Plants Flashcards
toxic principle of foxglove
digitalis glycosides (present in flowers, seeds and leaves)
mechanism of action of foxglove
interferes with Na/K ATPase –> decreased intracellular K and increased intracellular Na –> increased Ca (interferes with normal electrical conductivity in myocardium)
clinical signs of foxglove toxicity
vomiting, colic, diarrhea, anorexia, CV (bradycardia, arrhythmias, heart failure), weakness, depression, dyspnea, tremors, convulsions, coma, death
diagnosis of foxglove
ECG, plant in stomach contents
PM of foxglove
gastroenteritis
treatment of foxglove
emesis, activated charcoal, saline cathartic, symptomatic and supportive, digibind (human product with cross reactivity to plant toxins)
toxic principle of japanese yew
alkaloid taxine; taxine B (wood, bark, leaves, seeds) – not present in fleshy fruit
toxic principle of japanese yew
alkaloid taxine; taxine B (wood, bark, leaves, seeds) – not present in fleshy fruit
japanese yew mechanism of action
disrupts Na and Ca currents in myocytes by binding receptors; depress conduction of myocardial depolarization
susceptibility of japanese yew
equine are more susceptible than ruminants (but both are susceptible)
clinical signs of japanese yew poisoning
rapid onset, sudden death, weakness, trembling, dyspnea, bradycardia, arrhythmias, convulsion, collapse
diagnosis of japanese yew poisoning
ECG abnormalities; alkaloid screen to ID toxin in stomach;
PM of japanese yew poisoning
gastroenteritis, secondary pulmonary congestion and edema
treatment of japanese yew poisoning
GI decontamination, activated charcoal, fluids, seizure control, treat arrhythmias
toxic principle of rhododendron
glycoside grayanotoxin (all plant parts, especially leaves)
mechanism of action of rhododendron toxicity
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
clinical signs of rhododendron toxicity
salivation, projectile vomiting, diarrhea, anorexia, severe colic, depression, ataxia, paralysis, brady cardia, hypotension, arrhythmias
diagnosis of rhododendron toxicity
clinical signs and ID plant;
PM of rhododendron toxicity
degeneration of liver and kidneys (mild); GI irritation
treatment of rhododendron toxicity
aggressive GI decontamination, activated charcoal, symptomatic and supportive
toxic principle of jimson weed
tropane alkaloids (hyoscyamine, scopolamine, hyoscine) – all plant parts, especially seeds
mechanism of low dose jimson weed
competitive inhibitor of acetylcholine
mechanism of high dose jimson weed
direct CNS stimulation (crosses BBB rapidly)
clinical signs of jimson weed toxicity
atropine-like syndrome – mydriasis, anorexia, thirst, tachycardia, tachypnea, hypothermia, tremors, excitability, convulsions, death from resp paralysis
clinical signs of high dose jimson weed toxicity
hyperesthesia, apprehension, mania, vocalization
diagnosis of jimson weed toxicity
bioassay, pathology, drop of patients urine in the eye of clinic cat will cause mydriasis
diagnosis of jimson weed toxicity
bioassay, pathology, drop of patients urine in the eye of clinic cat will cause mydriasis
treatment of jimson weed toxicity
GI decontamination, activated charcoal, symptomatic/supportive, neostigmine (inhibits acetylcholinesterase)
toxic principle of castor bean
glycoprotein ricin (lectin) – stays in meal of bean
mechanism of action of castor bean
binds galacto-lipid and galacto-protein membrane components –> internalization –> cell death by inhibition of protein synthesis
clinical signs of castor bean toxicity
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
diagnosis of castor bean toxicity
clinical pathology and lesions
clinical pathology of castor bean toxicity
huge increase in PCV, panleukopenia, increased liver enzymes and bilirubin
PM of castor bean toxicity
hemorrhagic gastroenteritis
treatment of castor bean toxicity
GI decontamination, activated charcoal, fluids and electrolytes, GI protectants, grave prognosis
toxic principle of plants containing oxalates
calcium oxalate crystals are preformed in leaves and stems as insoluble salts
toxic principle of plants containing oxalates
calcium oxalate crystals are preformed in leaves and stems as insoluble salts +/- proteolytic enzymes
mechanism of action of plants containing oxalates
mechanical irritation from calcium oxalate raphides and proteolytic enzymes cause release of inflammatory mediators (histamine)
clinical signs of toxicity of plants containing oxalates
rapid onset of salivation, head shaking, oral pain, swelling of oral mucosa can lead to dyspnea, colic, vomiting, diarrhea
diagnosis of oxalate plant toxicity
clinical signs and ID plant
treatment of oxalate plant toxicity
rinse mouth, oral calcium (to precipitate some soluble oxalates), antihistamine, symptomatic/supportive
toxic principle of poinsettia
diterpene ester (milky white sap)
mechanism of action of poinsettia exposure
GIT irritation
clinical signs of poinsettia exposure
rapid onset of oral irritation leading to hypersalivation +/- head shaking, vomiting, diarrhea
diagnosis of poinsettia exposure
clinical signs, ID plant
treatment of poinsettia exposure
GI decontamination, activated charcoal, symptomatic/supportive
toxic principle of mistletoe
phoratoxin (NA); viscumin and viscotoxin (EU)
mechanism of action of mistletoe exposure
phoratoxin inhibits protein synthesis; viscumin agglutinates RBC and causes intravascular hemolysis; viscotoxin stimulates smooth and skeletal muscle
clinical signs of mistletoe exposure
delayed several hours for lectin to get into cell; colic, vomiting, diarrhea
diagnosis of mistletoe exposure
clinical signs and plant ID
treatment of mistletoe exposure
GI decontamination, activated charcoal, saline cathartic, symptomatic and supportive
toxic principle of autumn crocus
colchicine (alkaloid) – all parts esp. corm and seeds
mechanism of action of autumn crocus
binds to tubulin to disrupt microtubule dependent processes; rapidly dividing cells are most sensitive –> leaves cells arrested in metaphase
clinical signs of autumn crocus toxicity
delay of 12-24 hours; severe colic, vomiting, diarrhea, depression, weakness, ataxia, multiorgan failure (esp. liver, kidney), collapse, coma, death
diagnosis of autumn crocus toxicity
clinical signs, plant ID, clinical pathology (increased liver and renal enzymes)
diagnosis of autumn crocus toxicity
clinical signs, plant ID, clinical pathology (increased liver and renal enzymes, PM (gastroenteritis)
treatment of autumn crocus toxicity
GI decontamination (if observe eating plant), activated charcoal, fluids, electrolytes, anticholchicin is used in people
clinical signs of lily poisoning
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
Clin path of lily poisoning
increased BUN and creatinine, increased P and K, acidosis, glucosuria, proteinuria, granular casts
PM of lily poisoning
swollen, edematous kidneys; PCT necrosis, intact basement membrane (if cat lives kidney can regenerate)
diagnosis of lily poisoning
clin path and history
treatment of lily poisoning
emesis/gastric lavage in less than 6 hours; activated charcoal, IV fluids, supportive care
toxic principle of death camas
steroidal alkaloids including zygadenine and zygacine (all parts, esp. seeds)
death camas mechanism of action
induce arteriole dilatation –> hypotension; constriction of venules and slowing HR
susceptibility to death camas
sheep are especially susceptible
susceptibility to death camas
sheep are especially susceptible
clinical signs of death camas toxicity
often found death; salivation, colic, vomiting, tachypnea, trembling, ataxia, weak rapid pulse, hypothermia, weakness, depression, death with agonal struggling and jaw clamping
diagnosis of death camas toxicity
alkaloid screen of rumen contents
PM of death camas toxicity
pulmonary congestion and edema
treatment of death camas toxicity
impractical in field; symptomatic/supportive; grazing management
toxic principle of larkspur
diterpene alkaloids (methyllycaconitine and delphinine)
mechanism of action of larkspur toxicity
non-depolarizing, curare-like neuromuscular blocking agent; binds and blocks post-synaptic nicotinic cholinergic receptors at neuromuscular junctions
susceptibility to larkspur toxicity
sheep and horses are less susceptible than cattle
clinical signs of larkspur toxicity
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
diagnosis of larkspur toxicity
alkaloid screen of rumen contents
PM of larkspur toxicity
bloat and venous congestion
treatment of larkspur toxicity
impractical in field; supportive and symptomatic
toxic principle of water hemlock
cicutoxin
mechanism of action of water hemlock
potent direct acting neurotoxin that probably acts on GABA
susceptibility to water hemlock toxicity
cattle are most at risk; all species susceptible but causes emesis so pigs vomit it up
clinical signs of water hemlock toxicity
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
diagnosis of water hemlock toxicity
clinical pathology and histopath (increased muscle enzymes); ID plant
treatment of water hemlock toxicity
impractical in field; symptomatic and supportive
toxic principle of yellow star thistle
unidentified
mechanism of action of yellow star thistle
acts to destroy dopaminergic nigrostriatal pathway
mechanism of action of yellow star thistle
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
PM of yellow star thistle
ischemic necrosis of substantia nigra and globus pallidus in brain
susceptibility to yellow star thistle toxicity
equids are only susceptible
clinical signs of yellow star thistle toxicity
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
diagnosis of yellow star thistle toxicity
clinical signs, history, pathology
treatment of yellow star thistle toxicity
symptomatic and supportive; avoid exposure
toxic principle of horse tail
thiaminase (non-ruminants); not know in ruminants
mechanism of action of horse tail toxicity
break down of thiamine in GIT leading to vitamin B1 deficiency; thiamine is a cofactor in kreb’s cycle so interrupts energy production
clinical signs of horse tail toxicity
progressive weight loss but remain hungry, weakness, ataxia, staggering, general paresis, dyspnea, weak pulse, tremors –> convulsion, recumbency, coma, death
diagnosis of horse tail toxicity
response to treatment, clinical pathology, histopath (inflammation and edema of brain and meninges, edema of lungs)
treatment of horse tail toxicity
remove from source, supplement with good feed, thiamine hydrochloride treatment (vitamin B therapy)
treatment of horse tail toxicity
remove from source, supplement with good feed, thiamine hydrochloride treatment (vitamin B therapy)
toxic principle of bracken fern to non-ruminants
thiaminase
toxic principle of bracken fern to ruminants
aplastic anemia factor (glycoside ptaquiloside), enzootic hematuria factor (carcinogen ptaquiloside), cyanogenic glycoside
mechanism of action of bracken fern in non-ruminants
thiaminase induced thiamine deficiency
mechanism of action of bracken fern in ruminants
toxin acts on bone marrow causing and aplastic anemia; converted to carcinogen in bladder and causes DNA adduct formation
mechanism of action of bracken fern in ruminants
toxin acts on bone marrow causing and aplastic anemia; converted to carcinogen in bladder and causes DNA adduct formation
clinical signs of bracken fern in non-ruminants
progressive cachexia and neuro signs; ataxia, wide leg stance, knuckling, tremors, recumbency, convulsion and death
clinical signs of bracken fern toxicity in ruminants
aplastic anemia (sudden onset of depression, pyrexia,anorexia, emaciation, hemorrhage) or neoplastic syndrome (bladder TCC –> bleeding)
diagnosis of bracken fern toxicity
response to treatment in horses; clin path in ruminants and histopath
clinical pathology of bracken fern toxicity in ruminants
thrombocytopenia, leukopenia, blood in urine, petechial hemorrhage, bladder lesions with neoplastic syndrome
treatment of horses with bracken fern toxicity
thiamine hydrochloride treatment
treatment of cattle with bracken fern toxicity
symptomatic and supportive
toxic principles of lupine
qunolizidine alkaloids (lupinine) and teratogenic alkaloid (anagyrine)
mechanism of action of lupine toxicity
bind to nicotinic receptors causing CNS stimulation/depression; anagyrine causes arthrogryposis if dam is expose from days 40-70
susceptibility to lupine toxicity
sheep are most susceptible; others still susceptible though
clinical signs of lupine toxicity
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
diagnosis of lupine toxicity
clinical signs and plant ID
treatment of lupine toxicity
decontamination, supportive and symptomatic
toxic principle of false hellebore
steroidal alkaloids (acute) and cyclopamine (teratogenic)
mechanism of action of acute false hellebore toxicity
neurotoxins suspected
mechanism of action for teratogenic effect of false hellebore
selective inhibition of mitosis or migration of cells during embryogenesis
species susceptibility to false hellebore toxicity
sheep; congenital defects in lambs when ewes are exposed from days 12-14 of gestation
clinical signs of acute false hellebore toxicity
salivation, vomiting, diarrhea, weakness, ataxia, bradycardia, cyanosis, recumbency, convulsions, paralysis
clinical signs of teratogenic false hellebore toxicity
cyclopean malformations, prolonged gestation, cleft palate, hypoplasia of metacarpals/tarsals, tracheal stenosis
diagnosis of false hellebore toxicity
clinical signs and plant ID
treatment of false hellebore toxicity
GI decontamination, symptomatic and supportive
how do you manage sheep with false hellebore to prevent teratogenic effects
breed 5 weeks prior to exposure or expose after first frost
toxic principle of ponderosa pine
isocupressic acid and its variants
mechanism of action of ponderosa pine toxicity
may have decreased blood flow to bovine caruncles indicating sign of parturition – stimulates abortion by mimicking natural process
susceptibility to ponderosa pine toxicity
bison, cattle and llamas exposed for at least 3 days in last trimester
clinical signs of ponderosa pine toxicity
abortion 48 hour to 2 weeks after exposure
diagnosis of ponderosa pine toxicity
clinical signs, ID plant, pathology
treatment of ponderosa pine toxicity
nursing care for weak born calves; avoid exposure in critical period
toxic principle of group 1 astragalus (milkvetch)
selenium
mechanism of action of milkvetch
selenium is incorporated into cysteine and methionine in place of sulfur; Se metabolism produces ROS that damage cell membranes
clinical signs of acute milkvetch toxicity
same as acute Se
clinical signs of chronic milkvetch toxicity
same as chronic Se (alkali disease)
diagnosis of milkvetch toxicity
measure Se in plant
treatment of milk vetch toxicity
remove source, symptomatic/supportive, add sulfur to diet to bind selenium
toxic principle of group 2 astragulus (loco)
swainsonine (indolizidine alkaloid)
mechanism of action of group 2 astragulus (loco)
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
susceptibility to group 2 astragulus (loco)
horses are most susceptible; young are more severely effected (passed in milk)
clinical signs of group 2 astragulus (loco) toxicity
depression, anorexia, excitable with stimulation, circling, wander off, loss of herd instinct
diagnosis of group 2 astragulus (loco) toxicity
clinical signs, ID plant, clin path (lymphopenia, leukopenia)
treatment of group 2 astragulus (loco) toxicity
remove from source; mild cases recover, chronic don’t
toxic principle of st. johnswort
hypericin
toxic principle of st. johnswort
hypericin
mechanism of action of st. johnswort
direct acting photodynamic agent leading to primary photosensitization
clinical signs of st. johnswort toxicity
within 24 hours; erythema of non-pigmented skin, edema, vesiculation, desquamation and necrosis of epidermis; pyrexia, shock, hypotension
diagnosis of st. johnswort
rule out hepatogenous photosensitization; clinical signs and plant ID
treatment of st. johnswort toxicity
remove from source, terminate UV exposure, treat skin lesions like burns
which plants contain pyrrolizidine alkaloids
fiddleneck and tansy ragwort (senecio)
mechanism of action of pyrrolizidine alkaloids
toxin enters liver and is metabolized to pyrrole derivatives that bind cellular macromolecules; hepatocytomegaly and cell death result from binding of DNA
susceptibility to pyrrolizidine alkaloids
cattle and horses are most at risk; sheep are resistant
human health risk associated with pyrrolizidine alkaloids
carcinogenic alkaloids passed in milk
clinical signs of pyrrolizidine alkaloid toxicity
sudden hepatic insufficiency
clinical signs oh pyrrolizidine alkaloid toxicity in horse
cachexia, icterus, sleepy staggers, hepatic coma, biting things
clinical signs of pyrrolizidine alkaloid toxicity in cattle
nervousness, mania, colic, diarrhea, tenesmus, rectal prolapse, photosensitization
diagnosis of pyrrolizidine alkaloid toxicity
signs, alkaloid screen, pathology, histopath
treatment of pyrrolizidine alkaloid toxicity
symptomatic and supportive
