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Toxicology > Plants > Flashcards

Plants Flashcards

1
Q

toxic principle of foxglove

A

digitalis glycosides (present in flowers, seeds and leaves)

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2
Q

mechanism of action of foxglove

A

interferes with Na/K ATPase –> decreased intracellular K and increased intracellular Na –> increased Ca (interferes with normal electrical conductivity in myocardium)

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3
Q

clinical signs of foxglove toxicity

A

vomiting, colic, diarrhea, anorexia, CV (bradycardia, arrhythmias, heart failure), weakness, depression, dyspnea, tremors, convulsions, coma, death

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4
Q

diagnosis of foxglove

A

ECG, plant in stomach contents

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5
Q

PM of foxglove

A

gastroenteritis

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6
Q

treatment of foxglove

A

emesis, activated charcoal, saline cathartic, symptomatic and supportive, digibind (human product with cross reactivity to plant toxins)

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7
Q

toxic principle of japanese yew

A

alkaloid taxine; taxine B (wood, bark, leaves, seeds) – not present in fleshy fruit

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8
Q

toxic principle of japanese yew

A

alkaloid taxine; taxine B (wood, bark, leaves, seeds) – not present in fleshy fruit

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9
Q

japanese yew mechanism of action

A

disrupts Na and Ca currents in myocytes by binding receptors; depress conduction of myocardial depolarization

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10
Q

susceptibility of japanese yew

A

equine are more susceptible than ruminants (but both are susceptible)

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11
Q

clinical signs of japanese yew poisoning

A

rapid onset, sudden death, weakness, trembling, dyspnea, bradycardia, arrhythmias, convulsion, collapse

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12
Q

diagnosis of japanese yew poisoning

A

ECG abnormalities; alkaloid screen to ID toxin in stomach;

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13
Q

PM of japanese yew poisoning

A

gastroenteritis, secondary pulmonary congestion and edema

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14
Q

treatment of japanese yew poisoning

A

GI decontamination, activated charcoal, fluids, seizure control, treat arrhythmias

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15
Q

toxic principle of rhododendron

A

glycoside grayanotoxin (all plant parts, especially leaves)

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16
Q

mechanism of action of rhododendron toxicity

A

toxin binds and modified voltage gated Na channels on muscle membranes and nervous system –> leaves them in open position –> Na influx –> prolonged myocardial depolarization (paralysis); also increases intracellular Ca to have digitalis like effects on heart

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17
Q

clinical signs of rhododendron toxicity

A

salivation, projectile vomiting, diarrhea, anorexia, severe colic, depression, ataxia, paralysis, brady cardia, hypotension, arrhythmias

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18
Q

diagnosis of rhododendron toxicity

A

clinical signs and ID plant;

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19
Q

PM of rhododendron toxicity

A

degeneration of liver and kidneys (mild); GI irritation

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20
Q

treatment of rhododendron toxicity

A

aggressive GI decontamination, activated charcoal, symptomatic and supportive

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21
Q

toxic principle of jimson weed

A

tropane alkaloids (hyoscyamine, scopolamine, hyoscine) – all plant parts, especially seeds

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22
Q

mechanism of low dose jimson weed

A

competitive inhibitor of acetylcholine

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23
Q

mechanism of high dose jimson weed

A

direct CNS stimulation (crosses BBB rapidly)

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24
Q

clinical signs of jimson weed toxicity

A

atropine-like syndrome – mydriasis, anorexia, thirst, tachycardia, tachypnea, hypothermia, tremors, excitability, convulsions, death from resp paralysis

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25
Q

clinical signs of high dose jimson weed toxicity

A

hyperesthesia, apprehension, mania, vocalization

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26
Q

diagnosis of jimson weed toxicity

A

bioassay, pathology, drop of patients urine in the eye of clinic cat will cause mydriasis

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27
Q

diagnosis of jimson weed toxicity

A

bioassay, pathology, drop of patients urine in the eye of clinic cat will cause mydriasis

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28
Q

treatment of jimson weed toxicity

A

GI decontamination, activated charcoal, symptomatic/supportive, neostigmine (inhibits acetylcholinesterase)

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29
Q

toxic principle of castor bean

A

glycoprotein ricin (lectin) – stays in meal of bean

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30
Q

mechanism of action of castor bean

A

binds galacto-lipid and galacto-protein membrane components –> internalization –> cell death by inhibition of protein synthesis

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31
Q

clinical signs of castor bean toxicity

A

latent period of 10 hours to several days; severe colic, diarrhea, depression, thirst, sweating, weakness, fever, pronounced heartbeat, cyanosis, convulsions, recumbency, death from respiratory paralysis and multiorgan failure

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32
Q

diagnosis of castor bean toxicity

A

clinical pathology and lesions

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33
Q

clinical pathology of castor bean toxicity

A

huge increase in PCV, panleukopenia, increased liver enzymes and bilirubin

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34
Q

PM of castor bean toxicity

A

hemorrhagic gastroenteritis

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35
Q

treatment of castor bean toxicity

A

GI decontamination, activated charcoal, fluids and electrolytes, GI protectants, grave prognosis

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36
Q

toxic principle of plants containing oxalates

A

calcium oxalate crystals are preformed in leaves and stems as insoluble salts

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37
Q

toxic principle of plants containing oxalates

A

calcium oxalate crystals are preformed in leaves and stems as insoluble salts +/- proteolytic enzymes

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38
Q

mechanism of action of plants containing oxalates

A

mechanical irritation from calcium oxalate raphides and proteolytic enzymes cause release of inflammatory mediators (histamine)

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39
Q

clinical signs of toxicity of plants containing oxalates

A

rapid onset of salivation, head shaking, oral pain, swelling of oral mucosa can lead to dyspnea, colic, vomiting, diarrhea

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40
Q

diagnosis of oxalate plant toxicity

A

clinical signs and ID plant

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41
Q

treatment of oxalate plant toxicity

A

rinse mouth, oral calcium (to precipitate some soluble oxalates), antihistamine, symptomatic/supportive

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42
Q

toxic principle of poinsettia

A

diterpene ester (milky white sap)

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43
Q

mechanism of action of poinsettia exposure

A

GIT irritation

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44
Q

clinical signs of poinsettia exposure

A

rapid onset of oral irritation leading to hypersalivation +/- head shaking, vomiting, diarrhea

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45
Q

diagnosis of poinsettia exposure

A

clinical signs, ID plant

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46
Q

treatment of poinsettia exposure

A

GI decontamination, activated charcoal, symptomatic/supportive

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47
Q

toxic principle of mistletoe

A

phoratoxin (NA); viscumin and viscotoxin (EU)

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48
Q

mechanism of action of mistletoe exposure

A

phoratoxin inhibits protein synthesis; viscumin agglutinates RBC and causes intravascular hemolysis; viscotoxin stimulates smooth and skeletal muscle

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49
Q

clinical signs of mistletoe exposure

A

delayed several hours for lectin to get into cell; colic, vomiting, diarrhea

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50
Q

diagnosis of mistletoe exposure

A

clinical signs and plant ID

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51
Q

treatment of mistletoe exposure

A

GI decontamination, activated charcoal, saline cathartic, symptomatic and supportive

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52
Q

toxic principle of autumn crocus

A

colchicine (alkaloid) – all parts esp. corm and seeds

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53
Q

mechanism of action of autumn crocus

A

binds to tubulin to disrupt microtubule dependent processes; rapidly dividing cells are most sensitive –> leaves cells arrested in metaphase

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54
Q

clinical signs of autumn crocus toxicity

A

delay of 12-24 hours; severe colic, vomiting, diarrhea, depression, weakness, ataxia, multiorgan failure (esp. liver, kidney), collapse, coma, death

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55
Q

diagnosis of autumn crocus toxicity

A

clinical signs, plant ID, clinical pathology (increased liver and renal enzymes)

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56
Q

diagnosis of autumn crocus toxicity

A

clinical signs, plant ID, clinical pathology (increased liver and renal enzymes, PM (gastroenteritis)

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57
Q

treatment of autumn crocus toxicity

A

GI decontamination (if observe eating plant), activated charcoal, fluids, electrolytes, anticholchicin is used in people

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58
Q

clinical signs of lily poisoning

A

within 1-2 hours – vomiting, anorexia, lethargy, hypersalivation, depression; polyuria, ataxia, tremors, vocalization; 24-96 hours – oliguric or anuric ARF with uremic breath, dyspnea, recumbency

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59
Q

Clin path of lily poisoning

A

increased BUN and creatinine, increased P and K, acidosis, glucosuria, proteinuria, granular casts

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60
Q

PM of lily poisoning

A

swollen, edematous kidneys; PCT necrosis, intact basement membrane (if cat lives kidney can regenerate)

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61
Q

diagnosis of lily poisoning

A

clin path and history

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62
Q

treatment of lily poisoning

A

emesis/gastric lavage in less than 6 hours; activated charcoal, IV fluids, supportive care

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63
Q

toxic principle of death camas

A

steroidal alkaloids including zygadenine and zygacine (all parts, esp. seeds)

64
Q

death camas mechanism of action

A

induce arteriole dilatation –> hypotension; constriction of venules and slowing HR

65
Q

susceptibility to death camas

A

sheep are especially susceptible

66
Q

susceptibility to death camas

A

sheep are especially susceptible

67
Q

clinical signs of death camas toxicity

A

often found death; salivation, colic, vomiting, tachypnea, trembling, ataxia, weak rapid pulse, hypothermia, weakness, depression, death with agonal struggling and jaw clamping

68
Q

diagnosis of death camas toxicity

A

alkaloid screen of rumen contents

69
Q

PM of death camas toxicity

A

pulmonary congestion and edema

70
Q

treatment of death camas toxicity

A

impractical in field; symptomatic/supportive; grazing management

71
Q

toxic principle of larkspur

A

diterpene alkaloids (methyllycaconitine and delphinine)

72
Q

mechanism of action of larkspur toxicity

A

non-depolarizing, curare-like neuromuscular blocking agent; binds and blocks post-synaptic nicotinic cholinergic receptors at neuromuscular junctions

73
Q

susceptibility to larkspur toxicity

A

sheep and horses are less susceptible than cattle

74
Q

clinical signs of larkspur toxicity

A

often found dead; nervousness, excitability, disorientation, stiffness, muscle tremors, loss of motor control, convulsions, fall down hill, respiratory depression, bradycardia, hypotension death from resp paralysis

75
Q

diagnosis of larkspur toxicity

A

alkaloid screen of rumen contents

76
Q

PM of larkspur toxicity

A

bloat and venous congestion

77
Q

treatment of larkspur toxicity

A

impractical in field; supportive and symptomatic

78
Q

toxic principle of water hemlock

A

cicutoxin

79
Q

mechanism of action of water hemlock

A

potent direct acting neurotoxin that probably acts on GABA

80
Q

susceptibility to water hemlock toxicity

A

cattle are most at risk; all species susceptible but causes emesis so pigs vomit it up

81
Q

clinical signs of water hemlock toxicity

A

less than 15minute onset, found dead in 1 hour; salivation, apprehension, muscle twitching, jaw clamping, teeth grinding, spasmodic jerking, +/- running fits, seizures, death from respiratory paralysis

82
Q

diagnosis of water hemlock toxicity

A

clinical pathology and histopath (increased muscle enzymes); ID plant

83
Q

treatment of water hemlock toxicity

A

impractical in field; symptomatic and supportive

84
Q

toxic principle of yellow star thistle

A

unidentified

85
Q

mechanism of action of yellow star thistle

A

acts to destroy dopaminergic nigrostriatal pathway

86
Q

mechanism of action of yellow star thistle

A

acts to destroy dopaminergic nigrostriatal pathway that has coordinating and inhibiting effects on cerebral cortical pathways that control function of CN 5, 7 and 9

87
Q

PM of yellow star thistle

A

ischemic necrosis of substantia nigra and globus pallidus in brain

88
Q

susceptibility to yellow star thistle toxicity

A

equids are only susceptible

89
Q

clinical signs of yellow star thistle toxicity

A

sudden onset after prolonged exposure; hypertonicity of facial muscles, lower lip hangs, paralysis of tongue, yawning, head tossing, can’t prehend or chew food, emaciation, starvation, death

90
Q

diagnosis of yellow star thistle toxicity

A

clinical signs, history, pathology

91
Q

treatment of yellow star thistle toxicity

A

symptomatic and supportive; avoid exposure

92
Q

toxic principle of horse tail

A

thiaminase (non-ruminants); not know in ruminants

93
Q

mechanism of action of horse tail toxicity

A

break down of thiamine in GIT leading to vitamin B1 deficiency; thiamine is a cofactor in kreb’s cycle so interrupts energy production

94
Q

clinical signs of horse tail toxicity

A

progressive weight loss but remain hungry, weakness, ataxia, staggering, general paresis, dyspnea, weak pulse, tremors –> convulsion, recumbency, coma, death

95
Q

diagnosis of horse tail toxicity

A

response to treatment, clinical pathology, histopath (inflammation and edema of brain and meninges, edema of lungs)

96
Q

treatment of horse tail toxicity

A

remove from source, supplement with good feed, thiamine hydrochloride treatment (vitamin B therapy)

97
Q

treatment of horse tail toxicity

A

remove from source, supplement with good feed, thiamine hydrochloride treatment (vitamin B therapy)

98
Q

toxic principle of bracken fern to non-ruminants

A

thiaminase

99
Q

toxic principle of bracken fern to ruminants

A

aplastic anemia factor (glycoside ptaquiloside), enzootic hematuria factor (carcinogen ptaquiloside), cyanogenic glycoside

100
Q

mechanism of action of bracken fern in non-ruminants

A

thiaminase induced thiamine deficiency

101
Q

mechanism of action of bracken fern in ruminants

A

toxin acts on bone marrow causing and aplastic anemia; converted to carcinogen in bladder and causes DNA adduct formation

102
Q

mechanism of action of bracken fern in ruminants

A

toxin acts on bone marrow causing and aplastic anemia; converted to carcinogen in bladder and causes DNA adduct formation

103
Q

clinical signs of bracken fern in non-ruminants

A

progressive cachexia and neuro signs; ataxia, wide leg stance, knuckling, tremors, recumbency, convulsion and death

104
Q

clinical signs of bracken fern toxicity in ruminants

A

aplastic anemia (sudden onset of depression, pyrexia,anorexia, emaciation, hemorrhage) or neoplastic syndrome (bladder TCC –> bleeding)

105
Q

diagnosis of bracken fern toxicity

A

response to treatment in horses; clin path in ruminants and histopath

106
Q

clinical pathology of bracken fern toxicity in ruminants

A

thrombocytopenia, leukopenia, blood in urine, petechial hemorrhage, bladder lesions with neoplastic syndrome

107
Q

treatment of horses with bracken fern toxicity

A

thiamine hydrochloride treatment

108
Q

treatment of cattle with bracken fern toxicity

A

symptomatic and supportive

109
Q

toxic principles of lupine

A

qunolizidine alkaloids (lupinine) and teratogenic alkaloid (anagyrine)

110
Q

mechanism of action of lupine toxicity

A

bind to nicotinic receptors causing CNS stimulation/depression; anagyrine causes arthrogryposis if dam is expose from days 40-70

111
Q

susceptibility to lupine toxicity

A

sheep are most susceptible; others still susceptible though

112
Q

clinical signs of lupine toxicity

A

most cases have CNS depression with dyspnea, coma and death from respiratory paralysis; CNS stimulation shows as trembling, head pressing, teeth grinding, convulsions; crooked calf syndrome

113
Q

diagnosis of lupine toxicity

A

clinical signs and plant ID

114
Q

treatment of lupine toxicity

A

decontamination, supportive and symptomatic

115
Q

toxic principle of false hellebore

A

steroidal alkaloids (acute) and cyclopamine (teratogenic)

116
Q

mechanism of action of acute false hellebore toxicity

A

neurotoxins suspected

117
Q

mechanism of action for teratogenic effect of false hellebore

A

selective inhibition of mitosis or migration of cells during embryogenesis

118
Q

species susceptibility to false hellebore toxicity

A

sheep; congenital defects in lambs when ewes are exposed from days 12-14 of gestation

119
Q

clinical signs of acute false hellebore toxicity

A

salivation, vomiting, diarrhea, weakness, ataxia, bradycardia, cyanosis, recumbency, convulsions, paralysis

120
Q

clinical signs of teratogenic false hellebore toxicity

A

cyclopean malformations, prolonged gestation, cleft palate, hypoplasia of metacarpals/tarsals, tracheal stenosis

121
Q

diagnosis of false hellebore toxicity

A

clinical signs and plant ID

122
Q

treatment of false hellebore toxicity

A

GI decontamination, symptomatic and supportive

123
Q

how do you manage sheep with false hellebore to prevent teratogenic effects

A

breed 5 weeks prior to exposure or expose after first frost

124
Q

toxic principle of ponderosa pine

A

isocupressic acid and its variants

125
Q

mechanism of action of ponderosa pine toxicity

A

may have decreased blood flow to bovine caruncles indicating sign of parturition – stimulates abortion by mimicking natural process

126
Q

susceptibility to ponderosa pine toxicity

A

bison, cattle and llamas exposed for at least 3 days in last trimester

127
Q

clinical signs of ponderosa pine toxicity

A

abortion 48 hour to 2 weeks after exposure

128
Q

diagnosis of ponderosa pine toxicity

A

clinical signs, ID plant, pathology

129
Q

treatment of ponderosa pine toxicity

A

nursing care for weak born calves; avoid exposure in critical period

130
Q

toxic principle of group 1 astragalus (milkvetch)

A

selenium

131
Q

mechanism of action of milkvetch

A

selenium is incorporated into cysteine and methionine in place of sulfur; Se metabolism produces ROS that damage cell membranes

132
Q

clinical signs of acute milkvetch toxicity

A

same as acute Se

133
Q

clinical signs of chronic milkvetch toxicity

A

same as chronic Se (alkali disease)

134
Q

diagnosis of milkvetch toxicity

A

measure Se in plant

135
Q

treatment of milk vetch toxicity

A

remove source, symptomatic/supportive, add sulfur to diet to bind selenium

136
Q

toxic principle of group 2 astragulus (loco)

A

swainsonine (indolizidine alkaloid)

137
Q

mechanism of action of group 2 astragulus (loco)

A

inhibition of lysosomal enzymes involved in saccharide metabolism leading to accumulation of oligosaccharides in cells of brain and other organs that interferes with normal cell function

138
Q

susceptibility to group 2 astragulus (loco)

A

horses are most susceptible; young are more severely effected (passed in milk)

139
Q

clinical signs of group 2 astragulus (loco) toxicity

A

depression, anorexia, excitable with stimulation, circling, wander off, loss of herd instinct

140
Q

diagnosis of group 2 astragulus (loco) toxicity

A

clinical signs, ID plant, clin path (lymphopenia, leukopenia)

141
Q

treatment of group 2 astragulus (loco) toxicity

A

remove from source; mild cases recover, chronic don’t

142
Q

toxic principle of st. johnswort

A

hypericin

143
Q

toxic principle of st. johnswort

A

hypericin

144
Q

mechanism of action of st. johnswort

A

direct acting photodynamic agent leading to primary photosensitization

145
Q

clinical signs of st. johnswort toxicity

A

within 24 hours; erythema of non-pigmented skin, edema, vesiculation, desquamation and necrosis of epidermis; pyrexia, shock, hypotension

146
Q

diagnosis of st. johnswort

A

rule out hepatogenous photosensitization; clinical signs and plant ID

147
Q

treatment of st. johnswort toxicity

A

remove from source, terminate UV exposure, treat skin lesions like burns

148
Q

which plants contain pyrrolizidine alkaloids

A

fiddleneck and tansy ragwort (senecio)

149
Q

mechanism of action of pyrrolizidine alkaloids

A

toxin enters liver and is metabolized to pyrrole derivatives that bind cellular macromolecules; hepatocytomegaly and cell death result from binding of DNA

150
Q

susceptibility to pyrrolizidine alkaloids

A

cattle and horses are most at risk; sheep are resistant

151
Q

human health risk associated with pyrrolizidine alkaloids

A

carcinogenic alkaloids passed in milk

152
Q

clinical signs of pyrrolizidine alkaloid toxicity

A

sudden hepatic insufficiency

153
Q

clinical signs oh pyrrolizidine alkaloid toxicity in horse

A

cachexia, icterus, sleepy staggers, hepatic coma, biting things

154
Q

clinical signs of pyrrolizidine alkaloid toxicity in cattle

A

nervousness, mania, colic, diarrhea, tenesmus, rectal prolapse, photosensitization

155
Q

diagnosis of pyrrolizidine alkaloid toxicity

A

signs, alkaloid screen, pathology, histopath

156
Q

treatment of pyrrolizidine alkaloid toxicity

A

symptomatic and supportive

Toxicology (4 decks)

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