R E V I E W Flashcards
What is the “Threshold dose”?
Dose that is less than or equal to no detrimental effects measured
What is the most common route of toxicant exposure?
Oral (ingestion)
What is a dispositional antidote and what is an example?
Dispositional antidote alters the absorption of toxin, making it less available to tissues (activated charcoal)
0.30% = ____ ppm
3,000
KNOW ALL OF THE CALCULATIONS
!!!
What are the sources of nitrate? When are the levels the highest?
Sources are plants and commercial fertilizers or stored feces, accumulate in vegetative tissue, highest levels are just before flowering
What is an example of nitrate plant?
Forage Sorghum.
Also corn, wheat, oats, soybeans. Bermuda grass, Hay grasses and some weeds
Desiccation (wilting) of a plant will lower nitrate level of that plant. T/F
False!!! Will increase levels
Ruminants are the most susceptible to ____ toxicosis because the conversion of it in the rumen
Nitrate… they convert nitrate to nitrite in the rumen (which is the more toxic form)
Clinical signs of Nitrate poisoning….
Cyanosis, brownish cast to mm and dark, chocolate colored blood
Nitrate poisoning diagnosis—>
Weakness +/- hypoxia and chocolate brown blood
Tx of Nitrate toxicity:
Methylene blue
What test is done in the field for nitrate levels by testing the forages???
Diphenylamine test
Excess copper evaluation is done by this ratio..; what level is considered dangerous???
Cu:Mo ratio
>25:1 is dangerous
What’s the gold standard of testing for Copper toxicosis?
Liver biopsy
Copper toxicosis on necropsy will show this….
Gun metal blue kidneys, enlarged black/brown liver and spleen. Pale organs
Clinical signs of sulfur:
Violent purgation, colic, “Muddy” mucous membranes, ADR/lethargy
Necropsy shows what with sulfur toxicosis???
GI issues, congested liver and kidneys, excessive gas in GI tract (rotten egg smell bc of hydrogen sulfide)
Sulfur toxicosis in cattle is from _____ and ___ ____
Pasture and water sources (with high sulfate contents)
Signs assoc. sulfur = what condition?
signs assoc. with PEM (Polioencephalomacia)
What are the diagnosis of sulfur toxicosis:
Look at environment, do a full PE, check for lead poisoning
Treatment of PEM from sulfur toxicosis:
Thiamine, remove the animals from the possible source
Sodium Ion toxicosis water deprivation– Salt toxicity is directly related to low ____ _______. What species are most sensitive?
water consumption; swine are most sensitive
Clinical signs from sodium ion toxicosis/water deprivation:
Head pressing, disorientation, aimlessly walking/circling, blindness, dog sitting, paddling/seizures, death eventually
Pigs with salt poisoning = _____ ______
Eosinophilic meningoencephalitis
COWS LOVE ____
ARSENIC
Arsenic toxicosis:
Inorganic forms include:
!!!More toxic!!!!
Pesticides, insecticides, herbicides, cotton defoliants, insulation materials, and wood preservatives
Arsenic toxicosis:
Organic forms:
Herbicides (cacodylic acid, MSMA and DMSA) and feed additives
What are “The 3 D’s” associated with arsenic toxicosis?
Diarrhea, dehydration, death
Beside the 3 D’s, which also occurs as a clinical sign with arsenic toxicity?
Neuro signs
What is the Tx of arsenic toxicosis?
Activated charcoal, oil demulcents, FLUIDSSS!!!, sodium thiosulfate, dimercaprol (BAL)
Clinical signs of Mercury; what is the TX?
Stomatitis, loosening of teeth, ulcers, keratinization; no TX
Sorghum species and fruits are sources of ____
Cyanide (Prussic acid)
Cyanide/Prussic acid often follows ____ of plants
wilting
MM will be bright red with _____ poisoning
Cyanide
Cyanide toxicity signs—>
Bright red blood that clots slowly. Rumen contents will smell like “bitter almonds”.
Tx for cyanide poisoning—>
Sodium thiosulfate IV and repeat as needed. Also supportive care (O2) repeat as needed and may also have to do MB
Cyanide testing:
freeze lab sample to prevent further hydrolysis. DO A PICRATE test- test will turn bright yellow in presence of cyanide
Ionophore toxicity clinical signs:
Pulm. congestion, pleural effusion, cardiac necrosis, meningeal congestion
All mycotoxins are ______
Immunosuppressants
Mycotoxins often present as ___, subacute or ____ conditions.
Vague; chronic
Fusarium includes what subcategories?
Deoxynivalenol, Zearalenone, T2 toxin, Fumonisin
What are included as subcategory for Aspergillus?
Aflatoxin
What is a subcategory of Penicillium?
PR toxin
Aflatoxin- what is the primary organ that is targeted? What does this cause?
Liver is the primary target organ, leads to loss of proteins, improper antibody formation and decreased clotting factors. In humans, it is possible carcinogenic
Public health concerns involving Aflatoxin–>
Carcinogens, milk is monitored closely for M1 metabolites, 20ppb in feed is the legal limit
Fusarium toxins include:
Deoxynivalenol (T2 or DON) and Zearalenone (estrogenic effects)
Zearalenone mode of action:
functions as a weak estrogen and inhibits secretion and release of GnRH
Zearalenone causes what clinical signs in open/non pregnant young livestock?
Mammary enlargement
What species is most susceptible to Trichothecenes (T2, Don, or Vomitoxin)??
Cats
Trichothecenes lab diagnosis is what?
Anemia and leukopenia
Fumonisins cause….
Equine leukocephalamalacia
Ergotism MOA:
Initiates the contraction of smooth muscle and causes vasoconstriction, resulting in terminal necrosis of extremities. Inhibits release of prolactin (DMI and milk production DECREASES)
What are the clinical signs of Ergotism???
Psychoactive, abortions, paralysis, GI issues, gangrene of extremities, death
Xylitol aka ___ ____
Birch sugar
Xylitol primary target organ is ____ with indirect _____
Pancreas; hepatotoxicity
Xylitol MOA:
Stimulation of the pancreas to release insulin in a dose-dependent manner, causes hypoglycemia
Where is insulin stimulated for glucose intake?
Skeletal muscles (mostly) and some in adipose tissues
Is activated charcoal an effective tx for xylitol toxicity?
No because does not bind to the Xylitol
Cycad (sago palm) toxins are concentrated in _____
Seeds
Cycad (sago palm) toxin principles….
Cycasin
Microcystis aeruginosa aka
Blue green algae
What is the toxic principal of Microcystis aeruginosa???
Microcystin as a cyanotoxin
Microcystis aeruginosa TX–>
Cholestyramine (ion exchange resin)
Amanita phalloides (deadly amanita, death angel) Toxic principle and 3 clinical phases:
Toxic principle is Amanitins and phalloidins Clinical phases (in this progression/order): GI---> Hepatic --> Hepatorenal
What are the TX for Amanita?
SAM-e hepatoprotectants
Xanthium strumarium (cocklebur) and X. spinosum (sheepbur): what are the toxic parts?
Seed and seedlings in cotyledon stages
Xanthium strumarium (cocklebur), what is the toxin that is also a plant growth inhibitor?
Carboxyatractyloside is the toxin
X. Straumarium (cocklebur) most sensitive species is _____
Pigs (anddd then sheeps)
_______ plants are not toxic themselves but their metabolism in the body makes them toxic
PA plants
Chronic dietary exposure to this plant = PA toxicosis
Common ragwort/ragweed/ Senecio jacobaea
Ricinus communis is the castor bean plant and its seeds look like ticks. What is the toxic compound?
Phytotoxin (ricin)
Tetradymia toxin is:
Furanosesquiterpenes
Know mushroom stuff and bugs/stings/snakes lecture
!!!
Ionophores unique clinical signs-
rumensin (heart and skeletal musc. affected)
Bovatex (heart and pulm. system affected)
Lead toxicity unique clinical signs are….
Non regen. anemia, roaring, CNS issues, wing drop
Zinc toxicity unique clinical signs….
Intravascular regenerative hemolytic anemia and hemolysis
remember calculations
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