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Veterinary Toxicology > Final > Flashcards

Final Flashcards

1
Q

What is equine leukoencephalomalacia?

A

It is a condition caused by fumonisins, a mycotoxin produced from moldy corn

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2
Q

What is the main adverse affect of fumonisins?

A

They are hepatotoxic

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3
Q

What are the clinical signs of equine leukoencephalomalacia?

A
  1. Blindness
  2. Head pressing
  3. Aimless walking
  4. Stupor
  5. Glossopharyngeal paralysis
  6. Delirium
  7. Recumbency
  8. Seizures
  9. Death
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4
Q

Fumonisins cause ______ morbidity and _______ mortality in ________.

A

Low
High
Horses

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5
Q

What are the lesions that equine leukoencephalomalacia cause?

A

Subcortical white matter necrosis- can be bilateral or unilateral

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6
Q

What toxins can cause blindness in animals?

A
  1. Lead-Cattle
  2. Ivermectin
  3. Pyrethrins-Dogs/cats
  4. Metaldehyde-
  5. Fumonisin
  6. Salt
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7
Q

What substrate will grow fumonisin?

A

Corn

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8
Q

Why is fumonisin a public health concern? Aflatoxin?

A

It can cause esophageal cancer in humans

Alflatoxin is carcinogenic

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9
Q

How would you confirm a case of equine lueikoenceaphcalomalacia from fumonisin?

A

Screen corn by analyzing representative samples

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10
Q

What nicotinic products are the most hazardous and why?

A

Liquid cartridges and refills for e-cigarettes as they have concentrated levels of up to 2,000mg

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11
Q

What are the clinical signs of a nicotine toxicity?

A
  1. Vomiting
  2. Hyperactivity
  3. Tremors
  4. Seizures
  5. Respiratory paralysis leading to death
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12
Q

How long is the nicotine half life?

A

Short

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13
Q

How do you diagnose a nicotine toxicity?

A

Nicotine residues

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14
Q

What is the treatment for nicotine toxicity?

A

It is patient dependent, but should decontaminate with lavage/AC, control the CNS excitation and give oxygen support.

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15
Q

Which receptors does nicotine bind to?

A

Nicotinic acetylcholine receptors in the parasymphathetic and sympathetic nervous system

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16
Q

Which genetic issue is involved with ivermectin?

A

MDR1 (ABCB1) mutation in some dogs

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17
Q

Which species should you never use ivermectin in?

A

Turtle

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18
Q

What is the MOA of the MDR1 (ABCB1) mutation?

A

P-glycoprotein isn’t produced, so drugs can’t get pumped out of the blood brain barrier and end up staying in the CNS. In addition, the drug accumulates in the bile and kidney instead of being secreted.

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19
Q

If a dog has a MDR-1 mutation, what do you need to be aware of?

A

They can have multiple drug resistance, not just to ivermectin.

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20
Q

The half life of ivermectin varies in length due to three factors, what are these?

A
  1. Sensitive/non-sensitive patient

2. Hezterozygote or homozygote

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21
Q

What is the mechanism of action of ivermectin?

A

It targets the GABA and glutamate-gated chloride channels releasing inhibitory neurotransmitters.

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22
Q

What are the clinical signs of an ivermectin toxicity?

A
  1. Depression
  2. Lethargy/weakness/recumbency
  3. Tremors (high dose)
  4. Seizures (high dose)
  5. Reversible blindness
  6. Coma leading to death
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23
Q

How long can the clinical signs last with ivermectin toxicity?

A

Hours, days to weeks as it is hard to predict

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24
Q

A client tells you that she gives her horses oral ivermectin twice a year and now her dog is showing signs of depression, lethargy, recumbency and blindness. What may be going on?

A

Ivermectin toxicity

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25
Q

How would you chemically confirm an ivermectin toxicity?

A

You can only confirm exposure, but can use fat, liver, bile, feces and serum samples

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26
Q

What is the treatment for an ivermectin toxicity?

A
  1. Decontaminate with AC
  2. Aggressive supportive care
  3. Physostigmine (dogs/cats)
  4. IV lipid therapy
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27
Q

What is the prognosis of an ivermectin toxicity?

A

Most recover over 24 hours to 31 days and the severity of signs is not a good predictor of prognosis unless there are uncontrollable seizures.

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28
Q

What can you use physostigmine for?

A

Treatment for larkspur plant toxicity and ivermectin toxicity

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29
Q

Will IV lipid therapy help an animal with the MDR1 mutation that was given too much ivermectin?

A

It may not

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30
Q

An animal can experience salt toxicity if one of the following three circumstances are met…what are they?

A
  1. TOO much SALT intake
  2. TOO much SALT intake with WATER DEPRIVATION
  3. WATER DEPRIVATION
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31
Q

If ingested, which products can cause hypernatremia in animals?

A
  1. Whey
  2. Electrolyte supplement
  3. Play dough
  4. Ice melts
  5. Mixing errors
  6. If used as an emetic
  7. Crafts
  8. Ingesting sea water
  9. Paint balls
  10. Single or repeated AC doses
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32
Q

If a dog drinks too much water right after being hypernatremic, what can this cause?

A

Salt toxicity

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33
Q

What is the mechanism of salt toxicity?

A

Na is passively diffused into the CSF and neurons which leads to inhibition of glycolysis. Without the energy, active transport of Na won’t occur out of the CSF and neurons. Water then follow the Na into the CSF. The second the patient rehydrates, more water will follow the Na and cause cerebral edema and hemorrhage.

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34
Q

What are the clinical signs of salt toxicity?

A

CNS signs like wandering, circling, head pressing, blind, dog sitting, tremors, seizures, excessive thirst, vomiting, and death.

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35
Q

What pathological lesion will you see in pigs suffering from salt toxicity?

A

Eosinophilic meningoencephalitis

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36
Q

What are the clinical lesions associated with salt toxicity?

A
  1. Cerebral edema

2. Cerebral malacia

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37
Q

What tips off when taking a history would lead to a salt toxicity problem?

A
  1. Lack of water
  2. New feed
  3. Access to high salt sources
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38
Q

How could you confirm a salt toxicity?

A

Need to know the fluid/hydration status in order to interpret Na numbers that you see in the serum, CSF, and cerebrum..also look for lesions.

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39
Q

How do you treat a salt toxicity?

A
  1. SLOW rehydration
  2. Remove the source
  3. DO NOT GIVE ACTIVATED CHARCOAL
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40
Q

What are the 6 most common problems with mushroom ingestion?

A
  1. Gastroentertitis
  2. Muscarinic signs
  3. CNS excitation
  4. CNS depression
  5. Liver disease
  6. Renal disease
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41
Q

Which clinical sign is present with any mushroom ingestion?

A

Gastroenteritits

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42
Q

When dealing with a mushroom toxicity, what should you focus on?

A
  1. Preventing liver and renal disease
  2. Monitoring for CNS excitation/depression
  3. Treating muscarinic and gastroenteritis clinical signs
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43
Q

How would you treat an animal that ate muscarine mushrooms?

A
  1. Decontaminate via emesis and AC/sorbitol
  2. Administer atropine and maropitant to stop the vomiting
  3. Chem panal to establish baseline
  4. GI and Liver protectants
  5. Follow up chem penal at 48 hours and renal recheck in 10 days
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44
Q

How could you confirm the type of mushroom you are dealing with?

A

Email images and location to a mycologist so they can identify it

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45
Q

What kind of grass contains an endophytes that can contain ergovaline?

A

Tall fescue

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46
Q

What is the MOA of ergovaline?

A

Peripheral vasoconstriction and suppressing of prolactin secretion in large animals

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47
Q

What are the three syndromes that can be caused by fescue poisoning? What species and what time of year is this most likely to occur?

A
  1. Summer slump-cattle-summer
  2. Fescue foot-cattle-winter
  3. Reproductive problems-horse/ruminants-anytime of year
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48
Q

Why does fescue poisoning cause summer slump?

A

Vasoconstriction from the ergovaline leads to hyperthermia which leads to decreased feed intake, loss of body weight/condition, and abortions

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49
Q

Why does fescue poisoning cause fescue foot?

A

Vasocontriction from the ergovaline leads to ischemia necrosis and dry gangrene of the distal extremities and ears/tail, also causes abortions

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50
Q

Why does fescue poisoning lead to reproductive problems in horses and ruminants?

A

The suppressions of prolactin prolongs gestation leading to dysmature foals, agalactia and abortions.

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51
Q

How can you diagnose fescue poisoning?

A

Testing the hay or urine for ergovaline

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52
Q

What is domperidone used for?

A

its a dopamine antagonist that is used to treat summer slump and reproductive issues stemming from fescue poisoning.

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53
Q

What is the toxic principle of ergot?

A

Ergopeptide alkaloids:

  1. Ergotamine
  2. Ergonovine
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54
Q

You see a sclerotia body in grain, what is it?

A

Ergot, a mycotoxin

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55
Q

What can ergotamine and ergonovine do to the body of large animals? Which large animals?

A

Peripheral vasoconstriction

Cattle and swine

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56
Q

What form of ergot is the most dangerous? and why

A

Pelleted grain as the ergot gets crushed during processing, so it makes it hard to see.

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57
Q

What are the common clinical signs of ergot poisoning?

A
  1. Feed refusal
  2. Dry gangrene with lameness
  3. Agalactia leading to small/weak piglets
  4. Abortions
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58
Q

How can you confirm a diagnosis of ergot poisoning?

A

Analyze for ergopeptide alkaloids in the feed and look for sclerotia bodies

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59
Q

What characteristics determine the type of disease selenium poisoning causes?

A
  1. Form of selenium
  2. Duration and route of exposure
  3. Species affected
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60
Q

What are the acute clinical signs of selenium poisoning?

A
  1. Cardiac-myocardial necrosis
  2. Lung-pulmonary edem a
  3. Poliomyelomalacia (swine)
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61
Q

Which species is most sensitive to selenium poisoning?

A

Horses

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62
Q

What are the most common sources of selenium poisoning?

A
  1. Forages, especially obligate accumulators
  2. Supplements and mixing errors just as injectables and hay
  3. Water contamination
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63
Q

What can cause bobtailed disease?

A

Chronic selenium poisoning

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64
Q

What plant contains high amounts of selenium?

A

Locoweed

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65
Q

How is selenium poisoning analytically diagnosed antemortem and postmortem?

A 
Antemortem: 
1. Blood
2. Hair/hoof if chronic
Postmortem: 
1. Liver

And testing water

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66
Q

What is the treatment for selenium poisoning?

A

Supportive care of symptomatic patients

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67
Q

White muscle disease is caused by _________ and affects mainly __________. The main clinical sign seen is _________.

A

Selenium deficiency
Horses
Masseter muscle myopathy

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68
Q

What is paraquat?

A

Herbicide use to die plants out, especially popular with potatoes

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69
Q

Which species is most likely to be poisoned by paraquat?

A

Dog and sometimes large animals in recently treated areas

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70
Q

What is the MOA of paraquat?

A

It produces free radicals with the substrate being oxygen leading to cell death

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71
Q

What are the routes of exposure of paraquat?

A
  1. Oral leading to acute toxicity

2. Respiratory..accumulates in lung in 24 hours

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72
Q

How is paraquat excreted?

A

%70 unchanged in the urine

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73
Q

What the clinical signs of an acute paraquat toxicity?

A
  1. GIT: vomit and abdominal pain

2. Pulmonary: dyspnea and tachypnea

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74
Q

How do dogs normally die when poisoned with paraquat if its an acute manifestation?

A

From the pulmonary effects that cause dyspnea and tachypnea

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75
Q

What are the clinical signs of a chronic paraquat toxicity?

A
  1. Pulmonary: dyspnea from irreversible fibrosis

2. Renal: vomit and abdominal pain

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76
Q

How do dogs normally die when poisoned with paraquat if its a chronic manifestation?

A

Renal failure

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77
Q

If you did a necropsy on a dog that died from acute parquet poisoning, what would you see? Chronic?

A
  1. Hemorrhage of GIT and lungs
  2. Necrosis of GIT and lungs
  3. Heavy lungs
  4. Inflammation of the GIT

With chronic would also see fibrosis in lungs

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78
Q

You send samples into a pathologist for histology on a dog what died from chronic paraquat poisoning. What does the report say? What about an acute poisoning>

A

Chronic: Renal, adrenal and cardiac necrosis with interstitial lung fibroplasia

Acute: Hemmorrhage, edema and necrosis of the lung and GIT

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79
Q

What samples are best to test postmortem if you suspect paraquat poisoning?

Antemortem?

A
  1. Liver
  2. Kidney
  3. Lung

Urine, but only in acute disease

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80
Q

Why do animals start vomiting after they ingest paraquat?

A

It is an emetic

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81
Q

If a dog is asymptomatic after drinking paraquat, what should you do? Why is this scenario unlikely?

A

Decontaminate with activated charcoal and antiemetics

Paraquat is an emetic, so most animals will by symptomatic already.

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82
Q

How do you treat a symptomatic

paraquat toxicity patient?

A
  1. Antiemetic
  2. Activated charcoal
  3. Analgesics
  4. GI protectants
  5. IV fluids
  6. Oxygen supplementation
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83
Q

Why would you give IV fluids to a paraquat toxicity dog?

A
  1. Enhance excretion in the urine
  2. Decrease contact time in renal tubules
  3. Maintain hydration
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84
Q

Where can you find PTFR

A

Non stick cooking surfaces, lightbulbs, headlamps, irons, ironing board covers, and heaters

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85
Q

Which species is most sensitive to PTFR’s and what does it do to them?

A

Birds

Acute respiratory distress

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86
Q

At what temperature range can you be confident that PTFR fumes and particulates are not being expelled into the air?

A

less than 500 degrees F or 260 degrees C

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87
Q

How do you diagnose a PTFR toxicity when the pathological lesions are nonspecific and there are no tests for it?

A

Good history taking for sources

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88
Q

What plants can cause fog fever in cattle?

A
  1. 3-methyl-indole in grass
  2. Mustard
  3. Moldy sweet potatoes with ipomeanol
  4. Perilla mint
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89
Q

A horse is slobbering profusely , but you see nothing else wrong, what could be causing this?

A

Slaframine mycotoxin

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90
Q

Which plants can slaframine mycotoxin grow on?

A
  1. Red clover
  2. Alfalfa
  3. Legumes
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91
Q

What does DUMBSLED stand for?

A 
Diarrhea
Urination
Myosis 
Bradycardia 
Salivation 
Lacrimation 
Emesis 
Dyspnea
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92
Q

How can you diagnose and treat a slaframine toxicity?

A

Test the feed with representative samples, remember hot spots
Remove access to feed
Don’t treat with atropine

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93
Q

What is the mycotoxin called that is estrogenic, grows on grains and some grasses and hay and affects cattle and swine causing vulvovaginitis and mammary gland enlargement?

A

Zearalenone

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94
Q

What are the three main causes of seizures?

A
  1. Metabolic
  2. Structural
  3. Idiopathic epilepsy
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95
Q

What is the most common type of generalized seizure?

A

Tonic/clonic

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96
Q

What are the three types of seizures?

A
  1. Generalized
  2. Partial/focus
  3. Behavioral/psychological
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97
Q

If you see green, red, pink dyed wheat, think _______.

A

Strychnine

98
Q

What is strychnine?

A

It is a compound common in the PNW used as a rodenticide

99
Q

What is the MOA of strychnine?

A

It is a reversible antagonist of inhibitory NT glycine at postsynaptic sites in the spinal cord in medulla. It stimulates extensor muscles causing rigidity and tonic seizures .

100
Q

What is the onset time of and what are the clinical signs of strychnine poisoning?

A

Onset in 5-15 min.

  1. Extensor rigidity
  2. Tonic seizures via stimuli induction
  3. Hyperthermia
101
Q

How can you diagnose strychnine poisoning?

A

Since the lesions and clinical path are nonspecific, you must test the stomach contents, urine, and blood.

102
Q

A dog comes in and is experiencing extensor rigidity and intermittent tonic seizures. The owners say there was green stuff in the vomit before getting to the clinic. How are you going to treat this dog?

A

Since this is likely strychnine and the dog is already symptomatic, you need to control the seizures with:

  1. Methocarbamol
  2. Pentobarbital
  3. Diazepam

and keep the dog in a quiet, dark place while monitoring acidosis, lowering the body temp, giving oxygen and IV fluids with 24 hour surveillance.

103
Q

if a dog is asymptomatic for strychnine poisoning, what should you do first…after doing the math of course?

A

Decontaminate with activated charcoal as it binds strychnine very well.

104
Q

This is a molluscicide that is combined with an acetylcholinesterase inhibitor causing dumbsled signs in dogs. What is it?

A

Metaldehyde

105
Q

What are the clinical signs of an acute metaldehyde poisoning?

A
  1. Muscle tremors
  2. Becoming sensitive to external stimuli
  3. Tonic/clonic seizures
  4. Hyperthermia (shake and bake)
  5. Death due to respiratory failure
106
Q

Which toxin involved “shake and bake”?

A

Metaldehyde

107
Q

How would you diagnose a metaldehyde poisoning?

A
  1. Muscle tremor signs

2. Chemical analysis of the stomach contents ( freeze samples, they are volatile)

108
Q

What is the mycotoxin most likely found in the compost or garbage?

A

Penitrem A, a tremorgenic mycotoxin

109
Q

What are the sources of penitrem A?

A

Moldy food and decaying organic material especially nuts, cheese, and bread

110
Q

What are tremorgenic mycotoxins?

A

Toxins found in perineal rye grass and in moldy foods

111
Q

What are the clinical signs of a penitrem A toxicity?

A

Rapid onset of:

  1. Intention tremors
  2. Ataxia
  3. Tonic/clonic seizures
  4. Sensitivity to external stimuli
  5. Nystagmus
112
Q

Paraquat, Strychnine, metaldehyde and penitrem A all cause certain animals to have seizures, but what makes penitrem A different?

A

There is a cerebellar component with excitation- intention tremors and twitching

113
Q

How would you diagnose a penitrem A toxicity?

A

Look at the stomach contents for the source material and the chemically analyze it.

114
Q

What medication can be used to control tremors and seizures due to penitrem A and pyrethrins?

A

Methocarbamol

115
Q

Since animals that ingest penitrem A can become sensitive to external stimuli while under sedation, what do you want to do when treating them?

A

Weight the risks and benefits of decontamination versus controlling the tremors and providing supportive care

116
Q

If a dog ate moldy cherries, what issues could arise?

A
  1. GI mechanical upset
  2. Cyanide poisoning
  3. Tremorgenic mycotoxin poisoning
117
Q

What rodenticide has seen a 65% uptake in toxicity cases, has a very long half life, and has a very low toxic dose?

A

bromethalin

118
Q

What is the first few thing you want to do when a dog or cat ingests bromethalin?

A
  1. Do the math

2. Aggressively decontaminate with 4 doses of AC in 24 hours along with fluid to prevent hypernatremia

119
Q

What is the MOA of bromethalin?

A

It is an uncoupler of oxidative phosphorylation in mitochondria of the CNS leading to a drop in ATP production which produced fluid filled vacuoles between myelin sheaths leading to a paralytic/convulsant syndrome.

120
Q

What determines if a dog/cat what ingested bromethalin will experience the paralytic versus convulsant syndrome?

A

If less than the LD 50=paralytic syndrome

If more than the LD 50=convulsant syndrome

121
Q

What should be on your differential list when you are considering bromethalin poisoning?

WHY?

A
  1. Ionophores
  2. Macadamia nuts
  3. Intermediate syndrome with Organophosphates
  4. Methionine
  5. Tick paralysis
  6. Coonhound paralysis
  7. Botulism
  8. Myasthenia gravis

Hind limb paresis/paralysis

122
Q

What type of seiuzures do animals experience with bromethalin poisoning (the convulsant form)?

A

Tonic/clonic along with muscle tremors and hypersensitivity to external stimuli

123
Q

Which toxins involve hypersensitivity to external stimuli?

A
  1. Bromethalin
  2. Penitrem A
  3. Metaldehyde
  4. Strychnine
  5. Chlorinated hydrocarbon pesticides
124
Q

What is the range of clinical sign onset for bromethalin toxicity?

A

10 hours to 5 days, there is a lag phase to onset as it takes time to uncouple phophoralation

125
Q

If you see lesions with bromethalin toxicity, what will you see grossly and histologically when looking at the brain?

A

Edema and vacuolation( histology and this is time dependent, but electron microscopy may pick this up earlier)

126
Q

T/F: Even if you don’t see gross/histo lesions, you should never rule out bromethalin poisoning.

A

True

127
Q

Why is it so difficult to diagnosis bromethalin poisoning based on chemical analysis antemortem?

A

The stomach contents will be gone unless its very acute

128
Q

What sample should you test for bromethalin poisoning postmortem?

A

Fat

129
Q

Why do we give 4 doses of activated charcoal to a dog that ingested bromethalin? What else should we do?

A

It undergoes enterohepatic recirculation. Should also maintain hydration and provide good nursing care as they will be with you for several days not moving much.

130
Q

What does buttercup cause when ingested?

A

GI irritation

131
Q

What systems in the which species body does 1080 effect and what is 1080?

A

The GIT and central nervous system excitation in dogs

It is a rodenticide/coyote control product that is banned in the US

132
Q

What is the MOA of 1080?

A

It affects the Krebs cycle and ATP production

133
Q

How long does that lag phase past and what do you see clinically?

A

30min-2 hours: Wild barking/running with urination/defecation and seizure cycle that repeats getting more intense and severe cumulating in respiratory and cardiac arrest

134
Q

What clinically signs can 1080 cause in cattle?

A

Cardiac issues

135
Q

How is 1080 chemically analyzed?

A

Via testing of the urine and kidney

136
Q

What is the treatment for 1080 poisoning?

A

Its unrewarding and the prognosis is bad

137
Q

What is methionine?

A

It is the active ingredient in dog treats that changes the pH of urine so that it doesn’t discolor grass

138
Q

What are the clinical signs seen with methionine?

A
  1. Transient hind limb paralysis with abnormal posture
  2. Vomiting
  3. Ataxia aka cerebellar signs
139
Q

What are some treatments for methionine toxicity?

A
  1. IV fluid therapy
  2. Confinement
  3. Bicarbonate
  4. Emetics
140
Q

What are methylxanthines?

A
  1. Theobromine
  2. Caffeine
  3. Theophylline
141
Q

What contains theobromine?

A

Chocolate foods (remember those marijuana edibles)

142
Q

What contains caffeine?

A
  1. Coffee beans
  2. Chocolate
  3. No Doz medication
143
Q

The darker the chocolate gets, the _______ theobromine level.

A

Higher

144
Q

T/F: All dogs respond to the same toxic/lethal doses for theobromine.

A

False, there is a variation in toxic/lethal doses between individuals

145
Q

Why would you want to decontaminate a dog that ate chocolate (theobromine) with multiple doses of activated charcoal or cholestyramine?

A

Theobromine has a long half life and undergoes enterohepatic recirculation, it can be rapidly or slowly absorbed once release from its form.

146
Q

Why does theobromine increase heat rates and blood pressure?

A

It causes vasoconstriction and enhanced myocardial contraction

147
Q

After theobromine increased the heart rate, blood pressure, and ehances muscular excitability and muscle tremors, what will you see clinically?

A

CNS excitation with excessive urination, diarrhea, bloat, tachycardia leading to cardiac arrhythmias that waxes and wanes.

148
Q

What is that cause of death in theobromine toxicity?

A

Cardiac arrhythmias

149
Q

When diagnosing a theobromine toxicity, what are the steps you must take?

A
  1. Ask about potential exposure
  2. Do the math and remember variation between individuals
  3. Look for CNS, CV, GIT and urination signs
  4. DO chemical analysis on whatever you want
150
Q

A dog ate a bunch of chocolate, you did the math, and now need to treat…what do you do?

A
  1. Emesis
  2. Lavage
  3. AC 3 times in 24 hours
  4. Control the tremors and seizures
  5. Monitor with an ECG
  6. IV fluids
151
Q

What food items should be on your list when thinking about toxicities?

A
  1. Chocolate
  2. Raisins/grapes
  3. Marijuana
  4. Salt
  5. XIylitol
  6. Macadamia nuts
  7. Bracken fern
152
Q

What compound is found in glow jewelry that can cause excessive salivation, behavior changes, and act as an eye irritant in mainly cats?

A

Dibutyl phthalate

153
Q

How would you treat a cat that chew open a glow bracelet?

A

Rinse out the mouth/eye and bath the cat

154
Q

What can zinc sulfide/strontium aluminate be found in and what does it do?

A

Glow jewelry

Irritant that can cause neurologic issues

155
Q

Match these sources of lead and species of animal:

  1. Indoor birds A. Batteries
  2. Companion animals B. Shot
  3. Cattle C. Paint
  4. Waterfowl/raptors
A

Companion animals and indoor birds====PAINT

Cattle=====BATTERIES

Waterfowl/raptors======SHOT

156
Q

T/F: All species of animal suffer from an acute lead toxicity except humans and birds.

A

TRUE

157
Q

What type of environment does lead to to be in order to cause problems?

A

Acidic

158
Q

Why is lead so bad in pregnant animals?

A

It can remobilize Ca2+ out of bone

159
Q

What age animal is the most susceptible to lead poisoning?

A

Young because they have enhanced absorption and are curious and small

160
Q

What does lead bind to and what does this cause?

A

It binds to proteins on the surface of RBCs causing issues especially in the CNS/PNS, kidney, bone marrow, and GIT

161
Q

How is lead excreted?

A

Mainly in the bile, some in the urine

162
Q

Is lead poisoning a more chronic or acute issue and why?

A

Chronic as it has a long T1/2

163
Q

What is the main effect of lead in the bone marrow?

A

It causes the premature release of immature RBCs and then will lysis but no anemia unless its a very chronic issue like in waterfowl and raptors.

164
Q

What may be the only clinical sign you see with lead poisoning in small animals? What clinical signs may come after that initial sign?

A

GI irritant or lead colic

CNS signs like:

  1. Hysteria
  2. Hyperexcitability
  3. Intermittent seizures
165
Q

What effect does lead poisoning have on the CNS and PNS?

A

It increases vascular permeability leading to edema and demyelination of the peripheral nerves which can cause GIT stasis, wing paralysis and difficulty swallowing, blindness and seizures.

166
Q

What are the top differentials in an animal experiencing intermittent seizures?

A
  1. Hypoglycemia
  2. Portosystemic shunt
  3. Idiopathic epilepsy
  4. Lead toxicity
167
Q

What are the specific clinical signs you will see in cattle with lead poisoning?

A
  1. 90%=CNS and PNS signs like: blindness, eyelid snapping, inability to swallow and convulsions
  2. Acute death in calves
  3. Hyperthermia
168
Q

What is the main difference in clinical signs seen between companion animals, cattle and horses, and birds when they are experiencing lead toxicity?

A

Companion animals: GI signs first, CNS signs later with no PNS signs

Cattle: CNS and PNS signs first with GIT signs later along with hyperthermia and acute death in calves

Horses: Lethargy and laryngeal paralysis, but common to not see any signs

Avian: chronic GIT and PNS signs together like lethargy, anorexia, weak, diarrhea, crop stasis, impactions and wing paralysis

169
Q

On clinical pathology in a companion animal or cattle, what would you see evidence of with lead poisoning?

A

nRBC’s and evidence of regeneration with basophilic stippling, along with a lack of anemia (not this is not consistent or reliable). Sometimes will see tubular nephropathy showing glycosuria and proteinuria.

170
Q

Why would you take radiographs when dealing with a lead poisoning?

A

Lead is radio opaque and you must find the source and remove it in order to properly treat the patients.

171
Q

What are the gross lesions observed with lead toxicity?

A
  1. Cerebral edema

2. Pale-cooked muscle

172
Q

What are the microscopic lesions observed with lead toxicity?

A
  1. Polioencephalomalacia
  2. Intranuclear inclusions with lead precipitates
  3. Liver/kidney necrosis
173
Q

What part of the body in ruminants should you radiograph if you suspect lead poisoning?

A

Reticulum

174
Q

What samples would you use for a lead analysis antemortem and postmortem?

A

Antemortem: whole blood
Postmortem: kidney and liver

175
Q

How can you improve excretion of lead in the urine in small animals?

A

Combine succimer ( a chelator) with thiamine hydrochloride

176
Q

Which medication is really helpful to use as a treatment for lead poisoning in all animals, but especially cattle?

A

Thiamine

177
Q

How can you decontaminate an animal that ingested lead? What animals would this not work well with?

A
  1. Surgery
  2. Emetics
  3. Cathartics like MgSO4 aka epson salt

Very hard to decontaminate cattle and birds

178
Q

What is succimer used for?

A

It is an oral chelator of lead and arsenic that can be used in dogs, cats, and birds.

179
Q

What is CaEDTA used for?

A

The treatment of lead poisoning in cattle, birds, dogs and cats

180
Q

What is penicillamine used for?

A

It chelates copper and lead

181
Q

Why is succimer more effective to use in dogs, cats and birds for the treatment of lead poisoning than CaEDT?

A

There is no gut absorption

182
Q

What is the prognosis for lead poisoning?

A

In small animals, it is good, but in large animals is birds, its s not.

183
Q

Why would you want to inform the federal government agencies of a lead poisoning case?

A

It is a public health problem

184
Q

What are chlorinated hydrocarbons (organochlorines)?

A

Insecticides that contaminate the environment…remember DEET and silent spring?? It is a diffuse nervous stimulant.

185
Q

What is the MOA of chlorinated hydrocarbons?

A

They are lipid soluble and stable which means they can accumulate in the fat of animals and biologically magnify…as food chain gets higher, the concentration gets higher.

186
Q

What are the clinical signs of a chlorinated hydrocarbon toxicity?

A
  1. Early premonition period
  2. Muscle tremors of head/neck/body
  3. Tonic/clonic seizures (continuous/intermittent) with excessive response to external stimuli
187
Q

How can you test/diagnose for chlorinated hydrocarbons in animals?

A

Chemical residue testing in blood and fat post or antemortem

188
Q

How do you treat a chlorinated hydrocarbon toxicity in animals?

A

It is patient based, but steps include:

  1. Control tremors/seizures
  2. Decontaminate
  3. Make sure contaminated food animals are not consumed ( notify state vet)
189
Q

Cyanobacteria can cause hepatic damage, what what other complication can they cause?

A

Neurotoxicity

190
Q

What toxins found in cyanobacteria can act as neurotoxins? What is the difference?

A
  1. Anatoxin-a: mimic acetylcholine

2. Anatoxin-a(s)-inhibits acetylcholinesterase

191
Q

Which cyanobacterial toxin affects nicotinic receptors and which affects nictotinic and muscarinic?

A

Anatoxin-a mimics acetylcholine which affects nicotinic receptors
Anatoxin- a(s) inhibits acetylcholinesterase which affects both nicotinic and muscarinic receptors

192
Q

How common is it to have neurotoxic and hepatotoxic genera of cyanobacteria in the same population?

A

Not common

193
Q

What are the clinically signs of an anatoxin-a and anatoxin-a(s) toxicity?

A

All clinical signs are acute with rapid progression:

  1. Muscle tremors
  2. DUMBSLED
  3. Seizures
  4. Paralysis
  5. Death due to respiratory paralysis
194
Q

How can you diagnosis and test for neurotoxic cyanobacteria toxicity?

A
  1. History of exposure
  2. Acetylcholinesterase inhibitions blood screening tool
  3. Algae identification via light microscopy
  4. Test for the toxins in water and GIT
195
Q

How would you treat a symptomatic patient who ingested neurotoxic cyanobacteria from blue-green algae?

A
  1. Maintain adequate respiration with the ABC’s
  2. Supportive care and control tremors/seizures
  3. Cholestyramine because of bile sequestration in the GI tract
196
Q

What can you put in water to rid it of blue-green algae?

A

Cu sulfate

197
Q

What are organophosphates and carbamates

A

Insecticides which are relatively safe if people read the label before use

198
Q

What is the MOA of organophosphates and carbamates?

A

Acetylcholinesterase inhibitors/binders which cause acetylcholine to build up at the receptors leading to overstimulation of muscarinic and nicotinic receptors and CNS excitation.

199
Q

If muscarinic receptors are overstimulated like in the case of organophosphate/carbamate toxicity, what clinical signs will you see?

A

DUMBSLED

200
Q

If nicotinic receptors are overstimulated like in the case of organophosphate/carbamate toxicity, what clinical signs will you see?

A

Tremors and/or an intermediate syndrome

201
Q

What occurs when organophosphates/carbamates binds to AchE?

A

The AchE become phosphorylated, which is irreversible when a organophosphate does it, but reversible when a carbamate (carbalylated) does it. As the compound age, the irreversible bond strengthens and renders oxide treatment useless.

202
Q

What is the treatment goal when dealing with organophosphate/carbamate toxicity?

A

Enzyme recovery of AchE through oxime-induce reactivation of the AchE

203
Q

What three factors determine the onset of clinical signs with organophosphate.carbamate toxicity?

A
  1. Form
  2. Dose
  3. Route
204
Q

What are the main clinical signs of a organophosphate/carbamate toxicity? Will these signs be present all the time?

A
  1. Muscarinic signs=DUMBSLED
  2. Nicotinic signs=tremors
  3. CNS signs=excitation

Preponderance of evident and will not see all the signs, all the time.

205
Q

In what species of animals can organophosphates/carbamates affect?

A

ALL

206
Q

What clinical signs will you see in horses who have been poisoned with carbamates/organophosphates?

A
  1. Colic

2. Diarrhea

207
Q

What is the cause of death of animals suffering from organophosphate/carbamate toxicity? Why does this happen (4 reasons)?

A 
Respiratory failure due to: 
1. Increased bronchiole secretions
2. Bronchoconstriction
3 Paralysis of respiratory muscles 
4. Depression of respiratory center
208
Q

What other clinical sign can occur in dogs and cats who ingested organophosphates besides the CNS, muscarinic and nicotinic signs?

A

Pancreatitis

209
Q

Which plant has large amounts of carbamates in it?

A

Solanum (nightshade)

210
Q

How can you screen for a carbamate/organophosphate poisoning? what do the results tell us?

A
  1. Screen fro ChE inhibition:
    Inhibition =could be toxicity, but could also be a false positive due to anemia, BG-algae, or solanum
    No inhibition=could be false negative due to testing too soon, it hasn’t passed blood/brain barrier yet, or due to preservation of specimens
  2. Chemical residue tests in GIT and skin
211
Q

If a patient is symptomatic after ingesting carbamates/organophosphates, how should you treat?

A
  1. Atropine for muscarinic signs
  2. Oximes prior to aging to reactive enzyme
  3. DO not give diphenhydramine
212
Q

Why do you want to administer oximes to a organophosphate toxicity patient slowly?

A

It can cause cardiac arrest if given too fast.

213
Q

What is delayed neuropathy syndrome?

A

It is a syndrome caused by some organophosphates that causes ascending paralysis due to polyneuritis.

214
Q

What toxic differentials should be on your list when you think you are seeing delayed neuropathy syndrome?

A
  1. Organophosphate toxicity
  2. Macadamia nuts
  3. Bromethalin
  4. Ionosphores
  5. Methionine
215
Q

What is intermediate syndrome?

A

It is a disease sometimes caused by organophosphate/carbamate toxicity where the lipophilic compounds down regulate cholinergic receptors causing anorexia, nueromuscular weakness, and venture-flexion of the neck

216
Q

What chemical can be used to control nuisance birds and causes a nephrosis?

A

DRC-12 aka Starlicide

217
Q

What is avitrol

A

A toxin that can be used to control nuisance birds and is a neurotoxin.

218
Q

What are the group of insecticides/flea-tick repellants used in dogs and cats called?

A

Pyrethrins

219
Q

Which species is most sensitive to pyrethrins and therefore should not ever be exposed to it?

A

Cats

220
Q

How toxic are pyrethrins?

A

They have low mammalian toxicity, but depends on species

221
Q

What type of pyrethrin product can cause epidermal paresthesia leading to inflammatory contact dermatitis?

A

Pyrethroids in spot on products

222
Q

What can pyrethroids in spot on products cause?

A

Inflammatory contact dermatitis

223
Q

What is the MOA of pyrethrins?

A

CNS excitation, but not one MOA describes the clinical signs observed.

224
Q

What are the clinical signs of a pyrethrin toxicity?

A
  1. CNS excitation
  2. Salivation
  3. Tremors/twitching/parasthesia
  4. Agitate to subdued behavior due to paresthesia
  5. Temporary blindness in 30% cases
  6. Convulsions especially w/ high doses in cats
225
Q

How soon do we see the onset of clinical signs in pyrethrin cases? What is the route of exposure?

A

Within a few hours

Dermal

226
Q

How do you diagnose a pyrethrin toxicity? `

A
  1. History of use
  2. Clinical signs
  3. Rule out other things because no clin path or lesions
  4. Chemical residue analysis
227
Q

How do you treat a patient with a pyrethrin toxicity?

A
  1. Sedate patient
  2. Give a bath with mild dish soap and wash mouth
  3. AC/Cathartic/gastric lavage
  4. Control tremors/seizures
  5. Control rebound hypothermia
  6. IV lipid rescue therapy
  7. Apply vitamin E to application site
228
Q

What is the drug of choice for controlling tremors/seizures in animal that have ingested either pyrethrin or penitrem-A?

A

Methocarbamol

229
Q

What are the sources of NPN and what is it?

A

Non-protein nitrogen (urea) found in:

  1. Fertilizers
  2. Supplements like blocks, liquids, grain and cubes
230
Q

Why are cattle fed NPN’s?

A

Helps the cattle produce their own proteins

231
Q

What is NH3? What can it cause if inhaled?

A

Ammonia: pulmonary edema

232
Q

What occurs to urea once it is ingest by a ruminant?

A

Urea mixes with water (urease) in the rumen and produces ammonia (NH3) and CO2. The microflora take ammonia + carbohydrates and produced amino acids and proteins.

233
Q

What occurs if a ruminant ingest too much urea?

A

The microflora become overwhelmed by the amount of ammonia (NH3), so it is buffered to NH4 which increases the pH to 8-10 causing alkylosis. After awhile, the NH3 can’t be buffered anymore so it gets absorbed into the bloodstream causing hyperammonemia»>metabolic acidosis»>hyperkalemia induced cardiac failure

234
Q

What two things are needed in order for a cow to safely digest NPN’s?

A
  1. Adaptation period to feed

2. Carbohydrate source

235
Q

Why do we see bloat as a clinical sign in cattle that have ingested NPN’s?

A

The CO2 and NH3 produced from the urea and water in the rumen are gases.

236
Q

What are the clinical signs of an NPN toxicity?

A
  1. Bloat

2. Convulsions

237
Q

What criteria is needed to diagnose a NPN toxicity?

A
  1. Recent feed change or access to fertilizer
  2. Rumen pH of 8-10
  3. Confirmed high ammonia levels in blood/ocular fluid
  4. Urea presence in supplement
238
Q

What types of samples should be collected to confirm an NPN diagnosis? How should these be treated?

A
  1. Blood
  2. Ocular fluid

Collected within 30 min of death and FROZEN

239
Q

What is the treatment for an NPN toxicity?

A
  1. Cold water

2. Vinegar

240
Q

How soon after seeing clinical signs in a NPN toxicity should you treat the cattle?

A

20 minutes

241
Q

Why is cold water and vinegar used to treat an NPN toxicity?

A

Urease is pH and temperature dependent, so the cold water slow down the urease enzyme activity while vinegar provides protons the help convert NP3 into NH4.

242
Q

What condition does onion cause in dogs?

A

Red blood cell hemolysis with heinz’s bodies

Veterinary Toxicology (3 decks)

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