Exam three Flashcards
(271 cards)
1
Q
What are some properties of propylene glycol?
A
colorless, odorless, spooks like mineral oil, GRAS
2
Q
What are some sources of propylene glycol?
A
antifreeze, coolants, tobacco, electronic cigarettes
3
Q
What species are susceptible to propylene glycol toxicity?
A
dogs, *cats, cattle, horses
4
Q
Which is safer, propylene glycol or ethylene glycol?
A
propylene glycol
5
Q
How is propylene glycol absorbed?
A
via GI and inhalation
6
Q
How is propylene glycol metabolized?
A
in liver by alcohol dehydrogenase > lactaldehyde > lactic acid > pyretic acid
7
Q
How is propylene glycol excreted?
A
partly unchanged in urine
8
Q
What is the MOA of propylene glycol?
A
osmotic diuresis, CNS depression, encephalopathy, heinz body anemia in cats
9
Q
What are the clinical signs of propylene glycol toxicity?
A
ataxia and CNS depression, HB anemia in cats, muscle twitching
10
Q
What is seen on lab diagnosis of propylene glycol toxicity?
A
metabolic acidosis, hyperosmolarity, increased AG, hypoglycemia, low urine SG, HB anemia
11
Q
What is the treatment of propylene glycol toxicity?
A
emesis, activated charcoal, supportive treatment
12
Q
What are the sources of ethanol?
A
ingestion of beverages, rotten fruit, fermented bread dough, shampoo
13
Q
What is the source of methanol?
A
car windshield fluid antifreeze or paint remover
14
Q
What are the properties of ethanol/methanol?
A
volatile, irritant, highly lipid soluble
15
Q
How is ethanol/methanol absorbed?
A
PO and distributed in CNS - food delays absorption
16
Q
How is ethanol metabolized?
A
hepatic alcohol dehydrogenase > acetaldehyde > acetate > acetyl CoA > CO2 > water
17
Q
What is the MOA of ethanol/methanol
A
CNS depression, vasodilatior, emesis, metabolic acidosis, inhibits ADH, irritant of MM
18
Q
What are the clinical signs of ethanol toxicity?
A
CNS depression, abnormal behavior, vomiting, breath odor, hypothermia, tremor, ataxia, congested MM, PD, dehydration, death by respiratory failure, kidney and liver damage
19
Q
What lesions are seen with ethanol toxicity?
A
congestion go GI mucosa, liver, kidney, lungs
20
Q
What is seen on bloodwork of ethanol toxicity?
A
high blood alcohol levels, hypoglycemia
21
Q
What is the treatment for ethanol toxicity?
A
emetics, gastric lavage, NO AC, supporitve tx, monitor temp
22
Q
What is the antidote for methanol toxicity?
A
ethanol and fomepizole
23
Q
What are the uses of phenolic compounds?
A
disinfectants, household cleaners, antiseptics, lysol, derived from coal tar
24
Q
What species is more sensitive to toxicity of phenolic compounds?
A
cats due to deficiency of conjugation to glucuronic acid
25
How are phenolic compounds absorbed?
mostly from GIT, poorly from intact skin
26
How are phenolic compounds metabolized?
in liver by conjugation to glucaronic acid
27
How are phenolic compounds excreted?
metabolites in urine - can cause green or black urine
28
What is the MOA of phenolic compounds?
phenols denature and precipitate cellular proteins > direct irritation > coagulative necrosis - hepatotoxic, nephrotoxic, neurotoxic - stimulate respiratory center causing hyperventilation +/- respiratory alkalosis
29
What are the clinical signs to phenolic compound toxicity?
coagulative necrosis and ulceration on oral mucosa/skin, corneal ulcerations, ataxia, weakness, tremors, coma, methemoglobinemia, icterus, phenolic odor in breath/skin
30
What lesions are common in phenolic compound toxicity?
ulceration/necrosis of GI mucosa/skin, liver and kidney changes
31
What is seen in the lab diagnosis of phenolic compounds?
detected in urine, mixed with ferric chloride turns purple, hemolysis, methemoglobin, respiratory alkalosis, proteinuria, elevated serum liver enzymes
32
What is the detoxification of phenolic compounds?
emertics & gastric lavage is CONTRAINDICATED, use milk,egg whites followed by activated car coal and saline cathartics
33
What is used for decontamination of phenolic compounds?
PEG or glycerol and dish soap, flush eyes with isotonic, isothermic saline
34
What is used for supportive treatment of phenolic compounds?
NAC, methylene blue, ascorbic acid, fluids
35
What are the toxicity levels of different detergents?
lower > higher = nonionic, anionic, cationic detergents
36
What is the MOA of detergents?
direct irritation, corrosive, systemic toxicity by NM block > paralysis
37
What are the clinical signs with detergent toxicity?
nausea, vomiting, diarrhea, colic, shock, collapse, irritation
38
What is the treatment for detergent toxicity?
rinse with water, milk, egg whites, activated charcoal, supportive care -- emesis & gastric lavage CONTRAINDICATED
39
What is the toxic component in bleach?
sodium hypochlorite
40
What is the MOA of bleach toxicity?
release of chlorine or chloramine gas and hypochlorus acid > severe respiratory and eye irritation, corrosive to MM, oxidizing
41
What are the clinical signs of bleach toxicity?
oropharyngeal, GI, respiratory irritation, smell of chlorine
42
What is the treatment for bleach toxicity?
milk or water, wash dermal exposure with soap, supportive
43
What are the properties of xylitol?
sugar alcohol that looks and tastes like sugar
44
What are the uses of xylitol?
gum, candy, dental care, meds
45
Why should you not use human oral hygiene products in animals?
FDA doesn't require xylitol be listed on the label
46
What species are susceptible to xylitol toxicity?
dogs
47
How is xylitol absorbed?
GIT > glucose > glycogen in liver
48
What is the MOA of xylitol?
promotes insulin release resulting in hypoglycemia, large dose see liver failure, GI hemorrhage, DIC
49
What are the clinical signs of xylitol toxicity?
hypoglycemia w/i 30-60min, weakness, ataxia, collapse, seizures, lethargy, vomiting, liver failure, coagulopathy
50
What lesions are noted in xylitol toxicity?
none in hypoglycemic cases, in liver failure see petechial, ecchymotic or GI hemorrhages, hepatic necrosis
51
What is seen on lab work in xylitol toxicity?
hypoglycemia, high liver enzymes, prolonged PT/PTT, thrombocytopenia
52
How do you treat xylitol toxicity?
induce vomiting, 50%dextrose in 5% infusion, oral feeding of high carbs, fluids, liver protectants, transfusions for clotting factors
53
Where do methylxanthines come from?
caffeine, chocolate, coffee, tea, theophylline(tea), theobromine (cocoa beans)
54
What species are most susceptible to methylxanthine toxicity?
dogs mostly, cats too
55
How are methylxanthines absorbed and distributed?
from GI, distributed throughout body including CNS
56
How are methylxanthines metabolized?
by the liver > enterohepatic recycling
57
How are methylxanthines excreted?
in urine, unchanged and as metabolites
58
What is the MOA of methylxanthines?
phosphodiesterase inhibition > raise cAMP and competitive inhibition of adenosine receptors
cerebral cortical stimulation, seizures, myocardial contraction, smooth muscle relaxation and diuresis
caffeine stimulates release of catecholamines from adrenal medulla, respiratory, vasomotor and vagal centers
59
How long to clinical signs of methylxanthine toxicity last?
12-72 hours
60
What are the clinical signs of methylxanthine toxicity?
restlessness, hyperactivity, PU/PD, urinary incontinance, vomiting, tachycardia, hypertension, cardiac arrhythmias, respiratory failure, terminal seizures
61
What are the clinical signs of theophyline toxicity?
nausea, vomiting, abdominal pain, mild acidosis, tachycardia
62
When do the clinical signs of caffeine/theobromine start?
within 2 hours - can be delayed with chocolate ingestion
63
What are the signs of caffeine/theobromine toxicity?
restlessness, hyperactivity, panting, vomiting, tachycardia, weakness, ataxia, muscle tremors, hyperthermia, clonic convulsions, progression to arrhythmias, muscle rigidity, hyperreflexia, terminal seizures, coma
64
What lesions are seen in methylxanthine toxicity?
chocolate of caffeine products in GIT, gastroenteritis, congestion of organs
65
What is seen in lab diagnosis of methylxanthine toxicity?
low K, phis, Mg and elevated GLU - can detect in stomach contents, plasma, serum, urine, liver
66
How do you treat methylxanthine toxicity?
induce vomiting w/i 2-6 hours, activated charcoal up to 72hrs, IV fluids, empty bladder, supportive care
67
What are the non-toxic household chemicals?
silica gel packs, toilet water, lipstick, deodorant, conditioners, lotions, bath oils, children's toys
68
What are the sources of ammonia?
decomposing manure in confined animal houses, burning nylon/plastic, leaking hoses that spray ammonia
69
What properties does ammonia have?
sharp odor, heavier than air, soluble in water
70
What species are most susceptible to ammonia toxicity?
swine, poultry
71
What are the exposure amounts of ammonia?
smell 10ppm, eyes burn at 25-35ppm, 50ppm in animal housing, acute death at 5000ppm
72
How is ammonia absorbed and distributed
ammonia > ammonia hydroxide in contact with water (mm) also can be inhaled and distributed to tissues
73
What is the MOA of ammonia?
irritates mm, more resp infections, decreased growth, pulmonary edema, alkalosis and compensatory acidosis, inhibits TCA cycle, death by asphyxia
74
What are the clinical signs of ammonia toxicity?
red mm, lacrimation, sneezing, nasal discharge, eyes shut, decreased growth rate, dyspnea, cyanosis, clonic convulsions
75
How is chemical analysis made with ammonia toxicity?
no chemical analysis with gases
76
How do you treat ammonia toxicity?
remove source or free animals, soothing ointments, diuretics for pulmonary edema, treat secondary infections
77
Where does hydrogen sulfide come from?
decomposition of urine and feces in high volume farms, coal pits, gas wells, sulfur springs
78
What are some properties of hydrogen sulfide?
colorless, rotten egg odor, heavier than air, flammable, irritant
79
What happens when hydrogen sulfide comes in contact with mm?
H2S -> sulfuric acid -> sodium sulfide
80
What happens with hydrogen sulfide in the tissues and GI?
reacts to form balck/dark compounds
81
Where in liquid manure holding pits is hydrogen sulfide found?
retained in liquid and released when agitated
82
What are the concentrations of hydrogen sulfide?
smell 0.025, ocular irritation 20ppm, severe symptoms 50ppm, olfactory accommodation 200ppm, fatal 400ppm-1000ppm
83
How is hydrogen sulfide absorbed?
through lungs and GI, converted to alkali sulfides in blood
84
How is hydrogen sulfide excreted?
oxidized to sulfate and excreted in urine and feces
85
If hydrogen sulfide doesn't get excreted what happens to it?
trapped by natural disulfides (glutathione) in blood
86
What is the MOA of hydrogen sulfide?
irritates mm, inhibits cellular respiration by inhibiting cytochrome oxidate, stimulates chemoreceptors of carotid body interfering with respiratory drive
87
What are the clinical signs of hydrogen sulfide toxicity?
sudden collapse, cyanosis, dyspnea, death, irritation to mucosa
88
What lesions are noted in hydrogen sulfide toxicity?
blood dark and doesn't clot, dark black/green tissues, sewage odor
89
How do you treat hydrogen sulfide toxicity?
remove source, oxygen therapy, sodium nitrite IV, disulfides
90
Where does carbon monoxide come from?
CO by fires, space heater, propane powered stuff, automobile exhaust in confined space
91
What are the properties of carbon monoxide?
odorless and colorless
92
What species are more susceptible to CO toxicosis?
small animals as sentinels, fetus more sensitive
93
What is the MOA of CO toxicity?
combines with hemoglobin > carboxyhemoglobin which can't carry oxygen and interferes with release of oxygen carried by normal hemoglobin > hypoxia, death, competes with oxygen for binding sites on myoglobin, interfere with cellular respiration at mitochondrial level
94
What are the clinical signs of carbon monoxide toxicity?
sudden death, hypoxia, drowsiness, incoordination, dyspnea, coma
95
What lesions are seen with CO toxicity?
bright red blood, mm pink, brain edema, hemorrhage or necrosis > deafness
96
How can you diagnose CO toxicity in the lab?
measure CO in the air or % of carboxyhemoglobin in blood (stable in fridge for days) or fetal thoracic fluid
97
How do you treat CO toxicity?
oxygen, 5%CO2, blood transfusion, fluids for acidosis
98
What is the source of nitrogen oxide gas?
produced by incomplete reduction of nitrates during fermentation of silos
99
What are the properties of NO2 gas?
NO2 red/brown, N2O4 colorless, mixture of two is yellow/brown, heavier than air, forms layer on silage then settles down shute, gases form nitric acid and nitric oxide, smog converts NO and oxygen to NO2 and ozone
100
What are the levels of NO2 toxicity?
smell 1-3ppm, 50-150ppm irritation, 250-310ppm death in swine after 20mins
101
What happens when NO contact mm?
NO2 and N2O4 --> nitric acid that cross respiratory mucosa and cause cellular damage
102
What is the MOA of nitrogen oxide gases?
direct irritation, passes thru URT and causes damage in lungs, death by hypoxia
103
What are the clinical signs to nitrogen oxide toxicity?
respiratory signs
104
What lesions are seen in nitrogen oxide toxicity?
pulmonary edema, hemorrhage, emphysema and inflammation of bronchioles, cyanosis, methemoglobinemia and necrosis of skeletal muscles
105
How do you treat nitrogen oxide toxicity?
supportive - oxygen, diuretics, antioxidants, methylene blue IV
106
What is the source of sulfur oxide?
industrial pollutant
107
What are some properties of sulfur oxide?
irritant, coughing, choking and suffocation
108
What is the MOA of sulfur oxide?
irritant, bronchoconstriction, lung damage, death by hypoxia
109
What clinical signs are seen with sulfur oxide toxicity?
respiratory failure signs
110
How do you treat sulfur oxide toxicity?
supportive, oxygen therapy
111
Why is smoke more toxic now than it was previously?
use of synthetic building materials
112
What animals are more likely to present for smoke inhalation toxicity?
younger animals - older more likely to die
113
What is the LD50 of smoke inhalation?
none! depends on temp of fire, length of exposure, size of animal etc
114
What enhances the toxicity of smoke inhalation?
burns in respiratory tissue , heated air
115
What are the 3 combustion products in smoke inhalation?
simple asphyxiants, irritants, chemical asphyxiants
116
What do simple asphyxiants do?
occupy space at the expense of oxygen (CO2, methane, O2 deprived environment)
117
What do irritants do?
chemically react on contact w mm to cause local effects
118
What do chemical asphyxiants do?
produce toxic systemic effects at tissue distant from the lung
119
Which irritants have high water solubility?
acrolein, sulfer dioxide, ammonia, hydrogen chloride
120
Which irritants have intermediate water solubility?
chlorine, isocyanates
121
Which irritants have poor water solubility?
phosgene, nitrogen oxides
122
How does soot affect smoke inhalation toxicity?
soot binds to respiratory mucosa allowing other materials to adhere and react esp sulfur dioxide
123
Why is solubility an important factor in respiratory injury?
higher solubility affects upper airway and low solubility gets into lower airway and has delayed effect
124
What are the clinical signs of smoke inhalation?
cough, dyspnea, tachypnea, wheezing, tachycardia, hypoxemia, local irritation, CNS signs
125
When do signs of smoke inhalation appear?
may worsen after initial presentation, monitor for 8 hours to 24 hours
126
What lesions are seen with smoke inhalation?
burns, pulmonary changes, cerebral edema from CO poisoning
127
How do you treat smoke inhalation?
remove smoke, oxygen, B2 agonists for bronchoconstriction, NO steroids, cough suppressants or opioids
128
Where does petroleum come from?
sweet crude oil (gasoline, kerosine) sour crude oil (lubricating oil, gas oil) aliphatic hydrocarbons (methane, ethane, propane, gas, kerosene) aromatic hydrocarbons (paint, resin, glue, plastic)
129
What are some properties of petroleum?
irritant, oily, contain toxic materials, can have chlorinated naphthalenes > bovine skin hyperkeratosis
130
What species are the most susceptible to petroleum toxicity?
cattle, wildlife, small animals, horses
131
How is petroleum absorbed?
GI, skin and inhalation (inversely proportional to molecular weight, aromatic > aliphatic
132
How are petroleum products metabolized?
aliphatic by oxidation, aromatic by hydroxylation
133
How are petroleum products excreted?
aromatic in urine or bile, aliphatic by lungs
134
What is the MOA of petroleum toxicity?
aspiration pneumonia, chemical pneumonitis, GI irritation, CNS depression, liver/kidney damage, bone marrow suppression
135
What are the clinical signs of petroleum toxicity?
coughing, dyspnia, anorexia, fever, shivering, smell of oil
136
What lesions are seen in petroleum toxicity?
ulceration of tracheal mucosa, oil in GI or bronchioles, necrosis of liver and kidneys
137
What lab diagnosis can show petroleum toxicity?
detection of oil in GI, radiography of aspiration pneumonia
138
How do you treat petroleum toxicity?
remove oil, AC, supportive NO emetics or gastric lavage
139
Where is fluoride found?
insecticide, industrial toxicant, feed supplement
140
What are the properties of fluoride?
reacts w other compounds, affinity for calcium, aluminum, iron
141
What species is more common to see fluoride toxicity?
herbivores, esp dairy cattle - young animals
142
How is fluoride absorbed?
by GI and distributed throughout body
143
Where if fluoride stored?
in bones and teeth
144
How is fluoride excreted?
urine
145
What is the MOA of fluoride?
irritant on GI mucosa, hypocalcemia, coagulation defect, increased capillary permeability, delays mineralization of teeth and bones
146
What are the clinical signs of acute fluoride toxicity?
w/i 30 mins see gastroenteritis, stiffness, weakness, weight loss, seizures, respiratory and cardiac failure
147
What are the clinical signs of chronic fluoride toxicity?
6-12mths see lameness, spontaneous fractures, patchy brown teeth, anorexia, emaciation
148
What lesions are seen in fluoride toxicity?
GI, bone or teeth lesions depending on if chronic or acute
149
What specimen can be sent to test for fluoride toxicity?
bone, urine, feed and water
150
How do you treat fluoride toxicity?
balanced feed of calcium, phosphorus, bit D,
151
What is the MOA of the insoluble calcium oxalate plants?
calcium oxalate crystals penetrate oral mucosa causing irritation, enzymes cause release of histamine
152
What part of the insoluble calcium oxalate plants are toxic?
all parts
153
What is the MOA of soluble oxalate plants?
hypocalcemia and precipitation of insoluble calcium oxalates in soft tissues and kidney damage
154
What is the MOA of isocupressic acid plants?
vasoconstriction and decreases uterine blood flow that stimulates the release of fetal cortisol and abortion
155
What are the clinical signs of isocupressic acid plants?
abortion
156
What is the MOA of quinone plants?
primary photosensitization, photodynamic substance comes directly from the plant, substance in blood of the animal and exposure to sun in genetically predisposed animals - only in areas of light or unpigmented skin
157
What are the clinical signs of quinone plant toxicity?
erythema and pruritus, edema and necrosis of skin, secondary bacterial infections
158
What is the MOA of tannic acid plants?
tissue damage including GI lesions and kidney damage, both in ruminants, mainly GI in monogastrics
159
What are the clinical signs of tannic acid plant toxicity in cattle?
constipation, brown urine, anorexia, depression, rumen atony
160
What are the clinical signs of tannic acid plant toxicity in monogastrics?
mainly GI signs: colic, constipation, hemorrhagic diarrhea, hemoglobinuria, hematuria, icterus
161
What is the MOA of triterpene acid toxicity?
liver damage and hepatogenic photosensitization, lantadene A and B cause damage of bile canaliculi membranes and cholestasis, decreased elimination of phylloerythrin a metabolic of chlorophyll that causes photosensitization
162
What are the clinical signs of triterpene acid plant toxicity?
depression, anorexia, constipation, diarrhea, icterus, photophobia, erythema of skin, swelling, necrosis and sloughing
163
Which species are susceptible to triterpene acid plant toxicity?
ruminants, horses are resistant
164
What is the MOA of colchicine plant toxicity?
anti mitotic by binding to tubulin and inhibiting spindle formation during cell division, rapidly dividing cells are more sensitive
165
What are the clinical signs of colchicine toxicity?
many organs, GI signs, cardiovascular hypotension and cardiac arrhythmias, respiratory signs, renal failure, hepatic failure, seizure and neuronal signs, coagulopathies, myelosuppression
166
What is the MOA of diterpene alkaloid plant toxicity?
competitive blockade of the nicotinic receptors at the muscle endplate similar to curare
167
What are the clinical signs of diterpene alkaloid plant toxicity?
sudden death in cattle, muscle weakness/stiffness, staggering, bloating, collapse, cardiac arrhythmias
168
What is the treatment of diterpene alkaloid plant toxicity?
physostigmine or neostigmine
169
What is the MOA of the ergot alkaloid plants?
vasoconstriction and gangrene, uterine contraction
170
What is the MOA of indolizidine alkaloid plants?
inhibit lysosomal enzymes essentail for formation of proteins, alteration of cellular function in the brain and many other organs including endocrine and repro, heart and immune system, peripheral neuronal degeneration, respiratory signs, abnormal hoof and hair
171
What are the clinical signs of indolizidine alkaloid toxicity?
locoism disease - neuronal signs, depression, incoordination, ataxia, circling, abnormal behavior, infertility, congenital defects, heart failure, weight loss, poor performance, decreased immune function
172
Which species are more affected by locoism disease?
horses > cattle or sheep
173
What is the MOA of lycorine plant toxicity?
emetic and purgative
174
What are the clinical signs of lycorine plant toxicity?
GI signs, hypotension, large amounts cause muscle tremors and seizures
175
What is the MOA of muscarine plants?
stimulation of muscarinic cholinergic receptors, CNS stimulation
176
What is the treatment for toxicity of muscarine plants?
atropine is antidote, symptomatic treatment and decontamination
177
What is the MOA of piperidine alkaloid plants?
nicotinic effects, ganglionic and NM stimulation followed by ganglionic and neuromuscular blockade - prevents fetal movement > birth defects
178
What are the clinical signs of piperidine alkaloid plant toxicity?
ataxia, incoordination, birth defects
179
What is the MOA of pyridine alkaloid plants?
nicotine and lobe line act on nicotinic receptors at autonomic ganglia, NMJ and some synapses in the CNS, low doses cause depolarization, large doses cause blockade
180
What are the clinical signs of pyridine alkaloid plant toxicity?
rapid onset, excitation, salivation, lacrimation, V/D, tachypnea, muscle twitching/weakness, death by respiratory failure
181
What is the MOA of pyrrollizidine alkaloid plants?
hepatotoxic
182
What is the MOA of solanine and solanidine alkaloid plant toxicity?
GI, CNS, respiratory and cardiac
183
What is the MOA of taxine alkaloid plant toxicity?
cardiotoxic and GI
184
What is the MOA of tropane alkaloid plant toxicity?
x
185
What is the MOA of xanthine alkaloid plants?
blocks adenosine receptors, inhibits phosphodiesterase
186
What are the clinical signs of xanthine alkaloid plant toxicity?
salvation, vomiting, colic, diarrhea, CNS stimulation, convulsive seizures, muscle tremors, tachycardia, hypotension, urination
187
What is the MOA of anthraquinones plants?
purgative, skeletal and cardiac muscle degeneration, myoglobinuria, kidney damage, liver failure in horses
188
What is the MOA of carcinogenic glycoside plants?
hypercalcemia, calcification of the elastic tissues of the arteries, tendons, and ligaments as well as generalized increased density of the bones causing lameness
189
What is the MOA of carboxyatractyloside plant toxicity?
hepatotoxicty, excessive salivation, renal damage, hypoglycemia
190
What is the MOA of the cardiac glycoside plants?
cardiotoxic by inhibiting Na/K ATPase
191
What is the MOA of coumarin glycosides?
form dicoumarol in spoiled plants, hemorrhage due to antagonism of bit K by inhibiting bit K epoxide reductase resulting in deficiency of coat factors II, VII, IX and X
192
What is the MOA of cyanogenic glycoside plants?
release HCN on hydrolysis in damaged plants, HCN metabolized in liver to thiocyanates,
193
What happens in acute poisoning of cyanogenic glycoside plants?
inhibition of cytochrome oxidase and inhibition of cellular respiration, vasoconstriction, inhibition of glycolysis, inhibition of CAC, irritation of mucous membranes
194
What happens in chronic poisoning of cyanogenic glycoside plants?
neuronal degeneration, antithyroid effect
195
What is the MOA of cycasin plant toxicity?
have 3 toxins: cycasin a glycoside causes GI irritation and liver damage and is teratogenic, mutagenic and carcinogenic, B methyl amino L alanine (BMAA) is neurotoxic AA, unknown toxin may cause axonal degeneration in the CNS
196
What are the clinical signs of cycasin plant toxicity?
GI and liver disease or ataxia and CNS syndrome depending on amount and duration of exposure
197
What clinical signs are seen in dogs with cycasin plant toxicity?
GI and liver damage signs including vomiting, anorexia, diarrhea, depression, seizures
198
What clinical signs are seen in sheep with cycasin plant toxicity?
GI signs and weight loss
199
What clinical signs are seen in cattle with cycasin plant toxicity?
neuronal signs, ataxia, weakness, weight loss
200
What is the MOA of glucosinolate plant toxicity?
antithyroid
201
What is the MOA of nitropropanol glycoside plant toxicity?
inhibits enzymes of the krebs cycle and cellular oxidative phosphorylation
202
What clinical signs are associated with nitropropanol glycoside plant toxicity?
respiratory and neuro signs in cattle and sheep (cracker bees or roaring disease) - horses and rodents show neuro signs
203
What is the MOA of phytoestrogen plants?
bind to estrogen receptors causing infertility in females and males
204
What are the clinical signs of phytoestrogen plant toxicity?
infertility in females, decreased libido and feminization in males
205
What is the MOA of protoanemonin plants?
a volatile oil released by hydrolysis of the glycoside, causes severe irritation of the GI mucosa and dermatitis
206
What is the MOA of the ptaquiloside plants?
death of precursor cells in the bone marrow causing aplastic anemia in cattle and sheep, neoplasm in the urinary tract causing enzootic bovine hematuria, tumors of upper digestive tract and retinal degeneration on sheep (bright blindness)
207
What are the clinical signs in ptaquiloside plant toxicity?
aplastic anemia acutely, anorexia, hemorrhage, enzootic hematuria, tachycardia, death
208
What is the MOA of steroidal saponin plants?
liver damage and inability to eliminate phylloerythrin a metabolite of chlorophyll which acts as a photodynamic substance, hepatogenic photosensitization
209
What are the clinical signs of steroidal saponin plant toxicity?
signs of photosensitization and liver damage
210
What is the mechanism of action of gossypol plants?
cardiotoxic and secondary liver damage, destroys seminiferous reducing male fertility, binds to proteins, AA, and iron, only free gossypol is toxic, causes protein malnutrition, inhibits many enzymes and interferes with hemoglobin synthesis, heat changes the toxic free gossyol to the less toxic protein bound gossypol, iron salts decrease toxicity by increasing gossypol inactivation and excretion
211
What are the clinical signs of gossypol plant toxicity?
poisoning is chronic - not acute, signs of cardiac toxicity, male infertility
212
What species are more sensitive to gossypol plant toxicity?
monogastrics > ruminants
213
What is the MOA of copper plants?
liver damage, hemolysis, methemoglobinemia
214
What is the MOA of selenium plants?
acute = GI irritation and respiratory signs chronic = hoof and hair abnormalities
215
What is the MOA of acute nitrate plate toxicity?
GI irritation, nitrate > nitrite, cxydation of ferrous iron of hemoglobin to ferric iron and formation of methemoglobin, respiratory insufficiency, fetal methemoglobin and death > abortion
216
What is the MOA of chronic nitrate plate toxicity?
decreased progesterone during pregnancy and abortion, reduced performance
217
What is the MOA of dimethyl disulfide plants?
plant contains 5-methyl cysteine sulfide which is reduced by intestinal flora in mono gastric animals and rumen microflora to dimethyl disulfide, large amounts of dimethyl disulfide cause oxidation of RBC to form Heinz bodies which normally is prevented by glutathione
218
What are the clinical signs of dimethyl disulfide plants?
anemia, depression, hemoglobinemia, hemoglobinuria, icterus, cyanosis
219
What is the MOA of diterpene ester plants?
diterpenoid euphorbol esters cause direct irritation of the skin and mucous membranes, activate protein kinase C resulting in cell damage and enzyme dysfunction
220
What are the clinical signs of diterpene ester plant toxicity?
irritation and blistering of skin and GI mucosa > salivation, vomiting, and diarrhea w/ or w/o blood - signs usually mild in small animals but may be severe in large animals especially horses
221
What is the MOA of grayanotoxin plants?
binds to sodium channels in excitable cells, increases permeability of sodium ions and depolarization, irritates GI mucosa
222
What are the clinical signs of grayanotoxin plant toxicity?
GI signs, excessive salivation, V/D, regurgitation, colic, depression, tachycardia, tachypnea, seizures, fever, death by aspiration pneumonia
223
What is the MOA of lectin plants?
ricin and abrin are glycoproteins, inhibit cellular protein synthesis resulting in cell death
224
What are the clinical signs or lectin plant toxicity?
GI signs including hemorrhagic gastroenteritis
225
What is the MOA of meliatoxin plants?
enterotoxic, neurotoxic
226
What are the clinical signs of meliatoxin plant toxicity?
GI signs w/ or w/o blood, CNS and peripheral neuronal signs generally similar to nicotine poisoning, death is from respiratory failure
227
What is the MOA of propyl disulfide plants?
disulfides produce oxygen free radicals that cause damage of RBC membranes and hemolysis, free radicals also cause denaturation of hemoglobin resting in heinz bodies
228
What are the clinical signs of propyl disulfide plant toxicity?
anorexia, ataxia, tachycardia, tachypnea, dyspnea, icterus, abortion
229
What is the MOA of tetradymol plants?
induction of microsomal enzymes, causes liver damage that decreases elimination of phylloerythrin - a metabolite of chlorophyll, causes damage in microcirculation areas exposed to UV light and hepatogenic photosensitization in white skin
230
What are the clinical signs of tetradymol plant toxicity?
sudden anorexia, depression, incorrdination, dyspnea, icterus and head pressing, skin swelling, erythema, necrosis, sloughing, secondary bacterial infections
231
What is the MOA of thiaminase plants?
destroys thiamine in the diet and produces signs of thiamine deficiency in monogastrics (neurotoxic)
232
What is the MOA of triterpenoid saponin plants?
direct irritation of the GI mucosa
233
What are the clinical signs of triterpenoid saponin plant toxicity?
salivation, anorexia, V/D, colic, hypothermia
234
What is the MOA of resin plants?
irritation of the nervous or muscle tissue
235
What is the MOA of alsike clover and red clover toxicity?
hepatotoxicity and secondary photosensitization in horses only, also hepatic encephalopathy at large amount
236
What are the clinical signs of alsike clover and red clover plant toxicity?
lacrimation, photophobia, erythema, pruritis, edema, necrosis, sloughing of skin
237
What is the MOA of avocado?
cardiotoxicity in goats, horses, rabbits, and caged birds - noninfectious mastitis and agalactica in cattle, horses, goats, and rabbits
238
What is the MOA of black walnut?
ingestion of fresh shavings made from heartwood causes laminitis
239
What is the MOA of forage induced photosensitization plants?
secondary photosensitization due to liver damage, forage induced photosensitization in cattle due to cholestatic liver disease
240
What are the clinical signs of forage induced photosensitization plant toxicity?
lacrimation, photophobia, erythema, pruritis, edema, necrosis, sloughing of skin
241
What is the MOA of grape/raisin toxicity?
unknown toxin causes acute renal failure only in dogs, amount ingested 9oz-2lb per dog
242
What are the clinical signs of grape/raisin toxicity?
GI, vomiting, acute renal failure
243
What is the MOA of lily?
unknown toxin causes nephrotoxicity only in cats, GI irritation in cats and dogs - two leaves can poison cats!
244
What are the clinical signs of lily toxicity?
GI signs, salivation, vomiting, depression, anorexia, PU, anuria, death by renal failure
245
What is the MOA of pigweed?
acute nitrate poisoning causes methemoglobinemia, chronic nitrate poisoning causes abortion, soluble oxalates cause hypoglycemia and kidney damage, unknown toxin causes renal tubular nephrosis in ruminants, pigs, horses
246
What clinical signs are seen with pigweed toxicity?
hypocalcemia, depression, weakness, incoordination, renal failure
247
What is the MOA of red maple?
unknown toxin in dried leaves causes hemolytic anemia, hemoglo binemia, heinz body formation in horses, oxidation of the membranes of RBC and hemolysis, oxidized hemoglobin forms heinz bodies that damage cell membranes, hemoglobin may precipitate in renal tubules > renal failure
248
What are the clinical signs of red maple plant toxicity?
anorexia, depression, anemia, icterus, brown discoloration of mm, hemoglobinuria, dyspnea, cyanosis, death
249
What is the MOA of senna plants?
unknown myotoxin causes skeletal muscle myopathy and cardiomyopathy, seeds most toxic, anthraquinone glycoside is cathartic
250
What are the clinical signs of senna plant toxicity?
diarrhea/constipation, muscle weakness, recumbency, good appetite, myoglobinuria, coffee colored urine, tachycardia, death
251
What is the MOA of yellow stathistle and russian knappweed plants?
equine nigropallidal encephalomalacia or chewing disease, toxins may be sequiterpene lactones, aspartic acid and glutamic acid, toxins interact w dopamine transporter > death of dopaminergic neurons in brain esp substantial nigra and globes pallidus
252
What are the clinical signs of yellow stathistle and russian knappweed plant toxicity?
sudden onset inability to eat/drink, drowsiness interrupted by excitation, head down, dehydration
253
What is the MOA of macadamia nuts?
unknown and unknown toxin
254
What are the clinical signs of macadamia nut toxicity?
dogs ingest 3-6g/kg show signs in 12hrs - weakness esp hind limbs, depression, ataxia, tremors, hyperthermia, lameness, recumbency, vomiting, diarrhea, colic, pale mm - full recovery in 2 days
255
What are the sources of toad toxins?
cane or marine toad, colarado river toad - catecholamines and seotonin
256
What species are affected by toad toxicity?
dogs > cats, ferrets
257
How are toxins in toad toxicity absorbed?
from mm of mouth, gastric mucosa, conjunctiva, open skin wounds
258
How are toad toxins distributed?
all over body including CNS
259
How are toad toxins metabolized and excreted?
metabolized by MAO and COMT enzymes and undergo neuronal reuptake, eliminated in urine
260
What is the MOA of toad toxins?
direct irritation, inhibit Na/K ATPase, hallucinogenic effect, vasoconstrictor
261
What are the main organs effected in toad toxicity?
heart, blood vessels, CNS
262
What are the clinical signs of toad toxicity?
onset in a few mins, irritation, hyper salivation, brick red mm, vocalization, vomiting, neuro signs, cardiovascular signs
263
What is the treatment of toad toxicity?
flush mouth with water, activated charcoal, control seizures, atropine for bradycardia, supportive care
264
What US states have copperhead snakes?
everywhere except alaska, maine and hawaii
265
What species are exposed to snake toxicity?
dogs> cats, horses
266
What is the MOA of snake toxicity?
hyaluronidase causes venom to spread, phospholipase A2 disrupts cell membranes, uncouples phosphorylation and releases vasoactive amines, hematoxic, cardiotoxic, neurotoxic, hypocoagulation
267
What are the clinical signs of snake note toxicity?
rapid or delayed, edema, swelling, petechiation, necrosis
268
How do you treat snake note toxicosis?
don't touch site, makes absorption increase, IV catheter, monitor, polyvalent crotalid anti venom, diphnhydramine IV, fluids, blood transfusion,
269
What is the MOA of amphetamine toxicosis?
CNS stimulant, blocks reuptake of NE and dopamine, inhibits MAO, excitatory receptor agonist
270
What are the clinical signs of amphetamine toxicosis?
hyperactivity, restlessness, circling, tremors, hypersalivation, some animals show depression
271
What is the treatment for amphetamine toxicosis?
emesis, activated charcoal, pentobarbital/propofol for seizures, treat hyperthermia, fluids, urinary acidifiers
