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
Clinical signs of acute zinc toxicity
Occurs within a few days Vomiting Depression Anorexia Hemolytic anemia Jaundice Pancreatitis Enteritis, renal, hepatic, and pancreatic necrosis
Clinical signs of chronic zinc toxicity
Occurs most in cattle Onset time is several weeks PU/PD Diarrhea Anorexia Hemolytic anemia Lameness Gastric ulcers, renal tubule necrosis, hepatocyte necrosis
Diagnosing zinc toxicity
Serum zinc levels >10ppm Liver zinc >200ppm Decreased PCV, regen. Anemia, thrombocytopenia Heinz bodies Inc. kidney, liver, pancreatic enzymes Hemoglobinuria Radiographs for hardware ingestion
Treating zinc toxicity
Remove foreign body Emesis Fluids Omeprazole (Proton-pump inhibitor) H2 blocker
What is the 4th most common group of toxins that the Animal Poison Control Center receives calls for?
Household chemicals
Dow oven cleaner, easy off, drano, liquid plumber cause esophageal ulceration
Toxicity caused by ammonia, alcohols, chlorines, bleach, etc.
Clinical signs and treatment of soap/shampoo ingestion
Clinical signs: GI distress, vomiting, diarrhea
Treatment: DILUTION! Milk or water, fluid treatment
Clinical signs and treatment of scouring powder/bleach ingestion
Causes liquefactive necrosis
Clinical signs: vomiting, drooling, abdominal pain
Treatment: milk or water, gastroprotectants, activated charcoal and cathartics
NO EMESIS
Mechanism of action of disinfectants
Phenols: denature and precipitate cellular proteins this destroying all contacted cells
Pine oils: direct irritation to mucous membranes. Cats are more susceptible.
Clinical signs of disinfectant toxicosis
Phenols- corrosive burns of oral-esophageal pathway, vomiting, hypersalivation, ataxia, panting progresses to shock, cardiac arrhythmias, metHb, hepatic and renal damage, coma
Pine Oil- nausea, hypersalivation, bloody vomit, abdominal pain, ataxia, hypotension, respiratory depression, acute renal failure, pulmonary edema
Two types of disinfectants
Phenols
Pine Oils
Treatment of disinfectant toxicity
Dilute with gastroprotectants (milk or eggs)
Activated charcoal or cathartic
Methylene blue for MetHb
Supportive therapy
No emesis or lavage!
Toxicosis from automatic dishwasher detergent is mostly due to
High alkalinity (pH>10.5)
Examples of automatic dishwasher detergents
Cascade
Palmolive
All
Electrasol
Clinical signs of automatic dishwasher detergent toxicity
Vomiting Diarrhea Salivation GI pain Oral, esophageal, gastric erosions
Treatment of automatic dishwasher detergent toxicity
Dilution with milk or water
Analgesics
Possibly steroids for inflammation
Main reason toilet bowl cleaners are toxic
Acidic!
Contain sulfuric acid or hydrochloridic acid
Clinical signs of toilet bowl cleaner toxicity
Vomiting, salivation, dysphagia, abdominal pain, GI ulceration, dyspnea
Treatment of toilet bowl cleaner toxicity
Dilution with milk or water
Steroids if stricture
Symptomatic
NO emesis, lavage, activated charcoal or catharsis
What foods contain phytoestrogens?
Soybeans
Lentils
What is zearalenone
Mycotoxin produced by Fusarium spp. Often found with deoxynivalenol (DON)
Toxin production happens during storage ( is heat stable, resistant to mold, and most grains can be affected)
Affects most animals but chickens are resistant
Mechanism of zearalenone action
Estrogen receptor agonist
Alpha-zearalenone has a higher affinity for estrogen receptors
Causes “hyperestrogen “ syndrome (vulvogaginitis and estrogenic responses in swine)
Clinical signs of zearalenone toxicity in swine and ferrets
In ferrets and pigs, symptoms depend on sex and maturity
Males: decreased libido, infertility
Females: enlarged, swollen uteri, shrunken/cystic ovaries, swollen/reddened vulva, vaginal/rectal prolapse
Both: immunosuppression, liver damage, decreased litter size and birth weights
Clinical signs of zearalenone toxicity in cattle and sheep
Similar to swine/ferrets but also:
Males: regression of testis, feminization
Females: abortion, psuedo pregnancies
Diagnosis of zearalenone toxicity
Presence of >1-2ppm zearalenone in swine feed
Reversal of symptoms when feed is changed (7-10 days)
Treatment of zearalenone toxicity
Change feed
Activated charcoal or high fiber may reduce elimination times due to extensive enterohepatic recycling
