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Veterinary Toxicology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

How much copper do pennies made before 1983 have? What about after 1983?

A

90% and after 1983, they were mostly made of zinc.

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2
Q

What are the main sources of copper in food animals? What about small animals and exotics?

A

Feed and mineral mixes designed for cattle, poultry and swine….the sheep eat this and then get sick. In small animals, the main source is coins.

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3
Q

What are the gross pathological findings in an animal with copper toxicity?

A

Kidney: Acute, severe tubular nephrosis with hemoglobin casts due to intravascular hemolysis.
Liver: Acute, severe hepatocellular necrosis

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4
Q

Are chronic or acute exposures to copper more common? What is the route of exposure?

A

Chronic

Oral

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5
Q

What disease is associated with copper toxicity that has nothing to do with excessive amounts of copper?

A

Autosomal recessive copper storage disease

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6
Q

What will bind to copper, slow down its absorption and enhance its excretion in the bile?

A

Molybdenum and sulfur

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7
Q

What ratio of copper in the diet can lead to chronic problems with toxicity?

A

6-10:1

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8
Q

If there is a group of sheep exhibiting copper toxicity signs, the source of the toxicity is likely to be ________. If it is a single animal,, it is likely to be ________.

A

Primary

Secondary

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9
Q

Where is excess copper stored and excreted?

A

In the lysosomes and mitochondria of the liver. It is excreted in the bile bound to Mo and S.

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10
Q

What triggers copper to be released from the liver and what can it cause?

A

Stress stimulates the hepatoceullular cells to excrete copper which causes necrosis and elevated serum Cu leading to hemolysis (intra and extra)

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11
Q

If a group of sheep are experiencing copper toxicosis, when will the clinical signs show up?

A

They will show up abruptly and sporadically with nonspecific production losses occurring before severe signs

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12
Q

In small animals, how do the clinical signs typically show up for copper toxicity?

A

Chronic exposure with repeated bouts of hepatitis is most common to see. The acute condition is rare.

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13
Q

After running diagnostics on an animal with suspected copper toxicity, what will you see?

A
  1. Increased serum levels of GGT and AST
  2. Anemia due to hemolysis
  3. Hemoglobinemia/uria
  4. Hyperbilirubinemia/uria
  5. Methemoglobinema
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14
Q

On necropsy, you notice the liver is pale and enlarged, there is an distended gallbladder, and there is icteric, gun metal kidneys…this is a sheep. What toxin do you suspect?

A

Copper

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15
Q

What would you see on histopathy with copper toxicity?

A

Liver: Hepatic necrosis with varying patterns, pigment accumulation within kupffer cells, and sometimes won’t see any lesions if it is a chronic production case in large animals.
Kidney: Acute degeneration and necrosis with cast formation

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16
Q

Would collecting copper serum level help you out when trying to diagnose copper toxicity? Why/why not?

A

NO, copper accumulates in the liver, so it better to do a biopsy and histopath to asses copper concentration in the liver

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17
Q

What are the main components of an animals body that are adversely affected by copper toxicosis?

A
  1. GIT
  2. Liver
  3. RBC
  4. Kidney
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18
Q

How would you treat a small animal that is clinically affected by copper toxicity?

A
  1. Give liver protectants for a few weeks
  2. Corticosteroids
  3. Analgestics
  4. Give them a Mo-S sources
  5. Give them szinc
  6. Give them tetrathiomolybdate which is a chelator
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19
Q

List the most important liver protectants (6) you can give an animal?

A
  1. SAMe
  2. N-acetylcycsteine
  3. Milk Thistle
  4. Ursodiol
  5. Vitamine E
  6. Selenium
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20
Q

What is tetrathiomolybdate?

A

It is a copper chelator, very expensive but effective

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21
Q

Which breeds tend to suffer from copper storage diseases?

A

Dobermans
SKye terriers
Labradors

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22
Q

T/F: You will not see hepatocellular damage with hemolysis in a dog with a copper storage disease, but will see chronic bouts of intermittent hepatitis.

A

T

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23
Q

How would you treat a dog with a copper storage disease?

A

Zinc acetate and tridentine

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24
Q

What determines if a mycotoxin is produced (6) ?

A
  1. Mold genetics
  2. Substrate
  3. Temperature
  4. O2 concentration
  5. Mousture-huminidty
  6. Pre-existing damage to feed
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25
Q

T/F: All moldy feed contains mycotoxins and all feeds that contain mycotoxins are toxic.

A

F: Not all moldy feed contains mycotoxins and not all feeds that contain mycotoxins are toxic

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26
Q

When speaking to a client about mycotoxins, why would you never say, “ I think your herd is suffering from a mycotoxin?”

A

Mycotoxins cause distinct clinical disease, you need to be specific about which toxin you are talking about.

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27
Q

What types of aflatoxin is harmful?

A

B1 and M1

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28
Q

What is M1 alflatoxin?

A

It is the milk metabolite of B1 aflatoxin.

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29
Q

Where is aflatoxin found?

A

Corn and cottonseed aka GRAIN

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30
Q

Which species of animals are most susceptible to aflatoxin toxicity?

A

Cattle and dogs

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31
Q

How do dogs come into contact with aflatoxin?

A

Contaminated commercial dog food

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32
Q

What are the two main characteristics of aflatoxin that make it so harmful?

A
  1. Hepatotoxic (acute or chronic)

2. Carcinogenic

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33
Q

What are the main clinical signs you see with an acute alflatoxin toxicity?

A
  1. Vomiting
  2. Lethargy
  3. Anorexia
  4. Abdominal pain/weakness
  5. Icterus
  6. Petechiation/Ascites
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34
Q

If an animal presents to you with a drop in body weight, unthriftiness, drop in production, poor fertility and secondary photosensitization, is this more likely acute or chronic aflatoxin toxicity?

A

Chronic

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35
Q

You run some diagnostics on an animal with a suspected aflatoxin poisoning, what do you see?

A
  1. Increased ALT, AP and ASt
  2. Increased bile acids
  3. Hyperbilirubinemia/uria
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36
Q

How will a liver look that has been ravaged by aflatoxin?

A

Enlarged, friable, congested, ictus, OR shrunk and cirrhotic

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37
Q

How can you test feed stuff for aflatoxin?

A
  1. ELISA kits

2. Chromatography

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38
Q

How would you analyze aflatoxin in a patient?

A

Biopsy of the liver, kidney and lung

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39
Q

Why is it important to remember that there are “hot spots” in feed for aflatoxin?

A

Mold growth is not uniform, so there are hot spots throughout the feeds, so make sure you take multiple samples for different areas to have a representative sample.

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40
Q

You have a choice of sending your aflatoxin suspected feed to a lab to be tested. Do you choose a lab that sells binders along with the testing, or the lab that just tests?

A

The lab that just tests as its a conflict of interest to sell binders for the toxin you are testing for.

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41
Q

A dog comes in an you determine he is suffering from aflatoxin toxicity. How do you treat?

A
  1. Liver protectants (especially SAMe, silymarin, and ursodial)
  2. Supportive care
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42
Q

How could you remove aflatoxin from contained feed?

A

Add aluminosilicate to the feed and prevent mold growth from the very beginning

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43
Q

How does cyanobacteria grow…what does it need to get all crazy like?

A
  1. Freshwater
  2. Ubiquitous, stagnant-slowmoving water
  3. Low O2 concentration
  4. High nutrient concentration
  5. Quiet weather
  6. Warmish water temperature
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44
Q

Which are the top three nutrients that can contaminated water and cause the O2 levels to decrease?

A
  1. Nitrates
  2. Sulfates
  3. Phosphates
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45
Q

When can you see cyanobacteria and what does it look like?

A

You can see it all year round and it looks like a bloom…kinda like green paint and not slimy

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46
Q

What in the cyanobacteria can cause massive hepatic necrosis and hemorrhaging?

A
  1. Microcystin
  2. Nodularin
  3. Cylindrospermopsin
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47
Q

Which substance in cyanobacteria affects both the liver and the kidney?

A

Cylindrospermopsin

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48
Q

How soon will you see clinical signs from ingesting of blue green algae and what they they look like?

A

1-4 hours (acute onset) with vomiting, diarrhea, abdominal pain, pallor, recumbency, petechiation, edema, shock, dic and death

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49
Q

Which liver enzymes tend to be increased with a cyanobacteria toxicity?

A
  1. ALT
  2. BIle acids
  3. Bilirbinemia/uria
  4. Prolonged PT-PTT
  5. Low proteins and BUN
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50
Q

So, you think a dog is suffering from a cyanobacteria toxicity. How would you be certain they are?

A
  1. Figure out the water source and time of year it is
  2. Liver clinical signs
  3. Algal indentification from water or gastric contents
  4. Toxic analysis with kits for the water
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51
Q

Do you need to contact the department of health when you diagnose a cyanobacteria toxicity?

A

YES

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52
Q

If your patient is asymptomatic, but the you diagnose cyanobacteria toxicity, how do you treat?

A

Decontaminate and give cholestyramine

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53
Q

If give a dog liver protectants, IV fluids, coritocosteriods, and cholestyramine because they owner tells you they were swimming in a green pond earlier that day and they are showing signs of liver damage. What is going on?

A

A symptomatic cyanobacteria patient

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54
Q

How would you decontaminate an area with cyanobacteria blooms?

A

Spread Cu sulfate everywhere and/or change the underlying factors

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55
Q

Name the most common sources of iron that can potential poison an animal?

A
  1. Iron supplements
  2. Fertilizers
  3. Moss repellants
  4. Molluscicide
  5. Hand/food warmers (nonactivated)
  6. Oxygen-Moisture absorbers sachets (not activated)
  7. Birth control pills
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56
Q

Which form of iron causes poisoning?

A

The elemental form which is soluble

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57
Q

Which systems in the body will iron damage is too much is ingested?

A
  1. GIT
  2. Liver
  3. Vascular
  4. Cardiac
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58
Q

How is iron stored in the liver?

A

As ferritin/hemosiderin

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59
Q

How is iron absorbed into the body?

A

The animal eats it (oral) , the internal cells take it in, transferrin moves Fe around in the blood until it gets stored in the liver.

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60
Q

How soon will you see clinical signs in a patient that ingested too much iron? What is the first sign you will see?

A

Less than 6-8 hours

GIT issues like visiting and diarrhea

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61
Q

What clinical signs will you observe after 12-96 hours in an animal that is suffering from iron toxicity?

A

GIT
Liver ( elevated enzymes w/ dehydration)
Vascular
Cardiac

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62
Q

Where are the gross lesions seen in an animal suffering from iron toxicity?

A

Inflammation, hemorrhage and necrosis of the GIT, Liver and cardiac system

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63
Q

What are the two ways you can analytically determine if you are dealing with an iron toxicity? What can this help you determine?

A

Test the total serum Fe or the total Fe binding capacity

Helps determine is you need to chelate

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64
Q

If you take a radiograph of an animal that after a bunch of iron, what will you see?

A

You may see glomed up, radiopaque material in the GIT

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65
Q

Name the steps you would take when treating an animal with suffering from iron toxicity?

A
  1. Decontaminate aka emesis, lavage, cathartic (AC Doesn’t work well with elements)
  2. GI protectants
  3. IV fluids
  4. Liver protectants
  5. Chelate with deferoxamine
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66
Q

What can you use to chelate an animal with iron toxicity?

A

Deferoxamine

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67
Q

Name the four most important GI protectants you can give an animal?

A
  1. Sucralfate
  2. H2 antagonists
  3. Proton pump inhibitors
  4. Misoprostol
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68
Q

What is the number one thing you want to make sure an animal is receiving when they have ingested desiccant packs or oxygen moisture absorber sachets?

A

H20, they need to stay hydrated as it can make them constipated

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69
Q

Besides making sure an animal stays hydrated after eating desiccant packs, what else should you do to treat the patient?

A
  1. Induce emesis if appropriate

2. Administer a cathartic

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70
Q

What can be found in desiccant pack and oxygen moisture absorber sachets that is potentially toxic to animals?

A

Iron carbonate (50-70%)

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71
Q

How can you monitor an animal that ate a dessiccant pack to make sure they eliminate it?

A

Radiographs

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72
Q

What is the common clinical sign of an animal that eats an oxygen-moisture absorber sachet?

A

Mild GI upset

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73
Q

A dog eats a hand warmer, what is in the hand warmer that may be a problem and how to do get it out?

A

Iron!

Emesis and cathartic (milk of magnesia or bulk cathartic)…maybe some activated charcoal

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74
Q

Are non-activated or activated hand/food warmers more toxic?

A

Non activated

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75
Q

What inside birth control pills can cause problems for an animal that eats them?

A

The progesterone, especially if it is more 10mg/kg and iron

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76
Q

If a dog ate birth control pills, but the estrogen dose is less than 1mg/kg, do you need to worry?

A

NO

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77
Q

Where are the clinical signs for a animal that eats birth control pills?

A

Lethargy that resolves in 8-12 hours and GI upset. However, if the animal ingested more than 10/mg/kg, it can cause recumbency and seizures.

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78
Q

What is the main concern for animals that lick progesterone cremes off their owners?

A

Bone marrow and skin issues from chronic ingestion

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79
Q

Why is xylitol in a whole of products?

A

It is a sugar substitute that prevents fermentation and molding.

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80
Q

What contains xylitol that we have to worry about in veterinary medicine?

A

Gum, toothpaste, oral care products, baked good, candy, vitamins, and drugs.

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81
Q

What species is adversely affected by Xylitol and what are the main clinical signs?

A

Dogs

Decreased serum glucose levels, diarrhea, gas, ataxia,lethargy, seizures and liver disease

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82
Q

If xylitol is not the first sugar alcohol on the label, how much is in one piece of gum?

A

0.3g

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83
Q

If xylitol is the first sugar alcohol on the label, how much is in one piece of gum?

A

1.0g

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84
Q

How can you figure out the amount of xylitol in a product if the standard label amount isn’t right?

A

Call company or the poison control hotline

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85
Q

How does xylitol decrease glucose levels?

A

It increases insulin release

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86
Q

How long does it take for ingestion of xylitol to decrease glucose levels?

A

30-60 min

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87
Q

What comes first with xylitol poisoning…the hypoglycemia or the hepatic disease? Which causes death more frequently?

A

The hypoglycemia comes first, but the liver damage can cause death

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88
Q

When do the hepatic effects of xylitol set int and when do they peak? Why is this important to know?

A

9-12 hours and peak at 1-2 days

Need to give the patient liver protectants for at least 2-4 weeks

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89
Q

What toxin differentials cause weakness and CNS depression? ( 10)

A
  1. Ethylene glycol
  2. Propolyne glycol
  3. Di ethylene glycol
  4. Methanol
  5. Ethanol
  6. Sedatives like pentobarbital
  7. Marijuana
  8. Ivermectin
  9. Amitraz
  10. Xylitol
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90
Q

Besides hypoglycemia, what else will you see with a serum chem penal in a dog that has ingested xylitol? How long will this be apparent?

A

Hypokalemia and hypophosphatemia

Few days

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91
Q

Since xylitol cause hepatic damage, what will we see on clinical pathology?

A
  1. Elevated liver enzymes
  2. Hyperbilirubinemia
  3. Elevated bile acids
  4. Prolonged clotting times
  5. Hypocholesterolemia
  6. Hypoalbuminemia
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92
Q

Which toxins can cause hepatic necrosis on histology (8)?

A
  1. Aflatoxin
  2. Copper, zinc, and iron overdoses
  3. Mushrooms
  4. BG algae
  5. Carprofen
  6. Acetaminophen
  7. Plants
  8. Xylitol
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93
Q

Where are the 5 big causes of hypoglycemia?

A
  1. Xylitol
  2. Insulinoma
  3. Liver disease
  4. Septicemia
  5. Sitton on the clot aka letting the blood sit around before running diagnostic tests
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94
Q

If you wanted to test for xylitol analytically, what would you need?

A

The source material or stomach contents

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95
Q

What is the problem with ethylene glycol kits and xylitol?

A

Xylitol can show up as a false positive

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96
Q

If a dog is asymptomatic and ate a bunch of xylitol contains gum, how do you treat?

A

Decontaminate with emesis. lavage and a cathartic ( no AC..doesnt work)

make sure you monitor blood glucose for 12-48 hours every 2-6 hours

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97
Q

Before you send a asymptomatic xylitol eating patient home, what do you need to be sure of?

A

They dog needs to have bee euglycemic for 6 hours without supplementation

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98
Q

If a dog is exposed to more than 100-500 mg/mg of xylitol or is symptomatic, how would you treat?

A
  1. Give dextrose for 12-48 hours
  2. Administer liver protectants for 2-4 weeks
  3. Monitor c/s and clinical pathology of liver enzymes up to 72 hours and recheck at 1,2 and 4 weeks
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99
Q

If a dog presents in your clinic with persistent hyperthermia, weakness and panting, what should you think about other than heat stroke?

A

The dog may have gotten into some hops ( which can be fresh, spent or processed)

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100
Q

How would you treat a dog that ingested hops?

A

Try to decontaminate ( induce emesis) , give IV fluids, keep the dog cool, and try dantrolene.

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101
Q

What products could contain zinc phosphide?

A
  1. Rodenticide

2. Insecticide aka grain fumigant

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102
Q

What species of animal can be affected by zinc phosphide?

A

ALL

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103
Q

What routes do animals typically become poisoned by zinc phosphide?

A
  1. By ingesting bait or treated feed

2. Inhaling fumes from when water touches it

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104
Q

If you smell ammonia, rotten fish, acetylene, garlic odor, what should you do?

A

Zinc phosphide gas smells like these things so you need to get out of there fast.

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105
Q

If you inhale zinc phosphide fumes, what can occur?

A
  1. Pulmonary edema and increased RR
  2. Cardiac failure with increased HR
  3. CNS effects like ataxia, tremors, and seizures
  4. Liver failure
  5. Kidney failure
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106
Q

What is the first clinical sign you will see with a zinc phosphide oral ingestion?

A

Severe GIT pain with distension, anorexia, salivation, diarrhea, and vomiting

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107
Q

If a bunch of horses die extremely fast with few premonitory sings or lesions, what should you put on the top of your differential list?

A

Zinc phosphide

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108
Q

The stomach contents contain increased fine, phosphorus, aluminum and magnesium, what is this suggestive of?

A

Zinc phosphide poisoning

109
Q

How do you confirm diagnosis of zinc phosphide poisoning? How should you handle these samples?

A

Phosphine gas in stomach contents

Make sure you and your staff are in well ventilated areas, put the sample in an air tight container, and freeze it.

110
Q

In an asymptomatic patient who ingested zinc phosphide, how would you treat?

A

Decontaminate..aka emesis, lavage, and gives GIT protectants

111
Q

In a symptomatic patient who ingested since phosphide, how would you treat?

A
  1. Anti-emetic and follow with AC or gastric lavage
  2. GIT protectants
  3. IV fluids
  4. Lavage 5% sodium bicarbonate and antacids
112
Q

What are the five toxins that can be found in rodenticides?

A
  1. Anticoagulant rodenticides
  2. Bromethalin
    3 Cholecalciferol
  3. Strychnine
  4. Zinc phosphide
113
Q

Which plants contain arsenic?

A
  1. Helleborus
  2. Veratrum virile
  3. Epipactis
114
Q

What kind of arsenic is the most toxic?

A

Trivalent

115
Q

Which kind of arsenic is more common to encounter and what kind of clinical signs does it cause?

A

Inorganic

GIT systemic issues

116
Q

What are some sources of arsenic?

A
  1. Herbicide
  2. Old rodenticide
  3. Wood preservative (green wood )
  4. Ash
  5. Ant baits
  6. Natural element in soil and thermal hot springs
117
Q

What is the mechanism of action of arsenic in the body?

A

It is a capillary poison, so it binds oxidative enzymes that are associated with cellular respiration

118
Q

Is arsenic poisoning usually a chronic or acute issue? What are the clinical signs?

A

It is a parachute/acute/subacute.

  1. Abdominal pain
  2. Ataxia/weakness/lethargy
  3. Salivation/vomit/regurgitation/diarrhea
  4. Severe fluid loss and shock leading to acute cardiovascular collapse and death
119
Q

How would you diagnose arsenic toxicity antemortem?

A

Blood and urine, but since it has such a short 1/2 life, may be better to get a kidney biopsy as the arsenic may be gone already.

120
Q

How would you diagnose arsenic toxicity postmortem?

A

Liver, kidney and hair testing

121
Q

How would you treat an animal with arsenic poisoning?

A
  1. Treat the shock, so give lots of fluids

2. Administer succimer or BAL (dimercaprol chelators

122
Q

How does succimer/ BAL (dimercaprol ) work when dealing with arsenic?

A

They are chelators with lots of sulfur groups which pull the arsenic out of the body into the urine and bile

123
Q

What part of the body does the organic form of arsenic effect?

A

Peripheral nerve system damage

124
Q

What are Deoxynivalenol, vomitoxin, DAS a T2?

A

These are all trichothecene mycotoxins that are a big problem in production animals

125
Q

What determines if a mold produces a toxin when it comes to trichothecene mycotoxins?

A
  1. Type of substrate
  2. Genetics
  3. Environmental factors
126
Q

Where can we find trichothecene mycotoxins?

A

Wheat grain, less commonly in grass and hay

127
Q

Which species are the MOST susceptible to trichothecene mycotoxins?

A
  1. Cattle
  2. Swine
  3. Dogs
128
Q

A cow is showing signs of feed refusal, drop in weight, vomiting/regurgitation and diarrhea. The cattle are being fed wheat grain. What toxin could this be?

A

Vomitoxin or DON (trichothecene mycotoxins)

129
Q

How would you confirm diagnosis of a vomitoxin problem?

A

Test the feed after going through the HOT SPOTS and obtaining representative samples

130
Q

How do you treat a trichothecene mycotoxin problem?

A

Remove the source of the mycotoxin

131
Q

Your dog eats your steak, silica gel/celluose/polygel pack and all, what are you going to see?

A

Mild GI upset and dehydration

132
Q

How do you treat an animal that ate a meat diaper?

A

Keep them well hydrated and insure that it passes through the GI tract.

133
Q

Blister beetles contain _________, an amount that varies based on the species you are dealing with.

A

Cantharidin

134
Q

Why are beetles hanging out around large animals?

A

They follow grasshoppers around and feed on alfalfa hay

135
Q

Which large animals are most susceptible

to cantharidin poisoning?

A

Equine and Bovine

136
Q

How does cantharidin cause problems in horses and cattle?

A

It is a lipid soluble, highly irritating compound which penetrates cells and cause acantholysis. It is excreted unchanged in the urine.

137
Q

Why would you want to run a chem penal on a horse that you suspect is suffering from blister beetle poisoning?

A

Cantharidin can cause hypocalcemia and hypomagnesemia, so it may tip you off as to what is going on.

138
Q

How fast are animal affected by cantharidin and what are the clinical signs?

A

Abrupt onset with severe GIT distress, renal damage, CNS damage, myocardial damage, shock and death

139
Q

What gross pathological lesion will you typically see with blister beetle poisoning?

A

Congestion, inflammation, and hemorrhaging GIT and kidneys ( the lesion severity often doesn’t match the severity of the clinical signs)

140
Q

What microscopic lesions will you see with blister beetle poisoning?

A
  1. Gastroenteritis
  2. Nephritis
  3. Cystitis

All minimal to severe

141
Q

You do a postmortem exam on a horse and discover there is gesticulation of the non glandular portion of the gastric mucosa…what could this be?

A

Cantharidin (blister beetle poisoning)

142
Q

What is the most helpful diagnostic analysis that can be done to determine an animal has blister beetle poisoning and why?

A

A urine sample because 65% of the cantharidin is excreted unchanged in the urine

143
Q

How would you treat a cantharidin poisoning?

A
  1. Remove the source
  2. Assist in excretion via aggressive fluid therapy (urine) and mineral oil (fecal)
  3. Correct the fluid loss and provide maintenance fluids
  4. Correct the hypocalcemia and hypomagnesemia
  5. Manage pain
144
Q

What characteristic determine is a cationic detergent is toxic?

A
  1. The pH (less than 3 or more than 11)

2. The concentration

145
Q

A cat eats part of a unused dryer sheet, why might this be a problem?

A

Fresh dryer sheets can contain anywhere from 25-95% cationic detergent material which can be caustic/corrosive ad cause GIT inflammation and necrosis

146
Q

If a dryer sheet is used and an animal eats it, what are we most concerned with>

A

A foreign body issue, so make sure it passes

147
Q

If a patient is symptomatic after eating a cationic detergent, how do you treat?

A
  1. Give GI protectants

2. Give basic supportive care

148
Q

What are the component of basic supportive care for an animal that ingested cationic detergents?

A
  1. Analgesics
  2. Anti-inflammatories
  3. PEG tube
  4. Endoscopy
  5. Antibiotics
  6. Maintain fluid and electrolyte balance
149
Q

Other than dryer sheets, what other products may contain cationic detergents?

A
  1. Fabric softeners
  2. Germicides
  3. Sanitizers
  4. Potpourris
150
Q

Which phenoxy herbicide is the most commonly used and that we are concerned with?

A

2,4 D in weed and feed

151
Q

Which species of animals are susceptible to phenoxy herbicide and which is the most sensitive? Why?

A

ALL

DOGS

Renal tubules suck at secreting organic acids

152
Q

What are the top clinical signs you will see in a dog poisoned with 2,4 D?

A
  1. GIT ( anorexia, vomting, diarrhea) —usually self limiting and gone in 24 hours
  2. Neuromuscular ( ataxia, reluctance to move, myotonia)
153
Q

are phenoxy herbicide poisonings usually fatal? Why/Why not? What is the prognosis?

A

NO, unless there was a big spill in the yard, low exposure only cause self-limiting GI issues. It is rare to have high exposures.

Excellent prognosis

154
Q

What is the best way to test for phenoxy herbicide poisoning?

A

Test the serum and urine of the animal

155
Q

If an animal appears to be suffering from phenoxy herbicides, how would you treat the asymptomatic patient? Symptomatic?

A

AS:Decontaminate

S:

  1. Anti-emetic with AC/sorbitol or a lavage
  2. Diurese for 48 hours
  3. Supportive care
156
Q

Why does it not matter if an animal ate a dry cell battery or a lithium disc/button battery?

A

They both damage the mucosal lining of the GIT and need to come out.

157
Q

How long can you wait for a UNDAMAGED battery to pass in a dog that ingested one?

A

36 hours

158
Q

T/F: TO treat an animal that ate a batter, you would want to induce emesis, then give activated charcoal, then dilute, then radiograph, and then give GI protectants.

A

FALSE: DO NOT INDUCE EMESIS OR GIVE AC, you can do that rest. Batteries are corrosive, don’t want that shit coming back up the esophagus.

159
Q

Name the GI protectants again…

A
  1. Demulcents
  2. Sucralfate
  3. H2 antagonists
  4. Proton pump inhibitors (Omeprazole)
  5. Misoprostol
  6. Bulk cathartics
160
Q

What is the first thing you need to do when an animal comes in that ate an NSAID? Second thing?

A
  1. DO THE MATH (after getting the exam label from owner) to estimate the exposure does or how many pill that animal had to ingest to receive a toxic dose
  2. Induce emesis
161
Q

Name the three most common NSAID poisoning we see from most common to least.

A
  1. Ibuprofen
  2. Naproxen
  3. Carprofen
162
Q

How do small animals usually overdose on NSAIDS?

A
  1. The owner gives it to them thinking it will help
  2. The owner spills it
  3. Malicious
163
Q

NSAIDS all have similar MOAs, but what should you keep in mind about them that may be different?

A

They have different 1/2 lives, protein binding ability, enterohepatic recirculation requirements, excretory pathways and some are lipophilic. These factors can determine differences in treatment plans.

164
Q

How much more sensitive are cats to NSAIDS than dogs? `

A

8-10x

165
Q

What is the major MOA of NSAIDS?

A
  1. Inhibit PG synthetase activity
  2. Lead to a lack of GI2, and PGE2
  3. Gastric ulceration and renal necrosis
166
Q

What is unique about carprofen?

A

In DOGS, it inhibits platelet cyclooxygenase which decreases platelets aggregation and can cause an idiosyncratic reaction in the liver

167
Q

Why should you give a dog liver protectants if they have overdosed on carprofen?

A

It can cause there to be an idiosyncratic hepatic reaction

168
Q

Is ingeting NSAIDS an immediate emergency or can you take a few hours to treat?

A

Don’t need to treat right away, but at least within the first 2-6 hours (depends on the form of the NSAID)

169
Q

How soon will we see clinical signs after an animal overdoses on NSAIDS and what are they?

A

ACUTE

  1. GI upset (4-6 hours)
  2. GI ulceration (12 hr-4 days)
  3. Renal damage (12hr-5 days)
  4. Depression/lethargy and anorexia
170
Q

If an NSAID overdose is not treated, what pathological lesions may we start to see?

A

Hemoconcentration and further kidney and liver damage (liver if carprofen)

171
Q

What is the best way to diagnose an animal that has overdosed on NSAIDS?

A

Usually the exposure history is known, but you can also look at the GIT and renal signs. Serum levels are not useful

172
Q

So after you have induced emesis OR they already vomited and you gave an anti-emetic with activated charcoal (2x) and a cathartic (or gastric lavage), what will you do next in a patient that overdoses on NSAIDS?

A
  1. DO a CBC, chem profile, and U/A so you can monitor progress
  2. DIURESIS at 2-3x maintenance and at a minimum of 72 hours and administer fluid therapy
  3. Treat the gastric ulceration, renal disease and liver disease
173
Q

What are the reasons for performing aggressive diuresis (min 72 hours) on a NSAID overdose case?

A
  1. Some NSAIDS are water soluble so this enhances their excretion
  2. Enhances GFR which decreased the contact time between the cell and the toxin in addition to preventing tubular reabsorption
174
Q

Why would you choose to give cholestyramine instead of activated charcoal?

A

If you want to give some oral drugs, activated charcoal will render them useless.

175
Q

When administering GI protectants to an animal, which ones do you want to give first?

A

Start an H2 antagonist and a proton pump inhibitor at the same time as the omeprazole need to upregulate so it won’t work right away

176
Q

Which GI protectants are most useful to give after administering omepraxole and H2 antagonists?

A

Misprostole and Sucralfate

177
Q

Which GI protectant are good at protecting and treating the GI tract from ulcers and other damage?

A
  1. He antagonists
  2. Omepraxole
  3. Misoprostole
178
Q

How long should misoprotol be given?

A

5-7 days

179
Q

What parameters should you be monitoring in a dog that overdosed on NSAIDS?

A
  1. BUN/Creatine
  2. USG
  3. PCV
  4. TP
  5. Liver enzymes (carprofen)
180
Q

Which NSAIDS could you potential employ IV rescue therapy with?

A
  1. Naproxen
  2. Ibuprofen
  3. Maybe carprofen and phenylbutazone
181
Q

A dog eats a bunch of cough drops, what will you see? What is the cause of these clinical signs?

A

Abdominal discomfort, explosive diarrhea , and an anxious/agitate demeanor

Menthol and sugar

182
Q

What is acetaminophen used for?

Which species is most susceptible to a overdose?

A

Analgesic
Antipyretic

Dogs/Cats

183
Q

Should you ever use acetometophine in cats?

A

NOOOOOO, especially male cats

184
Q

What is the normal metabolism of acetometophine in dogs?

A

75% of it is conjugated with glucuronic acid and 20% into sulfates while the rest is excreted unchanged in the bile and urine

185
Q

What is the normal metabolism of acetometophine in cats?

A

90% of it turns into sulfates while only 1% is conjugated with glucuronic acid, and then a small amount is oxidized into a reactive intermediate which gets scavenged by glutathione and excreted in the urine.

186
Q

What is the overexposure pathway of acetometophine in dogs?

A

It overwhelms the detox pathway, which is glucuronidation, so more acetaminophen converts to the reactive intermediate depleting the glutathione supply.

187
Q

What is the overexposure pathway of acetometophine in cats?

A

It overwhelms the detox pathway, which is sulfaction, so more acetaminophine converts to the reactive intermediate, depleting the glutathione supply.

188
Q

What substance created when there is a acetometophine overexposure is responsible for the hepatic necrosis, red blood cell lysis, and methemoglobin clinical sign seen? What is responsible just for the methemoglobin?

A

The reactive intermediates

Para-aminophenol

189
Q

Which toxin causes there to be methemoglobin, but no lysis of RBCs?

A

Nitrate/nitrite

190
Q

Which toxins cause there to be no to very little methemoglobin, but lysis of the RBS?

A

Copper, ZInc, and red maple

191
Q

In cats, what is the first, second and third targets of the reactive intermediates created from overexposure of acetometophine?

A
  1. RBCs
  2. Liver
  3. KIdneys
192
Q

In dogs, what is the first, second and third targets of the reactive intermediates created from overexposure of acetometophine?

A
  1. Liver
  2. RBCs
  3. Kidneys
193
Q

Why do we see kidney damage with acetometophine overdose?

A

its secondary due to hypoxia….hypoxia because of the methemoglobin, hienz bodies, and hemolysis

194
Q

What are the main clinical signs and pathology we see in cats who have been exposed to excessive amounts of acetometophine?

A
  1. Weakness, lethargy, tachypnea, and cyanosis from the hypoxia due to the methemoglobin
  2. Salivation, vomiting, abdominal pain, and anorexia from the liver necrosis
  3. Convulsions and death
  4. Blood brown, white or cyanotic mucous membranes
  5. Facial and paw edema
195
Q

Why do we see facial and paw edema in cats/dogs with acetometophine toxicity?

A

Hypersensitivity reaction

196
Q

What are the main clinical signs and pathology we see in dogs who have been exposed to excessive amounts of acetometophine?

A
  1. Anorexia, vomiting, depression/lethargy, abdominal pain, icterus, increased liver enzymes and bile acids, decreased protein and clotting problems due to liver necrosis
  2. Hypoxemia and hypoxia form the RBC lysis
  3. Brown blood and white/cyanotic or muddy mucous membranes
  4. Facial and paw edema
197
Q

Why do dogs and cats die from acetometophine poisoning?

A

Hypoxia and inadequate perfusion to tissue, plus liver failure

198
Q

What are the top differentials for methemoglobinemia?

A
  1. Napthalene containing mothballs
  2. Nitrate in ruminants
  3. Dried maple leaves in horses
  4. Acetometophine overdose
  5. Other drugs
199
Q

What are the top differentials for RBS hemolysis?

A
  1. Immune mediated hemolysis in dogs
  2. Alllium spp.
  3. Zinc
  4. Copper
  5. Propylene glycol
  6. Rattlesnake venom
  7. Dried maples leaves in horses
  8. Acetometophin overdose
200
Q

What are the top differentials for toxin caused liver disease?

A
  1. Copper
  2. Zinc
  3. Iron
  4. Aflatoxin
  5. Cyanobacteria
  6. Mushrooms
  7. Xylitol
  8. Sago palm
  9. Acetometophine overdose
201
Q

What specific lesions do you see with acetometophine overdose?

A
  1. Hepatic necrosis
  2. Icterus
  3. Renal nephrosis
  4. Hemoglobin casts
202
Q

What is the best way to diagnose acetometophine overdose after you have gotten the exposure history, looked at the clinical signs and pathology, and looked at lesions?

A

Do a chemical analysis of serum

203
Q

How do you treat an asymptomatic patient that you think just ate a bottle of tylenol? What is the time frame you need to do this in?

A

Decontaminate via emesis, AC, cathartic, gastric lavage

Less than 2 hours!

204
Q

How do you treat a symptomatic patient that you think at a bottle of tylenol?

A
  1. Give them N-acetylcysteine which binds the toxins as its a precursor for glutathione
  2. Ascorbic acid and methylene blue
  3. Supportive care
  4. Liver protectants
  5. Monitor liver enzymes (chem panal)
205
Q

Why would you give ascorbic acid and /or methylene blue to an acetometophin eoverdose patient?

A

They convert methemoglobin to hemoglobin

206
Q

What is the prognosis of a symptomatic acetometophine overdose patient ?

A

Not good, often too late, but it depends on the dose and the degree of damage

207
Q

Your dog eats some gorilla glue (aka wood glue) and now you need to treat him, what do you do?

A

Radiographs and surgery, do not induce emesis and do not give anything per os.

208
Q

What is wood glue made out of and why is this a problem?

A

Polyurethanes,which expand, foam and cure when they come into contact with moisture

209
Q

How many chemical are on the market for anticoagulant rodenticides? What is different and the same between them?

A

11

Same MOAs, different 1/2 lives so have different toxicities and different lengths of treatment

210
Q

Which animals are most susceptible to anticoagulant rodent baits?

A

Dog and wildlife

211
Q

Step were taken to limit exposure of anticoagulant rodenticides, but why did this end up being a bad thing?

A

They replaced them with bromethalin which is worse

212
Q

Which type of anticoagulant rodenticide are dogs most commonly exposed to? What should you always assume it is if you don’t know for sure?

A

The long acting kind (95%)

213
Q

How do owls, hawks, and raptors become poisoned by anticoagulant rodenticides?

A

It a secondary poisoning from eating a lot of rodents and/or a residue problem

214
Q

What clotting factors is vitamin K a cofactor for in their activation?

A

2, 7, 9, and 10

215
Q

What converts inactive vitamins K into active vitamins K?

A

Vitamine K epoxide reductase

216
Q

How do anticoagulant rodenticides deplete the co-factors for the activation of clotting factors?

A

They inhibit vitamin K epoxide reductase which prevents the recycling of active vitamin K.

217
Q

If clotting factors are lost due to the inhibition

of vitamins K epoxide reductase, what occurs?

A

The patient will have prolonged clotting time which may show up even before clinical signs (12-16 hours after ingestion)

218
Q

When do the onset of clinical signs occur in anticoagulant rodenticide poisoning?

A

2-5 days

219
Q

Why three factors determine the clinical sings, clinical pathology, lesion and treatment of patients suffering from anticoagulant rodenticide poisoning?

A
  1. Hemorrhage site
  2. Speed of the hemorrhage
  3. Volume of the hemorrhage
220
Q

What is the percentage of patients that are poisoned by anticoagulant rodenticides
whom bleed into the lungs, thorax and mediastinum?

A

70%

221
Q

Where can an animal bleed from when poisoned with anticoagulant rodenticides?

A

ANYWHERE, most common from the lungs, thorax and mediastinum

222
Q

If an animal is bleeding from the lungs, what clinical signs will you see?

A
  1. Lethargy
  2. Anorexia
  3. Dyspnea
  4. Epitaxis
  5. Abnormal lung sounds (crackles/wheezes)
223
Q

If an animal is bleeding into the thoracic cavity and/or the mediastinum, what clinical signs will you see?

A
  1. Lethargy
  2. Dyspnea
  3. Drop dead with no signs
224
Q

What specific tests will be abnormal in an animal suffering from anticoagulant rodenticides poisoning?

A
  1. Anemia (possible)
  2. Thrombocytopenia
  3. Abnormal PT,PTT, and ACT (especially PT)
  4. Elevated fibrinogen and FDPs
  5. May not see any other changes if early
225
Q

Should you rule out an anticoagulant rodenticide poisoning if the animal is not anemic? What are the clinical signs of anemia?

A

NO

Low platelets, low protein, elevated liver enzymes, inflammatory leukogram, and elevated fibrinogen and FDPs

226
Q

What are the three causes of anemia?

A
  1. Loss
  2. Hemolysis
  3. Lack of RBC production
227
Q

What do you ALWAYS do when you radiograph a patient and see effusion and then want to do a tap?

A

CHECK CLOTTING TIMES, don’t want the patient to bleed out and then deliver plasma before removing the blood

228
Q

Why would you tap a patient that is suffering from anticoagulant rodenticide poisoning?

A

1 . Diagnostics

2. Alleviate distress

229
Q

What are the top differentials for an animals with prolonged PT, ACT, and and PTT?

A
  1. Anticoagulant rodenticides
  2. DIC
  3. Genetic defect of the common pathway
  4. Liver disease
230
Q

How would you confirm a diagnosis of anticoagulant rodenticide poisoning in a patient?

A

Via chemical confirmation, testing the blood and the liver.

231
Q

How do you treat a patient that just ate a bunch of anticoagulant rodenticide?

A
  1. DO the Math
  2. Decontaminate
  3. Give plasma and blood transfusions, plus IV fluids
  4. Vitamin K1
  5. Supportive care, especially O2 supplement
232
Q

How long and how much vitamin K1 should you give an anticoagulant rodenticide toxicity patient? `

A

High side of the dose, give it PO if you can, but SQ if you can’t, 4 weeks longs

233
Q

How long should you wait after giving vitamins K1 so monitor PT/PTT again?

A

24-36 hours

234
Q

What species of animal is most affected by acute nitrate poisoning?

A

Ruminants

235
Q

What species of animals are susceptible to performed nitrite?

A

All animals

236
Q

How do ruminants become poisoned by nitrate?

A

Ingestion of nitrate accumulating forage with the highest concentration at the bottom of the plant

237
Q

Which plants are good at concentrating nitrates?

A
  1. Amaranthus (pigweed)
  2. Chenopodium
  3. Oat hay
  4. Kochia (fireweed)
  5. Sorghum (sudan grass/johnson grass)
238
Q

What are the top risk factors for the ruminant when it comes to nitrate poisoning?

A
  1. High consumption rate
  2. Lack of adaptation in the rumen microbiota
  3. Older cows
  4. Cattle higher on the pecking order, get to food first and eat more of it
  5. Winter/spring months
239
Q

What re the top risk factors for a plant concentrating too much nitrate?

A
  1. Fertilization with mare, potato waste…
  2. Weather-droughs and frosts
  3. Soil and environmental factors
240
Q

What happens to nitrate when it enter the rumen? (NORMAL Situation)

A

It is converted to nitrite (which is 10x more toxic), the converted to ammonia which is used in the synthesis of proteins

241
Q

What happens to nitrate when it enters the rumen and there is too much?

A

The nitrite that was converted from the nitrate enters the bloodstream overwhelming method reductase, so methemoglobin forms .

242
Q

How fast do clinical signs of acute nitrate poisonings show up and how quickly can the animal die? Why?

A

30 min- 4 hours

4-6 hours

Nitrate is water soluble and has a short 1/2 life, so animals can recover quickly too

243
Q

Why is there such a wide range in clinical signs, from complete recovery to acute death, when dealing with ruminants who have ingested too much nitrate?

A

Some animals that ate more will succumb, while other that did not, may recover as the dose was not high enough. There is quick onset and recovery.

244
Q

When testing the feed for nitrates, what is the other differential that may show up on the test?

A

Chlorate

245
Q

How does the feed need to be tested for nitrates? What else can be tested in the environment?

A

Hot spots, needs to be representative.
Use a diphenylamine kit
Can test water

246
Q

Other than often seeing dead cattle without any prior clinical signs envy though they have been on the feed for weeks, what else can be seen in nitrate poisoning?

A

Abortions

247
Q

What is the best samples to take postmortem of a cow to diagnose nitrate poisoning? what about antemortem?

A

Eyeball

Serum or plasma and only if showing signs

248
Q

what is the treatment of choice in cattle suffering from acute nitrate poisoning?

A

Methylene blue

249
Q

If you can’t get hold of methylene blue to treat animals with acute nitrate poisoning, what should you do?

A

Do not stress them out, only treat the recumbent ones. You could try Bova-pro ( kinda like a probiotic for the rumen to help it break down the nitrate into ammonia).

250
Q

So your feed is full of nitrate, what do you do with it now?

A
  1. Dillute it

2. Feed it to monogastrics

251
Q

If you see a radio dense object on a radiograph, what does that tell us?

A

Something with metal is inside the animal, don’t know what kind of metal though.

252
Q

Which species of animals are most susceptible to zinc toxicity?

A

Small breed dogs less than 20 lbs, cats, birds and exotics

253
Q

What items have since in them that you need to worry about?

A
  1. US pennies made after 1983
  2. Toys
  3. Anything that is galvanized
  4. Zippers
  5. Jewelry
  6. Pens
254
Q

What is the most common way in which large animals become exposed to zinc?

A

Zinc sulfate footbath to treat for foot rot. If the animal stays in the bath too long and drink from it, can cause problems

255
Q

Is zinc toxicity more of an acute or chronic issue? How fast do we see clinical signs?

A

Acute

Within hours to a few days

256
Q

What are excretory pathways of zinc?

A
  1. Pancreas
  2. Liver-BILE
  3. Kidney-URINE
257
Q

What is the biggest clinical problem with zinc toxicity?

A

It can cause an acute hemolytic crisis due to the zinc causing oxidative damage to RBC’s .

258
Q

What are the main clinical signs seen with zinc toxicity?

A
  1. GIT signs like vomiting, lethargy and anorexia
  2. Pale mucous membranes/ blood due to anemia, pigmenturia, and icterus
  3. Nephrosis due to the hypoxia and zine , may see hemoglobin casts
  4. . Elevated liver enzymes from the hypoxia and zinc
  5. Elevated amylase and lipase due the pancreatic excretion of zinc
  6. DIC
  7. Angioedema of face and paws
259
Q

How can you diagnose a zinc toxicity?

A
  1. Radiographs, but don’t rule out if you don’t see anything
  2. Also, history of exposure
  3. Clinical sings and pathologies, along with lesions
  4. Chemical analysis of the serum or plasma antemortem
  5. Postmortem testing of the liver, kidney and pancreas
260
Q

How would you treat an animal with a zinc toxicity?

A
  1. Remove the source via decontamination (emesis, endoscopy, surgery, or manual removal)
  2. Diurese
  3. Blood transfusions and oxygen
  4. GIT protectants
  5. Monitor the PCV and for DIC every 3-4 hours
  6. Chelation if you can’t remove the source
261
Q

Why would you heavily diverse a patient that ate a bunch of pennies minted after 1983?

A

Keeps them hydrated and enhances recreation of the zinc with protects the kidneys from tubular nephrosis

262
Q

Which plant can cause cyclopedia in ruminants?

A

Veratrum californicum

263
Q

Which forms of mercury are the most common for animals to encounter? Which is worse?

A
  1. Inorganic (BAD)

2. Elemental

264
Q

What can inorganic mercury cause, as far as clinical signs go, in an animals?

A

Severe gastrointestinal damage and multi systemic issues

265
Q

What is the worse route of administration

for mercury?

A

Inhalation, causes morbidity pretty quickly

266
Q

What is the best treatment to administer to a dog that ate a mercury filled thermometer?

A

More concerned about the glass than the elemental mercury. Give GIT protectants and bulk cathartics, take radiographs and follow until all is passed within a day or so.

267
Q

What clinical signs can organic mercury exposure cause?

A
  1. Nervous system pathology
268
Q

Are snake plants safe? Why or why not?

A

Yes, they do contain calcium oxalate crystals , but they can not be absorbed; therefore, can’t cause renal disease.

Veterinary Toxicology (3 decks)

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