Musculoskeletal Toxicity Flashcards
1
Q
phenoxyacetic acid herbicides
A
- 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
Q
clinical signs of phenoxyacetic acid herbicide toxicity
A
-
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
Q
Diagnosis of phenoxyacetic acid herbicide toxicity
A
- 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
Q
Treatment of phenoxyacetic acid herbicide toxicity
A
- 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
Q
ergot alkaloids
A
- 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
Q
MOA of ergot toxicity
A
- 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
Q
Clinical signs of ergotism in cattle
A
- 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
Q
clinical signs of ergotism in horses
A
primary problem is abortions, weak foals, and prolonged gestation
9
Q
clinical signs of ergotism in pigs
A
infertility and early parturition
decreased milk production
10
Q
diagnosis of ergotism
A
- evidence of sclerotia in feed
- fescue in forage matter
- chemical analysis of feed and forage for ergot metabolites
11
Q
treatment of ergotism
A
- treat by removing source, prevent secondary infections
- Metoclopromide and domperidone increase prolactin secretion and normalize gestation in mares
12
Q
ionophores
A
- 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
Q
MOA of Ionophores
A
- 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
Q
Clinical signs of ionophores in horses and cattle
A
- 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
Q
clinical signs of ionophores in poultry, dogs, and cats
A
-
poultry
- down with legs and wings stretched out
-
dogs
- exhibit posterior paresis and paralysis with lasalocid
-
cats
- developed polyneuropathy from salinomycin
