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
T/F: Urea is very acidic
FALSE! Urea is BASIC
26
The species most susceptible to urea toxicosis
Ruminants
27
What is the most toxic of all non-protein nitrogen compounds?
Urea
28
Which is most sensitive to urea toxicosis? 3 year old bull 9 month old calf 3 week old calf
9 month old calf! Very young ruminants are TOLERANT to urea toxicosis!
29
Toxicity of urea can be increased by urease. What is an example of a feed rich in urease?
Soybeans
30
What is the normal rumen pH of ruminants?
5.0 - 6.5
31
T/F: At an increased urine pH (due to ingestion of excess urea), ammonia is in the ionized form and is absorbed
FALSE Ammonia is in the NON-IONIZED form and is absorbed
32
T/F: In urea toxicosis, non-ionized ammonia cross the BBB and placental barrier
TRUE
33
Urea ________ the pH of the rumen causing ammonia to exist in its non-ionized form which can then be absorbed into circulation
_increases_ | (more basic)
34
In urea toxicosis, the rumen pH is \_\_\_\_\_\_\_\_ while systemic pH is \_\_\_\_\_\_\_\_
In urea toxicosis, rumen pH is _increased_ while systemic pH is _decreased_ (systemic acidosis via ammonia!)
35
What 3 fluids can ammonia be found in for lab dx of urea toxicosis?
Whole blood Rumen fluid Vitreous fluid
36
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?_**
Urea Toxicosis
37
Which is the most common ionophore?
Monensin
38
Which species is most sensitive to the toxic effects of ionophores?
Horses!
39
This agent is absorbed 50% in ruminants and 100% in monogastrics
Monensin (Ionophore)
40
This agent does NOT accumulate in tissues when given in HIGH doses
Monensin (Ionophore)
41
How is monensin (ionophore) metabolized?
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
The main targest of monensin (ionophore) are
The mitochondria of highly energetic tissues: Myocardium Skeletal mm. Kidney Neurons Smooth mm.
43
Skeletal and cardiac muscle lesions are one of the most important clinical signs associated with toxicosis by this agent
Monensin (ionophore)
44
The best sample to send to a lab if ionophore (monensin) toxicity is suspected is
Sample of the FEED!
45
What abnormalities do you expect to see on blood work/biochem of an animal with monensin (ionophore) toxicosis?
Elevated CPK, AST, LDH and ALP Decreased serum Ca and K (first 12 hours) Increased PCV NO change in Na!
46
What are the normal Na levels in the plasma and CSF?
1. Plasma = 135 – 145 mEq/L 2. CSF = 130 – 140 mEq/L
47
Eosinophilic meningoencephalitis is pathognomonic for this toxicity in PIGS
Water deprivation/sodium toxicosis
48
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?_**
Water deprivation/sodium ion toxicosis
49
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?_**
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
What is the most toxic oxidative state of inorganic arsenic?
Trivalent (Arsenite)
51
Which species is the most susceptible to inorganic arsenic toxicosis?
Herbivores
52
Which entity is the most sensitive to damage by the toxic effects of inorganic arsenic toxicosis?
Capillary endothelial cells
53
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?
Inorganic arsenic toxicosis
54
How is inorganic arsenic toxicosis treated? (other than emeergency and supportive treatement and decontamination)
Demulcents (to coat gastric mucosa) and CHELATION therapy (**Kaolin-pectate** is the demulcent of choice) (**Dimercaprol** is the chelator of choice!)
55
What are the 2 main purposes for organic arsenic as a feed additive?
To improve weight gain and control enteric infections in swine and poultry
56
What type of organic arsenic is used to control enteric infections in pigs? In poultry?
1. Arsanilic acid – swine 2. Roxarsone – poultry
57
Toxicity of organic arsenic is enhanced by what 2 mechanisms?
Dehydration/Water deprivation Renal insufficiency
58
What is the MOA of organic arsenic?
Peripheral nerve demyelination and axonal damage
59
Blindness is a clinical sign seen with this organic arsenic agent
Only with **Arsanilic acid** (not Roxarsone)
60
The following clinical signs are caused by \_\_\_\_\_\_\_\_. Erythema in light-skinned pigs Muscle atrophy Microscopically, peripheral and optic nerves degeneration, demyelination, & gliosis
ORGANIC arsenic toxicosis
61
What are the 3 sources of copper toxicosis (chronic) in sheep?
Excess copper Molybdenum deficiency Sulfate deficiency
62
Normally, **molybdate** (MoO42‐) binds to **copper** (Cu2+) in tissues At a ratio of \_\_\_\_:\_\_\_\_ To form copper molybdate (CuMoO4) that is readily excreted in urine
**4:3** **molybdate:copper**
63
What is the normal copper to molybdenum ratio?
Normal copper:molybdenum ratio = **6:1**
64
Accumulation of copper in the liver is due to imbalances between
copper, molybdenum, and sulfate
65
Copper oxidizes hemoglobin in blood resulting in
Methemoglobinemia
66
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?_**
Copper toxicosis precipitated by the stress of being transported! GUNMETAL KIDNEYS and BLACKBERRY JAM SPLEEN
67
Sudden onset of hemoglobinuria, jaundice, and signs of shock and respiratory insufficiency in a sheep is most likely caused by
Cooper toxicosis!
68
Ammonium tetrathiomolybate and D‐penicillamine can be used to treat and prevent
Copper toxicosis in sheep
69
What breed of dog is most susceptible to chronic copper toxicosis due to an autosomal recessive disorder at 2 - 6 years old?
Bedlington Terriers
70
Elevated molybdenum can cause ________ deficiency
copper
71
What species is most susceptible to molybdenum toxicosis?
Cattle
72
In molybdenum toxocosis High levels of dietary sulfate\_\_\_\_\_\_\_ toxicity High levels of dietary copper *\_\_\_\_\_\_\_* toxicity
High levels of dietary sulfate *increases* toxicity Dietary copper *decreases* toxicity
73
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
MOLYBDENUM toxicosis!
74
The 6 Selenium deficiency diseases include:
White muscle disease (lambs) Nutritional muscle dystrophy (lambs) Hepatosis dietica (young pigs) Exudative diathesis (chicks) Nutritional pancreatic atrophy (chickens) Porcine Stress Syndrome
75
What are the 4 genus of plants that are considered seleniferous **obligate** accumulators?
* Astralagus* (locoweed, milk vetch) * Stanleya* (prince's plume) * Oonopsis* (golden wood) * Xylorrhiza* (woody aster)
76
What are the 3 genus of plants that are considered seleniferous **facultative** accumulators?
* Aster* * Atriplex* (saltbush) * Castilleja* (paintbrush)
77
\_\_\_\_\_\_\_\_\_ acts as antioxidant by prevention of peroxide accumulation through reduction of glutathione
Selenium
78
What is the most toxic form of selenium?
Organic selenium in plants
79
T/F: Selenium is teratogenic and is excreted in milk
TRUE
80