Toxins Q9

What the three categories of common toxins in dogs

food, medications, and other objects

What is the toxic component of chocolate

methylzanthine

Methylzanthine’s primary component

Theobromine

Methylzanthine’s secondary component

caffeine

Where are theobromine and caffeine absorbed?

GI tract

clinical signs of chocolate toxicity depends on what?

amount and type of chocolate

What would be the clinical signs for a small amount of chocolate ingested?

mild to moderate GI signs

what would be the clinical signs for a medium amount of chocolate ingested?

cardiac arrhythmias

what would be the clinical signs for a large amount of chocolate ingested?

seizures, life-threatening

name types of chocolate from most toxic to least

cocoa powder → Baker’s → Semisweet → instant cocoa mix → milk → white

what is the mechanism of toxicosis for chocolate

• behavioral change and CNS stimulation

• Cardiovascular abnormalities

• increased cardiac and skeletal muscle contractility

• death from cardiac arrhythmias, resp failures, or hyperthermia

overall clinical signs of chocolate toxicity

vomiting, polydipisia, restlessness, hyperthermia, ataxia

what is the timeframe of signs for chocolate ingestion

6-12hrs

what are the two main issues regarding chocolate toxicity signs

cardiovascular and CNS

how can you diagnose chocolate toxicity

recent exposure history

treatment of chocolate toxicity categories

1. decontamination

2. CNS signs

3. cardiac arrythmias

what are decontamination treatment options for chocolate toxicities

induce vomiting and activated charcoal

what does activated charcoal do?

decreased toxin absorption

what are the two CNS sign treatment options for chocolate toxicities

methocarbamol (muscle relaxer) and diazepam (mild sedative/seizure medication)

what are two cardiac arrythmias treatment options for chocolate toxicities

beta-blockers, lidocaine

prognosis for chocolate toxicities

generally good, guarded to poor if seizures or cardiac arrhythmias develop

when do signs resolve in chocolate toxicities usually

12-72 hours

what is the toxic component of raisins and grapes

tartaric acid

which is more toxic to dogs, raisins or grapes

raisins because they are more concentrated

mechanism of toxicosis of raisins and grapes

• renal tubular necrosis

• mineralization of kidneys, gastric mucosa, myocardium, lungs, and blood vessels

clinical signs of raisin/grape toxicity

anuria, anorexia, lethargy

what clinical sign can you expect within 12 hrs of ingestion of grapes/raisins

vomiting

what two clinical signs can you expect within 24 hrs of ingestion of grapes/raisins

anorexia and lethargy

onset of signs will be within how many hours post ingestion

6-12 hrs

what toxicity causes AKI

raisins and grapes

what are the bloodwork results for a raisin/grape toxicity

azotemia (increased BUN and creatinine) and increased phosphorus (hyperkemia)

what are the urinalysis results for raisin/grape toxicity

low urine specific gravity

xray results of grape/raisin toxicity

renamegaly (enlarged kidneys)

treatement of raisins/grape toxicity

decontamination, IV fluids!, supportive care, renal function monitoring

what are the decontamination options for the treatment of raisin/grape toxicity

induce vomiting, activated charcoal

prognosis of raisin/grape toxicity

varied, not all dogs develop AKI… poor with oliguria, anuria, ataxia, weakness

what is the toxic component of garlic/onions

thiosulfinates -→ dipropyl sulfides

what is more toxic: garlic or onions

garlic

mechanism of toxicosis

• oxide RBC membrane resulting in hemolysis

• poisoning can result from ingesting raw, dried,  powdered, or cooked

what type: raw, dried, powdered or cooked does NOT inactivated toxic principle

cooking or drying

most dogs would have to eat at least ___% (5G/KG) bodyweight to develop toxicosis

5%

clinical signs of garlic/onions

lethargy, pale mucous membranes, tachycardia, hemoglobinuria (red to brown urine)

onset of signs of garlic/onions - timeline

within 25 days post ingestion

bloodwork results of garlic/onion

anemia, heinz body formation, methemoglobinemia (brown serum)

urinalysis results of garlic/onion

hemoglobinuria (reddish - brown color)

treatment of garlic/onion toxicity

decontamination ± blood transfusion

decontamination treatment of garlic/onion toxicity

induce vomiting, activated charcoal

prognosis of garlic/onion toxicity

generally good, guarded with sever anemia

toxic component of sugar-free gum

xylitol

what are some things that xylitol is found in

gum, candy, peanut butters

xylitol causes a rapid, dose-dependent ________ release resulting in ______

xylitol causes a rapid, dose-dependent insulin release resulting in hypoglycemia

a really big dose of xylitol can cause what toxicity

hepatoxicity

clinical signs of xylitol

lethargy, vomiting, weakness, ataxia, seizures

bloodwork results of xylitol

hypoglycemia, increased ALT, hyperbilirubinemia, thrombocytopenia

treatment for xylitol toxicity

decontamination, IV dextrose, denamarin

prognosis for xylitol toxicity

good w/ control of hypoglycemia, guarded if hepatic necrosis and coagulopathy develops

marijuana toxic component

cannabinoids (specifically THC)

mechanism of toxicosis of marijuana

• THC acts on an unique receptor in the barin responsible for CNS effects

• clinical effects are often seen at low doses

clinical signs of marijuana toxicity

dilated pupils, ataxia, tremors, CNS depression

when will signs occur after ingestion of marijuana

30 minutes

diagnosis of marijuana toxicity

history and clinical signs ± urine drug tests

treatment of marijuana toxicity

decontamination and supportive care

what is the supportive care for marijuana toxicities

dark, quiet room

prognosis

excellent

what are common NSAIDs that are toxic

ibuprofen, aspirin, naproxen

Human NSAIDs commonly affect what in dogs

GI tract and kidneys

toxic mechanism of human NSAIDS

• inhibit cyclooxygenase enzyme leading to the blocking production of prostaglandins

• PG important for normal function of GI protection, renal blood flow

what commonly causes GI ulcers

human NSAIDs

clinical signs of human NSAIDs toxicity

abdominal pain, melena, hematemesis

severe toxicosis of human NSAIDS can cause what

dehydration, pale mucous membranes, ataxia, seizures

bloodwork results of NSAID tox

anemia from GI hemorrhage, azotemia, elevated ALT, bilirubin

treatment of NSAID tox

decontamination, IV fluids, supportive care

prognosis of human NSAID tox

• excellent with mild to moderate irritation/ulceration

• guarded to poor with GI perforation

• renal and liver effects are usually reversible if discovered and treated early

what are the three toxic components in rodenticides

warfarin, bromethalin, cholecalciferol

what does warfarin cause

bleeding - interferes with blood clotting (most common)

what does bromethalin cause

neurologic

what does cholecalciferol cause

calcification

when you are presented with a rodenticide case, what should you do

get active ingredient from product

clinical signs of warfarin toxicity

loss of appetite, depression, bleeding, panting

treatment of warfarin

vitamin K1 for 2-4 weeks

bromethalin clinical signs

muscle tremors, CNS depression, ataxia

treatment of bromethalin

decontimation, time and wishes

cholecalciferol produces…

excess calcium in the blood causing calcification of soft tissue throughout the body

clinical signs of cholecalciferol

loss of appetite, passing large amounts of urine, extreme thirst

treatment of cholecalciferol

decontamination, low calcium diet

toxic component of batteries

alkaline chemicals

• potassium hydroxide

• sodium hydroxide

mechanism of toxicosis of batteries

• causes corrosive injury on contact to tissues through the process called liquefaction necrosis

clinical signs of battery ingestion

abrasions/ulceration on the tongue/cheeks, drooling, lethargy

clinical signs start within what time of exposure of batteries

12hrs

xray for batteries

metal opacity

endoscopy for batteries

assess for GI ulceration

treatment for batteries

• drink water or milk 

• endoscopy or exploratory surgery

• may pass through but could need GI protectants

• pain meds for oral ulcerations

why can’t you induce vomiting for battery ingestion

can cause additional exposure to corrosive material

Signs of toxin exposure depends on the _____ and ______ of exposure

signs of toxin exposure depends on the toxin and route of exposure

examples of toxin signs in cats

GI signs, neuro signs, respiratory signs, skin signs, liver failure, kidney failure

what are the five important pieces/questions that it is important to answer?

1. what is the toxin/potential toxin?

2. What route was the pet exposed?

3. When was the exposure?

4. How much of the toxin was the pet exposed to?

5. What actions, if any, have already been done?

The solution to pollution is ___________!

dilution

what medications do you use to induce vomiting in dogs

apomorphine subconjunctival or intravenously

what medication is used to induce vomiting in cats

xylazine or dexdomitor

induce vomiting is usually most successful with toxins consumed within the last _____ hrs

2