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Preeti: Toxicology > Exam II: Organic Synthetic Herbicides, Fungicides, Feed/Water Toxicants, Metals and Minerals > Flashcards

Exam II: Organic Synthetic Herbicides, Fungicides, Feed/Water Toxicants, Metals and Minerals Flashcards

1
Q

Which species is most sensitive to the toxic effects of

phenoxy acids?

A

Dogs

(acute oral LD50 = 100 mg/kg)

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2
Q

_________ of urine enhances renal excretion

of phenoxy acids

A

Alkalization

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3
Q

Rumen stasis with ingested food

is a characteristic finding of toxicosis by this agent

A

Phenoxy acids

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4
Q

You have a farm with cows and pigs. You also have farm dogs that roam about.

All of a sudden, you notice that all of your animals

have diarrhea and are showing signs of muscle weakness

(the dog is mainly ataxic on the hindlimbs).

The dog’s diarrhea is bloody and both the dogs and the pigs are vomiting.

The cow has some ulcers in its mouth. Despite all of these neuro signs,

none of the animals are convulsing.

Elevated AP, LDH, and CPK are reported in blood samples.

What is your primary ddx?

A

Phenoxy acid toxicosis

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5
Q

This agent alters the metabolism of plants which increases

their toxicity by increasing accumulation of either nitrite or cyanide

A

phenoxy acids

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6
Q

The main mechanism for metabolism of phenoxy acids is

A

Hydrolysis

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7
Q

Paraquat and Diquat are __________ herbicides

A

Dipyridyl

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8
Q

T/F: Solutions of Dipyridyl herbicides are destroyed in acidic conditions

A

FALSE!

They are destroyed in ALKALINE conditions

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9
Q

What are 3 ways that Paraquat (dipyridyl) toxicity can be enhanced

A

Selenium/Vit E deficiency

Depletion of tissue Glutathione

Oxygen therapy

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10
Q

The toxicity of which agent can be increased by

supplementing oxygen

A

Paraquat (dipyridyl) herbicide

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11
Q

Paraquat binds strongly to ______

A

soil

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12
Q

T/F: Paraquat (dipyridly) herbicides are best absorbed via GIT and skin

A

FALSE!

Paraquat is poorly absorbed through GIT and skin!

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13
Q

This agent achieves highest concentration in the lungs, an

astonishing 10X the concentration of the rest of the body

A

Paraquat (dipyridyl)

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14
Q

The respiratory signs seen in subacute/chronic toxicosis

by Paraquat are due to ______________ and include:

Dyspnea, Tachypnea

Harsh respiratory sounds

Cyanosis

Reduced pulmonary compliance

A

progressive pulmonary fibrosis

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15
Q

At a puppy mill, several dogs present with dyspnea and tachypnea.

Some are cyanotic, and some are having seizures. A couple have ulcers on their

tongues. After treating one dog with fluids and oxygen, it died

and upon necropsy, you find significant

pulmonary congestion and hemorrhagic edema of the lungs.

The liver, kidneys, and spleen are all congested and enlarged.

What is your primary ddx?

A

PARAQUAT (Dipyridyl)

Oxygen therapy is CONTRAINDICATED…

you should not have given that dog oxygen!

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16
Q

T/F: Dermal exposure to the fungicide pentachlorophenol is the most

toxic route of exposure

A

TRUE

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17
Q

This agent can give off toxic vapors in toxic concentrations,

especially at high ambient temperatures

A

Pentachlorophenol (Fungicide)

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18
Q

Why is Pentachlorophenol (Fungicide)

not persistent in water, sewage, or soil?

A

Due to bacterial decomposition

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19
Q

Hyperthyroidism is a factor that can increase toxicity of this agent

A

Pentachlorophenol (Fungicide)

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20
Q

T/F: Antithyroid drugs can decrease toxicity of Paraquat

A

FALSE! Antithyroid drugs can decrease toxicity of

Pentachlorophenol (Fungicide)!

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21
Q

How is Pentachlorophenol (Fungicide) metabolized?

A

Via conjugation to glucoronic acid

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22
Q

In the hottest part of the summer, you decide to tear down an old barn on your property by the cow field in order to make room for the new “milkatorium”.

The next morning, you wake up to a HORRIFYING scene.

Some of your cows are dead, many of the others are in

respiratory distress and are overheated (have a fever).

You observe one cow die and rapidly go into rigor mortis.

You decide to draw blood and notice it is extremely dark in color.

What is your primary ddx?

A

Pentachlorophenol (Fungicide)

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23
Q

In the hottest part of the summer, you decide to tear down an old barn on your property by the cow field in order to make room for the new “milkatorium”.

The next morning, you wake up to a HORRIFYING scene.

Some of your cows are dead, many of the others are in

respiratory distress and are overheated (have a fever).

You observe one cow die and rapidly go into rigor mortis.

You decide to draw blood and notice it is extremely dark in color.

You rule out Nitrite toxicosis…Why?

A

Nitrite toxicosis also causes brown (dark) blood,

but there is no hyperthermia seen with nitrite toxicosis

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24
Q

Hyperkeratosis of the skin and

villous-like hyperplasia of the urinary bladder mucosa

are clinical signs associated with chronic toxicosis via this agent

A

Pentachlorophenol (fungicide)

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25
Q

T/F:

Urea is very acidic

A

FALSE!

Urea is BASIC

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26
Q

The species most susceptible to urea toxicosis

A

Ruminants

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27
Q

What is the most toxic of all non-protein nitrogen compounds?

A

Urea

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28
Q

Which is most sensitive to urea toxicosis?

3 year old bull

9 month old calf

3 week old calf

A

9 month old calf!

Very young ruminants are TOLERANT to urea toxicosis!

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29
Q

Toxicity of urea can be increased by urease.

What is an example of a feed rich in urease?

A

Soybeans

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30
Q

What is the normal rumen pH of ruminants?

A

5.0 - 6.5

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31
Q

T/F:

At an increased urine pH (due to ingestion of excess urea),

ammonia is in the ionized form and is absorbed

A

FALSE

Ammonia is in the NON-IONIZED form and is absorbed

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32
Q

T/F:

In urea toxicosis, non-ionized ammonia cross the BBB and placental barrier

A

TRUE

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33
Q

Urea ________ the pH of the rumen

causing ammonia to exist in its non-ionized form

which can then be absorbed into circulation

A

increases

(more basic)

34
Q

In urea toxicosis,

the rumen pH is ________

while systemic pH is ________

A

In urea toxicosis,

rumen pH is increased

while systemic pH is decreased

(systemic acidosis via ammonia!)

35
Q

What 3 fluids can ammonia be found in for

lab dx of urea toxicosis?

A

Whole blood

Rumen fluid

Vitreous fluid

36
Q

A farmer puts his herd of cows on a new feed supplement.

No more than 2 hours later, the cows are acting crazy!

Some are being aggressive, salivating, and grinding their teeth, while

others are in sternal recumbency while standing on their hind limbs!

One is convulsing and one has died. The dead cow is extremely bloated.

Despite all of this, there is no sign of diarrhea, and the newborn calves

seem unaffected.

What is your primary ddx?

A

Urea Toxicosis

37
Q

Which is the most common ionophore?

A

Monensin

38
Q

Which species is most sensitive to the toxic effects of ionophores?

A

Horses!

39
Q

This agent is absorbed 50% in ruminants

and 100% in monogastrics

A

Monensin (Ionophore)

40
Q

This agent does NOT accumulate in tissues when given in

HIGH doses

A

Monensin (Ionophore)

41
Q

How is monensin (ionophore) metabolized?

A

Rapidly by P-450 oxidative demethylation enyzymes in the liver

(Which is why HORSES are most sensitive…they have the

lowest oxidative demethylases of all the animals!)

42
Q

The main targest of monensin (ionophore) are

A

The mitochondria of highly energetic tissues:

Myocardium

Skeletal mm.

Kidney

Neurons

Smooth mm.

43
Q

Skeletal and cardiac muscle lesions are one of the most

important clinical signs associated with toxicosis by this agent

A

Monensin (ionophore)

44
Q

The best sample to send to a lab if ionophore (monensin) toxicity is suspected

is

A

Sample of the FEED!

45
Q

What abnormalities do you expect to see on blood work/biochem

of an animal with monensin (ionophore) toxicosis?

A

Elevated CPK, AST, LDH and ALP

Decreased serum Ca and K (first 12 hours)

Increased PCV

NO change in Na!

46
Q

What are the normal Na levels in the plasma and CSF?

A
  1. Plasma = 135 – 145 mEq/L
  2. CSF = 130 – 140 mEq/L
47
Q

Eosinophilic meningoencephalitis is pathognomonic for this

toxicity in PIGS

A

Water deprivation/sodium toxicosis

48
Q

On a dairy farm in the cold of winter in Wisconsin, cows in a field

present with circling and head-pressing, intermittent convulsive seizures,

blindness, deafness, and metabolic acidosis.

Upon necropsy of a dead cow, gastric inflammation and pinpoint ulcers

are seen, along with prominent cerebral edema.

What is your primary ddx?

A

Water deprivation/sodium ion toxicosis

49
Q

On a dairy farm in the cold of winter in Wisconsin, cows in a field

present with circling and head-pressing, intermittent convulsive seizures,

blindness, deafness, and metabolic acidosis.

Upon necropsy of a dead cow, gastric inflammation and pinpoint ulcers

are seen, along with prominent cerebral edema.

How would you treat these animals?

A

Small amounts of fresh water GRADUALLY over 2 – 3 days

(large amounts of water aggravate cerebral edema and can cause death)

This is water deprivation/sodium ion toxicosis

50
Q

What is the most toxic oxidative state of inorganic arsenic?

A

Trivalent (Arsenite)

51
Q

Which species is the most susceptible to inorganic arsenic toxicosis?

A

Herbivores

52
Q

Which entity is the most sensitive to damage

by the toxic effects of inorganic arsenic toxicosis?

A

Capillary endothelial cells

53
Q

Several cows in Farmer Ben’s herd present with the following:

Salivation, staggering, and depression.

A few have hemorrhagic diarrhea and mucosal shreds are seen in the diarrhea too.

Some of the cows seem to be paralyzed (just their hind limbs).

Microscopic evaluation shows capillary degeneration.

What is your primary ddx?

A

Inorganic arsenic toxicosis

54
Q

How is inorganic arsenic toxicosis treated?

(other than emeergency and supportive treatement and decontamination)

A

Demulcents (to coat gastric mucosa) and CHELATION therapy

(Kaolin-pectate is the demulcent of choice)

(Dimercaprol is the chelator of choice!)

55
Q

What are the 2 main purposes for organic arsenic

as a feed additive?

A

To improve weight gain and

control enteric infections in swine and poultry

56
Q

What type of organic arsenic is used to control enteric infections

in pigs? In poultry?

A
  1. Arsanilic acid – swine
  2. Roxarsone – poultry
57
Q

Toxicity of organic arsenic is enhanced by what 2 mechanisms?

A

Dehydration/Water deprivation

Renal insufficiency

58
Q

What is the MOA of organic arsenic?

A

Peripheral nerve demyelination and axonal damage

59
Q

Blindness is a clinical sign seen with this organic arsenic agent

A

Only with Arsanilic acid

(not Roxarsone)

60
Q

The following clinical signs are caused by ________.

Erythema in light-skinned pigs

Muscle atrophy

Microscopically, peripheral and optic nerves

degeneration, demyelination, & gliosis

A

ORGANIC arsenic toxicosis

61
Q

What are the 3 sources of copper toxicosis (chronic) in sheep?

A

Excess copper

Molybdenum deficiency

Sulfate deficiency

62
Q

Normally, molybdate (MoO42‐) binds to copper (Cu2+) in tissues

At a ratio of ____:____

To form copper molybdate (CuMoO4) that is readily excreted in urine

A

4:3

molybdate:copper

63
Q

What is the normal copper to molybdenum ratio?

A

Normal copper:molybdenum ratio = 6:1

64
Q

Accumulation of copper in the liver is due to imbalances between

A

copper, molybdenum, and sulfate

65
Q

Copper oxidizes hemoglobin in blood resulting in

A

Methemoglobinemia

66
Q

A sheep presents at necropsy. The cause of death is unknown.

The only history we have is that the sheep was transported from one farm to another recently. The findings from the necropsy are as follows:

Kidneys- enlarged, hemorrhagic, bluish-dark, friable

Spleen- blackish in color and enlarged

Liver- Enlarged, yellow, and friable

What is your primary ddx?

A

Copper toxicosis precipitated by the stress of being transported!

GUNMETAL KIDNEYS

and

BLACKBERRY JAM SPLEEN

67
Q

Sudden onset of hemoglobinuria, jaundice, and signs of shock and respiratory insufficiency in a sheep

is most likely caused by

A

Cooper toxicosis!

68
Q

Ammonium tetrathiomolybate and

D‐penicillamine can be used to treat and prevent

A

Copper toxicosis in sheep

69
Q

What breed of dog is most susceptible to chronic copper toxicosis

due to an autosomal recessive disorder at 2 - 6 years old?

A

Bedlington Terriers

70
Q

Elevated molybdenum can cause ________ deficiency

A

copper

71
Q

What species is most susceptible to molybdenum toxicosis?

A

Cattle

72
Q

In molybdenum toxocosis

High levels of dietary sulfate_______ toxicity

High levels of dietary copper _______ toxicity

A

High levels of dietary sulfate increases toxicity

Dietary copper decreases toxicity

73
Q

The following clinical signs result from _______ toxicosis:

Severe diarrhea (Greenish, with fluids and gas bubbles)

Rough hair coat and depigmentation (Achromotrichia), especially around the eyes (“spectacled” appearance)

Loss of weight, anemia

Osteoporosis and Lameness

Pica

Decreased libido in bulls

Infertility in cows

A

MOLYBDENUM toxicosis!

74
Q

The 6 Selenium deficiency diseases include:

A

White muscle disease (lambs)

Nutritional muscle dystrophy (lambs)

Hepatosis dietica (young pigs)

Exudative diathesis (chicks)

Nutritional pancreatic atrophy (chickens)

Porcine Stress Syndrome

75
Q

What are the 4 genus of plants that are considered seleniferous obligate accumulators?

A
  • Astralagus* (locoweed, milk vetch)
  • Stanleya* (prince’s plume)
  • Oonopsis* (golden wood)
  • Xylorrhiza* (woody aster)
76
Q

What are the 3 genus of plants that are considered seleniferous facultative accumulators?

A
  • Aster*
  • Atriplex* (saltbush)
  • Castilleja* (paintbrush)
77
Q

_________ acts as antioxidant by prevention of peroxide accumulation through reduction of glutathione

A

Selenium

78
Q

What is the most toxic form of selenium?

A

Organic selenium in plants

79
Q

T/F: Selenium is teratogenic and is excreted in milk

A

TRUE

80
Q
A

Preeti: Toxicology (6 decks)

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