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Toxicology > Hepatic, Dermal, and GI Toxins > Flashcards

Hepatic, Dermal, and GI Toxins Flashcards

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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
What are the signs of Microcystis aeruginosa (blue green algae) toxicity?
Gatroenteritis Hepatic: icterus and other secondary effects of acute liver failure Hepatogenous photosensitization
26
What is the lab diagnosis of Microcystis aeruginosa (blue green algae) toxicity?
Identification of algae from fresh or fixed samples Mouse bioassay High pressure liquid chromatography or gas chromatography
27
What is the treatment for Microcystis aeruginosa (blue green algae) toxicity?
Detoxification, supportive SAM-e/silibin Chloestyramine Procaine penicillin G-organic anion transporting polypeptide (oatp) competes with microcystin for entry in heptocyte
28
What is the Amanita phalloides?
Deadly amanita, death angel
29
What is the toxic principle of Amanita phalloides (deadly amanita)?
Amanita toxins and heptapeptide phallotoxins
30
What is the MOA of Amanita phalloides (deadly amanita)?
Amanita toxins: reduce protein synthesis by inhibiting RNA polymerase and transcription Heptapeptide phallotoxins: affect the hepatic cytocavitary
31
What is the toxic part of Amanita phalloides (deadly amanita)?
All. Stable to heat and drying
32
What species are affected by Amanita phalloides (deadly amanita)?
All
33
What is the time frame for Amanita phalloides (deadly amanita) toxicosis?
Acute
34
What are the clinical signs of Amanita phalloides (deadly amanita) toxicity?
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
What is the lab diagnosis of Amanita phalloides (deadly amanita) toxicity?
Elevated heptocellular enzymes, hyperbilirubinemia | Amatoxins: LC/MS
36
What are the lesions with Amanita phalloides (deadly amanita) toxicity?
Massive liver necrosis, iceterus, gastroenteritis, renal tubular necrosis
37
What is the treatment of Amanita phalloides (deadly amanita) toxicity?
Decontamination of the GI tract early: Emesis and charcoal
38
What is Xanthium strumarium?
Cocklebur
39
What is the toxic principle of Xanthium strumarium (Cocklebur)?
Carboxyatractyloside, Burs devalue wool
40
What is the MOA of Xanthium strumarium (Cocklebur)?
Glycoside- uncouples oxidative phosphorylation; produces hypoglycemia and hepatic damage
41
What is the toxic part of Xanthium strumarium (Cocklebur)?
Toxin in seed, recetly germinated cotyleons
42
What species are affected by Xanthium strumarium (Cocklebur)?
``` Pigs (most sensitive) Sheep Cattle Horse Fowl ```
43
What is the time frame of Xanthium strumarium (Cocklebur) toxicity?
Acute
44
What are the signs associated with Xanthium strumarium (Cocklebur) toxicity?
Depression, abdominal pain, anorexia, vomiting, weakness, coma, death blindness, convulsions
45
What are the lab diagnostics of Xanthium strumarium (Cocklebur) toxicity?
Increased hepatic enzymes, hypoglycemia
46
What are the lesions with Xanthium strumarium (Cocklebur) toxicity?
``` Gatroenteritis Hepatic cetrilobular hemorrhage Necrosis Tubular degenerations Seeding in GI tract ```
47
How can a diagnosis of Xanthium strumarium (Cocklebur) toxicity made?
Signs, lesions, accessibility, plants/burs in GI tract, burs in matted fur
48
What is the treatment for Xanthium strumarium (Cocklebur) toxicity?
Supportive
49
What is the prognosis for Xanthium strumarium (Cocklebur) toxicosis?
Guarded to poor
50
What is the prevention of Xanthium strumarium (Cocklebur) toxicosis?
Denying access to plants, destroy plants with herbicides
51
What are the different pyrrolizidine alkaloid (PA) plants?
``` Crotolaria (rattlebox) Senecio glabellus (Yellow top) ```
52
What are the toxic parts of PA plants?
All. Seeds and flowers are the most toxic, followed by leaves and stems
53
What is the time frame for toxicosis with PA plants?
Occurs from long-term consumption, leads to chronic liver failure
54
What animals are highly sensitive to PA plants?
``` Horses* Swine Cattle* Rat Chicken Sheep ```
55
What animals are less sensitive to PA plants?
``` Mouse Goats Quail Rabits Guinea pigs ```
56
What are the clinical signs of PA toxicosis?
Icterus, depression, anorexia Hepatic encephalopathy Type III or hepatogenous photosensitization
57
What is used for the diagnosis of PA toxicosis?
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
What are the lesions associated with PA toxicosis?
``` Portal fibrosis Megalocytosis Bile duct hyperplasia Bile stasis Nodular hyperplasia Hepatocellular necorsis Cirrhosis ```
59
What is the treatment of PA toxicosis?
Usually futile: serious damage by time animals recognized as ill Supportive care for hepatic failure
60
What is the prevention for PA toxicosis?
Herbicides | Pasture management
61
What is hepatic (type III) photosensitivty?
Photosensitization occurring secondary to liver disease caused by toxin
62
What plants can cause Type III or hepatogenous photosensitization?
``` Lantana camara (ornamenal) Tetradymia (horsebrush) ```
63
What are the photosensitization signs and lesions?
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
What is the toxin of Tetradymia?
Furanosesquiterpenes
65
What are the clinical signs associated with Tetradymia toxicosis?
Acute death from hepatic failure Chronic photosensitization if less hepatic damage Bighead
66
What species is commonly affected by Tetradymia toxicosis?
Sheep
67
What animals are primarily affected by Lantana toxicosis?
Grazing ruminants
68
What is the treatment of hepatic photosensitization?
With clinical signs, GI detoxification is ineffective | Supportive: liver damage, skin or eye dressings/antibiotics, keep eye out of sunlight
69
How can you prevent hepatic photosensitization?
Supplemental feeding | Reduce stocking rates on range
70
What causes primary photosensitization?
``` Hypericum perforatum (St. Johnswort) Ammi majus (Bishops weed) ```
71
What is the toxic principle of Hypericum perforatum (St. Johnswort)?
Hypericin
72
What is the toxic principle of Ammi majus (Bishops weed)?
Psoralens (furocoumarin)
73
What is the MOA of primary photosensitization?
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
What is Ricinus communis?
Castor bean
75
What is the toxic principle of Ricinus communis (castor bean)?
Phytotoxin (ricin), heat liable
76
What is the MOA of Ricinus communis (castor bean)?
Inhibits protein synthesis
77
What is the toxic part of Ricinus communis (castor bean)?
All; seeds most toxic
78
What species are affected by Ricinus communis (castor bean) toxicosis?
All | Horses, small animals > cattle, sheep, hogs
79
What is the time frame of Ricinus communis (castor bean) toxicosis?
Acute 12-24 hours
80
What are the signs of Ricinus communis (castor bean) toxicosis?
Colic, emesis, diarrhea
81
What ate the lesions with Ricinus communis (castor bean) toxicosis?
Minimal intoxication | With seed ingestion: severe reddening, edema, and necrosis of mucosa of GI tract especially stomach and small intestine
82
What is the treatment of Ricinus communis (castor bean) toxicosis?
Emesis detoxification using charcoal, and administration of fluids and electrolytes
83
What is the prevention of Ricinus communis (castor bean) toxicosis?
Don't plant where animals or children have access | Clip heads before mature

Toxicology (4 decks)

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