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Tox Final Exam > Toxic Principles in Plants > Flashcards

Toxic Principles in Plants Flashcards

1
Q

MOA of insoluble calcium oxalate?

A

plant cells have needle shaped calcium oxalate crystals that penetrate the oral mucosa and tongue

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2
Q

Clinical signs of insoluble calcium oxalate?

A

irritation of lips, mouth, throat, V+, some cases die of suffocation

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3
Q

MOA of soluble calcium oxalate?

A

bind to Ca and precipitation of insoluble calcium oxalates in soft tissues and kidney

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4
Q

Clinical signs of soluble calcium oxalate?

A

hypocalcemia, kidney damage

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5
Q

MOA of isocupressic acid?

A

vasoconstriction and decrease in uterine blood flow–increased fetal cortisol levels

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6
Q

Clinical signs of isocupressic acid?

A

abortion in cattle

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7
Q

MOA of quinone?

A

primary photosensitization

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8
Q

Clinical signs of quinone?

A

erythema and pruritus, edema, and necrosis of skin–secondary bacterial infections

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9
Q

MOA of tannic acid?

A

tissue damage including GI lesions and kidney damage

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10
Q

Clinical signs of tannic acid?

A

cattle–>constipation, brown urine, atony, anorexia, depression
monogastrics–>mainly GI

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11
Q

MOA of triterpene acid?

A

liver damage and hepatic photosensitization

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12
Q

Clinical signs of triterpene acid?

A

depression, anorexia, constipation, diarrhea, icterus, photophobia, erythema of skin, swelling, necrosis and sloughing

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13
Q

MOA of colchicine?

A

anti mitotic by binding to tubular and inhibiting spindle formation during cell division

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14
Q

Clinical signs of colchicine?

A

involves many organs

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15
Q

MOA of diterpene alkaloids?

A

Competitive blockade of the nicotinic receptors at the muscle endplate similar to curare

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16
Q

Clinical signs of diterpene alkaloids?

A
  • sudden death in cattle
  • Early signs are signs of neuromuscular blockade including muscle weakness, stiffness, staggering, bloating, recumbency, and collapse
  • Monkshood also show cardiac arrhythmias
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17
Q

Treatment for diterpene alkaloid toxicosis?

A

antidote is physostigmine or neostigmine

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18
Q

MOA and clinical signs of ergot alkaloids?

A

vasoconstriction and gangrene, uterine contraction

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19
Q

MOA of indolizidine alkaloids?

A

inhibition of lysosomal enzymes (decreased glycoproteins), peripheral neuronal degeneration (via nitropropanol glycoside also found in plants), abnormal hoof and hair (via selenium also found in plants)

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20
Q

Clinical signs of indolizidine alkaloids?

A

neuronal signs; depression, incoordination, ataxia, circling, abnormal behavior
infertility, congenital defects, heart failure, wt. loss, dec immune

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21
Q

MOA of lycorine?

A

emetic and purgative–bulb is most toxic

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22
Q

Clinical signs of lycorine?

A

anorexia, salivation, V+, D+, hypotension, muscle tremors/seizures

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23
Q

MOA of muscarine?

A

stimulation of muscarinic cholinergic receptors

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24
Q

Treatment of muscarine?

A

antidote is atropine, symptomatic tx and decontamination

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25
Q

MOA of piperidine alkaloids?

A

nicotinic effects starting w/ ganglionic and neuromuscular stimulation followed by ganglionic and neuromuscular blockade

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26
Q

Clinical signs of piperidine alkaloids?

A

ataxia, incoordination, birth defects (skeletal malformation and cleft palate)

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27
Q

MOA of pyridine alkaloids (nicotine and lobeline)?

A

Nicotine and lobeline act on nicotinic receptors at autonomic ganglia, neuromuscular junction and some synapses in the CNS. low doses cause depolarization. large doses cause blockade

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28
Q

Clinical signs of pyridine alkaloids (nicotine and lobeline)?

A
  • Rapid onset of clinical signs
  • Early signs are excitation, salivation, lacrimation, vomiting, diarrhea, and tachypnea
  • Muscle twitching, muscle weakness, and dyspnea • Death is due to respiratory failure
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29
Q

MOA of pyrrolizidine alkaloids?

A

hepatotoxic

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30
Q

MOA of solanine and solanidine alkaloids?

A

GI, CNS, respiratory, cardiac

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31
Q

MOA of taxine alkaloids?

A

cardiotoxic and GI

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32
Q

MOA of xanthine alkaloids (caffeine, theophylline, theobromide)?

A

blocking adenosine (A) receptors, inhibiting phosphodiesterase

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33
Q

Clinical signs of xanthine alkaloids (caffeine, theophylline, theobromide)?

A

salivation, V+, colic, D+, CNS stimulation, convulsive seizures, muscle tremors, tachycardia, hypotension, urination

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34
Q

MOA of anthraquinone?

A

purgative

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35
Q

MOA of calcinogenic glycosides (vit D analog)?

A

hypercalcemia; calcification of elastic tissues of the arteries, tendons and ligaments and increased density of bone

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36
Q

Clinical signs of carcinogenic glycosides (vit D analog)?

A

lameness

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37
Q

MOA of carboxyatractyloside (sulfated glycoside)?

A

hepatotoxicity, renal damage, hypoglycemia, excessive salivation

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38
Q

MOA of cardiac glycoside?

A

cardiotoxic by inhibiting Na/K ATPase

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39
Q

MOA of coumarin glycoside?

A

form dicoumarol in spoiled plants. inhibit vit K epoxide reductase resulting in deficiency of coag factors 2, 7, 9, 10

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40
Q

Clinical signs of coumarin glycoside?

A

hemorrhage

41
Q

MOA of cyanogenic glycosides?

A

Acute–>inhibition of cytochrome oxidase and inhibition of cellular respiration, vasoconstriction, inhibition of glycolysis, inhibition of citric acid cycle, irritation of MM
Chronic–>neuronal degeneration

42
Q

MOA of cycasin?

A

glycoside that causes GI irritation and liver damage, teratogenic, mutagenic, carcinogenic, beta-methylamino-L-alanine (BMAA)–>neurotoxic AA, unknown toxin–>axonal degeneration in CNS

43
Q

Clinical signs of cycasin?

A

GI and liver disease syndrome or ataxia and CNS syndrome

44
Q

MOA of glucosinolate (thiocyanate glycoside)?

A

antithyroid

45
Q

MOA of nitropropanol glycoside?

A

inhibits enzymes of the Krebs cycle and cellular oxidative phosphorylation

46
Q

Clinical signs of nitropropanol glycoside?

A

cattle and sheep–>respiratory and neuro signs (cracker heels or roaring dz)
horses and rodents–>neuro signs

47
Q

MOA of phytoestrogens?

A

bind to estrogen receptors causing infertility in females and males

48
Q

Clinical signs of phytoestrogens?

A

infertility in females, decreased libido and feminization in males

49
Q

MOA of protoanemonin?

A

volatile oil released by hydrolysis of the glycoside

50
Q

Clinical signs of protoanemonin?

A

severe irritation of the GI mucosa and dermatitis

51
Q

MOA ptaquiloside?

A

death of precursor cells in BM, neoplasm in the UT, tumors in the URT and retinal degeneration

52
Q

Clinical signs of ptaquiloside?

A

aplastic anemia, enzootic hematuria

53
Q

MOA of steroidal saponins?

A

liver damage and inability to eliminate phylloerythrin, a metabolite of chlorophyll which acts as a photodynamic substance–hepatogenic photosensitization

54
Q

Clinical signs of steroidal saponins?

A

signs of photosensitization and liver damage

55
Q

MOA of gossypol?

A

cardiotoxic and secondary liver damage, destroys seminiferous tubules, binds to proteins, AA, and iron

56
Q

Clinical signs of gossypol?

A

chronic–>cardiotoxic, male infertility

monogastrics more sensitive

57
Q

MOA of molybdenum?

A

signs of copper deficiency including watery bubbly diarrhea, wasting, depigmentation, demyelination, osteoporosis

58
Q

MOA of copper?

A

liver damage, hemolysis, methemoglobinemia

59
Q

MOA of selenium?

A

acute–>GI irritation and respiratory signs

chronic–>hoof and hair abnormalities

60
Q

MOA of nitrate?

A

acute–>GI irritation. nitrate is reduced to nitrite by nitrate reductase. nitrite causes oxidation of ferrous iron of hemoglobin to ferric iron and formation of methemoglobin. Respiratory insufficiency signs d/t inability of the blood to carry oxygen. fetal methemoglobinemia and death causing abortion.
chronic–> decreased progesterone during pregnancy and abortion. reduced performance

61
Q

MOA of dimethyl disulfide?

A

oxidation of RBCs

62
Q

Clinical signs of dimethyl disulfide?

A

anemia, depression, hemoglobinuria, hemoglobinemia, icterus, cyanosis

63
Q

MOA of diterpene esters?

A

activate protein kinase C resulting in cell damage and enzyme dysfunction

64
Q

Clinical signs of diterpene esters?

A

irritation and blistering of GI mucosa–>salivation, V+, D+ (maybe w/ blood)

65
Q

MOA of grayanotoxins?

A

binds to Na channels in excitable cells, increased permeability and depolarization, irritation of GI mucosa

66
Q

Clinical signs of grayanotoxins?

A

GI signs, depression, recumbancy, tachycardia, tachypnea, seizures, fever. death d/t aspiration pneumonia

67
Q

MOA of lectin (phytotoxin, toxalbumin)?

A

inhibit cellular protein synthesis resulting in cell death

68
Q

Clinical signs of lectin (phytotoxin, toxalbumin)?

A

GI signs including hemorrhagic gastroenteritis

69
Q

MOA of meliatoxin?

A

enterotoxic, neurotoxic

70
Q

Clinical signs of meliatoxin?

A

GI signs (maybe w/ blood), CNS and peripheral neuronal signs similar to nicotine poisoning, death from respiratory failure

71
Q

MOA of propyl disulfide?

A

oxygen free radicals–>damage RBC membranes–>heinz bodies

72
Q

Clinical signs of propyl disulfide?

A

anorexia, ataxia, tachycardia, tachypnea, dyspnea, icterus, onion odor, abortion

73
Q

MOA of tetradymol?

A

liver damage and inability to eliminate phylloerythrin, a metabolite of chlorophyll which acts as a photodynamic substance, hepatogenic photosensitization

74
Q

Clinical signs of tetradymol?

A

sheep–>anorexia, depression, incoordination, dyspnea, icterus, head pressing, skin swelling, erythema, necrosis, sloughing, secondary bacT infections

75
Q

MOA of thiaminase?

A

destroys thiamine in the diet and produces signs of thiamine (vit B1) deficiency in mono gastric animals (neurotoxic)

76
Q

MOA of triterpenoid saponins?

A

direct irritation of GI mucosa

77
Q

Clinical signs of triterpenoid saponins?

A

salivation, V+, anorexia, D+, colic, hypothermia

78
Q

MOA of resin or resinoids?

A

irritation of nervous or muscle tissue

79
Q

MOA of alsike clover and red clover ingestion?

A

hepatotoxicity and secondary photosensitization in horses only, hepatic encephalopathy at large amount

80
Q

Clinical signs of alsike clover and red clover ingestion?

A

lacrimation, photophobia, erythema, pruritus, edema, necrosis, sloughing of skin

81
Q

MOA of avocado ingestion?

A

cardiotoxicity in goats, horses, rabbits and caged birds. non infectious mastitis and agalactia in cattle, horses, goats and rabbits.

82
Q

MOA of black walnut ingestion?

A

ingestion of fresh shavings made form heartwood (used in bedding) causes laminitis

83
Q

MOA of forage induced photosensitization?

A

primary photosensitization and secondary photosensitization due to liver damage

84
Q

Clinical of forage induced photosensitization?

A

lacrimation, photophobia, erythema, pruritus, edema, necrosis, sloughing of skin

85
Q

MOA of grape and raisin ingestion?

A

unknown toxin causes renal failure only in dogs

86
Q

Clinical signs of grape and raisin ingestion?

A

GI signs including V+ followed by signs of ARF

87
Q

MOA of lily ingestion?

A

unknown toxin causes renal failure only in cats, GI irritation in dogs and cats

88
Q

Clinical signs of lily ingestion?

A

GI signs including salivation, V+, depression and complete anorexia, PU followed by anuria and death from RF

89
Q

MOA of pigweed ingestion?

A

acute–>nitrate causing methemoglobin
chronic–>nitrate causing abortion
soluble oxalate–>hypocalcemia and kidney damage
unknown–>renal tubular damage in ruminants, pigs, horses

90
Q

Clinical signs of pigweed ingestion?

A

depression, weakness, incoordination, renal failure

91
Q

MOA of red maple leaf ingestion?

A

unknown toxin in dried leaves–>hemolytic anemia, hemoglo binemia, heinz bodies

92
Q

Clinical signs of red maple leaf ingestion?

A

anorexia, depression, anemia, icterus, brown MM, hemoglobinuria, dyspnea, cyanosis, death

93
Q

MOA of senna ingestion?

A

unknown mechanism–>skeletal muscle myopathy and cardiomyopathy
anthroquinone–>cathartic

94
Q

Clinical signs of senna ingestion?

A

D+, muscle weakness, recumbancy, good appetite, myoglobinura, coffee colored urine, tachycardia, death

95
Q

MOA of yellow star thistle and russian knapweed ingestion?

A

toxins interact w/ dopamine transporters resulting in death of dopaminergic neurons in the brain

96
Q

Clinical signs of yellow star thistle and knapweed ingestion?

A

equine nigropallidal encephalomalacia (ENE) or chewing dz

97
Q

MOA of macadamia nut ingestion?

A

unknown and the toxin is unknown

98
Q

Clinical signs of macadamia nut ingestion?

A

dog–>weakness in hindlimbs, depression, ataxia, tremors, hyperthermia, lameness, recumbency, V+, colic, D+, pale MM
full recovery in 2 days

99
Q

What are the plants that cause mechanical injury?

A

cactus family, jimsonweed seed pods, cocklebur seed pods

Tox Final Exam (9 decks)

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