EXAM II Flashcards
Different types of industrial petroleum. What are the 4 categories?
Short-chain aliphatics.
Long chain aliphatics.
Chlorinated aliphatic hydrocarbon.
Aromatic hydrocarbons.
Which of the industrial petroleum has the lowest toxicity?
Short-chain aliphatics.
Which of the industrial petroleum causes aspiration pneumonia?
Long chain aliphatics.
Which of the industrial petroleum causes CNS toxicity?
Chlorinated aliphatic hydrocarbons.
Which of the industrial petroleum causes bone marrow suppression?
Aromatic hydrocarbons.
T/F. Horses are most susceptible to crude petroleum substances. Rodents are most frequently poisoned with refined petroleum products (pesticides). Small animals are highly susceptible to oil spills.
False.
Cattle are most susceptible.
Small animals are frequently poisoned with refined petroleum products.
Terrestrial and aquatic wildlife and birds are susceptible oil spills.
Describe toxicokinetics of industrial petroleum.
Absorbed through ingestion, inhalation, skin.
T/F. Absorption for industrial petroleum is inversely proportional to molecular weight.
True.
T/F. Aliphatic hydrocarbons are more readily absorbed than polycyclic aromatic hydrocarbons.
False. Polycyclic aromatic hydrocarbons are more readily absorbed.
What is the MOA of industrial Petroleum?
Aspiration pneumonia or chemical pneumonitis.
GI (direct irritation > V+, colic, D+).
Systemic effects (MAIN: CNS depression; Liver/kidney damage, bone marrow suppression, cardiac arrhythmias/cardiac arrest).
What is aspiration pneumonia?
Bronchopneumonia that develops due to the entrance of foreign materials into the bronchial tree, usually involves oral or gastric contents due to V+ or regurgitation.
What are CS/Lesions of industrial Petroleum?
Signs of aspiration pneumonia, smell of oil/kerosene, oil in feces (GI/resp), low temp oil hydrocarbon causes CNS signs; ulceration in trachea.
Alphatic hydrocarbons: necrosis of liver/kidney.
What are lab Dx for industrial Petroleum?
Oil in GI (floats); anemia, leukopenia, thrombocytopenia due to aromatic hydrocarbons; radiographic changes of aspiration pneumonia.
What are Dx for industrial Petroleum? What is Ddx for it?
Presence of oil in the lungs/GI tract.
DDx: pneumonia (bacterial).
What are tx for industrial Petroleum?
Removal of oil by soap and warm water, activated charcoal/mineral oil, symptomatic/supportive therapy (fluid therapy, antibiotics, blood transfusion), rest.
T/F. Emetics, gastric lavage, glucocorticoids are used to treat industrial Petorleum.
False. Contraindicated due to aspiration pneumonia.
What is MOA of Non-industrial Fluoride?
Binds to tooth enamel by replacing hydroxyl molecule and makes the tooth more resistant to acid attack from plaque bacteria and sugars.
T/F. There is a danger of adding in Non-industrial fluoride.
False. No studies show.
What are uses of Industrial Fluoride?
Pesticide/Insecticides.
T/F. Sodium fluoride and sodium fluorosilicate are highly toxic. Sodium fluoroaluminate has a low toxicity. Hydrofluoric acid is an industrial toxicant.
True.
What are the sources of exposure of industrial fluoride?
Forages, pastures, water, feed, and mineral supplements are contaminated.
FLUORIDE IS A NORMAL CONSTITUENT OF FORAGES (Herbaceous parts of plants accumulate large amounts but not seeds).
What are the properties of industrial fluoride?
Reacts with variety of other organic acid/inorganic compounds.
Strong affinity for CALCIUM, aluminum and iron.
T/F. Acute fluoride toxicosis is the most common.
False. Chronic fluoride toxicosis is the most common (mostly seen in dairy cattle).
What are the factors influencing chronic fluoride toxicity?
Type and solubility of fluoride (soluble is more toxic: NaF > CaF2).
Age (young animals more sensitive; crosses placenta but fetus not affected).
What is the toxicokinetic of industrial fluoride?
Readily absorbed through GI and distributed throughout the body > bind up Ca2+ > stored in the bones and teeth > excreted in the urine.
What is the MOA of industrial fluoride?
Acute toxicosis: GI MUCOSA, inhibition of MITOCHONDRIAL ENZYMES (cellular resp.)
Chronic toxicosis: alteration and delaying mineralization of teeth (black discoloration, osteoporosis, damage to teeth).
CS/Lesions of industrial fluoride?
Acute toxicosis (rare): rapid onset, GI (bleeding, salivation, V+), seizure (edema), stiffness, weight loss, death from resp/cardiac failure. Chronic toxicosis (more common): slow onset, lameness/painful stiff gait, bony protrusions on legs, spontaneous fractures (osteoporosis), deformed legs/limbs.
What is lab Dx for industrial fluoride?
Chemical analysis: bone biopsy, sample feed and water, microscopic and radiographic changes of bone, elevated urine levels (recent exposure).
What is Clinical Dx for industrial fluoride? What is ddx for industrial fluoride toxicosis?
History, intermittent lameness, dental and skeletal lesions, and fluoride analysis.
Ddx: Vit. D deficiency, low PTH/low Ca.
What is the tx for industrial fluoride?
PREVENTION more important!
No known method.
Aluminum salts, calcium carbonate > binding to fluoride > excrete out.
Monitor feed and water (source of contamination).
T/F. Products with low boiling points are less toxic for industrial petroleum because they are poorly absorbed.
False.
Why does iron deficiency anemia develop very rapidly in nursing piglets rears in confinement?
Low body storage of iron in newborn pig, low iron content of sow’s colostrum and milk, elimination of contact with iron from soil, rapid growth.
What are the tx options for nursing piglets with iron deficiency anemia?
2-3 days after birth: iron dextran (IM or SC > don’t overdose); mix iron in feed or in drinking water; provide natural source of iron in soil.
What is the source of Nitrogen Oxide Gases?
Incomplete reduction (Dentrification) of nitrates during fermentation process in silos “Silo filler’s disease”:
What are the properties of Nitrogen Oxide gases? (NO2 and N2O4)
NO2: reddish brown; heavier than air but as dense as air (forms layers on top of silage and settles down the chute).
N2O4: colorless.
Mixture of the two is yellow/yellow-brown and has an irritating chlorine like odor.
Water (low solubility), gases form HNO3 and NO > sunlight converts NO + O2 to NO2 and ozone (may produce resp. damage).
What is the toxicity of Nitrogen Oxide Gases?
Long exposure to a few ppm can lower resistant to resp. infections.
T/F. Chronic exposure to low concentration of nitrogen oxide gases is more toxic than brief or acute exposure.
False. Brief or acute exposure of nitrogen oxide gases is more toxic.
What is Etylene glycol commonly used for?
ANTIFREEZE, coolant, industrial solvent, Rust remover, ingredient for various things (color film processing fluids, motor oil, snow globes, brake fluid), windshield de-icing agents.
T/F. Ethylene glycol is more toxic than propylene glycol.
True.
I am dihydric alcohol, soluble in water, sweet, colorless, odorless, lowers the freezing point of water. Who am I
Ethylene Glycol.
T/F. Some commercial antifreeze products have phosphate rust inhibitor.
True.
What is the main route of exposure of ethylene glycol?
Ingestion
T/F. EG intoxication is the first most common cause of fatal poisoning in animals.
False. SECOND MOST COMMON.
T/F. Mortality rate in dogs are high (50-70%) and more cases seen in fall, winter, and spring in NA
True
Which species are most sensitive to EG toxicosis? Which species is the most susceptible?
Sensitive: humans and cats.
Susceptible: dogs
What is MOA of EG toxicosis?
GIT (absorption delayed by food) > distributed all over (CNS). EG oxidized by Alcohol DH > glycoaldehyde > oxidized by Aldehyde DH > Glycolic acid > oxidized by Aldehyde DH > glyoxylic acid (TOXIC metabolite) > metabolized to oxalic acid > binds to Ca2+ to form insoluble calcium oxalate crystals and hypocalcemia > damage the kidney; metabolites for several days; small amount EG is excreted unchanged in urine.
Half life 11 hrs in dogs and shorter in cats.
What does Ethylene Glycol cause (MOA)? Toxic metabolite (Glycolic acid) cause?
EG: GI irritation, increased serum osmolality, CNS depression.
Toxic metabolites: metabolic acidosis and acute renal failure.
How does EG toxicosis affect CNS? What happens to CNS?
Inhibiton of resp, glucose metabolism, serotonin metabolism, alteration of amine concentration.
Ca oxalate deposition.
Marked cerebral edema in later stage in humans.
What is the major mechanism of EG toxicosis that causes death in animals?
Acute renal failure.
What are the early signs of EG toxicosis? (30min-12 hour)
Systemic acidosis. Nausea/V+, anorexia, CNS signs, renal signs, increased heart, dehydration, PUPD, coma, death.
Cats are markedly depressed and do not usually show polydipsia.
What is the MOA of acute renal failure during EG toxicosis?
Ca Oxalate monohydrate crystal form within renal tubules
What are the later signs of EG toxicosis (24-72h dogs, 12-24h cats)?
If survived acute form > oliguric renal failure.
When get really sick: V+, anorexia, depresion, severe lethargy, coma, seizures, oliguira and renal pain.
Stages are shorter duration in cats.
Early signs may not be noticed by O.
What are gross lesions/microscopic lesions of EG toxicosis?
Gross: Hemorrhagic GI, pulmonary edema, pale and swollen kidneys with gray or yellow streaks.
Microscopic: yellow birefringent rosette-shaped Ca oxalate crystals in the kidney or urine and in perivascular spaces in the brain..
Increased serum osmolality (happens early; osmolar gap), increased anion gap (metabolic acidosis) > 40-50meq/L.
Dilute urine, hypocalcemia (no CS due to unbound state of ionized Ca2+), hyperglycemia, acute renal failure changes (increased BUN, Crea, hyperphosphatemia, hyperkalemia), increased PCV, TP, birefringent Ca oxalate (monohydrate) crystals in urine sediment (absence does not rule out), glycolic acid in serum, sodium fluorescein (wood’s lamp).
Lab Dx for EG toxicosis.
Chemical analysis of EG.
EG in blood, urine, renal (1-6 hours > before it’s metabolized). Check the specific of the test kit you’re using.
What is the difference between Kacey EG test kit and Catachem TG test? Local human labs?
Kacey (a test strip): 30min-14 hours, plasma only, FALSE + CAN RESULT FROM PROPYLENE GLYCOL, MANNITOL, SORBITAL, GLYCERAL, AND ETHANOL.
Catachem: NO FALSE - WITH ETHANOL, varabile interference propylene glycol (quantitative test doesn’t cross-react with PG, qualitative test might have PG interference).
Human labs: differentiate between EG, PG, ethanol; turnaround time is a limiting factor.
DDX for EG toxicosis?
Toxin induced renal failure and other causes of renal failure (obstruction, infection).
What is the specific antidote for EG toxicosis?
Inhibitors of alcohol dehydrogenase (most effective within 3 hrs of EG ingestion): Fomepizole (4-MP), ethanol 20%.
T/F. Fomepazole cause a false positive result on the Kacey EG test?
False.
T/F. Activated charcoals are less active for alcohols and metals.
True.
What doesn’t Fomepizole (4-MP) cause? What are some side effects of this?
CNS depression, diuresis, hyperosmolality or interfere with EG tests.
Side effects: tachypnea, salivation and trembling.
T/F. Femepizole has a faster recovery than ethanol tx.
True.
What is the mechanism of ethanol 20% tx during EG toxicosis? What are the side effects of ethanol 20% tx?
Ethanol has a higher affinity for alcohol DH than EG.
Side effects: CNS depression and increases blood osmolality.
Not used after 24 hours PI.
What are additional therapy of EG toxicosis?
Thiamine + pyridoxine enhance metabolism of glyoxylic acid to non-toxic end products.
What is the supportive therapy of EG toxicosis?
Sodium bicarbonate for acidosis, fluid therapy (5% dextrose), Calcium borogluconate (ionized hypocalcemia for dehydration, increase tissue perfusion, promote diuresis; not used in ogliuric/anuric patients), mannitol, hemodialysis.
Prognosis for EG toxicosis.
Early tx (Dogs: 5-8 hour; Cats: 3 hours) has good prog. Grave when azotemic.
What is the toxicokinetics of Nitrogen Gases?
Animal quarters that develop the irritant odor or yellow haze in the air must not be entered.
NO2/N2O4 form nitric acid when contact with MM > cross resp. mucosa > cellular damage of the lungs.
MOA of Nitrogen oxide gases.
Lung damage may be due to reaction with polyunsaturated FA’s of lung cellular lipids > death is from hypoxia.
What are CS/lesions of nitrogen oxide gas toxicosis?
Resp. signs (similar to ammonia poisoning), cyanosis, Methb, necrosis of skeletal m.
What is methemoglobin?
A form of hemoglobin where ferric iron has a lower binding affinity for O2 than ferrous iron.
What is tx for Nitrogen oxide Gas toxicosis?
Supportive (fresh air, O2, diuretics if pulmonary edema, antioxidants).
Methylene blue IV for methemoglobinemia.
Ointments for MM.
What is prog. of Nitrogen Oxide Gases?
Acutely exposed to high concentration > low.
Chronic exposure to lower concentration > high.
What are the sources of sulfur oxide gases?
SO2 and SO3 industrial pollutants (fossil fuel combustion @ power plants and industrial facilities).
Properties of Sulfur Oxide gases.
Sharply irritant to MM because the form sulfurous and sulfuric acids on contact with water. Odor causes coughing, choking and suffocation
What is MOA of Sulfur Oxide?
Direct irritation of the MM and reflex bronchoconstriction, lung damage, death is due to hypoxia.
What are CS/lesions of Sulfur oxide?
Similar to other toxic gases (irritation to MM, effects of resp.).
What is dx/tx of sulfur oxide gases?
Similar to other toxic gases (ventilation with O2).
T/F. Older dogs are more likely to present for smoke inhalation but recover. Younger dogs are more likely to perish.
False. Younger dogs are more exposed but recover. Older dogs are more likely to perish.
How come there is no LD50 for smoke inhalation?
Significant variability: mixture of substances burning/combusting, temp of the fire, length of exposure, availability of O2, size of the animal, no typical smoke.
How are combustion products classified?
Simple asphyxiants and Chemical asphyxiants
What is the difference between simple and chemical asphyxiants?
Simple: inert (CO2) gases or vapors (displace O2 in air, low concentration > little in physiologic effect).
Chemical: prevent uptake of O2 (CO) > produce toxic local and systemic effects, IRRITANTS, reactive on contact with MM to cause local effects.
What are combustion products of simple asphyxiants?
CO2, methane, O2-DEPRIVED ENVIRON.
What are combustion products of chemical asphyxiants?
CO (most serious systemic; CHANGES IN O2 - CARRYING CAPACITY OF Hb), Hydrogen cyanide, hydrogen sulfides, nitrogen oxides.
What are CS of smoke inhalation (respiratory, CV, CNS)?
Respiratory: cough, dyspnea, tachypnea, rales, wheezing, crackles.
CV: tachycardia, hypoxemia, hypotension, dysrrhythmias.
CNS: seizures, ataxia, confusion, edema.
Mucosal ulceration, inflammation upper resp/eyes, soot on nose/mouth/throat, cornea abrasions, surface burns.
CO poisoning.
What is the initial workup for smoke inhalation?
History, initial presentation, vials, O2 status (cyanosis or distress), ophthalmic evaluation, acid/base status, carxocyhemoglobin or methemoglobin, thoracic x-rays.
What is the tx for smoke inhalation?
Removal from smoke environ, O2 support, beta agonists for bronchoconstriction, no steroids and cough suppressants, remove soot from skin, maintain airway potency/ventilation.
When do you want to intubate for smoke inhalation?
Before acute airway compromise and compensate (early).
SpO2
T/F. Sulfur dioxide adheres highly to soot.
True.
Name all organic synthetic herbicides.
Amides, Benzoic acid, Carbamates, Dinitroanilines, Diphenyl esters, Dipyridyle/Bipyridyls, nitriles, Organoarsenicals, Phenoxy acids, Phthalamic acids, Thiocarbamates, Triazines
What are the sources of phenoxy derivatives of FA’s (2,4-D) Toxicosis?
Accidental ingestion of concentrates or sprays, grazing freshly sprayed pastures, access to fresh sprayed lawns.
T/F. All animals (including young, old, sick animals) do not get poisoned by sprayed forages with 2,4-D.
False. Young, old, sick animals may get poisoned.
Which animals are most susceptible to 2,4-D toxicosis? Which animals are the most sensitive to 2,4-D toxicosis?
Susceptible: Dogs and cattle.
Sensitive: Dogs
Properties. Alter the metabolism of plants (increases toxicity by increasing accumulation of nitrate or cyanide from soil). Improve palatability. Not stable in the environ. Not degraded by rumen microflora and do not alter rumen microflora. Irritant to GI mucosa (see ulcers in oral cavity). Who am I?
2,4-D
What is the toxicokinetics of 2,4-D toxicosis?
Ingestion or inhalation > distributed all over the body (including brain) > metabolized by hydrolysis > excreted unchanged in urine.
Half lives are short but longer in dogs.
T/F. Acidification of urine enhances renal excretion of 2,4-D.
False. Alkalinization of urine enhances renal excretion.
What is the MOA of 2,4-D?
UNKNOWN; uncouple oxidative phosphorylation > CNS signs.
Irritation of the GI mucosa (ulcers), affect skeletal muscle membranes (NM) in dogs.
Lesions of 2,4-D toxicosis?
NONSPECIFIC.
GI, liver, kidney damage.
Rumen stasis with ingested food is a characteristic finding.
What is found in lab. diagnosis for 2,4-D toxicosis?
Chem. analysis: expensive and time consuming; specimens in forage, water, kidney, urine, liver, stomach, feces.
Elevated AP, LDH, CPK (muscle damage) levels
What is dx for 2,4-D toxicosis?
Difficult from CS and lesions.
History of ingestion.
Chemical analysis helpful; rule out other dieases.
What is the tx for 2,4-D toxicosis?
NO SPECIFIC ANTIDOTE.
Detoxification (wash skin with soap and water; activated charcoal).
Supportive and symptomatic tx (fluids, antidirrheals and rumenatorics).
T/F. Diquat is RUP and Paraquat is GUP.
False. Paraquat is RUP and Diquat is GUP.
What are the sources of paraquat toxicosis?
Ingestion of concentrates, malicious.
Properties. Unstable, rapidly INactivated by light and soil. The salts are soluble in water. Solutions are stable in neural or acid conditions but destroyed by alkali. Binds strongly to soil. Caustic to MM. Who am I?
Paraquat toxicosis.
Which species is the most susceptible to paraquat toxicosis?
Dogs
What enhance toxicity of paraquat?
Selenium-vitamin E deficiency, depletion of tissue glutathione, and O2 therapy.
What is the toxicokinetics of paraquat?
(Diquat is poorly absorbed in GI tract).
Paraquat absorbed through ingestion and inhalation > distributed all over (not much in CNS but high in lungs) > excreted unchanged in urine.
T/F. 2,4-D toxicosis is a lung poison whereas paraquat toxicosis is a CNS posion.
False. 2,4-D toxicosis affects GI, kidney, liver, CNS whereas paraquat toxicosis is a lung poison.
MOA. REDUCED BY NADPH to produce singlet O2 > reacts with lipids of the cell membranes to for hydroperoxides > production of free radicals and membrane damage and cellular degeneration, necrosis of lung tissue.
Paraquat toxicosis.
What are CS/lesions of paraquat toxicosis?
Acute toxicosis: early signs (GI signs) and delayed signs (resp signs), lingual ulcers (foul odor).
Subacute or chronic toxicosis: usually die or resp signs due to progressive pulmonary fibrosis.
Microscopic lesions follow gross lesions.
Where are specimens found for acute and chronic toxicosis of paraquat? radiographic changes?
Acute: stomach and urine.
Chronic: lungs.
Mild lung changes in the radiograph.
What is the tx for paraquat toxicosis?
NO SPECIFIC ANTIDOTE. Detoxification: activated charcoal is preferred, Bentonite or Fuller's earth orally; emetics, saline cathartics. Supportive tx: Fluid therapy to support kidney function, hemodialysis/peritoneal dialysis. Biochemical antagonists (antioxidants): Acetylcysteine (most common), ascorbic acid, niacinr/riboflavin, orgotein.
T/F. Fluid therapy and O2 are good supportive tx for all herbicide toxicosis.
False. Fluids are only used for 2,4-D toxicosis. Both are contraindicated in paraquat toxicosis because O2 increases lung damage and fluids enhance kidney damage if oliguria/anuria.
T/F. None of the tx is likely to be much help unless begun within 24 hours of exposure in paraquat toxicosis.
True.
What are fungicides?
Prevent or tx fungal infections in plants. Low toxicity if correctly used. Accidental exposure to large amounts cause toxicosis in livestock and pets.
T/F. Pentachlorophenol (PCP) is often used in wood preserving solutions and is an ongoing problem.
False. Restricted use/banned.
Not a problem in open areas (vapor gets diluted).
Properties. Chlorinated hydrocarbon. Soluble in oils and organic solvents. Volatile can give off toxic vapors in toxic concentration in high temps (confined areas). Not persistent in environ. Irritant to MM, respiratory, skin.
PCP toxicosis.
What are the factors that increase toxicity of PCP?
High temp (shake and bake), oily or organic solvent vehicles, previous exposure, poor condition, newborn, and hyperthyrodism.
What are the factors that decrease toxicity of PCP?
Cold temp, antithyroid drugs, presence of body fat.
Toxicokinetics of PCP toxicosis?
Ingestion, inhalation, SKIN > distributed throughout body with ACCUMULATION in fat > metabolized by conjugation to glucuronic acid (deficient in cats) > excreted in urine.
What is MOA of PCP toxicosis?
Uncouples oxidative phosphorylation > increases O2 demand more than supply > overheating, metabolic acidosis, dehydration.
What are CS of PCP toxicosis?
Acute: no signs may seen (too fast); fever, tachycardia, dyspnea, cyanosis, seizure, death.
Newborn: hyperthermia, skin irritation, death.
Chronic: weight loss, decreased milk production, anemia, fetal malformation and abortions.
What is the pathopneumonic lesion of PCP toxicosis?
RAPID RIGOR MORTIS.
Dark blood and other signs the same as herbicides; hyperkeratosis of the skin and villous like hyperplasia of bladder in chronic cases.
Lab Dx of PCP toxicosis.
Chem analysis: blood/urine (antemortem), kidney/skin (PM).
DDx of PCP toxicosis.
Heat stroke (history), toxicants causing resp. insufficient.
What is the tx for PCP toxicosis?
NO SPECIFIC ANTIDOTE.
Removal of animals from site of exposure.
Detoxification: emetics, gastric lavage with NaHCO3, activated charcoal, soap and water bath.
Supportive and symtomatic therapy: O2, lower body temp, fluids and electrolytes for dehydration and acidosis, antibiotics and vit for secondary infection.
