Musculoskeletal & Pulmonary Flashcards
What are Phenoxyacetic Acid Herbicides?
2,4-D (Scott’s weed and feed), 2,4,5-T, Silvex
Low toxicity in most animals
Dogs most susceptible
Mechanism of action of phenoxyacetic acid herbicides?
Unknown
Clinical signs of phenoxyacetic acid herbicide toxicosis
GI- vomiting diarrhea, ulceration (often only signs in dogs)
Muscle- reluctance to move, rigid muscles, ataxia, weakness, seizure, rumen atony, MYTONIA with serious toxicosis
Renal tubular degeneration
Hepatic necrosis
Diagnosis of phenoxyacetic acid herbicide toxicosis
Oral and GI ulcers Enteritis, rumen stasis Congestion of kidney/liver Hyperemia of lymph nodes Liver damage Chemical analysis of serum, urine
Treatment of phenoxyacetic acid herbicide toxicosis
GI emesis or lavage Bathe Activated charcoal Cathartic Ion trapping
What is ergot?
Alkaloid produced in small grains where seeds are replaced by sclerotia (look like mouse droppings)
Mechanism of action of ergot toxicity
Dopamine serotonin receptor agonist which produce hallucinations
Leads to decreased prolactin secretion
Cause smooth muscle contraction (uterus and peripheral vasculature which cause abortion and ischemia) -> sever reproductive problems
Clinical signs of ergotism (cattle, horses, pigs)
Cattle: Reduced feed intake, weight gain, heat intolerance, retained winter coat (“summer slump”), necrotizing ergotism, fat necrosis, poor reproductive performance
Horses: Abortion, weak foals, prolonged gestation
Pigs: infertility, early parturition, decreased milk production
What is necrotizing ergotism?
Lameness, gangrene of extremities, sloughing of feet, ears, and tail during cold weather “Fescue foot”
Diagnosis of ergotism
Evidence of sclerotia in feed
Fescue in forage matter
Chemical analysis of feed and forage for ergot metabolites
Treatment of ergotism
Remove source, prevent secondary infection
Metoclopromide and domperidone to increase prolactin secretion and normalize gestation
What are ionophores?
Compounds that form lipid-soluble complexes with cations and facilitate ion transport across specific membranes
Used as an antibiotic
Used to improve milk production
Mechanism of action of ionophore toxicity
Act by increasing intracellular Na+ and Ca++ which leads to mitochondrial swelling and cell death
Usually a result of feed-mixing errors
Horse most sensitive, poultry least sensitive
Clinical signs of ionophore toxicity
Horses: anorexia, colic, profuse sweating on flanks, incoordination, weakness
Cattle: same as horses but with diarrhea and respiratory difficulty
Poultry: down with legs and wings stretched out
Dogs: posterior paralysis from lasalocid
Cats: polyneuopathy from salinomycin
Diagnosis of ionophore toxicity
Increased muscle enzymes and myoglobinuria
Elevated AST, CK, LDH, ALP, BUN, bilirubin
Decreased K and Ca
Chemical analysis of feed and water (not blood)
Treatment of ionophore toxicity
No specific treatment or antidote
FEED CHANGE
Supportive therapy
Characteristics of tetanus (clostridium tetani)
Mostly affects cattle
Usually caused by spores in puncture wounds or can be ingested
Mechanism of action of tetanus
Toxin acts by blocking release of GABA and glycine (inhibitory transmitters)
Results in overstimulation of muscles leading to stiffness and tetany
Clinical signs of tetanus
Stiffness, reluctance to move Twitching, tremors Lockjaw Unsteady gait with stiff, held out tail Bloat is common in ruminants Later signs include collapse, spasm, death
Treatment of tetanus
Antitoxin is available but only useful at very early stages of toxicity
Supportive therapy
Poor prognosis
Common respiratory toxins
Ventilatory muscle paralysis:
Botulism, tetanus, snake venom, OP insecticides, strychnine
Respiratory center depression:
Barbiturates, opioids, ethylene glycol, hypnotics, sedatives, tricyclic antidepressants, crude oil
