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Toxicology > GI and Reproductive Toxins > Flashcards

GI and Reproductive Toxins Flashcards

1
Q

NSAIDs

A
  • Include aspirin, ibuprofen, naproxen
  • absorbed well from the stomach and intestinal mucosa
  • Dogs are sensitive to ibuprofen (25 mg/kg)
  • Cats are sensitive to aspirin (25 mg/kg) due to lack of glucuronidation
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2
Q

MOA of NSAIDs

A
  • Inhibit COX-1 and COX-2 which make prostaglandins
  • Uncouple oxidative phosphorylation at high doses
    • increase lactic acid, metabolic acidosis
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3
Q

COX-1 actions

A

Create prostaglandins that protect gastric mucosa and help with hemostasis

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4
Q

COX-2 actions

A

Create prostaglandins that mediate pain, inflammation, and fever

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5
Q

MOA of NSAID toxicity

A
  • GI and RENAL
  • Cause gastric ulceration
  • Cause renal toxicity mainly by the inhibition of prostaglandin synthesis and renal blood flow (analgesic nephropathy)
    • vasoconstructive acute renal failure
    • acute interstitial nephritis
    • fluid and electrolyte imbalanes
    • renal papillary necrosis
    • chronic renal failure
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6
Q

clinical signs of acute aspirin toxicity

A
  • Nausea, vomiting (may be blood tinged), anorexia
  • Fever and respiratory stimulation with high doses
  • Depression (muscle weakness, ataxia), lethargy, seizure, coma
  • Acidosis with anion gap
  • Reduced renal flow, renal failure
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7
Q

clinical signs of chronic aspirin toxicity

A
  • Gastric irritation and ulceration most common
  • Anemia, bone marrow depression
  • Heinz bodies, thrombocytopenia in cats
  • toxic dose for dogs is 50 mg/kg/day
  • toxic dose for cats is 25 mg/kg/day
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8
Q

Naproxen clinical signs

A
  • Vomiting (sometimes bloody)
  • black tarry stool
  • diarrhea
  • anorexia, weakness, lethargy
  • painful abdomen
  • pale gums
  • more rare: facial twitching (cats), seizures, depression, coma
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9
Q

diagnosis of NSAID toxicity

A
  • Hx and clinical signs
    • GI irritation, lethargy, anemia
    • in cases of perforation due to ulcers, signs will include abdominal pain, shock, dark red mm, tachycardia
  • Anion gap due to acidosis (for salicylates)
  • Increased liver enzymes, jaundice
  • Increased blood clotting time
  • Acute renal failure
    • renal tubular casts in urine sediment (incr. BUN, creat)
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10
Q

treatment of NSAID toxicity

A
  • Induced emesis and activated charcoal several times
  • Address GI ulceration and acute renal failure as necessary
    • use ranitidine or similar H2-blocker, or sucralfate and misoprostol for a few weeks to heal or prevent ulcers
  • Supportive care (watch for and treat acidosis, hyperkalemia, correct electrolyte and glucose levels, increase renal blood flow and maintain urine flow)
  • Consider transfusion for animals with significant hemorrhage/severe anemia
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11
Q

arsenic

A
  • The #1 priority pollutant
  • Sources:
    • insecticides
    • medicine
    • food production (chicken and swine feed additive)
    • electronics
    • shellfish
    • water
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12
Q

inorganic arsenicals

A
  • mechanism of action depends on form
    • Pentavalent
    • Trivalent
  • Causes serious toxicity to GI epithelium and capillary endothelium leading to enteritis and shock
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13
Q

pentavalent MOA

A
  • *Reduced and metabolized in the rumen** and:
    1. reduces available metabolic energy
    2. some gets converted to the trivalent form, producing toxicosis
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14
Q

trivalent MOA

A
  • binds to -SH groups and disrupts cellular metabolism and inhibits oxidative phosphorylation enzymes, reducing metabolism
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15
Q

clinical signs of inorganic arsenic poisoning

A
  • Depends on dose
  • Acute/sub-acute exposure
    • intense abdominal pain, gastroenteritis
    • weakness, staggering gait
    • salivation, trembling
    • vomiting (dogs)
    • PU/PD progressing to oliguria and anuria
    • dehydration, thirst
    • posterior paresis
    • cold extremities due to poor perfusion
    • subnormal temps
    • may live for 1-3 days
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16
Q

Lesions associated with inorganic arsenic toxicity

A
  • At very high exposure, may not see any lesions
  • Brick red gut (abomasum in ruminants)
  • Fluid GI contents, sometimes foul smelling
  • Soft yellow liver, red congested lungs
  • Damage to glomerulus and tubules in kidney
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17
Q

diagnosis of inorganic arsenic toxicity

A
  • Consider whenever there is sudden onset of gastroenteritis or sudden death, especially dead animals found in or near water
  • Liver or kidney arsenic > 5ppm
  • Should also examine stomach contents or vomitus for arsenic
  • Readily absorbed from GI tract, rapidly excreted
    • take samples early
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18
Q

Treatment of inorganic arsenic toxicity

A
  • GI decontamination
    • if no symptoms, emesis followed by activated charcoal with a cathartic
  • Begin chelation therapy
    • the classic chelating antidote for arsenic toxicosis is dimercaprol: compete with -SH groups for available arsenic
    • sodium thiosulfate before clinical signs
  • Supportive therapy
    • demulcents (sucralfate or kaopectate)
    • fluids for dehydration ,shock, reduced renal function
  • Prognosis is poor once symptoms occur
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19
Q

zinc

A
  • Found in all galvanized metals: nuts, bolts, wire (hardware ingestion)
  • Post-1982 pennies
    • 96% zinc
    • big problems in zoos
    • one of the most common household hazards called into ASPCA
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20
Q

MOA of zinc

A
  • When zinc enters the stomach’s acidic environment, free zinc is released, forming zinc salts
    • zinc salts have a direct corrosive effect to stomach and intestinal mucosa
  • Oxidative damage that leads to hemolysis
  • Toxicity usually seen in dogs and aquatic organisms (seal at the zoo)
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21
Q

clinical signs of acute zinc toxicity

A
  • occurs within a few days
  • vomiting (especially with ointment)
  • depression, anorexia
  • hemolytic anemia
  • jaundice
  • pancreatitis
  • lesions
    • enteritis
    • renal, hepatic, and pancreatic necrosis
22
Q

clinical signs of chronic toxicity

A
  • Occurs most often in cattle
  • Onset time is several weeks
  • Signs include
    • PU/PD
    • diarrhea
    • anorexia
    • hemolytic anemia
    • lameness
    • lesions (gastric ulcers, renal tubular necrosis, hepatic necrosis)
23
Q

diagnosis of zinc toxicity

A
  • Serum zinc levels >10 ppm
    • use blue top tube for collecting blood and syringes without rubber due to zinc in lubricant
  • liver zinc > 200 ppm
  • decreased PCV, regenerative anemia, thrombocytopenia
  • Heinz bodies reported in 33% of canine patients
  • elevated liver, kidney, and pancreatic enzymes
  • hemoglobinuria
  • radiographs for hardware ingestion
24
Q

treatment of zinc toxicity

A
  • Removal of foreign bodies
  • Emesis if not contraindicated
  • Primarily symptomatic
    • fluids for renal failure, dehydration
    • blood products for hemolytic anemia
  • Initiate treatment with proton pump inhibitors, or H2 blockers
    • will help to decrease systemic absorption of zinc salts
    • can also administer gastroprotectants for irritation/ulceration
25
Q

soap and shampoo clinical signs

A

vomiting and diarrhea

26
Q

soap and shampoo treatment

A

dilution with milk or water

rarely ever fatal

27
Q

scouring powder/bleach toxicity

A

due to alkalinity-corrosive effect on skin and mucous membranes

28
Q

MOA of scouring powder/bleach

A

causes liquefactive necrosis that penetrates deep layers of mucous membranes

29
Q

clinical signs of scouring powder/bleach

A

vomiting and abdominal pain

30
Q

treatment of scouring powder/bleach

A
  • Diluting with milk or water
  • Emesis and lavage not good
  • activated charcoal and cathartics except with very caustic exposures
31
Q

phenol disinfectants MOA

A

Phenol denatures and precipitates cellular proteins thus destroying all contacted cells

32
Q

pine oil disinfectant MOA

A
  • Pine oil disinfectant MOA
  • Directly irritating to mucous membranes.
  • Detoxified by glucuronidation so cats are more susceptible
33
Q

phenol toxicity clinical signs

A
  • Corrosive burns or oral-esophageal pathway, vomiting, hypersalivation, ataxia, panting
  • Progresses to shock, cardiac, arrhythmias, methemoglobinemia, hepatic and renal damage, coma
34
Q

pine oil toxicity clinical signs

A

Nausea, hyersalivation, bloody vomit, abdominal pain, ataxia, hypotension, respiratory depression, acute renal failure, pulmonary edema

35
Q

phenol toxicity treatment

A
  • Demulcents (milk or eggs)
  • Not gastric lavage or emesis or activated charcoal
  • Supportive therapy including IV fluids and resp support
  • 1% methylene blue for methemoglobinemia
36
Q

pine oil treatment

A
  • Dilute with milk, egg whites, or water
  • Because of aspiration pneumonia, emesis and lavage are contraindicated
  • Follow dilution with activated charcoal or cathartic
  • Supportive therapy including renal perfusion, acid-base and electrolyte balance
37
Q

automatic dishwater detergent toxicity

A

Due mostly to high alkalinity (pH >10.5)

38
Q

clinical signs of automatic dishwasher detergent

A

vomiting, diarrhea, salivation, GI pain, and oral, esophageal, gastric erosions

39
Q

treatment of automatic dishwasher detergent

A

Dilution with milk or water, analgesics and possibly steroids for inflammation

40
Q

toilet bowel cleaner toxicity

A

they are acidic - containing sulfuric acid or hydrochloric acid

41
Q

clinical signs of toilet bowl cleaner toxicity

A

vomiting, salivation, dyspnea, dysphagia, abdominal pain, GI ulceration

42
Q

treatment of toilet bowel cleaner toxicity

A
  • dilution with milk or water, steroids if stricture possible, symptomatic
  • emesis, lavage, activated charcoal and catharsis CONTRAINDICATED
43
Q

ammonia, oven cleaners, drain cleaner toxicity

A

alkaline products that cause caustic ulceration at pH around 12

44
Q

clinical signs of ammonia, oven cleaners, and drain cleaner toxicity

A

vomiting, salivation, dysphagia, abdominal pain, GI ulceration, dyspnea

45
Q

treatment of ammonia, oven cleaners, and drain cleaner toxicity

A

dilution with milk or water, steroids if stricture possible, symptomatic

46
Q

phytoestrogens

A
  • Large animal toxins
  • most affect reproductive system
  • Found in foods like lentils, beans, clover
47
Q

zearalenone

A
  • mycotoxin
  • metabolite of Fusarium spp, often found with deoxynivalenol
  • Most grains can be affected, toxin production occurs mostly during storage
  • Heat stable and resistant to most mold retardants
48
Q

animals affected by zearalenones

A

most animals: pigs, cattle, sheep

chickens are resistant

49
Q

MOA of zearalenones

A
  • estrogen receptor agonists
  • alpha-zearalenol has a higher affinity for estrogen receptors than endogenous estrogen
50
Q

clinical signs of zearalenol

A
  • “hyperestrogen” syndrome
  • In pigs and ferrets: symptoms depend on sex and maturity
    • decrease male libido, infertility
    • enlarged, swollen uteri
    • shrunken and/or cystic ovaries
    • necrosis or reddening of the tail
    • vulva swelling and reddening
    • vaginal and rectal prolapse
    • immunosuppression and liver damage
    • decreased litter size and birth weights
  • similar signs in cattle and sheep: males regressed testis and feminization, females have abortions and pseudopregnancy
51
Q

diagnosis of zearalenol toxicity

A
  • presence of greater than 1-2 ppm zearalenone in swine feed
  • Reversal of symptoms when feed is changed
  • may take 7-10 days due to long half life of zearalenone
52
Q

treatment of zearalenol toxicity

A

activated charcoal or high fiber may reduce elimination times due to extensive enterohepatic recycling

Toxicology (8 decks)

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