Quiz Flashcards

1
Q

What body system does Sago Palm (Cycas revoluta) affect?

A

Liver

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2
Q

What is the toxic part of cycad plants?

A

All parts are toxic, but the seeds especially

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3
Q

What is the toxic principle in cycads?

A

Cycasin (a glycoside)

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4
Q

What body system does Coontie (Arrowroot, Zamia spp.) affect?

A

Liver

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5
Q

What are the primary clinical signs associated with cycad toxicity?

A
  1. G.I. signs
  2. Hepatotoxicity: jaundice, coagulation problems, dark urine
  3. Neurotoxicity: ataxia, posterior paralysis and knuckling in sheep
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6
Q

What is Zamia staggers?

A

Neurotoxicity associated with cycad poisoning

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7
Q

What is the toxic principle responsible for the neurologic signs in cycad toxicity?

A

BMAA

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8
Q

What is the treatment for cycad toxicity?

A

Medications (anti-seizure, vitamin K, intestinal protectants like NAC)

Supportive therapy (fluids and electrolytes)

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9
Q

What are the main genera of plants that have pyrrolizidine alkaloids (PAs) as their toxic principle (that we talk about in the class)?

A

Senacio (groundsel, ragwort) and Crotalaria (rattlebox)

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10
Q

What is the specific toxic principle in rattlebox?

A

Alkaloid monocrotalene

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11
Q

What are the hallmarks of PA toxicosis (4)?

A
  1. Hepatocytomegaly
  2. Hepatic necrosis
  3. Bile duct hyperplasia
  4. Fibrotic or cirrhotic changes
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12
Q

What are the clinical signs of PA toxicity?

A

Liver signs (weight loss, poor appetite, jaundice)

Secondary hepatogenous photosensitization

Neurologic signs (“sleepy staggers”)

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13
Q

What is the treatment for PA toxicity and is it often effective?

A

Supportive therapy, but it’s not usually helpful once the animals are showing clinical signs of toxicity

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14
Q

When is lantana most toxic?

A

After flowering due to immature fruits

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15
Q

What is the toxic principle in lantana?

A

Lantadene (a triterpenoid)

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16
Q

What are the clinical signs of lantana toxicity?

A

G.I. distress, constipation, secondary photosensitization

On necropsy, the liver will be swollen and green due to bile accumulation

17
Q

What are the two mechanisms for bracken fern (Pteridium aquilinum) toxicity?

A
  1. thiaminase (monogastrics, esp. horses)

2. myelosuppression (ruminants)

18
Q

What are clinical signs of thiaminase toxicity?

A

Scruffy appearance, tremors, convulsions, death

19
Q

What is the treatment for thiaminase toxicity?

A

Thiamine!

This doesn’t work for cows/sheep because of their rumen

20
Q

How does myelosuppression present in bracken fern toxicity in ruminants?

A

Acute hemorrhagic syndrome due to bone marrow suppression (hemolytic anemia, hematuria, lots of unpleasant-ness)

21
Q

What can happen with very long term bracken fern exposure in ruminants (1-6 years)?

A

Carcinoma of the bladder and G.I. tract

22
Q

What is the toxic principle in Allium spp. (onions, garlic)?

A

N-propyl disulfide

23
Q

What is the treatment for Allium toxicity?

A

N-acetyl cysteine (NAC) or ascorbic acid

24
Q

What body system do Allium spp. affect?

A

Hematopoetic system

25
Q

What is the toxic principle in red maple (Acer rubrum)?

A

Unknown, but likely Gallic acid

26
Q

What species does red maple affect?

A

Horses

27
Q

What can you see on a blood smear to diagnose red maple toxicity?

A

Heinz bodies

28
Q

What disease does white sweet clover (Melitotus alba) cause?

A

Sweet clover bleeding disease

29
Q

How does white sweet clover cause toxicity?

A

Dicoumerol inhibits Vitamin K synthesis (just like in some rat poisons)