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Toxicology > Final > Flashcards

Final Flashcards

1
Q

Regarding classification of toxicity, 50-500 mg/kg is considered how toxic?

A

MODERATELY

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2
Q

Regarding classification of toxicity, 1-50 mg/kg is considered how toxic?

A

HIGHLY

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3
Q

Regarding classification of toxicity, how toxic is 0.5-5g/kg?

A

SLIGHTLY

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4
Q

Regarding classification of toxicity, how toxic is 5-50g/kg?

A

PRACTICALLY NONTOXIC

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5
Q

1mg/kg or less is considered how toxic?

A

EXTREMELY

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6
Q

What is the NORMAL Copper/molybdenum ratio?

A

6:1

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7
Q

3 things that can cause chronic copper toxicosis in sheep?

A
  1. Excess copper (feed, soil/plants)
  2. Molybdenum deficiency
  3. Unavailability of Sulfate
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8
Q

What is the primary organ system involved in ACUTE copper toxicosis?

A

GI; vomiting, colic, hemorrhagic diarrhea

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9
Q

What is the primary organ system involved in CHRONIC copper toxicosis?

A

LIVER—>degeneration/necrosis

  • release from liver/excess copper in blood—>oxidation of RBCs—>hemolysis
  • *also oxidizes Hb—>MtHb
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10
Q

What regions may we find excess Molybdenum in the soil?

A

Florida, California, Oregon, Nevada

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11
Q

What is the specific antidote for chronic copper toxicosis?

A

Ammonium tetrathiomolybate
(IV or SC, for 3 Tx every other day)

Also, D-penicillamine

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12
Q

Specific antidote for Molybdenum toxicosis?

A

Copper glycinate SC

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13
Q

What is the specific antidote for Nitrate and Nitrite toxicosis?

A

Methylene blue 1% (for metHb)

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14
Q

Primary organ system involved in molybdenum toxicosis?

A

GI (wasting)

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15
Q

What region(s) is known for selenium-DEFICIENT soil?

A

Northwest, northeast, southeast, Great Lakes

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16
Q

What dosage is required for Selenium toxicosis?

A

0.1 mg/kg

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17
Q

Primary organ system involved in ACUTE selenium toxicosis?

A

GI and respiratory

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18
Q

Primary organ system involved in SUBACUTE Selenium toxicosis?

A

GI and CNS (“blind staggers” in cattle)

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19
Q

Primary organ system involved in CHRONIC selenium toxicosis?

A

Integument (hair, hooves)

*also called “Alkali dz”

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20
Q

Nitrate-accumulating plants?

A 
Sweet clover
Alfalfa
Wheat
Corn
PIGWEED
Sunflower
Oats
Sorghum
Beets
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21
Q

Species most susceptible to nitrate poisoning?

A

Ruminants

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22
Q

In large animals, ingestion of cyanogenic plants may cause cyanide poisoning. What are some of these plants?

A

Wild cherry (Prunus spp.)
Sudan grass
Johnson grass
Sorghums

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23
Q

What species is most susceptible to cyanide poisoning?

A

Ruminants (then sheep, horses, and swine)

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24
Q

How fast is the onset in acute cyanide poisoning and what are the signs? (Primary organ system involved)

A

PERacute or acute; extremely rapid!

Respiratory

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25
Q

What is the primary organ system involved in CHRONIC cyanide poisoning?

A

CNS

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26
Q

Specific antidote for Cyanide toxicosis?

A

Sodium nitrite 20% or sodium thiosulfate 20%

Vinegar in cold water orally to slow microbial hydrolysis

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27
Q

Most susceptible species to soluble oxalate toxicosis?

A

Sheep and cattle

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28
Q

Primary organ system involved in soluble oxalate toxicosis?

A

Renal (Ca2+ oxalate precipitation in renal tubules)

CNS (mm.twitching, coma, convulsions)

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29
Q

Plants that contain large amount of soluble oxalates?

A 
PIGWEED
Beet,
Sorrel,
Rhubarb,
Lamb’s quarters,
Halogeton
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30
Q

Specific antidote for deterrence alkaloids (buttercup family, larkspur, delphinium)?

A

Physostigmine or Neostigmine

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31
Q

INsoluble calcium oxalate plants?

A

Arum Family (Araceae)

  • Chinese evergreen
  • flamingo plant
  • Alocacia
  • dumcane varieties
  • peace lily
  • calla lily
  • caladium
  • jack-in-the-pulpit
  • cuckoo pint
  • philodendron varieties
  • skunk cabbage
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32
Q

What are some differential diagnoses for soluble oxalate toxicosis?

A

Rumen acidosis (but the pH of rumen in oxalate is ALKALINE)

Milk fever (but lesions are not as prominent as oxalate)

Hypocalcemia

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33
Q

Quinones (St. John’s wort, etc.) share the MOA of what….?

A

Primary photosensitization

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34
Q

Primary organ system involved in insoluble calcium oxalate toxicosis?

A

Upper GI

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35
Q

Primary organ system involved in isocupressic acid toxicosis?

What are some plants that have this component?

A

Reproductive; abortion

Ponderosa pines, Monterey cypress

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36
Q

Primary organ system involved in tannic acid toxicosis in ruminants?

A

GI and Renal

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37
Q

Primary organ systems involved in tannic acid toxicosis in monogastrics?

A

GI

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38
Q

T or F:

Horses are resistant to Triterpene acids.

A

TRUE

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39
Q

Primary organ involved in triterpene acid toxicosis in ruminants?

A

LIVER

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40
Q

What are some plants that contain triterpene acids?

A

Lantana, yellow sage, vervain family

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41
Q

T or F:

Diterpene alkaloids have an MOA similar to curare.

A

TRUE; competitive blockade of the Nicotinic receptors at the muscle endplate

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42
Q

Primary organ involved in gossypol (cottonseed) toxicosis?

A

Cardiac

Secondary liver damage

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43
Q

What is an example of a plant containing carboxyatractyloside (sulfated glycoside)?
What’s its MOA?

A

Cocklebur (xanthium strumarium)

Hepatotoxic

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44
Q

How are cardiac glycosides cardiotoxic?

A

Inhibit the Na/K/ATP-ase pump!

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45
Q

Examples of cardiac glycosides?

A 
Foxglove
Oleander
Periwinkle
Desert rose
Frangipani
bridal bouquet
Milkweed
Christmas Kallanchoe
46
Q

Primary organ involved in coumarin glycoside toxicosis?

A

BLOOD; form dicoumarol in spoiled plants—>hemorrhage due to antagonism of vitamin K by inhibiting Vit K Epoxide reductase —>deficiency of coagulation factors (II, VII, IX, and X)

47
Q

Acute toxicosis from cyanogenic glycosides would lead us to believe what primary organ is involved?

A

Respiratory

48
Q

Chronic toxicosis from cyanogenic glycosides would lead us to believe what primary organ system is involved?

A

CNS

49
Q

Of the 3 toxins cycad palms (of the cycasin family), only 2 are known. What are the primary organ systems they involve?

A

Cycasin: GI and liver

Beta-methylamino-L-alanine(BMAA): CNS

50
Q

What is sodium picrate paper test used to diagnose?

A

Cyanide

51
Q

What is nitrate poisoning associated with?

A

Abortions and MetHb-nemia

52
Q

Toxic principle of oak trees?

A

Tannic acid

53
Q

Plant known for being similar to warfarin?

A

Sweet clover

54
Q

Rattlebox has what toxic principle?

A

Pyrrolizidine alkaloids

55
Q

Toxic principle for azaleas?

A

Grayanotoxins

56
Q

What toxic plant is known for causing diarrhea/vomiting, as well as cardiac arrhythmias?

A

Oleander

57
Q

What plant causes neurodegeneration and demyelination in the CHRONIC stage?

A

Elderberry

58
Q

Selenium-containing plant located in Wyoming and out west?

A

Prince’s plume

59
Q

Vitamin K Tx time period for a SECOND generation Anticoagulation rodenticide?

A

4 weeks

60
Q

Clinical application: dog’s lab results come back after poisoning…
Elevated: calcidiol, calcitriol, serum [Ca2+] and [P]
Decreased: PTH

What’s at the top of our differential list?

A

Cholecalciferol

61
Q

What do we think of with Bromethalin toxicosis?

What should we avoid?

A

Affects brain + spinal cord; monitor fluid and electrolytes during Tx; consider activated charcoal

DO NOT give emetics if toxin has been in the system for ~3 hours

62
Q

What goes with lethal synthesis?

A

Hepatic bioactivation

63
Q 
What toxicosis would we diagnose if we see:
Hyperosmolality,
Increased anion gap,
Heinz bodies on blood smear,
Metabolic acidosis
A

PROPYLENE GLYCOL

64
Q

Diterpene alkaloid Larkspur, competitively blockades what receptors at what location? How do we treat?

A

Nicotinic Rs at the MUSCLE ENDPLATE (similar to curare);

Treat with physostigmine

65
Q

What family does locoweed belong to?

A

Indolizidine alkaloids

66
Q

T or F:

Day lily causes hepatotoxicity

A

False

67
Q

How do we treat canine arrhythmias for chocolate toxicosis?

A

Beta blockers!

68
Q

What drugs may increase warfarin toxicity?

A

Aspirin
Sulfonamides
Steroids
Thyroxine

69
Q

Sensitivity to anticoagulant rodenticides according to species in DECREASING Order…

A

Pigs>dogs/cats> ruminants> horses> chickens

70
Q

Ingestion of plants that have been sprayed with the recommended levels of 2,4-D herbicides may cause poisoning in livestock…
But WHY?

A

Accumulation of toxic levels of nitrate in the plant

71
Q

The first clinical signs in organophosphate poisoning are mainly due to…?

A

Muscarinic stimulation

72
Q

If we do not know the type of anticoagulant rodenticide, how long should we treat with Vitamin K1?

A

3-4 weeks

73
Q

T or F:
Warfarin acts as an anticoagulant in-vivo and in vitro by inhibiting vitamin K epoxide reductase, inhibiting activation of vitamin K-dependent clotting factors.

A

Falseee

74
Q

What do carbamate and organophosphate pesticides have in common?

A

Similar sources of poisoning,
Lipid soluble/can penetrate intact skin,
Quickly eliminated,
Clinical signs due to excess ACh

75
Q

T or F:

Use acepromazine to treat organophosphate poisoning in dogs.

A

FALSE

76
Q

How does 2-PAM antagonize the toxic effects of organophosphate?

A

Deactivation of acetylcholinesterase

77
Q

Route of choice for Vitamin K administration?

A

PO

78
Q

MOA of anticoagulant rodenticides?

A

Inhibit ACTIVATION OF precursor proteins of clotting factors (II, VII, IX, X)

79
Q

Best sample for chemical analysis, to help confirm a Dx of cholecalciferol toxicosis in a live GSD?

A

Serum

80
Q

What might we think if we saw these clin path changes:

Hypercalcemia,
Hyperphosphatemia
Hypokalemia,
Elevated Crea & BUN

A

Cholecalciferol

81
Q

What is peculiar about toxicity from the insecticide parathion in cattle?

A

It’s LESS toxic to young calves (30 day old), than adult cattle…

82
Q

We’re trying to confirm diagnosis of organophosphate in a live cow. What’s the best sample to submit to tox lab?

A

Whole blood

83
Q

Anticoagulant effects of warfarin rodenticide can be reversed immediately by what?

A

Intravenous whole fresh blood infusion

84
Q

What do PCP and ergot (Claviceps purpurea) have in common?

A

Chronic toxicosis with PCP generally has similar clinical signs as Ergot (in cattle)

85
Q

What do warfarin and spoiled sweet clover (Melilotus spp) have in common?

A

May cause similar clinical signs

86
Q

A blood lead concentration reported as 50mg/dL is equal to _____ ppm.

A

500 ppm

87
Q

What is the most common cause of acute death in cholinesterase inhibitor toxicity?

A

Respiratory failure

88
Q

T or F:
Phenoxy acetic acid herbicides are plant hormones that change plant metabolism resulting in increasing toxicity of plants by improving plant palatability and increasing toxin content.

A

TRUE

89
Q

Acute toxicosis of dipyridyl herbicides:

What would we see?

A

Vomiting, anorexia, depression, production of free radicals that damage tissue

And in HIGH doses, maybe cause ataxia, dyspnea, and seizures

90
Q

T or F:
Paraguay is a plant hormone that alters the metabolism of plants which increases their toxicity and improves palatability

A

Falseee

91
Q

Name the toxicant:

If the dog survives the acute phase (3hours), s/he will develop liver failure.

A

Metaldehyde

92
Q

Signs of CNS stimulation and GI irritation in a DOG,

And heart failure in a HORSE….

Is most indicative of which toxicant?

A

Fluoroacetate

93
Q

T or F:

Repeated exposure to small amounts of strychnine over time is more toxic than large single exposure.

A

FALSE

94
Q

A toxicant that has the following lesion in most species:

Gastroenteritis (may be hemorrhagic)
Pulmonary congestion/edema,
Congestion of liver and kidney,
Dead fish odor (acetylene odor) in stomach

A

Zinc phosphide

95
Q

What toxicant would we think of if we saw elevated citrate in the kidney tissue or blood?

A

Fluoroacetate

96
Q

What rodenticide is MOST likely to cause increased ICP and posterior paralysis?

A

Bromethalin

97
Q

What is pamidronate disodium?

A

Welll… it’s a bisphosphonate and it acts as a specific inhibitor of bone resorption

98
Q

Most sensitive animals to zinc phosphide toxicosis?

A

Caged birds

99
Q

T or F:
Dipyridyl herbicides are plant hormones that change metabolism resulting in increasing toxicity of plants by improving plant palatability and increasing toxin content.

A

False

100
Q

What toxicant do we think of when we see signs of respiratory insufficiency and overheating (and somehow we know that it’s BY MOA of uncoupling oxidative phosphorylation and blocking/decreasing ATP)?

A

PCP

101
Q

What toxicosis would the following blood chemistry best characterize in ruminants?

A

Acidosis,
Hyperkalemia,
Hyperglycemia,
Elevated BUN

102
Q

Onset clinical signs in urea toxicosis?

A

0.5-3 hours! Fast af

103
Q

T or F:

Grain overload is highly likely to elevate rumen pH.

A

False.

104
Q

A feedlot steer that survived an overdose of monensin in the feed was found dead 3 weeks later. If the death was related to the monensin toxicity, what was the cause?

A

Cardiac fibrosis and insufficiency as a result of cardiac muscle necrosis (during the acute toxicosis)

105
Q

Pretty much pathognomonic evidence of water deprivation/sodium ion toxicosis in swine is……

A

Eosinophilic meningoecephalitis

106
Q

Species most sensitive to ethylene glycol poisoning….

A

Kitty cats

107
Q

T or F:

Propylene glycol is highly likely to cause systemic acidosis.

A

False

108
Q

How long after ingestion of ethylene glycol (resulting in toxicosis) in the dog, does acute renal failure result?

A

24-72 hours

109
Q

In addition to antidotal treatment of ethylene glycol poisoning, what other treatment is important?

A

Sodium bicarbonate

110
Q

What is the recommended cheating agent for lead toxicosis in pet birds?

A

Dimercaptosuccinic acid (succimer)

Toxicology (1 decks)

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