Toxicology Q1 607

what are properties of mercury

pure metallic form is non-toxic but inhalation of vapors are toxic---interact by inactivating sulfhydryl enzymes and interfere with cellular metabolism

what are the properties of DDT

readily absorbed into soils and river sediments, lipophilic

what are the 4 basic components of a risk assessment

toxicant identification, toxicant evaluation, exposure evaluation, and risk estimation

if no witnessed exposure, what 4 things should be asked

when were they last normal, duration of signs, other pets in house affected, any initial signs that are no longer apparent

what are the 7 questions for an ecological risk assessment

who, what, where did it come from, how, what does the body do and how is that impacted by other factors, what are the ecological effects, and how long does it take to cause toxic effect

what product can induce vomiting in cats

alpha-2 agonists like xylazine and dexmedetomidine but with risk of serious CNS depression

why should a cathartic be used after activated charcoal

because bound toxicant can eventually be released due to weak binding and be reabsorbed

how do you treat grape toxicity

fluids

why are cats more sensitive to NSAID toxicosis

they cannot do glucuronidation well which is needed to metabolize the drugs in the liver

what about blister beetles makes them toxic

they have cantharidin that makes them a strong vesicant to create blisters on mucosal surfaces

how do lipophilic chemicals become trapped in the adipose

they have high entrapment in the middle of the lipid bilayer due to their lipid qualities and low leakage out of the bilayer

what products can be used with dogs to induce vomiting

3% hydrogen peroxide, apomorphine, ropinirole

what is the treatment for NSAID toxicity

GI protectant proton pump inhibitor and fluids

what are effects of NSAID toxicity

GI upset, ulceration, reduced renal blood flow, renal failure, CNS signs

what are the categories of toxins of companion animals

accessibles mostly, nutrition, natural toxins, and commercial poisons

define ion trapping

acidifying the urine helps remove basic drugs, alkalizing urine helps remove acidic drugs

what are the effects of soluble oxalate toxicity

acutely hypocalcemia, chronically chronic renal failure

where can toxicants be stored in the body

adipose tissue, liver, plasma, bone, and kidney

breeds, causes, clinical signs, treatment of copper toxicity in DOGS

bedlington terriers, westies, and skye terriers have defect in Cu metabolism...dobermans can have chronic active hepatitis---no hemolytic crisis, weight loss, elevated liver enzymes, nodular liver---D-penicillamine or trientine with addition of zinc in diet

what species should saline cathartics not be used with

birds and reptiles

what species should enemas not be used with

birds due to their cloaca

who does lily toxicity apply to

cats

define toxicant identification

characterization of innate adverse toxic effects of different agents---physical/chemical properties, exposure properties, and host factors

define toxicant evaluation

characterization of relationship between doses and incidences of adverse effects in exposed population---calculate dose effect, include safety factor to build in uncertainty due to not every individual being the same

clinical signs and treatment of pit vipers

coagulopathy, tissue destruction, hypotension, neurotoxicosis, echinocytes---do not use cold packs, give IV fluids, use antivenins

how do grapes cause toxicity

contain tartaric acid that dogs cannot transport well and it gets stuck in their renal tubular cells to cause obstructive nephropathy

what can metabolism of a toxicant lead to

decreased activity (detoxification), increased activity (bioactivation), and changed distribution

what is the goal of toxicant evaluation

determine what dose of the toxicant causes an adverse resposne

what do you do after risk assessment has been perfomed

develop a risk management protocol

what is the treatment for cholecalciferol toxicity

diurese with NaCl or give bisphosphonates to stop reabsorption of bone

who does grape toxicity affect most profoundly

dogs

define threshold dose

dose at which effects are first observed

what is the bird's eye view of toxicology

environment over ecosystem over event

what is the treatment for ethylene glycol toxicity

ethanol (everclear or clear vodka) or 4MP

what are the principle routes of elimination of toxicants

fecal, urinary, and exhalation

sources, pathogenesis, clinical signs, treatment of copper toxicity in SHEEP

feeding calf, horse, poultry or swine diet, or pasture fertilized with swine or poultry manure---copper gets stored in liver, kidney, and brain in excess and when stressed, Cu is released into blood stream causing hemolysis---gun metal blue kidneys---ammonium tetrathiomolybdate and monitor det for Cu, Mo, and S

what kinds of lilies are toxic to cats

flowers with lilium or hemerocallis in the species name

how do you treat lily toxicity

fluids to maintain urine output

what is important to know about ocular dilution with toxicants

flush with large quantities, flush for 20-30 minutes, do not use get the red out products, and use tepid tap water, normal saline, or artificial tears

when is an endoscope useful

for those that cannot vomit

who is most susceptible to blister beetles

horses

species, clinical signs, and treatment of red maple

horses and equid species---hemolysis, brown urine, secondary renal failure, tachypnea, depression---blood transfusions

sources, function, clinical signs, and treatment of cyanide

house fires, plants like peach pits, cherry and apple seeds, fresh or dried leaves from trees---stops tissue utilization of oxygen---rapid onset with cherry red venous blood---hydroxycobalamine or sodium nitrite with sodium thiosulfate

what are some clinical effects of DDT

in birds: reproductive problems, eggshell thinning---fish: membrane function and enzyme disruption---invertebrates: reproductive, developmental, CV, and neurological changes

causes, pathogenesis, clinical signs, treatment of carbon monoxide

incomplete combustion---Hb binds to CO to create carboxyhemoglobin with decreased offloading of O2 to tissues---cherry red color of skin and mucus membranes, drowsiness, incoordination---hyperbaric oxygen chamber

when should you NOT use emetics

ingestion of a caustic substance or corrosive, or petroleum or oily things due to risk of aspiration, or with animals that cannot vomit

what are the 3 main routes of absorption

inhaled, oral, contact

pathogenesis, clinical signs, diagnosis, treatment of anticoagulants

inhibit vitamin K epoxide reductase from recycling vitamin K to create 2, 7, 9, 10 coagulation factors---hemorrhage, first generation rapidly excreted, second gen one feeding sufficient...takes 3-7 days to see clinical signs...initially, lethargy, then dyspnea and bleeding anywhere in body---monitor PT 48-72 hours...in horses PTT goes up in first 24 hours---treat with vitamin K1 orally and clotting factors for hemorrhage

how does DDT cause issues in organisms

interfering with mitochondrial metabolism by disrupting ETC and energy production which affects the whole system

what should be used for avian dermal exposures

liquid hand dish washing detergent on feathers

what should be used to get rid of oily toxicants on skin

liquid hand dish washing detergent, not shampoo

how do microplastics negatively affect the environment as a whole

marine wildlife consume and damage organs or get entrapped...habitat is disrupted...humans consume the wildlife

define exposure evaluation

measurement or estimation of intensity, frequency, and duration of exposures to particular toxicants---exposure source, exposure route, exposure duration, exposure dose

what are the effects of ethylene glycol toxicity

metabolic acidosis, renal tubular injury, hypocalcemia

clinical signs of acetaminophen

methemoglobinemia, hepatic necrosis

what should never be used on feathers

mineral oil

what is important to know about emetics

most animals only vomit up 40-75% of stomach contents, its useful for ingestion within 30-90 minutes in most substances, generally more effective when there is food in stomach

what are the effects of blister beetle toxicity

mouth ulcers causing horses not to eat and bladder ulcers

what are the categories of toxins of livestock and horses

nutrition mostly, accessibles, natural toxins, and commercial poisons

what can be used to remove sticky, non-water soluble compounds

oily substances

sources, clinical signs, treatment of propyl disulfide

onions, garlic, chives, leeks, shallots---hemolysis, secondary renal failure, lethargy, tachy, pale mm---blood transfusion

sources, clinical signs, diagnosis, treatment of zinc toxicity

pennies, nuts and bolts, galvanized metals, monopoly pieces---oxidative damage to RBCs, hemolysis, secondary renal failure---serum zinc conc. in royal blue tube, radiography of zinc objects---remove zinc by vomiting if immediately, otherwise surgical or endoscopic

which methods should not be used to induce vomiting

pharyngeal stimulation, saltwater

what are the 3 Ps of toxicology

planet, pet, people

what are the most common types of microplastics

polyethylene, polystyrene, and polypropylene

what is the goal of decontamination

preventing absorption by changing kinetics and being performed on an asymptomatic animal

define risk

probability that a particular hazard will occur under specific exposure conditions

define risk assessment

process by which hazard, exposure, and risk are determined using epi and tox data

what is important to remember with dermal exposures in species like reptiles

return animal to optimal humidity and temp after cleaning

what is the risk equation

risk = toxicity x exposure

how do we evaluate the risk of morbidity and mortality of toxicant exposure

risk assessment

species, sources, pathogenesis, clinical signs, and treatment of nitrates

ruminants most susceptible---fertilizers, plants, water---formation of methemoglobin that can't carry O2---tachy, brown mm, brown blood---methylene blue IV but has 180 day withdrawal period...raise cutter bar in field

what plants contain soluble oxalate

shamrock, rhubarb, dock/curly dock, halogeton, greasewood, beets, and lambsquarters

what are the effects of cholecalciferol toxicity

soft tissue mineralization, renal failure, marked increase in serum Ca and P

what 3 things should be asked if there was a witnessed exposure

substance and strength, amount, and how long ago

what does the pattern of distribution depend on

the chemical properties of the toxicant

where do most toxicant exposures in animals come from

the environment

what happens as the higher the dose becomes with a dose response curve

the more severe the response

what does the dose response curve allow us to establish

the toxicant was the cause of effects, lowest dose at which effects occur, and rate at which injury progresses

what does distribution, metabolism, and elimination of a toxicant depend on

the toxicant's physiochemical properies