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Toxicology > Exam II > Flashcards

Exam II Flashcards

1
Q

Organic synthetic herbicides: source

A

ingestion of concentrates or sprays, grazing/access to freshly sprayed pastures/lawns

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2
Q

Organic synthetic herbicides: toxicity

A

cattle, dogs most susceptible. Dogs more sensitive, LD50 100 mg/kg

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3
Q

Organic synthetic herbicides: clinical signs

A

Non specific GI and NM. High doses= rapid onset

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4
Q

Organic synthetic herbicides: diagnosis

A

Chemical analysis $$$. Elevated ALP, LDH, CPK. Hx important.

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5
Q

Organic synthetic herbicides: treatment

A

No specific antidote. Wash skin, activated charcoal. Supportive and symptomatic

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6
Q

Paraquat and diquat: source

A

Ingestion of concentrates, malicious poisoning

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7
Q

Paraquat and diquat: toxicity

A

LD50 25-75 mg/kg in cats, dogs, pigs, sheep, humans.

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8
Q

Paraquat and diquat: clinical signs

A

Acute: vomiting, anorexia, depression. High doses= ataxia, dyspnea, seizures. Delayed= respiratory signs

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9
Q

Paraquat and diquat: diagnosis

A

Lesions in respiratory tract, lingual ulcers. Liver, kidney spleen enlarged. Chem analysis of plant, stomach contents, urine. Mild rad changes in lungs. History.

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10
Q

paraquat and diquat: treatment

A

No specific antidote. Detox: emetics, activated charcoal, saline catchertics. Supportive tratment- fluid therapy, dialysis. Antioxidants

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11
Q

paraquat and diquat: prognosis

A

Guarded to grave, especially if treatment begins >24 hours post-exposure

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12
Q

Pentachlorophenol (fungicide): source

A

treated wood, contaminated feed/water

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13
Q

Pentachlorophenol (fungicide): toxicity

A

LD 50 100-200 mg/kg in domestic animals. Chronic 40-70 mg/kg

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14
Q

Pentachlorophenol (fungicide): clinical signs

A

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

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15
Q

Pentachlorophenol (fungicide): diagnosis

A

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.

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16
Q

Pentachlorophenol (fungicide): treatment

A

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.

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17
Q

Pentachlorophenol (fungicide): prognosis

A

If survive initial 24 hrs, fair chance of recovery

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18
Q

Non-protein nitrogen: source

A

Urea as feed additive, contamination by urea fertilizer, ammonium salt and ammoniated feed products

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19
Q

Non-protein nitrogen:toxicity

A

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.

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20
Q

Non-protein nitrogen: clinical signs

A

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.

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21
Q

Non-protein nitrogen: diagnosis

A

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.

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22
Q

Non-protein nitrogen: treatment

A

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

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23
Q

Ionophore: source

A

anticoccidial, growth promoter, eating feeds with higher than recommended levels, malicious poisoning in horses

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24
Q

Ionophore: toxicity

A

all animals susceptible, equine most sensitive, cattle intermediate, poultry are least.

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25
Q

Ionophore: clinical signs

A

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

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26
Q

Ionophore: diagnosis

A

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

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27
Q

Ionophore: treatment

A

No specific antidote, remove medicated feed, activated charcoal, mineral oil, saline cathartics. IV fluid and e-lytes, K+, monitor cardiac function, reduce stress

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28
Q

Ionophore:prognosis

A

Survive can lead to myocardial scarring and necrosis, horses may not reach previous performance

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29
Q

Water deprivation/sodium ion: source

A

In feed, drinking water, excess sodium and water deprivation

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30
Q

Water deprivation/sodium ion: toxicity

A

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.

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31
Q

Water deprivation/sodium ion: clinical signs

A

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.

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32
Q

Water deprivation/sodium ion: diagnosis

A

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

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33
Q

Water deprivation/sodium ion: treatment

A

Small amounts of fresh water gradually over 2-3 days. IV fluid and furosemide in small animals, anticonvulsants in small animals

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34
Q

Water deprivation/sodium ion: prognosis

A

Poor. 50% mortality

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35
Q

Inorganic arsenic: source

A

ant and roach bait, wood preservative, pesticides, contaminated pastures

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36
Q

Inorganic arsenic: toxicity

A

Lethal oral dose 1-25 mg/kg in most species. Chronic toxicosis not documented

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37
Q

Inorganic arsenic: clinical signs

A

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.

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38
Q

Inorganic arsenic: diagnosis

A

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

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39
Q

Inorganic arsenic: treatment

A

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

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40
Q

Inorganic arsenic: prognosis

A

Grave if not treated early

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41
Q

Organic arsesnic: source

A

feed additives

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42
Q

Organic arsesnic: toxicity

A

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.

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43
Q

Organic arsesnic: clinical signs

A

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.

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44
Q

Organic arsesnic: diagnosis

A

Lesions: swine- erythema, muscle atrophy (chronic), nerve degeneration, demyelination, gliosis. Chem analysis of suspected feed, liver, kidney.

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45
Q

Organic arsesnic: treatment

A

No specific antidote, withdrawal of organic arsenicals, supportive therapy- fluids, vitamins, antibiotics (2ndry infection)

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46
Q

Copper: source

A

Acute: ingestion of high concentrations of copper. Chronic in sheep: excess copper in feed/soil or molybdenum deficiency

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47
Q

Copper: toxicity

A

Accumulation in liver when molybdenum is less than 1-2 ppm or sulfate unavilable, liver damage, stress

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48
Q

Copper: clinical signs

A

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

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49
Q

Copper: diagnosis

A

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.

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50
Q

Copper: treatment

A

acute treatment: supportive and symptomatic therapy. Chronic: ammonium tetrathiomolybate, D-penicillamine, sheep rations contain Cu/Mo 6:1

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51
Q

Molybdenum: source

A

soil rich in Mo or contaminated by industry or fertilizers, plants can accumulate. Or copper deficiency.

52
Q

Molybdenum: toxicity

A

Cattle most susceptible, seen in sheep. Horses and pigs resistant. Max diet level 5-10 ppm

53
Q

Molybdenum: clinical signs

A

severe diarrhea 8-10 days post exposure, rough hair coat and depigmentation around eyes, weight loss, anemia, osteoporosis, exotosis, lameness, pica, infertility

54
Q

Molybdenum: diagnosis

A

Clinical signs, elevated Mo in blood and liver, decreased Cu in blood and liver

55
Q

Molybdenum: treatment

A

copper glycinate SC, copper sulfate added to diet

56
Q

Selenium: source

A

selenium rich soil, feed supplements, injectable selenium-vit E, antioxidant supplements, shampoo for dermatitis, plants

57
Q

Selenium: toxicity

A

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

58
Q

Selenium: clinical signs (acute)

A

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.

59
Q

Selenium: clinical signs (chronic)

A

Chronic: rough hair coat, hoof deformities, lameness, partial blindness, anemia, lethargy, emaciation, infertility and birth defects

60
Q

Selenium: diagnosis

A

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.

61
Q

Selenium: treatment

A

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

62
Q

Selenium: prognosis

A

poor when acute, animals die quickly

63
Q

Lead: source

A

paint, old batteries, plumbing, galvanized wire, linoleum, ceramics, contamination from industry, lead shot, lead weights, fishing sinkers

64
Q

Lead: toxicity

A

young more sensitive than adults. Cattle, horses, pets, waterfowl, other birds. Dogs more susceptible due to eating habits. Goats, swine and chickens more resistant.

65
Q

Lead: clinical signs

A

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.

66
Q

Lead: diagnosis

A

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

67
Q

Lead: treatment

A

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

68
Q

Lead: prognosis

A

Guarded- better if caught early. House pets as sentinels

69
Q

Zinc: source

A

pennies, galvanized metals, batteries, jewelry, zinc oxide skin ointments, overdose dietary zinc

70
Q

Zinc: toxicity

A

cattle, sheep, horses, cats, dogs, ferrets, aviary birds. Acute LD50 100 mg/kg. Chronic >2000 ppm in the diet

71
Q

Zinc: clinical signs

A

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.

72
Q

Zinc: diagnosis

A

Lesions- gastritis, gastric ulcers, liver damage, reneal tubular casts, pancreatitis

73
Q

Zinc: treatment

A

Decon: remove foreign bodies, cathartics. Supportive care: blood transfusion, oxygen therapy, fluid therapy, treat renal failure, pancreatitis. Chelation, but not in dogs

74
Q

Zinc: prognosis

A

Favorable with early dx and treatment

75
Q

Iron: source

A

Oral supplements, fertilizers, snail baits, hand warming pads. Poorly soluble iron products not hazardous.

76
Q

Iron: toxicity

A

More toxic IV, less toxic orally. 20-60 mg/kg moderate, >60 mg/kg severe, >200 mg/kg lethal

77
Q

Iron: clinical signs

A

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.

78
Q

Iron: diagnosis

A

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.

79
Q

Iron: treatment

A

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

80
Q

Iron: prognosis

A

Prognosis depends on severity of clinical signs, good in animals treated early, guarded to poor in animals with severe clinical signs

81
Q

Ammonia gas: source

A

decomposing manure, burning nylon, anhydrous ammonia in fertilizer

82
Q

Ammonia gas: toxicity

A

5000 ppm can cause acute death, 50-75 ppm decreased ability to clear bacteria from lungs, 100 ppm decreased growth rate of young animals

83
Q

Ammonia gas: clinical signs

A

Red mucous membranes, lacrimation, coughing/sneezing, nasal discharge, decreased growth rate and egg production, dyspnea (pulmonary edema), cyanosis, CNS stim, clonic convulsions

84
Q

Ammonia gas: diagnosis

A

Lesions: see clinical signs. Labs: chem analysis not routinely w/ toxic gases. Odor of ammonia.

85
Q

Ammonia gas: treatment

A

Remove source of NH3, keep premises clean and well ventilated. Fresh air, soothing ointments, antibiotics to prevent 2ndry infections, diuretics for pulmonary edma

86
Q

Hydrogen Sulfide: source

A

contaminated forages and pastures, waterways, feed and mineral supplements, rich soil

87
Q

Hydrogen Sulfide: toxicity

A

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.

88
Q

Hydrogen Sulfide: clinical signs

A

Collapse, cyanosis, dyspnea, anoxic convulsions, death. Lower concentration- irritation of eyes, resp mucosa, lungs

89
Q

Hydrogen Sulfide: diagnosis

A

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.

90
Q

Hydrogen Sulfide: treatment

A

remove source of H2S. Sodium nitrite IV. Oxygen therapy, ventilation, supportive care.

91
Q

Carbon Monoxide: source

A

fires, propane powered equipment, car exhaust in confined spaces.

92
Q

Carbon Monoxide: toxicity

A

Uncommon. Dogs, cats, livestock, chickens. >1000 ppm can cause clinical signs, death with 1 hr exposure. Fetus more sensitive

93
Q

Carbon Monoxide: clinical signs

A

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.

94
Q

Carbon Monoxide: diagnosis

A

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)

95
Q

Carbon Monoxide: treatment

A

If time, oxygen or 5% CO2 administered with positive pressure. Blood transfusion, Fluids for acidosis.

96
Q

Carbon Monoxide: prognosis

A

Bad if acute

97
Q

Nitrogen Oxide: source

A

Incomplete reduction of nitrates during fermentation in silos.

98
Q

Nitrogen Oxide: toxicity

A

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.

99
Q

Nitrogen Oxide: clinical signs

A

Resp signs similar to ammonia. Lesions- pulmonary edema, hemorrhage, emphysema and inflammation of bronchioles, cyanosis, necrosis of skeletal muscles, methemoglobinemia.

100
Q

Nitrogen Oxide: diagnosis

A

History and clinical signs

101
Q

Nitrogen Oxide: treatment

A

supportive treatment- fresh air, O2, diuretics (pulmonary edema), antioxidants, methylene blue IV for methemoglobinemia, ointment for mucous membranes.

102
Q

Nitrogen Oxide: prognosis

A

Bad for animals acutely exposed to high concentration, better for animals chronically exposed to lower concentrations.

103
Q

Sulfur Oxide: source

A

industrial pollutants, fossil fuel combustion

104
Q

Sulfur Oxide: toxicity

A

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.

105
Q

Sulfur Oxide: clinical signs

A

irritation to mucous membranes, effect on respiration.

106
Q

Sulfur Oxide: diagnosis

A

similar to other toxic gases

107
Q

Sulfur Oxide: treatmet

A

similar to other toxic gases

108
Q

Petroleum Products: source

A

Fuels, solvents, inerts, lubricants. Gasoline, kerosene, lubricating oils, fuel oils, oil spills

109
Q

Petroleum Products: toxicity

A

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.

110
Q

Petroleum Products: clinical signs

A

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.

111
Q

Petroleum Products: diagnosis

A

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

112
Q

Petroleum Products: treatment

A

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

113
Q

Petroleum Products: prognosis

A

Depends on severity, if severe aspiration, guarded to poor bc of persistence of oil in lungs

114
Q

Fluorine: source

A

contaminated forages and pastures, waterways, feed and mineral supplements, rich soil

115
Q

Fluorine: toxicity

A

Chronic most common, dairy cattle most susceptible. Large animal toxicity at 40-60 ppm.

116
Q

Fluorine: clinical signs (acute)

A

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.

117
Q

Fluorine: clinical signs (chronic)

A

Chronic: alteration and delaying mineralization of teeth/bone. Lameness/stiff gait. Bony protrusions, osteoporosis.

118
Q

Fluorine: diagnosis

A

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

119
Q

Fluorine: treatment

A

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

120
Q

Ethylene glycol: source

A

antifreeze

121
Q

Ethylene glycol: toxicity

A

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.

122
Q

Ethylene glycol: clinical signs

A

Itself: direct GI irritation, increased serum osmolality, CNS depression. Toxic metabolites: metabolic acidosis, acute renal failure

123
Q

Ethylene glycol: diagnosis

A

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.

124
Q

Ethylene glycol: treatment

A

Detox: activated charcoal within 4 hrs. Specific antidotes, inhibitors of alcohol dehydrogenase- Fomepizole. Ethanol 20% IV. Supportive: NaCO3 for acidosis. Fluid therapy

125
Q

Ethylene glycol: prognosis

A

Early treatment has good prognosis. Once azotemic, prognosis is grave

Toxicology (2 decks)

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