Hepatic, Dermal, and GI Toxins Flashcards
What are sources of xylitol?
Peanut butter Baked goods Desserts Toothpaste, other oral car products Sugar-free gums and candies
What is xylitol toxic to?
Dogs and ferrets
Where does rapid absortion of xylitol come from?
Stomach
What is the MOA of xylitol?
Stimulates the pancreas to release insulin
Rapid hypoglycemia
What is the hypoglycemic dose of xylitol in dogs?
0.1 g/kg bw (stick of gum has 0.3-0.4 g xylitol)
What is the onset of xylitol toxicity?
30-60 minutes
What are the clinical signs and lesions associated with xylitol?
Weakness Ataxia Collapse Seizures Acute hepatic necrosis May develop coagulopathy: petechial or ecchymotic hemorrhages
What is the clinical pathology associated with xylitol?
Hypoglycemia
Liver enzymes normal if dog can mobilize glycogen; otherwise, increased ALT, AST, GGT within 2-3 hours
Hypokalemia
Later PT and PTT increased
What is used to diagnose xylitol toxicity?
History of ingestion
Identification of fragments of chewing gum or other sources of xylitol
Profound hypoglycemia
Elevated liver enzymes
What is the treatment of xylitol toxicity?
Deconatmination: emesis and administration of activated charcoal
Replenish dextrose
Poor prognosis is severe hepatic necrosis
What are the toxic principles of cycad (Sago palm)?
Glycosides (hepatotoxin): cycasin, macrozamin Amino acids (neprotoxin): β-methylamino-L-alanine Unknown toxicants (neutrotoxin)
What is the MOA of cycad?
Glycosides: irritate GI tract/hepatic necrosis
Amino acids: ataxia in rats; not the cause of neurotoxins in cattle/sheep
What is the toxic part of cycad?
Ceoncentrated in seeds, leaves
What species are affected by cycad?
All, especially dogs
What is the time frame for cycad toxicosis?
Acute, within 12 hours
What are the clinical signs associated with cycad toxicity?
Vomiting and gastroenteritis followed by octerus and coagulopathy
Weakness, ataxia, paresis-cattle ruminants only
What is the lab diagnosis of cycad toxicity?
Increased ALT, AST, ALP, GGT, bilirubin
What are the lesions associated with cycad toxicity?
Centrilobular necrosis, bile retention, icterus, ecchymotic hemorrhages
Ruminants: demyelination and axon degeneration of spinal cord
What is the treatment for cycad toxicity?
Supportive
What is Microcystis aeruginosa?
Blue green algae
What is the toxic principle of Microcystis aeruginosa (blue green algae)?
Microcystin
What is the MOA of Microcystis aeruginosa (blue green algae)?
Collapse of hepatocyte structure
What are the species affected by Microcystis aeruginosa (blue green algae)?
All, including waterfowl
What is the time frame of Microcystis aeruginosa (blue green algae) toxicosis?
Acute
What are the signs of Microcystis aeruginosa (blue green algae) toxicity?
Gatroenteritis
Hepatic: icterus and other secondary effects of acute liver failure
Hepatogenous photosensitization
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
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
What is the Amanita phalloides?
Deadly amanita, death angel
What is the toxic principle of Amanita phalloides (deadly amanita)?
Amanita toxins and heptapeptide phallotoxins
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
What is the toxic part of Amanita phalloides (deadly amanita)?
All. Stable to heat and drying
What species are affected by Amanita phalloides (deadly amanita)?
All
What is the time frame for Amanita phalloides (deadly amanita) toxicosis?
Acute
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
What is the lab diagnosis of Amanita phalloides (deadly amanita) toxicity?
Elevated heptocellular enzymes, hyperbilirubinemia
Amatoxins: LC/MS
What are the lesions with Amanita phalloides (deadly amanita) toxicity?
Massive liver necrosis, iceterus, gastroenteritis, renal tubular necrosis
What is the treatment of Amanita phalloides (deadly amanita) toxicity?
Decontamination of the GI tract early: Emesis and charcoal
What is Xanthium strumarium?
Cocklebur
What is the toxic principle of Xanthium strumarium (Cocklebur)?
Carboxyatractyloside, Burs devalue wool
What is the MOA of Xanthium strumarium (Cocklebur)?
Glycoside- uncouples oxidative phosphorylation; produces hypoglycemia and hepatic damage
What is the toxic part of Xanthium strumarium (Cocklebur)?
Toxin in seed, recetly germinated cotyleons
What species are affected by Xanthium strumarium (Cocklebur)?
Pigs (most sensitive) Sheep Cattle Horse Fowl
What is the time frame of Xanthium strumarium (Cocklebur) toxicity?
Acute
What are the signs associated with Xanthium strumarium (Cocklebur) toxicity?
Depression, abdominal pain, anorexia, vomiting, weakness, coma, death blindness, convulsions
What are the lab diagnostics of Xanthium strumarium (Cocklebur) toxicity?
Increased hepatic enzymes, hypoglycemia
What are the lesions with Xanthium strumarium (Cocklebur) toxicity?
Gatroenteritis Hepatic cetrilobular hemorrhage Necrosis Tubular degenerations Seeding in GI tract
How can a diagnosis of Xanthium strumarium (Cocklebur) toxicity made?
Signs, lesions, accessibility, plants/burs in GI tract, burs in matted fur
What is the treatment for Xanthium strumarium (Cocklebur) toxicity?
Supportive
What is the prognosis for Xanthium strumarium (Cocklebur) toxicosis?
Guarded to poor
What is the prevention of Xanthium strumarium (Cocklebur) toxicosis?
Denying access to plants, destroy plants with herbicides
What are the different pyrrolizidine alkaloid (PA) plants?
Crotolaria (rattlebox) Senecio glabellus (Yellow top)
What are the toxic parts of PA plants?
All. Seeds and flowers are the most toxic, followed by leaves and stems
What is the time frame for toxicosis with PA plants?
Occurs from long-term consumption, leads to chronic liver failure
What animals are highly sensitive to PA plants?
Horses* Swine Cattle* Rat Chicken Sheep
What animals are less sensitive to PA plants?
Mouse Goats Quail Rabits Guinea pigs
What are the clinical signs of PA toxicosis?
Icterus, depression, anorexia
Hepatic encephalopathy
Type III or hepatogenous photosensitization
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
What are the lesions associated with PA toxicosis?
Portal fibrosis Megalocytosis Bile duct hyperplasia Bile stasis Nodular hyperplasia Hepatocellular necorsis Cirrhosis
What is the treatment of PA toxicosis?
Usually futile: serious damage by time animals recognized as ill
Supportive care for hepatic failure
What is the prevention for PA toxicosis?
Herbicides
Pasture management
What is hepatic (type III) photosensitivty?
Photosensitization occurring secondary to liver disease caused by toxin
What plants can cause Type III or hepatogenous photosensitization?
Lantana camara (ornamenal) Tetradymia (horsebrush)
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”
What is the toxin of Tetradymia?
Furanosesquiterpenes
What are the clinical signs associated with Tetradymia toxicosis?
Acute death from hepatic failure
Chronic photosensitization if less hepatic damage
Bighead
What species is commonly affected by Tetradymia toxicosis?
Sheep
What animals are primarily affected by Lantana toxicosis?
Grazing ruminants
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
How can you prevent hepatic photosensitization?
Supplemental feeding
Reduce stocking rates on range
What causes primary photosensitization?
Hypericum perforatum (St. Johnswort) Ammi majus (Bishops weed)
What is the toxic principle of Hypericum perforatum (St. Johnswort)?
Hypericin
What is the toxic principle of Ammi majus (Bishops weed)?
Psoralens (furocoumarin)
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
What is Ricinus communis?
Castor bean
What is the toxic principle of Ricinus communis (castor bean)?
Phytotoxin (ricin), heat liable
What is the MOA of Ricinus communis (castor bean)?
Inhibits protein synthesis
What is the toxic part of Ricinus communis (castor bean)?
All; seeds most toxic
What species are affected by Ricinus communis (castor bean) toxicosis?
All
Horses, small animals > cattle, sheep, hogs
What is the time frame of Ricinus communis (castor bean) toxicosis?
Acute 12-24 hours
What are the signs of Ricinus communis (castor bean) toxicosis?
Colic, emesis, diarrhea
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
What is the treatment of Ricinus communis (castor bean) toxicosis?
Emesis detoxification using charcoal, and administration of fluids and electrolytes
What is the prevention of Ricinus communis (castor bean) toxicosis?
Don’t plant where animals or children have access
Clip heads before mature
