Nephro, hepatotoxicity, GI, dermal Flashcards by Madison Warner

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

young oak leaves or green acorns

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

Lily toxicity

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

Identify common sources of ethylene glycol

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

How well did you know this?

Not at all

Perfectly

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

alcohol dehydrogenase
ethylene glycol isnt toxic, its metabolites are

How well did you know this?

Not at all

Perfectly

ethylene glycol toxicity stage 1

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)

How well did you know this?

Not at all

Perfectly

Stage 2 ethylene glycol toxicity

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

How well did you know this?

Not at all

Perfectly

Stage 3 ethylene glycol toxicity

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

Explain how acetaminophen toxicity affects the liver and red blood cells

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

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

Explain how animals are exposed to harmful algae blooms

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

How well did you know this?

Not at all

Perfectly

Explain how animals are exposed to aflatoxin

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

How well did you know this?

Not at all

Perfectly

Know which aflatoxin metabolite gets excreted in milk

Aflatoxin M1

Recognize which animals are more susceptible to aflatoxin-induced hepatotoxicity

Dogs, poultry, young pigs

Recognize which animals are more susceptible to aflatoxin-induced hepatotoxicity

Dogs, poultry, young pigs

Describe how xylitol causes hypoglycemia in dogs

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!

Describe how xylitol causes hypoglycemia in dogs

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!

Explain how xylitol toxicosis affects serum potassium levels in dogs

Hypokalemia – excess insulin release stimulates cells to take up potassium

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

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)

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

euglycemia

normal blood glucose

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

N-Acetylcysteine SAM-e

Know what toxins/toxicants cause gastrointestinal toxicity in animals

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

Know what toxins/toxicants cause dermal toxicity in animals

Plants Causing Photosensitization Corrosive Agents Blister Beetles (Cantharidin))

Know which mycotoxin causes “Slobber Syndrome”

slaframine

Describe the mechanism of toxicity of the rodenticide zinc phosphide

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

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

rotten fish smell

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

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

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

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**

Know how animals are exposed to blister beetles

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

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

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**

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

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

slobber syndrome aka "Black Patch Disease"

Explain how animals are exposed to slaframine

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

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

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**

Know which animals are most sensitive to the mycotoxin deoxynivalenol

dogs and pigs

Describe the common clinical signs associated with deoxynivalenol toxicity

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