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Toxicology > Hepatic, Dermal, and GI Toxins > Flashcards

Hepatic, Dermal, and GI Toxins Flashcards

1
Q

What are sources of xylitol?

A 
Peanut butter
Baked goods
Desserts
Toothpaste, other oral car products
Sugar-free gums and candies
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2
Q

What is xylitol toxic to?

A

Dogs and ferrets

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3
Q

Where does rapid absortion of xylitol come from?

A

Stomach

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4
Q

What is the MOA of xylitol?

A

Stimulates the pancreas to release insulin

Rapid hypoglycemia

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5
Q

What is the hypoglycemic dose of xylitol in dogs?

A

0.1 g/kg bw (stick of gum has 0.3-0.4 g xylitol)

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6
Q

What is the onset of xylitol toxicity?

A

30-60 minutes

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7
Q

What are the clinical signs and lesions associated with xylitol?

A 
Weakness
Ataxia
Collapse
Seizures
Acute hepatic necrosis
May develop coagulopathy: petechial or ecchymotic hemorrhages
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8
Q

What is the clinical pathology associated with xylitol?

A

Hypoglycemia
Liver enzymes normal if dog can mobilize glycogen; otherwise, increased ALT, AST, GGT within 2-3 hours
Hypokalemia
Later PT and PTT increased

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9
Q

What is used to diagnose xylitol toxicity?

A

History of ingestion
Identification of fragments of chewing gum or other sources of xylitol
Profound hypoglycemia
Elevated liver enzymes

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10
Q

What is the treatment of xylitol toxicity?

A

Deconatmination: emesis and administration of activated charcoal
Replenish dextrose
Poor prognosis is severe hepatic necrosis

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11
Q

What are the toxic principles of cycad (Sago palm)?

A 
Glycosides (hepatotoxin): cycasin, macrozamin
Amino acids (neprotoxin): β-methylamino-L-alanine
Unknown toxicants (neutrotoxin)
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12
Q

What is the MOA of cycad?

A

Glycosides: irritate GI tract/hepatic necrosis

Amino acids: ataxia in rats; not the cause of neurotoxins in cattle/sheep

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13
Q

What is the toxic part of cycad?

A

Ceoncentrated in seeds, leaves

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14
Q

What species are affected by cycad?

A

All, especially dogs

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15
Q

What is the time frame for cycad toxicosis?

A

Acute, within 12 hours

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16
Q

What are the clinical signs associated with cycad toxicity?

A

Vomiting and gastroenteritis followed by octerus and coagulopathy
Weakness, ataxia, paresis-cattle ruminants only

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17
Q

What is the lab diagnosis of cycad toxicity?

A

Increased ALT, AST, ALP, GGT, bilirubin

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18
Q

What are the lesions associated with cycad toxicity?

A

Centrilobular necrosis, bile retention, icterus, ecchymotic hemorrhages
Ruminants: demyelination and axon degeneration of spinal cord

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19
Q

What is the treatment for cycad toxicity?

A

Supportive

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20
Q

What is Microcystis aeruginosa?

A

Blue green algae

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21
Q

What is the toxic principle of Microcystis aeruginosa (blue green algae)?

A

Microcystin

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22
Q

What is the MOA of Microcystis aeruginosa (blue green algae)?

A

Collapse of hepatocyte structure

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23
Q

What are the species affected by Microcystis aeruginosa (blue green algae)?

A

All, including waterfowl

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24
Q

What is the time frame of Microcystis aeruginosa (blue green algae) toxicosis?

A

Acute

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25
Q

What are the signs of Microcystis aeruginosa (blue green algae) toxicity?

A

Gatroenteritis
Hepatic: icterus and other secondary effects of acute liver failure
Hepatogenous photosensitization

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26
Q

What is the lab diagnosis of Microcystis aeruginosa (blue green algae) toxicity?

A

Identification of algae from fresh or fixed samples
Mouse bioassay
High pressure liquid chromatography or gas chromatography

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27
Q

What is the treatment for Microcystis aeruginosa (blue green algae) toxicity?

A

Detoxification, supportive SAM-e/silibin
Chloestyramine
Procaine penicillin G-organic anion transporting polypeptide (oatp) competes with microcystin for entry in heptocyte

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28
Q

What is the Amanita phalloides?

A

Deadly amanita, death angel

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29
Q

What is the toxic principle of Amanita phalloides (deadly amanita)?

A

Amanita toxins and heptapeptide phallotoxins

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30
Q

What is the MOA of Amanita phalloides (deadly amanita)?

A

Amanita toxins: reduce protein synthesis by inhibiting RNA polymerase and transcription
Heptapeptide phallotoxins: affect the hepatic cytocavitary

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31
Q

What is the toxic part of Amanita phalloides (deadly amanita)?

A

All. Stable to heat and drying

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32
Q

What species are affected by Amanita phalloides (deadly amanita)?

A

All

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33
Q

What is the time frame for Amanita phalloides (deadly amanita) toxicosis?

A

Acute

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34
Q

What are the clinical signs of Amanita phalloides (deadly amanita) toxicity?

A

Gastrointestinal: 8-36 hours latency followed by abdominal pain, GI signs
Hepatic: apparent recovery from GI phase; in 1-3 days severe hepatic failure with hepatic necrosis, icterus, and coagulopathy

35
Q

What is the lab diagnosis of Amanita phalloides (deadly amanita) toxicity?

A

Elevated heptocellular enzymes, hyperbilirubinemia

Amatoxins: LC/MS

36
Q

What are the lesions with Amanita phalloides (deadly amanita) toxicity?

A

Massive liver necrosis, iceterus, gastroenteritis, renal tubular necrosis

37
Q

What is the treatment of Amanita phalloides (deadly amanita) toxicity?

A

Decontamination of the GI tract early: Emesis and charcoal

38
Q

What is Xanthium strumarium?

A

Cocklebur

39
Q

What is the toxic principle of Xanthium strumarium (Cocklebur)?

A

Carboxyatractyloside, Burs devalue wool

40
Q

What is the MOA of Xanthium strumarium (Cocklebur)?

A

Glycoside- uncouples oxidative phosphorylation; produces hypoglycemia and hepatic damage

41
Q

What is the toxic part of Xanthium strumarium (Cocklebur)?

A

Toxin in seed, recetly germinated cotyleons

42
Q

What species are affected by Xanthium strumarium (Cocklebur)?

A 
Pigs (most sensitive)
Sheep
Cattle
Horse
Fowl
43
Q

What is the time frame of Xanthium strumarium (Cocklebur) toxicity?

A

Acute

44
Q

What are the signs associated with Xanthium strumarium (Cocklebur) toxicity?

A

Depression, abdominal pain, anorexia, vomiting, weakness, coma, death blindness, convulsions

45
Q

What are the lab diagnostics of Xanthium strumarium (Cocklebur) toxicity?

A

Increased hepatic enzymes, hypoglycemia

46
Q

What are the lesions with Xanthium strumarium (Cocklebur) toxicity?

A 
Gatroenteritis
Hepatic cetrilobular hemorrhage
Necrosis
Tubular degenerations
Seeding in GI tract
47
Q

How can a diagnosis of Xanthium strumarium (Cocklebur) toxicity made?

A

Signs, lesions, accessibility, plants/burs in GI tract, burs in matted fur

48
Q

What is the treatment for Xanthium strumarium (Cocklebur) toxicity?

A

Supportive

49
Q

What is the prognosis for Xanthium strumarium (Cocklebur) toxicosis?

A

Guarded to poor

50
Q

What is the prevention of Xanthium strumarium (Cocklebur) toxicosis?

A

Denying access to plants, destroy plants with herbicides

51
Q

What are the different pyrrolizidine alkaloid (PA) plants?

A 
Crotolaria (rattlebox)
Senecio glabellus (Yellow top)
52
Q

What are the toxic parts of PA plants?

A

All. Seeds and flowers are the most toxic, followed by leaves and stems

53
Q

What is the time frame for toxicosis with PA plants?

A

Occurs from long-term consumption, leads to chronic liver failure

54
Q

What animals are highly sensitive to PA plants?

A 
Horses*
Swine
Cattle*
Rat
Chicken
Sheep
55
Q

What animals are less sensitive to PA plants?

A 
Mouse
Goats
Quail
Rabits
Guinea pigs
56
Q

What are the clinical signs of PA toxicosis?

A

Icterus, depression, anorexia
Hepatic encephalopathy
Type III or hepatogenous photosensitization

57
Q

What is used for the diagnosis of PA toxicosis?

A

History: chronic dietary exposure to plant materials
Clinical signs and gross lesions
Detection of PA in plant material and pyrroles in blood and liver

58
Q

What are the lesions associated with PA toxicosis?

A 
Portal fibrosis
Megalocytosis
Bile duct hyperplasia
Bile stasis
Nodular hyperplasia
Hepatocellular necorsis
Cirrhosis
59
Q

What is the treatment of PA toxicosis?

A

Usually futile: serious damage by time animals recognized as ill
Supportive care for hepatic failure

60
Q

What is the prevention for PA toxicosis?

A

Herbicides

Pasture management

61
Q

What is hepatic (type III) photosensitivty?

A

Photosensitization occurring secondary to liver disease caused by toxin

62
Q

What plants can cause Type III or hepatogenous photosensitization?

A 
Lantana camara (ornamenal)
Tetradymia (horsebrush)
63
Q

What are the photosensitization signs and lesions?

A

Time: 1-3 days
Early: eryhtemia, edema, puritis, photophobia, hyperesthesia
Later: exudation of serum, formation of vesicles, ulceration, exfoliation of damaged epidermis, blindness
Reduced feed intake and cessation of nursing and breeding
Sheep: edema of ears and face “big head”

64
Q

What is the toxin of Tetradymia?

A

Furanosesquiterpenes

65
Q

What are the clinical signs associated with Tetradymia toxicosis?

A

Acute death from hepatic failure
Chronic photosensitization if less hepatic damage
Bighead

66
Q

What species is commonly affected by Tetradymia toxicosis?

A

Sheep

67
Q

What animals are primarily affected by Lantana toxicosis?

A

Grazing ruminants

68
Q

What is the treatment of hepatic photosensitization?

A

With clinical signs, GI detoxification is ineffective

Supportive: liver damage, skin or eye dressings/antibiotics, keep eye out of sunlight

69
Q

How can you prevent hepatic photosensitization?

A

Supplemental feeding

Reduce stocking rates on range

70
Q

What causes primary photosensitization?

A 
Hypericum perforatum (St. Johnswort)
Ammi majus (Bishops weed)
71
Q

What is the toxic principle of Hypericum perforatum (St. Johnswort)?

A

Hypericin

72
Q

What is the toxic principle of Ammi majus (Bishops weed)?

A

Psoralens (furocoumarin)

73
Q

What is the MOA of primary photosensitization?

A

Molecules go directly to surface of skin
Molecules at surface of unpigmented skin fluoresce when struck by long wave UV
Creates unstable energized molecules which collide with other cell constituents
Creates free radicals
Free radicals damage cell membranes

74
Q

What is Ricinus communis?

A

Castor bean

75
Q

What is the toxic principle of Ricinus communis (castor bean)?

A

Phytotoxin (ricin), heat liable

76
Q

What is the MOA of Ricinus communis (castor bean)?

A

Inhibits protein synthesis

77
Q

What is the toxic part of Ricinus communis (castor bean)?

A

All; seeds most toxic

78
Q

What species are affected by Ricinus communis (castor bean) toxicosis?

A

All

Horses, small animals > cattle, sheep, hogs

79
Q

What is the time frame of Ricinus communis (castor bean) toxicosis?

A

Acute 12-24 hours

80
Q

What are the signs of Ricinus communis (castor bean) toxicosis?

A

Colic, emesis, diarrhea

81
Q

What ate the lesions with Ricinus communis (castor bean) toxicosis?

A

Minimal intoxication

With seed ingestion: severe reddening, edema, and necrosis of mucosa of GI tract especially stomach and small intestine

82
Q

What is the treatment of Ricinus communis (castor bean) toxicosis?

A

Emesis detoxification using charcoal, and administration of fluids and electrolytes

83
Q

What is the prevention of Ricinus communis (castor bean) toxicosis?

A

Don’t plant where animals or children have access

Clip heads before mature

Toxicology (4 decks)

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