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1. Specialty - Reading List > Toxicities > Flashcards

Toxicities Flashcards

1
Q

Lathyrus hirsutus(Caley Pea) Intoxication in a Herd of Horses

Holbrook et al, JVIM 2015

A

Results: Bermuda grass hay consumed by the horses contained large quantities of mature Lathyrus hirsutus. Acute clinical signs conform to earlier descriptions of Lathyrus hirsutus intoxication in cattle. Residual neurologic signs were characterized by incoordination in the rhythmicity of multiple gaits. Evidence of mild neurogenic muscle atrophy was recognized in 1 of 5 horses biopsied.

Conclusions and Clinical Importance: Caley Pea intoxication may occur within days of seed pod consumption. The neurologic signs are unique and suggest involvement of the upper motor neuron system and regions of the spinal cord influencing voluntary motor movement. Drought conditions during plant growth may increase the risk of toxicosis

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2
Q

Poisonweed

Staggerweed

A

delphinium

larkspur

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3
Q

delphinium:

toxin and mechanism

A

NEUROTOXIN

Diterpene alkaloid (methyllyca-conitine)

Mechanism: NMB –> resp paralysis

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4
Q

delphinium: toxic part

A

it flowers early, so poisonings occur in spring or fall

early growth or dried parts are worse - less bad after flowering happens

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5
Q

delphinium suceptibility

A

Cattle > horses > sheep

LD50 cattle is 0.5% BW = 17g/kgBW

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6
Q

delphinium CS

A

NEUROTOXIN

Sudden death
CNS signs, aspiration pneumonia, bloat, constipation, regurg, salivation

Death d/t resp paralysis/bloat  animals fall w/ head downhill
Fatalities within 3-4hrs

Lesions: nonspecific; bloat, congestion, pneumonia, GI inflamm

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7
Q

delphinium TX

A

Prognosis: guarded

(1) AC + SC
(2) Physostigmine (rarely have enough)
(3) Turn head uphill
(4) Relieve bloat
(5) Abx for asp pneumonia

Prevention: move to new pasture, spot spray, revegetate

*An affected animal may be mistaken for a grass tetany case; however, treatment with magnesium exacerbates the effect of larkspur’s toxins at the neuromuscular junction and should be avoided.

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8
Q

Lathyrus hirsutus

A

sweet pea vetchlings

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9
Q

Osteolathyrism

Neurolathyrism

A

Lathyrus hirsutus

sweet pea vetchlings

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10
Q

Lathyrus hirsutus / Osteolathyrism

A

neurotoxin of cattle in the SE US

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11
Q

Lathyrus hirsutus: toxin and mechanism

A

Aminopropionic acid derivative

Mechanism: interferes with glutamate receptors in the brain, causing influx of Ca2+ into cells = cell death

Heat-labile = cook it to destroy!

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12
Q

Lathyrus hirsutus: clinical signs

A

NEUROTOXIN

Neurolathyrism: neuronal degeneration; mm rigidity, paralysis, bradycardia; horse: abnormal gait, hopping gait, tying-up, head low, laryngeal hemiplegia

Osteolathyrism: cattle –> lameness after 3-5d; boney Δ
Horses –> skeletal deformities and aortic rupture (defective cartilage/connective tissue)

–>Holbrook case report

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13
Q

poison hemlock

A

Conium maculatum

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14
Q

Conium maculatum: toxin and mechanism

A 
Piperidine alkaloids (like nicotine): conine
EXTREMELY TOXIC; LD50 < 10g/kg

Mechanism: Direct cholinergic effects (antagonist and agonist) – large dose causes skeletal m stimulation followed by neuromuscular blockade and paralysis

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15
Q

Conium maculatum: toxic part

A

Young plants = LOW alkaloid concentrations

Roots, stem, leaves and fruit = toxic

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16
Q

Conium maculatum: clinical signs

A

Nicotinic: salivation, bloating, tachycardia progressing to incoordination and colic

2’ cardiac arrhythmias

Teratogen: 1st trimester = cleft palate, brain/face problems, arthrogryposis, hydrocephalus : Seen in cattle that consumed between 40-70 day gestation

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17
Q

Lathyrus hirsutus: TX

A

Prognosis: full recovery OR chronic

(1) Gastric lavage
(2) AC + SC
(3) Symptomatic + supportive therapy

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18
Q

Conium maculatum: TX

A

1) Emetics (don’t repeat if vomited)
(2) Gastric lavage
(3) AC + SC
(4) Resp support (IPPV or Dopram)
(5) Diazepam (seizures)

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19
Q

Water hemlock

A

(Cicuta maculatum or Cicuta douglasii)

Among most poisonous plants in US

also toxic to humans

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20
Q

Water hemlock: toxin and mechanism

A

Cicutoxin (unsaturated alcohol)  seizurigenic
EXTREMELY TOXIC
2oz kill sheep
8-10oz kill cow

Mechanism: Acts directly on CNS as a violent convulsant (GABA antagonist)

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21
Q

water hemlock: toxic part

A

stem and root

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22
Q

water hemlock: CS

A

Seizurigenic: rapid onset (15-60min) –> salivation, abdominal pain, tremors, seizures –> death due to respiratory failure

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23
Q

water hemlock: TX

A

Prognosis: good if survive 2hrs (excrete alcohol)
Control seizures
Alcohol molecule size too small for AC

Tx with barbituates to control seizures

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24
Q

jimson weed

A 
Belladonna alkaloids:
Jimson weed (Datura stramonium)
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25
Q

Belladonna alkaloids exposure:

A

seed contamination of grain, plant contamination of forage

all plant parts are toxic

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26
Q

Belladonna alkaloids : toxin and mechanism

A

Belladonna alkaloids = antimuscarinic:
Belladonna (Atropa) –> atropine

Mechanism: competitive antagonism at muscarinic receptors preventing acetylcholine binding

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27
Q

Belladonna alkaloids: CS

A

mostly toxic to ruminants

Antimuscarinic: tachycardia, tachypnea dry skin, ↓salivation, mydriasis (can be topical), blurred vision, hyperthermia, ↓feed, tremors, bloat, recumbancy

28
Q

Belladonna alkaloids: TX

A

(1) Physostigmine
(2) Emetic/AC

CS resolve within 24hrs – death is rare

29
Q

Yellow Star Thistle

A

(Centauria solstitialis)

Russian Napweed

30
Q

Yellow Star Thistle: toxin and mechanism

A

Unknown
NOT HIGHLY TOXIC

**only toxic to horses
signs after grazing 30-90d (hundreds of ##)

Contains a neurotoxin destroys dopaminergic nigrostriatal pathway – inhibiting effects on cerebral cortex pathways that control prehension and chewing (CN’s V, VII, IX)

31
Q

Yellow Star Thistle: CS

A

Mixed CNS: hypertonic facial/lip mm, tongue lolling, head tossing, dysphagia, immerse head in water to drink  death 2’ starvation
Lesions: pathognomonic bilaterally symmetric nigropallido-encephalomalacia – liquefactive necrosis in globus pallidus and substantia nigra

“Sardonic grin” is class term used to describe facial lesions

32
Q

Yellow Star Thistle: TX

A

Irreversible once symptomatic euthanize

33
Q

Locoweeds

A

(Astragalus spp, Oxytropis sericea)

34
Q

Most destructive to livestock of all poisonous plants

A

locoweed

whole plant is toxic

35
Q

Locoism: toxin and mechanism

A

Locoism:alkaloid swainsonine inhibits mannosidase  brain accumulation of oligosaccharides (generalized lysosomal storage disease of CNS)

36
Q

Locoism: CS

A

Methemoglobinemia  fetlock knuckling (cracker heels), dyspnea, cyanosis, death (24hrs); abortion (fetal Hgb sensitive); brown blood
Locoism:  CNS dep, dullness, emaciation, ataxia, then excitement;
reduced fertility (cattle); abortion
Teratogen: skeletal problems

37
Q

Locoism: TX

A

Selenosis: no tx; allow to excrete; soft bedding; change diet

Locoism: improve feed; horses = euthanize

38
Q

Cardiac Glycoside Mechanism

A

Inhibit membrane sodium-Potassium-ATPase pumps – intracellular sodium increases and potassium decreases – changes in ions flux decreases electrical conductivity = arrhythmias

Used therapeutically to increase myocardial contractility (by decrease intracellular sodium, increases intracellular calcium through Na:Ca Exchanger – more calcium available to actin-myosin apparatus

39
Q

Nerium oleander

A

Oleander

Toxin = cardiac glycoside

40
Q

Oleander suceptibility

A

ruminants on ionophores are MORE susceptible

41
Q

CARDIAC GLYCOSIDE CS

A

Early (GI) = projectile vomiting, diarrhea; bloating, salivation

Later (CV): hypotension, bradycardia,Vtach, SVT, conduction probs

Even later: sudden death

Death hrs or days after ingestion

Lesion: cardiac mm necrosis

42
Q

CARDIAC GLYCOSIDE TX

A

MEDICAL EMERGENCY

(1) Emetics
(2) AC + SC
(3) AVOID K+ in tx
(4) Manage cardiac effects for 1-3d (drugs designed for animals w/ pre-existing cardiomyopathy) = unless lethal arrhythmia, don’t be too aggressive w/ heart

Treating arrhythmias: Bradycardia: atropine
Heart block: phenytoin
Tachyarrhythmia: propranolol

Digitalis Abs (FAD antibody): Digibind (works well but $$$)

43
Q

Milkweed

A

Asclepias spp
Toxin = Cardenolides (Cardiac glycoside)

AFFECTS SHEEP

44
Q

Nerium Oleander
Asclepias / Milkweed
Taxus cuspidate / Japanese Yew
Zigadenus / Black Snakeroot / Death Camas

A

Cardio toxins

45
Q

Taxus cuspidate

A

Japanese yew

Toxin = Taxine A and B

cardio toxic

46
Q

Zigadenus spp

A

Black snakeroot
Death camas

Toxin = steroidal alkaloids

cardio toxic

47
Q

Veratrum spp

A

teratogen in sheep

toxin = cyclopamine, veratramine

48
Q

Lantana, Crotalaria, and Ragwort and Groundsel are all

A

hepatotoxins

49
Q

Crotalaria / Senecio: toxin and mechanism

A

Pyrrolizidine alkaloids –> pyrrole derivatives (must be bioactivated) –> irreversible liver damage (hepatocyte DNA alkylation, megalocytosis)

50
Q

Crotalaria / Senecio: CS

A

Hepatic veno-occlusive dz –> icterus, ascites, edema–> fibrosis

Liver necrosis and death: bipsy – triad of fibrosis, bile duct proliferation and megalocytosis

51
Q

Ragwort mechanism

A

Pyrroles crosslink DNA – antimitotic effect and hepatocytes can’t divide = replaced by connective tissue = megalocytosis

52
Q

Perilla frutescens

A

Perilla mint

53
Q

Perilla mint: toxin and mechanism

A

Perilla ketone (similar to 4-ipomeanol from moldy sweet potatoes) –> reactive metabolite in Clara cells –> lung damage (especially alveolar Type I cells; proliferation of type II pneumocytes = interstial pneumonia)

54
Q

perilla mint: CS

A 
Acute bovine pulmonary emphysema & edema (ABPE)
Respiratory distress (grunt on exhale), nasal discharge, cyanosis, hypersalivation

Lesions: pulmonary fibrosis, emphysema, edema, congestion

55
Q

perilla mint: TX

A

No specific antidote
Hard to reverse once CS
Supportive: steroids, antihistamines, abx
Prevention: eliminate

Ddx for ABPE: moldy sweet potatoes, lush pasture (3-methylindole)

56
Q

Pteridium aquilinum

A

bracken fern

57
Q

bracken fern: toxin and mechanism

A

Ptaquiloside – primary carinogen

Causes bone marrow supp  ↓neut/plt/anemia
SE: thiaminase  thiamine deficiency (horses and pigs = NOT cattle)

58
Q

bracken fern: CS

A

Bone marrow: hemorrhage on mucus membranes, hyphema, melena, anemia

Thiamine deficiency: anorexia, wt loss, weakness, ataxia, crouching stance, arched neck in horses

polioencephalomalacia (ruminants)

Bladder neoplasia = Red water disease (cattle/sheep)

59
Q

Veratrum tenuipetalum; V. californicum”

A

Hellebore

Over 50 alkaloids – some are teratogenic

Sheep: if consumed on 14th day of gestation = CYCLOPS LAMP (Boards ?) and monkey faced facial deformities
After 30-35 days, shortened limbs

60
Q

bracken fern exposure

A

Common in South East US

Exposure: fresh plant or dried in hay (young fronds palatable)
More likely in dry years

61
Q

bracken fern tx

A

give thiamine

62
Q

Organophosphates and carbamates

A

Both are acetylcholinesterase (AChE) inhibitors w similar chemical effects

Carbamates are esters of carbamic acid

OPs are esters of phosphoric acid

63
Q

Organophosphates and carbamates: mechanism of action

A

Can enter body through oral, dermal or resp route

Bind and inhibit the AChE (and other cholinesterases) within the nervous system, the neuromuscular junctions and blood, causing an accumulation of the acetyl choline neurotransmitter at postsynaptic receptors

OP’s considered irreversible inhibitors of the enzymes, whereas carbamates are reversible inhibitors of AChE

64
Q

Muscarinic signs of AChE inhibition

A

vomiting, dyspnoea, colic, salivation, lacrimation, urination, diarrhoea, miosis, tracheobronchial secretion, lung oedema, cyanosis

65
Q

Nicotinic signs of AChE inhibition

A

twitching of muscles, tremors, followed by convulsions, and seizures which can finally progress to paresis and even paralysis

66
Q

Organophosphates and carbamates: diagnosis

A

atropine test dose – preanaesthetic dose of 0.02 mg/kg IV à if HR decreases and mydriasis occurs, it is not an OP or carbamate poisoning

antidote tx for OP: atropine sulphate and pyridine 2-aldoxime methochloride (2-PAM)

  • -atropine will control muscarinic R associated signs. 0.22 mg/kg (1/4 dose given IV, remainder IM or SC)
  • -2-PAM will control the nicotinic signs. 2-aldoxime methochloride reactivates the AChE enzyme and can control nicotinic and CNS associated signs. Has to be administered within 24 h of exposure. Dose in horses is 20 mg/kg slow IV, repeated q 4-6 h. Not recommended for carbamate toxicosis because this drug has less affinity for carbamates and the AChE inhibition is usu rapidly reversible
67
Q

metalaldehyde toxicity

A

Cyclic tetramer of acetaldehyde

Toxicity characterised by CNS signs, metabolic acidosis and resp alkalosis

Exact mechanisms unknown, but decrease in the conc of the inhibitory NT GABA, noradrenaline and serotonin (5-hydroxytryptamine, 5-HT) as well as increased monoamine oxidase activity may be involved

CS usu within 15 min to a few hours: agitation, ataxia, hypersalivation, hyperaesthesia, muscle spasms, profuse sweating, convulsions, tachycardia and hyperpnoea. Signs of severe and unrelenting colic also reported.

Death, usu dt resp failure, can occur within a few hours of ingestion and oft preceded by violent convulsions

1. Specialty - Reading List (9 decks)

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