Musculoskeletal & Pulmonary Flashcards

1
Q

What are Phenoxyacetic Acid Herbicides?

A

2,4-D (Scott’s weed and feed), 2,4,5-T, Silvex
Low toxicity in most animals
Dogs most susceptible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mechanism of action of phenoxyacetic acid herbicides?

A

Unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Clinical signs of phenoxyacetic acid herbicide toxicosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diagnosis of phenoxyacetic acid herbicide toxicosis

A
Oral and GI ulcers
Enteritis, rumen stasis
Congestion of kidney/liver
Hyperemia of lymph nodes
Liver damage
Chemical analysis of serum, urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Treatment of phenoxyacetic acid herbicide toxicosis

A
GI emesis or lavage
Bathe 
Activated charcoal
Cathartic
Ion trapping
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is ergot?

A

Alkaloid produced in small grains where seeds are replaced by sclerotia (look like mouse droppings)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Mechanism of action of ergot toxicity

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Clinical signs of ergotism (cattle, horses, pigs)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is necrotizing ergotism?

A

Lameness, gangrene of extremities, sloughing of feet, ears, and tail during cold weather “Fescue foot”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diagnosis of ergotism

A

Evidence of sclerotia in feed
Fescue in forage matter
Chemical analysis of feed and forage for ergot metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment of ergotism

A

Remove source, prevent secondary infection

Metoclopromide and domperidone to increase prolactin secretion and normalize gestation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are ionophores?

A

Compounds that form lipid-soluble complexes with cations and facilitate ion transport across specific membranes

Used as an antibiotic

Used to improve milk production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mechanism of action of ionophore toxicity

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Clinical signs of ionophore toxicity

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diagnosis of ionophore toxicity

A

Increased muscle enzymes and myoglobinuria
Elevated AST, CK, LDH, ALP, BUN, bilirubin
Decreased K and Ca
Chemical analysis of feed and water (not blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment of ionophore toxicity

A

No specific treatment or antidote
FEED CHANGE
Supportive therapy

17
Q

Characteristics of tetanus (clostridium tetani)

A

Mostly affects cattle

Usually caused by spores in puncture wounds or can be ingested

18
Q

Mechanism of action of tetanus

A

Toxin acts by blocking release of GABA and glycine (inhibitory transmitters)

Results in overstimulation of muscles leading to stiffness and tetany

19
Q

Clinical signs of tetanus

A
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
20
Q

Treatment of tetanus

A

Antitoxin is available but only useful at very early stages of toxicity
Supportive therapy
Poor prognosis

21
Q

Common respiratory toxins

A

Ventilatory muscle paralysis:
Botulism, tetanus, snake venom, OP insecticides, strychnine

Respiratory center depression:
Barbiturates, opioids, ethylene glycol, hypnotics, sedatives, tricyclic antidepressants, crude oil