Toxicology Flashcards
(87 cards)
1
Q
What is a Toxicant?
A
Any substance that when introduced into or applied onto the body can interfere with the life processes of cells of the organism
May be of biologic origin, manufactured chemicals, or naturally occurring chemicals
2
Q
What is Decontamination?
A
The process of removing or neutralizing injurious agents
3
Q
What is Chelation?
A
Chelation therapy is the use of chelating agents to detoxifypoisonousmetal agents such asmercury,arsenic, andlead by converting them to a chemically inert form that can be excreted without further interaction with the body.
4
Q
What does LD 50 stand for?
A
Lethal Dose 50
5
Q
Order of handling a poison emergency.
A
- Assessment of the patient’s condition
- Stabilization of vital functions
- Decontamination
- Control Clinical Signs
- Provide Nursing Care
6
Q
What is external exposure decontamination?
A
Ocular Irrigation, Bathing with cool water in mild dishwashing detergent, shaving.
7
Q
What Emetics agents can you use?
A
Hydrogen Peroxide 3%
Syrup of Ipecac
Apomorphine hydrochloride
Xylazine
8
Q
What Decontamination method absorbs a chemical toxicant?
A
Activated Charcoal
9
Q
In what instance can you not use activated charcoal?
A
animals that have ingested caustic materials. These materials are not absorbed systemically, and the charcoal may make it more difficult to see oral and esophageal burns.
10
Q
What is used to enhance elimination?
A
Cathartics
11
Q
What kind of Cathartics are there?
A
Saline cathartics
Sorbitol
Bulk cathartics
Pumpkin
Metamucil
12
Q
When eliminating toxins from the lower gastrointestinal tract what do we use?
A
Enemas
13
Q
What should be used
A
in cases of caustic or petroleum distillate ingestion
14
Q
When would we use Enterogastric Lavage?
A
when potentially lethal oral exposures have occurred. Examples: strychnine, metaldehyde, tricyclic antidepressants
15
Q
What does a topical allergy look like?
A
mild redness or hair loss at the application site
16
Q
What is this the definition of? Ingestion of bitter-tasting products result in excessive salivation
A
Taste Reactions
17
Q
Topical Insecticide used in k-9 Advantage
A
Imidacloprid
18
Q
Topical Insecticide used in Frontline?
A
Fiproni
19
Q
What happens when Permethrin is applied to a cat?
A
Severe reaction if the permethrin product applied, Seizures and Tremors
20
Q
How do you treat Permerthrin poisoning in cats?
A
Control seizures with Methocoarbamol (other products used: Diazepam, Propofol), bath, Supportive care for thermoregulation, dehydration, nutrition, should continue until full recovery
21
Q
Who can Fipronil cause death in?
A
Rabbits: reports of lethargy, anorexia, convulsions, death
22
Q
How is absorbed? and the lethal dose?
A
Systemically, >1600mg/kg
23
Q
What is in chocolate that makes it toxic?
A
theobromine and caffeine, which are both classified as methylxanthines
24
Q
What are the clinical sign of chocolate poisoning?
A
hyperactivity, tachycardia, tachypnea, trembling and potentially death, vomiting, diarrhea, excessive thirst, increased urination, lethargy
25
General Rule of Thumb for chocolates?
The more bitter the more toxic
26
How do you treat Chocolate poisining?
stabilize, decontaminate, supportive care
27
How does onions cause toxicity?
cause oxidative RBC damage, leading to hemolytic anemia
28
Clinincal Signs of Onion poisoning
hemolytic anemia, hemoglobinuria, vomiting, weakness, pallor
29
How do you treat Onion poisoning?
Decontamination if recent exposure
Monitor PCV, whole blood transfusions if warranted,
Supportive care (IVF, Nutrition, Etc.) until fully recovered
30
What happens when an animal ingest rising bread dough?
Can be life-threatening as the heat from the animals’ body causes the dough to rise in the stomach
Ethanol is produced as it rises, causing it to expand several times its original size
31
Clinical Signs of Rising Bread dough?
ethanol toxicosis and foreign body obstruction: severe abdominal pain, bloat, vomiting, incoordination, depression
32
What Happens if an animal ingest grapes or raisins?
May cause kidney failure if eaten in any quantity
33
Clinical signs of tobacco poisoning
develop quickly: excitement, tachycardia, tachypnea, salivation, vomiting, diarrhea Clinical signs after the initial excitability may progress to shallow breathing, muscle weakness, tremors, depression, collapse, coma, death.
Death is due to respiratory paralysis
34
What is Xylitol? and the clinical signs associated with it.
sugar substitute: hypoglycemia secondary to the release of insulin; liver failure and coagulopathy
Hypoglycemia: weakness, ataxia, depression, vomiting occur within 30 min of ingestion
CHEM may reveal elevate ALT and ALP and/or liver failure within 18-72 hr of ingestion
35
Why is Xylitol toxic to dogs?
Xylitol does not stimulate the release of insulin from the pancreas in humans. However, when non-primate species like dogs eat something containing xylitol, the xylitol is quickly absorbed into the bloodstream, resulting in a potent release of insulin from the pancreas.
36
What to do when a pet ingest acids?
Corrosive and can produce burns on contact w/ tissue (skin, mouth, GI tract) Tx: dilution!!! Attempt to increase pH
Tx: supportive care of burn
37
What do you need to know about ingestion of alkali products?
Cause DEEPER lesions than acidic compounds
Severity depends on concentration, amount ingested, pH and duration of contact w/ tissues pH <11: serious corrosive injury is unlikely
pH > 12.5: can cause ulceration (esophageal)
pH>14: can cause erosion/perforation(esophageal)
Tx: Stabilize, Supportive
38
What all can detergents be?
be nonionic, anionic, cationic
39
What do need to know about Ainonic detergents?
shampoos, dishwashing/laundry detergents, electric dishwashing detergent;
toxicity low, usually limited to: cutaneous, ocular, oral, GI irritation;
may be caustic if combined w/ other chemicals
40
What do you need to know about Cationic detergents?
fabric softeners, potpourri oils, hair mousse, conditioners, germicides, sanitizers, disinfectants;
rapidly absorbed and may produce severe local and systemic toxicities;
cats may get oral ulcerations, stomatitis at concentrations of 1% or less
41
What is the first aid of exposure to corrosive agents
Ocular: Flushing 20-30 min; eye is then examined by DVM and Tx accordingly
Dermal: bathe animal ASAP w/ mild soap; Topical irritation examined by DVM and Tx accordingly
Ingestion:
DO NOT INDUCE VOMITING!!!
Oral dilution w/ milk or water
DVM evaluate for oral, esophageal, lower GI ulcerations and Tx accordingly
Supportive Care w/ IVF, serial labs, Nutritional Support, Etc..
42
Zinc poisoning?
, US pennies minted since 1983
One penny can cause zinc poisoning in a small dog!PU/PD, hemoglobinuria, diarrhea, weight loss, anemia, vomiting, weakness, cyanosis, seizures, death
Diagnosis: Radiographic findings, serum zinc levels may be obtained using plastic syringes w/ no rubber grommets and stored in Royal blue top Vacutainers, post-mortem pancreatic analysis
Treatment:
Remove the source of zinc from GI tract via sx or endoscopy;
activated charcoal is not effective; bulk cathartics (peanut butter, mineral oil, corn oil) may aid in removal from the GI tract;
IVF, nursing care, serial lab work, nutrition
43
Lead poisoning?
Sources: paint, toys, drapery weights, linoleum, batteries, plumbing, galvanized wire, stained glass, lead shot, foil from champagne bottles, improperly glazed bowls
Pathology: GI tract, renal, hepatic, nervous system; lead combines w/ RBC and makes them fragile, resulting in anemia, capillary damage
Clinical Signs: vague: lethargy, weakness, anorexia, regurgitation, polyuria, ataxia, circling, convulsions
Diagnosis: Rads may reveal metallic object, blood levels, evaluation of RBC morphology for basophilic stippling and cytoplasmic vacuolization
Treatment:
Remove lead particles via bulk-diet, surgery or endoscopy
CaEDTA for chelation
Supportive care: IVF, Seizure Control, Etc.. Until full recovery
44
Poisoning of mothballs
Veterinary treatment of mothball ingestion is always required
Composed of either 100% naphthalene or 99% paradichlorobenzene
Naphthalene more toxic
Pathology: Heinz-body anemia, hemolysis, methemoglobinemia; affects liver, RBC, CNS
45
Clinical SIgns of Fly bait
“SLUDGE”: Salivation, Lacrimation, Urination, Defecation, GI cramping, Emesis
Clinical Signs may occur w/I minutes of ingestion
46
What is the antidote to fly bait poisoning?
Atropine and 2-PAM
47
Antidote for systemic insecticides?
Atropine and 2-PAM
48
What is poisonous in Snail bait?
Metaldehyde
49
What is poisonous about Gopher and Mole bait?
May contain zinc phosphide, which is converted to phosphine gas in the stomach
Released phosphine gas results in severe respiratory distress
50
Three main types of rat bait
Anticoagulants
Bromethalin
Cholechalciferol
51
Pathology of Anticoagulants
anticoagulant rodenticides act by competitive inhibition of vitamin K epoxide reductase, thereby halting the recycling of Vitamin K. This results in blood clotting abnormalities and can result in spontaneous hemorrhage
52
Antidote for anticoagulants
Vitamin K
53
Clinical signs for anticoagulant toxicity
Prolonged clotting times (Prothrombin Time (PT)) as early as 36-72 hr post ingestion
Spontaneous hemorrhage beyond 72 hr (petechiae, scleral hemorrhage, SQ hematomas, hemothorax, etc..)
Other clinical signs may not be evident for at least 5-10 days post ingestion: weakness, pale MM, dyspnea, coughing, swollen joints
54
Pathology of Bromethalin
causes a reduction in ATP which is necessary to maintain the Na-K pump. When this pump fails, fluid builds up, leading to fluid-filled vacuoles between myelin sheaths. This leads to decreased nerve impulse conduction.
55
Clinical signs pf Bromethalin toxicity
occur within 24 hr to 2 weeks and include muscle tremors, seizures, hyperexcitability, forelimb extensor rigidity, ataxia, CNS depression, loss of vocalization, paresis, paralysis and death
56
Tx of Bromethalin
Aggressive decontamination: repeated doses of activated charcoal every 8-12 hrs
Supportive care for clinical signs: diazepam, methocarbamol, diphenhydramine, mannitol, furosemide, corticosteroids, IVF therapy
Poor Px for animals showing severe signs
Gingko Biloba???
57
Pathology for Cholecalcifferol
Cholecalciferol (Vitamin D3) increases intestinal absorption of Ca, stimulates bone resorption, and enhances kidney resorption of Ca. This results in serum calcium increase, which leads to kidney failure, CVS abnormalities and tissue mineralization.
58
Clinical signs for Cholecalciferol
delayed onset of 18-38 hr; vomiting, depression, diarrhea, anorexia, PU/PD, cardiac arrhythmias
kidney failure results from Ca deposition in the kidneys (elevated BUN/CREA)
59
Tx for Cholecalciferol
Aggressive decontamination, repeated doses of activated charcoal every 8-12 hr
Supportive care: IVF to enhance diuresis, furosemide and prednisolone may be added to promote diuresis
Pamidronate inhibits bone resorption of Ca
Salmon Calcitonin may decrease serum hypercalcemia
60
Types of antifreeze products
Methanol
Propylene Glycol
Ethylene Glycol
61
What do you need to know about Methanol
Most commonly found in windshield washer fluids
Pathology: methanol’s metabolite, formaldehyde, is oxidized to formic acid, which results in systemic acidosis Small exposures (chewing on a bottle) will only cause mild GI upset
Large exposures: supportive care for metabolic acidosis
62
What do you need to know about Glycol.
Main ingredient in the “safer” antifreeze forms
Three times LESS toxic than Ethylene Glycol (EG)
No clinical signs after a dog given 20ml/kg
Toxic quantities: liver damage, renal insufficiency possible
Clinical Signs: CNS depression, muscle weakness, ataxia, seizures, metabolic acidosis
63
What do you need to know about Ethylene Glycol
Most dangerous form of antifreeze; most commercial forms of antifreeze contain 95-97% EG
EG is rapidly absorbed from the GI tract; in dogs, peak blood concentrations of EG occur within 3 hr of ingestion. Approximately 50% of ingested EG is excreted unchanged by the kidneys; however, a series of oxidation reactions in the liver and kidneys metabolize the remaining EG. Toxic metabolites of EG cause severe metabolic acidosis and renal tubular epithelial damage.
64
Clinical signs of Ethylene Glycol
Stage 1: This occurs within 30 minutes to 12 hours, and looks similar to alcohol poisoning. Signs of walking drunk, drooling, vomiting, seizing, and excessive thirst and urination may be seen.
Stage 2: This occurs within 12-24 hours post-exposure, and clinical signs seem to “resolve” when in fact more severe internal injury is still occurring.
Stage 3: In cats, this stage occurs 12-24 hours after ethylene glycol exposure. In dogs, this stage occurs 36-72 hours post-ingestion. During this stage, severe acute kidney failure is occurring. Signs of inappetance, lethargy, drooling, halitosis (secondary to kidney failure), coma, depression, vomiting, and seizures may be seen.
65
Diagnosis of Ethylene Glycol
Serum Chemistry, Acid-Base
Commercial EG kit that can be run as early as 30 min after ingestion up to 72 hours after ingestion. (detects levels > 50mg/dl)
Idexx Laboratory
activated charcoal may cause false positive as some forms contain propylene glycol…..
66
Treatment of Ethylene Glycol
Decontamination for recent exposure only
<1 hr: induction of emesis
1-3 hr: activated charcoal, gastric lavage
Supportive Care: IVF diuresis, control clinical signs. Fomepizole is the preferred treatment in dogs but is not effective in cats. It inhibits alcohol dehydrogenase.
Ethanol can be used in dogs and cats. It competes with EG as a substrate for alcohol dehydrogenase.
Side effects: CNS depression, ataxia, metabolic acidosis
67
What Ethenols are used to treat Ethylene Glycol?
Vodka (80 Proof)
Grain Alcohol (190 Proof)
68
What NSAID is toxic to cats
Tylenol!
69
Clinical signs of Acetaminophen Toxicosis
Methemoglobin values increase within 2–4 hours, followed by Heinz body formation.
Clinical signs include depression, cyanosis, weakness, tachypnea, vomiting, methemoglobinemia, hypothermia, facial or paw edema, and death.
Clinical signs of methemoglobinemia may last 3–4 days. Hepatic injury may not resolve for several weeks.
No dose is safe in cats since they are deficient in glucuronyl transferase.
70
Clinical signs of aspirin overdose
depression, vomiting, GI ulceration, increased bleeding times, hematemesis, anorexia, hypothermia, tachypnea; may progress to muscular weakness, pulmonary and cerebral edema, hypernatremia, hypokalemia, ataxia, coma, death.
71
What does ibroprophen cause?
gastric ulcers
72
Symptoms of Marijuana toxicity
Prolonged depression, vomiting, incoordination, sleepiness or excitation, hypersalivaton, dilated pupils, low blood pressure, low body temperature, seizure, coma, death (rare)
73
What to know about Azaleas
contain substances known as grayantoxins, which lead to cardiovascular dysfunction
Clinical signs: abdominal pain, cardiac arrhythmias, vomiting, drooling, diarrhea, weakness and depression of the central nervous system in animals.
Severe azalea poisoning could ultimately lead to coma and death from cardiovascular collapse.
Signs occur within 4-12 hr of ingestion and may persist for days
74
What to know about Cardiac Glycosides
Oleander , Foxglove
All parts of Nerium oleander are considered to be toxic, as they contain cardiac glycosides that have the potential to cause serious effects—including gastrointestinal tract irritation, abnormal heart function, hypothermia and even death.
Clinical signs develop within several hr of ingestion and may persist for several days
Clinical signs usually involve the GI tract and cardiovascular system
75
What to know about Castor Beans
Castor Bean The poisonous principle in Ricinus communis is ricin, a highly toxic protein that can produce severe abdominal pain, drooling, vomiting, diarrhea, excessive thirst, weakness and loss of appetite. Severe cases of poisoning can result in dehydration, muscle twitching, tremors, seizures, coma and death.
Ricin is one of the most potent plant toxins known
All parts of the plant are toxic, but the seeds are the most potent
76
What to know about lillies
Members are considered to be highly toxic to cats. While the poisonous component has not yet been identified, it is clear that with even ingestions of very small amounts of the plant, severe kidney damage could result.Affected cats vomit w/i a few hours of exposure, then the vomiting subsides and the cat may appear clinically normal or the cat may be depressed and anorexic
Within 24-72 hr, oliguric to anuric renal failure may occur, accompanied by vomiting, depression, dehydration
Laboratory data may reveal elevated BUN/CREA as early as 12-18 hr post ingestion
Death from acute kidney failure possible within 3-6 post ingestion
77
Tx for Lilly poisoning
Veterinary care: stabilize, decontaminate, supportive care
Early decontamination and aggressive IVF therapy can prevent kidney failure
Delaying tx >18 hrs results in a grave Px
78
What to know about Sago Palms
All parts of Cycas Revoluta are poisonous, but the seeds or "nuts" contain the largest amount of toxin.
The ingestion of just one or two seeds can result in very serious effects, which include vomiting, diarrhea, depression, seizures and liver failure.
79
What are Calcium-Oxalate-Containing Plants
Calla lily (Zanteseschia spp)
Elephant Ears (Caladium spp)
Dumb Cane
Mother-in-law’s tongue
Peace Lily (Stathiphyllum spp)
80
Pathology of Calcium-Oxalate-Containing Plants
Calcium oxalate crystals expelled in the mouth upon chewing, resulting in oropharyngeal edema
81
Clinical signs of Calcium-Oxalate-Containing Plants
oral irritation, burning of lips, mouth, tongue, drooling, vomiting, difficulty swallowing
82
Clinical Signs of Red Maple
Horses often die within 18-24 hr of ingestion of wilted leaves
Horses that remain alive for 18-24 hr after ingestion of wilted leaves will be severely depressed and cyanotic and produce dark red or brown urine.
The mucous membranes are blue to brown from poor oxygenation
They suffer intravascular and extravascular hemolysis
83
Diagnosis of Red Maple toxicity
Dx: based on CS, blood work includes methemoglobinemia, which gives the blood a brown color if exposure is recent, Heinz body formation on RBCs, which can seen on a blood smear, and an elevation of liver and kidney value
84
Tx of Red Maple Toxicity
If exposure is within a few hours, activated charcoal can be administered through a nasogastric tube
Mineral oil may also be administered to decrease the absorption of the toxin when activated charcoal is not available.
Other treatments include IV fluid therapy to flush and maintain the function of the kidneys, steroids, and possibly blood transfusions and oxygen therapy if needed
85
What to know about Bracken Fern
Enzootic hematuria is the most common result of bracken fern poisoning.
Primarily affects cattle and, less frequently, sheep. Poisoning most often occurs during late summer when other feed is scarce, or when animals are fed hay containing bracken fern.
Poisoning requires prolonged exposures; affected livestock must ingest bracken fern for several weeks to years before disease develops.
86
Clinical signs of Enzootic hematuria
Affected cattle are weak, rapidly lose weight, and develop pyrexia (106°–110°F)
Calves often have difficulty breathing, with pale mucous membranes. Hemorrhages vary from minor mucosal petechia to effusive bleeding, and at times large blood clots form that may be passed in the feces.
Coagulation is prolonged, and bleeding may be pronounced and excessive even at small wounds such as small insect bites or minor scratches.
Once animals develop clinical disease, poisoning is almost always fatal.
Mortality rate in cattle >90%
87
What to know about Bracken Fern. Bracken Staggers.
first recognized as a neurologic disease when horses consumed contaminated hay.Clinical signs in horses include anorexia, weight loss, incoordination, and a crouching stance while arching the back and neck with the feet placed wide apart. When the horse is forced to move, trembling muscles are noted.
These changes are due to bracken fern thiaminases. The resulting disease is similar to vitamin B1 deficiency, therefore most animals respond to thiamine therapy
