Urinary Toxicology, Pt. 2 Flashcards
What are some oxalate-containing plants that are nephrotoxic? What animals are most susceptible?
- beets and docks (Rumex spp.)
- Halogeton spp.
- lamb’s quarter (Chenopodium spp.)
- greasewood (Sarcobatus)
- rhubarb (Rheum spp.)
- soursob (Oxalis cernua)
- Setaria, Kochia, Amaranthus
livestock (mostly sheep and cattle) and companion animals
What is the mechanism of toxicity of oxalate-containing plants? What is partly responsible for renal cell damage?
soluble oxalates bind to serum calcium to form calcium oxalate, which cases hypocalcemia and crystalizes in the kidney, causing tubular necrosis
free radical production (scavengers were shown. to reverse renal damage
What causes clinical signs associated with oxalate-containing plant toxicosis? What are the most common clinical signs?
hypocalcemia
- muscle tremors, tetany, seizures
- weakness, incoordination, reluctance to move, recumbency
- depression coma
- rumen atony, bloat
- teeth grinding, slobbering
- bradycardia
- vomiting, increased BUN and weight loss in those that do not die acutely
How is oxalate-containing plant toxicosis diagnosed? What 3 treatments are recommended?
plant identification, calcium oxalate crystals in kidneys, oxalate in forage
- SMALL ANIMALS: induce emesis and give dairy products, like milk or yogurt to bind oxalate
- dicalcium phosphate:sodium chloride (1:3) binds oxalates in gut
- IV fluid in animals with renal insufficiency
What species is especially susceptible to Lilium and Hemerocallis (lily) toxicity? What is the toxic principle?
cats
unknown water-soluble toxin found in the leaves and flowers
What is the mechanism of toxicity of Lilium and Hemerocallis (lily)? What are the 2 components necessary for acute renal failure?
renal tubular epithelial cell damage
- direct action of the toxin(s) on the renal tubular epithelium resulting in cellular damage
- severe dehydration due to polyuria
When are most cases of Lilium and Hemerocallis (lily) toxicity common? What are the initial and later clinical signs?
1-3 weeks after Easter
- INITIALLY: depression, vomiting, anorexia, salivation, progressive weakness
- LATER: PU followed by dehydration, anuria,and recumbency
What treatment is recommended for anuric patients with Lilum and Hemerocallis (lily) toxicity?
- correct dehydration and impose fluid diuresis (2-3x amount of maintenance)
- peritoneal dialysis or hemodialysis
What species is most susceptible to grape and raisin toxicity?
dogs, maybe cats and ferrets
all types and colors of grapes/raisins are toxic and toxic dosage varies widely
What is thought to be the toxic principle of grapes and raisins? What are 3 reasons this is hypothesized?
tartaric acid and potassium bitartrate
- toxicity of potassium bitartrate is characterized by similar clinical signs and proximal renal tubule damage as grapes and raisins
- exposure to tamarinds, which are uniquely ricj in tartaric acid, cause similar severe vomiting and acute renal failure in dogs as grapes and raisins
- grapes contain high levels of both, with levels varying depending on growing conditions and ripeness
What are 5 other additional toxins suspected to be present in grapes/raisins?
- ochratoxin
- flavonoids
- polyphenols
- tannins
- monosaccharides
Why is rapid absorption of grape and raisin toxins suspected? What describes why a clear dose-response curve has not been established yet?
toxicosis has rapid onset
variation in the number of toxic principles or varying sensitivities among individual dogs
Where is the injury to the kidneys most concentrated with grape/raisin toxicity? What does this result in? What may explain the variability in toxicosis?
proximal renal tubular epithelium
idiosyncratic reaction resulting in hypovolemic shock and renal ischemia
variability in tartaric acid and potassium bitartrate in grape types, different growing conditions, and ripeness
What clinical sign is first noted with grape/raisin toxicity? What develops?
vomiting within 6-12 hr of ingestion, likely due to direc effect of the toxins on the GIT or from uremia secondary to renal failure
- diarrhea, anorexia, lethargy
- abdominal pain, weakness, dullness
- dehydration isosthenuria, oliguria/anuria
- increased BUN and creatinine within 24 hours
- hypercalcemia, hyperphosphatemia, hyperkalemia
- anuric renal failure leads to death or euthanasia
What treatments are used to combat renal failure in grape/raisin toxicity? What symptomatic/supportive treatments are recommended?
- Furosemide
- Dopamine
- Mannitol
- hemodialysis/peritoneal dialysis
VOMITING - antiemetics
IV FLUIDS - monitor central venous pressure in anterior vena cava and uring production for potential fluid overloas
What is Amphotericin-B? What is the major factor that limits its use?
antifungal - Fungizone, Amphotec, AmBisome used to treat candidiasis, aspergillosis, and histoplasmosis
nephrotoxicity