Exam two Flashcards
1
Q
What is methaldehyde used for?
A
snail, slug and insect killer, fuel for camp stoves
2
Q
What kind of pesticide is methaldehyde?
A
RUP
3
Q
What are the properties of methaldehyde?
A
irritant, flammable powder, poorly soluble in H20, soluble in oil
4
Q
How long can products release methaldehyde?
A
10-14 days under moderately moist conditions
5
Q
What animals are susceptible to methaldehyde toxicity?
A
dogs, cats, livestock, horses
6
Q
Which route makes methaldehyde most toxic?
A
inhalation
7
Q
What happens to methaldehyde in the stomach?
A
some undergoes acid hydrolysis to acetaldehyde and both can be absorbed from GIT
8
Q
Do methaldehyde and acetaldehyde cross the BBB?
A
YES
9
Q
What is the elimination half life of metaldehyde?
A
~27 hours
10
Q
What can decrease toxicity of methaldehyde?
A
enzyme inducers like phenobarbital
11
Q
How is acetaldehyde metabolized?
A
by hepatic aldehyde dehydrogenase and converted to CO2 and exhaled
12
Q
What is the MOA of methaldehyde?
A
metaldehyde > acetaldehyde, then concentration is higher than capability of liver to oxidize it, methaldehyde decreases brain GABA, NE and 5HT and increases MAO (breaks down more)
13
Q
What contributes to toxicity of methaldehyde?
A
hyperthermia due to muscle tremors, metabolic acidosis
14
Q
What is the cause of early death in methaldehyde toxicity?
A
respiratory failure within 4-24 hours
15
Q
What is seen in dogs that survive acute phase of methaldehyde toxicity?
A
liver failure, damage, cirrhosis
16
Q
When is the onset of action for methaldehyde toxicity?
A
w/i 3 hours
17
Q
What are the clinical signs of methaldehyde toxicity?
A
salivation, vomiting, diarrhea, tachycardia, reversible blindness, convulsive seizures, CNS depression
18
Q
If an animal recovers from methaldehyde toxicity, what is the time frame?
A
2-3 weeks
19
Q
What lesions are found in methaldehyde toxicity?
A
formaldehyde odor in stomach contents, methaldehyde granules may be visible in GI, petechial and ecchymotic hemorrhages in GI
20
Q
What lab work can be done to confirm methaldehyde toxicity?
A
look for methaldehyde/acetaldehyde in stomach contents
21
Q
How do you diagnose methaldehyde toxicity?
A
history, clinical signs, odor, lab analysis
22
Q
What is the antidote for methaldehyde toxicity?
A
none
23
Q
How do you treat methaldehyde toxicity?
A
emetics, gastric lavage, activated charcoal, enemas, anticonvulsants, respiratory support, muscle relaxants, fluid therapy, monitor and manage temp
24
Q
How is phenoxy2,4,D used?
A
herbicide, turf, agent orange
25
How does 2,4,D alter the metabolism of plants?
increases toxicity by increasing accumulation of nitrate or cyanide and improves palatability
26
How long does 2,4,D live in the environment?
not stable in environment
27
How is 2,4,D affected by the rumen?
not degraded by rumen microflora and don't alter microflora, irritant to GI mucosa
28
What species are most susceptible to 2,4,D toxicity?
cattle and dogs
29
How is 2,4,D absorbed/distributed?
absorbed well from GI and poorly from skin - distributed all over body
30
What is the half life of 2,4,D?
a few hours (can be up to 4 days in dogs)
31
How is 2,4,D metabolized?
hydrolysis
32
How id 2,4,D excreted?
unchanged in urine, alkalization of urine enhances this
33
What is the MOA of 2,4,D toxicosis?
irritates GI mucosa, uncouples oxidative phosphorylation, affects skeletal muscle membranes in dogs
34
What clinical signs are seen w 2,4,D toxicosis?
GI and neuromuscular
35
What lesions are seen in 2,4,D toxicosis?
GI damage, degeneration of renal tubules, rumen stasis
36
What lab tests help with diagnosis?
elevated kidney levels, ALP, LDH, CK and checking forage, water, liver and stomach contents
37
How do you diagnose 2,4,D toxicity?
history of ingestion, chemical analysis, rule out other diseases
38
What is the antidote for 2,4,D?
none
39
How do you treat 2,4,D toxicity?
wash skin, activated charcoal, IV fluids, alkalinize urine
40
What are the dipyridyl herbicides?
paraquat (RUP) and diquat (GUP) broad spectrum herbicides
41
How well do dipyridyl herbicides live in the environment?
unstable, rapidly inactivated by light and soil, soluble in water but not alcohol, hydrocarbon solvents
42
What pH destroys dipyridyl herbicides?
alkaline
43
What species are susceptible to dipyridyl herbicide toxicity?
all esp dogs
44
What increases dipyridyl herbicide toxicity?
selenium vit D deficiency, depletion of tissue glutathione and oxygen therapy and preexisting renal failure
45
How is paraquat absorbed, distributed and excreted?
absorbed from GI and skin, distributed all over esp in lung, excreted unchanged in urine
46
How is diquat absorber?
poorly absorbed from GI
47
Where is paraquat selectively sequestered?
in alveolar cells - after 4hrs [ ] 10x other organs, 30-80x plasma after 4-10 days
48
What is the diphasix efflux?
initial rapid 1/2 life followed by slow phase as chemical is released from lung storage pool
49
What is the MOA of paraquat and diquat?
reduced by NADPH to produce singlet oxygen > reacts w lipids of membranes to form hydroperoxides > production of free radical and membrane damage and cellular degeneration and necrosis
50
What are the clinical signs of the first phase of acute herbicide toxicosis?
vomiting, anorexia, irritation of topical exposure, -- ataxia, dyspnea and seizures at high doses
51
What are the clinical signs of the second phase of acute toxicosis in herbicide toxicity?
renal failure and hepatocellular necrosis, reversible renal injury
52
What are the clinical signs of the third phase of acute toxicosis in herbicide toxicity?
initially damage to the alveoli and consequent pulmonary edema, tachypnea, dyspnea, harsh respiratory sounds
53
What happens in subacute or chronic toxicosis of herbicides?
survive initial exposure > lungs undergo proliferative/fibrotic stage after 7 days and <30mmHg
54
What lesions are commonly seen with herbicide toxicosis?
respiratory tract and GIT lesions, pulmonary chanfes, lung may be shrunken and fibrotic if chronic, lingual ulcers
55
What lab work is done for herbicide toxicosis?
plant, stomach contents and urine sent to lab, mild changes in lungs on rads
56
How soon after herbicide toxicosis does the normal present negative?
48hours
57
How do you diagnose paraquat and diquat toxicity?
history, clinical signs, lesions, lab
58
What is the antidote for paraquat and diquat toxicity?
none
59
How do you treat paraquat and diquat toxicity?
emetics, oral adsorbants, saline cathartics, supportive treatment, hemodialysis
60
What is contraindicated in early treatment of paraquat and diquat toxicity?
oxygen! may increase lung damage
61
What are the biochemical antagonists for paraquat and diquat toxicity?
orgotein, acetylcysteine, ascorbic acid, niacin or riboflavin
62
How soon must treatments for herbicide toxicity begin to have much of an effect?
within 24 hours of exposure
63
What are fungicides used for?
prevent or treat fungal infections in plants
64
What are the fungicides?
chlorophenols and nitrophenols, pentachlorophenol (PCP)
65
What is the toxicity of fungicides like in animals?
usually low toxicity unless exposed in large amount
66
What is pentachlorophenol used for?
a wood preservative, protects from fugus and insects
67
What is the most toxic exposure of pentachlorophenol?
vapors penetrateing intact skin, dermal exposure
68
What ways can animals become poisoned by pentachlorophenol?
inhalation, licking wood, ingestion, vapors penetrating intact skin
69
How soluble is pentachlorophenol?
not in water, soluble in pils and organic solvents
70
What did older preparations of pentachlorophenol contain?
dioxins - carcinogenic and teratogenic
71
What factors increase toxicity of pentachlorophenol?
high temp, oily or organic solvent vehicles, previous exposure, poor condition, newborn, hyperthyroid
72
What factors decrease pentachlorophenol toxicity?
cold temp, antithyroid drugs, presence of body fat
73
How is pentachlorophenol absorbed?
GI, inhalation, intact skin
74
What is the half life of pentachlorophenol?
1.5-2 days
75
How is pentachlorophenol excreted?
as glucuronides or unchanged in urine
76
What is the MOA of pentachlorophenol?
uncouples oxidative phosphorylation and blocks or decreases ATP > overheating, metabolic acidosis and dehydration
77
What clinical signs are seen with pentachlorophenol toxicosis?
irritation of eye, respiratory or GI mucosa and intact skin, neurotoxic due to decreased cellular energy, CNS simulation and seizures
78
What signs of acute pentachlorophenol toxicity are seen in pigs?
hyperthermia, skin irritation and rapid death
79
What are the signs of chronic pentachlorophenol toxicity?
weight loss, decreased milk production, anemia, fever, respiratory distress
80
What lesions are seen in pentachlorophenol toxicosis?
rapid rigor mortis, local irritaiton, pulmonary congestion, dark blood
81
What lab diagnosis can be done in pentachlorophenol toxicosis?
chemical test of blood in urine (or kidney and skin if dead)
82
How do you diagnose pentachlorophenol toxicity?
history, signs, lesions, chemical analysis
83
What is the antidote for pentachlorophenol toxicity?
none
84
How do you treat pentachlorophenol toxicity?
removal of animal from site, emetics, activated charcoal, bath, oxygen therapy, lower temp, IV fluids, antibiotics
85
Where does non-protein nitrogen come from?
urea as feed additive, urea fertilizer, ammonium salts in feed products
86
What pH enhances hydrolysis of urea by urease?
alkaline -- urea is basic
87
What species are most effected by non-protein nitrogen toxicity?
ruminants, horses
88
What compound is the most toxic of all NPN compounds?
urea
89
What age of animals are more sensitive to NPN toxicity?
<1year but 3-6weeks are tolerant
90
What increases toxicity of NPN?
fasting, dehydration or low water intake, between 6weeks-1yr, feeds rich in urease, hepatic insufficiency, diet low in energy and protein but high in fiber
91
What does too much urea and ammonia result in?
elevation of rumen pH in non-ionized form (BAD)
92
In NPN toxicity, what happens once non-ionized ammonia is absorbed?
converted by liver to urea > excreted in urine > too much = hyperammonemia
93
Why is non-ionized ammonia more toxic to animals?
crosses cell membranes, BBB, and placenta
94
What is the MOA of NPN toxicosis?
urea > ammonia, ammonia inhibits CAC > lack in energy > decreased cellular respiration and tissue damage
95
What is the cause of death in NPN toxicity?
cardiac failure or respiratory failure --> RAPID
96
What are the clinical signs of NPN toxicity?
RAPID onset of restlessness, muscle tremors, salivation, colic, bloat, sternal recumbency while standing on hind limbs, convulsions, death within 1-2hours
97
What are the lesions associated in NPN toxicity?
none- ammonia odor, vascular damage, dead animals are bloated
98
How do you diagnose NPN toxicity in the lab?
analysis of feed for urea content, ammonia in whole blood or rumen fluid, or frozen specimens
99
What is found in blood chemistry and rumen pH in NPN toxicity?
elevated rumen pH alkalotic, acidic blood
100
How do you diagnose NPN toxicity?
history, clinical signs, ammonia odor, lab
101
How do you treat NPN toxicity?
relieve bloat, acetic acid or vinegar to ruminants, sodium bicarb, normal saline
102
Which animals do you treat for NPN toxicity?
not showing signs yet - every 4-5hours for 48hours, ones showing signs die quickly, usually can't treat in time
103
What are ionophores used for?
anti-coccidia, growth promotor, antibiotics, monensin for milk production efficiency
104
What is the solubility of ionophores like?
slightly soluble in water, soluble in organic solvents and oils - microphilic
105
What are sources of ionophores?
monensin, eating feed with high levels, malicious poisoning
106
What species are susceptible to ionophore toxicity?
all, equines most, then cattle, poultry least
107
Are cattle levels of ionophores toxic to horses?
NO
108
What increases ionophore toxicity?
tiamulin, chloramphenicol, erythromycin, sulfonamides, cardiac glycosides
109
What is the difference between ruminants and mongastrics absorption of ionophores?
monogastrics absorb all but ruminants absorb 50%
110
How are ionophores distributed?
throughout body, blood and tissue levels are small, doesn't accumulate
111
How are ionophores metabolized and excreted?
metabolized by P-450 in liver, excreted in bile
112
What is the MOA of ionophores?
disrupt electrochemical gradients targeting mitochondria of highly energetic tissues, influx of sodium-ionophore complex increasing intracellular Na and Ca >decreased ATP, cell death, free radicals released
113
What organs/tissues are most affected by ionophore toxicity?
myocardium, kidneys
114
What is the onset of ionophore toxicity?
rapid
115
What are the clinical signs of ionophore toxicity?
GI, skeletal, cardiac --> anorexia, colic, hyperventilation, tachyarrythmias, diarrhea, ataxia, dyspnea, death, resting on knees with wings and legs outward in birds
116
What lesions are seen in ionophore toxicity?
cardiac and skeletal muscle lesions - pale white patchy areas on muscle
117
What is the lab diagnosis for ionophores?
feed and GI contents best for detection, look for ppb levels
118
What is seen on clinical pathology of ionophores?
increase enzymes, CPK, AST, LDH, ALP - decreased Ca, K, increased PCV -- Na often normal
119
How do you diagnose ionophore toxicity?
history, clinical signs, lesions, lab
120
What poisonous plants are toxic to skeletal muscle?
coffee senna, coyotillo, white snakeroot
121
What are the cardiotoxic plants?
oleander, taxus, milkweed, vetch
122
What is the antidote for ionophores?
none
123
How do you treat ionophore toxicity?
remove medicated feed, activated charcoal, mineral oil, saline cathartics, symptomatic treatment, do NOT stress horses
124
How do animals get water deprivation?
feedining brine, whey or garbage, ingestion of salt licks, drinking water containing salt, overcrowding, frozen water, lack of water, medicated (unpalatable) water
125
What effect does salt have on animals?
taste is attractive, mild irritant to mucous membranes
126
How much salt can animals tolerate in feed?
>10% salt in feed if they have free access to water
127
What species are susceptible to water deprivation?
pigs, cattle and poultry mostly, dogs less
128
How is salt absorbed?
by GI and distributed all over body - enters brain by passive diffusion and removed by active transport
129
How is excess sodium excreted?
in urine, as long as there is enough water
130
What is the MOA of water deprivation?
dehydration increases plasma sodium and cerebral spinal fluid - high sodium in brain inhibits anaerobic glycolysis resulting in lack of energy for active transport
131
What happens with sodium trapped in the brain?
attracts water because of osmotic gradient > cerebral edema and brain damage
132
What are the clinical signs of water deprivation?
early constipation and thirst, vomiting, PU, metabolic acidosis, seizures, circling, head pressing, blindness
133
What lesions are seen in water deprivation that are pathognomonic?
eosinophilic meningoencephalitis is pathognomonic in PIGS ONLY and only within 24 hours of exposure - disappears after
134
What other lesions could be seen with water deprivation?
fluid in body cavities, organ edema, cerebral edema
135
What is used for lab diagnosis of water deprivation?
serum and CSF concentrations, salt in feed
136
How do you diagnose water deprivation?
history, encephalitic signs, lesions and lab diagnosis
137
How do you treat water deprivation?
give small amounts of fresh water - large amount can kill them by causing more cerebral edema, IV fluids, furosemide, anticonvulsants
138
What is the prognosis of water deprivation?
poor, mortality 50%
139
What is the source of acute copper toxicosis?
ingestion of high concentrations of copper - feed additives, in soil
140
Why is acute heavy metal toxicity bad?
very small amount can cause toxicosis, irritants, poor penetrated of membranes, small amount that is absorbed can cause toxicosis because of potency
141
Which heavy metal crosses the BBB and causes CNS damage?
lead
142
What are the clinical signs of acute copper toxicosis?
rapid onset of GI signs, dehydration, shock
143
What species is chronic copper poisoning common in?
sheep > cattle, due to lower maliptinum in sheep that enhance copper toxicosis
144
What is the treatment for acute copper toxicosis?
supportive and symptomatic therapy
145
What enhances excess copper in the body?
molybdenum deficiency
146
How do you get molybdenum deficiency?
unavailability of sulfate
147
What is the normal ratio of copper to molybdenum
6:1
148
Why does chronic copper toxicosis occur?
molybdenum deficiency makes copper accumulate in liver
149
How long does chronic copper accumulation take in sheep?
2-10 weeks
150
How is copper excreted?
bile
151
What is the MOA of copper toxicosis?
accumulation in liver causes liver degeneration and necrosis, release > excess copper in blood, oxidation or RBC > hemolysis crisis, oxidizes hemoglobin to methemoglobin
152
What are the clinical signs of chronic copper toxicity?
weakness, anorexia, icturus, hemoglobunuria, dyspnea, shock
153
What lesions are seen with chronic copper toxicity?
liver is enlarged, friable, kidneys are enlarged, hemorrhagic, spleen enlarged and dark brown/black
154
How do you diagnose chronic copper toxicosis?
history, sudden onset hemoglobinuria, jaundice
155
What are the DDX for chronic copper toxicity?
hemolytic agents, poisonous plants, snake venom, infectious dz,
156
How do you treat chronic copper toxicity?
add molybdate to sheep rations or pastures, ammonium tetrahiomolybate, D-penicillamine, supplemental zinc
157
What dog breed is susceptible to chronic copper toxicosis?
bedlington terrier - recessive disorder at 2-6 years, also westie, skye terriers, dobermans
158
How do animals get molybdenum toxicity?
excess molybdenum in soil, plants, industrial contamination, fertilizer OR copper deficiency
159
What species are susceptible to molybdenum toxicity?
cattle most, seen in sheep, horses and pigs resistance
160
What increases molybdenum toxicity?
high levels of dietary sulfate, low levels of copper
161
How is molybdenum absorbed and excreted?
absorbed from GI, excreted in milk in toxic levels
162
What is the MOA of molybdenum toxicosis?
copper deficiency > involved in hematopoesis, CT metabolism, myelin formation in newborn animals, pigmentation, bone formation
163
How long does it take to see signs of molybdenum toxicity?
a few days after exposure, 8-10 days for diarrhea
164
What are the clinical signs of molybdenum toxicity?
green/yellow non-hemorrhagic diarrhea, rough hair coat esp around eyes, decreased weight, anemia, decreased fertility
165
What is seen in lab on molybdenum toxicity?
look for high molybdenum or low copper, OR decreased cytochrome oxidase (indicates low copper)
166
How do you treat molybdenum toxicity?
copper glycinate SC, copper sulfate added to diet
167
Where does inorganic arsenic come from?
ant/roach bait, wood preservative, insecticides, herbicides, fungicides, paint, pigments, detergents
168
What is the oxidative state of inorganic arsenic?
3 oxidative states: elemental, trivalent arsenite, pentavalent arsenate
169
Which form of inorganic arsenic is most toxic?
trivalent - arsenite
170
How fast is inorganic arsenic toxicosis?
acute or per acute
171
What species are susceptible to arsenic toxicosis?
most herbivores, dogs, rarely swine, chickens
172
Is inorganic or organic arsenic more toxic?
inorganic more toxic
173
Why is pentavalent dangerous when metabolized?
it is inverted to trivalent in vivo - more toxic
174
How is inorganic arsenic absorbed?
GI, intact skin, inhalation - distributed all over body, higher in kidney and liver
175
Does inorganic arsenic cross the BBB?
poorly
176
How is inorganic arsenic excreted?
urine w/i 48 hours, feces, milk, saliva, sweat
177
What is the MOA of inorganic arsenic?
trivalent binds to 2-SH groups of lipoic - inhibits glycolysis and CAC, locally corrosive, tissues rich in oxidative enzymes, capillary endothelial cells most sensitive
178
What are the clinical signs of PERACUTE inorganic arsenic toxicity?
severe rapid colic, collapse, death,
179
What are the clinical signs of ACUTE inorganic arsenic toxicity?
rapid onset, severe colic, staggering, vomiting, hemorhagic diarrhea, hematuria - corrosive effects, death in 1-3 days
180
What are the clinical signs of SUBACUTE inorganic arsenic toxicity?
colic, anorexia, posterior paralysis
181
What are the classical lesions of inorganic arsenic toxicity?
GI mucosal edema and hemorrhage, liver and kidney damage, capillary degeneration, skin lesions and blistering
182
What is the best specimen for chemical analysis of inorganic arsenic?
urine for antemortem
| liver and kidney in postmortem
183
What on bloodwork can indicate inorganic arsenic toxicity?
increased PCV, increased BUN
184
How do you treat inorganic arsenic toxicity?
emergency and supportive treatment (fluids, treat acidosis), fluids and electrolytes
185
What ways can you decontaminate inorganic arsenic toxicity?
gastric lavage, mineral oil, activated charcoal, demulcents to coat mucosa - emetics CONTRAINDICATED because of corrosives if seeing clinical signs
186
What compound is used in chelation therapy for inorganic arsenic toxicity?
dimercaprol (BAL) **treat and gets worse, metabolizes and gets in blood
187
What are the side effects of dimercaprol used in inorganic arsenic toxicity?
vomiting, tremors, convulsions, shock, coma, death **can get at therapeutic doses
188
What are organic arsenicals used for?
feed additives to improve weight gain
189
What species is arsanilic acid used in?
swine
190
What species is roxarsone used in?
poultry
191
How do animals get organic arsenic toxicity?
overdose, prolonged use, contraindications in sick animals
192
What is the classification of damage in organic arsenicals?
peripheral neural toxicity
193
What enhances toxicity or organic arsenic?
dehydration, water deprivation, renal insufficiency
194
How are organic arsenics absorbed?
through GI and distributed throughout body
195
How is organic arsenic excreted?
unchanged in urine
196
What is the MOA of organic arsenic?
unknown but beleve due to peripheral neuronal damage and demylination
197
What are the clinical signs of organic arsenic (arsanilic acid) in swine?
3-5 days, incoordination, ataxia, partial paralysis but still GOOD appetite, NO GI SIGNS, erythema, blindness
198
What are the clinical signs of organic arsenic toxicity (arsanilic acid) in poultry?
anorexia, depression, coma, death
199
What are the clinical signs of roxarsone toxicity in swine?
sudden onset, hyperexcitability, tremors, collapse, coma, death, NO blindness
200
What are the clinical signs of roxarsone toxicity in poultry?
incoordination and ataxia
201
What lesions are seen with organic arsenic toxicity?
erythema in light skin pigs, muscle atrophy
202
What is the best specimen to test for organic arsenic toxicity?
feed, GI - otherwise levels may be low because of absorption
203
What is the antidote for organic arsenic?
none
204
How do you treat organic arsenic toxicity?
withdrawal, supportive therapy --> if demylination will be permanent damage,
205
How long does recovery of organic arsenic take?
2-4 weeks
206
What does selenium deficiency cause?
white muscle dz, nutritional muscle dystrophy, hepatitis dietetic, exudative diathesis, nutritional pancreatic atrophy, porcine stress syndrome
207
What areas get selenium deficient soil?
northwest, northeast, southeast, great lakes
208
What is the requirement of selenium?
0.1mg/kg
209
What is selenium used for?
feed supplement, injectable, supplements, medicated shampoos, seleniferous plants
210
What is the palatability of selenium plants?
unpalatable, smell like rotting garlic
211
What are the seleniferous plants?
astragalus, stanleya, oonopsis, xylorrhiza
212
How does selenium effect mucous membranes?
irritant
213
What type of soil enhances the formation of selenate?
arid alkaline soil of great planes
214
How does diet effect toxicity of selenium?
reduced by high protein diet and ingestion of other things that bind Se like copper
215
How is selenium absorbed?
SI, distributed throughout body esp. to liver, kidney, spleen
216
Chronic exposure of selenium leads to high concentrations where?
hair and hoof
217
Does selenium cross the placenta?
yes, also in milk
218
What is the MOA of selenium?
oxidative damage, free radicals, irritant
219
How is selenium excreted?
mostly urine, also bile
220
What increases biliary excretion of selenium?
arsenic
221
What causes death in acute and subacute toxicosis of selenium?
cardiogenic shck, respiratory insufficiency from pulmonary edema
222
What causes death in chronic toxicosis of selenium?
starvation and thirst from weakness and loss of hooves, lameness
223
What are the clinical signs of acute toxicosis of selenium?
GI signs, respiratory signs, neuro signs esp if injected
224
What are the clinical signs of chronic toxicosis of selenium?
hoof and hair falling out/apart
225
What are the clinical signs of subacute toxicosis of selenium?
mix of acute and chronic signs - see hoof and hair problems with respiratory and cardiovascular issues - may see blind staggers
226
What lesions are seen in swine with selenium toxicosis?
porcine focal symmetrical poliomalacia
227
What lesions are seen in acute selenium toxicosis?
hemorrhagic gastroenteritis, gut contents smell like rotten garlic or horseradish
228
What is used for lab diagnosis of selenium toxicity?
blood, kidney and liver for acute
| hoof and hair if chronic
229
How do you treat acute selenium toxicosis?
saline cathartics, symptomatic therapy, acetylcysteine
230
What should you do to prevent selenium toxicosis?
regularly test soil, remove animals from seleniferous areas, add copper to diet, add organic arsenicals to diet
231
What is the difference between nitrate and nitrite?
nitrate NO3 is absorbed from soil by plant and is converted to nitrite NO2, nitrite > ammonia >AA> plant protein
232
When animals ingest plants, do they get nitrate or nitrite?
BOTH
233
How does nitrate accumulate in the plant?
when rate of nitrate to nitrite is reduced and continuation of nitrate uptake from soil
234
What plant species favor nitrate accumulation?
sweet clover, alfalfa, wheat, corn
235
What soil conditions enhance nitrate uptake?
rains, moisture, acid soil, low soil molybdenum, sulfur or phosphorus, low soil temp, soil aeration
236
What part of the plant contains the highest [ ] of nitrate?
the stalk closest to ground, seed and flower has least
237
What age of plants have more nitrate?
younger
238
What are the nitrate accumulating plants?
pigweed, oats, beets, johson grass, sudan grass, milo, corn, maize, lambs quarters, sweet clover, alfalfa, wheat, sunflower
239
What is nitrate and nitrite used for?
fertilizers, sodium nitrite IV as vasodilator
240
What is the most important property of nitrate/nitrite?
nitrate > nitrite by nitrate reductase
241
Are nitrates/nitrites palatable?
yes, salty
242
How does nitrate toxicity occur?
develops over time
243
What species is most affected by nitrate poisoning?
ruminants, horses sensitive to IV nitrite, pigs are resistant
244
Which is more toxic; nitrate or nitrite?
nitrite is 10x more toxic than nitrate
245
Why are ruminants so susceptible to nitrate toxicity?
factors that stimulate rumen microflora increase nitrate reductase activity > increases toxicity
246
What factors of the animal increases nitrate toxicity?
younger animal, with anemia and methemoglobinemia
247
What is the 1/2 life of nitrite? Nitrate?
<1hr, nitrate 4-48hr
248
What is the MOA of nitrate toxicosis?
oxidation > hemoglobin turns to methemoglobin and can't carry oxygen
249
At what level of methemoglobin does death occur from anoxemia?
80-90%
250
What are the clinical signs of nitrate toxicity?
sudden death, rapid breathing, dyspnea, ataxia, cyanosis, convulsions with a fast onset, abortion
251
What lesions are noted in nitrate toxicity?
congestion, brown/chocolate blood
252
What samples are taken for chemical analysis of nitrate and nitrate toxicity?
forage, hay, water for nitrate
ocular fluid if died for a few hours for nitrate
serum, plasma, urine, rumen contents for nitrate if alive
253
How do you diagnose nitrate/nitrite toxicity?
diphenylamine indicate >5,000ppm - not a final test, also look for methemoglobinemia
254
How do you treat methemoglobinemia?
methylene blue 1% IV (but NOT cats) changes methemoglobin back to hemoglobin
255
How do you treat nitrate/nitrite toxicity?
methylene blue 1%, activated charcoal, ruminal lavage, oral antibiotics
256
What are the cyanogenic plants?
wild choke cherry (prunus), sudan grass, johnson grass, sorghums
257
What is the most common cause of cyanide poisoning?
large animals eating plants containing cyanide
258
What are the causes of cyanide toxicity?
gas as a rodenticide, fertilizers, plants
259
In cyanide poisoning, what is the most toxic part of the plant?
the seeds
260
What is the characteristic odor of cyanide?
bitter almond of ammoniacal
261
What does the cyanide radical bind with to form complexes?
ferric ion, cupric and molybdenum
262
What species are more susceptible to cyanide toxicity?
ruminants > horses and swine and sheep
263
What releases cyanine in plants?
stress, plant damage
264
Where are cyanogenic glycosides concentrated in plants?
most in seeds, leaves, bark, stems, fruit
265
What age of plant has more glycoside?
young and growing
266
What type of soil increases glycoside?
high nitrogen, low phosphorus
267
How is HCN absorbed?
from GI, inhalation or intact skin and distributed throughout body
268
How is HCN excreted?
in urine or expired air (can measure HCN in urine)
269
What is the MOA of acute cyanide toxicity?
excess CN in blood binds ferric acid blocking electron transport, inhibiting cells to use O2 > anoxia in brain
270
What effects does cyanide have on the body?
metabolic acidosis, inhibits CAC, prominent vasoconstrictor, neuronal damage, irritation
271
What is the MOA of chronic cyanide toxicity?
neuronal degeneration and demyelination of spinal cord and brain
272
What are the clinical signs of acute cyanide poisoning?
nausea, vomiting, colic, diarrhea, seizures, muscle tremors, cyanosis, tachypnea,
273
How soon do animals die after clinical signs of cyanide toxicity?
4-5mins
274
What are the clinical signs of chronic cyanide poisoning?
paralysis, neuronal degeneration, incontinance, cystitis, wobbly gate, muscular weakness
275
What lesions are seen in cyanide toxicity?
MM bright red, cherry red blood, clots very slowly or not at all, petechial hemorrhages, plant in rumen, smell of cyanide
276
How can you detect cyanide?
must FREEZE sample (leaves quickly) brain is best, heart, blood, rumen contents -- also see elevated thiocyanate levels in urine, lactic acidosis and increased AG, sodium picrate paper test
277
What preserves cyanide in ruminal contents?
1-3% solution of mercuric chloride
278
What confirms diagnosis of cyanide toxicity?
chemical analysis
279
What is the treatment for cyanide toxicity?
sodium nitrite 20% IV - improves perfusion by vasodilation, sodium thiosulfate, oxygen, vinegar, mineral oil
280
What plants contain soluble oxalate?
halogeton, sarcobatus, amarantus, chenopodium, oxalis, rumex
281
Besides plants, what else is soluble oxalate in?
rust remover, bleach, tanning solution, fungi, ethylene glycol
282
What species are most susceptible to soluble oxalate?
sheep and cattle (but microflora in rumen can detoxify oxalates to carbonates and bicarbonates)
283
Which part of the plant is highest in soluble oxalate?
leaves, then seeds, then stems
284
What can decrease toxicity of soluble oxalates?
food in rumen, calcium, absence of fungi
285
What is the MOA of soluble oxalate toxicity?
SO combine w calcium > insoluble ca oxalate > hypocalcemia > crystals in tubules
286
What are the clinical signs of soluble oxalate toxicity?
onset a few hours of colic, depression, muscle twitch, rapid breathing, coma, death, oligouria, hyperkalemia, cardiac failure
287
What occurs in animals that survive acute sodium oxalate toxicity?
chronic tubular nephrosis and polyuria
288
What lesions are seen in soluble oxalate toxicity?
presence in rumen, excess fluid in abdomen and thorax, emphysema, blood tinged froth in mouth and esophagus, kidneys show dark red cortex and medulla
289
What is the laboratory diagnosis for soluble oxalate toxicity?
presence of Ca oxalate crystals in kidney tubules, hypocalcemia, high BUN
290
How do you treat soluble oxalate toxicity?
activated charcoal of lime water, calcium gluconate IV, saline glucose, supplement calcium salts, supportive therapy for nephrosis (usually of little values once clinical signs seen)
291
Where does lead come from?
paint, bullets, gas etc. being phased out - contaminated pastures,
292
How is lead absorbed?
not easily metabolized, nay 1-2 absorbed from GIT, normally forms insoluble compounds - dermal absorption is poor, inhalation is good
293
What pH conditions favor dissolution of lead?
acid conditions
294
What species are most susceptible to lead toxicity?
cattle, horses, pets, waterfowl, birds
295
What species are more resilient to lead toxicity?
goats, swine, chicken
296
What age of animal are more susceptible to led toxicsis?
younger because of more sensitive and greater absorption and immature BBB
297
What other compounds decrease absorption of lead?
calcium, zinc, protein
298
Does lead cross the BBB?
yes, more in younger animals, and placenta
299
How long does lead stay in soft tissues?
4-6 weeks then stored in bone and stays for several years
300
How is lead excreted?
urine, bile, milk at toxic levels
301
What are the target tissues of lead toxicity?
CNS, GIT and blood
302
What is the MOA in lead toxicosis?
replace zinc in some enzymes, interferes with GABA in CNS, competes with calcium ions and alters Ca movement across membranes
303
What is the time frame for the onset of clinical signs in lead toxicity?
hours,days,weeks or months depending on amount and species
304
What are the clinical signs of lead toxicity?
anorexia, salvation, vomiting, diarrhea, pharyngeal paralysis, CNS paralysis, anemia
305
What microscopic lesions are seen in lead toxicity?
cerebral cortical necrosis and poliomalacia in cattle, acid fast eosinophilc intranuclear inclusion bodies in renal tubular epithelium or hepatocytes
306
What is the antimortem specimen of choice in lead toxicity?
whole blood, liver, kidney and GI
307
What is seen on the bloodwork in lead toxicity?
increased nRBCs, basophilic stippling of erythrocytes, increased zinc protoporphyrin, florescence of plasma porphyrins under UV light
308
How do you treat lead toxicity?
fluid therapy, was hsurface, remove lead from gut BEFORE chelation
309
What is avoided in the treatment of lead toxicity?
activated charcoal not recv (doesn't bind) sulfate/mg cathartics may bind with lead to form lead sulfate
310
What is the chelating agent of choice for lead?
calcium disodium EDTA, but only for 5 days due to kidney damage, after break can use again
311
What can be given with chelation in lead toxicity?
dimercaprol prior to EDTA to improve the effect, D penicillamine, dimercaptosuccunuc acid
312
What is used for supportive treatment in lead toxicity?
thiamine, taurine, glucocorticoids, mannitol, zinc, barbituates, fluids
313
What are the sources of zinc?
galvanized containers, wire, nuts, batteries, jewlery, pennies, ointments
314
How many pennies can cause subacute toxicity in dogs?
5 pennies
315
What pH environment increases zinc release and absorption?
acidic
316
What decreases GI absorption of zinc?
Ca, Cu, Fe, phytate, fiber - competition for absorption sutes
317
What organs does zinc accumulate in?
pancreas, liver, kidney, spleen
318
How is zinc excreted?
feces, bile, saliva, sweat, urine
319
What is the MOA of zinc?
GI irritant, interferes with enzymes, direct damage to cell membranes, interferes with absorption of copper and iron, hemolytic anemia
320
What are the main organs affected in zinc toxicity?
RBC, liver, kidney, pancreas
321
What are the clinical signs of zinc toxicity?
GI upset, hemolytic anemia, icterus, hemoglobinuria, azotemia, hyperphosphatemia, decreased milk production, lameness
322
What lesions are seen in zinc toxicity?
gastric ulcers, liver damage, renal casts
323
What tube is used for chemical analysis of zinc toxicity?
dark blue top - use serum, liver, kidney, pancreas, urine
324
How do you treat zinc toxicity?
remove foreign body, cathartics, supportive care
325
What is the chelating agent for zinc toxicity?
calcium disodium EDTA or D-penicillamine
326
What are the sources of iron?
supplements, snail baits, hand warmers, fertilizers
327
Which types of iron are more irritant?
organic < inorganic
| ferrous < ferric
328
Which type of iron is more toxic, parenteral or oral?
parenteral > oral
329
What happens when iron is absorbed?
absorbed ferrous iron > ferric > binds to transferrin in plasma, distributed throughout body
330
What factor is important for toxicosis of iron?
going over carrying capacity
331
What does free iron cause?
saturation of transferrin resulting in free circulating iron
332
Hoe does excretion of iron change during toxicosis?
it doesn't! = problem
333
What effect does free iron have in the body?
direct cellular damage to GIT, liver, cardiovascular system
334
Where does circulating free iron accumulate?
in liver, causes mitochondrial damage and liver damage, systemic acidosis and shock
335
What is the MOA of iron toxicity?
circulating free iron > free radical lipid per oxidation > damage to membranes > increased vascular permeability > coagulopathy, vasodilation, shock
336
What are the clinical signs of per acute iron toxicosis?
anaphylactic reaction, shock, death within minutes
337
What are the clinical signs of acute iron toxicosis?
depression, shock, acidosis, death within hours
338
What are the stages to iron toxicosis?
1- GI upset
2 - apparent recovery
3- most serious, coagulation disorders, hepatic failure
4 - GI obstruction with fibrosing repair of GI
339
What are the lesions noted in iron toxicity?
yellow/broen discoloration at LN, GI ulcers, congestion of liver and kidney
340
What is seen on chemical analysis of iron toxicity?
no hemolysis, increased saturation of total iron binding capacity
341
How do you treat iron toxicity?
decontaminate GI w/i 4hours of ingestion, supportive treatment, (activated charcoal doesn't work)
342
What precipitates iron?
milk of magnesia
343
What is the specific chelator for iron?
desferoxamine
344
What is ethylene glycol found in?
antifreeze, coolant, windshield de-ice
345
How is ethylene glycol absorbed?
in GI, distributed to all tissues, metabolized to toxic metabolites in liver
346
How is ethylene glycol metabolized?
oxidized by alcohol dehydrogenase > glycoaldehyde > glycol acid > glycoxylic acid > oxalic acid, glycine, formic acid, hippuric acid, benzoic acid
347
What happens to oxalic acid in the body?
binds to serum calcium to form insoluble calcium oxalate crystals and hypocalcemia
348
What is the MOA of ethylene glycol itself?
direct GI irritaion, increased serum osmolality, CNS depression
349
What is the MOA of toxic metabolites of ethylene glycol?
metabolic acidosis and acute renal failure, CNS damage and failure, cerebral edema
350
What are the clinical signs of ethylene glycol toxicity?
nausea, vomiting, CNS depression, PU/PD, dehydration, renal failure, lethargy, renal pain, oliguria, coma, death
351
What lesions are seen with ethylene glycol toxicity?
hemorrhagic gastroenteritis, pulmonary edema, pale swollen kidneys
352
What is seen on the lab work in ethylene toxicity?
increased serum osmolality, increased anion gap, low USG, low blood pH, hypocalcemia, hyperglycemia, azotemia, increased PCV and TP, crystals in urine, serum glycol acid
