Toxicants Affecting the Liver & GI II (13) Flashcards
What is the MOA of xylitol toxicity in dogs?
Dogs sees xylitol as glucose → drives insulin response → lowers glucose instead → hypokalemia
What are the primary effects of xylitol toxicity in dogs?
hypoglycemia - develop within 30 minutes
liver injury - 1-2 days later
What is the toxicant in dieffenbachia (dumbcane)?
calcium oxalate crystals (raphides) produce physical damage to skin and mucous membranes in which they contact
hypocalcemia and crystallize in renal tubules, resulting in kidney damage
What is the MOA for oxalate toxicity?
Chewing the leaves and stems causes sharp crystals, called raphides, to be forcibly ejected from idioblast cells in the plant.
The crystals usually don’t dissolve but ingestion of the juice of the plant or water in which plants
are rooted can result in hypocalcemia and renal tubular damage
What are clinical signs of oxalate toxicity?
Immediate response is evidence of pain in the mouth, head shaking, intense salivation, unusual vocalization
What does oxalate toxicity cause?
stomatitis, toxic dose depends on the degree the plant tissue was chewed
What are the toxicants in pokeweed?
saponins and oxalates, phytolaccotoxin
What is the MOA of pokeweed?
irritation of the mucosal surface
What is pokeweed?
a traditional southern Appalachian food
What are clinical signs of pokeweed?
oral irritation, excessive salivation, vomiting, colic, bloody diarrhea, depression, prostration, and death
mild to severe gastroenteritis
What is the toxicant in the castor plant?
ricin
What is the MOA of the castor bean?
Ricin is transported into the cells by endocytosis → in cytoplasm can migrate into the ER → depurinates the 28S ribosomes in rRNA = protein synthesis ceases and the cell dies
Also interferes with Ca2+ transport
What are clinical signs of castor bean toxicity?
GI tract: intestinal mucosa: diarrhea, vomiting, decreased nutritional absorption, increased bacterial infections and hemorrhagic gastroenteritis
What is the toxicant in buttercup?
Ranunculin converted to protoanemonin
What is the MOA of buttercup toxicity?
Ranunculin is converted to protoanemonin by release of plant enzymes during mastication → is a potent drying agent (vesicant) that irritates mucous membranes of the GI system
What are clinical signs of buttercup toxicity?
Irritation to the mouth and upper GI tract, swelling of the muzzle and lips
What is the toxic principle of autumn crocus?
colchicine - found mostly in corms and seeds
What is the MOA of colchicine toxicity regarding autumn crocus?
interferes with spindle formation in normally dividing cells
rapidly dividing cell such as epithelium are most affected
What are the toxic principles of red clovers - slaframine toxicity?
mycotoxins slaframine and swainsonine
What are clinical signs of slaframine toxicity?
salivation (slobbers) in most animals
Look at this
What is cyclooxygenase?
exists in the tissue as constitutive isoform (COX-1)
at site of inflammation, cytokines stimulates the induction of the 2nd isoform (COX-2)
most currently used NSAIDs are somewhat selective for COX-1 but selective COX-2 inhibitors are available
What are NSAIDs?
diverse group of chemicals that all inhibit cyclooxygenase
resultant inhibition of prostaglandin synthesis
What happens if prostaglandin synthesis is inhibited?
GIT damage (dyspepsia, gastritis)
What happens if you drop COX-1?
don’t have that lining
What do NSAIDs also inadvertently inhibit, along with prostaglandin synthesis?
decreases GFR because blocking prostaglandins which are vasodilators
What are common adverse effects to NSAIDs?
