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Veterinary Toxicology > Mixed CNS Toxicants > Flashcards

Mixed CNS Toxicants Flashcards

1
Q

What is the difference between pyrethrins and pyrethroids? What are they most commonly seen in?

A
  • PYRETHRIN = natural insecticides produced by pyrethrum (Chrysanthemum) flowers
  • PYRETHROIDS = synthetic

flea control products - major cause of poisoning in small animals

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2
Q

What do pyrethrins and pyrethroids cause in insects?

A

rapid knockdown effect

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3
Q

What is the difference between Type I and II pyrethroids? What is commonly added to Type II pyrethroids?

A

Type II pyrethroids have an extra cyano group, which enhances insecticidal activity

synergists (piperonyl butoxide, sesamex, piperonyl cyclonene) to increase stability and effectiveness by inhibiting CYP450 metabolism

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4
Q

What species are susceptible to pyrethroid toxicity? Which is especially sensitive and more likely to be poisoned? Why?

A

cats, dogs, fish

cats - low glucuronidation capacity due to UDP-glucuronosyltransferase deficiency

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5
Q

How does absorption of pyrethroids vary? Why does it have low oral toxicity?

A

GI = 70%
DERM = <2%

rapid hydrolysis in the GIT and high lipophilicity allows rapid and wide distribution

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6
Q

Where are pyrethroids metabolized? How does this happen?

A

liver

oxidation, hydrolysis, and conjugation with glucuronide (deficient in cats), glycine, sulfate, taurine, or glutamate

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7
Q

What toxicant is able to increase the toxicity of pyrethroids? How?

A

OPs inhibit hydrolysis in the liver, leading to accumulation

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8
Q

What are 3 mechanisms of toxicity of pyrethroids?

A
  1. slow down closing and prolong opening of voltage-sensitive Na+ channels
  2. direct action on sensory nerve endings causing repetitive firing and paresthesia
  3. inhibit voltage-gated Cl- channels
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9
Q

How does the mechanism of toxicity of Type I and II pyrethroids compare?

A

TYPE I = repetitive firing prolongs the opening of Na+ channels for short periods

TYPE II = membrane depolarization prolongs the opening of Na+ channels for longer periods of time

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10
Q

What happens at high doses of Type II pyrethroids?

A

antagonizes GABA-gated Cl- channels, causing seizures

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11
Q

What are common clinical signs of pyrethroid toxicity? What is commonly seen in cats?

A
  • depression or hyperexcitability*
  • convulsions, muscle tremors
  • paresthesia
  • ataxia
  • anorexia, diarrhea, vomiting, salivation
  • bradycardia, dyspnea, hyperthermia
  • sudden death by respiratory failure

ear twitching, paw shaking, shivering, mydriasis

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12
Q

How can pyrethroid toxicity be differentiated from OP and CM toxicity?

A
  • atropine test
  • ChE activity
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13
Q

When is emesis contraindicated in pyrethroid toxicity? When is activated charcoal used?

A

if the product contains petroleum distillates

if a spot-on product was ingested by a cat

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14
Q

What are the 2 common symptomatic treatments for pyrethroid toxicosis? What is avoided?

A
  1. Diazepam/Phenobarbital for seizures
  2. Methocarbamol for severe muscle tremors and seizures

Atropine - causes CNS stimulation

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15
Q

Why must thermoregulation for pyrethroid toxicosis be done carefully?

A

hyperthermia from excess muscle activity can rapidly become hypothermia during treatment

  • hypothermia enhances nervous activity by slowing Na+ channel kinetics
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16
Q

What is bromethalin commonly used for?

A

anticoagulant rodenticide-resistant mice and rats

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17
Q

Which species are most susceptible to bromethalin toxicity?

A

cats*, dogs, rabbits

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18
Q

How is bromethalin absorbed, metabolized, and excreted?

A

rapid absorption from GIT

metabolized by mixed function oxidases in the liver to desmethyl-bromethalin, its toxic metabolite

lipophilic and slowly eliminated via bile

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19
Q

What species is highly resistant to bromethalin toxicity? Why?

A

guinea pigs

has decreased N-demethylase activity, which decreases the metabolism into desmethyl-bromethalin

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20
Q

What is the mechanisms of toxicity of bromethalin?

A

uncouples oxidative phosphorylation in CNS mitochondria, decreasing ATP production and diminishing Na+/K+-ATPase activity allowing Na+ to flow into cells —> cerebral edema and high CSF pressure

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21
Q

How does bromethalin affect nerve impulses and the brain?

A

causes the formation of fluid-filled vacuoles in myelin sheaths, decreasing nerve impulse conduction

induces membrane lipid peroxidation

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22
Q

What clinical signs appear upon low-dose exposure to bromethalin?

A
  • depression*
  • tremors
  • hindlimb ataxia and paresis
  • vomiting
  • vocalization in cats
  • lateral recumbency
  • anisocoria
  • behavioral changes
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23
Q

What clinical signs appear upon high-dose exposure to bromethalin?

A
  • hyperexcitability*
  • severe muscle tremors
  • hyperthermia
  • running fits, circuling
  • seizures
  • CNS depression and death
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24
Q

What 2 postures are associated with high-dose exposure to bromethalin?

A
  1. Schiff-Sherrington - rigid forelimbs and flaccid paralysis of hindlimbs
  2. decerebrate - hindlimb extensor rigidity and forelimb flexion
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25
Q

What postmortem lesion is seen in bromethalin toxicity?

A

diffuse white matter vacuolization in the CNS

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26
Q

What cathartic is recommended for bromethalin toxicity? What is avoided?

A

saline cathartics

magnesium-containing solutions to prevent CNS depression

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27
Q

What 3 drugs are recommended to treat cerebral edema from bromethalin toxicity?

A
  1. diuretics (furosemide, mannitol)
  2. methylprednisolone
  3. dexamethasone
28
Q

What method of treatment was especially helpful in the treatment of bromethalin toxicity in the Pit Bull terrier?

A

IV lipid emulsion

29
Q

What has increased the incidence of antidepressant toxicosis in animals? What are 3 antidepressants of concern?

A
  • increased use in humans has increased the chance of exposure in dogs and cats
  • used to treat behavioral problems in pets, like Clomipramine for separation anxiety in dogs

tricyclic antidepressants, selective serotonin reuptake inhibitors, monoamine oxidase inhibitors

30
Q

What is the mechanism of action of tricyclic antidepressants? What is its most life-threatening effect? What other effect does it have?

A

inhibits the reuptake of biogenic amines (serotonin, NE, dopamine) centrally to potentiate their effects

anticholinergic effect inhibits cardiac Na+ channels causing arrhythmias

antihistaminic effect causes vascular α1-adrenergic blockade and vasodilation

31
Q

What is the most common clinical sign of tricyclic antidepressant toxicity? What else can occur?

A

hyperactivity and seizures followed by depression and a semi-comatose state

  • ataxia
  • lethargy
  • behavioral changes (disorientation, anxiety, aggression)
  • hyper/hypothermia
  • mydriasis, ileus, vomiting
  • cardiac arrhythmias, hypotension
  • shock, death
32
Q

What is charcteristic of the safety of tricyclic antidepressants?

A

narrow safety margin

33
Q

What is the preferred method of decontamination in tricyclic antidepressant toxicosis?

A

(considered an emergency, treat immediately!)

  • activated charcoal, cathartic, gastric lavage for large ingestions
  • emesis is not preferable
34
Q

Why is Atropine not recommended to use for bradycardia in tricyclic antidepressant toxicosis?

A

may potentiate anticholinergic effects

35
Q

What is recommended for seizures seen in tricyclic antidepressant toxicosis? What if this is not successful?

A

Diazepam

induce anesthesia with a Barbiturate

36
Q

What does fumonisin cause? What is the major source? Predisposing factor?

A

equine leukoencephalomalacia (ELEM), blind staggers

mycotoxins produced by the fungi of Fusarium spp. in corn and corn-based foods (B1 is the dominant toxin)

conditions that promote fungal growth and toxin production, like midsummer droughts, early wet falls, early frosts, and delayed harvests

37
Q

Where does fumonisin typically accumulate? How is it excreted?

A

liver, kidney, intestine

feces, with only trace amounts in the urine and bile

38
Q

What 4 species are most susceptible to fumonisin toxicity?

A
  1. horses**
  2. ponies
  3. donkeys
  4. pigs
39
Q

What is the mechanism of toxicity of fumonisin?

A
  • inhibits sphinganine and sphingosine N-acyltransferase, impairing sphingolipid synthesis
  • this causes the accumulation of sphinganine and sphingosine with a decrease in the production of sphingolipids
  • this impairs cell-to-cell communication and signaling
  • also causes the loss of membrane structure, disrupting the barrier function of endothelial cells leading to edema and hemorrhage
40
Q

What additional mechanism of toxicity is seen in pigs with fumonisin toxicity?

A

inhibition of cardiac calcium channels leading to left-sided heart failure and pulmonary edema

41
Q

What clinical syndrome is seen in horses with fumonisin toxicity?

A

NEUROTOXIC SYNDROME with 7-90 day onset, showing mania, depression, and death

  • frenzy
  • anorexia
  • ataxia
  • blindness
  • holding head low, head pressing
  • paralysis of lips and tongue
  • stupor, hyperesthesia
  • terminal convulsions and death
42
Q

What is seen in equine survivors of neurotoxic syndrome caused by fumonisin toxicity?

A

permanent CNS damage

43
Q

What syndrome is characteristic of swine with fumonisin toxicity? What causes this? What clinical signs are commonly seen?

A

porcine pulmonary edema (PPE) - pulmonary hypertension with transudation of fluids resulting in interstitial pulmonary edema and hydrothorax

  • dyspnea, cyanosis
  • weakness, recumbency
  • death often within 24 hours
  • surviving pregnant sows may abort
44
Q

What happens to swine exposed to sublethal exposure to fumonisin?

A

hepatotoxicosis with reduced growth and icterus

45
Q

How can fumonisin toxicosis be avoided?

A

carefully examine corn used in feed for mold and avoid using any moldy cobs

  • can be difficult because corn may not be grossly moldy
46
Q

In what states is Centaurea (yellow starthistle, Russian knapweed) commonly seen? Why is it extremely common here?

A

Western US - CA, ID, OR, CO, WA

it grows aggressively, has no natural enemies, and is costly to eliminate

47
Q

What 3 neurotoxins are produced by Centaurea?

A
  1. sesquiterpene lactones - repin
  2. excitotoxins - aspartic and glutamic acid
  3. DDMP
48
Q

What are the 2 mechanisms of toxicity of DDMP in Centaurea?

A
  1. interacts with dopamine transporter and causes the selective death of dopaminergic neurons, especially in the substantia nigra and globus pallidus
  2. causes damage to neural areas supporting cranial nerves V, VII, IX, and XII

(similar to Parkinson’s)

49
Q

What species is most susceptible to Centaurea toxicosis? What is required for toxicosis?

A

horses - require prolonged and large dietary intake, but has an abrupt onset

(animals were normal the previous day and now canot eat or drink)

50
Q

What disease does Centaurea toxicity cause? What clinical signs are seen?

A

nigropallidal encephalomalacia - chewing disease

  • excessive tone of facial and lip muscles
  • depression with periods of excitability
  • yawning, mouth held open with tongue out
  • chewing movements without ability to chew and swallow
  • head tossing
  • inability to drink, dunks head into water and tips head back
  • pitting edema, dehydration, death by starvation
51
Q

What is the toxic principle of Locoweeds? What 3 species commonly cause toxicosis?

A

indolizidine alkaloid, swainsonine

  1. Astragalus
  2. Oxytropis
  3. Swainsona
52
Q

How can locoweed toxicosis affect fetuses and nursing animals? When does toxicosis occur?

A

swainsonine can cross the placental barrier and be secreted unchanged in milk

chronic ingestion

53
Q

What are the 2 mechanisms of actions of locoweed toxicosis?

A
  1. inhibits lysosomal α-D-mannosidase, impairing catabolism of mannose-containing oligosaccharides, causing their accumulation in the lysosomes in the brain, thyroid, and other tissues, resulting in impairment of cellular function (like mannosidosis in humans and cattle)
  2. inhibits Golgi mannosidase II, causing disruption of glycoprotein processing, which leads to dysfunctional cellular adhesion molecules, circulating hormones, and membrane receptors and the accumulation of oligosaccharide-glycosylated proteins
54
Q

What are the most common clinical signs of locoweed toxicosis? What species are most susceptible?

A

LOCOISM - “crazy”

  • depression, circling, ataxia, belligerency, nervousness, aggressiveness, stargazing, loss of flocking instinct (sheep), convulsions
  • weight loss due to impaired liver, thyroid, and pancreas
  • reproductive problems (birth defects, abortions)

HORSES - “loco” horses are useless or dangerous/unsafe to ride

55
Q

How is locoweed toxicosis diagnosed? How is it treated?

A
  • history and evident of consumption of locoweeds (examine feces and rumen contents)
  • clinical signs
  • swainsonine in serum and low serum α-mannosidase activity

no proven effective treatment - remove animals from pasture

56
Q

What are the major sources of lead?

A
  • lead-based products, like paints, batteries, lubricants, toys, sinkers, and bullets
  • forage growing in lead-contaminated soil
  • tetraethyl lead in gasoline (discontinued)`
57
Q

What species are most commonly affected by lead toxicosis? What species is resistant? What makes lead poisoning limited in other species?

A
  • cattle, dogs, waterfowl
  • swine

reduced accessibility, more selective eating habits, lower susceptibility

58
Q

What is the most common exposure to lead? What affects absorption? How is it distributed?

A

oral - Pb-containing objects may be retained in reticulum in cattle

physical form and route of exposure - metallic < salts < organic, with greater absorption in the young

90% bound to RBCs with increased distribution to bone, teeth, liver, brain, and kidney, and across the BBB

59
Q

How is most ingested lead excreted?

A

via feces before absorption

  • some in urine and bile
60
Q

What are 6 mechanisms of toxicity of lead?

A

MULTI-SYSTEM TOXICANT

  1. inhibits thiol-containing enzymes
  2. displaces Zn and Fe in metalloenzymes
  3. lowers GABA concentrations and inhibits NMDA glutamate receptors in CNS
  4. inhibits membrane-associated ion pumps
  5. competes with and mimics Ca ions
  6. inhibits hemoglobin and RBC synthesis by blocking δ-aminolevulinic acid dehydratase and ferrochelatase
61
Q

What are the most common CNS and GI signs of lead toxicity in cattle?

A

CNS - seizures, depression followed by hyperesthesia and aggression, blindness, circling, head pressing, ataxia, muscle spasms

GI - vomiting, reduced motility, salivation, colic, anorexia, rectal sphincter paresis, tucked abdomen, bloat, diarrhea

62
Q

What clinical signs are associated with lead toxicosis in waterfowl?

A

paracute death or chronic disease with…..

  • anorexia
  • emaciation
  • muscle atrophy
  • weakness
  • dysphonia
  • depression
  • coma
63
Q

What signs predominate in lead toxicosis in dogs/cats? What clinical signs are seen?

A

GI upset

  • anorexia, colic, emesis
  • salivation
  • diarrhea/constipation
  • anxiety, barking, jaw champing
  • ataxia, blindness, muscle spams
  • opisthotonos, convulsions, depression
64
Q

What occurs following chronic lead poisoning in horses? What clinical signs are seen?

A

segmental demyelination causing lower lip paresis and recurrent laryngeal nerve paralysis (roaring)

dysphagia, weight loss, depression, weakness, colic, diarrhea, death

65
Q

What are 4 ways to diagnosis lead toxicity? What can be done postmortem?

A
  1. blood tests detecting Pb levels in whole blood (>0.6 ppm or 0.35-0.6 with clinical signs diagnostic)
  2. urine Pb levels (>0.75 ppm diagnostic; levels increase greatly after EDTA treatment)
  3. RBC ALAD activity and urinary ALA levels
  4. radiography detect Pb objects in GI tract

lesions + Pb levels in liver or kidney

66
Q

How is decontamination done with lead toxicosis? What therapy is used for treatment?

A
  • remove Pb-containing foreign bodies from GIT via rumenotomy, gastrotomy, or endoscopy
  • emesis, gastric lavage, cathartic, enema, WBI

chelation with Ca-EDTA, D-penicillamine, succimer (DMSA) - bind Pb into a soluble form excreted in urine

67
Q

What supportive therapy is recommended for seizures, cerebral edema, and CNS signs following lead toxicosis?

A

Diazepam

Mannitol, Furosemide

Thiamine

Veterinary Toxicology (29 decks)

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