Lecture 22 Flashcards

(41 cards)

1
Q

What are the general characteristics of organophosphates and carbamates?

A

-wide variety of products
-some products are so safe they are directly applied to animals
-others are considered weapons of mass destruction due to danger levels

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2
Q

What is the pathophysiology of OP/carbamate toxicity?

A

-inhibit acetylcholinesterase enzymes in nervous and muscle tissue
-effect is excess ACh and overstimulation of post-synaptic neuron or muscle
-OP induces irreversible AChE binding; must produce all new AChE to recover
-carbamates bind AChE reversibly

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3
Q

What are the muscarinic clinical signs of OP toxicity?

A

-salivation*
-lacrimation*
-urination*
-diarrhea*
-miosis
-vomiting
-colic
-dypsnea

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4
Q

What are the nicotinic clinical signs of OP toxicity?

A

-muscle fasciculation
-weakness

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5
Q

What are the CNS signs of OP toxicity?

A

-nervousness
-ataxia
-apprehension
-seizures

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6
Q

What causes death due to OP toxicity?

A

-respiratory collapse
-continuous seizures

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7
Q

How is OP toxicity diagnosed?

A

-history and clinical signs
-measurement of AChE inhibition activity in blood or brain tissue
-measurement of OP/CM compounds in feed, stomach/rumen contents, or tissues

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8
Q

What are the two main treatments for OP toxicity?

A

*atropine:
-muscarinic ACh receptor blocker
-doses repeated to effect
-stop dosing when pupils re-dilate, salivation stops, and animal brightens

*2-PAM:
-reactivates AChE
-want to give as soon as possible
-best used for OP toxicity only; not CM

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9
Q

What other treatments can be used in the case of OP toxicity?

A

-decontamination; stomach evacuation if under 2 hours, activated charcoal if over 2 hours
-bathing in dermal contact cases
-diazepam to reduce muscle tremors and seizures
-anesthesia and barbiturates to control seizures
-ventilation

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10
Q

What are the general characteristics of pyrethrins/pyrethroids?

A

-come from chrysanthemums
-pyrethrins are natural derivatives; pyrethroids are synthetic derivatives
-pyrethroids are more toxic
-typically combined with piperonyl butoxide
-oral route is worse than topical

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11
Q

What is the pathophysiology of pyrethroid toxicity?

A

-force sodium channels to remain open longer
-sodium channels kept open produce hyper-excitable neurons
-chloride, calcium, and GABA channels are also impacted

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12
Q

What are the clinical signs of pyrethroid toxicity?

A

-salivation
-vomiting
-hyperexcitability
-muscle fasciculation
-weakness
-seizures
-dyspnea
-recumbency
-death

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13
Q

Which systems can be affected by chronic pyrethroid exposure?

A

*pre-pubertal females:
-disruption of reproductive endocrine function
-disruption of reproductive development

*adult bulls:
-poor sperm production in bull studs

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14
Q

How is pyrethroid toxicity diagnosed?

A

-history and clinical signs
-measurement of insecticide residues in tissue or blood

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15
Q

What is the treatment for pyrethroid toxicity?

A

-most signs resolve with time
-symptomatic/supportive care; esp. seizure control
-activated charcoal
-avoid oil-based oral treatments
-bathing for dermal exposures

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16
Q

What are the characteristics of organochlorines?

A

-among the most ecologically toxic chemicals ever used
-most are banned from use in the US; may still be able to get lindane lice treatment
-class that contains DDT

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17
Q

What is the pathophysiology of organochlorine toxicity?

A

-general CNS stimulants
-alter the polarization of the neuron and reduce the excitation threshold; easier for neuron to fire
-prevent GABA from binding its receptor; prevents inhibition of excitatory signals

18
Q

How do organochlorines affect birds?

A

bioaccumulate in fat and affect egg shell thickness

19
Q

What are the clinical signs of organochlorine toxicity?

A

-salivation
-vomiting
-hyperexcitability
-ataxia
-tremors
-apprehension
-seizures
-abnormal movements

20
Q

How is organochlorine toxicity diagnosed?

A

-history and clinical signs
-measurement of toxin in blood or tissue
-fat biopsy is a relevant sample due to accumulation

21
Q

What is the treatment for organochlorine toxicity?

A

-symptomatic and supportive care
-seizure control
-activated charcoal
-bathing and clipping hair
-REPORT; OCs are tightly regulated in US

22
Q

What are the characteristics of neonicotinamides?

A

-used in flea/tick medications and crop applications
-class of insecticide considered safe for non-target species
-includes imidacloprid, dinotefuran, and nitenpyram

23
Q

What is the pathophysiology of neonicotinamide toxicity?

A

binds post-synaptic nicotinic receptors

24
Q

What are the clinical signs of neonicotinamide toxicity?

A

-neuro. signs
-depression
-tremors
-impaired pupillary function
-ataxia
-hypothermia
-death
-hepatotoxicity

25
How is neonicotinamide toxicity diagnosed and treated?
*diagnosis: -history and clinical signs -measurement of compound in blood *treatment: -supportive care -mild cases resolve with time
26
What are the characteristics of paraquat?
-desiccant used on crops -toxic only in immediate exposures -inactivated when dry or bound to soil compounds -use is restricted by permit
27
How do animals become exposed to paraquat?
-contact with improperly stored concentrates -aerial drift directly onto animals or their pastures while still wet
28
What is the pathophysiology of paraquat toxicity?
-selectively concentrated by alveolar epithelial cells -induces free radical formation and oxidative change -snowball effect; injury leads to more injury until acute resp. distress syndrome and fibrosis occur
29
Which conditions result from paraquat toxicity?
-ARDS -interstitial pneumonia
30
What are the clinical signs of paraquat toxicity?
-dyspnea -pulmonary edema -cyanosis -lingual ulcers -death up to 30 days after exposure; ARDS acutely, fibrosis later on
31
How is paraquat toxicity diagnosed?
-history and clinical signs -measurement of compound in blood and tissues
32
What is the treatment for paraquat toxicity?
-selenium and vitamin E -anti-inflammatories/steroids -diuretics -mannitol diuresis -avoid O2 and excessive fluid admin. -activated charcoal
33
What are the characteristics of glyphosphate?
-associated with non-Hodgkin's lymphoma in people -farm workers at greater risk -general exposure risk is unknown -follow labels, wear gloves, and only use it on calm, dry days
34
What are the characteristics of petroleum?
-livestock mostly encounter petroleum products through ingestion -crude oil is classified as light or heavy oil -light oil contains more volatile compounds like gasoline, kerosene, diesel, and naphtha -more volatile compounds are more toxic -livestock like the taste and willingly consume it
35
What is the pathophysiology of petroleum toxicity?
directly caustic and toxic to many cell types -CNS -renal -repro -resp. -GI -cardiac -hepatic
36
What are the acute signs of petroleum toxicity?
-bloat -emesis -bloody diarrhea -oily feces -petroleum odor to breath and feces -weakness -ataxia -depression -hyperthermia -dyspnea
37
What are the subacute signs of petroleum toxicity?
-depression -pneumonia -anorexia -constipation -ileus -recumbency -abortion -weight loss -lethargy -petroleum odor to breath and feces
38
What are the chronic signs of petroleum toxicity?
-lethargy -anorexia -weight loss/poor condition -poor repro. -chronic cough -abortion -laminitis -chest/abdominal pain -cachexia
39
How is petroleum toxicity diagnosed?
-history and clinical signs -gasoline odor to breath -measurement of compounds in rumen fluid, blood, or feces
40
What are the clin. path. findings in the case of petroleum toxicity?
*elevated liver enzymes -AST -GGT -SDH *elevated BUN and creatinine
41
What is the treatment for petroleum toxicity?
-supportive care for pet animals -activated charcoal -euthanasia -lifetime withdrawal for meat or milk from affected animals