Exam II Flashcards
Organic synthetic herbicides: source
ingestion of concentrates or sprays, grazing/access to freshly sprayed pastures/lawns
Organic synthetic herbicides: toxicity
cattle, dogs most susceptible. Dogs more sensitive, LD50 100 mg/kg
Organic synthetic herbicides: clinical signs
Non specific GI and NM. High doses= rapid onset
Organic synthetic herbicides: diagnosis
Chemical analysis $$$. Elevated ALP, LDH, CPK. Hx important.
Organic synthetic herbicides: treatment
No specific antidote. Wash skin, activated charcoal. Supportive and symptomatic
Paraquat and diquat: source
Ingestion of concentrates, malicious poisoning
Paraquat and diquat: toxicity
LD50 25-75 mg/kg in cats, dogs, pigs, sheep, humans.
Paraquat and diquat: clinical signs
Acute: vomiting, anorexia, depression. High doses= ataxia, dyspnea, seizures. Delayed= respiratory signs
Paraquat and diquat: diagnosis
Lesions in respiratory tract, lingual ulcers. Liver, kidney spleen enlarged. Chem analysis of plant, stomach contents, urine. Mild rad changes in lungs. History.
paraquat and diquat: treatment
No specific antidote. Detox: emetics, activated charcoal, saline catchertics. Supportive tratment- fluid therapy, dialysis. Antioxidants
paraquat and diquat: prognosis
Guarded to grave, especially if treatment begins >24 hours post-exposure
Pentachlorophenol (fungicide): source
treated wood, contaminated feed/water
Pentachlorophenol (fungicide): toxicity
LD 50 100-200 mg/kg in domestic animals. Chronic 40-70 mg/kg
Pentachlorophenol (fungicide): clinical signs
Irritation of eye, respiratory, GI mucosa, intact skin. Neurotoxic effects, high exposure- CNS stimulation/seizures. Acute- hyperthermia, tachycadia, dyspnea, cyanosis, death. Chronic- weight loss decreased milk, anemia, fetal malformation/abortion
Pentachlorophenol (fungicide): diagnosis
Lesions: rapid rigor mortis, irritation of skin/mucous membranes, pulmonary congestion, degenerate liver, kidney, brain, dark blood.
Chem analysis of blood, urine, kidney, skin.
Clinical signs: rapid overheating, respiratory distress.
Pentachlorophenol (fungicide): treatment
No specific antidote. Remove from site of exposure. Detox: emetics, gastric lavage w/ 5% NaCO3, activated charcoal, soap and water. Supportive: oxygen therapy, lower bosy temp, IV fluids, prevent 2ndry infection.
Pentachlorophenol (fungicide): prognosis
If survive initial 24 hrs, fair chance of recovery
Non-protein nitrogen: source
Urea as feed additive, contamination by urea fertilizer, ammonium salt and ammoniated feed products
Non-protein nitrogen:toxicity
Ruminants most susceptible, horses also. Urea is most toxic. Non-adapted toxic dose 0.45 g/kg. Lethal dose in adapted animals 1-1.5 g/kg.
Non-protein nitrogen: clinical signs
Increase in blood ammonia, lactate, glucose, BUN, systemic acidosis. Death due to cardiac or respiratory failure. Restlessness, aggression, muscle tremors, salivtion, teeth grinding, colic, bloat, rumen stasis, convulsion, death.
Non-protein nitrogen: diagnosis
Lesions due to vascular damage, congestion and degeneration in liver and kidneys. Ammonia odor.
Lab: anaysis of feed for urea content, ammonia in whole blood, rumen fluid, vitreous fluid.
Non-protein nitrogen: treatment
Relieve bloat. Vinegar to cattle, sheep, goats, followed by cold water. Repeat every 4-5 hr for 48 hrs. Normal saline for dehydration, NaCO3 IV for acidosis, rumenotomy
Ionophore: source
anticoccidial, growth promoter, eating feeds with higher than recommended levels, malicious poisoning in horses
Ionophore: toxicity
all animals susceptible, equine most sensitive, cattle intermediate, poultry are least.
Ionophore: clinical signs
Horses: rapid onset, anorexia, sweating, colic, depression, incoordination, hyperventilation, tachycadia, tachyarrythmias, prostration and death. Cattle: anorexia, diarrhea, depression, labored breathing, ataxia, prostration, death. Poultry: anorexia, diarrhea, ataxia, odd posture, decreased egg production. Dogs: ataxia, muscle weakeness, respiratory paralysis, dysuria, constipation, depression
Ionophore: diagnosis
Lesions: cardiac muscle in horses, skeletal muscle in sheep, swine, dogs, both in cattle and poultry. Chem analysis of feed, GI contents, liver. Elevated liver enzymes, decreased serum Ca and K, increased PCV
Ionophore: treatment
No specific antidote, remove medicated feed, activated charcoal, mineral oil, saline cathartics. IV fluid and e-lytes, K+, monitor cardiac function, reduce stress
Ionophore:prognosis
Survive can lead to myocardial scarring and necrosis, horses may not reach previous performance
Water deprivation/sodium ion: source
In feed, drinking water, excess sodium and water deprivation
Water deprivation/sodium ion: toxicity
Acute dose 2.2 g/kg in horses, cattle and swine. 6 g/kg in sheep. 4 g/kg in dogs. Can tolerate 10% w/ free access to water. Pigs, poultry, cattle most susceptible. Dogs are less susceptible.
Water deprivation/sodium ion: clinical signs
Constipation and thirst, vomiting, polyuria, metabolic acidosis. Intermittent convulsive seizures. Circuling, pivoting, head-pressing, blindness, deafness, inability to eat or drink. Poultry- depession, ascites and collapse.
Water deprivation/sodium ion: diagnosis
Lesions: gastric congestion, inflammation with pinpoint ulcers. Fluid in body cavities, edema in organs and brain. Eosinophilic meningoencephalitis in pigs. Serum and CSF [Na+], 2000 ppm [Na+] in brain
Water deprivation/sodium ion: treatment
Small amounts of fresh water gradually over 2-3 days. IV fluid and furosemide in small animals, anticonvulsants in small animals
Water deprivation/sodium ion: prognosis
Poor. 50% mortality
Inorganic arsenic: source
ant and roach bait, wood preservative, pesticides, contaminated pastures
Inorganic arsenic: toxicity
Lethal oral dose 1-25 mg/kg in most species. Chronic toxicosis not documented
Inorganic arsenic: clinical signs
Peracute: sudden death, colic. Acute: rapid onset, severe colic, staggering, salivation, vomiting, thirst, watery diarrhea (+/- hemorrhagic, hematuria), death in 1-3 days. Subacute: colic, anorexia, depression, diarrhea, dehydration, partial paralysis of hind limbs, death in several days.
Inorganic arsenic: diagnosis
Lesions: GI mucosal edema and hemorrhage with sloughing and perforation, liver and kidney damage, capilary degeneration, skin exposure- skin lesions and blistering. Chem analysis: Urine antemortem, liver and kidney postmortem. More than 7-10 ppm in liver/kidney is strong indication. Increased PCV and BUN
Inorganic arsenic: treatment
Fluids, e-lytes, transfusion, treat acidosis, prevent 2ndry infection and stress. Decon: gastric lavage (early), mineral oil and activated acharcoal, no emetics/cathartics, demulcents to coat GI mucosa. Chelation- BAL not 100% effective, may increase tox, follow dosing carefuly. Chemet less effective but safer than BAL
Inorganic arsenic: prognosis
Grave if not treated early
Organic arsesnic: source
feed additives
Organic arsesnic: toxicity
organic less toxic than inorganic, 500 ppm Arsanilic acid for 7-10 days toxic in swine, 250 ppm Roxarsone for 7-10 day toxic in swine.
Organic arsesnic: clinical signs
Arsanilic acid: acute onset, 3-5 days. Incoordination, ataxia, partial paralysis, blindness, erythema, sensitivity to sunlight. In poultry, anorexia, depression, coma, death. Roxarsone: swine- sudden onset, marked hyperexcitability, tremors, collapse, coma, death, no blindness. Poultry: incoordination and ataxia.
Organic arsesnic: diagnosis
Lesions: swine- erythema, muscle atrophy (chronic), nerve degeneration, demyelination, gliosis. Chem analysis of suspected feed, liver, kidney.
Organic arsesnic: treatment
No specific antidote, withdrawal of organic arsenicals, supportive therapy- fluids, vitamins, antibiotics (2ndry infection)
Copper: source
Acute: ingestion of high concentrations of copper. Chronic in sheep: excess copper in feed/soil or molybdenum deficiency
Copper: toxicity
Accumulation in liver when molybdenum is less than 1-2 ppm or sulfate unavilable, liver damage, stress
Copper: clinical signs
Acute: rapid onset of severe GI signs due to corrosive action. Chronic: sudden onset of weakness, anorexia, pale mucous membranes, icterus, hemoglobinuria, fever, dyspnea and shock
Copper: diagnosis
acute: clinical signs Chronic: lesions- icterus, hemolysis, methemoglobinemia, liver enlarged, yellow and friable, kidneys enlarged, hemorrhagic, bluish, friable. Chem analysis: elevated Cu in serum/whole blood, liver, kidney. Elevated liver enzymes.
Copper: treatment
acute treatment: supportive and symptomatic therapy. Chronic: ammonium tetrathiomolybate, D-penicillamine, sheep rations contain Cu/Mo 6:1
Molybdenum: source
soil rich in Mo or contaminated by industry or fertilizers, plants can accumulate. Or copper deficiency.
Molybdenum: toxicity
Cattle most susceptible, seen in sheep. Horses and pigs resistant. Max diet level 5-10 ppm
Molybdenum: clinical signs
severe diarrhea 8-10 days post exposure, rough hair coat and depigmentation around eyes, weight loss, anemia, osteoporosis, exotosis, lameness, pica, infertility
Molybdenum: diagnosis
Clinical signs, elevated Mo in blood and liver, decreased Cu in blood and liver
Molybdenum: treatment
copper glycinate SC, copper sulfate added to diet
Selenium: source
selenium rich soil, feed supplements, injectable selenium-vit E, antioxidant supplements, shampoo for dermatitis, plants
Selenium: toxicity
3.3 mg/kg in horse, 10 mg/kg in cattle, 17 mg/kg in swine. Subacute for swine, 20-50 ppm for 3 or more days. Chronic for horses, cattle and swine is 5-10 ppm for weeks/months
Selenium: clinical signs (acute)
Clinical signs acute: colic, bloat, dark watery diarrhea, labored respiration, fluid in lungs, bloody froth, cyanosis, fever, polyuria, mydriasis. Neurologic signs- mydriasis and incoordination. Cattle: poor appetite, wandering, circling then depression, incoordination, anorexia then colic, hypothermia, emaciation, clouded corneas/blindness, paresis, coma, death. Swine: porcine focal symmetrical poliomyelomalacia, incoordination, lameness, paralysis, alopecia, hoof abnormalities.
Selenium: clinical signs (chronic)
Chronic: rough hair coat, hoof deformities, lameness, partial blindness, anemia, lethargy, emaciation, infertility and birth defects
Selenium: diagnosis
Acute: hemorrhagic gastroenteritis, congestion, pulmonary edema, hydrothorax. Subacute in swine: focal symmetrical poliomyelomalacia Chronic: abnormal hooves, cardiac damage, hepatic necrosis. Lab: elevated selenium in blood, liver, kidney, hair, hoof.
Selenium: treatment
Acute: saline cathartics, symptomatic- oxygen, treat for pulmonary edema andd circulatory shock, acetylcysteine. Chronic and subacute: prevention is key- soil and forage levels tested, add copper, protein and sulfur containing protein
Selenium: prognosis
poor when acute, animals die quickly
Lead: source
paint, old batteries, plumbing, galvanized wire, linoleum, ceramics, contamination from industry, lead shot, lead weights, fishing sinkers
Lead: toxicity
young more sensitive than adults. Cattle, horses, pets, waterfowl, other birds. Dogs more susceptible due to eating habits. Goats, swine and chickens more resistant.
Lead: clinical signs
Hours to months to develop clinical signs. Mainly GIT, hematologic, CNS signs. Vomiting, colic, diarrhea, constipation, megaesophagus. Anemia, basophilic stippling of erythrocytes. CNS- anxiety, hyperexcitability, vocalization, head pressing, seizures, blindness, pharyngeal paralysis, CNS depression.
Lead: diagnosis
Lesions: gross non-specific, lead objects in GIT. Microscopic- may see cerebral cortical necrosis and poliomalacia in cattle, eosinophilic intranuclear inclusion bodies in renal tubular epithelium or hepatocytes. Lab: whole blood concentration >0.35 ppm, kidney and liver >10 ppm. Increased nRBCs. Increased urinary lead- kidney damage
Lead: treatment
Stabilize patient- fluids and e-lytes. Eliminate Pb, remove from gut before chelation. Cathartics- magnesium sulfate to accelerate defecation. Calcium disodium EDTA most common- give IV and monitor kidneys. DMSA- oral, doesn’t bind essential minerals, less nephrotoxic. Treat neuro signs
Lead: prognosis
Guarded- better if caught early. House pets as sentinels
Zinc: source
pennies, galvanized metals, batteries, jewelry, zinc oxide skin ointments, overdose dietary zinc
Zinc: toxicity
cattle, sheep, horses, cats, dogs, ferrets, aviary birds. Acute LD50 100 mg/kg. Chronic >2000 ppm in the diet
Zinc: clinical signs
RBC, liver, kidney, pancreas most affected. Intravascular hemolysis, hemoglobinemia/uria. Renal injury. Accumulation and turnover in pancreas, liver, kidney, spleen, male repro organs. Vomiting, anorexia, lethargy, abdominal pain, diarrhea, pica, BUN, hyperphosphatemia.
Zinc: diagnosis
Lesions- gastritis, gastric ulcers, liver damage, reneal tubular casts, pancreatitis
Zinc: treatment
Decon: remove foreign bodies, cathartics. Supportive care: blood transfusion, oxygen therapy, fluid therapy, treat renal failure, pancreatitis. Chelation, but not in dogs
Zinc: prognosis
Favorable with early dx and treatment
Iron: source
Oral supplements, fertilizers, snail baits, hand warming pads. Poorly soluble iron products not hazardous.
Iron: toxicity
More toxic IV, less toxic orally. 20-60 mg/kg moderate, >60 mg/kg severe, >200 mg/kg lethal
Iron: clinical signs
Per acute: anaphylactoid reaction, shock, death.
Acute: depression, shock, acidosis, death. Lesions: yellow-brown discoloration at injection site, GI ulceration, hemorrhagic enteritis, congestion of liver and kidney, liver necrosis, icterus, hemoglobinuria. Chem: elevated serum iron, increased PCV, acidosis, hemoglobinuria, shock.
Iron: diagnosis
Per acute: anaphylactoid reaction, shock, death. Acute: depression, shock, acidosis, death. Lesions: yellow-brown discoloration at injection site, GI ulceration, hemorrhagic enteritis, congestion of liver and kidney, liver necrosis, icterus, hemoglobinuria. Chem: elevated serum iron, increased PCV, acidosis, hemoglobinuria, shock.
Iron: treatment
Treatment: GI decon- effective w/in 4 hrs, emesis or gastric lavage, milk of magnesia. Supportive- IV fluids, GI protectants, anaphylactoid reaction treatments. Chelation therapy- only severe toxicosis and within 12 hrs, continuous IV infusion
Iron: prognosis
Prognosis depends on severity of clinical signs, good in animals treated early, guarded to poor in animals with severe clinical signs
Ammonia gas: source
decomposing manure, burning nylon, anhydrous ammonia in fertilizer
Ammonia gas: toxicity
5000 ppm can cause acute death, 50-75 ppm decreased ability to clear bacteria from lungs, 100 ppm decreased growth rate of young animals
Ammonia gas: clinical signs
Red mucous membranes, lacrimation, coughing/sneezing, nasal discharge, decreased growth rate and egg production, dyspnea (pulmonary edema), cyanosis, CNS stim, clonic convulsions
Ammonia gas: diagnosis
Lesions: see clinical signs. Labs: chem analysis not routinely w/ toxic gases. Odor of ammonia.
Ammonia gas: treatment
Remove source of NH3, keep premises clean and well ventilated. Fresh air, soothing ointments, antibiotics to prevent 2ndry infections, diuretics for pulmonary edma
Hydrogen Sulfide: source
contaminated forages and pastures, waterways, feed and mineral supplements, rich soil
Hydrogen Sulfide: toxicity
20 ppm- occular irritation, 50 ppm- severe symptoms, 200 ppm- olfactory accomodation, 400 ppm- sudden exposure could be quickly fatal, 1000 ppm- rapid unconsciousness and death in 1 hr. Mammals all similar, poultry resistant.
Hydrogen Sulfide: clinical signs
Collapse, cyanosis, dyspnea, anoxic convulsions, death. Lower concentration- irritation of eyes, resp mucosa, lungs
Hydrogen Sulfide: diagnosis
Lesion- compatible w/ clinical signs. Dark blood, may not clot. Tissues dark or greenish purple. Sewage odor of carcass. GI contacts black or dark gray.
Hydrogen Sulfide: treatment
remove source of H2S. Sodium nitrite IV. Oxygen therapy, ventilation, supportive care.
Carbon Monoxide: source
fires, propane powered equipment, car exhaust in confined spaces.
Carbon Monoxide: toxicity
Uncommon. Dogs, cats, livestock, chickens. >1000 ppm can cause clinical signs, death with 1 hr exposure. Fetus more sensitive
Carbon Monoxide: clinical signs
Binds to hemoglobin- greater affinity than O2. Sudden death. Hypoxia, drowsiness, incoordination, dyspnea, lethargy, coma with 30-60% COHb. Death at 60-70% COHb. Moderate concentrations increases stillborn fetuses.
Carbon Monoxide: diagnosis
Lesions- blood and mucous membranes normal color. Acute cases- no significant lesions. Chronic- brain edema, hemorrhage, necrosis, deafness. Labs: measure CO in air, % COHb in blood (correlation to clinical signs poor)
Carbon Monoxide: treatment
If time, oxygen or 5% CO2 administered with positive pressure. Blood transfusion, Fluids for acidosis.
Carbon Monoxide: prognosis
Bad if acute
Nitrogen Oxide: source
Incomplete reduction of nitrates during fermentation in silos.
Nitrogen Oxide: toxicity
A few ppm can lower resistance to respiratory infections. 50-150 ppm causes mild to moderate irritation of eyes and upper resp mucosa. 250-310 ppm for 10 minutes causes swine death in 20 min-1 hr. Brief or acute exposure to high concentrations is more toxic than chronic exposure to low concentration.
Nitrogen Oxide: clinical signs
Resp signs similar to ammonia. Lesions- pulmonary edema, hemorrhage, emphysema and inflammation of bronchioles, cyanosis, necrosis of skeletal muscles, methemoglobinemia.
Nitrogen Oxide: diagnosis
History and clinical signs
Nitrogen Oxide: treatment
supportive treatment- fresh air, O2, diuretics (pulmonary edema), antioxidants, methylene blue IV for methemoglobinemia, ointment for mucous membranes.
Nitrogen Oxide: prognosis
Bad for animals acutely exposed to high concentration, better for animals chronically exposed to lower concentrations.
Sulfur Oxide: source
industrial pollutants, fossil fuel combustion
Sulfur Oxide: toxicity
500 ppm fatal to cats in 30-60 minutes, 500 ppm for 1 hr dangerous to grazing animals, 5-40 ppm for 8 days causes poisoning in pigs.
Sulfur Oxide: clinical signs
irritation to mucous membranes, effect on respiration.
Sulfur Oxide: diagnosis
similar to other toxic gases
Sulfur Oxide: treatmet
similar to other toxic gases
Petroleum Products: source
Fuels, solvents, inerts, lubricants. Gasoline, kerosene, lubricating oils, fuel oils, oil spills
Petroleum Products: toxicity
Lethal dose based on aspiration pneumonia: sweet crude oil 48 ml/kg, sour crude oil 74 ml/kg. Short chain low toxicity, long-chain cause aspiration pneumonia, chlorinated aliphatic hydrocarbon toxic to CNS. Aromatic hydrocarbons cause bone marrow suppression.
Petroleum Products: clinical signs
Irritation of GI mucosa: vomiting, colic, diarrhea. Systemic effects: CNS depression, liver/kidney damage, cardiac arrhythmias/arrest. Aspiration pnuemonia: shivering, incoordination, anorexia, weightloss, fever, coughing, dyspnea, abnormal lung sounds.
Petroleum Products: diagnosis
Lesions: typical of apsiration pnuemonia, ulceration of tracheal mucosa, oil in bronchi/GIT, degeneration and necrosis of liver and kidneys. Labs: oil in GI contents, anemia, leukopenia, thrombocytopenia
Petroleum Products: treatment
Removal of oil with soap/water, activated charcoal, mineral oil, symptomatic and supportive therapy- respiratory support, antibiotics, fluid therapy, blood transfusion. Do not- emetics, gastric lavage, steroids
Petroleum Products: prognosis
Depends on severity, if severe aspiration, guarded to poor bc of persistence of oil in lungs
Fluorine: source
contaminated forages and pastures, waterways, feed and mineral supplements, rich soil
Fluorine: toxicity
Chronic most common, dairy cattle most susceptible. Large animal toxicity at 40-60 ppm.
Fluorine: clinical signs (acute)
Acute: caustic effect on GI mucosa, hypocalcemia, coag defect, inhibition of mitochondrial enzymes- hypoxia and cell death. Gastroenteritis, urination and defecation. CNS stimulation, clonic seizures. Respiratory and cardiac failure=death.
Fluorine: clinical signs (chronic)
Chronic: alteration and delaying mineralization of teeth/bone. Lameness/stiff gait. Bony protrusions, osteoporosis.
Fluorine: diagnosis
Lesions: acute: hemorrhagic gastroenteritis, hemorrhage, congestion and edema. Chronic: dental lesions in developing teeth, bilateral bone lesions. Chem analysis: bone, levels >1500 ppm. Sample feed/water
Fluorine: treatment
Can’t mobilize fluoride from bone, tolerance can be increased by a new balance intake of calcium, phosphorus, vit D. Aluminum salts, CaCO2 and defluoridated phosphate orally to form insoluble compounds in gut. Dilute with non-contaminated feed or water
Ethylene glycol: source
antifreeze
Ethylene glycol: toxicity
Cats and dogs commonly, swine and poultry also have been poisoned. 1.4 ml/kg in humans, cats. 4.2-6.6 ml/kg in dogs. 7-8 ml/kg in poultry.
Ethylene glycol: clinical signs
Itself: direct GI irritation, increased serum osmolality, CNS depression. Toxic metabolites: metabolic acidosis, acute renal failure
Ethylene glycol: diagnosis
Lesions: gross- hemorrhagic gastroenteritis, pulmonary edema, pale/swollen kidneys. Microscopic- calcium oxalate crystals in kidney/urine. Lab: increased serum osmolality, increased anion gap, low USG, acidemia, hypocalcemia, hyperglycemia, increased creatinine BUN, hyperphosphatemia, hyperkalemia, increase PCV and TP, calcium oxalate crystals in urine. Detection of EG in blood, urine and renal tissue.
Ethylene glycol: treatment
Detox: activated charcoal within 4 hrs. Specific antidotes, inhibitors of alcohol dehydrogenase- Fomepizole. Ethanol 20% IV. Supportive: NaCO3 for acidosis. Fluid therapy
Ethylene glycol: prognosis
Early treatment has good prognosis. Once azotemic, prognosis is grave
