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2. Smith and EIM > Toxicants > Flashcards

Toxicants Flashcards

1
Q

cyanogenic plants

A
  • sudden death
  • bright red MMs, bright red venous blood
  • cyanosis, dyspnea, muscle twitching, staggering, convulsions, coma
  • contain hydrogen cyanide
  • Tx= sodium thiosulfate, sodium nitrate
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2
Q

nitrate accumulating plants

A
  • sudden death
  • weak, drowsy, chocolate MMs, tremors, tachycardia/tachypnea, staggers
  • Tx= methylene blue
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3
Q

copperweed

A
  • sudden death

- oxytentia acerosa

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4
Q

death camas

A
  • zigadenus
  • sudden death
  • salivation, bloody froth, vomiting, muscle weakness, staggers, tachycardia
  • Tx= atropine
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5
Q

dogbane

A
  • apocynum
  • contains cymarin
  • sudden death, blue MMs
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6
Q

easter lily

A
  • zephyranthes atamasca

- sudden death, staggering, D+

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7
Q

false hellbore, skunk cabbage

A
  • veratrum
  • contain cyclopamine, cyclopasine, jervine
  • sudden death, salivation and frothing, weak, V+, tachyarrhythmias

teratogen - cyclops lambs

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8
Q

fitweed

A
  • corydais
  • containe isoquinolone alkaloid
  • sudden death, neuro signs
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9
Q

foxglove

A
  • digitalis purpurea
  • contains digitoxin, digitalin, digoxin, saponins, alkaloids
  • sudden death
  • colic, melena, anorexia, PU, arrhythmias
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10
Q

jimsonweed, thornapple

A
  • datura stramonium
  • contain tropane alkaloids
  • sudden death, colic, ileus, D+, mydriasis, tachycardia, anorexia, spasms, seizures, PU
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11
Q

larkspur

A
  • delphinium
  • contains alkaloids
  • sudden death, weakness, staggers, twitches, bloat, tachyarrhythmias
  • die within 3 hrs
  • range cattle

-Tx= IV phyostigmine, neostigmine

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12
Q

milkvetches

A
  • astragalus
  • contain miserotoxin
  • SUDDEN DEATH, NEURO
  • acute resp distress, emphysema, wheezing, drooling
  • goose stepping, knuckling, collapse
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13
Q

milkweed

A
  • asclepias
  • contain cardenolides
  • sudden death, depression, weakness, resp paralysis
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14
Q

mistletoe

A
  • containe amines, toxic proteins

- sudden death, colic, D+, bradycardia, hypotension

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15
Q

nightshade

A
  • solanum
  • contains solanine and other glycoalkaloids
  • sudden death, dyspnea w/ exp grunt, salivation, weak and trembling
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16
Q

perilla mint

A
  • perilla frutescens
  • contains perilla ketone, egomaketone, isoegomaketone
  • sudden death, acute resp distress
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17
Q

poison hemlock

A
  • conium maculatum
  • contains coniine, gamma coniceine, cyanapine
  • sudden death, trembling, ataxia, resp paralysis, abortion or birth defects
  • Tx= ATROPINE
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18
Q

rayless goldenrod

A
  • isocoma
  • contain tremetol
  • sudden death, trembling legs and nose, stiff gait, constipation, urine dribbling, acetone breath
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19
Q

sweet clover

A
  • melilotus
  • contains coumarin, converted to dicoumarol by molds
  • sudden death, hemorrhage
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20
Q

white snakeroot

A
  • eupatorium rugosum
  • contains tremetol
  • sluggish behaviour, acetone breath, melena, constipation, dysphagia, tachyarrhythmias, CHF, myoglobinuria
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21
Q

plant poisoning of range cattle

A

1) locoweed

2) tall larkspur

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22
Q

blocks molecular oxygen transfer in cytochrome oxidase systems in mitochondria, causing tissue anoxia

A

cyanide

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23
Q

causes of nitrate accumulation in plants

A
  • fertiizer
  • photosynthesis is impaired by shade or prolonged cloudiness
  • drought, frost, hail
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24
Q

bracken fern

A
  • pteridium aquilinum
  • contains ptaquiloside
  • neuro signs, thrombocytopenia, bladder and GI cancer

-Tx= thiamine

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25
Q

castor bean

A
  • ricinus communis
  • contains ricin
  • neuro signs, bloody D+, tenesmus, colic
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26
Q

horse nettle

A
  • solanum carolinense
  • contains solanine
  • neuro signs

-Tx = physostigmine

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27
Q

horse tail or scouring rush

A
  • equisetum
  • contains aconitic acid, palustrine, thiaminase
  • neuro, paresis

-Tx = thiamine

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28
Q

Jamaican nettle tree

A
  • contains trema toxin and ammonia

- blindness, signs of hyperammonemia

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29
Q

johnson grass

A
  • sorghum halepense
  • contains hydrocyanide
  • neuro, posterior ataxia, urinary incontinence and cystitis
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30
Q

locoweed

A
  • astragalus and oxytropis
  • containe swainsonine
  • neuro, abnormal behaviour, abortion, reduced fertility, skeletal malformations
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31
Q

lupine

A
  • contain piperidine, quinolizidine

- neuro, frothing, dyspnea, birth defects

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32
Q

oak

A
  • quercus
  • contains gallotannins
  • neuro, ileus, mouth ulcers, mucosal discoloration, patchy sweating, dark urine
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33
Q

yellow star thistle

A
  • centaurea solstitalis
  • contains sesquiterpene lactones
  • neuro signs, twitching lips, tongue flicking, chewing, poor prehension, facial paralysis
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34
Q

4 syndromes of milkvetch

A

1) sudden death from methemoglobinemia, cattle and sheep
2) respiratory dz and emphysema, sheep
3) neuro
4) selenium toxicosis

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35
Q

tremetol

A
  • cumulative effects on skeletal and cardiac muscle

- white snakeroot, rayless goldenrod, and burrow weed

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36
Q

atypical myopathy

A
  • box elder seeds - Hypoglycin A
  • damages mitochondria, impairs lipid metabolism in muscle cells, –> cell death
  • weakness, recumbency, myoglobinuria
  • dysphagia, choke, colic
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37
Q

plants containing cardiac glycosides

A

milkweed, dogbane, indian hemp, blue-eyed grasses, foxglove, hellbores, hyacinth, oleander, periwinkle

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38
Q

important plants that damage myocardium in large animals

A

yew, avocado, death camas, and summer pheasant eye

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39
Q

PA

A
  • loss of appetite, lethargy, D+, constipation, icterus, photosensitization
  • liver failure
  • HE
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40
Q

oleander

A
  • tachycardia
  • severe gastroenteritis, diarrhea, abdominal pain
  • sweating, weakness
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41
Q

red clover

A
  • mold slaframine

- slobbers, bloat, D+, blindness, abortion, laminitis

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42
Q

enzootic hematuria

A 
bracken fern (ptaquiloside)
-carcinogenic to bladder epithelium
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43
Q

alsike clover

A

-hepatic encephalopathy or photosensitization

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44
Q

plants containing PAs

A 
groundsel (senecio)
heliotrope 
houndstongue (cynoglossum)
kochia
patersons curse (echiu plantagineum)
rattlebox, rattlepod (crotalaria)
tansy ragwort (senecio)
tarweed, fiddleneck (amsinckia)
vipers bugloss (echium vulgare)
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45
Q

ergot alkaloids + fescue

A

claviceps purpurea

-failure to develop udder, agalactia, prolonged gestation, placental abnormalities, dystocia

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46
Q

ergot alkaloids + livestock

A
  • vasoconstriction
  • gangrene and lameness in cold weather
  • heat stroke
  • summer slump
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47
Q

perilla mint in ruminants

A
  • compounds are bioactivated in the lung

- cause atypical interstitial pneumonia and acute resp distress

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48
Q

common photosensitization plants

A

st johns wort (hypericum perforatum)
buckwheat (fagopyrum)
dutchmans breeches, bishops weed, rain lily, spring parsley, giant hog weed, cow parsnip (heracleum)

49
Q

syndromes of excess selenium

A

1) acute toxicosis
2) blind staggers
3) chronic alkali disease

50
Q

oxalate poisoning is most common in

A

sheep

  • sequestration of ca and mg
  • tetany or flaccid paralysis
51
Q

most common cyanobacterial dz (algae)

A

acute hepatotoxicosis from microcystin exposure

-hypovolaemia, shock, blood loss into disentegrated liver lobules and hepatocyte emboli traveling to lungs

52
Q

aflatoxins

A
  • aspergillus flavus and parasiticus, corn, nuts, cottonseed
  • hepatic insult/failure
  • cancer
53
Q

zearalenone

A
  • corn, wheat, barley

- hyperestrogenism

54
Q

fumonisins

A
  • corn
  • equine leukoencephalomalacia = moldy corn poisoning
  • swine = pulmonary edema
  • hepatic dz
55
Q

bovine bonkers

A
  • ammoniated feed

- hyperexcitability

56
Q

action of organophosphates and carbamates

A
  • acetylcholinesterase inhibitor
  • AcH accumulates at junctions and causes excessive synaptic action
  • nervous and skeletal muscle signs

-Tx= pralidoxime chloride (2-PAM)

57
Q

Monensin

A

Ionophore Antibiotic
Biologically active compound (produced by a fungus in nature)​
​
Uses: coccidiostat (poultry) and for feed efficiency (cattle)​
​Mechanism: selective transport Na+ and K+ ions b/w intra and extracellular spaces​​
​
Horses most sensitive to toxicosis​

58
Q

Monensin Toxicity

A
  1. LD50 in horses 1-2mg/kg​
    ​
  2. Primary target organ = heart, severe mitochondrial damage​
    ​
  3. Dx samples: the feed itself, serum, liver, GI content, feces​
    ​
  4. Tx: laxatives / charcoal, vit E / Se, IVFT and electrolytes / acid-base correction​
    (there is no antidote)​
59
Q

Clinical Presentations of Monensin Tox

A

Peracute toxicity (death within hours):​
Severe hemoconcentration, hypovolemic shock​
​
Acute toxicity:​
feed aversion, colic, watery feces, intermittent sweating, stiffness, progressive muscle weakness (especially hindquarters), ataxia, recumbency, tachycardia, hypotension, dyspnea, polyuria​
​
Survive sublethal dose: ​
Reduced athletic performance, ill-thriftiness, cardiac failure (tachycardia, AF)​
myocardial sarcolemma damaged and replaced by fibrous tissue

60
Q

Lasalocid​

A

Accepts monovalent AND divalent cations​

CS, Dx and Tx similar to monensin toxicosis ​

Ataxia + paresis and paralysis​

Least toxic ionophore, LD50 21.5mg/kg

61
Q

Salinomycin

A

Accepts just monovalent cations (like monensin)​

CS, Dx and Tx similar to monensin toxicosis ​

Lethal dose not provided in text

62
Q

Ionophore Toxicity

A

Critical evaluation of cardiac function of any previously intoxicated horse​ that is destined to return to some form of athletic endeavor is judicious.

63
Q

NITRATES AND NITRITES

A

Nitrate poisoning is common in ruminants but rare in horses ​

Nitrates naturally undergo microbial decomposition to nitrites​

Risk is when horses are exposed to preformed nitrite ​— ingesting feed / water where nitrates have decomposed to yield large amounts of nitrites (both are water soluble)​

Moist haystacks, water troughs, farm ponds, silages, pig swills​

Clinical signs related to severe oxygen deficiency

64
Q

Clinical signs of nitrate toxicity become evident when ___% of hemoglobin is oxidized to methemoglobin?

A

30-40%

65
Q

Nitrate Toxicity

A

Vasodilation leads to hypotension and decreased CO​

Dx:​ Test forage/feed/water for nitrate or nitrite​
Blood test for methemoglobin (quickly, not stable)​
Ocular fluid on post mortem ​

Tx:​ Methylene blue 4.4mg/kg as 1% solution with isotonic saline​
Repeat in 30min if needed​
Vitamin C - less effective alternative​
Supportive – oxygen, laxatives / charcoal ​

66
Q

Cyanide CS

A

Affected animals commonly are found dead ​— anoxia in the brain​

*Tachypnea, panting/gasping, excitement, salivation, lacrimation, muscle tremors, defecation, urination, mydriasis. Followed by convulsions, death​
​
Horses surviving > 90 - 120 minutes after exposure usually survive ​
Don’t need further treatment ​

67
Q

what toxic syndrome does ingestion of black walnut shavings cause in horses?

A

laminitis

Horses have a favourable prognosis for recovery if they are removed quickly from the offending bedding.

68
Q

horses with chronic wild jasmine ingestion develop lameness and weight loss despite a good appetite. what else can affected horses develop?

A

Hypercalcemia and renal failure

Solanaceae family plants contain a potent steroid glycoside ​

  • Vitamin D– like activity​
  • Normal vitamin D negative feedback mechanism bypassed ​
  • Excessive Ca and P absorption at level of the GIT​ exceeds renal capacity to excrete ​
  • Soft tissue mineralization (dystrophic calcification)​ of flexor tendons, suspensory ligament, other elastic tissues​
  • Renal azotemia and hypercalcemia (phosphorus may be WNL)
69
Q

the toxic mechanism of tall fescue is

A

fungal endophyte that grows within the stem, leaf sheaths, and seeds

ergopeptine alkaloids: Ergovaline and ergosine

70
Q

AT WHAT POINT IN GESTATION ARE PREGNANT MARES SUSCEPTIBLE TO TOXICITY BY INFECTED FESCUE? ​

A

late >300 days

71
Q

summer slump or summer syndrome​

A

also caused by tall fescue

characterized by anorexia, weight loss, poor hair quality, pyrexia, and hypersalivation. ​

72
Q

SIGNS OF IODINE TOXICOSIS

A

A: nasal discharge due to increased respiratory tract secretions​
B: excessive lacrimation​
C: intermittent non-productive cough​
D: nonpruritic generalized alopecia and scaling

73
Q

Carbamate Pesticides

A

CS of toxicity in horses reflect muscarinic and nicotinic cholinergic overstimulation:
profuse salivation, severe GI, hypermotility, severe pain, abdominal cramps and diarrhea, excessive lacrimation, miosis, sweating, dyspnea, cyanosis, and urinary and fecal incontinence. Affected animals also may cough frequently as a sign of excessive accumulation of respiratory tract secretions.

The signs reflected by nicotinic overstimulation include excessive stimulation of the skeletal muscles. The muscles of the face, eyelids, and tongue, in addition to the general musculature, may twitch. Some animals exhibit signs of generalized tetany that causes them to walk in a stiff-legged fashion. This hyperactivity may be followed by weakness and paralysis of the skeletal muscles​
​
Diagnosis can be made based on history to exposure, clinical signs, and response to atropine.

74
Q

organophosphates cause death by ?

A

asphyxia

the combined effects of nicotinic, muscarinic, and central cholinergic overstimulation or receptor paralysis. These effects include hypotension, bradycardia, bronchoconstriction and excessive bronchial secretion, inability of the respiratory muscles to work properly, cyanosis, and central respiratory depression. The animal actually dies of asphyxia.​

75
Q

Strychnine

A

Clinical signs appear within 10mins - 2hrs

—Initial signs include apprehension, nervousness, and muscle stiffness​
—Later signs are tetanic spasms – extreme extensor muscle rigidity​
—Death occurs when the spasm become more frequent until exhaustion or anoxia​
—The entire clinical episode typically lasts 2 hours

76
Q

Levamisole Toxicity

A

Is effective in eliminating lungworms, ascarids, and adult pinworms from horses. The drug also has been used in human beings and other animal species in an attempt to enhance immune system function. ​

Clinical signs occur within 1 hour of administration and include hyperexcitability, muscle tremors, hyperactivity, excessive sweating, and lacrimation. Recumbency may follow these signs, but animals that recover generally appear normal within 12 hours after exposure.​

77
Q

Nicotine Toxicity

A

Large doses result in a descending paralysis of the CNS​

Death results from respiratory failure caused by paralysis of the diaphragm and chest muscles​

The effects of a sublethal dose should diminish in a few hours​

78
Q

why are urea and non protein nitrogens (added to ruminant feed in addition to other uses) toxic in horses?

A

Hydrolyzed to AMMONIA

79
Q

Bracken Fern

A
  1. The toxic agent is Thiaminase​
  2. Horses can exhibit signs even If they have not ingested the plant for 2-3 weeks​
  3. Signs begin after ingesting the plant continuously for 30-60 days​
  4. Toxicity results in the systemic accumulation of a variety of metabolites, including pyruvate and lactate. ​–> thiamine deficiency
80
Q

which plants are implicated in nigropallidal encephalomalacia?

A

A) yellow star thistle (Centaurea solstitialis) ​

B) russian knapweed (Acroptilon repens) ​

C) Centaurea melitensis ​

81
Q

Jimson weed contains

A

Tropane alkaloids (atropine, scopalomine)–mydriasis, tachycardia, decreased gut sounds​

82
Q

Castor bean (Ricinus communis)​ contains

A

​Ricinnoleic aci–60S ribosome disruption, RBC agglutination​

83
Q

Nightshade (Solanum spp)​ contains

A

​Solanine–salivation, colic, increased borborygmi, diarrhea, mydriasis, depression, weakness​

84
Q

Pokeweed (Phylotacca americana)​ contains

A

Phytolaccine, mitogens–GI irritation, hemorrhagic gastritis, hemagglutionation, mitotic activity​

85
Q

Phosphorous Toxicity

A

Toxic signs start within hours of ingestion, undergo a latent period of 48 -96 hours, then recur​

initially shows as severe colic, GI irritation, occasional diarrhea, arrhythmias, cyanosis, shock, coma, death

late signs = liver dysfunction, including icterus and bleeding from the gingiva, GI, or kidney​

86
Q

Locoweed

A

Horses may have progressive clinical signs over several years due to addiction to the plant​

Clinical signs include lethargy, weight loss, incoordination, and nervousness under stress​

Indolizidine alkaloids, swainsonine, and swainsonine N-oxide are the suspected toxic agents​

The alkaloids, which may be due to an endophyte in the plant, cause vacuolization of the kidneys first (as early as 4 days), followed by the CNS by 8 days. If removed vacuoles go away, but exposure for >30 days results in permanent vacuolization in all tissues EXCEPT cardiac and skeletal muscle. Swainsonine is an alpha-mannosidase inhibitor, which causes oligosaccharide build-up in lysosomes​

Mild cases may resolve 1-2 weeks after plant removal, but chronic cases generally do not recover​

87
Q

Zinc Toxicosis

A

A) gradual onset lameness and stiffness​​
C) joint swellings​
C) osteochondrosis

88
Q

three clinical syndromes attributed to selenium toxicity

A

B) Acute (within 6 hrs): sweating, diarrhea, tachycardia, tachypnea, mild pyrexia, lethargy, and mild to severe colic, death in 24 hours; may be “dumb” before death​

C) Chronic (weeks – months): blind staggers, aimless wandering or circling, muscle weakness, incoordination, respiratory difficulty, and decreased vision, paralysis and death​

D) Alkali disease (weeks – months): initially lameness and swelling of the coronary bands; anorexia and mild depression –> transverse cracking of the hoof wall, loss of hair from mane and tail​

89
Q

Several horses in a herd become lame and have dark and discolored skin on the fetlocks with a line of demarcation. These areas are cool. Skin in some horses is sloughing. Other horses are showing signs of colic. What is the most likely causative agent?

A

Ergotism (Claviceps purpurea)

Ergotamine is a vasoactive substance that causes arterial and venous constriction and may damage capillary endothelium

90
Q

Iron tox mechanism

A

Toxicity occurs when serum iron levels exceed the iron-binding capacity of transferrin. Free circulating iron then damages blood vessels, may cause erosion and ulceration of the stomach and intestine, causes hepatocellular necrosis and fatty degeneration of the myocardium, and can produce cerebral edema

91
Q

What are the main clinical signs seen with sorghum toxicity?​

A

hindend ataxia and urinary incontinence​

92
Q

CS of VitD toxicity

A

A) depression, anorexia, weakness​
B) PU/PD​
C) murmurs and tachycardia​
D) stiffness and reduced mobility​

93
Q

What body system is affected by vit K3 toxicity?

A

acute renal failure

94
Q

Mercury Intoxication

A

acute – ARF, oliguria and depression, GI irritation​

chronic – oral ulceration, progressive respiratory difficulty, terminal azotemia​

treatment is with activated charcoal, dimercaprol, and supportive

95
Q

Nigropallidal Encephalomalacia​ - onset of signs is

A

always sudden

beginning w variable degrees of impairment of eating and drinking​

96
Q

Nigropallidal Encephalomalacia - Characteristic necropsy findings

A

bilaterally symmetric, and sharply defined softening and necrosis in areas of the globus pallidus and substantia nigra ​

97
Q

LEUKOENCEPHALOMALACIA

A

Most cases occur from late autumn through early spring, and most outbreaks have been associated with a dry growing period followed by a wet period​

ingestion of mycotoxin fumonsin B1 produced by molds on corn –> neurologic and hepatoxic syndromes ​

The onset of clinical signs is abrupt after 3-4 weeks of daily ingestion​

Older animals are more likely to be affected than younger animals ​

Neuro syndrome: incoordination, aimless walking, intermittent anorexia, lethargy, depression, blindness , head pressing –> may be followed by hyperexcitability, belligerence, extreme agitation, profuse sweating, delirium. Recumbency and clonic-tetanic convulsions possible before death. ​

Hepatotoxic syndrome - swelling of lips and nose, somnolence, severe icterus, petechiae of mucous membranes, abdominal breathing, cyanosis. Affected horses acute onset csx w death within hours to days. ​

Typical gross lesions: liquefactive necrosis, degeneration of cerebral hemispheres – degenerative changes also possible in brainstem, cerebellum, spinal cord. Bilateral or unilateral lesions. ​

98
Q

Lead sensitivity

A

Horses are much more sensitive than cattle to prolonged, low-dose exposure to lead,

but

much less sensitive than cattle to short-term exposure of large doses

99
Q

Lead Poisoning

A

primarily peripheral nerve dysfunction - motor nerves at greater risk​

—Depression and wt loss worsen over time​
—Laryngeal and pharyngeal paralysis, dysphagia, dysphonia, and proprioceptive deficits​
—Progressively may exhibit flaccidity of rectal sphincter; paresis of lower lip; and difficulty in prehension, mastication and deglutition. Aspiration pneumonia common, also intermittent fine muscle tremors ​
—Terminally: severe incoordination, anorexia, emaciation, and almost complete pharyngeal, and oesophageal paralysis w the inability to swallow food and water. ​

Intoxication primarily through ingestion

Peripheral neuropathy associated with Pb toxicosis in horses thought to be caused by peripheral nerve segmental demyelination, which impedes nerve impulse conduction and contributes to clinically observed signs. ​

100
Q

Oleander

A

sudden death

do not give calcium

101
Q

cyclops lamb

A

veratrum californicum
false hellebore
cyclopamine teratogen

102
Q

alkali disease

A

—Chronic excessive selenium ingestion
—skin and hoof abnormalities
—livestock in areas with seleniferous soils, such as the Great Plains
—Common seleniferous plant species with this potential include primary selenium accumulator plants, such as milkvetch (Astragalus spp.)

103
Q

enzootic hematuria in cattle

A

Bracken fern’s toxin, ptaquiloside, is carcinogenic to bladder epithelium

104
Q

TOXIN:

nephritis with necrosis and renal tubular casts is observed, possibly leading to acute renal failure

A

oak poisoning

105
Q

microcystins

A

produced by multiple cyanobacteria and detected in fresh and coastal waters worldwide

106
Q

most commonly reported cyanotoxin poisoning in large animals is

A

acute hepatotoxicosis subsequent to microcystin exposure

107
Q

the ____ is the target organ of aflatoxin metabolites in all species

A

liver

108
Q

two species most suceptible to fumonisin

A

horses and swine

109
Q

who is susceptible to zeralenone

A

perpubertal gilts

possibly first calf heifers

110
Q

the pathogenesis of clinical signs associated with dietary exposures to EAs can generally be explained in terms of:

A

vasoconstriction (ruminants) and/or hypoprolactinemia (mares)

111
Q

mechanism behind summer slump, dry gangrene, fescue foot, gangrenous ergotism

A

vasoconstriction!

112
Q

Copper causes ____ hemolysis

A

Intravascular

113
Q

___ are most sensitive to copper

A

Sheep, often chronic by getting the wrong species feed

114
Q

How does copper kill sheep?

A

Methemoglobin
Anemic from hemolysis
Pigment trashes the kidneys

115
Q

Nitrate vs cyanide

A

Nitrate = brown blood

Cyanide = cherry red blood

116
Q

Calves not thriving, can’t thermo regulate

A

Summer slump

Fescue

117
Q

Onion, brassica

A

Hemolysis

Heinz body anemia

118
Q

Pine needles

A

Late term abortion in cattle

2. Smith and EIM (22 decks)

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