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TOXICOLOGY > 13 – NSAIDs and Acetaminophen > Flashcards

13 – NSAIDs and Acetaminophen Flashcards

1
Q

Intro and important info to gather

A
  • common misconception that if it is safe for humans = safe for pets
  • any drug is toxic if dose is high enough
  • dose-dependent vs. idiosyncratic drug reactions
  • *active ingredient
  • *strength/composition
  • *estimated amount ingested
  • *time ingested
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2
Q

*NSAIDs: exposure scenarios

A
  • Overdose of prescribed medication
  • Combination therapy
  • Accidental ingestion of improperly stored medications
  • Well-meaning owner gives human OTC NSAID
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3
Q

What are the most common NSAID toxicoses in companion animals?

A
  • *OTC NSAIDs
  • Ibuprofen and naproxen
    o Easily accessible and available, lack of understanding of risk
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4
Q

NSAIDs: target organs

A
  • *GIT, kidneys, CNS
  • *exacerbated with dehydration
  • Hepatotoxicity possible
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5
Q

NSAIDs: mechanism

A
  • Inhibition of COX expression=decreased prostaglandin production
    o Decrease GIT mucosal and renal blood flow
    o Decrease mucosal barrier repair and cell turnover
    o Decrease GI immune function
    o Decrease GI mucosal protection: bicarbonate, mucus secretion
  • *relevant toxicokinetic: many are highly protein bound and undergo enterohepatic recirculation
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6
Q

NSAIDs: companion animals (cats >dogs)

A
  • *consider cats TWICE as sensitive as dogs
    o Deficient hepatic glucuronide conjugation
  • Clinical presentations
    o Cats: renal failure
    o Dogs: GI ulcers
  • **ferrets are very sensitive to ibuprofen
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7
Q

NSAIDs: large animals

A
  • Horses: narrow margin of safety
    o Ponies and foals considered more sensitive
  • Uncommon in cattle and small ruminants
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8
Q

NSAIDs: onset

A
  • Within hours to days (dose-dependent)
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9
Q

*NSAIDs: clinical features, GI

A
  • Anorexia, abdominal pain
  • Vomiting and diarrhea (“coffee grounds”)
  • Dehydration, hypovolemia
  • Underlying pathology (ulcers)
    o Risk of GI perforation and septic peritonitis
    o Pale MM
  • Tachypnea, tachycardia
  • Horses: colic, diarrhea, fever, anorexia
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10
Q

*NSAIDs: clinical features, renal

A
  • Painful abdomen, PU/PD
  • Underlying pathology: acute renal insufficiency secondary to hypoperfusion
  • Characteristic PM lesion in companion animals: *renal papillary necrosis
  • *horses: right dorsal colitis
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11
Q

*NSAIDs: clinical features, CNS

A
  • Depression
  • Ataxia
  • Stupor or obtundation
  • Seizures
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12
Q

NSAIDs: death form (clinical features)

A
  • GI perforation secondary to ulceration
  • Acute kidney injury and renal failure
  • CNS toxicosis
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13
Q

NSAIDs: clinical pathology

A
  • Dehydration
  • +/- decreased total protein and anemia
  • Leukocytosis with left shift
  • Renal dysfunction
  • Right dorsal colitis (horses): hypoalbuminemia
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14
Q

NSAIDs: carprofen

A
  • Idiosyncratic hepatopathy
  • Acute hepatic necrosis
  • Good prognosis with D/C drug and prompt medical treatment
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15
Q

NSAIDs: aspirin (acetylsalicylic acid)

A
  • 2 presentations
  • Cats very sensitive: glucuronide conjugation
  • Similar presentation to other NSAIDs
  • High dose
    o Uncouples oxidative phosphorylation: pyrexia leading to hyperthermia, panting, seizures
    o Salicylates inhibits thromboxane production: bleeding is possible
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16
Q

NSAIDs: management

A
  • No specific antidote
  • Decontamination if not contraindicated
  • Aggressive symptomatic and supportive care
    o Gastroprotectants, renal support, CNS, frequent monitoring
  • Other things to consider
    o IVLE for severely affected patients (CNS)
    o Therapeutic plasma exchange due to high protein binding
    o Horses: low stress, reduce work/exercise, low bulk diet
17
Q

NSAIDs: diagnosis

A
  • History of exposure
  • Quantification in blood or urine
  • Imaging: loss of serosal detail if peritonitis
18
Q

NSAIDs: DDx

A
  • Bleeding: anticoagulant rodenticides
  • GI ulcers: corrosive products
  • Acute kidney insufficency: grapes/raisins, lilies
  • CNS depression: ethylene glycol, acetone, xylitol, ivermectin
19
Q

NSAIDs: prognosis

A
  • Companion animals: excellent with prompt medical attention
  • If perforation=grave prognosis
20
Q

Acetaminophen

A
  • Common OTC pain reliever
    o COX-3 inhibitor: hypothalamus
  • Previously recommended for dogs at LOW dose
  • Common reason for presentation to the ER at the VMC
21
Q

Acetaminophen: exposure scenarios

A
  • Accidental ingestion
  • *lack of owner knowledge
22
Q

Acetaminophen: mechanism

A
  • *bioactivation reaction
    o Production of reactive metabolite=depletion of cellular glutathione and oxidative injury
    o Damage to proteins and cell membranes
23
Q

Acetaminophen: target organs

A
  • Blood: cats
  • Liver: cats and dogs
24
Q

Acetaminophen: why are there species differences?

A
  • Cats, ferrets&raquo_space; dogs
  • *cats have deficient glucuronidation capacity and more readily saturated sulfation capacity
25
Acetaminophen: dose-response
- *NO safe dose for cats - Dogs: over 50mg/kg warrants decontamination and monitoring
26
Acetaminophen: onset
- Within 4-12 hours of ingestion - Within 24-36hrs: progression to hepatic necrosis, methemoglobinemia, oxidative damage hemolytic anemia o Yellow, brown MM o Jaundice, abdominal pain o CNS involvement: tremors, seizures, coma o *Can be fatal!
27
Acetaminophen: clinical features
- Vomiting, anorexia, diarrhea - Depression, lethargy - Tachypnea, tachycardia - Chemosis, facial edema, paw swelling
28
Acetaminophen: clinical pathology
- Regenerative anemia - *Blood smear: HEINZ BODIES - Metabolic acidosis - (met)hemoglobinuria
29
Acetaminophen: PM
- Hepatomegaly with enhanced reticular pattern - Jaundice
30
Acetaminophen: histo
- Severe centrilobular hepatic necrosis - Renal tubular nephrosis
31
Acetaminophen: management
- Decontamination if NOT contraindicated - *antidote: N-acetylcysteine - Symptomatic and supportive care o Fluids, oxygen o Hemolytic anemia: blood transfusion o Hepatoprotectants o MetHb: methylene blue - Other treatments to consider: cimetidine, vit C, bioflavonoids
32
What is the mechanism of N-acetylcysteine?
- Increases hepatic glutathione synthesis - Enhances sulfation - Directly binds NAPQI (reactive metabolite)??
33
Acetaminophen: diagnosis
- History of exposure, compatible C/S and clinical pathology findings o Some labs can analyze for it in blood and urine
34
DDx for MetHb: acetaminophen
- Oxidizing agents o Heinz bodies: zinc, skunk musk, mothballs, phenolics, garlic/onion o Liver damage: sago palm, death cap mushroom, aflatoxin, microcystin
35
Acetaminophen: prognosis
- Variable - Any cat with any exposure: at least guarded - Severe liver damage with no response to treatment=grave

TOXICOLOGY (20 decks)

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