Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Toxicology > Exam three > Flashcards

Exam three Flashcards

1
Q

What are some properties of propylene glycol?

A

colorless, odorless, spooks like mineral oil, GRAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some sources of propylene glycol?

A

antifreeze, coolants, tobacco, electronic cigarettes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What species are susceptible to propylene glycol toxicity?

A

dogs, *cats, cattle, horses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which is safer, propylene glycol or ethylene glycol?

A

propylene glycol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is propylene glycol absorbed?

A

via GI and inhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is propylene glycol metabolized?

A

in liver by alcohol dehydrogenase > lactaldehyde > lactic acid > pyretic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is propylene glycol excreted?

A

partly unchanged in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the MOA of propylene glycol?

A

osmotic diuresis, CNS depression, encephalopathy, heinz body anemia in cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the clinical signs of propylene glycol toxicity?

A

ataxia and CNS depression, HB anemia in cats, muscle twitching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is seen on lab diagnosis of propylene glycol toxicity?

A

metabolic acidosis, hyperosmolarity, increased AG, hypoglycemia, low urine SG, HB anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the treatment of propylene glycol toxicity?

A

emesis, activated charcoal, supportive treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the sources of ethanol?

A

ingestion of beverages, rotten fruit, fermented bread dough, shampoo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the source of methanol?

A

car windshield fluid antifreeze or paint remover

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the properties of ethanol/methanol?

A

volatile, irritant, highly lipid soluble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is ethanol/methanol absorbed?

A

PO and distributed in CNS - food delays absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is ethanol metabolized?

A

hepatic alcohol dehydrogenase > acetaldehyde > acetate > acetyl CoA > CO2 > water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the MOA of ethanol/methanol

A

CNS depression, vasodilatior, emesis, metabolic acidosis, inhibits ADH, irritant of MM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What lesions are seen with ethanol toxicity?

A

congestion go GI mucosa, liver, kidney, lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is seen on bloodwork of ethanol toxicity?

A

high blood alcohol levels, hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the treatment for ethanol toxicity?

A

emetics, gastric lavage, NO AC, supporitve tx, monitor temp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the antidote for methanol toxicity?

A

ethanol and fomepizole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the uses of phenolic compounds?

A

disinfectants, household cleaners, antiseptics, lysol, derived from coal tar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What species is more sensitive to toxicity of phenolic compounds?

A

cats due to deficiency of conjugation to glucuronic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How are phenolic compounds absorbed?

A

mostly from GIT, poorly from intact skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How are phenolic compounds metabolized?

A

in liver by conjugation to glucaronic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How are phenolic compounds excreted?

A

metabolites in urine - can cause green or black urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the MOA of phenolic compounds?

A

phenols denature and precipitate cellular proteins > direct irritation > coagulative necrosis - hepatotoxic, nephrotoxic, neurotoxic - stimulate respiratory center causing hyperventilation +/- respiratory alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the clinical signs to phenolic compound toxicity?

A

coagulative necrosis and ulceration on oral mucosa/skin, corneal ulcerations, ataxia, weakness, tremors, coma, methemoglobinemia, icterus, phenolic odor in breath/skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What lesions are common in phenolic compound toxicity?

A

ulceration/necrosis of GI mucosa/skin, liver and kidney changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is seen in the lab diagnosis of phenolic compounds?

A

detected in urine, mixed with ferric chloride turns purple, hemolysis, methemoglobin, respiratory alkalosis, proteinuria, elevated serum liver enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the detoxification of phenolic compounds?

A

emertics & gastric lavage is CONTRAINDICATED, use milk,egg whites followed by activated car coal and saline cathartics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is used for decontamination of phenolic compounds?

A

PEG or glycerol and dish soap, flush eyes with isotonic, isothermic saline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is used for supportive treatment of phenolic compounds?

A

NAC, methylene blue, ascorbic acid, fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the toxicity levels of different detergents?

A

lower > higher = nonionic, anionic, cationic detergents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the MOA of detergents?

A

direct irritation, corrosive, systemic toxicity by NM block > paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the clinical signs with detergent toxicity?

A

nausea, vomiting, diarrhea, colic, shock, collapse, irritation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the treatment for detergent toxicity?

A

rinse with water, milk, egg whites, activated charcoal, supportive care – emesis & gastric lavage CONTRAINDICATED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the toxic component in bleach?

A

sodium hypochlorite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the MOA of bleach toxicity?

A

release of chlorine or chloramine gas and hypochlorus acid > severe respiratory and eye irritation, corrosive to MM, oxidizing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the clinical signs of bleach toxicity?

A

oropharyngeal, GI, respiratory irritation, smell of chlorine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the treatment for bleach toxicity?

A

milk or water, wash dermal exposure with soap, supportive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the properties of xylitol?

A

sugar alcohol that looks and tastes like sugar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the uses of xylitol?

A

gum, candy, dental care, meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Why should you not use human oral hygiene products in animals?

A

FDA doesn’t require xylitol be listed on the label

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What species are susceptible to xylitol toxicity?

A

dogs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How is xylitol absorbed?

A

GIT > glucose > glycogen in liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the MOA of xylitol?

A

promotes insulin release resulting in hypoglycemia, large dose see liver failure, GI hemorrhage, DIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the clinical signs of xylitol toxicity?

A

hypoglycemia w/i 30-60min, weakness, ataxia, collapse, seizures, lethargy, vomiting, liver failure, coagulopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What lesions are noted in xylitol toxicity?

A

none in hypoglycemic cases, in liver failure see petechial, ecchymotic or GI hemorrhages, hepatic necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is seen on lab work in xylitol toxicity?

A

hypoglycemia, high liver enzymes, prolonged PT/PTT, thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How do you treat xylitol toxicity?

A

induce vomiting, 50%dextrose in 5% infusion, oral feeding of high carbs, fluids, liver protectants, transfusions for clotting factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Where do methylxanthines come from?

A

caffeine, chocolate, coffee, tea, theophylline(tea), theobromine (cocoa beans)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What species are most susceptible to methylxanthine toxicity?

A

dogs mostly, cats too

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How are methylxanthines absorbed and distributed?

A

from GI, distributed throughout body including CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How are methylxanthines metabolized?

A

by the liver > enterohepatic recycling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How are methylxanthines excreted?

A

in urine, unchanged and as metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the MOA of methylxanthines?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How long to clinical signs of methylxanthine toxicity last?

A

12-72 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the clinical signs of methylxanthine toxicity?

A

restlessness, hyperactivity, PU/PD, urinary incontinance, vomiting, tachycardia, hypertension, cardiac arrhythmias, respiratory failure, terminal seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the clinical signs of theophyline toxicity?

A

nausea, vomiting, abdominal pain, mild acidosis, tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

When do the clinical signs of caffeine/theobromine start?

A

within 2 hours - can be delayed with chocolate ingestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the signs of caffeine/theobromine toxicity?

A

restlessness, hyperactivity, panting, vomiting, tachycardia, weakness, ataxia, muscle tremors, hyperthermia, clonic convulsions, progression to arrhythmias, muscle rigidity, hyperreflexia, terminal seizures, coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What lesions are seen in methylxanthine toxicity?

A

chocolate of caffeine products in GIT, gastroenteritis, congestion of organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is seen in lab diagnosis of methylxanthine toxicity?

A

low K, phis, Mg and elevated GLU - can detect in stomach contents, plasma, serum, urine, liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How do you treat methylxanthine toxicity?

A

induce vomiting w/i 2-6 hours, activated charcoal up to 72hrs, IV fluids, empty bladder, supportive care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the non-toxic household chemicals?

A

silica gel packs, toilet water, lipstick, deodorant, conditioners, lotions, bath oils, children’s toys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the sources of ammonia?

A

decomposing manure in confined animal houses, burning nylon/plastic, leaking hoses that spray ammonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What properties does ammonia have?

A

sharp odor, heavier than air, soluble in water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What species are most susceptible to ammonia toxicity?

A

swine, poultry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the exposure amounts of ammonia?

A

smell 10ppm, eyes burn at 25-35ppm, 50ppm in animal housing, acute death at 5000ppm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How is ammonia absorbed and distributed

A

ammonia > ammonia hydroxide in contact with water (mm) also can be inhaled and distributed to tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is the MOA of ammonia?

A

irritates mm, more resp infections, decreased growth, pulmonary edema, alkalosis and compensatory acidosis, inhibits TCA cycle, death by asphyxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are the clinical signs of ammonia toxicity?

A

red mm, lacrimation, sneezing, nasal discharge, eyes shut, decreased growth rate, dyspnea, cyanosis, clonic convulsions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How is chemical analysis made with ammonia toxicity?

A

no chemical analysis with gases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How do you treat ammonia toxicity?

A

remove source or free animals, soothing ointments, diuretics for pulmonary edema, treat secondary infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Where does hydrogen sulfide come from?

A

decomposition of urine and feces in high volume farms, coal pits, gas wells, sulfur springs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What are some properties of hydrogen sulfide?

A

colorless, rotten egg odor, heavier than air, flammable, irritant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What happens when hydrogen sulfide comes in contact with mm?

A

H2S -> sulfuric acid -> sodium sulfide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What happens with hydrogen sulfide in the tissues and GI?

A

reacts to form balck/dark compounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Where in liquid manure holding pits is hydrogen sulfide found?

A

retained in liquid and released when agitated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the concentrations of hydrogen sulfide?

A

smell 0.025, ocular irritation 20ppm, severe symptoms 50ppm, olfactory accommodation 200ppm, fatal 400ppm-1000ppm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

How is hydrogen sulfide absorbed?

A

through lungs and GI, converted to alkali sulfides in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How is hydrogen sulfide excreted?

A

oxidized to sulfate and excreted in urine and feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

If hydrogen sulfide doesn’t get excreted what happens to it?

A

trapped by natural disulfides (glutathione) in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is the MOA of hydrogen sulfide?

A

irritates mm, inhibits cellular respiration by inhibiting cytochrome oxidate, stimulates chemoreceptors of carotid body interfering with respiratory drive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are the clinical signs of hydrogen sulfide toxicity?

A

sudden collapse, cyanosis, dyspnea, death, irritation to mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What lesions are noted in hydrogen sulfide toxicity?

A

blood dark and doesn’t clot, dark black/green tissues, sewage odor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

How do you treat hydrogen sulfide toxicity?

A

remove source, oxygen therapy, sodium nitrite IV, disulfides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Where does carbon monoxide come from?

A

CO by fires, space heater, propane powered stuff, automobile exhaust in confined space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What are the properties of carbon monoxide?

A

odorless and colorless

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What species are more susceptible to CO toxicosis?

A

small animals as sentinels, fetus more sensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the MOA of CO toxicity?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the clinical signs of carbon monoxide toxicity?

A

sudden death, hypoxia, drowsiness, incoordination, dyspnea, coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What lesions are seen with CO toxicity?

A

bright red blood, mm pink, brain edema, hemorrhage or necrosis > deafness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

How can you diagnose CO toxicity in the lab?

A

measure CO in the air or % of carboxyhemoglobin in blood (stable in fridge for days) or fetal thoracic fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

How do you treat CO toxicity?

A

oxygen, 5%CO2, blood transfusion, fluids for acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What is the source of nitrogen oxide gas?

A

produced by incomplete reduction of nitrates during fermentation of silos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What are the properties of NO2 gas?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What are the levels of NO2 toxicity?

A

smell 1-3ppm, 50-150ppm irritation, 250-310ppm death in swine after 20mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What happens when NO contact mm?

A

NO2 and N2O4 –> nitric acid that cross respiratory mucosa and cause cellular damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is the MOA of nitrogen oxide gases?

A

direct irritation, passes thru URT and causes damage in lungs, death by hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What are the clinical signs to nitrogen oxide toxicity?

A

respiratory signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What lesions are seen in nitrogen oxide toxicity?

A

pulmonary edema, hemorrhage, emphysema and inflammation of bronchioles, cyanosis, methemoglobinemia and necrosis of skeletal muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

How do you treat nitrogen oxide toxicity?

A

supportive - oxygen, diuretics, antioxidants, methylene blue IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is the source of sulfur oxide?

A

industrial pollutant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What are some properties of sulfur oxide?

A

irritant, coughing, choking and suffocation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is the MOA of sulfur oxide?

A

irritant, bronchoconstriction, lung damage, death by hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What clinical signs are seen with sulfur oxide toxicity?

A

respiratory failure signs

110
Q

How do you treat sulfur oxide toxicity?

A

supportive, oxygen therapy

111
Q

Why is smoke more toxic now than it was previously?

A

use of synthetic building materials

112
Q

What animals are more likely to present for smoke inhalation toxicity?

A

younger animals - older more likely to die

113
Q

What is the LD50 of smoke inhalation?

A

none! depends on temp of fire, length of exposure, size of animal etc

114
Q

What enhances the toxicity of smoke inhalation?

A

burns in respiratory tissue , heated air

115
Q

What are the 3 combustion products in smoke inhalation?

A

simple asphyxiants, irritants, chemical asphyxiants

116
Q

What do simple asphyxiants do?

A

occupy space at the expense of oxygen (CO2, methane, O2 deprived environment)

117
Q

What do irritants do?

A

chemically react on contact w mm to cause local effects

118
Q

What do chemical asphyxiants do?

A

produce toxic systemic effects at tissue distant from the lung

119
Q

Which irritants have high water solubility?

A

acrolein, sulfer dioxide, ammonia, hydrogen chloride

120
Q

Which irritants have intermediate water solubility?

A

chlorine, isocyanates

121
Q

Which irritants have poor water solubility?

A

phosgene, nitrogen oxides

122
Q

How does soot affect smoke inhalation toxicity?

A

soot binds to respiratory mucosa allowing other materials to adhere and react esp sulfur dioxide

123
Q

Why is solubility an important factor in respiratory injury?

A

higher solubility affects upper airway and low solubility gets into lower airway and has delayed effect

124
Q

What are the clinical signs of smoke inhalation?

A

cough, dyspnea, tachypnea, wheezing, tachycardia, hypoxemia, local irritation, CNS signs

125
Q

When do signs of smoke inhalation appear?

A

may worsen after initial presentation, monitor for 8 hours to 24 hours

126
Q

What lesions are seen with smoke inhalation?

A

burns, pulmonary changes, cerebral edema from CO poisoning

127
Q

How do you treat smoke inhalation?

A

remove smoke, oxygen, B2 agonists for bronchoconstriction, NO steroids, cough suppressants or opioids

128
Q

Where does petroleum come from?

A

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
Q

What are some properties of petroleum?

A

irritant, oily, contain toxic materials, can have chlorinated naphthalenes > bovine skin hyperkeratosis

130
Q

What species are the most susceptible to petroleum toxicity?

A

cattle, wildlife, small animals, horses

131
Q

How is petroleum absorbed?

A

GI, skin and inhalation (inversely proportional to molecular weight, aromatic > aliphatic

132
Q

How are petroleum products metabolized?

A

aliphatic by oxidation, aromatic by hydroxylation

133
Q

How are petroleum products excreted?

A

aromatic in urine or bile, aliphatic by lungs

134
Q

What is the MOA of petroleum toxicity?

A

aspiration pneumonia, chemical pneumonitis, GI irritation, CNS depression, liver/kidney damage, bone marrow suppression

135
Q

What are the clinical signs of petroleum toxicity?

A

coughing, dyspnia, anorexia, fever, shivering, smell of oil

136
Q

What lesions are seen in petroleum toxicity?

A

ulceration of tracheal mucosa, oil in GI or bronchioles, necrosis of liver and kidneys

137
Q

What lab diagnosis can show petroleum toxicity?

A

detection of oil in GI, radiography of aspiration pneumonia

138
Q

How do you treat petroleum toxicity?

A

remove oil, AC, supportive NO emetics or gastric lavage

139
Q

Where is fluoride found?

A

insecticide, industrial toxicant, feed supplement

140
Q

What are the properties of fluoride?

A

reacts w other compounds, affinity for calcium, aluminum, iron

141
Q

What species is more common to see fluoride toxicity?

A

herbivores, esp dairy cattle - young animals

142
Q

How is fluoride absorbed?

A

by GI and distributed throughout body

143
Q

Where if fluoride stored?

A

in bones and teeth

144
Q

How is fluoride excreted?

A

urine

145
Q

What is the MOA of fluoride?

A

irritant on GI mucosa, hypocalcemia, coagulation defect, increased capillary permeability, delays mineralization of teeth and bones

146
Q

What are the clinical signs of acute fluoride toxicity?

A

w/i 30 mins see gastroenteritis, stiffness, weakness, weight loss, seizures, respiratory and cardiac failure

147
Q

What are the clinical signs of chronic fluoride toxicity?

A

6-12mths see lameness, spontaneous fractures, patchy brown teeth, anorexia, emaciation

148
Q

What lesions are seen in fluoride toxicity?

A

GI, bone or teeth lesions depending on if chronic or acute

149
Q

What specimen can be sent to test for fluoride toxicity?

A

bone, urine, feed and water

150
Q

How do you treat fluoride toxicity?

A

balanced feed of calcium, phosphorus, bit D,

151
Q

What is the MOA of the insoluble calcium oxalate plants?

A

calcium oxalate crystals penetrate oral mucosa causing irritation, enzymes cause release of histamine

152
Q

What part of the insoluble calcium oxalate plants are toxic?

A

all parts

153
Q

What is the MOA of soluble oxalate plants?

A

hypocalcemia and precipitation of insoluble calcium oxalates in soft tissues and kidney damage

154
Q

What is the MOA of isocupressic acid plants?

A

vasoconstriction and decreases uterine blood flow that stimulates the release of fetal cortisol and abortion

155
Q

What are the clinical signs of isocupressic acid plants?

A

abortion

156
Q

What is the MOA of quinone plants?

A

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
Q

What are the clinical signs of quinone plant toxicity?

A

erythema and pruritus, edema and necrosis of skin, secondary bacterial infections

158
Q

What is the MOA of tannic acid plants?

A

tissue damage including GI lesions and kidney damage, both in ruminants, mainly GI in monogastrics

159
Q

What are the clinical signs of tannic acid plant toxicity in cattle?

A

constipation, brown urine, anorexia, depression, rumen atony

160
Q

What are the clinical signs of tannic acid plant toxicity in monogastrics?

A

mainly GI signs: colic, constipation, hemorrhagic diarrhea, hemoglobinuria, hematuria, icterus

161
Q

What is the MOA of triterpene acid toxicity?

A

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
Q

What are the clinical signs of triterpene acid plant toxicity?

A

depression, anorexia, constipation, diarrhea, icterus, photophobia, erythema of skin, swelling, necrosis and sloughing

163
Q

Which species are susceptible to triterpene acid plant toxicity?

A

ruminants, horses are resistant

164
Q

What is the MOA of colchicine plant toxicity?

A

anti mitotic by binding to tubulin and inhibiting spindle formation during cell division, rapidly dividing cells are more sensitive

165
Q

What are the clinical signs of colchicine toxicity?

A

many organs, GI signs, cardiovascular hypotension and cardiac arrhythmias, respiratory signs, renal failure, hepatic failure, seizure and neuronal signs, coagulopathies, myelosuppression

166
Q

What is the MOA of diterpene alkaloid plant toxicity?

A

competitive blockade of the nicotinic receptors at the muscle endplate similar to curare

167
Q

What are the clinical signs of diterpene alkaloid plant toxicity?

A

sudden death in cattle, muscle weakness/stiffness, staggering, bloating, collapse, cardiac arrhythmias

168
Q

What is the treatment of diterpene alkaloid plant toxicity?

A

physostigmine or neostigmine

169
Q

What is the MOA of the ergot alkaloid plants?

A

vasoconstriction and gangrene, uterine contraction

170
Q

What is the MOA of indolizidine alkaloid plants?

A

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
Q

What are the clinical signs of indolizidine alkaloid toxicity?

A

locoism disease - neuronal signs, depression, incoordination, ataxia, circling, abnormal behavior, infertility, congenital defects, heart failure, weight loss, poor performance, decreased immune function

172
Q

Which species are more affected by locoism disease?

A

horses > cattle or sheep

173
Q

What is the MOA of lycorine plant toxicity?

A

emetic and purgative

174
Q

What are the clinical signs of lycorine plant toxicity?

A

GI signs, hypotension, large amounts cause muscle tremors and seizures

175
Q

What is the MOA of muscarine plants?

A

stimulation of muscarinic cholinergic receptors, CNS stimulation

176
Q

What is the treatment for toxicity of muscarine plants?

A

atropine is antidote, symptomatic treatment and decontamination

177
Q

What is the MOA of piperidine alkaloid plants?

A

nicotinic effects, ganglionic and NM stimulation followed by ganglionic and neuromuscular blockade - prevents fetal movement > birth defects

178
Q

What are the clinical signs of piperidine alkaloid plant toxicity?

A

ataxia, incoordination, birth defects

179
Q

What is the MOA of pyridine alkaloid plants?

A

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
Q

What are the clinical signs of pyridine alkaloid plant toxicity?

A

rapid onset, excitation, salivation, lacrimation, V/D, tachypnea, muscle twitching/weakness, death by respiratory failure

181
Q

What is the MOA of pyrrollizidine alkaloid plants?

A

hepatotoxic

182
Q

What is the MOA of solanine and solanidine alkaloid plant toxicity?

A

GI, CNS, respiratory and cardiac

183
Q

What is the MOA of taxine alkaloid plant toxicity?

A

cardiotoxic and GI

184
Q

What is the MOA of tropane alkaloid plant toxicity?

A

x

185
Q

What is the MOA of xanthine alkaloid plants?

A

blocks adenosine receptors, inhibits phosphodiesterase

186
Q

What are the clinical signs of xanthine alkaloid plant toxicity?

A

salvation, vomiting, colic, diarrhea, CNS stimulation, convulsive seizures, muscle tremors, tachycardia, hypotension, urination

187
Q

What is the MOA of anthraquinones plants?

A

purgative, skeletal and cardiac muscle degeneration, myoglobinuria, kidney damage, liver failure in horses

188
Q

What is the MOA of carcinogenic glycoside plants?

A

hypercalcemia, calcification of the elastic tissues of the arteries, tendons, and ligaments as well as generalized increased density of the bones causing lameness

189
Q

What is the MOA of carboxyatractyloside plant toxicity?

A

hepatotoxicty, excessive salivation, renal damage, hypoglycemia

190
Q

What is the MOA of the cardiac glycoside plants?

A

cardiotoxic by inhibiting Na/K ATPase

191
Q

What is the MOA of coumarin glycosides?

A

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
Q

What is the MOA of cyanogenic glycoside plants?

A

release HCN on hydrolysis in damaged plants, HCN metabolized in liver to thiocyanates,

193
Q

What happens in acute poisoning of cyanogenic glycoside plants?

A

inhibition of cytochrome oxidase and inhibition of cellular respiration, vasoconstriction, inhibition of glycolysis, inhibition of CAC, irritation of mucous membranes

194
Q

What happens in chronic poisoning of cyanogenic glycoside plants?

A

neuronal degeneration, antithyroid effect

195
Q

What is the MOA of cycasin plant toxicity?

A

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
Q

What are the clinical signs of cycasin plant toxicity?

A

GI and liver disease or ataxia and CNS syndrome depending on amount and duration of exposure

197
Q

What clinical signs are seen in dogs with cycasin plant toxicity?

A

GI and liver damage signs including vomiting, anorexia, diarrhea, depression, seizures

198
Q

What clinical signs are seen in sheep with cycasin plant toxicity?

A

GI signs and weight loss

199
Q

What clinical signs are seen in cattle with cycasin plant toxicity?

A

neuronal signs, ataxia, weakness, weight loss

200
Q

What is the MOA of glucosinolate plant toxicity?

A

antithyroid

201
Q

What is the MOA of nitropropanol glycoside plant toxicity?

A

inhibits enzymes of the krebs cycle and cellular oxidative phosphorylation

202
Q

What clinical signs are associated with nitropropanol glycoside plant toxicity?

A

respiratory and neuro signs in cattle and sheep (cracker bees or roaring disease) - horses and rodents show neuro signs

203
Q

What is the MOA of phytoestrogen plants?

A

bind to estrogen receptors causing infertility in females and males

204
Q

What are the clinical signs of phytoestrogen plant toxicity?

A

infertility in females, decreased libido and feminization in males

205
Q

What is the MOA of protoanemonin plants?

A

a volatile oil released by hydrolysis of the glycoside, causes severe irritation of the GI mucosa and dermatitis

206
Q

What is the MOA of the ptaquiloside plants?

A

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
Q

What are the clinical signs in ptaquiloside plant toxicity?

A

aplastic anemia acutely, anorexia, hemorrhage, enzootic hematuria, tachycardia, death

208
Q

What is the MOA of steroidal saponin plants?

A

liver damage and inability to eliminate phylloerythrin a metabolite of chlorophyll which acts as a photodynamic substance, hepatogenic photosensitization

209
Q

What are the clinical signs of steroidal saponin plant toxicity?

A

signs of photosensitization and liver damage

210
Q

What is the mechanism of action of gossypol plants?

A

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
Q

What are the clinical signs of gossypol plant toxicity?

A

poisoning is chronic - not acute, signs of cardiac toxicity, male infertility

212
Q

What species are more sensitive to gossypol plant toxicity?

A

monogastrics > ruminants

213
Q

What is the MOA of copper plants?

A

liver damage, hemolysis, methemoglobinemia

214
Q

What is the MOA of selenium plants?

A

acute = GI irritation and respiratory signs chronic = hoof and hair abnormalities

215
Q

What is the MOA of acute nitrate plate toxicity?

A

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
Q

What is the MOA of chronic nitrate plate toxicity?

A

decreased progesterone during pregnancy and abortion, reduced performance

217
Q

What is the MOA of dimethyl disulfide plants?

A

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
Q

What are the clinical signs of dimethyl disulfide plants?

A

anemia, depression, hemoglobinemia, hemoglobinuria, icterus, cyanosis

219
Q

What is the MOA of diterpene ester plants?

A

diterpenoid euphorbol esters cause direct irritation of the skin and mucous membranes, activate protein kinase C resulting in cell damage and enzyme dysfunction

220
Q

What are the clinical signs of diterpene ester plant toxicity?

A

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
Q

What is the MOA of grayanotoxin plants?

A

binds to sodium channels in excitable cells, increases permeability of sodium ions and depolarization, irritates GI mucosa

222
Q

What are the clinical signs of grayanotoxin plant toxicity?

A

GI signs, excessive salivation, V/D, regurgitation, colic, depression, tachycardia, tachypnea, seizures, fever, death by aspiration pneumonia

223
Q

What is the MOA of lectin plants?

A

ricin and abrin are glycoproteins, inhibit cellular protein synthesis resulting in cell death

224
Q

What are the clinical signs or lectin plant toxicity?

A

GI signs including hemorrhagic gastroenteritis

225
Q

What is the MOA of meliatoxin plants?

A

enterotoxic, neurotoxic

226
Q

What are the clinical signs of meliatoxin plant toxicity?

A

GI signs w/ or w/o blood, CNS and peripheral neuronal signs generally similar to nicotine poisoning, death is from respiratory failure

227
Q

What is the MOA of propyl disulfide plants?

A

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
Q

What are the clinical signs of propyl disulfide plant toxicity?

A

anorexia, ataxia, tachycardia, tachypnea, dyspnea, icterus, abortion

229
Q

What is the MOA of tetradymol plants?

A

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
Q

What are the clinical signs of tetradymol plant toxicity?

A

sudden anorexia, depression, incorrdination, dyspnea, icterus and head pressing, skin swelling, erythema, necrosis, sloughing, secondary bacterial infections

231
Q

What is the MOA of thiaminase plants?

A

destroys thiamine in the diet and produces signs of thiamine deficiency in monogastrics (neurotoxic)

232
Q

What is the MOA of triterpenoid saponin plants?

A

direct irritation of the GI mucosa

233
Q

What are the clinical signs of triterpenoid saponin plant toxicity?

A

salivation, anorexia, V/D, colic, hypothermia

234
Q

What is the MOA of resin plants?

A

irritation of the nervous or muscle tissue

235
Q

What is the MOA of alsike clover and red clover toxicity?

A

hepatotoxicity and secondary photosensitization in horses only, also hepatic encephalopathy at large amount

236
Q

What are the clinical signs of alsike clover and red clover plant toxicity?

A

lacrimation, photophobia, erythema, pruritis, edema, necrosis, sloughing of skin

237
Q

What is the MOA of avocado?

A

cardiotoxicity in goats, horses, rabbits, and caged birds - noninfectious mastitis and agalactica in cattle, horses, goats, and rabbits

238
Q

What is the MOA of black walnut?

A

ingestion of fresh shavings made from heartwood causes laminitis

239
Q

What is the MOA of forage induced photosensitization plants?

A

secondary photosensitization due to liver damage, forage induced photosensitization in cattle due to cholestatic liver disease

240
Q

What are the clinical signs of forage induced photosensitization plant toxicity?

A

lacrimation, photophobia, erythema, pruritis, edema, necrosis, sloughing of skin

241
Q

What is the MOA of grape/raisin toxicity?

A

unknown toxin causes acute renal failure only in dogs, amount ingested 9oz-2lb per dog

242
Q

What are the clinical signs of grape/raisin toxicity?

A

GI, vomiting, acute renal failure

243
Q

What is the MOA of lily?

A

unknown toxin causes nephrotoxicity only in cats, GI irritation in cats and dogs - two leaves can poison cats!

244
Q

What are the clinical signs of lily toxicity?

A

GI signs, salivation, vomiting, depression, anorexia, PU, anuria, death by renal failure

245
Q

What is the MOA of pigweed?

A

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
Q

What clinical signs are seen with pigweed toxicity?

A

hypocalcemia, depression, weakness, incoordination, renal failure

247
Q

What is the MOA of red maple?

A

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
Q

What are the clinical signs of red maple plant toxicity?

A

anorexia, depression, anemia, icterus, brown discoloration of mm, hemoglobinuria, dyspnea, cyanosis, death

249
Q

What is the MOA of senna plants?

A

unknown myotoxin causes skeletal muscle myopathy and cardiomyopathy, seeds most toxic, anthraquinone glycoside is cathartic

250
Q

What are the clinical signs of senna plant toxicity?

A

diarrhea/constipation, muscle weakness, recumbency, good appetite, myoglobinuria, coffee colored urine, tachycardia, death

251
Q

What is the MOA of yellow stathistle and russian knappweed plants?

A

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
Q

What are the clinical signs of yellow stathistle and russian knappweed plant toxicity?

A

sudden onset inability to eat/drink, drowsiness interrupted by excitation, head down, dehydration

253
Q

What is the MOA of macadamia nuts?

A

unknown and unknown toxin

254
Q

What are the clinical signs of macadamia nut toxicity?

A

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
Q

What are the sources of toad toxins?

A

cane or marine toad, colarado river toad - catecholamines and seotonin

256
Q

What species are affected by toad toxicity?

A

dogs > cats, ferrets

257
Q

How are toxins in toad toxicity absorbed?

A

from mm of mouth, gastric mucosa, conjunctiva, open skin wounds

258
Q

How are toad toxins distributed?

A

all over body including CNS

259
Q

How are toad toxins metabolized and excreted?

A

metabolized by MAO and COMT enzymes and undergo neuronal reuptake, eliminated in urine

260
Q

What is the MOA of toad toxins?

A

direct irritation, inhibit Na/K ATPase, hallucinogenic effect, vasoconstrictor

261
Q

What are the main organs effected in toad toxicity?

A

heart, blood vessels, CNS

262
Q

What are the clinical signs of toad toxicity?

A

onset in a few mins, irritation, hyper salivation, brick red mm, vocalization, vomiting, neuro signs, cardiovascular signs

263
Q

What is the treatment of toad toxicity?

A

flush mouth with water, activated charcoal, control seizures, atropine for bradycardia, supportive care

264
Q

What US states have copperhead snakes?

A

everywhere except alaska, maine and hawaii

265
Q

What species are exposed to snake toxicity?

A

dogs> cats, horses

266
Q

What is the MOA of snake toxicity?

A

hyaluronidase causes venom to spread, phospholipase A2 disrupts cell membranes, uncouples phosphorylation and releases vasoactive amines, hematoxic, cardiotoxic, neurotoxic, hypocoagulation

267
Q

What are the clinical signs of snake note toxicity?

A

rapid or delayed, edema, swelling, petechiation, necrosis

268
Q

How do you treat snake note toxicosis?

A

don’t touch site, makes absorption increase, IV catheter, monitor, polyvalent crotalid anti venom, diphnhydramine IV, fluids, blood transfusion,

269
Q

What is the MOA of amphetamine toxicosis?

A

CNS stimulant, blocks reuptake of NE and dopamine, inhibits MAO, excitatory receptor agonist

270
Q

What are the clinical signs of amphetamine toxicosis?

A

hyperactivity, restlessness, circling, tremors, hypersalivation, some animals show depression

271
Q

What is the treatment for amphetamine toxicosis?

A

emesis, activated charcoal, pentobarbital/propofol for seizures, treat hyperthermia, fluids, urinary acidifiers

Toxicology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions