EXAM II Flashcards
(313 cards)
1
Q
Different types of industrial petroleum. What are the 4 categories?
A
Short-chain aliphatics.
Long chain aliphatics.
Chlorinated aliphatic hydrocarbon.
Aromatic hydrocarbons.
2
Q
Which of the industrial petroleum has the lowest toxicity?
A
Short-chain aliphatics.
3
Q
Which of the industrial petroleum causes aspiration pneumonia?
A
Long chain aliphatics.
4
Q
Which of the industrial petroleum causes CNS toxicity?
A
Chlorinated aliphatic hydrocarbons.
5
Q
Which of the industrial petroleum causes bone marrow suppression?
A
Aromatic hydrocarbons.
6
Q
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.
A
False.
Cattle are most susceptible.
Small animals are frequently poisoned with refined petroleum products.
Terrestrial and aquatic wildlife and birds are susceptible oil spills.
7
Q
Describe toxicokinetics of industrial petroleum.
A
Absorbed through ingestion, inhalation, skin.
8
Q
T/F. Absorption for industrial petroleum is inversely proportional to molecular weight.
A
True.
9
Q
T/F. Aliphatic hydrocarbons are more readily absorbed than polycyclic aromatic hydrocarbons.
A
False. Polycyclic aromatic hydrocarbons are more readily absorbed.
10
Q
What is the MOA of industrial Petroleum?
A
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).
11
Q
What is aspiration pneumonia?
A
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.
12
Q
What are CS/Lesions of industrial Petroleum?
A
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.
13
Q
What are lab Dx for industrial Petroleum?
A
Oil in GI (floats); anemia, leukopenia, thrombocytopenia due to aromatic hydrocarbons; radiographic changes of aspiration pneumonia.
14
Q
What are Dx for industrial Petroleum? What is Ddx for it?
A
Presence of oil in the lungs/GI tract.
DDx: pneumonia (bacterial).
15
Q
What are tx for industrial Petroleum?
A
Removal of oil by soap and warm water, activated charcoal/mineral oil, symptomatic/supportive therapy (fluid therapy, antibiotics, blood transfusion), rest.
16
Q
T/F. Emetics, gastric lavage, glucocorticoids are used to treat industrial Petorleum.
A
False. Contraindicated due to aspiration pneumonia.
17
Q
What is MOA of Non-industrial Fluoride?
A
Binds to tooth enamel by replacing hydroxyl molecule and makes the tooth more resistant to acid attack from plaque bacteria and sugars.
18
Q
T/F. There is a danger of adding in Non-industrial fluoride.
A
False. No studies show.
19
Q
What are uses of Industrial Fluoride?
A
Pesticide/Insecticides.
20
Q
T/F. Sodium fluoride and sodium fluorosilicate are highly toxic. Sodium fluoroaluminate has a low toxicity. Hydrofluoric acid is an industrial toxicant.
A
True.
21
Q
What are the sources of exposure of industrial fluoride?
A
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).
22
Q
What are the properties of industrial fluoride?
A
Reacts with variety of other organic acid/inorganic compounds.
Strong affinity for CALCIUM, aluminum and iron.
23
Q
T/F. Acute fluoride toxicosis is the most common.
A
False. Chronic fluoride toxicosis is the most common (mostly seen in dairy cattle).
24
Q
What are the factors influencing chronic fluoride toxicity?
A
Type and solubility of fluoride (soluble is more toxic: NaF > CaF2).
Age (young animals more sensitive; crosses placenta but fetus not affected).
25
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.
26
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).
27
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.
```
28
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).
29
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.
30
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).
31
T/F. Products with low boiling points are less toxic for industrial petroleum because they are poorly absorbed.
False.
32
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.
33
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.
34
What is the source of Nitrogen Oxide Gases?
Incomplete reduction (Dentrification) of nitrates during fermentation process in silos "Silo filler's disease":
35
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).
36
What is the toxicity of Nitrogen Oxide Gases?
Long exposure to a few ppm can lower resistant to resp. infections.
37
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.
38
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.
39
T/F. Ethylene glycol is more toxic than propylene glycol.
True.
40
I am dihydric alcohol, soluble in water, sweet, colorless, odorless, lowers the freezing point of water. Who am I
Ethylene Glycol.
41
T/F. Some commercial antifreeze products have phosphate rust inhibitor.
True.
42
What is the main route of exposure of ethylene glycol?
Ingestion
43
T/F. EG intoxication is the first most common cause of fatal poisoning in animals.
False. SECOND MOST COMMON.
44
T/F. Mortality rate in dogs are high (50-70%) and more cases seen in fall, winter, and spring in NA
True
45
Which species are most sensitive to EG toxicosis? Which species is the most susceptible?
Sensitive: humans and cats.
Susceptible: dogs
46
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.
47
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.
48
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.
49
What is the major mechanism of EG toxicosis that causes death in animals?
Acute renal failure.
50
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.
51
What is the MOA of acute renal failure during EG toxicosis?
Ca Oxalate monohydrate crystal form within renal tubules
52
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.
53
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..
54
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.
55
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.
56
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.
57
DDX for EG toxicosis?
Toxin induced renal failure and other causes of renal failure (obstruction, infection).
58
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%.
59
T/F. Fomepazole cause a false positive result on the Kacey EG test?
False.
60
T/F. Activated charcoals are less active for alcohols and metals.
True.
61
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.
62
T/F. Femepizole has a faster recovery than ethanol tx.
True.
63
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.
64
What are additional therapy of EG toxicosis?
Thiamine + pyridoxine enhance metabolism of glyoxylic acid to non-toxic end products.
65
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.
66
Prognosis for EG toxicosis.
```
Early tx (Dogs: 5-8 hour; Cats: 3 hours) has good prog.
Grave when azotemic.
```
67
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.
68
MOA of Nitrogen oxide gases.
Lung damage may be due to reaction with polyunsaturated FA's of lung cellular lipids > death is from hypoxia.
69
What are CS/lesions of nitrogen oxide gas toxicosis?
Resp. signs (similar to ammonia poisoning), cyanosis, Methb, necrosis of skeletal m.
70
What is methemoglobin?
A form of hemoglobin where ferric iron has a lower binding affinity for O2 than ferrous iron.
71
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.
72
What is prog. of Nitrogen Oxide Gases?
Acutely exposed to high concentration > low.
| Chronic exposure to lower concentration > high.
73
What are the sources of sulfur oxide gases?
SO2 and SO3 industrial pollutants (fossil fuel combustion @ power plants and industrial facilities).
74
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
75
What is MOA of Sulfur Oxide?
Direct irritation of the MM and reflex bronchoconstriction, lung damage, death is due to hypoxia.
76
What are CS/lesions of Sulfur oxide?
Similar to other toxic gases (irritation to MM, effects of resp.).
77
What is dx/tx of sulfur oxide gases?
Similar to other toxic gases (ventilation with O2).
78
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.
79
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.
80
How are combustion products classified?
Simple asphyxiants and Chemical asphyxiants
81
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.
82
What are combustion products of simple asphyxiants?
CO2, methane, O2-DEPRIVED ENVIRON.
83
What are combustion products of chemical asphyxiants?
CO (most serious systemic; CHANGES IN O2 - CARRYING CAPACITY OF Hb), Hydrogen cyanide, hydrogen sulfides, nitrogen oxides.
84
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.
85
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.
86
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.
87
When do you want to intubate for smoke inhalation?
Before acute airway compromise and compensate (early).
| SpO2
88
T/F. Sulfur dioxide adheres highly to soot.
True.
89
Name all organic synthetic herbicides.
Amides, Benzoic acid, Carbamates, Dinitroanilines, Diphenyl esters, Dipyridyle/Bipyridyls, nitriles, Organoarsenicals, Phenoxy acids, Phthalamic acids, Thiocarbamates, Triazines
90
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.
91
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.
92
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
93
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
94
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.
95
T/F. Acidification of urine enhances renal excretion of 2,4-D.
False. Alkalinization of urine enhances renal excretion.
96
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.
97
Lesions of 2,4-D toxicosis?
NONSPECIFIC.
GI, liver, kidney damage.
Rumen stasis with ingested food is a characteristic finding.
98
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
99
What is dx for 2,4-D toxicosis?
Difficult from CS and lesions.
History of ingestion.
Chemical analysis helpful; rule out other dieases.
100
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).
101
T/F. Diquat is RUP and Paraquat is GUP.
False. Paraquat is RUP and Diquat is GUP.
102
What are the sources of paraquat toxicosis?
Ingestion of concentrates, malicious.
103
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.
104
Which species is the most susceptible to paraquat toxicosis?
Dogs
105
What enhance toxicity of paraquat?
Selenium-vitamin E deficiency, depletion of tissue glutathione, and O2 therapy.
106
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.
107
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.
108
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.
109
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.
110
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.
111
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.
```
112
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.
113
T/F. None of the tx is likely to be much help unless begun within 24 hours of exposure in paraquat toxicosis.
True.
114
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.
115
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).
116
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.
117
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.
118
What are the factors that decrease toxicity of PCP?
Cold temp, antithyroid drugs, presence of body fat.
119
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.
120
What is MOA of PCP toxicosis?
Uncouples oxidative phosphorylation > increases O2 demand more than supply > overheating, metabolic acidosis, dehydration.
121
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.
122
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.
123
Lab Dx of PCP toxicosis.
Chem analysis: blood/urine (antemortem), kidney/skin (PM).
124
DDx of PCP toxicosis.
Heat stroke (history), toxicants causing resp. insufficient.
125
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.
126
What is the prog for PCP toxicosis?
Survives 24 hours > complete recovery fair.
127
What are Feed and Water related toxicants?
Non protein nitrogen (NPN), Ionophore, Water deprivation-sodium salt.
128
What are the sources of Ammonia (NH3)?
Decomposing manure in confined animal houses, burning nylon/plastics, anhydrous ammonia used in fertilizer.
129
Properties. Has a characteristic sharp oder. Heavier than air. Soluble in water and reacts with hydroxyl ions in moist MM > irritant and caustic. Who am I?
Ammonia (NH3)
130
Which animals are the most susceptible to ammonia toxicity?
Swine and poultry
131
What is Toxicokinetics/MOA of ammonia?
Inhalation > Ammonia to ammonium hydroxide. Direct irritation of MM, increased susceptibility to resp. infections due to continuous irritation, decreased growth of young animals, alkalosis and compensatory acidosis, inhibit TCA cycle, Death.
132
T/F. Death of ammonia toxicosis due to hypocalcemia.
False. Partly due to asphyxia and partly due to electrolyte/cellular metabolic effects.
133
What are CS of ammonia toxicosis?
RED MM, lacrimation, coughing, sneezing, nasal discharges, keeping eyes shut, decreased growth rate and egg production, dyspnea.
Terminal signs: cyanosis, CNS stimulation and convulsions.
134
T/F. Lesions of ammonia toxicosis is compatible with CS.
True.
135
T/F. Chemical analysis is very important for toxic gases.
False. Chemical analysis are not routinely made with toxic gases.
136
What are dx of ammonia toxicosis?
ODOR of ammonia.
137
What is ddx for ammonia toxicosis?
Dz that cause respiratory insufficiency.
138
What are txs for ammonia toxicosis?
Removal of NH3, fresh air for dyspnea, soothing ointments to the eyes, antibiotics for secondary infection, diuretic for pulmonary edema.
139
What are the sources of Hydrogen Sulfide (H2S)?
Liberated from decomposition of urine and feces in waste pits, by products of industry, liquid manure holding pits (swine), natural gas and crude oil production, burning rubber.
140
T/F. H2S is the most dangerous sewage gas.
True.
141
T/F. Acute hydrogen sulfide poisoning is directly responsible for more deaths in open animal facilities than any other gas.
False. More deaths in CLOSED animals facilities.
142
T/F. Although H2S is very toxic to animals, humans are usually not affected.
False. Human deaths are reported accidents associated with animal and industrial facilities.
143
What is toxicokinetics of H2S?
Inhalation and Ingestion > H2S converted to alkali sulfides in blood > excreted in urine or feces; some sulfides may be trapped by natural disulfides (glutathione) in the blood.
144
What is MOA of H2S?
Direct irritation of MM, inhibition of cellular respiration by inhibiting cytochrome oxidate, stimulation of the chemoreceptors of the carotid body interfering with resp. drive.
145
What are CS of H2S? (large vs. small)
Large concentrations: sudden collapse, cyanosis, dyspnea, anoxic convulsions and rapid death.
Small concentrations: irritation to ocular, resp. mucosa and lungs as in ammonia.
146
What are the lesions of H2S?
Compatible with CS.
Blood is dark and don't clot, tissues are dark and may not clot, carcass may have odor of H2S (Sewage), GI contents may be black or dark gray and have sewage odor.
147
Properties. Colorless and has an odor of rotten eggs. Heavier than air. Flammable. Irritant. Reacts with silver, iron, lead and other metals to form black or dark colored compounds.
H2S toxicosis.
148
How do you dx H2S?
Characteristics of H2S odor and the color of blood and tissues.
149
What is ddx for H2S?
As for ammonia.
150
What are tx for H2S?
Removal of the source, sodium nitrite IV (form methemoglobin that binds the radical and reactivate cytochrome oxidase), O2 therapy, ventilation, supportive tx.
Management: monitor animals when agitation of pit started, shut off pump, do not rescue animals immediately.
151
T/F. H2S is one of the ingredients for flatus.
True.
152
What is the source for Carbon Monoxide (CO)?
Accidental exposure from fires, propane powered equipment, portable cookers, de-icers, automobile exhaust in confined spaces.
153
What are two properties of CO?
Odorless and colorless.
154
T/F. CO toxicosis is one of the most common gas toxicosis.
False. Toxicosis is uncommon.
155
T/F. CO toxicosis. Older animals are more sensitive than fetus.
False. Fetus is more sensitive.
156
What does Canary in the coal mine mean for CO toxicosis?
Smaller animals have faster breathing rate and smaller Vd so may show toxicity before humans.
157
Which animals are susceptible to CO toxicosis?
Dog, cat, livestock, and chickens.
158
What is MOA of CO?
CO combines with Hb to form COHb (cannot carry O2) and this interferes with release of O2 carried by normal Hb > death from hypoxia (competes with O2 for binding sites on myoglobin > worsened hypoxia).
Interfere with cellular resp at the mitochondrial level > free radical formation.
159
What are CS of CO toxicosis?
Sudden death.
Low exposure: hypoxia, drowsiness, incoordination, dyspnea, lethargy, coma (nonspecific signs).
High exposure: death.
Moderate exposure: stillborn fetuses in swine and lambing barns.
160
What are the lesions of CO?
Blood is bright red and MM is healthy pink.
Acute cases: no significant lesions.
Chronic cases: brain edema, hemorrhage, necrosis > deafness in dogs and cats.
161
What are lab dx of CO toxicosis?
Measuring CO in air, percentage of carboxyhemoglobin in the blood (correlation with CS is poor, stable in whole blood for a few days if refrigerated, concentration in fetal thoracic fluid).
162
What is tx for CO toxicosis?
IF THERE IS TIME FOR TX.
| O2 or 5% CO2 in O2 with IPPV, blood transfusion, recovery may/not occur, fluids for acidosis (bicarb is controversial).
163
What is the main source of Non-Protein Nitrogen (NPN) Toxicosis?
Increased urea = increased ammonia OR decreased soluble CHO.
| UREA IS THE MOST TOXIC.
164
T/F. Decreased temp or acidified environ can increase NPN toxcosis.
False. Increased temp and alkalinized environ can increase NPN toxicosis.
165
What are factors that affect toxicity of urea?
Species, compounds, feeding management, age, diet, liver function, Intake of feed/water.
166
Which animals are most susceptible to NPN toxicosis?
Ruminants.
167
T/F. Older animals are more tolerant than younger animals to NPN toxicosis.
False. Younger animals are more tolerant than older animals.
168
Which factors increase toxicity of NPN toxicosis?
Fasting, dehydration, feeds rich in urease (soybeans), hepatic insufficiency, diet low in energy/protein but high in fiber.
169
What is the toxicokinetics of NPN toxicosis?
Too much urea/ammonia > elevation of rumen pH (ammonia in non-ionized form) > absorbed and converted to urea by the liver > if supply exceeds demand > hyperammonemia > crosses cell membranes (BBB/placenta).
Ammonia inhibits citric acid cycle > Increase lactate, blood glucose, BUN, serum K and P, transaminases and PCV.
170
T/F. The death caused by urea toxicosis is due to cardiac or resp. failure.
True
171
What are CS/lesions of NPN toxicosis?
RAPID ONSET.
restless, aggression, salivation, colic, bloat, rumen stasis, convulsions, death.
Congestion in liver, kidney; ammonia odor.
Dead animals are bloated.
172
Lab dx for NPN toxicosis?
Urea in feed, ammonia in blood/rumen fluid/vitreous fluid, elevated rumen pH.
Specimens (except blood) should be frozen immediately.
173
What are ddx for NPN toxicosis?
Colic (inorganic arsenic), lead, metaldehyde, and chlorinated hydrocarbon pesticides, organophosphate, grain engorgement, nitrate poisoning, enterotoxemia, and cyanide poisoning.
174
What are the txs for NPN toxicosis?
BLOAT SHOULD BE RELIEVED FIRST.
Acetic acid or vinegar to ruminants followed by a large cold water (making rumen more acidic), repeat 4-5 hrs for 2 days.
Saline for dehydration, NaHCO3 for acidosis, rumenotomy.
Management: increase other vitamins, consistent feeding, increase palatability.
175
What is the prog. for NPN toxicosis?
BAD!
176
What are the uses of ionophore toxicosis?
Anticoccidial in livestock, growth promoter feed in cattle, reduction of bloat and rumen acidosis, prevention of bovine pulmonary edema.
177
What is the most common source of Ionophore toxicosis?
Monensin (banned in turkeys)
178
Properties. Carboxylic acid derivatives antibiotics. Slightly soluble in water and soluble in organic solvents and oil. Form lipid-soluble complexes with polar cations that are transported across cellular membranes.
Ionophore toxicosis (includ monensin, lasalocid, salinomycin, narain, semduramicin).
179
T/F. Urea is more toxic than monensin.
False. Monensin is more toxic than urea.
180
Which animal is most sensitive to monensin?
Equine
181
T/F. All animals are susceptible to ionophore toxicosis. Concurrent administration of other drugs (antibiotics, cardiac glycosides) increase toxicosis.
True
182
Why is monensin very toxic to horses compared to other animals?
Usually rapidly metabolized by P-450 oxidative demethylation enzymes in the liver and excreted mainly in bile.
Horse: Slower metabolism because they have low oxidative demethylases and they do not have gall bladder to eliminate.
183
What is MOA of ionophore toxicosis?
Targets mitochondria of highly energetic tissues.
Increased Na+ influx (into the cell) > increased intra-Ca2+ levels > injures tissues.
Catecholamine release > free radicals > sarcolemmal membrane damage.
184
T/F. Monensin toxicosis. Horses usually show skeletal muscle signs whereas cattle show mostly GI signs.
False.
Horse: GI, cardiac, resp. signs; RAPID ONSET (die fast).
Cattle: skeletal muscle signs
185
What is the best sample for chemical analysis for ionophore toxicosis?
Feed (GI contents, liver, feces).
186
What are the things you find in clin pathology for ionophore toxicosis?
Elevated enzymes of muscle origin (CPK, AST); elevated LDH, AP; increased PCV, decreased serum Ca2+ and K+.
187
What is ddx for ionophore toxicosis?
Myopathy, neuropathy, cardiotoxic conditions.
Horses: colic, cantharidin toxicosis, azoturia.
Cattle: Vit E/Se deficiency, poisonous plants (oleander, coffee senna).
188
What is tx for ionophore toxicosis?
NO SPECIFIC ANTIDOTE.
Remove source, decreasing absorption (activated charcoal, mineral oil, cathartics), symptomatic tx (fluid/electrolyte, potassium, monitor cardiac function).
Horses should not be ridden for several months.
Vit E/Se can decrease muscle damage.
189
What is prog. for ionophore toxicosis?
Horses that survive may suffer from myocardial damage and necrosis; may not reach previous performance.
190
What are the sources of water deprivation-sodium ion toxicosis?
Feeding garbage, ingestion of salt licks/ice melts, drinking water with salt, overcrowding, frozen water, unpalatable water, lack of water.
191
T/F. Water deprivation-sodium ion toxicosis is usually due to water deprivation, not providing excess of salt.
True.
192
T/F. Salt taste is not attractive and does not cause irritation to animals.
False. Salt taste is attractive to animals and cause irritation of MM.
193
Which animals are most susceptible to water deprivation-sodium ion toxicosis?
Pigs, cattle, and poultry (dogs are less susceptible)
194
What is the toxicokinetics/MOA of water deprivation-sodium ion toxicosis?
Salt absorbed through GI > distributed all over the body (CNS by passive and removed by active transport but this lacks) > if excess of salt > hypertonicity > attracts water > cerebral edema.
195
What are CS of water deprivation-sodium ion toxicosis?
Early: constipation and thirst (difficult to detect).
Intermitten convulsive seizures (not elicitable by external stimuli), head pressing, circling, blindness, deafness, inability to drink/feed.
196
What are the lesions of water deprivation-sodium ion toxicosis?
MOST IMPORTANT: Eosinophilic meningoencephalitis only in PIGS within 24 HOURS.
Edema, gastric congestion/inflammation with ulcers.
197
What are lab dxs for water deprivation-sodium ion toxicosis?
Increased Na concentration in serum and CSF.
| Salt in feed.
198
What are ddx for water deprivation-sodium ion toxicosis?
Encephalitic diseases, chlorinated hydrocarbon insecticides, roxarsone, pseudorabies.
199
How do you tx water deprivation-sodium ion toxicosis?
Giving small amount of fresh water (2-3 days), iV fluids (5% dextrose), furosemide, anticonvulsants.
200
Why can't you give large amounts of water to water deprived animals?
May kill the animal by aggravating cerebral edema.
201
What is prog. for water deprivation-sodium ion toxicosis?
POOR (mortality is 50%).
| Depends on severity of brain signs.
202
What is the most common source of lead toxicosis?
Lead-based paints. Other sources: pesticides, lead shots (wildlife), contaminated pasture from industry.
203
Properties. Not degraded in the environment. NOT easily metabolized. Only about 1-2% absorbed from the GI tract due to insoluble compound formation. Acid conditions favor dissolution. Who am I
Lead toxicosis
204
T/F. Lead toxicosis is uncommon.
False. One of the common toxicosis.
205
T/F. Older dogs are more sensitive to lead toxicosis and more susceptible than puppies.
False. Pups are more frequently poisoned (eating habits) and more sensitive (absorption through immature BBB).
206
Which species are resistant to lead toxicosis?
Goats, swine, chickens.
207
T/F. Chronic toxicosis is the most common in lead toxicosis.
False. subacute is most common.
208
What is toxicokinetics/MOA of lead toxicosis?
Oral absorption is poor and increased by acidity > transported as lead proteinate on the erythrocyte membrane > distributed all over the body (CNS/placenta) > mainly excreted in urine (some in bile/milk); stays in tissues for a few weeks and stays in bone for a few years.
NOT KNOWN.
Binds with SH, COOH, NH2 > inhibits proteins and replace zinc in some enzymes.
209
Which factors decrease absorption of lead?
Calcium, zinc, protein (they all use the same active transport > competition).
210
What is the target/CS for lead toxicosis?
Depend on amount, species, other factors (may take short or long).
GI, CNS (excitability in small animals and depression in horses and sheep), hematopoietic system (anemia) in chronic.
211
T/F. Acute exposure of lead toxicosis causes anemia due to inhibition of key enzymes in heme synthesis. delay in erythrocyte maturation, shortening the life span of erythrocytes.
False. Chronic exposure does.
212
What are the lesions of lead toxicosis?
Gross: nonspecific, lead in Gi.
Microscopic: cerebral cortical necrosis and poliomalacia in cattle; eosinophilic intranuclear inclusion bodies in renal and hepatocytes.
213
How do you dx lead toxicosis?
Chemical: blood lead more than 0.4ppm (doesn't correlate with CS).
Hematology: Nucleated RBC's, basophilic stippling (dogs), fluorescence of plasma prophyrins.
Radiograph: objects in GI, metaphyseal sclerosis in young animals (chronic).
Urinalysis: increased ALA-D, urinary lead following EDTA administration.
214
What are ddx for lead toxicosis?
Chlorinated hydrocarbons, urea, OP and carbamates, other conditions.
215
How do you tx lead toxicosis?
STABILIZE PATIENT FIRST.
Chelation: Calcium EDTA (BAL before EDTA improves effect > crosses BBB, enhance renal of lead), DMSA and Succimer for birds, D-penicillamine PO.
Supportive and symptomatic: thiamine, glucocorticoids, mannitol, zinc, diazepam, barbiturates, fluid.
Decontamination: magnesium sulfate (osmotic cathartic), surfical removal of lead.
216
What are two different types of Industrial petroleum?
Crude oil: sweet crude oil (48 ML/KG), rich in low temp (gas, kerosene, naphtha).
Sour crude oil (74ML/KG): high sulfur high temp (lubricating oil and gas oil).
217
What are the types of refined petroleum products in industrial petroleum?
Alphatic hydrocarbons: short-chain aliphatics (methane, ethane).
Long chain aliphatics: gas, kerosene, mineral oil.
Chlorinated aliphatic hydrocarbons: chloroform, carbon tetrachloride, dry cleaning and degreasing solutions.
Aromatic or polycyclic aromatic hydrocarbons: paints, glues, plastics (Benzene).
218
Are plastics a product of industrial petroleum?
Yes. Manufactured from hydrocarbon gas liquids and natural gas > not crude oil!
Byproducts or petroleum refining and natural gas processing.
219
T/F. Properties of industrial petroleum. Both crude oil and refined products are HIGHLY IRRITANT to skin and MM. Can cause bovine skin HYPERKERATOSIS (thickening of the stratum corneum).
True.
220
What are the physicochemical properties of industrial petroleum?
High boiling points > non-toxic, more volatile > more toxic through inhalation (low boiling points, low viscosity and low surface tension have more pneumotoxic effects).
221
What are the main sources of zinc toxicosis?
Ingestion of zinc containing pennies/products.
222
Who are the most susceptible to zinc toxicosis?
Ruminants, pets, aviary.
223
Properties. I am an essential dietary element. I am also a component of many important enzymes and proteins. I bind to -SH group and phosphate. I am widely distributed in the environment. I am important for functioning of taste and smell receptors. Who am I?
Zinc.
224
What is toxicokinetics of zinc toxicosis?
20-30% of ingested zinc is absorbed in GI by CARRIER-MEDIATED PROTEIN > 2/3 bound to albumin and 1/3 binds to beta2-macroglobulin (returns to circulation) > accumulates in LIVER, kidney, pancreas, spleen, reprod. organs > excreted mainly in feces (bile, saliva, sweat, and urine).
225
What increases absorption of zinc? What decrease absorption of zinc?
Acid environment, proteins, aminoa acids, EDTA increases absorption.
Ca, Cu, Fe, phytate, fiber decrease absorption.
226
What is MOA of zinc toxicosis?
NOT KNOWN.
| Effect on RBC (HEMOLYTIC ANEMIA), liver, kidney, pancreas.
227
What are acute, subacute, chronic CS of zinc toxicosis? What are other CS/lesions?
GI: cellular irritation/damage (gastritis, ulcers)
Hematologic: RBC damage
Renal: cell damage.
Lameness/stiffness in foal, decreased weight/milk production in livestock.
228
What are lab dx for zinc toxicosis?
HEMOLYTIC ANEMIA, icterus, hemoglobinuria, azotemia, hypercreatinemia, and hyperphosphatemia.
Decreased copper in liver in chronic toxicosis.
Radiographs: objects in the GI tract.
Use trace element tubes for analysis.
229
What is dx of zinc toxicosis?
History or a meal FB.
230
How do you treat zinc toxicosis?
Decontamination: cathartics, surgical removal.
Supportive care: blood transfusion, O2, fluid, furosemide, mannitol, dopamine for acute renal.
Chelation (NOT 1ST CHOICE): EDTA, D-penicillamine.
231
What is prog for zinc toxicosis?
Early dx and tx > good.
| Severe hemolytic anemia > guarded.
232
T/F. In canines, zinc levels fall very quickly after source is removed.
True.
233
Sources of INorganic arsenic toxicosis?
Ant/roach bait, wood preservatives, -cides, paint, detergents, building materials.
234
Properties. I exist in 3 oxidative states (elemental, trivalent, and pentavalent). I react with -SH group. Who am I?
Inorganic Arsenic Toxicosis
235
What are the different types of inorganic arsenic toxicosis? What is the lethal dose?
Peracute, acute, or subacute toxicosis.
| Lethal dose? 1-25mg/kg
236
T/F. Herbivores, swine, and chickens are most susceptible to inorganic arsenic toxicosis. Horses can get poisoned by ant and roach baits.
False. HERBIVORES are most susceptible (swine and chickens are rarely poisoned). Dogs can get poisoned by ant and roach bait.
237
T/F. Inorganic trivalent is more toxic than pentavalent. Pentavalent is more toxic than organic. Pentavalent is converted to trivalent in-vivo.
True.
238
What is the toxicokinetics of inorganic arsenic toxicosis?
Ingestion, inhalation, skin > distributed all over the body (higher concentrations in liver and kidney, hair, skin, hoof); poorly crosses BBB > pentavalent reduced in the liver to trivalent and partly metabolized in the liver and kidney by methylation > excreted in urine (48 hours).
239
T/F. Milk from poisoned cows contains toxic levels from inorganic arsenic.
True.
240
What is MOA of inorganic arsenic toxicosis?
Trivalent binds to 2-SH groups of lipoic (essential cofactor for decarboxylation of keto acids) > inhibition of citric acid.
Pentavalent uncouples oxidative phosphorylation and interfere with vit. B1 and B6.
Local corrosive effect. Intestines, liver, kidney, capillary endothelial cells are most sensitive.
241
What are CS of inorganic arsenic toxicosis? (Peracute/Acute/Subacute)
Peracute: sudden death or severe colic, collapse, death.
Acute: Rapid onset, severe colic, salivation, V+, watery D+ (hemorrhagic), hematuria, death in 1-3 days.
Subacute: Colic, anorexia, depression, D+ with blood, paralysis of hindlimb, death in several days.
242
What are the lesions of inorganic arsenic toxicosis?
Gi edema and hemorrhage with sloughing and perforation.
Liver and kidney damage.
Capillary degeneration.
Skin lesions and blistering due to skin exposure.
243
How do you dx inorganic arsenic toxicosis?
URINE FOR ANTEMORTEM.
LIVER/KIDNEY FOR PM.
GI contents, V+, feces, milk; increased PCV, BUN.
244
What are tx for inorganic arsenic toxicosis?
Emergency and supportive tx: fluids, acidosis tx, vitamins, antibiotics, analgesics, dopamine.
Decontamination: gastric lavage (only early), mineral oil, activated charcoal, emetics/strong cathartics, demulcents to coat GI (kaolin-pectin).
Chelation therapy: Dimercaprol (BAL: choice), Dimercaptosuccinic acid (DMSA)
245
What is prog. for inorganic arsenic toxicosis?
Guarded if not treated early.
246
What is ddx for inorganic arsenic toxicosis?
Irritant plants, urea, pesticides, monensin, OP, hypomagnesemia, enteric bacterial and viral diseases.
247
How do you dx inorganic arsenic toxicosis?
History, signs of sudden onset bloody D+, mucosal shreds, lesions, lab dx.
248
What is the use of organic arsenicals?
Improve weight gain and feed efficiency and to control enteric infections in swine and poultry.
249
Which is the main organic arsenical used in swine? Poultry?
Swine: Arsanilic acid.
Poultry: Roxarsone.
250
What is the main CS caused by organic arsenicals in swine and poultry?
Peripheral Neuronal toxicity (PNT): locomotor signs > stumbling, ataxia.
251
Properties. I am phenylarsonice acid (benzenarsonic acid) derivative. I'm in the pentavalent oxidation state. Who am i?
Organic Arsenicals toxicosis.
252
T/F. Organic pentavalent arsenicals are more toxic than inorganic arsenic.
False. Less toxic.
253
What enhances organic arsenical toxicosis?
Dehydration, water deprivation, and renal insufficiency.
254
What is the toxicokinetics/MOA of organic arsenicals?
Small amounts absorbed in GI > distributed throughout the body > excreted unchanged in urine.
UNKNOWN.
Peripheral nerve demyelination > similar to vitamin B deficiency.
255
What are CS of are arsanilic acid in swine and poultry? What are CS of Roxarsone in swine and poultry?
Arsanilic acid - swine: PNT with good appetite; hour or days to develop. Poultry: Anorexia, depression, coma, death.
Roxarsone - poultry: PNT. Swine: marked hyperexcitability, no blindness.
256
What are the lesions of organic arsenicals?
No lesions > lesions only due to neuronal degeneration.
| Swine: erythema in light skin pigs, muscle atrophy in chronic, demyelination in nerves.
257
What are lab and regular dx for organic arsenicals?
Lab: specimens of feed, liver, kidney.
Dx: history, CS, microscopic nerve demyelination, chem analysis.
258
What is tx for organic arsenicals?
NO SPECIFIC ANTIDOTE.
Withdrawal of organic arsenicals.
Supportive therapy: water, fluid, vitamins, antibiotics.
Recovery make take 2-4 weeks.
259
What are the uses of iron?
Oral iron supplements, parenteral iron prep, mineral fortified fertilizers, hand warmers, O2 absorbing sachets.
260
T/F. IV of iron toxicosis is most toxic and oral is the least toxic.
True.
261
Properties. I am needed in diet in small amounts. I am a heavy metal. I present as elemental, divalent or trivalent.
Iron toxcosis.
262
T/F. Inorganic iron is less irritant and less astrigent than organic. Ferric iron is less irritant and less astrigent than ferrous iron.
False.
Organic is less irritant/astrigent than inorganic.
Ferrous is less irritant/astrigent than ferric iron.
263
T/F. When assessing the potential toxicity of an iron overdose, the amount of elemental iron in product ingested must be determined.
True.
264
What is the toxicokinetics of iron toxicosis?
Ferrous iron absorbed through GI using carrier mechanism (rate limiting factor) > oxidized to ferric iron > binds to transferring in plasma and is distributed throughout body > only a small amount is excreted in urine.
265
T/F. Chronic overdose overwhelms the selective absorption mechanism causing absorption of toxic concentrations of iron, causing free radicals.
False. Acute overdose.
266
What is MOA of iron toxicosis?
Circulating free iron causes free radicals > GI (direct corrosion), liver, CV.
Injectable iron causes peracute anaphylactoid reaction and rapid death due to histamine release.
267
What are parenteral prep CS/lesions of iron toxicosis? Oral prep?
```
Parenteral prep (peracute and acute toxicosis): yellowish brown discoloration @ inj. sites.
Oral prep (GI ulceration and hemorrhage enteritis; congestion of liver and kidney, icterus): Acute - Stage 1 (V+, D+, GI hemorrhage), Stage 2 (Apparent recovery > don't fall for it!), Stage 3 (metabolic acidosis, coag disorders, hepatic failure > MOST SERIOUS), stage 4 (GI obstruction due to secondary to fibrosing of GI tract).
```
268
What are lab findings of iron toxicosis?
Chem. analysis: elevated serum iron.
| Increased PCV, acidosis, hemoglobinuria, abdominal radiograph.
269
How do you tx iron toxicosis? (GI decontamination, supportive tx, chelation therapy)
GI decontamination: within 4 hours of ingestion, emesis, gastric lavage before CS, milk of magnesia to precipitate iron.
Supportive tx: fluids, GI protectants (sulcralfate).
Chelation therapy (not the 1st choice): only in severe within 12 hours, DEFEROXAMINE (Desferal) by IV.
Anaphylatic shock with epi, O2, antihistamine.
270
What is prog for iron toxicosis?
Depends on severity. Good in animals treated early.
271
What are the CS of acute copper toxicosis?
Rapid onset of severe GI signs.
272
What are the sources of chronic copper toxicosis in sheep?
Excess copper, molybdenum deficiency, unavailability of sulfate.
273
T/F. Chronic copper toxicosis is very common in both sheep and cattle.
False. Only sheep.
274
Properties. Normally, Molybdate binds to me in tissues at a ratio of 4:3 that is excreted in urine. Rumen sulfates and sulfites are reduced to sulfides that binds to me, reducing absorption. Accumulation of me in the liver is due to imbalances between me, molybdenum, and sulfate.
Copper.
275
What is toxicity of chronic copper toxicosis?
Happens when deficient in molybdenum or sulfate is unavailable (accumulation requires 1-2 weeks of exposure) Liver damage causes copper accumulation in hepatocytes (secondary). Stress cause sudden loss of copper to blood.
276
Absorbed from intestine > carried by serum and erythrocytes to tissues > liver removes most of it from blood > bound to hepatic lysosomes, mitochondria, and nucleus > excreted by bile. Toxicokinetics of what?
Chronic Copper Toxicosis.
277
What is MOA of chronic copper toxicosis?
Liver degeneration and necrosis, hemolytic anemia, oxidizes Hb to metHb (cannot carry O2).
278
What is CS of chronic copper toxicosis?
Sudden onset of weakness, pale MM, anorexia, icterus, hemoglobinemia, fever, dyspnea, and shock.
279
What are the lesions of chronic copper toxicosis?
Gunmetal kidneys (kidneys enlarged, hemorrhagic, bluish dark, friable), blackberry jam spleen (spleen enlarged, dark brown to black).
280
What are lab dx of chronic copper toxicosis?
Elevated serum or whole blood (AM), liver function test (PM) for elevated liver enzymes.
281
What are ddx for chronic copper toxicosis?
Hemolytic agents (Zinc, naphthalene, DMSO, guaifenesin, acemteophen0, poisonous plants (onion, gossypol, red maple), snake venoms, infectious diseases.
282
What are tx of chronic copper toxicosis?
Ammonium tetrathiomolybate, D-penicillamine, molybdenized copper phosphate, addition of molybdate/ammonium molybdate, supplemental zinc.
283
What breed dog is genetically prone to chronic copper toxicosis? what is the tx?
```
Bedlington terrier (2-6 years of age).
Blood transfusion (don't need to do this if dog doesn't show CS).
```
284
T/F. Molybdenum toxicosis is usually a problem in cattle. Horses and pigs are resistant.
True.
285
What are the sources of molybedenum toxicosis?
Excess molybedenum, copper deficiencies.
286
Properties. I am an essential trace element. I am a component of xanthine oxidase > converts the purine xanthine to uric acid. Elevated me interferes with copper absorption. Excess me cause copper deficiency.
Molybdenum toxicosis.
287
What increases molybdenum toxicity? What decreases molybdenum toxicity?
Sulfate increases toxicity. Copper decreases toxicity.
288
What is toxicokinetics of molybdenum toxicosis?
Absorbed from the GI tract; excreted in milk in toxic levels.
289
What are CS of molybdenum toxicosis?
Severe D+ (greenish with fluids and gas bubbles), hair coat depigmentation, anemia, osteoporosis, exotosis, lameness, decreased libido in bulls and infertility in cows.
Microscopic anemia due to copper deficiency.
290
What are lab dx of molybdenum toxicosis?
Elevated molybdenum in blood and liver, decreased copper in blood and liver, decreased cytochrome oxidase activity.
291
What are ddx of molybdenum toxicosis?
Selenium, argetism, fluoride, frost bite, ergot.
292
What are tx for molybdenum toxicosis?
Copper glycinate SC/IM, copper sulfate added to diet.
293
What are Se deficiency diseases?
White muscle disease in lambs, hepatosis dietetica in young pigs, exudative diathesis in chicks, nutritonal pancreatic atrophy in chickens, porcine stress syndrome in pigs.
294
Northewest, Northeast, Southeast, Great lakes are rich in Se.
False. Deficient in Se (do not get toxicosis).
295
Seleniferous plants. Who am I? Accumulate up to 15,000ppm Se, require Se for growth. Include Astragalus, Stanleya, Oonopsis.
Obligate accumulators.
296
Seleniferous plants. Accumulate up to 1-25ppm. Accumulate Se passively in Se-rich soil (alkaline soil). include in soil, wheat, oats, barley, grass, and hay.
Passive accumulators. THE MOST COMMON SOURCE.
297
Seleniferous plants. Accuulate up to 25-100ppm. do not require Se but they can accumulate it. Aster, Airiplex, Castilleja plants.
Facultative accumulators.
298
Properties. I am a component of glutathione peroxidase. I'm an antioxidant. I'm found in 5-deiodinase (converts from T4 to T3). I am an irritant to MM like other metals.
Selenium toxicosis.
299
What is the toxicity in order (highest to lowest)? Selenate, selenite, synthetic organoselenium compounds, selenide, organic selenium in plants.
Organic Se in plants (bad odor, unpalatable) > selenate = selenite > selenide > synthetic organoselenium compounds > elemental Se (nontoxic).
300
What reduces Se toxicity?
High protein diet and ingestion of other elements that bind to Se such as Cu.
301
What is MOA of Se toxicity?
```
Acute or subacute death due to respiratory. Chronic death due to starvation and thirst. Decrease in tissue gluthathione and ascrobic acid. Se replaces sulfur in AA's. Decrease ATP in chronic.
Crosses placenta (teratogenic) and arsenic increases biliary excretion of this.
```
302
Acute CS of Se toxicity? Subacute? Chronic?
Acute: Oral (GI signs, resp signs, death), Parenteral (neurological signs).
Subacute: Resp, GI, hair/hoof losses (blind staggers in cattle; swine: PROCINE FOCAL SYMMETRICAL POLIOMYELOMALACIA).
Chronic (ALKALI DZ): bobbed tail dz, hoof deformities, rough hair coat, birth defects.
303
What are lab dx of Se toxicity?
Elevated Se, blood or plasma glutathione peroxidase activity (AM) correlates well with blood Se, Hoof and hair (PM).
304
What are ddx of Se toxicity?
Paraquat, pneumonia, fluoride toxicosis, molybdenum toxicosis.
305
What are tx for acute Se toxicity?
Cathartics, symptomatic therapy (O2), acetylcysteine, arsenic increases elimination and Cu/Zn decrease absorption.
306
What are prevention of subacute and chronic?
Forages tested regularly, remove from animals, Addition of Cu/organic arsenicals and high protein diet.
307
What is prog. of Se toxicosis?
Poor in acute due to quick death.
308
Name one fungicide.
Pentochlorophenol (PCP)
309
Name herbicides.
Phenoxy derivatives of fatty acids (2,4-D) and Dipyridyl herbicides (paraquat/diquat).
310
Name three feed and water related toxicants.
NPN (urea), Ionophore (monensin), H2O deprived-Na+.
311
Name one common household product.
Ethylene Glycol.
312
What are the metals and minerals that can cause toxicosis?
Iron, Inorganic arsenicals, organic arsenicals, lead, zinc, copper, molybdenum, Selenium.
313
Name five toxic gases.
Ammonia, hydrogen sulfide, carbon monoxide, nitrogen oxide, sulfur oxides.
