Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are Methylxanthine Alkaloids?

A
  • Natural Product:
    • Caffeine
    • Theobromine
    • Theophylline
  • In food, beverages, medications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the sources of Theobromine?

A
  • Chocolate products or byproducts
  • Cocoa Mulch
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Urine dribbling is a common sign of what 2 toxicities?

A
  • Theobromine (chocolate)
  • Weed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the sources of Theophylline?

A
  • Tea
  • Human pharmaceutical
    • used to treat bronchoconstriction and cough
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is Methylxanthine Alkaloids toxicosis diagnosed?

A
  • Hx, clinical signs
  • Detection of alkaloids
    • urine
    • serum
    • stomach content
    • liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What Herbicides are toxic to animals?

A
  • Phenoxy Herbicides
  • Dinitro Herbicides
  • Paraquat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are Phenoxy Herbicides?

A
  • Mimic plant growth regulator IAA
    • Indol-3-acetic acid
  • Selective
  • 2,4-D
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the Absorption and Distribution of Phenoxy Herbicides?

A
  • Absorption - rapid, readily absorbed
  • Distribution - wide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How is Phenoxy Herbicides metabolized and excreted?

A
  • Metabolism - not appreciably metabolized
  • Excretion - Urine, little to no accumulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions