4.2 Lab Flashcards
what does ingestion of grapes and raisins cause in dogs/cats? what is a troubling dose? treatment?
- causes renal damage (proximal renal tubules) > possible anuric renal failure (can be fatal)
- Variable effect; some dogs unharmed by quantities of grapes that have killed other dogs
- As few as 4-5 grapes can harm a small dog, 1lb grapes for a large breed dog; 3g/kg of raisins
- Vomiting (direct effect? or from uremia?)
- Death or euthanasia common if treatment is delayed – prognosis is poor
- Goal is to minimize absorption (emesis, charcoal) and perfuse kidneys (IV fluids with diuretic for 72 h)
probable harmful component in grapes? what other substance can this be found in, sometimes?
proposed that tartaric acid and its salt, potassium bitartrate, are the toxic principles in grapes leading to acute renal failure in dogs.
- The ASPCA Animal Poison Control Center received several reports of dogs exposed to potassium bitartrate (cream of tartar) in homemade playdough products
issues caused by consumption of macadamia nuts? toxic dose? treatment?
- Unknown toxin causes weakness, lethargy, joint swelling & pain
- As little as 1 nut (2g) /kg BW can induce clinical signs of toxicity
- Onset in 4-24 hours, signs generally resolve completely within 48h without treatment
- Emesis induction may be helpful if performed early
- No fatalities recorded
where are methylxanthines found? what problems do they cause? how can they cause death? treatment and prognosis?
Caffeine, theobromine (chocolate, cocoa), theophylline (tea)
* Dogs readily consume chocolate (theobromine)
> Baking chocolate and cocoa powder most toxic (approx 10 times more potent)
* Stimulation of CNS, skeletal muscle, cardiac tissue
> Restlessness, vomiting, tremors
> Tachypnea, tachycardia, diarrhea, polyuria
> Seizures & arrhythmias are common
* Death is from arrhythmia or resp failure, within 24 hrs (sometimes delayed a few days)
* No specific antidote: decontamination, hydration, seizure management
* Prognosis good if treated early (within 3-4 hours of ingestion)
where do we find xylitol? what problems does it cause? what are clinical signs and mechanism of toxicity?
Sugar free gum, mouthwash, candy, toothpaste
* Does not affect humans or cats, absorbed very slowly
* Absorbed very rapidly in dogs
* Onset of signs in 15-30 minutes: dose dependent INSULIN SPIKE, then acute drop in blood sugar (hypoglycemia)
* Severe liver toxicity and failure > death (unknown mechanism)
how to treat xylitol consumption? what should we monitor?
- Only induce emesis if within 30 minutes (b/c rapidly absorbed)
- AC doesn’t bind well
- Baseline blood glucose level, liver values, electrolytes, CBC
- Repeat in 8-12 hr, monitor blood glucose ever 2 hours
- IV dextrose for hypoglycemia
alternative names for xylitol
“Birch Sugar” “Birch Sap” “Wood sugar”
when is battery consumption an issue? what damaging effects can occur? how should we treat?
If small, may pass through without any issues
> 20 mm likely to lodge in esophagus – leak
corrosive substances – perforation
Larger dry cell batteries (alkaline or acidic + various metals)
Leakage of alkali more damaging than acids
Radiographs to diagnose
>36 hours or lodged in esophagus – remove by endoscopy or surgery
Damaged by chewing – remove immediately
how might an animal ingest zinc? what problem can this cause? how can we diagnose and treat? prognosis?
US pennies from 1982 on (and Canadian pennies from 1997-2001) are >95% zinc
Galvanized metal objects (nuts, bolts, nails, toys)
Acute GI distress (vomiting, diarrhea, anorexia, abdominal
pain)
Hemolytic anemia (icterus, hemoglobinemia, hemoglobinuria)
Radiographs reveal radio-opaque objects in the GI tract
Hepatic necrosis, renal tubular nephrosis, pancreatitis, DIC
may occur
Remove zinc object and supportive care +/- blood transfusions
Prognosis is guarded
how might an animal ingest lead? what is the impact of consumption? what are the clinical signs? how should we treat?
Old paint chips, paint dust (1978): up to 50% lead by weight
Toys, lead fishing sinkers, stained glass windows or lamps, lead bullets
Chronic exposure: inhibition of heme production, increased RBC fragility > anemia
Acute exposure: increased intracellular Ca levels > neuronal cell death, renal damage, GI smooth muscle spasticity
GI UPSET (vomiting, anorexia) +/- CNS signs
Remove lead object (if found), chelate w/ EDTA, D- penicillamine, or succimer (succimer facilitates urinary excretion of lead)
Manage seizures
Wash lead dust off fur
how does nicotine ingestion affect an animal? how can we treat?
Stimulation of nicotine receptors in CNS: vomiting, hypersalivation, bradycardia, defecation, miosis (constriction of pupils)
CNS excitement/tremors, then depression
Neuromuscular blockade of diaphragm/intercostal
muscles may cause death
Decontamination and supportive care (no specific antidote)
what animals are sensitive to non-stick cookware? why? effects?
“Teflon” and “Silverstone” pans
PTFE (polytetrafluoroethylene)
Release of fluoride containing gases when heated
“Polymer fever” in humans (flu-like)
Caustic to airways, birds are highly sensitive
Acute respiratory distress > death (usually found dead)
issues associated with fluoride consumption? chronic vs acute signs. treatment?
High concentration exposure over long period of time (chronic exposure in cattle) interferes with calcium metabolism
> Reduces mineralization of bone: painful joints, fractures
> Can also cause severe dental irregular wear and discoloration
High concentration exposure, acute (dogs): such as in toothpaste
> Acute fluoride exposure at high concentrations will cause corrosive damage to tissues
> GI upset: nausea, vomiting, abdominal pain
> Treatment is supportive
issues associated with advil (ibuprofen) consumption?
An acute single ingestion of 100–125 mg/kg can lead to vomiting, diarrhea, nausea, abdominal pain, and anorexia.
Renal failure may follow dosages of 175–300 mg/kg.
CNS effects (ie, seizures, ataxia, depression, coma) in addition to renal and GI signs can be seen at dosages >400 mg/kg.
Dosages >600 mg/kg are potentially lethal in dogs.
How rapidly is ibuprofen absorbed following ingestion?
30 minutes to 3 hours
What are the main adverse effects of NSAIDs?
1: gastric mucus LOW, gastric acid HIGH > ulceration and hemorrhage
2: renal vasoconstriction, inhibition of platelet function
3: hepatotoxicity - idiosyncratic
why do NSAIDs damage the kidney? why are dogs with chronic renal failure more susceptible to renal related side effects?
we know that COX-2 is expressed in kidney and so kidneys can be affected whether the NSAID’s are more broad spectrum or COX-2 selective.
COX-2 takes over more homeostatic mechanisms in dogs with chronic renal failure as well, so they are even more susceptible to renal related side effects.
how can we attempt decontamination and treatment in the case of ibuprofen ingestion?
How can we attempt decontamination?
-Emesis
-Activated charcoal
- Cathartic
What broad categories of supportive care is our treatment plan going to involve?
-IV fluids
-Gastric protectants to minimize ulcer formation
E.g. proton pump inhibitor e.g. omeprazole
H2 blocker e.g. ranitidine;
Misoprostol – a PGE1 analogue which stimulates gastric bicarbonate and mucus secretion and inhibits gastric acid secretion
What is the toxic compound of chocolate? What is the mechanism of action?
Methylxanthines: theobromine, caffeine, theophylline
Although the concentration of theobromine in chocolate is 3–10 times that of caffeine, both constituents contribute to the clinical syndrome seen in chocolate toxicosis
Methylxanthines: theobromine and caffeine mechanism of toxicity? result?
competitively inhibit cellular adenosine receptors, resulting in CNS stimulation, diuresis, and tachycardia.
Methylxanthines also increase intracellular calcium levels by increasing cellular calcium entry and inhibiting intracellular sequestration of calcium by the sarcoplasmic reticulum of striated muscle.
The net effect is increased strength and contractility of skeletal and cardiac muscle.
Additionally, methylxanthines increase circulating levels of epinephrine and norepinephrine and compete for benzodiazepine receptors
Why does xylitol cause hypoglycemia? what other issue does it cause?
In dogs, and perhaps rabbits and ferrets, it is absorbed extremely quickly.
The immediate result is that it fools the pancreas into releasing a huge spike of insulin, which is quickly followed by a precipitous drop in blood sugar (acute hypoglycemia) since there isn’t really any surplus sugar for the insulin to work on.
The next problem, which isn’t quite as well understood, is severe (and often fatal) liver toxicity and failure.
what timeframe should we induce emesis within for xyletol consumption? is activated charcoal useful?
Do not do if ingestion >30 min since very rapidly absorbed and may further stress/compound hypoglycemia.
Activated charcoal is of questionable efficiency
important diagnostics to get after xyletol consumption?
blood glucose, a baseline liver profile
effect of N- acetyl-cysteine on acetaminophen toxicity
peed conjugation of toxic metabolites
Minimum tissue collection from carcasses should include:
Liver
Kidney
Brain
Fat
Urine
GI content
List of samples to be collected from live animals that are suspected of being poisoned:
Whole blood
Serum
Urine
Stomach content
Feed (if suspect)
why are dogs more sensitive to cannabis than humans?
- DOGS HAVE MORE CANNABINOID RECEPTORS IN THE BRAIN VS. HUMANS
most common clinical signs from marijuana ingestion? less common?
- Most common:
– CNS depression, ataxia, bradycardia (tachycardia if involving chocolate), urinary incontinence, vomiting
– Agitation, glazed expression/dilated pupils - Less common:
– Vocalizing, diarrhea, hypothermia, hypersalivation, hyperesthesia, seizures, coma
treatment for marijuana toxicity?
- Decontamination: emesis, AC
- Supportive care: no specific antidote – Body temperature
– Heart rate, blood pressure - Agitation: butorphanol
- Lipid therapy?
– Not routinely recommended
are dogs likely to die after marijuana ingestion?
- Two deaths reported related to cannabis overdose in dogs
– Both complicated cases
– Both involved baked goods w/ very
concentrated butter - The minimum lethal oral dose for dogs for THC is more than 3 g/kg
– To put this into perspective, a 10 kg dog eating joints with approx. 15% THC content (150mg/g) would have to eat 200 joints.
