic shck, respiratory insufficiency from pulmonary edema

222
Q

What causes death in chronic toxicosis of selenium?

A

starvation and thirst from weakness and loss of hooves, lameness

223
Q

What are the clinical signs of acute toxicosis of selenium?

A

GI signs, respiratory signs, neuro signs esp if injected

224
Q

What are the clinical signs of chronic toxicosis of selenium?

A

hoof and hair falling out/apart

225
Q

What are the clinical signs of subacute toxicosis of selenium?

A

mix of acute and chronic signs - see hoof and hair problems with respiratory and cardiovascular issues - may see blind staggers

226
Q

What lesions are seen in swine with selenium toxicosis?

A

porcine focal symmetrical poliomalacia

227
Q

What lesions are seen in acute selenium toxicosis?

A

hemorrhagic gastroenteritis, gut contents smell like rotten garlic or horseradish

228
Q

What is used for lab diagnosis of selenium toxicity?

A

blood, kidney and liver for acute

hoof and hair if chronic

229
Q

How do you treat acute selenium toxicosis?

A

saline cathartics, symptomatic therapy, acetylcysteine

230
Q

What should you do to prevent selenium toxicosis?

A

regularly test soil, remove animals from seleniferous areas, add copper to diet, add organic arsenicals to diet

231
Q

What is the difference between nitrate and nitrite?

A

nitrate NO3 is absorbed from soil by plant and is converted to nitrite NO2, nitrite > ammonia >AA> plant protein

232
Q

When animals ingest plants, do they get nitrate or nitrite?

A

BOTH

233
Q

How does nitrate accumulate in the plant?

A

when rate of nitrate to nitrite is reduced and continuation of nitrate uptake from soil

234
Q

What plant species favor nitrate accumulation?

A

sweet clover, alfalfa, wheat, corn

235
Q

What soil conditions enhance nitrate uptake?

A

rains, moisture, acid soil, low soil molybdenum, sulfur or phosphorus, low soil temp, soil aeration

236
Q

What part of the plant contains the highest [ ] of nitrate?

A

the stalk closest to ground, seed and flower has least

237
Q

What age of plants have more nitrate?

A

younger

238
Q

What are the nitrate accumulating plants?

A

pigweed, oats, beets, johson grass, sudan grass, milo, corn, maize, lambs quarters, sweet clover, alfalfa, wheat, sunflower

239
Q

What is nitrate and nitrite used for?

A

fertilizers, sodium nitrite IV as vasodilator

240
Q

What is the most important property of nitrate/nitrite?

A

nitrate > nitrite by nitrate reductase

241
Q

Are nitrates/nitrites palatable?

A

yes, salty

242
Q

How does nitrate toxicity occur?

A

develops over time

243
Q

What species is most affected by nitrate poisoning?

A

ruminants, horses sensitive to IV nitrite, pigs are resistant

244
Q

Which is more toxic; nitrate or nitrite?

A

nitrite is 10x more toxic than nitrate

245
Q

Why are ruminants so susceptible to nitrate toxicity?

A

factors that stimulate rumen microflora increase nitrate reductase activity > increases toxicity

246
Q

What factors of the animal increases nitrate toxicity?

A

younger animal, with anemia and methemoglobinemia

247
Q

What is the 1/2 life of nitrite? Nitrate?

A

<1hr, nitrate 4-48hr

248
Q

What is the MOA of nitrate toxicosis?

A

oxidation > hemoglobin turns to methemoglobin and can’t carry oxygen

249
Q

At what level of methemoglobin does death occur from anoxemia?

A

80-90%

250
Q

What are the clinical signs of nitrate toxicity?

A

sudden death, rapid breathing, dyspnea, ataxia, cyanosis, convulsions with a fast onset, abortion

251
Q

What lesions are noted in nitrate toxicity?

A

congestion, brown/chocolate blood

252
Q

What samples are taken for chemical analysis of nitrate and nitrate toxicity?

A

forage, hay, water for nitrate

ocular fluid if died for a few hours for nitrate

serum, plasma, urine, rumen contents for nitrate if alive

253
Q

How do you diagnose nitrate/nitrite toxicity?

A

diphenylamine indicate >5,000ppm - not a final test, also look for methemoglobinemia

254
Q

How do you treat methemoglobinemia?

A

methylene blue 1% IV (but NOT cats) changes methemoglobin back to hemoglobin

255
Q

How do you treat nitrate/nitrite toxicity?

A

methylene blue 1%, activated charcoal, ruminal lavage, oral antibiotics

256
Q

What are the cyanogenic plants?

A

wild choke cherry (prunus), sudan grass, johnson grass, sorghums

257
Q

What is the most common cause of cyanide poisoning?

A

large animals eating plants containing cyanide

258
Q

What are the causes of cyanide toxicity?

A

gas as a rodenticide, fertilizers, plants

259
Q

In cyanide poisoning, what is the most toxic part of the plant?

A

the seeds

260
Q

What is the characteristic odor of cyanide?

A

bitter almond of ammoniacal

261
Q

What does the cyanide radical bind with to form complexes?

A

ferric ion, cupric and molybdenum

262
Q

What species are more susceptible to cyanide toxicity?

A

ruminants > horses and swine and sheep

263
Q

What releases cyanine in plants?

A

stress, plant damage

264
Q

Where are cyanogenic glycosides concentrated in plants?

A

most in seeds, leaves, bark, stems, fruit

265
Q

What age of plant has more glycoside?

A

young and growing

266
Q

What type of soil increases glycoside?

A

high nitrogen, low phosphorus

267
Q

How is HCN absorbed?

A

from GI, inhalation or intact skin and distributed throughout body

268
Q

How is HCN excreted?

A

in urine or expired air (can measure HCN in urine)

269
Q

What is the MOA of acute cyanide toxicity?

A

excess CN in blood binds ferric acid blocking electron transport, inhibiting cells to use O2 > anoxia in brain

270
Q

What effects does cyanide have on the body?

A

metabolic acidosis, inhibits CAC, prominent vasoconstrictor, neuronal damage, irritation

271
Q

What is the MOA of chronic cyanide toxicity?

A

neuronal degeneration and demyelination of spinal cord and brain

272
Q

What are the clinical signs of acute cyanide poisoning?

A

nausea, vomiting, colic, diarrhea, seizures, muscle tremors, cyanosis, tachypnea,

273
Q

How soon do animals die after clinical signs of cyanide toxicity?

A

4-5mins

274
Q

What are the clinical signs of chronic cyanide poisoning?

A

paralysis, neuronal degeneration, incontinance, cystitis, wobbly gate, muscular weakness

275
Q

What lesions are seen in cyanide toxicity?

A

MM bright red, cherry red blood, clots very slowly or not at all, petechial hemorrhages, plant in rumen, smell of cyanide

276
Q

How can you detect cyanide?

A

must FREEZE sample (leaves quickly) brain is best, heart, blood, rumen contents – also see elevated thiocyanate levels in urine, lactic acidosis and increased AG, sodium picrate paper test

277
Q

What preserves cyanide in ruminal contents?

A

1-3% solution of mercuric chloride

278
Q

What confirms diagnosis of cyanide toxicity?

A

chemical analysis

279
Q

What is the treatment for cyanide toxicity?

A

sodium nitrite 20% IV - improves perfusion by vasodilation, sodium thiosulfate, oxygen, vinegar, mineral oil

280
Q

What plants contain soluble oxalate?

A

halogeton, sarcobatus, amarantus, chenopodium, oxalis, rumex

281
Q

Besides plants, what else is soluble oxalate in?

A

rust remover, bleach, tanning solution, fungi, ethylene glycol

282
Q

What species are most susceptible to soluble oxalate?

A

sheep and cattle (but microflora in rumen can detoxify oxalates to carbonates and bicarbonates)

283
Q

Which part of the plant is highest in soluble oxalate?

A

leaves, then seeds, then stems

284
Q

What can decrease toxicity of soluble oxalates?

A

food in rumen, calcium, absence of fungi

285
Q

What is the MOA of soluble oxalate toxicity?

A

SO combine w calcium > insoluble ca oxalate > hypocalcemia > crystals in tubules

286
Q

What are the clinical signs of soluble oxalate toxicity?

A

onset a few hours of colic, depression, muscle twitch, rapid breathing, coma, death, oligouria, hyperkalemia, cardiac failure

287
Q

What occurs in animals that survive acute sodium oxalate toxicity?

A

chronic tubular nephrosis and polyuria

288
Q

What lesions are seen in soluble oxalate toxicity?

A

presence in rumen, excess fluid in abdomen and thorax, emphysema, blood tinged froth in mouth and esophagus, kidneys show dark red cortex and medulla

289
Q

What is the laboratory diagnosis for soluble oxalate toxicity?

A

presence of Ca oxalate crystals in kidney tubules, hypocalcemia, high BUN

290
Q

How do you treat soluble oxalate toxicity?

A

activated charcoal of lime water, calcium gluconate IV, saline glucose, supplement calcium salts, supportive therapy for nephrosis (usually of little values once clinical signs seen)

291
Q

Where does lead come from?

A

paint, bullets, gas etc. being phased out - contaminated pastures,

292
Q

How is lead absorbed?

A

not easily metabolized, nay 1-2 absorbed from GIT, normally forms insoluble compounds - dermal absorption is poor, inhalation is good

293
Q

What pH conditions favor dissolution of lead?

A

acid conditions

294
Q

What species are most susceptible to lead toxicity?

A

cattle, horses, pets, waterfowl, birds

295
Q

What species are more resilient to lead toxicity?

A

goats, swine, chicken

296
Q

What age of animal are more susceptible to led toxicsis?

A

younger because of more sensitive and greater absorption and immature BBB

297
Q

What other compounds decrease absorption of lead?

A

calcium, zinc, protein

298
Q

Does lead cross the BBB?

A

yes, more in younger animals, and placenta

299
Q

How long does lead stay in soft tissues?

A

4-6 weeks then stored in bone and stays for several years

300
Q

How is lead excreted?

A

urine, bile, milk at toxic levels

301
Q

What are the target tissues of lead toxicity?

A

CNS, GIT and blood

302
Q

What is the MOA in lead toxicosis?

A

replace zinc in some enzymes, interferes with GABA in CNS, competes with calcium ions and alters Ca movement across membranes

303
Q

What is the time frame for the onset of clinical signs in lead toxicity?

A

hours,days,weeks or months depending on amount and species

304
Q

What are the clinical signs of lead toxicity?

A

anorexia, salvation, vomiting, diarrhea, pharyngeal paralysis, CNS paralysis, anemia

305
Q

What microscopic lesions are seen in lead toxicity?

A

cerebral cortical necrosis and poliomalacia in cattle, acid fast eosinophilc intranuclear inclusion bodies in renal tubular epithelium or hepatocytes

306
Q

What is the antimortem specimen of choice in lead toxicity?

A

whole blood, liver, kidney and GI

307
Q

What is seen on the bloodwork in lead toxicity?

A

increased nRBCs, basophilic stippling of erythrocytes, increased zinc protoporphyrin, florescence of plasma porphyrins under UV light

308
Q

How do you treat lead toxicity?

A

fluid therapy, was hsurface, remove lead from gut BEFORE chelation

309
Q

What is avoided in the treatment of lead toxicity?

A

activated charcoal not recv (doesn’t bind) sulfate/mg cathartics may bind with lead to form lead sulfate

310
Q

What is the chelating agent of choice for lead?

A

calcium disodium EDTA, but only for 5 days due to kidney damage, after break can use again

311
Q

What can be given with chelation in lead toxicity?

A

dimercaprol prior to EDTA to improve the effect, D penicillamine, dimercaptosuccunuc acid

312
Q

What is used for supportive treatment in lead toxicity?

A

thiamine, taurine, glucocorticoids, mannitol, zinc, barbituates, fluids

313
Q

What are the sources of zinc?

A

galvanized containers, wire, nuts, batteries, jewlery, pennies, ointments

314
Q

How many pennies can cause subacute toxicity in dogs?

A

5 pennies

315
Q

What pH environment increases zinc release and absorption?

A

acidic

316
Q

What decreases GI absorption of zinc?

A

Ca, Cu, Fe, phytate, fiber - competition for absorption sutes

317
Q

What organs does zinc accumulate in?

A

pancreas, liver, kidney, spleen

318
Q

How is zinc excreted?

A

feces, bile, saliva, sweat, urine

319
Q

What is the MOA of zinc?

A

GI irritant, interferes with enzymes, direct damage to cell membranes, interferes with absorption of copper and iron, hemolytic anemia

320
Q

What are the main organs affected in zinc toxicity?

A

RBC, liver, kidney, pancreas

321
Q

What are the clinical signs of zinc toxicity?

A

GI upset, hemolytic anemia, icterus, hemoglobinuria, azotemia, hyperphosphatemia, decreased milk production, lameness

322
Q

What lesions are seen in zinc toxicity?

A

gastric ulcers, liver damage, renal casts

323
Q

What tube is used for chemical analysis of zinc toxicity?

A

dark blue top - use serum, liver, kidney, pancreas, urine

324
Q

How do you treat zinc toxicity?

A

remove foreign body, cathartics, supportive care

325
Q

What is the chelating agent for zinc toxicity?

A

calcium disodium EDTA or D-penicillamine

326
Q

What are the sources of iron?

A

supplements, snail baits, hand warmers, fertilizers

327
Q

Which types of iron are more irritant?

A

organic < inorganic

ferrous < ferric

328
Q

Which type of iron is more toxic, parenteral or oral?

A

parenteral > oral

329
Q

What happens when iron is absorbed?

A

absorbed ferrous iron > ferric > binds to transferrin in plasma, distributed throughout body

330
Q

What factor is important for toxicosis of iron?

A

going over carrying capacity

331
Q

What does free iron cause?

A

saturation of transferrin resulting in free circulating iron

332
Q

Hoe does excretion of iron change during toxicosis?

A

it doesn’t! = problem

333
Q

What effect does free iron have in the body?

A

direct cellular damage to GIT, liver, cardiovascular system

334
Q

Where does circulating free iron accumulate?

A

in liver, causes mitochondrial damage and liver damage, systemic acidosis and shock

335
Q

What is the MOA of iron toxicity?

A

circulating free iron > free radical lipid per oxidation > damage to membranes > increased vascular permeability > coagulopathy, vasodilation, shock

336
Q

What are the clinical signs of per acute iron toxicosis?

A

anaphylactic reaction, shock, death within minutes

337
Q

What are the clinical signs of acute iron toxicosis?

A

depression, shock, acidosis, death within hours

338
Q

What are the stages to iron toxicosis?

A

1- GI upset
2 - apparent recovery
3- most serious, coagulation disorders, hepatic failure
4 - GI obstruction with fibrosing repair of GI

339
Q

What are the lesions noted in iron toxicity?

A

yellow/broen discoloration at LN, GI ulcers, congestion of liver and kidney

340
Q

What is seen on chemical analysis of iron toxicity?

A

no hemolysis, increased saturation of total iron binding capacity

341
Q

How do you treat iron toxicity?

A

decontaminate GI w/i 4hours of ingestion, supportive treatment, (activated charcoal doesn’t work)

342
Q

What precipitates iron?

A

milk of magnesia

343
Q

What is the specific chelator for iron?

A

desferoxamine

344
Q

What is ethylene glycol found in?

A

antifreeze, coolant, windshield de-ice

345
Q

How is ethylene glycol absorbed?

A

in GI, distributed to all tissues, metabolized to toxic metabolites in liver

346
Q

How is ethylene glycol metabolized?

A

oxidized by alcohol dehydrogenase > glycoaldehyde > glycol acid > glycoxylic acid > oxalic acid, glycine, formic acid, hippuric acid, benzoic acid

347
Q

What happens to oxalic acid in the body?

A

binds to serum calcium to form insoluble calcium oxalate crystals and hypocalcemia

348
Q

What is the MOA of ethylene glycol itself?

A

direct GI irritaion, increased serum osmolality, CNS depression

349
Q

What is the MOA of toxic metabolites of ethylene glycol?

A

metabolic acidosis and acute renal failure, CNS damage and failure, cerebral edema

350
Q

What are the clinical signs of ethylene glycol toxicity?

A

nausea, vomiting, CNS depression, PU/PD, dehydration, renal failure, lethargy, renal pain, oliguria, coma, death

351
Q

What lesions are seen with ethylene glycol toxicity?

A

hemorrhagic gastroenteritis, pulmonary edema, pale swollen kidneys

352
Q

What is seen on the lab work in ethylene toxicity?

A

increased serum osmolality, increased anion gap, low USG, low blood pH, hypocalcemia, hyperglycemia, azotemia, increased PCV and TP, crystals in urine, serum glycol acid

Toxicology (4 decks)

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