4.4 Lab - Toxic Plants cont. Flashcards

1
Q

what type of liver toxins can be found in plants, and what plants are they found in?

A

Plants containing:
* Pyrrolizidine alkaloids (ragwort, houndstongue)
* Unknown hepatotoxins (alsike clover etc.)
* Amatoxins (cytotoxic mushrooms – will talk
about at end of the lab)
* Microcystins (blue-green algae/cyanobacteria – already discussed)

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2
Q

what do Pyrrolizidine alkaloids do to the body?

A

Hepatotoxic, impairs cell division (megalocytosis)

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3
Q

what type of toxin is found in ragwort? what does it do? what species does it affect? what are the clinical signs and lesions?

A
  • Toxin: Pyrrolizidine alkaloids
  • Species susceptible: cattle, horses
  • Part of plant: All above ground parts
  • Clinical signs:
  • Acute: colic, tachycardia, death
  • Chronic: photosensitization, weigh loss, liver failure, hepatic encephalopathy, jaundice, death
  • Lesions: Chronic liver disease, fibrosis, bile duct proliferation, megalocytosis
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4
Q

acute clinical signs of pyrrolizidine alkaloid toxicity?

A
  • Acute: colic, tachycardia, death
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5
Q

chronic clinical signs of pyrrolizidine alkaloid toxicity?

A

photosensitization, weigh loss, liver failure, hepatic encephalopathy, jaundice, death

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6
Q

what type of toxin is found in red maple? what species is susceptible?

what clinical signs will we see?

A
  • Toxin: gallic acid
  • Species susceptible: horses
  • Part of plant: wilted or dried leaves (older wilted leaves contain more than spring leaves!)
  • C/S: depression, anemia, icterus, cyanosis, hemoglobinuria
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7
Q

what is the pathogenesis of gallic acid? what lesions will we see?

A

gallic acid
> converted to PYROGALLOL in the ileum of the horse
> oxidation of hemoglobin
> produces methemoglobin and causes hemolysis with Heinz body formation
➝ anemia, icterus, hemoglobinuria
> periacinar hepatic necrosis; hemoglobinuric nephrosis

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8
Q

What treatment can be offered to a horse that has eaten red maple and what is the prognosis? what should we watch out for?

A
  • Supportive care; including intravenous fluids, blood transfusions, and oxygen therapy. - Because red maple leaf toxicity compromises the horse’s ability to carry oxygen in its blood, affected horses should be kept quiet in a stall while being treated.
  • Secondary complication of red maple leaf toxicity is acute kidney failure due to the by- products of red blood cell breakdown (hemoglobin and methemoglobin)
  • “hemoglobinuric nephrosis”
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9
Q

plants that cause hemolysis, other than red maple. what is their mechanism and what is the result?

A

Onions (and garlic!)
* Allium spp.
* Dogs, cattle, others
* N-propyl disulfide: Oxidative damage to erythrocytes; Heinz bodies
* Hemoglobinemia, hemoglobinuria, anemia

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10
Q

what type of toxins damage bone marrow and blood, and in what ways? what plants are these found in?

A
  • Red blood cell membrane injury/hemolysis (*red
    maple, onions, Brassicas (turnips, kale, rapeseed))
  • Myelosuppression (*bracken fern)
  • Clotting abnormalities (mouldy sweet clover)
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11
Q

what type of issues does bracken fern cause? what toxins does it contain? what species are susceptible?

A

Myelosuppression

Toxins:
* Type I thiaminase
* Ptaquiloside

Species susceptible:
* Cattle (neoplasia, bone marrow suppression)
* Horses (neurologic)
* Sheep (bright blindness)

  • Part of plant: all, fresh or dry
  • Not palatable, but will be eaten if no other forage available.

Karen’s way of remembering this toxin: Ptaquiloside sounds like it should suppress inhibitions, not bone marrow.

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12
Q

clinical signs of braken fern consumption in cattle

A
  • Fever, anorexia, anemia, leukopenia, thrombocytopenia, hemorrhages, melena
    (“bovine enzootic hematuria”)
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13
Q

lesions associated with bracken fern consumption in cattle

A
  • Generalized hemorrhage, anemia, aplastic marrow; abomasal ulceration
  • Urinary bladder lesions – hemorrhage, inflammation, hyperplasia, papilloma, carcinoma or hemangioma in cattle exposed to lower doses for 1-6 years.
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14
Q

what does bracken fern consumption cause in horses? what are the associated clinical signs and lesions?

A
  • Thiamine deficiency d/t thiaminases
  • Similar to Vit B1 deficiency, respond to thiamine therapy
  • C/S: Weight loss, depression, weakness, incoordination (“bracken staggers”), wide stance, twitching, arrhythmias, recumbency, convulsions, death.
  • Lesions: nonspecific, pericardial/epicardial hemorrhage
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15
Q

types of nephrotoxins and plants that contain them:

A
  • Oxalates (red-root pigweed, rhubarb)
  • Tannins (oak)
  • Unknown toxins (*lily, *grape)
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16
Q

what species are susceptible to lily toxins? what are clinical signs? what are the lesions?

A
  • Toxin: unknown
  • Species susceptible: Cats
  • C/S: Depression, vomiting, renal failure

Lesion: acute renal tubular necrosis
-kidney injury will lead to dehydration, further vomiting and finally reduced and then no urine production

17
Q

Treatment options for cats who ingest lilies? prognosis?

A
  • Chances of survival are increased with aggressive decontamination and fluid diuresis within 18 hours of exposure
  • Successful treatment includes initiation of fluid diuresis before the onset of anuric renal failure.
  • Prognosis is excellent if fluid diuresis is started before anuric renal failure has developed.
  • Once anuria develops, peritoneal dialysis or hemodialysis is the only potential treatment, and the cat will likely have chronic kidney failure
18
Q

what is a teratogen?

A

is any agent that causes an abnormality following fetal exposure during pregnancy.

19
Q

what are some examples of teratogenic plants?

A
  • Milk vetches, locoweeds, lupines
  • False hellebore
20
Q

what does false hellebore contain that is teratogenic? what animals does it affect? what are the clinical signs?

A
  • Contains teratogenic alkaloids such as cyclopamine
  • Sheep (and occasionally goats, alpacas and cattle) when ingested at day 14 gestation
  • Often they do not abort and will retain the pregnancy until a stillbirth occurs
  • Multiple clinical signs – called “monkey face“ lambs, holoprosencephaly, cyclopia, anopthalmia, cleft palate; shortened maxilla, arthrogryposis, shortened long bones
  • Toxin causes interference with body patterning via sonic-hedgehog signaling.
21
Q

what are a some types of toxins that mushrooms can contain?

A
  • Cytotoxins Most important
  • Autonomic nervous system toxins
  • Central nervous system toxins
  • Gastrointestinal irritants
21
Q

what are a some types of toxins that mushrooms can contain?

A
  • Cytotoxins Most important
  • Autonomic nervous system toxins
  • Central nervous system toxins
  • Gastrointestinal irritants
22
Q

what type of toxins are found in cytotoxic mushrooms? what is mechanism? what are clinical signs and lesions?

A

eg Amanita phalloides, amanita verna
HIGH risk

  • Toxin: cyclopeptide amatoxins
  • Mechanism: inhibit RNA polymerase, block protein
    synthesis, signal apoptosis

C/S: Four phases
* Latent period 6-24 hours
* Severe GI signs – pain, vomiting, bloody diarrhea
* Second latent period mimicking recovery
* In 36-84 hours – fulminant hepatic, renal failure, death.

  • Lesions: periacinar to massive hepatic necrosis, renal tubular necrosis
23
Q

what type of toxin does amanita muscaria contain?

A

Ibotenic acid, muscimol – act on two
major neurotransmitters of the central nervous system: glutamic acid and GABA
 Results in these have psychoactive toxic properties (hallucinations)

 Dogs can result in acute gastrointestinal distress that precedes a potentially life-threatening central neurologic syndrome characterized by seizures, tremors, and somnolence
 Dogs like to eat these because apparently they smell like fish