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Toxicology (Spring 2017) > Toxic Plants in Large Animals > Flashcards

Toxic Plants in Large Animals Flashcards

1
Q

Which species does yellow star thistle affect?

A

Horses

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2
Q

Where is yellow star thistle located?

A

Western/upper midwest

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3
Q

What is the clinical onset of signs associated with yellow star thistle like?

A

Abrupt

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4
Q

What are the clinical signs associated with yellow star thistle?

A
  1. Involuntary chewing movements
  2. Food falling from the mouth
  3. Twitching of the tongue and lips
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5
Q

How does yellow star thistle cause death?

A

Starvation

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6
Q

What are the lesions associated with yellow star thistle?

A
  1. Necrosis of globus pallidus
  2. Necrosis of substantia nigra

“Nigropallidal encephalomalacia”

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7
Q

What is the treatment for yellow star thistle toxicity?

A

None - recommend euthanasia

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8
Q

Yellow start thistle requires ____-____% BW for toxicosis.

A

59 - 200% (requires an extended period of consumption)

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9
Q

What component of Locoweeds causes the clinical signs?

A

Swainsonine

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10
Q

What is the MOA of swainsonine in Locoweeds?

A

Is it an enzyme inhibitor

Inhibits alpha-D mannosidase and golgi mannosidase II –> oligosaccharides buildup in lysosomes of brain cells –> generalized lysosomal storage disease ensues

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11
Q

True or False: Swainsonine crosses the placenta, but is absorbed rather slowly.

A

True/False: Swainsonine does cross the placenta, but it is RAPIDLY absorbed.

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12
Q

True or False: Swainsonine is secreted in the milk.

A

TRUE

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13
Q

True or False: Swainsonine is excreted in the urine unchanged.

A

TRUE

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14
Q

Describe the onset of signs associated with locoweed consumption.

A

Signs usually only observed after several weeks of consumption

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15
Q

What type of signs would you see in a horse due to locoweed consumption?

A

Neurological signs: ataxia, circling, proprioceptive deficits

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16
Q

What type of signs would you see in a cow or sheep due to locoweed consumption?

A

Reproductive problems: abortion, testicular atrophy, decreased spermatogenesis

Sheep: blindness, star gazing

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17
Q

What type of lesions would you see with locoism?

A

Vacuolation of neurons, renal tubular epithelia, and macrophages

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18
Q

True or False: The vacuolation associated with locoism is IRREVERSIBLE.

A

FALSE: The vacuolation is reversible.

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19
Q

Which species are most severely affected by Jimson weed?

A
  1. Pigs

2. Horses

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20
Q

What is the toxic principle of Jimson weed?

A

Tropane alkaloid

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21
Q

What is the MOA of Jimson weed?

A

Anticholinergic effects at muscarinic receptors in the CNS

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22
Q

What would the clinical signs of Jimson weed consumption be?

A

Similar to an atropine overdose:

  1. Decreased salivation
  2. GI stasis
  3. Mydriasis
  4. Tachycardia
  5. Muscle twitching
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23
Q

How would you treat a Jimson weed toxicity?

A
  1. GI detoxification

2. Physostigmine

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24
Q

What is the toxic principle of Lupine (Bluebonnet)?

A

Quinolizidine alkaloid

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25
Q

Lupanine is a quinolizidine alkaloid. To which receptors does it bind?

A
  1. Nicotinic

2. Muscarinic

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26
Q

Anagyrine is a quinolizidine alkaloid. How does this affect cattle?

A

Teratogenic alkaloid in cattle (NOT in sheep however)

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27
Q

What are the clinical signs associated with Lupinus spp. in sheep?

A
  1. Labored breathing
  2. Salivation
  3. Head pressing
  4. Ataxia
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28
Q

What causes death with Lupinus spp. (Lupine, Bluebonnet)?

A

Respiratory paralysis

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29
Q

What are the clinical signs associated with Lupine/Bluebonnet consumption in the cow?

A
  1. Salivation

2. Teeth grinding

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30
Q

Consumption at what point during gestation causes problems in calves?

A

Days 38 - 70 of gestation

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31
Q

What causes “crooked calf disease”?

A

Lupinus spp.

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32
Q

What is the toxic principle of Poison hemlock?

A

Piperidine alkaloids

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33
Q

___% BW of poison hemlock is lethal in cattle.

A

0.5%

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34
Q

___% BW of poison hemlock is lethal in sheep.

A

1%

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35
Q

When do clinical signs occur after consumption of poison hemlock?

A

Within 1 hour

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36
Q

When does death occur following consumption of poison hemlock?

A

Within 2-3 hours

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37
Q

What is the cause of death associated with poison hemlock consumption?

A

Respiratory failure (respiratory paralysis)

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38
Q

What type of lesions would you see in adult animals following poison hemlock toxicity?

A

NONE

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39
Q

How would you diagnose a poison hemlock toxicity?

A

Detect piperidine alkaloids in (1) stomach content, (2) serum, or (3) urine.

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40
Q

Where is Larkspur located within the U.S.?

A

Western U.S.

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41
Q

What is the toxic principle of Larkspur?

A

Diterpene alkaloids

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42
Q

What is the MOA of Larkspur?

A

Blocks action of nicotinic acetylcholine receptors

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43
Q

At what point does Larkspur have high toxicity and low palatability?

A

When young

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44
Q

What are the clinical signs associated with Larkspur?

A
  1. Bloat (inability to eructate)
  2. Sudden death
  3. Stiffness, weakness, staggering, ataxia, paralysis, tremors
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45
Q

Which species is more susceptible to Larkspur toxicity, cattle or sheep?

A

Cattle

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46
Q

How would you treat a Larkspur toxicity?

A

Cholinesterase inhibitor (physostigmine)

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47
Q

What is the toxic principle of water hemlock?

A

Aliphatic alcohol

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48
Q

What toxin is found in water hemlock?

49
Q

What is the MOA of cicutoxin in water hemlock?

A

Blocks GABA receptors

50
Q

Which parts of the water hemlock plant are toxic?

A
  1. Roots
  2. Young leaves

Mature plant foliage is virtually non-toxic

51
Q

What are the clinical signs associated with water hemlock?

A
  1. Violent seizures

2. Rapid death

52
Q

Water hemlock toxicity resembles what other toxicity previously described in class?

A

Strychnine

53
Q

What is the toxic principle of white snakeroot?

A

High molecular weight alcohol

54
Q

What plant contains tremetone?

A

White snakeroot

55
Q

True or False: Tremetone from white snakeroot is not secreted in milk.

A

FALSE: Tremetone is secreted in milk.

56
Q

What type of necrosis does white snakeroot cause?

A

Myonecrosis (cardiac > skeletal)

57
Q

What are the clinical signs associated with white snakeroot?

A
  1. Offspring show signs first (as toxin is secreted in milk)
  2. Reluctance to move
  3. Muscle tremors
  4. CRT > 3 sec.
  5. Dark urine
  6. Acetone breath
58
Q

Why the dark urine with white snakeroot toxicity?

A

Myonecrosis - break down of myocytes

59
Q

What would you see on lab work with white snakeroot toxicity?

A
  1. Myoglobinuria
  2. Elevated CK
  3. Elevated liver enzymes
60
Q

What is the toxic principle of the Yew shrub?

A

Taxine alkaloids

61
Q

What type of toxin is the yew plant (taxine alkaloids)?

A

Cardiotoxic

62
Q

Which parts of the yew plant are toxic?

A

All parts, except the aril

63
Q

Taxine alkaloids are not cardiac glycosides. They work directly on cardiac myocyte ion channels to ____ conduction or depolarization.

64
Q

When would you see onset of clinical signs associated with Yew plants?

A

Within 2-4 hours

65
Q

What type of gross lesions are associated with Yew plants?

A

Little to none (minimal lesions)

66
Q

Which specie(s) is(are) affected by red maple?

67
Q

What is the toxic principle of red maple?

A

Pyrogallol

68
Q

what is the proposed pathway for red maple toxicosis in the horse?

A

Tannic acid –> gallic acid –> pyrogallol –> methemoglobinemia once absorbed into the bloodstream

69
Q

When in the body is tannic acid converted to gallic acid and gallic acid converted to pyrogallol?

70
Q

What is the toxic principle of rape/kale?

A

Dimethyl disulfide

71
Q

What is the MOA of dimethyl disulfide (rape/kale)?

A

Oxidizes hemoglobin –> heinz body formation –> hemolytic anemia

72
Q

Clinical signs of rape/kale toxicosis are similar to clinical signs of what other toxicity?

73
Q

What are the 5 forms of disease associated with bracken fern toxicity?

A
  1. Bright blindness (sheep)
  2. Enzootic hematuria
  3. Bone marrow aplasia
  4. Bracken staggers
  5. Chronic exposure (carcinogenic)
74
Q

What is the toxic principle of bracken fern?

A

Ptaquiloside

75
Q

Which species are most affected by the bone marrow aplasia form of bracken fern toxicity?

76
Q

Which species are most affected by the enzootic hematuria form of bracken fern toxicity?

A

Sheep and cattle

77
Q

What is the toxic principle of sweet clover?

A

Coumarin glycoside

78
Q

What is the MOA of dicoumarol?

A

Acts as a vitamin K antagonist.

Inhibits epoxide reductase.

Reduces formation of vitamin K-dependent coagulation factors.

79
Q

What are the clinical signs associated with sweet clover toxicity?

A
  1. Hemorrhaging
  2. Anemia
  3. Pallor
  4. Hematomas
80
Q

How would you treat a sweet clover toxicity?

A
  1. Fresh blood
  2. Fresh plasma
  3. Vitamin K1
81
Q

Describe PT, PTT, and platelet numbers associated with sweet clover toxicity.

A

Elevated PT

Elevated PTT

Normal platelets

82
Q

True or False: Only the roots of the veratrum spp. are toxic.

A

FALSE: All parts of the veratrum plant are toxic.

83
Q

Although there are over 50 steroidal alkaloids of the veratrum spp., name 2.

A
  1. Cevanine

2. Jervanine

84
Q

Which of the following is a neurotoxin, cevanine or jervanine?

85
Q

Which of the following is teratogenic, cevanine or jervanine?

86
Q

Which of the following is the most important jervanine alkaloid of the vertrum spp., cyclopamine, cycloposine, jervine? Why?

A

Cyclopamine: interferes with intercellular signaling during embryogenesis and organogenesis.

87
Q

Teratogenesis occurs when ewes are exposed to Veratrum spp. from day ___ to day ___ of gestation.

88
Q

In order for a fetus to develop cyclops, a ewe would have to consume veratrum on what day of gestation?

89
Q

Which species is resistant to pyrrolizidine alkaloids?

90
Q

What are the acute clinical signs of pyrrolizidine alkaloid toxicity?

A
  1. Hepatic insufficiency

2. Icterus

91
Q

What are the chronic clinical signs of pyrrolizidine alkaloid toxicity?

A
  1. Hepatic encephalopathy
  2. Emaciation
  3. Icterus
  4. Photosensitivity
92
Q

What are the microscopic lesions you would see with pyrrolizidine alkaloid toxicity?

A
  1. Bile duct proliferation
  2. Hepatocytomegaly
  3. Bridging periportal fibrosis
93
Q

What is the treatment for pyrrolizidine alkaloid toxicity?

94
Q

Which species is most affected by the cocklebur?

95
Q

What is the toxic principle of the cocklebur?

A

Carboxyatractyloside

96
Q

What is the MOA of carboxyatractyloside (cocklebur)?

A

Inhibits oxidative phosphorylation in mitochondria –> block ATP production –> cellular damage of hepatocytes and PCTs

97
Q

Where are cockleburs located?

A

All over the U.S.

98
Q

What would be the lab findings consistent with cocklebur ingestion?

A
  1. Elevated liver enzymes

2. Hypoglycemia

99
Q

What would be gross lesions consistent with cocklebur ingestion?

A

Pale liver with enhanced lobular pattern and centrilobular hemorrhages

100
Q

What is the main species affected by oak?

101
Q

What is the toxic principle of oak?

A

Metabolites of tannic acid

102
Q

What would you see on lab work (blood work or UA) with oak poisoning?

A
  1. Increased BUN
  2. Increased creatinine
  3. Increased phosphorous
  4. Hematuria
  5. Proteinuria
  6. Protein casts
103
Q

What type of gross lesions would you expect with oak toxicity?

A
  1. Ascites
  2. Hydrothorax
  3. Hemorrhagic/ulcerative gastroenteritis
  4. Acorns in rumen
104
Q

How would you prevent oak toxicity if cattle have access to oak trees?

A

Provide grain mix containing 10% calcium hydroxide

105
Q

What type of lesions would you expect with redroot pigweed?

A

Acute tubular necrosis affecting both proximal and distal tubules

106
Q

What are the clinical signs assocaited with redroot pigweed?

A
  1. Sternal recumbancy
  2. Incoordination
  3. Weakness
  4. Ascites
107
Q

When would clinical signs occur after consumption of redroot pigweed?

A

Within 5-10 DAYS

108
Q

Which species is most affected by black walnut?

109
Q

When do clinical signs from black walnut develop?

A

Within 24 hours of exposure (ingestion)

110
Q

True or False: Black walnut disease is fatal.

A

FALSE: Nonfatal disease

111
Q

What are the clinical signs associated with black walnuts in horses?

A
  1. Laminitis (rotation of P3)
  2. Limb edema
  3. Increased temp, HR, digital pulse, and hoof temperature
112
Q

What 3 factors are necessary for photosensitization to occur?

A
  1. Susceptible skin (nonpigmented)
  2. Exposure to sun
  3. Presence of photodynamic pigment in skin
113
Q

Which species are at greatest risk for St. John’s wort toxicity?

A

Herbivores

114
Q

Which species are at greatest risk for Buckwheat toxicity?

A

Herbivores

115
Q

What is the photodynamic pigment of st. john’s wort?

116
Q

What is the photodynamic pigment of buckwheat?

117
Q

What are the clinical signs of photosensitization?

A
  1. Photosensitization
  2. Pruritus
  3. Erythema
  4. Blindness
  5. Sloughing of damaged cells
118
Q

What is the MOA of a primary photosensitization?

A

Toxic quinones are absorbed following ingestion –> circulate to cutaneous vasculature –> activated by light wavelengths of 540-610 nm –> form singlet oxygen –> vascular injury

119
Q

What is the MOA of a secondary photosensitization?

A

Severe liver damage or biliary obstruction –> phylloerythrin not excreted into bile –> acts as a phtodynamic pigment

Toxicology (Spring 2017) (15 decks)

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