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Toxicology > Unit 2 - Toxic Plants in Large Animals I > Flashcards

Unit 2 - Toxic Plants in Large Animals I Flashcards

1
Q

What species are affected by Yellow Star thistle/Russian knapweed toxicosis?

A

Horses only

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2
Q

T/F: Fresh or dried Yellow Star Thistle is toxic.

A

True

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3
Q

What is the indicated toxic principle of Yellow Star Thistle?

A

Sequiterpine lactones

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4
Q

What do sesquiterpine lactones do?

A

Depletes glutathione which results in oxidative damage, mitochondrial dysfunction and neuronal death

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5
Q

What clinical signs are associated with Yellow Star thistle toxicosis?

A

Involuntary chewing moments, food falling from mouth
Depression
Inability to eat

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6
Q

How is Yellow Star thistle toxicosis diagnosed?

A

Clinical signs

History of exposure

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7
Q

What is necessary for horses to get Yellow Star thistle toxicosis?

A

They need to have an extended period of consumption - high intake over 30+ days

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8
Q

What lesion does Yellow Star thistle cause?

A

Nigropallidal encephalomalacia

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9
Q

How is Yellow Star thistle toxicosis treated?

A

There is no treatment - euthanasia is recommended

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10
Q

When do perennials grow?

A

In spring/summer

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11
Q

T/F: Locoweed or milkvetch is typically eaten when other forages are not present.

A

False - it is palatable and nutritious and may be eaten even when other forages are present

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12
Q

What is the toxic principle of locoweeds?

A

Indolizidine alkaloid -Swainsonine

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13
Q

Where is swainsonine located in locoweeds?

A

In all parts of the plant - it is highest in leaves, flowers, and seedpods

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14
Q

Swainsonine is ______ absorbed, crosses the _____, is secreted in _____, and excreted _______ in ________.

A 
Rapidly
placenta
milk
unchanged
urine
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15
Q

What is the MOA of swainsonine?

A
  1. Inhibits alpha-D-mannosidase and Golgi mannosidase II
  2. Accumulation of oligosaccharides in lysosomes of cells in the brain and other tissues
  3. Generalized lysosomal storage disease ensues
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16
Q

What species are affected by locoweed toxicosis?

A

Cattle, horses, sheep, goats, and elk

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17
Q

When do clinical signs due to Locoweed toxicosis occur?

A

After several weeks of consumption

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18
Q

How do sheep with Locoweed toxicosis typically appear?

A

Blind with stargazing behavior

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19
Q

What clinical signs are associated with Locoweed toxicosis in horses?

A

Neurologic signs - depression, procioceptive deficits, circling, ataxia, and falling over backwards

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20
Q

What clinical signs are associated with Locoweed toxicosis in cattle and sheep?

A

Reproductive problems - abortions, fetal resorption, skeletal malformations, testicular atrophy, and decreased spermatogenesis

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21
Q

What lesions are associated with Locoweed toxicosis?

A

Vacuolation of neurons, renal tubular epithelia, and macrophages

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22
Q

What species are affected by Jimson weed?

A

All species - pigs and horses are worse

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23
Q

What do Jimson weed plants look like?

A

2-5 feed high with simple irregular toothed leaves

Tubular flowers with 2-4

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24
Q

T/F: Jimson weed is normally palatable

A

True

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25
Q

What part of Jimson weed is toxic?

A

The entire plant - but it is concentrated in seeds

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26
Q

What is the toxic principle of Jimson weed?

A

Tropane alkaloid

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27
Q

What is the MOA of tropane alkaloid?

A

Anticholinergic effects at muscarinic receptors in the CNS

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28
Q

Jimson weed appears like an ______ overdose.

A

Atropine

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29
Q

What clinical signs are associated with Jimson weed toxicosis?

A

Reduced secretions
Mydriasis/blindness
Muscle twitching, incoordination, paralysis
GI stasis, tachycardia, urine retention

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30
Q

How is Jimson weed toxicosis treated?

A

Physostigmine

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31
Q

What other plants have similar effects to Jimson weed?

A

Mandrake and deadly nightshade

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32
Q

What do lupine and bluebonnet look like?

A

Flowers are generally blue, but yellow or white in some species

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33
Q

What are the toxic principles of lupine?

A

Quinolizidine alkaloids - Lupanine and anagyrine

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34
Q

What does Lupanine do?

A

Bind nicotinic and muscarinic receptors

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35
Q

What does Anagyrine do?

A

Teratogenic alkaloid in cattle

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36
Q

When do clinical signs due to Lupine/Blue bonnet toxicosis occur?

A

Within 1-3 hours post ingestion

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37
Q

What clinical signs are associated with Lupine/Blue bonnet toxicosis in sheep?

A 
Labored breathing pattern
Depression, salivation, ataxia
Clonic spasms, head pressing, tremors, seizures and coma
Death due to respiratory paralysis
\+/- transient excitement/aggression
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38
Q

What clinical signs are associated with lupine/blue bonnet toxicosis in cattle?

A

Salivation/bruxism

Congenital defects

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39
Q

When during gestation does eating lupine/blue bonnet toxicosis result in congenital defects in cattle?

A

38-70 days

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40
Q

What congenital defects are associated with Lupine/blue bonnet toxicosis?

A

Misaligned joints/arthrogryposis

Neck, back, and cleft palate

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41
Q

What are the features of poison hemlock?

A

Hollow stems and parsely-like alternate, dissected leaves

Flowers occur in small, white, umbrella-shaped clustures

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42
Q

What is the toxic principle for poison hemlock?

A

Piperidine alkaloids

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43
Q

What do piperidine alkaloids do?

A

Initial stimulation followed by severe depression of neuromuscular junctions and autonomic ganglia

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44
Q

What components of the poison hemlock plant are toxic?

A

Toxins are highest in root, vegetative parts in spring, and decrease in summer

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45
Q

When do clinical signs due to poison hemlock occur?

A

Within 1 hour of consumption

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46
Q

What clinical signs are associated with poison hemlock toxicosis?

A

Death from respiratory failure
Salivation, abdominal pain, muscle tremors, and incoordination
Dilated pupils, prolapse of nictitating membrane
Weak pulse
Frequent urination and defecation
Coma without convulsions

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47
Q

How is poison hemlock toxicosis diagnosed?

A

Detection of alkaloid in stomach content, serum, and urine

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48
Q

How is poison hemlock toxicosis treated?

A

Emetics/cathartics early are important
Mineral oil or charcoal
Maintain airway. respiratory support

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49
Q

What species are susceptible to water hemlock toxicosis?

A

Cattle, horses, sheep, and people

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50
Q

What does water hemlock look like?

A

Two to eight, thick, tuberous roots
Alternate leaves with toothed edges
White flowers

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51
Q

What is the toxic principle of water hemlock?

A

Aliphatic alcohol

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52
Q

What is the MOA of aliphatic alcohol?

A

Blocks GABA receptors

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53
Q

What parts of water hemlock are toxic?

A

Roots, young leaves

54
Q

What clinical signs are associated with water hemlock toxicosis?

A

Chewing, teeth grinding, ataxia
Progress to violent seizures
Rapid death

55
Q

How is water hemlock toxicosis diagnosed?

A

plant ID and confirmed consumption

56
Q

How is water hemlock toxicosis treated?

A

Generally not feasible

57
Q

What is the toxic principle of Larkspur?

A

Diterpene alkaloids

58
Q

What species are susceptible to Larkspur toxicosis? Resistant?

A

Susceptible - cattle, rarely horses

Resistant - sheep/goats

59
Q

Tall larkspur has (low/high) toxicity when young, but (low/high) palatability. When it is mature it is the exact opposite.

A

high; low

60
Q

What is the MOA of Larkspur toxicosis?

A

Blocks the action of nicotinic acetylcholine receptors within CNS and NM junctions

61
Q

When is the greatest risk of Larkspur toxicosis?

A

During flowering and fruit formation

62
Q

What clinical signs are associated with Larkspur toxicosis?

A

Sudden death
Stiffness, weakness, staggering, ataxia, paralysis, tremors, recumbence
Impaired eructation

63
Q

How is Larkspur toxicosis treated?

A

With a cholinesterase inhibitor - Physostigmine

Manage bloat

64
Q

How is Larkspur toxicosis managed/prevented?

A

Large flocks of sheep can be used to trample

or eat larkspur before bringing in cattle to graze

65
Q

What species are affected by milkweed?

A

Cattle, horses, and small ruminants

66
Q

What is the toxic principle of milkweed?

A

Cardiac glycosides

67
Q

What is the MOA of cardiac glycosides?

A

They inhibit Na/K ATPase pumps affecting myocardial conduction and contractility
Certain species produce a neurotoxin

68
Q

What part of the milkweed is toxic?

A

All parts, green or dry

69
Q

What clinical signs are associated with milkweed toxicosis?

A

Staggering, weakness, muscle fasciculation, SEIZURES
Colic/bloat, excess salivation, dyspnea, mydriasis
Rapid, weak pulse
Coma, death

70
Q

How is milkweed toxicosis diagnosed?

A

Identifying plants in the rumen

71
Q

What does white snakeroot look like?

A

2-4 feet tall
heart-shaped, 3-6 inch serrated leaves
crowned with composite flowers

72
Q

What is the toxic principle of white snakeroot?

A

Tremetone

73
Q

Tremetone is toxic when ______, secreted in ______, and induces _______.

A

Dried
milk
myonecrosis

74
Q

T/F: Toxic effects of white snakeroot are cumulative

A

True

75
Q

What clinical signs are associated with white snakeroot toxicosis?

A 
Reluctance to move/sluggish behavior
Muscle tremors 
CRT >3 sec
Dark urine: myoglobin
Acetone odor to breath
76
Q

What additional clinical signs do horses show with white snakeroot toxicosis?

A

Sweating, jugular pulses, arrythmia

77
Q

What laboratory findings are associated with snakeroot toxicosis?

A

Myoglobinuria, elevated CK, elevated liver enzymes (AST and ALT)

78
Q

How is white snakeroot toxicosis treated?

A 
Detox with charcoal and cathartics
Good nursing care and nutrition
Treat cattle for ketosis
Avoid consumption of milk
Monitor EKG in horses
79
Q

What species are susceptible to the Yew plant?

A

All

80
Q

What does the Yew plant look like?

A

Common ornamental evergreen shrub - small, flat lanceolate leaves and seed cones with a fleshy red covering

81
Q

What is the toxic agent of the Yew plant?

A

Taxine alkaloids

82
Q

Where are taxine alkaloids located in the Yew plant?

A

Bark, leaves, and seeds

It is higher in older leaves

83
Q

What part of the Yew is highly toxic if chewed?

A

The seeds

84
Q

What is the suspected MOA of Yew?

A

Depress conduction or depolarization - direct action on cardiac myocyte ion channels

85
Q

Most cases of Yew toxicosis occur due to what?

A

Clippings from bushes

86
Q

When is the onset of clinical signs do to Yew toxicosis?

A

Onset 2-4 hours post ingestion in ruminants

87
Q

What may be the only sign of Yew toxicosis?

A

Sudden death may be the only sign

88
Q

What clinical signs, if they occur, are associated with Yew toxicosis?

A

Nervous signs including trembling, dyspnea, incoordination, reluctance to move, and collapse
Acute cardiac failure - bradycardia and jugular pulses
Gastroenteritis and diarrhea

89
Q

How is yew toxicosis diagnosed?

A

Presence of yew leaves in rumen or stomach
Microscopic exam of stomach contents
Chemical assay

90
Q

What is the prognosis for yew toxicosis?

A

Guarded to grave

91
Q

How is yew toxicosis treated?

A

Activated charcoal +/- cathartic
Rumen lavage or rumenotomy and removal of rumen content
Atropine for bradycardia

92
Q

What species are affected by Red maple toxicosis?

A

Horses

93
Q

What is the toxic principle of red maple?

A

Tannic acid

94
Q

Where is tannic acid found?

A

In wilted or dried red maple leaves

95
Q

What is the MOA of tannic acid?

A

It is converted into gallic acid into the ileum and then to pyrogallol
Pyrogallol is absorbed into the blood stream causing methemoglobinemia

96
Q

What does red maple toxicosis induce?

A

Heinz body formation
Methemoglobinemia
Intravascular hemolysis

97
Q

What clinical signs are associated with red maple toxicosis?

A 
Weakness
Tachypnea
Tachycardia
Icterus
Cyanosis
Hemoglobinuria
98
Q

How is red maple toxicosis treated?

A

History of exposure
Clinical signs
Laboratory findings

99
Q

How is red maple toxicosis treated?

A

IV fluids
Oxygen
Blood transfusion

100
Q

What is the toxic principle of rapeseed and kale?

A

Dimethyl disulfide

101
Q

What species are affected by rapeseed or kale toxicosis?

A

cows

102
Q

What is the MOA of dimethyl disulfide?

A
  1. Oxidizes hemoglobin
  2. Heinz body formatino
  3. Hemolytic anemia
103
Q

What clinical signs are associated with kale or rapeseed toxicosis?

A

The same as Red maple or allium

Diagnostics and treatment is the same

104
Q

What species are affected by sorghum and sudan grass toxicosis?

A

Ruminants

105
Q

What is the toxic prinicple of Sorghum and sudan grass?

A

Dhurrin

106
Q

What is the amount of Dhurrin dependent on?

A

Climate, stage of growth, speed of growth, and fertility of plant

107
Q

Where is the highest concentration of Dhurrin?

A

In leaves

108
Q

What is the MOA of dhurrin?

A
  1. Damage to plant cells
  2. Enzymes convert non-toxic dhurrin to toxic prussic acid
  3. Prussic acid is absorbed into the blood stream
  4. Cells cannot utilize oxygen
109
Q

What clinical signs are associated with Sorghum and Sudan grass toxicosis?

A

Tachypnea, tachycardia, dyspnea, and arrhythmia
Collapse, bright red mucus membrane
Trembling, spasms, convulsions, death from respiratory paralyssi

110
Q

How is Sorghum and Sudan grass toxicosis diagnosed?

A

History of recent exposure and clinical signs
Detection of cyanide in rumen/blood/feed
Detection of thiocyanate in urine

111
Q

How is Sorghum and sudan grass toxicosis treated?

A

Amyl nitrate (inhaled) + Sodium nitrite (IV, fast) + sodium thiosulfate (IV, slow) + sodium thiosulfate (oral

112
Q

What are some other options for Sorghum and Sudan grass toxicosis treatment?

A

Hydroxycobalamin, 4-DMAP, EDTA, and Methylene blue

113
Q

What species are susceptible to bracken fern toxicosis?

A

Cattle and sheep

Pigs, horses, and other species are also susceptible

114
Q

When does bracken fern toxicosis typically occur?

A

In times of drought where better forages are not available

115
Q

Disease due to bracken fern is dependent on _____, _____, and the _____ affected.

A

Dose, duration, species

116
Q

What are the forms of disease caused by bracken fern toxicosis?

A 
Bone marrow aplasia/anemia
Enzootic hematuria
Bracken staggers
Bright blindness
Chronic low-level exposure
117
Q

What laboratory findings are associated with bracken fern bone marrow aplasia/anemia?

A

Thrombocytopenia, anemia, and neutropenia

118
Q

Bracken fern bone marrow aplasia/anemia mostly affects ______ that have had _______ consumption in a _____ period of time.

A

Cattle
Heavy
short

119
Q

What is the toxic principle for all forms of bracken fern toxicois?

A

Ptaquiloside

120
Q

What species are affected by enzootic hematuria?

A

Cattle and sheep

121
Q

T/F: Enzootic hematuria due to bracken fern toxicosis is rapid and due to little exposure

A

False - it requires prolonged exposure

122
Q

Bracken staggers is basically _____ deficiency that affects ______ and _____. It requires consumption of approximately _____% of their diet for 2-3 weeks.

A

thiamine
horses
pigs
25%

123
Q

What clinical signs are associated with bracken disease?

A

Neuro disease - uncoordinated, wide stance, unable to treat

124
Q

What is the lesion that causes bright blindness?

A

Progressive retinal degeneration

125
Q

Chronic low-level exposure of Bracken fern occurs over ___ to ____ years. It is a ______ agent that causes neoplasia in ruminants. It is excreted in _____.

A

2-4
carcinogenic
milk

126
Q

What is the toxic principle of sweet clover?

A

Melilotoside

127
Q

Melilotoside + fungi =

A

dicoumarol

128
Q

What is the MOA of dicoumarol?

A

It is a vitamin K antagonist that inhibits epoxide reductase - reduced coag factors II, VII, IX, and X

129
Q

When is the onset of clinical signs due to sweet clover toxicosis?

A

Several days

130
Q

What clinical signs are associated with sweet clover toxicosis?

A

Large hematomas, anemia, weakness, pallor, prolonged hemorrhage

131
Q

How is sweet clover toxicosis diagnosed?

A

Elevated PT and PTT

Platelet numbers are normal

132
Q

How is sweet clover toxicosis treated?

A

Fresh blood or plasma

Vitamin K1

Toxicology (32 decks)

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