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

Unit 2 - Toxic Plants in Large Animals II Flashcards

1
Q

What plants cause respiratory effects in large animals?

A

Perilla mint and moldy sweet potatoes

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2
Q

What species are susceptible to perilla mint toxicosis?

A

Cattle and horses

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3
Q

When do problems with perilla mint typically occur?

A

In late summer with lack of other forage

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4
Q

What is the toxic principle of perilla mint?

A

Perilla ketone

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5
Q

What does perilla ketone do?

A

It damages endothelial cells and type I pneumocytes

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6
Q

What does perilla mint toxicosis result in?

A

Atypical interstitial pneumonia

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7
Q

When do clinical signs associated with perilla mint toxicosis occur?

A

1-2 days after consumption

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8
Q

What clinical signs are associated with perilla mint toxicosis?

A

Acute onset of dyspnea, extension of head and neck

Froth around the mouth and nose

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9
Q

What clinical signs are associated with severe cases of perilla mint toxicosis?

A

Collapse and death during handling/restraint

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10
Q

How is perilla mint toxicosis treated?

A

Corticosteroids, diuretics, and NSAIDs

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11
Q

What lesions does perilla mint toxicosis cause?

A

Non-collapsing lungs, rib impressions on lung surface, and emphysema

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12
Q

What is the prognosis for perilla mint toxicosis?

A

Good if animals survive past 2-3 days

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13
Q

What is the toxic principle of moldy sweet potatoes?

A

4-ipomeanol

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14
Q

What does 4-ipomeanol do?

A

Damages endothelial cells and type I pneumocytes

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15
Q

T/F: The mechanism, clinical signs, and lesions of Perilla mint and moldy sweet potatoes are the same.

A

True

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16
Q

What is the prognosis of moldy sweet potato toxicosis?

A

Guarded to poor

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17
Q

What are the teratogenic species in sheep that result in cyclopsia?

A

Veratrum californicum, Veratrum viridae, and Veratrum japonicum

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18
Q

What do Veratrum species look like?

A 
Coarse erect herb
1-2 meters tall
Stems are unbranched, leafy throughout
Long leaves
Numerous flowers
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19
Q

What parts of the Veratrum plants are toxic?

A

All of them - especially the roots

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20
Q

What are the two toxic components of Veratrum species and what effects are they responsible for?

A

Cevanine alkaloids - neurotoxic

Jervanine alkaloids - teratogenic

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21
Q

What is the MOA of cevanine alkaloids?

A

Bind open voltage-selective Na channels

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22
Q

What is believed to be the most important jervanine alkaloid in Veratrum toxicosis and what is its MOA?

A

Cyclopamine - interferes with intercellular signalling and patterning during embryogenesis and organogenesis

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23
Q

What clinical signs are associated with acute cases of Veratrum poisoning?

A

Onset 2-3 hours post ingestion
Excessive salivation
Ataxia, collapse
Death in severe cases

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24
Q

Teratogenesis occurs when ewes are exposed to Veratrum species from day ___ to ____ of gestation. Cyclops occurs if consumption is on day ____ and limb and tracheal defects occur when consumption is from day ___ to ___. _____ lip and _______, as well as syndactyly are possible.

A 
12-30
14
28-33
cleft
palate
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25
Q

What plants are commonly associated with pyrrolizidine alkaloids?

A

Ragwort, rattlepod, and hound’s tongue

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26
Q

What species are commonly affected by pyrrolizidine alkaloids? More resistant?

A

Cattle and horses - young are more susceptible

More resistant

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27
Q

When are pyrrolizidine alkaloids generally consumed?

A

In drought conditions

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28
Q

Where are pyrrolizidine alkaloids located in the plant?

A

In all parts of the plant - highest in flowers

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29
Q

What is the MOA of pyrrolizidine alkaloids?

A

They are converted by mixed function oxidases to toxic pyrroles that are detoxified and rapidly excreted
Others are activated and remain in th eliver where they inhibit mitosis

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30
Q

What acute gross lesions are associated with pyrrolizidine alkaloids?

A

Signs of liver failure - icterus and edema

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31
Q

What chronic gross lesions are associated with pyrrolizidine alkaloids?

A

Firm nodular liver, cirrhosis, icterus, +/- photosensitivity

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32
Q

What microscopic lesions are associated with pyrrolizidine alkaloid toxicosis?

A

Heopatocytomegaly
Bridging periportal fibrosis
Bile duct proliferation

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33
Q

How is pyrrolizidine alkaloid toxicosis treated?

A

Supportive care for liver failure

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34
Q

What clinical signs are associated with acute high doses of pyrrolizidine alkaloids?

A

Hepatic insufficiency
Icterus
Anorexia
Depression

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35
Q

What clinical signs are associated with chronic low doses of pyrrolizidine alkaloids?

A

Chronic hepatopathy - weight loss, emaciation, +/- icterus
Hepatic encephalopathy - aimless walking, head pressing, coma
Photosensitivity

36
Q

T/F: Pyrrolizidine alkaloids cannot cross the placenta but can pass into milk.

A

False - it can do both

37
Q

What species are the most often affected by Cocklebur toxicosis? Other species?

A

Swine are the most often affected

Cattle and sheep are also susceptible

38
Q

What is the toxic principle of Cocklebur toxicosis?

A

Carboxyatractyloside

39
Q

Where is carboxyatractyloside located in Cocklebur plants?

A

In seeds and cotyledons

40
Q

What is the MOA of carboxyatractyloside?

A
  1. Competitively inhibits oxidative phosphorylation in mitochondria
  2. Block ATP production
  3. Cellular damage
  4. Hepatocytes and PCTs highly susceptible to damage
41
Q

What clinical signs are associated with cocklebur toxicosis?

A

Depression, abdominal pain
Convulsions/seizures
Opisthotonus
Apparent blindness

42
Q

What laboratory findings are associated with cocklebur toxicosis?

A

Elevated liver enzyems

hypoglycemia

43
Q

What gross lesions are associated with cocklebur toxicosis?

A

Pale liver with enhanced lobular pattern and centrilobular hemorrhages
Presence of burs in the stomach/rumen

44
Q

What histologic lesions are associated with cocklebur toxicosis?

A

Hepatic necrosis and hemorrhage centrilobular to midzonal

Renal tubular degeneration and necrosis

45
Q

How is cocklebur toxicosis diagnosed?

A

Detection in stomach content

46
Q

How is cocklebur toxicosis treated?

A

Supportive care and oral detoxification

47
Q

What species are most commonly affected by oak tree toxicosis?

A

Cattle mainly - spring calves are often poisoned in the fall by acorns

There are a few reports in horses

48
Q

What is the toxic principle for oak tree toxicosis?

A

Metabolites of tannic acid

49
Q

What percentage of a cows diet needs to be oak in order to be toxic?

A

> 50%

50
Q

What are the 3 mechanisms of oak tree toxicosis?

A

Direct toxicity to GI epithelium
Hydrolyzed tannins are absorbed and damage endothelium
Metabolites of ingested tannins are toxic to proximal tubular epithelium

51
Q

What clinical signs are associated with early oak tree toxicosis (2 days)?

A

Anorexia, dullness, rumen atony, constipation, melena

52
Q

What clinical signs are associated with early oak tree toxicosis 3-7 days post exposure?

A

Weak, prostrate, icterus, hematuria, and dehydration

53
Q

What serum chemistry findings are associated with oak tree toxicosis?

A

Increased BUN, creatinine, phosphorus

54
Q

What urinalysis findings are associated with oak tree toxicosis?

A

Hematuria, proteinuria, protein casts

55
Q

What gross lesions are associated with oak tree toxicosis?

A

Ascites, hydrothorax
Perirenal blood tinged edema
Hemorrhagic and ulcerative gastroenteritis
Acorns in rumen

56
Q

What microscopic lesions are associated with oak tree toxicosis?

A

Coagulation necrosis of proximal convoluted tubules

Regeneration

57
Q

How is oak tree toxicosis treated?

A

Remove from access to oak
Activated charcoal or mineral oil
Fluids to correct dehydration/acidosis

58
Q

What species does redroot pigweed primarily affect?

A

Pigs

Cattle, sheep, and goats are also susceptible

59
Q

What season is Redroot pigweed toxicosis common in?

A

Mid june to late summer

60
Q

What is the toxic principle and MOA for Redroot pigweed?

A

Unknown toxic principle

causes acute renal tubular necrosis

61
Q

What clinical signs are associated with Redroot pigweed toxicosis?

A

Posterior weakness, incoordination, and sternal recumbency (5-10 days post ingestion)
Death

62
Q

What gross lesions are associated with Redroot pigweed toxicosis?

A

Perirenal edema +/- hemorrhage

Ascites

63
Q

What histologic lesions are associated with Redroot pigweed toxicosis?

A

Acute tubular necrosis affecting both proximal and distal tubules

64
Q

What plants are commonly associated with soluble oxalates?

A

Halogeton, greasewood, beets, dock, pigweed, lamb’s quarters, and rhubarb

65
Q

What species are commonly associated with soluble oxalate toxicosis?

A

Sheep > cattle

All species are susceptible

66
Q

What are soluble oexalates?

A

Sodium and potassium

67
Q

What is the MOA of soluble oxalates?

A
  1. Soluble oxalates are rapidly absorbed
  2. Complex with serum calcium to form calcium oxalate
  3. Excreted in the kidney and crystalize
68
Q

What clinical signs are associated with soluble oxalate toxicosis?

A 
Onset: 2-6 hours
Dullness, depression
Abdominal pain, rumen atony
Twitching bruxism
Ataxia, prostration, coma
69
Q

What gross lesions are associated with soluble oxalate toxicosis?

A

Ascites, hydrothorax

70
Q

What microscopic lesions are associated with soluble oxalate toxicosis?

A

Oxalate nephrosis

Crystals within vessel walls

71
Q

What species are affected by black walnut toxicosis?

A

Primarily horses

72
Q

What is the pathogenesis of black walnut toxicosis?

A

It is suspected that the wood has a vasoactive effect with ischemia, reperfusion, and reperfusion injury

73
Q

What clinical signs are associated with black walnut toxicosis?

A

Reluctance to move w/in 24 hours of exposure
Depression
Increased temperature, heart and respiratory rate, digital pulses and hoof temperature
Lower limb edema
Severe laminitis with continued exposure

74
Q

How is black walnut toxicosis diagnosed?

A

History of recent exposure acute clinical disease

75
Q

How is black walnut toxicosis treated?

A

Nonfatal disease
Remove animal from offensive breeding immediately
Oral detox
Treat limb edema and laminitis

76
Q

What factors are necessary for photosensitization to occur?

A
  1. presence of photodynamic pigment in the skin
  2. Exposure to sunlight
  3. Areas of susceptible skin
77
Q

What are the two major forms of photosensitization?

A

Primary - performed photodynamic agent is ingested

Secondary - a photodynamic secondary metabolite is not cleared by the liver

78
Q

What clinical signs are associated with photosensitization?

A

Photosensitization - photophobia
Pruritus and erythema - non pigmented areas are affected most commonly
Blindness
Sloughing of damaged skin

79
Q

How is photosensitization treated?

A

Removal from the source
Keep animals out of sunlight
Antibiotics for secondary bacterial infections
Ointments, anti-inflammatories prn for tissue swelling

80
Q

What toxins are involved in the pathogenesis of photosensitization?

A

Quinones

Phylloerythrin

81
Q

What species are at a higher risk for St. Johns wort toxicosis?

A

Herbivores > all other species

82
Q

What is the toxic principle of St. Johns wort?

A

Hypericin - photodynamic pigment

83
Q

What species are affected by buckwheat toxicosis?

A

All species, but herbivores are at a greater risk

84
Q

What is toxic principle of St. John’s wort?

A

Fagopyrin

85
Q

T/F: The toxic agents of St. John’s wort and buckwheat are both slowly eliminated from the body and have cumulative effects

A

TRUE

Toxicology (32 decks)

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