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Toxicology > At home poisonings > Flashcards

At home poisonings Flashcards

1
Q

What were the top 10 pet toxins in 2019?

A
  1. OTC medications
  2. Human prescription medications
  3. Foods
  4. Chocolate
  5. Veterinary products
  6. household products
  7. Rodenticides
  8. Plants
  9. Insecticides
  10. Garden Products
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2
Q

What critical information is needed for poisonings?

A
  • Full trade name of the product-bring in the container
    • Ingredient list: both active and inert
      • Concentration of ingredients
  • Amount of exposure of the product the animal contacted
  • Clinical signs and progression in relation to time of exposure
  • Treatments given by the owner….if any
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3
Q

What is ethylene glycol?

A
  • Antifreeze - 95%
  • Dilute 50% with water for use in engines
  • Major killer of pets
  • Can be difficult to recognize and treat
  • Must act quickly
  • High death rate >75%
  • can be used as a malicious poison
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4
Q

What are the toxic levels of Ethylene glycol?

A
  • Cats:
    • 1.5 mL EG/kg = 5.45 mL (8lb cat)
    • Oxalic Acid
  • Dogs:
    • 4.6 mL EG/kg
    • 9.5 mL/kg ⇢ death in as little as 12 hours
  • Cattle:
    • 6-10 mL/kg lethal
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5
Q

What is the MOA of ethylene glycol?

A
  • Absorbed intact
    • Peak blood levels in 1-4 hrs
    • Initially mild CNS depression (like ethanol)
  • Rapidly metabolized by liver enzyme alcohol dehydrogenase to:
    • toxic organic acids ⇢ acidosis
    • Hypocalcemia
    • Calcium oxalate crystals in kidney
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6
Q

What are the clinical signs of ethylene glycol toxicosis?

A
  • Acute (1st) stage (30minutes -12 hrs)
    • Vomiting, ataxia, depression, PU/PD
    • Inebriation
  • 2nd stage (12-24-72 hrs)
    • Severe depression (acidosis)
    • Vomiting, dehydration
    • Oliguria with isosthenuria; miosis, coma
    • Occasional seizures due to hypocalcemia
  • 3rd Stage:
    • Oliguria renal failure
    • Acidosis
    • Uremia
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7
Q

How is Ethylene glycol toxicosis diagnosed?

A
  • CBC:
    • Dehydration: ⇡ PCV, ⇡ serum protein
    • Stress leukogram: neutrophilia and lymphopenia
  • Dx:
    • Serum hyperosmolarity, large anion gap (3*48hrs)
    • Hyperglycemia, hyperkalemia, hypocalcemia
    • Elevated BUN, creatinine, phosphorus (phosphate rust inhibitor)
    • Low USG
  • Laboratory:
    • Urine pH <6.5
    • Sever metabolic acidosis
    • Hypocalcemia, approximately 50% of cases
    • Calcium oxalate crystalluria
  • Calcium Oxalate Nephrosis (visualized with polarized light)
  • Detection of EG in Serum
    • Ethylene Glycol Test Kit, PRN Pharmacal
      • Most effective early in the disease while EG still present
      • False positives with Propylene Glycol and Glycerol
  • Gas Chromatography/Mass Spectrometry
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8
Q

What is the treatment for Ethylene glycol toxicosis?

A
  • Reduce further absorption:
    • emetics, activated charcoal, cathartics within 1-2 hrs
  • Increase excretion, correct dehydration - IV fluids
  • Combat acidosis - Na bicarb
  • Block EG metabolism, alcohol dehydrogenase (ADH) start within 1-2 hrs after ingestion
  • 4-MP (fomepizole) (4-methyl pyrazole) available as Antizol-Vet
    • Antidote $$$$
  • Ethanol (20% in slow IV fluids) used in the past but can cause respiratory depression. Competitive inhibitor of ADH
    • Preferred antidote for cats
    • IV until very inebriated
  • Hemodialysis
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9
Q

What is Fomepizole?

A
  • 4-MP
  • Preferred treatment in dogs
  • Needs to be used within 8 hours of ingested of EG
  • Not recommended as an alternative to ethanol in cats
  • $$$$
  • 1gm/ml (1.5 ml vial)
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10
Q

What is the effect of the antidote in Ethylene glycol toxicosis?

A
  1. Ethylene glycol
  2. alcohol dehydrogenase
  3. glycoaldehyde
  4. glycolic acid
  5. glyoxalic acid
  6. oxalic acid
  7. Ca oxalate crystals
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11
Q

What are Methylxanthine Alkaloids?

A
  • Natural Product:
    • Caffeine
    • Theobromine
    • Theophylline
  • In food, beverages, medications
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12
Q

What is the MOA of Methylxanthine Alkaloids?

A
  • Competitive antagonism of adenosine on adenosine receptors
    • Bronchodilation
    • Vasoconstriction
    • Tachycardia
    • CNS stimulation
  • Increases amounts of intracellular Ca
  • Inhibits Phosphodiesterase
  • Increases cAMP ⇢ release of catecholamines
  • Stimulates the sympathetic nervous system
  • “Bouncing Dog”
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13
Q

What are the pharmacologic outcomes of Methylxanthine Alkaloids?

A
  • Cerebral stimulants
    • hyperactivity, agitation, seizures
  • Myocardial stimulant
    • tachycardia
  • Increased motor activity, over response to stimuli, tremors
  • Diuretic = Polyuria
  • GI irritation = vomiting, diarrhea
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14
Q

What is the toxic level of caffeine?

A
  • Lethal dose:
    • Dogs 110-200 mg/kg (LD50 140 mg/kg)
    • Cats 80-150 mg/kg
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15
Q

What are the sources of Theobromine?

A
  • Chocolate products or byproducts
  • Cocoa Mulch
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16
Q

What are the different levels of Theobromine in common chocolates?

A
  • Baking chocolate 390-450 mg/oz
  • Cocoa 400-737 mg/oz
  • Cocoa bean mulch 56-850 mg/oz
  • Special dark sweet choc chips 207 mg/oz
  • Milk chocolate 44-60 mg/oz
  • White chocolate 0.25 mg/oz
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17
Q

What are the toxic levels of Theobromine?

A
  • LD50 dogs 250-500 mg/kg
    • Lethal dose as low as 115mg/kg
  • A 10 kg (22lb) dog could be poisoned by 2.25 oz baking chocolate (~½ common 4oz bars)
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18
Q

What is the half life of theobromine and what are the implications of the half-life?

A
  • 17.5 hours
  • More time to decontaminate animal
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19
Q

What are the clinical effects of Theobromine?

A
  • Strong Cardiac Stimulant
    • tachycardia @ 200-300bpm
    • Arrhythmias
    • premature ventricular contractions
  • CNS: excitement, hyperreflexia, seizures
  • May also have vomiting & urinary incontinence
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20
Q

Urine dribbling is a common sign of what 2 toxicities?

A
  • Theobromine (chocolate)
  • Weed
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21
Q

What are the sources of Theophylline?

A
  • Tea
  • Human pharmaceutical
    • used to treat bronchoconstriction and cough
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22
Q

How is Methylxanthine Alkaloids toxicosis diagnosed?

A
  • Hx, clinical signs
  • Detection of alkaloids
    • urine
    • serum
    • stomach content
    • liver
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23
Q

What is the treatment for Methylxanthine Alkaloids toxicosis?

A
  • Artificial Respiration
  • Emetic, lavage, activated charcoal
  • Control seizures
  • Monitor the heart
  • Lidocaine for VPCs in dogs (Propranolol in cats)
  • Beta blockers as needed
  • Fluids
  • Residual effects unlikely
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23
Q

What is the treatment for Methylxanthine Alkaloids toxicosis?

A
  • Artificial Respiration
  • Emetic, lavage, activated charcoal
  • Control seizures
  • Monitor the heart
  • Lidocaine for VPCs in dogs (Propranolol in cats)
  • Beta blockers as needed
  • Fluids
  • Residual effects unlikely
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24
Q

What Herbicides are toxic to animals?

A
  • Phenoxy Herbicides
  • Dinitro Herbicides
  • Paraquat
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25
Q

What are Phenoxy Herbicides?

A
  • Mimic plant growth regulator IAA
    • Indol-3-acetic acid
  • Selective
  • 2,4-D
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26
Q

What are the toxic levels of Phenoxy herbicides?

A
  • Cattle:
    • Acute 200 mg/kg
    • 10-30 days 100mg/kg
    • Chronic 2000 ppm in diet
  • Dogs
    • Acute 100 mg/kg
    • 10-30 days 25 mg/kg
    • Chronic 500 ppm in diet
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27
Q

What is the Absorption and Distribution of Phenoxy Herbicides?

A
  • Absorption - rapid, readily absorbed
  • Distribution - wide
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28
Q

How is Phenoxy Herbicides metabolized and excreted?

A
  • Metabolism - not appreciably metabolized
  • Excretion - Urine, little to no accumulation
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29
Q

What is the MOA of Phenoxy Herbicide toxicosis?

A
  • Uncouples oxidative phosphorylation
  • Inhibits protein synthesis
    • Ribonuclease synthesis inhibition
  • Decreases chloride conductance in dogs
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30
Q

What are the clinical signs of Phenoxy Herbicides toxicosis?

A
  • Dogs:
    • Vomiting, diarrhea
    • Myotonia, ataxia, posterior weakness, periodic spasms, muscle weakness
  • Cattle:
    • Anorexia
    • Rumen atony
    • Bloat
    • diarrhea
    • oral ulceration
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31
Q

How is Phenoxy Herbicide toxicosis diagnosed?

A
  • Elevations in liver and muscle enzymes
    • ALP, CPK
  • Gross lesions
    • Swollen, friable liver
    • Congested kidneys
    • Oral ulcers
    • Moderate tubular injury on histopath
  • Chemical analysis
    • Forage
    • Rumen/gastric content
    • Urine
32
Q

What tis the treatment for Phenoxy Herbicide toxicosis?

A
  • Detox
    • Emesis & activated charcoal
    • Dermal exposure - wash with soap and water
    • Diuresis
  • No specific antidote
  • Bland, high quality diet
33
Q

What are dinitro herbicides?

A
  • Dinitroanilines and Dinitrophenols
  • Dinitroanilines often used as pre-emergent
  • Uncouple oxidative phosphorylation
  • Banned since 1987
34
Q

What is the MOA of dinitro herbicides?

A
  • Uncouples phosphorylation
    • Prevent ADP conversion to ATP
35
Q

What are the clinical signs of dinitro herbicide toxicosis?

A
  • Tachypnea
  • weakness
  • ataxia
  • disorientation
  • hyperthermia
36
Q

what is the treatment for dinitro herbicide toxicosis?

A
  • No antidote
  • Thermoregulation, supportive care
37
Q

What is Paraquat?

A
  • Dipyridyl class - Desiccant
  • Non-selective
  • Degrades in sunlight
  • Quick-kill defoliation
  • binds to clays and is inactivated in soil
  • Often mixed with Diquat
38
Q

What is the absorption and distribution of paraquat?

A
  • Absorption:
    • water soluble with ~20% absorbed
    • Remainder excreted in feces
    • Commonly prepped with emetics or bitters
  • Distribution:
    • Rapidly and selectively sequestered in Type I and II
    • Lung have 10x concentration compared to other tissues
39
Q

How is Paraquat metabolized and excreted?

A
  • Not readily metabolized
  • Excreted in urine
40
Q

What is the MOA of Paraquat?

A
  • Most ingested paraquat is excreted unchanged
  • Remainder undergoes cyclic redox reactions
  • Produces Oxygen and Hydroxyl groups
  • Free radical damage to membrane lipids
    • Alveolar cells
    • Proximal tubular epithelium
    • Concentrates can produce dermal lesions
41
Q

What are the toxic levels of Paraquat?

A
  • 25-75 mg/kg PO in domestic animals
  • 290 mg/kg in Turkeys
  • Dogs fed 170 ppm in diet for 60 days
    • Anorexia
42
Q

What is the clinical picture of Paraquat toxicosis?

A
  • High dose - systemic poisoning
    • Early vomiting
    • Death in 1-4 days due to acute pulmonary edema
    • Renal failure, Hepatocellular damage
  • Subacute Poisoning:
    • slower onset 5-10 days
    • Pulmonary edema
    • Respiratory failure
  • Low Dose - irreversible pulmonary fibrosis
    • weeks after exposure
  • Tachypnea, dyspnea, rales
  • Hypoxia, cyanosis, etc
43
Q

How is Paraquat toxicosis diagnosed?

A
  • Clinical signs and exposure
  • Gros lesions in lungs
    • Congestion, emphysema, hemorrhage, atelectasis
  • Histopathology
    • Necrosis of type 1 epithelium, edema, hemorrhage
    • Fibrosis of alveolar surface
    • Renal tubular degeneration
  • Analytical testing - urine is best for 2-3 days
    • Stomach content/vomitus
44
Q

What is the treatment of Paraquat toxicosis?

A
  • No antidote
  • Early - decontamination
  • Bentonite clay - absorbent
  • Supportive care
    • Respiratory support - hypoxic ventilation
      • Adding O2 may enhance oxidative effects
    • Fluids - can exacerbate pulmonary edema
  • Prognosis - guarded
45
Q

What are some common herbicides that are NOT toxic?

A
  • Roundup (glyphosate)
    • toxicity related to surfactant
    • Ocular irritant
  • Atrazine
  • Carbamates
    • less toxic than insecticide preparations
46
Q

What are the toxic chemicals in fungicides?

A
  • Captan
  • Copper sulfate
  • Formaldehyde
  • Thiram
  • Triphenyltinhyroxide
47
Q

What is Avitrol?

A
  • 4-Aminopyridine
  • Used in feedlots to keep birds away
  • Restricted use
  • Enhances ACh release at synapses
    • Neuromuscular juntion
    • Birds become disoriented
    • Emit distress cries
      • drives other birds away
48
Q

What are the toxic levels of Avitrol?

A
  • LD50s:
    • Rat 20 mg/kg
    • Mouse 10 mg/kg
    • Dog 3.7 mg/kg
    • Horse 3 mg/kg
49
Q

What is the clinical picture associated with Avitrol toxicosis?

A
  • Acute onset ~15min
  • Tremors
  • Incoordination
  • Convulsions
  • Seizures
  • Cardiorespiratory distress
50
Q

How is Avitrol toxicosis diagnosed?

A
  • Clinical signs
  • Exposure
  • Analysis in stomach content/vomitus/liver
  • Convulsant panel at D-lab
    • Strychnine
    • Nicotine
    • Caffeine
    • 4-aminopyridine
51
Q

What is the treatment for Avitrol toxicosis?

A
  • Supportive therapy
    • Activated charcoal
    • Fluids
    • Thermoregulation
    • Prevent further
    • exposure
52
Q

What is Starlicide?

A
  • 3-chloro-4-methyaniline (3-chloro-p-toluidine)
  • Starlings, gulls, and other birds
  • Mammals less sensitive
  • Nephrotoxin
  • Proximate nephrotoxic mechanisms are not defined
  • LD50 for starlings is 3.88 mg/kg bwt
  • High chronicity factor
    • 4.7 ppm over 30days vs 1 ppm for 90 days
53
Q

How is Starlicide toxicosis diagnosed?

A
  • Crop/stomach content
  • Liver and kidney
  • Histology:
    • Tubular necrosis of epithelial cells
54
Q

Is there a treatment for stralicide toxicosis?

A
  • supportive care
  • guarded prognosis
55
Q

What is Metaldehyde?

A
  • Moluscicide (slugs and snails)
    • often combined with methiocarb (carbamate)
  • Dogs find the baits attractive
    • toxic dose 200-600 mg/kg
  • Suppresses GABA production
    • lack of inhibition of CNS neuronal activity
56
Q

What are the toxicokinetics of metaldehyde?

A
  • Low water solubility - insoluble in fat
  • Uncertain metabolism - old lit sas it forms acetaldehyde
    • acetaldehyde believed converted to CO2 and exhaled
  • Cyt P450 inducers protect against toxicity
  • T½ in humans is 27 years
57
Q

What is the MOA of metaldehyde?

A
  • Hydrolysis to acetaldehyde
  • Reduced brain Na, 5-HT, and 5-HIA
    • Low Na & 5HT lowers seizure threshold
  • Increased monoamnine oxidase activity
  • Decrease in brain GABA
    • reduced GABA increases seizures
  • Hyperthermia prominent
58
Q

What are the toxic levels of metaldehyde?

A
  • LD50:
    • Dogs 210-600 mg/kg
    • Cats 207 mg/kg
  • Lethal:
    • Cattle 200 mg/kg
    • horses 60-100 mg/kg
  • Ducks & chickens MLD 300&500 mg/kg
  • Lower doses can cause signs - a few pellets can produce signs in small puppies
  • Unlikely to cause relay toxicosis
59
Q

What is the clinical picture associated with metaldehyde toxicosis?

A
  • Acute - minutes to hours
  • Anxiety
  • Incoordination
    • muscle tremors ⇢ continuous spasms ⇢ seizures
  • Hyperesthesia, opisthotonus
  • Excitement may alternate with depression
  • Hyperthermia (108F), tachypnea, acidosis
  • Cats also show mydriasis, nystagmus
  • Muscarinic signs from OP’s or carbamates
60
Q

How is metaldehyde toxicosis diagnosed?

A
  • History of exposure
  • Acute neurologic signs with hyperthermia & parasympathetic characteristics
  • Stomach contents (odor of acetylene), bait, serum, urine for dx testing
  • Keep samples frozen
  • Lesions: general, difficult to interpret
  • GI inflammation
  • Congestion/hemorrhage - non-specific
  • Histo: hepatocellular swelling, neuronal degeneration
61
Q

What is the prognosis of Metaldehyde toxicosis?

A
  • Prognosis:
    • death 4-24 hrs post ingestion
    • Respiratory failure
    • >50% of cases die
    • Early aggressive detoxification and therapy essential
62
Q

What is the treatment for Metaldehyde toxicosis?

A
  • Evacuate gut: gastric lavage, enemas
  • Stop absorption - activated charcoal
  • Control tremors - diazepam, barbiturates
    • phenobarbital, methocarbamol
    • ketamine anesthesia
  • Supportive Care
    • Fluids, A/B balance, thermoregulation
63
Q

What are the common differentials for Metaldehyde toxicosis?

A
  • Strychnine - acute, tremors, rigidity
  • Zinc phosphide - vomit, running, seizures
  • Bromethalin - delayed signs, tremor, ataxia
  • OP-Carbamates - SLUD signs + tremors
  • Pyrethrins - acute, continuous tremors
  • 4-Aminopyridine - HR increase, tremors, temp
  • Blue-green algae (anatoxins) - peracute, salivation, diarrhea
64
Q

What is Rotenone?

A
  • Natural insecticide, alkaloid
  • Extract of Derris root
  • Unstable in sunlight and air
  • Flea control, premise insecticides, cattle grubs,, Ticks, lice
  • Toxic to fish (75 ug/L)
65
Q

What is the MOA of Rotenone?

A
  • Inhibit electron transport - interferes with ATP synthesis
66
Q

What are the toxic levels of Rotenone?

A
  • Enhanced by combo with pyrethrins/pyrethroids
  • Acute PO LD50 300 mg/kg in dogs
67
Q

What are the clinical signs of Rotenone toxicosis?

A
  • Vomiting
  • lethargy
  • dyspnea
  • tremors-seizures
  • hypoglycemia
68
Q

How is Rotenone toxicosis diagnosed?

A
  • Detect compound in vomitus, blood, urine, feces
69
Q

How is Rotenone toxicosis treated?

A
  • Decontaminate:
    • Diazepam
    • Dextrose IV
    • Oxygen
70
Q

What is Imidacloprid?

A
  • insecticide
    • fleas, lawn grubs, termites, crop seeds
71
Q

What is the MOA of Imidacloprid?

A
  • Block post-synaptic nicotinic acetylcholine receptors in insects
72
Q

What is the toxic level of imidicloprid?

A
  • No issues with 5x dose in dogs, potential hair loss at application site with 10x dose
  • Dogs tolerate 500ppm in diet for a year
  • Rapid clearance 95% in 24 hours
73
Q

What is the MOA of Fipronil?

A
  • GABA inhibition in insects
  • Potential excitation in dogs
74
Q

what is the toxic level of Fipronil?

A
  • No substantiated reports of toxicosis in dogs
75
Q

What is Hydramethylnon?

A
  • Insecticide
    • Cockroach and ant baits
76
Q

What is the MOA of Hydramethylnon?

A
  • Stop ATP synthesis in insects
77
Q

What is the toxic level of hydramethylnon?

A
  • Low mammalian toxicity
  • 40 pound dog would have to eat ~240 trays
  • Foreign body from plastic tray bigger concern
78
Q

What are IGRs?

A
  • Methoprene
    • Prevents metamorphosis into adult
    • Dog LD50 >5000mg/kg
  • Lufenuron
    • Inhibits deposition of chitin in eggs and exoskeleton of fleas
      *

Toxicology (25 decks)

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