Ornamental and house plants Flashcards
True lilies
Lilium spp, Hemerocallis spp
-only toxic in cats
-entire plant
Lily cat exposure scenarios
-chewing on plant
-drinking vase water
-rubbing against pollen
Mechanism of lily toxicity
Unknown
-targets the kidneys
Onset of lily toxicity
-within a few hours post exposure
Lily toxicity early clinical signs
-vomiting
-hypersalivation
-anorexia
-after vomiting, cat is depressed
Lily toxicity clinical signs 24-72 hours
Rapid deterioration = development of oliguric to anuric renal failure
-PU/PD
-anorexia, depressed, vomiting resumes
-enlarged painful kidneys on palpation
*Death or euthanasia within 3-6days
Clinical pathology signs for true lily toxicity
Acute kidney injury
-12hrs: azotemia, increased Ca, P
-24hrs: tubular casts, proteinuria, glucosuria, isosthenuria
Post mortem findings of true lily toxicity
-swollen and congested kidneys
-peri renal hemorrhage and edema
-will se proximal tubular degeneration and necrosis
True lily toxicity management
-Decontamination (emesis, A/C if not contraindicated); dermal for pollen removal
-IVFT ASAP & urinary catheter to monitor urine
-monitor chem panel, UA
-euthanasia if anuria develops
Diagnosis of true lily toxicity
-lily present in same house as cat
-pollen on muzzle
-evidence of chewed plant
-plant parts in vomit
-clinical signs/history
DDx of lily toxicity
-ethylene glycol poisoning
-vita D
-NSAIDs
-aminoglycosides
Prognosis of true lily toxicity
-fluids before anuric renal failure= good
-delayed treatment or anuric renal failure- poor
-no treatment=grave
Cardiac glycosides
-foxglove
-lily of the valley
-oleander
-milkweed
-Kalanchoe
*all species susceptible; often exposed from clippings, fallen leaves, hay contamination, gardens
Oleander
“flower within a flower”
Mechanism of cardiac glycosides
Cardenolide group of cardiotoxins
-inhibits Na-K ATPase leading to increased Ca availability= dysrhythmias and bradycardia
Toxicity levels of cardiac glycosides
Only need a few leaves or seeds
but in horses 10-20 leaves of oleander
Cardiac glycosides toxicity onset
within 30mins to hours of ingestion
Clinical signs of cardiac glycosides
-lethargic, dull, discomfort
-vomiting, abdominal pain, diarrhea
*ruminant bloat, horse colic
-lower dose: positive inotropy, negative chronotopy=bradycardia
-higher dose: negative dromotopy= AV block, sinus tachycardia and Vtach
-cold extremities, sweating, dyspnea
-tremors, ataxia, mydriasis
-sudden death with exertion
-survival= permanent heart damage
Clinical pathology of cardiac glycoside toxicity
-hyperkalemia
-increased CK, LDH
-increased cardiac troponins
PM of cardiac glycoside toxicity
-cardiomyopathy and necrosis
-pulmonary edema and congestion, cardiac petechiation, ecchymoses, gastroenteritis
-histo: myocardial necrosis, hemorrhage
Management of cardiac glycosides
-Decontamination
-antidote: anti-digoxin Fab antibody fragment
-IVFT
-anti-arrhythmic drugs (Atropine for bradycardia, Lidocaine for tachyarrhythmias)
-oxygenation, bloodwork, etc.
Diagnosis of cardiac glycosides
-history of accessibility to plant
-plant present in vomit or stomach contents
-diagoxin assay
DDx for cardiac glycosides and yew
-ionophore toxicity
-rhododendron
-yew
-acute selenium toxicosis
-death camas
-endocarditis
-colic
-fluoroacetate
Prognosis of cardiac glycosides
-Livestock typically found dead
-response to treatment and supportive care indicates prognosis
-if survival for more than 24hrs than improved prognosis
Yew
-all parts are toxic all year round EXCEPT fruit
-most poisonings in livestock because clippings tossed in pens
Yew
Toxin of yew
Taxine alkaloids (taxine A+B)
Target and mechanism of yew
Target= heart
Mechanism= inhibits Na and Ca exchange in myocardium resulting in decreased electrical conduction and acute heart failure
Onset of yew
Within mins to a few hours after ingestion
Acute yew symptoms
Most often just found dead
Subacute Yew symptoms
-GI irritation
-CV signs: bradycardia, weak pulse, jugular distension, wide QRS, depressed P wave
-CNS: tremors, ataxia, convulsions, collapse
Death= 24-48hrs
Cause of death of yew
Diastolic standstill
Lesions of yew
-no lesions if acute
-Heart and lungs= hemorrhage, edema, congestion
-subchronic heart failure and myocardial fibrosis
-stomach and rumen contents= yew plants
Management of yew
-no antidote
-low stress handling
-supportive care:atropine, fluids, antiarrhythmics
Diagnosis of yew
-history of access to yew
-presence of yew in stomach/rumen
-detection of taxine alkaloids in animal tissues
Prognosis of yew toxicity
Grave to poor in livestock
