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47 Cards in this Set
- Front
- Back
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What is the toxin that causes acute bovine pulmonary emphysema (fog fever)?
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3-MI
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When do animals normally get acute bovine pulmonary emphysema?
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Cattle moved from marginal pasture in fall or spring to lush pasture
Lush pasture Contains more tryptophan -Rumen microbes not adapted to L-tryptophan--> 3- methylindole---> lung damage |
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What's the MOA of 3-MI?
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Damages pneumocytes
Proliferation of fetal type II Pneumocytes Type II pneumocytes have more gas diffusion distance--> fluid in alveoli |
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What is the main clinical sign of 3- MI toxicity?
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Acute respiratory distress syndrome within 2 weeks of pasture change
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Do bovine with acute bovine pulmonary emphysema cough?
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No, or minimal coughing
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What are 6 clinical signs of acute bovine pulmonary emphysema?
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1) Acute respiratory distress syndrome
2) "dyspnea" 3) Expiratory grunt or groan 4) Frothing from mouth 5) Open mouth breathing 6) Entire lung field involved |
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What are 4 pathologies associated with acute bovine pulmonary emphysema?
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1) Lungs wet and heavy---> pulmonary alveolar edema
2) Pulmonary interstitial emphysema 3) Hyalin membranes 4) Type II pneumocytes |
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How do you diagnose acute bovine pulmonary emphysema?
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History of change to lush pasture
-no specific lab changes |
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Why do you have to be VERY careful about treating cows with acute bovine pulmonary emphysema?
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Stress of handling the animal may kill them more than treatment will save them
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What are 4 possible components of treating acute bovine pulmonary emphysema?
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1) Remove from pasture
2) Flunixin meglamine (banamine) 3) Corticosteroids, dexamethasone 4) Atropine?? |
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What are 5 ways you can prevent acute bovine pulmonary emphysema?
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1) Place in dry lot on hay a few days before putting on pasture
2) Limit pasture to a few hours during first few days 3) Cut pasture first 4) Delay pasture until 1st frost 5) Strip grazing |
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What are 5 toxins that cause atypical interstitial pneumonia or proliferative pneumonias?
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1) Purple mint
2) Moldy sweet potatoes 3) Silo gases, NO2 4) Fungus contaminated plants 5) Brassica spp. ??? |
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What is the mold that produces the toxin that causes moldy sweet potato toxicity? what is the name of the mycotoxin?
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Fusarium solani produces mycotoxin furanoterpenold toxin
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What are the 4 clinical signs of proliferative pneumonia caused by moldy sweet potato toxicity?
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1) Could be pasture or stabled
2) Severe dyspnea 3) Often a grunt at end of expiration 4) Entire lung are involved -abnormal lung sounds -**not just cranial ventral as w/ broncho-pneumonia |
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How do you diagnose moldy sweet potato toxicity?
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History of consuming plant
Lungs look like ABPEE |
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Why do you have to be very very careful when treating animals with moldy sweet potato toxicity?
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Don't stress the animal into death due to hypoxia
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What drugs can you use to treat moldy sweet potato toxicity?
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Flunixin megalamine (banamine)
Corticosteroids, dexamethasone |
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What is the source of paraquat and diquat?
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Commonly used dipyridyl herbicide that kills vegetation by inhibiting photosynthesis
-only used by licensed applicators |
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What is the most common circumstance of paraquat toxicity in people & animals?
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Involves ingestion of concentration formulations
-hateful poisoning w/ meatballs |
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In dogs, only about 25% to 28% of orally administered paraquat is absorbed and the remainder is _________.
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Excreted unchanged in feces
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What is the mode of action of paraquat?
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Absorbed paraquat undergoes extensive cyclic oxidation-reduction reactions in mammalian tissues, this redox cycling produces oxygen & hydroxyl and the ensuing *****free radical mediated damage to cellular macromolecules
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**What macromolecule is most affected by free radical damage from paraquat metabolism and therefore responsible for most of the toxic effects?
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**Membrane lipids
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The ______ (organ) selectively accumulate paraquat, and therefore contain higher concentrations than other tissues.
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Lungs
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What damage is done to the lungs from paraquat poisoning?
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Selective accumulation of paraquat develops into pulmonary edema & other lung damage, leading to fibrosis
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What is the primary cause of death due to high doses of paraquat?
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Death occurs 1-4 days after ingestion due to a combination of acute pulmonary edema****** and other things..
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What are the clinical signs of subacute paraquat toxicity?
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Poisoning w/ a slower onset of organ failure and eventual death from pulmonary edema and respiratory failure
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What are the clinical signs of low doses of paraquat?
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Late, irreversible pulmonary fibrosis syndrome w/ death ensuing several days to several weeks after exposure
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What is the primary pathophysiology of tissue damage from paraquat toxicity?
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Selective paraquat accumulation sites
-contact of mucosal surfaces & skin w/ concentrated paraquat solutions may result in marked tissue damage |
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How is paraquat toxicity usually diagnosed?
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Combination of *clinical history, results of a *histologic examination of affected tissues & detection of paraquat in tissue or bait samples
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What are the primary lesions related to paraquat toxicity?
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Pulmonary edema
Renal failure |
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What is the treatment for paraquat toxicity?
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No specific antidote
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What is the prognosis of paraquat toxicity?
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Overall prognosis=POOR
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What is diquat?
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A rapidly acting contact herbicide used to control aquatic weeds * destroy potato halums before harvesting
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What are some common formulations of diquat?
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Liquids, aqueous concentrates, water soluble mixtures w/ paraquat
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True or false. Diquat accumulates in the lungs.
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False, no affinity for lung tissue- that is paraquat
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What organs take up diquat?
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GI tract, liver & kidney
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With minimal toxic concentrations diquat can produce signs in ___ days in cattle and ____ days in sheep.
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8 days= cattle
3 days= sheep |
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What are the clinical signs of diquat toxicity? (5)
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Anorexia, vomiting, diarrhea, GI distention, severe loss of water into lumen of GI tract
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High exposure to diquat concentrations will elicit _____ damage & accumulate in the _____.
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Elicit liver damage
Accumulate in kidneys |
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True or false. Diquat is not cumulative in body tissues.
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True
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What is usually the most helpful diagnostic aid for diquat toxicity?
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History of diquat herbicide exposure
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What clinical pathology will you see with diquat toxicity?
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ALT increased w/ liver damage
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What are 2 components of diquat treatment?
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1) Decontaminate
2) Supportive therapy -diuresis w/ mannitol or furosemide may be helpful |
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In diquat poisoning the main problems are associated with _____ and ______ damage.
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Brain & kidney
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*What should you avoid using for treatment of a patient with diquat toxicity?
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Oxygen is contraindicated early in diquat poisoning
-oxygen administration may cause increased formation of oxyradicals |
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What are 3 ways to decontaminate an animal with diquat toxicity?
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1) Induce emesis w/in 30-60 m
-in DOGS 2) Perform gastric lavage -in DOGS 3) Administer adsorbent |
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What is the prognosis of diquat toxicity?
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Guarded to poor w/ high levels
Animals have a good prognosis for recovery in 1-2 weeks w/ prompt treatment |
