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DWT exam 3 > Nephro, hepatotoxicity, GI, dermal > Flashcards

Nephro, hepatotoxicity, GI, dermal Flashcards

1
Q

Know which is more toxic to ruminants: older oak leaves and brown (older) acorns or young oak leaves and green (young) acorns

A

young oak leaves or green acorns

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2
Q

Explain the mechanism by which the toxins in oak leaves and acorns cause gastrointestinal irritation and nephrotoxicity in ruminants

A

Toxins: Gallotannins (tannic acid, gallic acid, pyrogallol)
Rumen microflora metabolize gallotannins to acids
* Bind and precipitate proteins > Gastrointestinal tract and kidneys
* Damage to proximal tubules in kidneys

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3
Q

Lily toxicity

A

Cats!
nephrotoxic
Vomiting, anorexia, lethargy, dehydration
Renal failure with polyuria, oliguria, or anuria
CNS signs: Ataxia, tremors, seizures

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4
Q

Know what toxins are suspected to be the nephrotoxic agents in grapes and raisins

A

Mostly dogs
tartaric acid and potassium bitartrate
Dogs have rapid absorption and high renal elimination of these compounds
Vomiting, diarrhea, lethargy, dehydration

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5
Q

Explain the mechanism of toxicity of cholecalciferol (vitamin D3) rodenticide and Describe how cholecalciferol (vitamin D3) affects calcium hemostasis in an animal and explain how this causes nephrotoxicity

A

Calcitriol increases Ca2+ absorption in GI, renal tubules, bone resorption
too much Ca2+ = bleeding, calcification of tissues, tubular necrosis (alters Ca2+ pump activity)

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6
Q

Identify common sources of ethylene glycol

A

Antifreeze, deicing agents, solvents, paints, brake fluids, toilet bowl antifreeze

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7
Q

Know the enzyme that acts as the rate-limiting step in the metabolism of ethylene glycol

A

alcohol dehydrogenase
ethylene glycol isnt toxic, its metabolites are

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8
Q

ethylene glycol toxicity stage 1

A

Stage 1: 30 minutes to 12 hours post-ingestion
* Neurological Signs
Un-metabolized ethylene glycol = alcohol
Progressive CNS signs: “Drunk” > ataxic
Sedation to mild depression
Muscle fasciculations, coma (high doses)
Hypothermia (nervous system depression)
* Gastrointestinal Signs
Nausea, vomiting, salivation
Ethylene glycol is a gastrointestinal irritant
* Polydipsia and increased urination (polyuria)

Treatment: Ethanol given within 3-6 hours prevents acute kidney injury (AKI)

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9
Q

Stage 2 ethylene glycol toxicity

A

12 to 24 hours post-ingestion
Cardiopulmonary Signs
* Tachypnea, tachycardia
* Severe metabolic acidosis

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10
Q

Stage 3 ethylene glycol toxicity

A

24 to 72 hours post-ingestion in dogs
12 to 24 hours post-ingestion in cats
Nephrotoxicity
* Oliguria = rapid reduction in urine output, abnormally small volume produced
* Seizures

Too late for ethanol treatment

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11
Q

Identify the recommended treatment for ethylene glycol toxicity and describe the mechanism by which this product/drug treats ethylene glycol toxicity

A

Early emesis, gastric lavage
Supportive care: IV fluids, GI protectants

Ethanol given within 3-6 hours prevents acute kidney injury (AKI)
* 20% ethanol with saline IV
* competitive inhibitor for alcohol dehydrogenase

If ethylene glycol is prevented from being metabolized (in the liver) it can be excreted via the kidneys as ethylene glycol with little toxicity

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12
Q

Explain how acetaminophen toxicity affects the liver and red blood cells

A

metabolized in liver to toxic metabolites
* Lipid peroxidation/RBC oxidation
* Binds mitochondrial and cellular proteins, DNA

 Hepatotoxicity (bind to liver proteins)
Methemoglobinemia (oxidative injury)

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13
Q

Identify which animal is most susceptible to acetaminophen toxicity and explain why

A

cats
sensitive to phenols
Cats have low hepatic levels of glucuronyltransferase (metabolize the toxic metabolites)

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14
Q

Explain how harmful algae blooms can be toxic to animals and Know the toxin in blue-green algae that was discussed in class that causes hepatotoxicity in animals

A

Microcystins =Hepatotoxic
* Acute (death is most common sign)
* Induces oxidative stress
* Inhibit protein phophatases 1 and 2A
* Increases phosphorylation of cytoskeletal proteins in liver > liver cell apoptosis

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15
Q

Explain how animals are exposed to harmful algae blooms

A

Algal blooms in freshwater
Inhalation of “water” droplets
Dogs swimming in ponds
Cows drinking contaminated water

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16
Q

Explain how animals are exposed to aflatoxin

A

produced by fungus (aspergillus)
Ingestion of contaminated food
* Moldy peanuts or moldy bread
* Corn most common source

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17
Q

Know which aflatoxin metabolite gets excreted in milk

A

Aflatoxin M1

18
Q

Recognize which animals are more susceptible to aflatoxin-induced hepatotoxicity

A

Dogs, poultry, young pigs

18
Q

Recognize which animals are more susceptible to aflatoxin-induced hepatotoxicity

A

Dogs, poultry, young pigs

19
Q

Describe how xylitol causes hypoglycemia in dogs

A

Potent stimulator of insulin secretion in dogs
* 6 times that of glucose

Canine pancreas interprets xylitol as glucose > releases insulin
Insulin cannot bind xylitol > binds glucose instead!

20
Q

Describe how xylitol causes hypoglycemia in dogs

A

Potent stimulator of insulin secretion in dogs
* 6 times that of glucose

Canine pancreas interprets xylitol as glucose > releases insulin
Insulin cannot bind xylitol > binds glucose instead!

21
Q

Explain how xylitol toxicosis affects serum potassium levels in dogs

A

Hypokalemia – excess insulin release stimulates cells to take up potassium

22
Q

Explain what supportive treatment is used to correct for hypoglycemia in dogs with xylitol toxicosis

A

Emesis (1 to 6 hours post-ingestion)
* Gum stays in stomach longer
* However! It is absorbed rapidly (especially the pure formulation)
* **Do not induce if patient is hypoglycemic **
* Weakness may increase aspiration pneumonia risk
* Emesis is not recommended in patients that ingest 100% xylitol products > 40 minutes prior to clinic > clinical signs and aspiration risk

Activated charcoal not beneficial
If Hypoglycemia:
* I.V. fluids with 2.5 – 5 % dextrose supplementation
* Monitor blood glucose every 2 hours for the 12 hours…
* Patient should maintain euglycemia for 6 hours without supplementation before discharge

If Hepatotoxicity:
* Monitor liver values at 12, 24, and 48 hours
* Monitor for secondary coagulopathy
* If increased clotting times, give fresh/frozen plasma and vitamin K1
* Hepatoprotectants (N-Acetylcysteine, SAM-e) 2 to 4 weeks may be needed
* long term monitoring (up to 4 weeks)

22
Q

Explain what supportive treatment is used to correct for hypoglycemia in dogs with xylitol toxicosis

A

Emesis (1 to 6 hours post-ingestion)
* Gum stays in stomach longer
* However! It is absorbed rapidly (especially the pure formulation)
* **Do not induce if patient is hypoglycemic **
* Weakness may increase aspiration pneumonia risk
* Emesis is not recommended in patients that ingest 100% xylitol products > 40 minutes prior to clinic > clinical signs and aspiration risk

Activated charcoal not beneficial
If Hypoglycemia:
* I.V. fluids with 2.5 – 5 % dextrose supplementation
* Monitor blood glucose every 2 hours for the 12 hours…
* Patient should maintain euglycemia for 6 hours without supplementation before discharge

If Hepatotoxicity:
* Monitor liver values at 12, 24, and 48 hours
* Monitor for secondary coagulopathy
* If increased clotting times, give fresh/frozen plasma and vitamin K1
* Hepatoprotectants (N-Acetylcysteine, SAM-e) 2 to 4 weeks may be needed
* long term monitoring (up to 4 weeks)

23
Q

euglycemia

A

normal blood glucose

24
Q

Know the recommended hepatoprotectants (treatments) that can be used to treat animals with hepatotoxicity

A

N-Acetylcysteine
SAM-e

25
Q

Know what toxins/toxicants cause gastrointestinal toxicity in animals

A

NSAIDs
Corrosive Agents
Batteries
Zinc/Aluminum Phosphide
Deoxynivalenol
Blister Beetles (Cantharidin)
Insoluble Oxalate-Containing Plants
Heavy Metals

26
Q

Know what toxins/toxicants cause dermal toxicity in animals

A

Plants Causing Photosensitization
Corrosive Agents
Blister Beetles (Cantharidin))

27
Q

Know which mycotoxin causes “Slobber Syndrome”

A

slaframine

28
Q

Describe the mechanism of toxicity of the rodenticide zinc phosphide

A

Hydrolysis when in contact with moist environment or stomach acid > Liberation of toxic phosphine gas
Corrosive and direct irritant to GIT and lungs
Reactive oxygen species = cell damage/death
Inhibits aerobic respiration > Cells undergo anaerobic respiration producing lactic acid = Metabolic acidosis and systemic organ damage

29
Q

Describe the characteristic odor of vomitus/gastrointestinal contents that is associated with zinc phosphide exposure

A

rotten fish smell

30
Q

Know what clinical condition occurs in horses with NSAID toxicity and Know which NSAID is more frequently implicated in causing this clinical condition and the mechanism

A

long term use (can be normal use) > ulcers> protein losing enterocolopathy
* disrupts mucosa in intesting
* malabsorption
* lose proteins into GI tract

phenylbutazone, banamine

31
Q

Know the toxin present in blister beetles and explain how this toxin causes toxicity in animals

A

Toxin = Cantharidin

Mechanism of Toxicity:
* powerful vesicant (blistering agent) > severe chemical burns
* Absorbed by lipid membranes in epidermal cells
* Causes release of serine proteases (enzymes that break peptide bonds in proteins)
* Loss of cell connection between keratinocytes = blistering of skin

32
Q

Know how animals are exposed to blister beetles

A

Toxicity due to ingestion of beetle in hay – get swarms in the hay
Cantharidin is released from crushed beetles

33
Q

Know the difference between primary photosensitization and secondary photosensitization with regard to exposure to photosensitizing plants

A

Primary: Occurs when skin becomes more susceptible to UV light damage
* Photons of light react with photodynamic compounds from the plants
* Reaction causes release of free radicals that damage cell membranes leading to skin ulceration, edema, or necrosis

Secondary: heptotoxicity
* Pyrrolizidine alkaloids are broken down by the liver to toxic metabolites (toxic pyrroles)
* Phylloerythrin enters the blood stream and reaches the skin and reacts with sunlight resulting in severe skin burns

34
Q

Describe the appearance of the light-colored areas of the skin on animals with photosensitization

A
35
Q

Describe the clinical sign most commonly associated with exposure to the mycotoxin slaframine

A

slobber syndrome aka
“Black Patch Disease”

36
Q

Explain how animals are exposed to slaframine

A

Issues in livestock and horses arise when red clover is infected with Rhizoctonia leguminicola fungus

37
Q

Explain what deoxynivalenol is and how animals are exposed to this toxin

A

AKA DON or “vomitoxin” (mycotoxin)
Produced by Fusarium spp. molds or fungi growing with heavy rainfall or high humidity in: Corn, Wheat, Barley, Oats
Vomitoxin is stable throughout the manufacturing process used to make pet and livestock food

38
Q

Know which animals are most sensitive to the mycotoxin deoxynivalenol

A

dogs and pigs

39
Q

Describe the common clinical signs associated with deoxynivalenol toxicity

A

Onset of feed refusal and vomiting within 2-3 hours post-ingestion

DWT exam 3 (14 decks)

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