Musculoskeletal Toxicity Flashcards Preview

Toxicology > Musculoskeletal Toxicity > Flashcards

Flashcards in Musculoskeletal Toxicity Deck (23):
1

phenoxyacetic acid herbicides

  • 2,4-D (Scott's weed and feed)
  • Low toxicity in most animals
  • Affected animals usually exposed to concentrate or predisposed through kidney damage or genetics
  • MOA unknown

2

clinical signs of phenoxyacetic acid herbicide toxicity

  • GI effects (often only signs in dogs)
    • vomiting, diarrhea may be bloody, oral and GI ulcerations
  • Muscle effects
    • hesitates to move, rigid skeletal muscles
    • ataxia, weakness, posterior weakness
    • seizures at high doses
    • myotonia with serious toxicosis***
    • rumen atony
  • Renal tubular degeneration
  • Hepatic necrosis

3

Diagnosis of phenoxyacetic acid herbicide toxicity

  • oral and GI ulcers
  • enteritis, rumen stasis
  • congestion of kidney/liver
  • hyperemia of lymph nodes
  • clinical pathology (liver damage)
  • chemical analysis of serum, urine

4

Treatment of phenoxyacetic acid herbicide toxicity

  • GI (emesis, lavage) or dermal (bath) decontamination
  • activated charcoal/cathartic
  • ion-trapping to enhance excretion
    • 1-2 mEq/kg NaHCO3 if kidneys normal
  • Prognosis is good for treated animals

5

ergot alkaloids

  • Produced in small grains (barley, rye, wheat, oat) by Claviceps purpurea, similar alkaloids produced by endophytic fungus in tall fescue
  • in infected grains, the seeds are replaced by sclerotia (look like mouse droppings)
  • fescue infection not detectable by the naked eye
  • at least 40 alkaloids have been ID'd including ergovaline, ergonovine, ergotamine, and LSD

6

MOA of ergot toxicity

  • Alkaloids are dopamine serotonin agonists which produce hallucinations
  • Activity at dopamine receptors in pituitary lead to decreased prolactin secretion
  • Smooth muscle contraction, especially in uterus and peripheral vasculature, may be due to alpha-adrenergic antagonist activity - cause abortion and ischemia

7

Clinical signs of ergotism in cattle

  • reduced feed intake and weight gain, heat intolerance, retain winter coat ("summer slump")
  • necrotizing egotism
    • lameness, gangrene of extremities that may result in sloughing of feet, ears, and tail during cold weather "fescue foot"
  • fat necrosis
  • poor reproductive perfomance

8

clinical signs of ergotism in horses

primary problem is abortions, weak foals, and prolonged gestation

9

clinical signs of ergotism in pigs

infertility and early parturition
decreased milk production

10

diagnosis of ergotism

  • evidence of sclerotia in feed
  • fescue in forage matter
  • chemical analysis of feed and forage for ergot metabolites

11

treatment of ergotism

  • treat by removing source, prevent secondary infections
  • Metoclopromide and domperidone increase prolactin secretion and normalize gestation in mares

12

ionophores

  • Compounds that form lipid soluble complexes with cations
    • facilitate specific ionic transport across membranes
  • Used as antibiotic (monensin, salinomycin)
    • monensin used in beef and dairy industry to prevent coccidiosis and prevent bloat
  • Approved for use in dairy cattle
  • Several marketed and off label uses

13

MOA of Ionophores

  • Act by increasing intracellular Na and Ca, leads to mitochondrial swelling and cell death, especially in muscle
  • Usually a result of feed-mixing errors
  • Among non-target species, horse most susceptible
    • results from consumption of ionophore containing poultry or cattle feed
  • Poultry are the least sensitive to ionophore toxicity

14

Clinical signs of ionophores in horses and cattle

  • Usually occur 12-72 hours after ingestion
  • anorexia is a common clinical sign in all animals
  • horses present with anorexia, colic, profuse sweating on flanks
    • may be in-coordinated and weak
  • cattle are similar to horses but with diarrhea and respiratory difficulty

15

clinical signs of ionophores in poultry, dogs, and cats

  • poultry
    • down with legs and wings stretched out
  • dogs
    • exhibit posterior paresis and paralysis with lasalocid
  • cats
    • developed polyneuropathy from salinomycin

16

diagnosis of ionophores

  • increased muscle enzymes and myoglobinuria
  • elevated AST, CK, LDH, alkaline phosphatase, BUN, Bilirubin
  • decreased K and Ca (most pronounced in horses)
  • chemical analysis of feeds, liver (not blood)
  • differentiate from other causes of colic: vit E and Se deficiency, white snakeroot, blister beetle, gossypol, botulism

17

treatment of ionophores

  • No specific treatment or antidote
  • Feed change to non-ionophore must be made immediately until all diagnostic procedures are completed
  • Offer supportive therapy (fluid and electrolyte replacement)
  • Recovered animals may die later due to exercise intolerance

18

tetanus

  • Mostly affects cattle
  • Usually caused by spores in puncture wounds, can be ingested

19

MOA of tetanus

  • Toxin acts by blocking release of GABA and glycine (inhibitory neurotransmitters)
  • Results are overstimulation of muscles leading to stiffness and tetany

20

clinical signs of tetanus

  • Stiffness and reluctance to move
  • Twitching and tremors of the muscles
  • Lockjaw
  • Unsteady gait with stiff held out tail
  • Bloat is common in ruminants
  • Later signs: collapse, spasm, death

21

treatment of tetanus

  • Antitoxin is available but only of value at the very early stages
  • Supportive therapy
  • Prognosis is very poor
  • Vaccination available

22

Common respiratory toxins that cause ventilatory muscle paralysis

  • Botulism
  • tetanus
  • snake venom
  • OP insecticides
  • strychnine

23

Common respiratory toxins that can cause respiratory center depression

  • Barbituates, opiates/opiods
  • Ethylene glycol
  • hypnotics, sedatives
  • tricyclic antidepressants
  • crude oil