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Veterinary Toxicology > Cardiovascular Toxicology, Pt. 2 > Flashcards

Cardiovascular Toxicology, Pt. 2 Flashcards

1
Q

What is the source of gossypol? What is it? Where is the toxin most concentrated?

A

cotton plants, like Gossypium —> seed, seed meal, seed cake

bi-naphthyl-aldehyde, which makes the cotton plant more insect-resistant

the glands within the seeds

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2
Q

Why is cotton seed widely used in livestock feed? What is it deficient in?

A

it is economical and high in protein, fiber, fat, and energy

  • essential amino acids: lysine and tryptophan
  • vitamins A and D
  • minerals: calcium
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3
Q

What species are most susceptible to gossypol toxicity? What is an exception? Why are other species resistant?

A

monogastrics, except horses

ruminants - gossypol binds to soluble protein components in rumen liquor of ADULTS (young are still susceptible)

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4
Q

What are the 2 forms of gossypol? What causes exposure? Where does is accumulate?

A

free and bound —> free form is more bioavailable and toxic

oral ingestion

plasma, heart, liver, muscle, and testis, BUT NOT milk

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5
Q

What is the mechanism of toxicity of gossypol?

A

causes cardiac muscle destruction and interferes with conduction by affecting potassium movement, resulting in focal myocardial necrosis

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6
Q

What are 5 additional mechanisms of toxicity of gossypol other than focal myocardial necrosis?

A
  1. anti-fertility - damage spermatogenic epithelium, decreases sperm motility, suppresses estradiol and progesterone
  2. chelates iron and causes RBC lysis - anemia
  3. binds amino acids in the GIT making them unavailable for absorption
  4. inhibits protein synthesis
  5. induces nutritional deficiencies - vitamin A and E, calcium, and amino acids
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7
Q

What are common misdiagnoses of gossypol toxicity in lambs and pigs?

A

LAMBS - sudden death caused by over-eating

PIGS - chronic labored breathing (thumping) unresponsive to antibiotics caused by pneumonia

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8
Q

What are common clinical signs of gossypol toxicity? What do cattle present with?

A
  • gradual heart failure: edema, jugular vein distension, congestion
  • anorexia, weakness
  • rough hair coat
  • poor-doer
  • reproductive problems, decrease in fertility

decreased heat tolerance and hemoglobinuria

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9
Q

How is gossypol toxicity diagnosed? What postmortem lesions are most important?

A
  • history of extended feeding of cottonseed meal or cottonseed products
  • clinical signs: sudden death, chronic dyspnea
  • lack of response to antibiotic therapy
  • analytical detection of significant concentrations of free gossypol in feed

signs of cardiomyopathy

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10
Q

What is the best symptomatic treatment of gossypol toxicity? Why is activated charcoal and cathartics of little value?

A
  • remove source - withdraw cottonseed products from diet
  • treat heart failure and pulmonary edema
  • give nutritional supplements, especially vitamin A, iron, lysine, and protein

toxicosis is associated with chronic exposure and is cumulative in nature

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11
Q

What are the 2 most common toxic toads in North America? Where are they primarily found? What animals are most susceptible?

A
  1. Rhinella marina - cane/marine toad
  2. Bufo alvarius - Colorado River toad

FL, TX, CO, AZ, HI

dogs, sometimes cats and ferrets

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12
Q

What is the major toxic principle of toad poisoning? What are 4 others?

A

bufadienolides - bufagenins and bufotoxins are structurally similar to cardiac glycosides

  1. bufotenine
  2. catecholamines - dopamine, EPI, NE
  3. serotonin
  4. indolealkylamines
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13
Q

What causes variability in toxicity in toad poisoning?

A

size of dog and size/species of toad (1mg/kg)

  • severe toxicosis with small dogs encountering larger toads, since they have larger parotid glands, allowing them to produce more secretions and toxins
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14
Q

When exposure to toad poisoning most common? How do toads intoxicate prey?

A

summer, fall, and periods of high humidity

  • toxins are produced and stored in the parotid glands along the neck and parascapular region
  • when mouthed/bitten, toads release toxins in a thick milky-white substance via pores on the glands
  • toxins are rapidly absorbed via the buccal mucous membranes, GIT mucosa, broken skin, and conjunctiva
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15
Q

What are the mechanisms of toxicity of the toxic principles of toad poisoning?

A
  • bufadienolides: cardiac glycoside-like and inhibits Na/K ATPase and voltage-gated Na, K, and Ca channels, disrupting excitable cells
  • bufotoxins: vasoconstriction
  • bufotenine: systemic pressor activity (increases BP) and hallucinogen
  • indolealkylamines: hallucinogenic
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16
Q

What is the mechanism of toxicity of catecholamines found in toad poisoning? What other toxin does it work synergistically with?

A

arrhythmogenic

bufadienolides - produces greater cardio-respiratory effects

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17
Q

What is the characteristic clinical sign of toad poisoning? What else is seen?

A

brick-red buccal cavity MM and hypersalivation + cardiac glycoside-like effects (arrythmias)

  • vomiting, vocalization
  • pawing and foaming at the mouth
  • anxiety, disorientation, ataxia
  • blank stare, mydriasis, nystagmus
  • hyeractivity, hyperesthesia
  • opisthotonus, convulsions, seizures
  • tachypnea, hyperthermia, acidosis, hyperkalemia
    (rapid onset with death in 15 mins)
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18
Q

What are 4 differential diagnoses that should be considered with toad poisoning?

A
  1. toxicosis with acute onset: metaldehyde, methylxanthines, oleander, foxglove, pyrethrins/pyrethroids, anticholinesterase insecticides
  2. ingestion of acids and alkalis
  3. heat stroke, trauma
  4. antidepressants, sympathomimetics
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19
Q

How should decontamination with toad poisoning be done?

A
  • flush mouth with copious amounts of water rostrally to avoid ingestion before seeking veterinary care
  • with severe signs, oral lavage is done after stabilization, anesthesia, and insertion of a cuffed ET tube
  • activated charcoal and cathartics are also advised
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20
Q

How is tachycardia caused by toad poisoning treated? What should be done for patients with pre-existing heart disease? Unresponsive patients?

A

Propranolol —> monitor ECG

use lower doses of Propranolol

Lidocaine, Phenytoin, Procainamide

21
Q

What is used to treat patients with marked bradycardia following toad poisoning? When is this contraindicated?

A

Atropine, Dopamine

hypersalivation - may worsen tachycardia and decrease dilution of toxins

22
Q

What is used to treat seizures/tremors/agitation, hyperkalemia, metabolic acidosis, and respiratory acidosis following toad poisoning?

A

Diazepam, Barbiturates

insulin, glucose, sodium bicarbonate

crystalloid IV fluids, sodium bicarbonate (pH < 7.1)

positive pressure ventilation

23
Q

What antidote may be of value for toad poisoning? What can increase excretion?

A

Digibind (not clinically tested for toad toxicosis)

IV lipid emulsion reduces the toxicity of the more lipophilic constituents of toad secretion, like bufodienolides

24
Q

What is the source of ergot alkaloids? What are the 2 types? What species are susceptible?

A

fungus Claviceps purpurea that invades grasses, like rye, oats, barley, canary, brome, and triticale

  1. ergopeptine alkaloids - ergotamine, ergovaline, ergosine, ergocristine, ergocornine
  2. ergoline alkaloids - lysergic acid, ergonovine, lysergol

cattle, sheep, swine, horses

25
Q

Where in the grass is ergot commonly found/concentrated?

A

sclerotia/ergot bodies - dark compacts of hardened fungal (Claviceps) mycelia with ergot alkaloids

26
Q

How are the toxic principles of ergot excreted?

A
  • ergopeptine alkaloids: bile
  • ergoline alkaloids: urine
27
Q

What is the mechanism of toxicity of ergot alkaloids?

A

interact with biogenic amines (NE, serotonin, dopamine) causing….

  • inhibition of D1 vasodilatory receptors and agonism of α1-adrenergic and serotonin receptors leading to vasoconstriction, ischemia, and gangrene formation
  • stimulation of D2 receptors in anterior pituitary, which decreases prolactin secretion
28
Q

What causes the clinical signs associated with ergot toxicosis? What 4 clinical signs are most common?

A

vasoconstriction and decreased prolactin

  1. gangrenous/cutaneous ergotism - lameness, swelling, sloughing of feet below fetlocks (+/- ears, tail)
  2. hyperthermia
  3. reproductive syndrome - agalactia, prolonged gestation, dystocia, abortions
  4. nervus syndrome - more common in carnivores, horses, and sheep, possible caused by tremorgenic mycotoxins
29
Q

Gangrenous ergotism:

A
30
Q

How is ergotism diagnosed?

A
  • detection of C. purpurea sclerotia in plant tissues and feed
  • ergot alkaloid concentrations in forage/hay/processed feeds
  • analysis of animal tissues
  • clinical signs
31
Q

What is key to successful ergotism treatment? What are common ways to do this?

A

early recognition

  • remove animals from grass sources and more to a dry,warm environment
  • treat secondary bacterial infection
32
Q

What is the source of fescue toxicosis?

A

Festuca arundinacea (tall fescue), a major forage grass common in eastern USA

33
Q

What toxic principles are found in fescue? What relationship does it have with the grass?

A

ergot alkaloids, ergoline and ergopeptine (ergovaline = 90%), produced by endophytic fungus, Neotyphodium coenophialum

MUTUALISTIC - fungus generates toxins that make fescue resistant to drought, insects, nematodes, fungi, and herbivores and fescue provides a proper environment and nutrients to fungus

34
Q

What causes fescue toxicosis? What are the mechanisms of toxicity?

A

interacts with biogenic amines

  • D1 receptor inhibition
  • α1-adrenergic and serotonergic receptor agonism
  • stimulation of D2 receptors, resulting in
35
Q

What are the 3 results of D1 receptor inhibition and α1-adrenergic and serotonergic receptor agonism in fescue toxicity?

A
  1. vasoconstriction - impaired thermoregulation, impaired circulation to placenta, extremities, and abdominal/pelvic fat
  2. uterine contraction due to α1-adrenergic effects
  3. decreased feed intake
36
Q

What are the 5 results of D2 receptor stimulation in fescue toxicity?

A
  1. decreased prolactin secretion from pituitatry - impaired lactogenesis and agalactia
  2. impaired steroidogenesis due to low progesterone and high estradiol causing reproductive problems
  3. decreased feed intake and inability to shed winter hair coat
  4. impaired metabolism of lipids and carbohydrates
  5. dysregulation of thermoregulatory center causing hypothermia or hyperthermia
37
Q

What species are the most susceptible to fescue toxicosis? What 4 syndromes have been described?

A

horses > cattle> sheep

  1. fescue foot
  2. summer slump
  3. fat necrosis
  4. reproductive and lactation problems
38
Q

When is fescue foot most common? What is it characterized by?

A

cattle in later fall or winter - hypothermic conditions

progressive lameness

39
Q

What are the 2 major steps to fescue foot? What limbs are most commonly affected?

A
  1. swelling and reddening of coronary band with knuckling of pastern joints, arching of the back, and weight shifting
  2. ischemic necrosis above the foot and other extremities, like ears and tails

hind limbs

40
Q

What is the most common complaint with summer slump? What are 4 characteristics of this syndrome?

A

cattle/sheep ADR

  1. reduced feed intake, growth, and milk production
  2. reduced conception and calving rates
  3. impaired thermoregulatory ability with heat intolerance, hyperthermia, and tachypnea resulting in behavioral changes (more time under shade or at watering holes/ponds)
  4. rough hair coat, lethargy, diarrhea
41
Q

Summer slump:

A

fescue toxicosis!

42
Q

When is fat necrosis (lipomatosis) most common in fescue toxicosis? What is it associated with? What does it result in?

A

ruminants - mature cattle with prolonged exposure

hard necrotic fat in abdominal and pelvic cavities palpable transrectally, but are normally seen postmortem

digestive and genitourinary signs due to obstruction and/or constriction - hystocia, bloat, nephrosis, uremia

43
Q

In what animals is reproduction and lactation syndrome common with fescue toxicosis? What are the primary problems?

A

cattle, sheep, horses

abortion, stillbirth, agalatia

44
Q

What 8 clinical signs are common in horses with reproductive and lactation syndrome with fescue toxicosis? What causes them?

A
  1. decreased conception rate
  2. prolonged gestation with increased fetal size
  3. minimal signs of impending parturition - no waxing (colostrum leakage) or udder development
  4. red-bag presentation - foal preceded by chorioallantois
  5. dystocia
  6. weak foals
  7. edema of fetal membranes
  8. retained placenta

dysregulation of hormones - decreased prolactin and progesterone and increased estradiol

45
Q

What must be ruled out before fescue poisoning disgnosis? What should be done with animals affected?

A

foot rot, frost bite, injuries

remove animals from infected fescue - may be impractical due to lack of alternative forages and sources of hay

46
Q

What drugs acting on receptors are commonly used for symptomatic treatment of fescue toxicosis? In what animals is this not approved for?

A
  • D2 antagonist: Metclopramide
  • α1-adrenergic antagonist: Prazosin
  • α1-adrenergic and serotonin blocker: Phenoxybenzamine

food animals - side effect, drug residue concerns

47
Q

What is recommended for agalactia and prolonged gestation in mares with fescue toxicity? What is their mechanism of action?

A
  • Domperidone (Equidone)
  • Perhenazine
  • Sulpiridie
  • Acepromazine
  • Reserpine*

antagonize D2 receptors or deplete dopamine*

48
Q

What is the difference between ergotism and fescue toxicosis?

A

ERGOTISM = C. purpurea, parasitism, more prevalent in late summer when seed heads of grasses mature

FESCUE TOXICOSIS = N. coenophialum, mutualism, most common in late fall and winter

Veterinary Toxicology (29 decks)

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