GI & Repro Flashcards
Examples of NSAIDs that cause toxicity
Aspirin, ibuprofen, naproxen
Dogs are sensitive to ibuprofen
Cats are sensitive to aspirin due to glucuronidation
Mechanism of action of NSAID toxicity
Inhibition of prostaglandin synthesis and renal blood flow (analgesic nephropathy) Vasoconstrictive acute renal failure Acute interstitial nephritis Fluid and electrolyte imbalanced Renal papillary necrosis Chronic renal failure
Uncoupled oxidative phosphorylation at high doses
Increases lactic acid
Metabolic acidosis
Clinical signs of aspirin toxicity
Acute: Nausea, vomiting, anorexia Fever, respiratory stimulation Depression, lethargy, seizure, coma Acidosis with anion gap Renal failure
Chronic: Gastric irritation and ulceration Anemia Heinz bodies Thrombocytopenia
Clinical signs of naproxen toxicity
Bloody vomit Black tarry stool Diarrhea Anorexia Weakness Lethargy Painful abdomen Pale gums Facial twitching, seizures, depression, coma
Diagnosis of NSAID-induced toxicity
Clinical signs Increased anion gap Increased liver enzymes, jaundice Prolonged clotting time Acute renal failure (renal tubular casts)
What would you find on necropsy that would be typical of chronic NSAID-induced toxicity?
Gastric ulcers
Treatment of NSAID-induced toxicity
Induce emesis and activated charcoal
Address GI ulceration and acute renal failure (ranitidine, sucralfate)
Supportive care
Transfusion?
What is the #1 priority pollutant?
Arsenic
Sources of arsenic exposure
Insecticides Medicine Food production Electronics Shellfish Water
Mechanism of action of arsenic toxicity
Pentavalent and trivalent forms
Pentavalent: reduced and metabolized in rumen
- Reduces available metabolic energy
- Some gets converted into trivalent form, which produces toxicosis
Trivalent:binds to -SH groups -> disrupts cellular metabolism and inhibits oxidative phosphorylation
Causes serious toxicity to GI epithelium and capillary endothelium leading to enteritis and shock
Clinical signs of arsenic poisoning
Intense abdominal pain, gastroenteritis, vomiting
Weakness, staggering gait
PU/PD, oliguria, anuria, dehydration, thirst
Blood related: cold extremities due to poor perfusion
CNS-related: salivation, trembling, depression, posterior paresis
Lesions associated with arsenic toxicity
Brick red gut (abomasum in ruminants)
Fluid GI contents, sometimes foul smelling
Soft, yellow liverRed, congested lungs
Kidney damage
Diagnosis of arsenic toxicity
Sudden onset of gastroenteritis or sudden death, especially near standing water
Liver or kidney has arsenic >5ppm
Should also examine stomach contents or vomitus
Readily absorbed from GI tract, rapidly excreted
Treatment of arsenic toxicity
GI decontamination
Chelation therapy with dimercaprol
Supportive therapy
Prognosis is guarded to poor
Sources of zinc that commonly cause toxicosis
Any galvanized metals: nuts, bolts, wire (hardware ingestion)
Pennies made after 1982 (96% zinc)
Topical ointments (desiring, sunscreen)
Mechanism of action of zinc toxicity
Formation of zinc salts in stomach, which has corrosive effect
Oxidative damage causes hemolysis
Usually seen in dogs and aquatic organisms