Exam 2 Flashcards
T/F Some oils contain chlorinated naphtalenes and can cause bovine skin hyperkeratosis
TRRUUUUEEE
Which has more toxicity, petroleum products with high or low boiling points?
low boiling points (and low viscosity, surgace tension) have more pneumotoxic effects and impaired respiration
Short chain aliphatics have ____ toxicity
low
Long chain aliphatics cause
aspiration pneumonia
Chlorinated aliphatic hydrocarbons cause toxicity on
the CNS
aromatic hydrocarbons cause
bone marrow suppression
What species are most susceptible to crude petroleum substances?
cattle
Toxicokinetics of petroleum
- absorbed from GI mucosa, skin and inhalation
- absorption is inversely proportional to molecular weight
- polycyclic aromatic hydrocarbons are more readily absorbed than aliphatic hydrocarbons
MoA of Petroleum
aspiration pneumonia or chemical pneumonitis
Lab dx of petroleum toxicity
oil in feces will float
anemia, leukopenia, thrombocytopenia
rads- aspiration pneumonia
Can you give emetics, gastric lavage or glucocorticoids to tx petroleum toxicosis?
No
T/F Fluoride is a normal constituent of forages
True, especially legumes
Which part of the plant accumulates large amounts of fluoride?
Herbaceous parts (not seeds)
Fluoride has a strong affinity for ______
calcium
T/F Acute fluoride toxicosis is most common
False- chronic is more common
MoA of acute fluoride toxicosis
*caustic effect on GI mucosa
*Inhibition of mitochondrial enzymes
hypocalcemia
coag defect
increased capillary permeability
MoA of chronic toxicosis
alteration and delaying mineralization of teeth
Clinical signs associated with chronic fluoride toxicosis
lameness, bony protrusion on legs
spontaneous fractures
teeth look nasty
emaciation, rough hair coat
What is the best specimen for chemical analysis of fluoride toxicosis?
bone
What is the most dangerous sewage gas?
H2S
MoA of H2S
direct irritation of mm
inhibition of cellular respiration by inhibiting cytochrome oxidate
stimulation of chemoreceptors of the carotid body interfering w/ resp drive (hypernea -> breathe off all its CO2-> recover or die from asphyxiation)
Clinical signs of H2S toxicity
collapse, cyanosis, dyspnea, anoxic convulsions, rapid death
lower conc signs of irritation to ocular, resp mucosa and lungs as in pneumonia
MOA of CO
CO combines w/ hemoglobin to form carboxyhemoglobin which can’t carry O2 -> death from hypoxia
Lesions w/ CO
blood- bright red
mm- pink
(won’t always see this though)
MoA for Nitrogen oxide gases
direct irritation of mm -> soluble so can pass through upper resp tract and cause damage to lungs -> lung damage -> death from hypoxia
CS/Lesions for nitrogen oxide gases
Resp signs (similar to ammonia poisoning) pulmonary edema, cyanosis, methemoglobinmeia
Tx for nitrogen oxide gases
methylene blue IV (for methemoglobinemia)
supportive tx
ointments for mm
MoA of smoke inhalation
simple aphyxiants displace O2 in air
chemical asphyxiants prevent uptake of oxygen
irritants obviously irritate things
T/F Sulfur dioxide adheres highly to soot
T
3 things that increase toxicity in Paraquat poisoning
vit e/sel deficiency
decreased tissue glutathione
O2 therapy
Lesions w/ Paraquat/Diquat toxicity?
lingual ulcers
lungs look like liver- hepatization
Which is more susceptible to urea poisoning, equine or bovine?
ruminants/bovine
The usual concentration of urea is ___ % of the grain ration and ___% of the total ration
3 % grain
1% total ration
T/F Urea toxicosis has no characteristic lesions
true
What’s the best sample to send in for lab dx of urea poisoning?
vitreous fluid
2-4D are cattle or dogs more sensitive
dogs
What lab values will be increased with 2-4 D poisoning?
ALP, LDH, CPK