FA3 Toxicology > Lecture 12 > Flashcards

Lecture 12 Flashcards

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1
Q

What is this plant and its characteristics?

A

foxglove; Digitalis purpurea
-herb with toothed leaves
-tubular pendant flowers that have spots inside
-toxins are digoxin and digitoxin

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2
Q

What is the mechanism of toxicity for foxglove and other cardiac glycosides?

A

-reversibly inhibit sodium-potassium ATPase pumps within myocytes
-inhibition leads to increased intracellular sodium levels
-build-up leads to a shift of sodium extracellularly via exchange for calcium ions
-influx of calcium and increased myocyte contractility result
-increased vagal tone leads to decreased frequency of cardiac contractions via prolonged conduction from SA and AV nodes
-end result is arrhythmias; both tachyarrhythmias and bradyarrhythmias

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3
Q

What are the clinical signs of foxglove toxicity?

A

*cardiac conduction abnormalities leading to arrhythmias:
-bradyarrhythmias with ventricular premature contraction
-AV block
-bidirectional ventricular tachycardia
-ventricular fibrillation

*GI disruption:
-salivation
-nausea
-vomiting
-bloody diarrhea
-abdominal pain

*weakness
*hypotension
*collapse
*death
*terminal seizures

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4
Q

How is foxglove toxicity diagnosed?

A

-clinical signs and proximity to cardiac glycoside plants
-presence of any type of arrhythmia with GI disturbance
-ECG showing “sagging” or “scooped” ST segment

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5
Q

What are the treatment steps for foxglove toxicity?

A

*treat arrhythmia:
-atropine for bradyarrhythmia
-lidocaine for AV block

*activated charcoal to decrease further absorption

*supportive care for GI disturbance
-monitor electrolytes
-ensure no hyperkalemia

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6
Q

What is this plant and what are its characteristics?

A

Japanese yew; Taxus japonicus
-evergreen shrubs or small trees with glossy, rigid, dark green, linear leaves
-form red to yellow fruits; each contain a single seed
-primarily in northwest, Great Lakes area, and northeast
-all parts of plant are toxic, both fresh or dry
-highest toxic conc. are found in leaves in the winter

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7
Q

What is the mechanism of toxicity for Japanese yew?

A

-affects monogastrics the worst; also cattle and horses
-contains multiple alkaloids; most importantly taxine A and B
-taxines are calcium channel blockers
-calcium channel blockade results in cardiac depression via AV nodal conduction depression
-result is second and third degree AV blocks, prolonged diastole, and eventual complete diastolic cardiac arrest
-hypotension occurs
-GI peristalsis is inhibited

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8
Q

What are the clinical signs of Japanese yew toxicity?

A

acute:
-animals found dead

subacute:
-ataxia
-muscle tremors
-recumbency
-convulsions
-bradycardia
-dyspnea

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9
Q

How is Japanese yew toxicity diagnosed?

A

-identification of yew in digestive tract
-presumptive based on proximity/history of exposure and sudden death

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10
Q

How is Japanese yew toxicity treated in subacute cases?

A

*decontamination
-emetics
-activated charcoal
-gastric lavage
-rumenotomy

*IM atropine

*other supportive care as indicated

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11
Q

How is Japanese yew toxicity prevented?

A

never plant yew hedgerows around animal enclosures

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12
Q

What is this plant and its characteristics?

A

white snakeroot; Eupatorium rugosum
-2 to 5 foot tall shrubs with serrated leaves
-small white flowers in flat-topped clusters at ends of branches
-seen throughout eastern US; mostly wooded regions
-toxic both fresh or dry

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13
Q

What is the mechanism of toxicity for white snakeroot?

A

-affects ruminants and horses
-tremetol accumulates over time; toxicity signs begin once 5-10% bodyweight is consumed
-inhibits citrate synthase in krebs cycle; causes hypoglycemia and ketoacidosis
-secondary neurologic impairment
-degeneration of cardiac myocytes and conduction abnormalities lead to arrhythmias and death
-skeletal myocyte degeneration; leads to “staggers”
-can be passed through milk to young animals and humans

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14
Q

What are the clinical signs of white snakeroot toxicity in horses?

A

-myocardial necrosis
-congestive heart failure
-tachycardia
-ventral edema
-jugular pulsation
-sudden death

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15
Q

What are the clinical signs of white snakeroot toxicity in ruminants?

A

-gradual onset
-depression
-weakness
-tremors
-delirium
-“acetone breath”
-death 2-10 days after signs begin

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16
Q

How is white snakeroot toxicity diagnosed?

A

-presence of clinical signs with ketosis and proximity to plant
-degenerative myopathy of cardiac and skeletal muscle at necropsy
-tremetol levels analyzed in post-mortem liver and kidney samples

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17
Q

What is the treatment for white snakeroot toxicity?

A

supportive care based on clinical signs

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18
Q

What is this plant and its characteristics?

A

nightshade; Solanum spp.
-herbs/shrubs with either simple or compound ovate to lanceolate leaves
-radially symmetrical flowers with 5 petals arranged in a 6-10 mm star
-smooth round fruits that turn black when ripe
-all parts toxic; immature berries most toxic

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19
Q

What is the mechanism of toxicity for nightshade as it relates to the neurologic system?

A

-affects ruminants and horses
-steroidal, tropane alkaloids competitively block acetylcholine at muscarinic receptors
-inhibition of parasympathetic nervous system leads to dry mouth, decreased GI motility, dilated pupils, tachycardia, agitation, lethargy, convulsions, and coma
-solanine promotes intracellular calcium release; leads to calcified tissues, lameness, and weight loss
-alkaloids function as GI irritants and cause diarrhea

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20
Q

What are the clinical signs of nightshade intoxication in ruminants?

A

*cholinergic signs:
-agitation
-lethargy
-delirium
-seizure
-coma
-pupil dilation
-tachycardia
-incoordination
-ataxia
-paresis/paralysis
-death

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21
Q

What are the clinical signs of nightshade intoxication in horses?

A

*GI signs:
-dry mouth
-anorexia
-nausea
-colic
-diarrhea

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22
Q

How is nightshade toxicity diagnosed?

A

proximity to plants and associated clinical signs

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23
Q

What is the treatment for nightshade toxicity?

A

-physostigmine
-activated charcoal
-supportive care based on clinical signs

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24
Q

What is this plant and its characteristics?

A

water hemlock; Cicuta maculata
-thick, parsnip-like roots that exude yellow, thick, oily liquid when cut
-hollow, erect stems up to 1-2 meters tall
-occasional purple stripes on stems
-white flower clusters terminally
-grow in wet habitats
-tubers are most toxic part; remainder of plant is non-toxic after drying

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25
What is the mechanism of toxicity for water hemlock?
-affects cattle and horses -circutoxin is rapidly absorbed via mucous membranes and from GI tract -toxin is a non-competitive GABA antagonist in the central nervous system -results in continued neuronal depolarization causing continued, violent grand mal seizures and resp. failure
26
What are the clinical signs of water hemlock toxicity?
-progression from salivation to muscle twitching to violent tetanic seizures -ataxia -dyspnea -rapid eye blinking -collapse -pale lesions in heart and long digital extensor muscles due to myocardial degeneration and replacement fibrosis
27
How is water hemlock toxicity diagnosed?
identification of water hemlock in rumen and/or stomach of animals that died suddenly
28
What is the treatment for water hemlock in animals that survive to possible treatment?
-diazepam to control seizures -sodium pentobarbitol -induce vomiting or perform gastric lavage -artificial respiration -dilute acetic acid given orally
29
How is water hemlock toxicity prevented?
-avoid the plant -hand pull from pastures to ensure removal of roots
30
What is this plant and its characteristics?
larkspur; Delphinium spp. -blue to purple flowers that are bilaterally symmetrical and on the terminal end of erect stems in summer -stems are hollow with long leaves -fruit follicles split open to release numerous dark brown seeds -most common in Rocky Mountains -most toxic when young and flowering
31
What is the mechanism of toxicity for larkspur?
-cattle most susceptible; also affects horses -sheep and goats are resistant -curare-like anticholinergic alkaloid competitively inhibits acetylcholine at alpha-1 nicotinic sites -results in neuromuscular blockade at post-synaptic neuromuscular junctions -patients experience muscle weakness and paralysis
32
What are the clinical signs of larkspur toxicity?
-sudden death -muscle weakness -trembling -wide-base stance -stiffness -paresis -periodic collapse -seizures -resp. paralysis -bloat -arrhythmia
33
How is larkspur toxicity diagnosed?
-sudden death of cattle in summer at high altitudes with proximity to plant -ruminal contents containing > 3mg/g of material consistent with toxicity
34
What is the treatment for larkspur toxicity?
-do not force animals to move faster than desired -physostigmine -maintain animal in standing position if possible; sternal if needed -rumen trocharization or ororuminal tube to alleviate bloat
35
How is larkspur toxicity prevented?
-do not allow cattle to graze in areas with larkspur until seed pods shatter -have large flocks of sheep graze in field prior to introducing cattle -herbicides -supplement cattle with commercial minerals
36
What is this plant and its characteristics?
locoweeds; Oxytropis or Astagalus spp. -many different species in North America -basal leaves that are silvery blue with silver/white hairs -flowers produced on leafless stalks in racemes; butterfly-like in shape -seeds contained in pods -ingestion is habit-forming
37
What is the locoism mechanism of toxicity for locoweeds?
-most common presentation in horses -swainsonine inhibits carbohydrate breakdown in the brain by inhibiting glycosidase -leads to formation of cytoplasmic vacuoles (lysosomal storage disease) -toxicity is chronic and develops after weeks of ingestion -effects are reversible until structural damage occurs
38
What is the nitrotoxicosis mechanism of toxicity for locoweeds?
-more common in ruminants -acute disease is uncommon; due to nitrate accumulation and methemoglobin production -miserotoxin causes spinal cord demyelination and hind-end proprioceptive ataxia within 7-10 days of ingestion (chronic) -increased toxicity in ruminants due to ruminal microflora
39
What is the selenosis mechanism of toxicity for locoweeds?
-occurs in horses and ruminants -unpleasant garlic-like odor compared to other locoweeds -acute disease rare but possible -chronic disease results from alkali toxicosis
40
What are the clinical signs of locoism from locoweeds?
-depression -dull appearing eyes -incoordination -aberrant behavior -emaciation/weight loss -death -repro. failure -abortion -birth defects
41
What are the clinical signs of nitrotoxicosis from locoweeds?
acute: -methemoglobinemia -weakness -tachypnea -dyspnea -coma -death -emphysema chronic: -spinal cord demyelination -generalized weakness -incoordination -hind-end proprioceptive ataxia -"cracker heels"/clicking of dewclaws when walking -knuckling and/or goose-stepping
42
What are the clinical signs of selenosis from locoweeds?
acute: -diarrhea -hyperthermia -tachycardia -myocardial necrosis -tachypnea -dyspnea -pulmonary congestion, hemorrhage, or edema -pulmonary alveolar vasculitis -abnormal posture/recumbency -death chronic: -rough hair coat -weight loss -abnormal hoof growth -lameness -dermatitis -polioencephalomalacia (swine)
43
How is locoweed toxicity diagnosed?
-swainosine testing on serum -presence of vacuolation in brain, liver, lymph nodes, thymus, and/or uterus -forage, blood, liver, and kidney testing for selenium
44
What is the treatment for locoweed toxicity?
*locoism: -no specific treatment -recovery possible in acute cases; not in chronic cases -reserpine to decrease clinical signs *chronic selenosis: -feed diets with low selenium and adequate copper and sulfur
45
How is locoweed toxicity prevented?
-avoid grazing on locoweed pastures -ensure appropriate stocking densities
46
What is this plant and its characteristics?
yellow star thistle; Centaurea solstitialis -branching herb up to 3 feet tall with densely haired leaves -yellow disc flowers at ends of stems and surrounded by stiff spines -found in western US -seeds remain viable after passing through GI tract -only affects equines; mostly late summer or early fall -toxic dry and fresh
47
What is the mechanism of toxicity for yellow star thistle?
-toxicity arises from chronic consumption of 60-100% bodyweight -unknown toxin causes nigropallidal encephalomalacia -impairment to muscles supplied by cranial nerves 5, 7, and 9 -believed that toxin inhibits dopamine transporter system in brain to inhibit nerves associated with prehension and chewing
48
What are the clinical signs of yellow star thistle toxicity?
-abrupt onset despite toxicity being chronic -facial muscles become hypertonic; fixed/wooden facial expression -inability to eat or drink -involuntary chewing with empty mouth -chewing and dropping food -behavioral changes -aspiration pneumonia
49
How is yellow star thistle toxicity diagnosed?
-horses unable to prehend and chew -post-mortem findings of nigropallidal encephalomalacia
50
What is the treatment for yellow star thistle toxicity?
-no known treatment; brain lesions are permanent -euthanasia recommended so animal does not starve to death
51
What is this plant and its characteristics?
poison hemlock; Conium maculatum -ornamental herb reaching 1 to 2.5 meters tall -stout, rigid, hollow stems with purple spots -large, carrot-like tap-root -triangular, serrated, fern-like leaves -small, white, clustered flowers -foul odor -only toxic when fresh -seeds are most toxic
52
What is the mechanism of toxicity for poison hemlock?
-coniine blocks motor end plates of skeletal muscles -results in flaccid paralysis, ataxia, salivation, and resp. failure -blocks spinal cord reflexes -no convulsions or seizures -results in teratogenicity in pregnant swine and cattle
53
What are the clinical signs of poison hemlock toxicity?
-anxiety -tachycardia -muscle weakness -fasciculations -ataxia -incoordination -depression -recumbency -collapse -3rd eyelid prolapse and impaired vision -salivation -vomiting -diarrhea -death -teratogenesis
54
How is poison hemlock toxicity diagnosed?
sudden death in animals seen eating plant or with plant found in GI tract
55
What is the treatment for poison hemlock toxicity?
-no specific treatment -resp. support and other supportive care -gastric lavage and/or activated charcoal
56
How is poison hemlock toxicity prevented?
-avoid plant -pull plant by hand to ensure root removal
57
What is this plant and its characteristics?
Lupinus spp. -stemmy herbs with lanceolate leaflets that grows in spring -flowers in early to mid summer are white to purple-blue and formed on ends of branches -flat seed pods form in late summer and early fall -found throughout the US; often after overgrazing or fire -seeds are most toxic
58
What is the mechanism of toxicity for Lupinus spp.?
-sheep > cattle and horses > goats (resistant) -quinolizidine alkaloids induce nicotinic effects -anagyrine alkaloid causes teratogenesis in cattle -anagyrine also stops uterine motility and causes cleft palate formation
59
What are the clinical signs of Lupinus spp. toxicity?
*nicotinic effects: -salivation -incoordination -head-pressing -aimless wandering -excitement -muscle tremors -seizures -dyspnea -recumbency -death *crooked calf syndrome: -contracture malformations -scoliosis -torticollis -immobile elbow joints
60
How is Lupinus spp. toxicity diagnosed?
clinical signs and proximity to plants
61
What is the treatment for Lupinus spp. toxicity?
-no specific treatment -symptomatic supportive care
62
How is Lupinus spp. toxicity prevented?
avoid grazing pregnant cattle on flowering/seed pod Lupinus spp. during first 3 months of gestation
63
What is this plant and its characteristics?
skunk cabbage; Veratrum spp. -coarse, erect plants 1 to 2.5 meters tall with short roots -smooth, broad leaves with parallel veins -numerous small, green-white flowers at pinnacle of stalk -typically in Western US at high altitudes -all parts toxic; most toxic when young in early spring
64
What is the mechanism of toxicity for skunk cabbage?
-primarily affects sheep; camelids and cattle also affected -veratrines and cevanines bind sodium channels to delay closure, causing cardio. and resp. effects -cyclopamines and jervanines are teratrogenic; cause monkey-faced lamb syndrome and/or still births
65
What are the teratogenic effects of skunk cabbage based on timing of ingestion?
Gestation day 14: classic cyclopean deformity Day 17-18: hindlimb motor nerve paralysis Day 12-30: craniofacial deformities Day 30-36: shortened legs from metacarpal/tarsal bone hypoplasia
66
What are the clinical signs seen in adult sheep due to skunk cabbage toxicity?
-excessive salivation -vomiting -ataxia -collapse -death
67
How is skunk cabbage toxicity diagnosed?
-lambs born/still-born with cyclops deformities -lambs born with shortened legs -lambs that die due to absent trachea
68
What is the treatment for skunk cabbage toxicity?
-atropine for neuro. signs -activated charcoal
69
What is the prevention for skunk cabbage toxicity?
do not allow ewes to have access to plant in the first trimester
70
What is this plant and its characteristics?
ponderosa pine; Pinus pondersoa -evergreen tree that grows > 60 meters tall -most prevalent pine in western US -needles are soft, grow in clusters, and reach 8 to 20 cm in length -pinecones are brown and 7 to 15 cm long -fresh and dried needles are toxic if consumed over several days
71
What is the mechanism of toxicity for ponderosa pine?
-only affects pregnant cattle -needles contain isocupressic acid -induces abortion by decreasing blood flow to uterus and causing fetal death -typically occurs during last trimester in late fall, winter, or early spring -higher risk of abortion with prolonged ingestion and the needles being ingested closer to term
72
What are the clinical signs of ponderosa pine toxicity?
-"pine needle abortion" characterized by weak uterine contractions, incomplete cervical dilation, dystocia, excessive discharge, and/or uterine bleeding -calves that are stillborn or small and weak -retained fetal membranes -agalactia -metritis
73
How is ponderosa pine toxicity diagnosed?
-presence of late term abortions and proximity or suspicion of pine needle ingestion
74
How is ponderosa pine toxicity treated?
-treatment of retained fetal membranes, agalactia, and/or metritis -no specific treatment to prevent abortions
75
How is ponderosa pine toxicity prevented?
avoid grazing around pine needles; provide other forage options
76
What is this plant and its characteristics?
milkweed; Asclepias spp. -milky sap or latex within stems -leaves are either 6-12 cm, broad, and narrow OR linear leaves < 2-4 cm wide -flowers range from green-white to yellow-red and are arranged terminally -flowers have 2 5-parted whorls of petals -seeds have silky tufts of white hair -toxic fresh or dry -most toxic during rapid growth
77
What are the mechanisms of toxicity for milkweed?
*affects ruminants *cardenolides: -type of cardiac glycoside *galitoxin: -neurotoxin with unknown mechanism -resin-like substance
78
What is the cardiovascular syndrome caused by milkweed?
-weakness -dyspnea -arrhythmia -GI effects -sudden death -NO seizures
79
What is the neurologic syndrome caused by milkweed?
-severe colic -profound depression -muscle tremors -weakness -incoordination -ataxia -seizure -resp. failure -death
80
How is milkweed toxicity diagnosed?
-no specific ante- or post-mortem signs -plants in proximity to animals with signs -plant in stomach of animals post-mortem
81
How is milkweed toxicity treated?
-no specific treatment -remove animals from plants -provide water, non-contaminated hay, and shade -IV fluid therapy -atropine/anti-arrhythmic agents
FA3 Toxicology
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