17 – Toxic Ornamental Plants and Houseplants Flashcards
1
Q
True Lilies
A
- Lilium, Hemerocallis
- *only toxic to CATS
- *Parts of plants: ENTIRE PLANT
- Exposure
o Chewing leaves or petals, drinking vase water or rubbing against pollen (typical=bouquet brought into the house)
2
Q
True Lilies: toxin and mechanism
A
- Unknown
3
Q
True Lilies: toxicity
A
- *any ingestion or exposure is clinically significant to cats
4
Q
True Lilies: target organ
A
- Kidneys
5
Q
True Lilies: clinical features
A
- Onset: within a few hours post-exposure
- Earliest: vomiting, hypersalivation, anorexia
- 24-72 hours: rapid deterioration=development of aliguric to anuric renal failure
o PU/PD: oliguria, anuria, uremia
o Anorexia, depression, vomiting resumes
o Abdominal palpation: enlarged, painful kidneys - Death and euthanasia within 3-6 days
6
Q
True Lilies: clinical pathology
A
- Indicative of acute kidney injury
o Within 12hrs: azotemia, increased Ca and P
o Within 24hrs: tubular casts, proteinuria, glucosuria, isosthenuria
7
Q
True Lilies: post mortem
A
- Swollen and congested kidneys
- Peri-renal hemorrhage and edema
8
Q
True Lilies: management
A
- Decontamination: emesis, AC if not contraindicated
- *IVFT ASAP=48hrs! (maybe SC at home?)
- Dermal decontamination: remove pollen from fur/muzzle
- Frequent monitoring of chem panel, UA, and urinary output
- If anuria develops=dialysis or euthanasia
9
Q
True Lilies: diagnosis
A
- Lilies present in same household as cat
- Presence of pollen on muzzle
- Evidence of chewing on plant
- Plant parts in vomitus
- Compatible clinical signs
10
Q
True Lilies: DDx
A
- Ethylene glycol poisoning
- Vit D
- NSAIDs
- Aminoglycosides
11
Q
True Lilies: prognosis
A
- Fluids before anuric renal failure=good
- Delayed treatment and/or anuric renal failure=poor
- No treatment=grave
12
Q
Cardiac glycosides
A
- Numerous species of plants
o *most common in animals=OLEANDER
o Foxglove
o Lily of the valley
o Milkweed
o Kalanchoe spp. - All species susceptible
13
Q
Cardiac glycosides: exposure
A
- Clippings
- Fallen leaves
- Hay contamination
- Access to garden
14
Q
Cardiac glycosides: mechanism
A
- CARDIOTAXINS
- Inhibit Na/K ATPase
o Increased vagal tone=bradycardia - Toxicity: a few leaves or seeds can be fatal (10-20 oleander leaves in horse)
- Dried plants remain toxic
15
Q
Cardiac glycosides: clinical features
A
- Within 30mins
- Lethargic, dull, signs of discomfort
- GI: nausea, vomiting, abdominal pain, diarrhea
o Ruminate: bloat
o Horses: colic - Low dose: bradycardia
- High dose: tachycardia
- Cold extremities, sweating, dyspnea
- CNS: tremors
- Sudden death with exertion
- If survives: permanent heart damage possible
16
Q
Cardiac glycosides: clinical pathology
A
- Hyperkalemia
- Increased CK, LDH
- Increased cardiac tamponins
17
Q
Cardiac glycosides: postmortem
A
- Cardiomyopathy and necrosis
o Pulmonary edema and congestion, cardiac petechiation and ecchymoses, gastroenteritis
18
Q
Cardiac glycosides: management
A
- Decontamination if not contraindicated
- Antidote: anti-digoxin Fab antibody fragment
- Supportive care: IVFT, anti-arrhythmic drugs
o Atropine, lidocaine
o Hyperkalemia: insulin/dextrose - Close monitoring of ECG/BP, oxygenation, bloodwork
19
Q
Cardiac glycosides: diagnosis
A
- Cardiotoxic plants accessible to pets/livestock
- Presence of plants in vomitus/stomach contents/rumen contents
- Detection of cardiotoxins in tissues/serum: Ex. oleandrin (US not Canada)
- Digoxin assay
20
Q
Cardiac glycosides: DDx
A
- Ionophore toxicity
- Rhododendron
- Yew
- Acute selenium toxicosis
- Death comas
- Endocarditis
- Colic (horses)
- Fluoroacetate
21
Q
Cardiac glycosides: prognosis
A
- Livestock typically found dead
- Response to treatment and supportive care dictates prognosis
o Survival >24hrs improves prognosis
22
Q
Yew
A
- Common ornamental shrub in North America
- All parts are toxic, except the fruit
o Toxic year round - *most poisonings are in livestock
23
Q
*Yew: target
A
- Heart
24
Q
Yew: mechanism of action
A
- Inhibit sodium and calcium exchanged in the myocardium
o Decreased electrical conduction=acute heart failure
25
Q
Yew: clinical features
A
- Onset: within minutes to a few hours following ingestion
- Acute: *MOST often found dead
- SUBACUTE
o GI irritation
o CV: lethargy, dyspnea, bradycardia, weak pulses, jugular distension
o CNS signs: tremors, ataxia, convulsions, collapse
o Death within 24-48 hrs of ingestion - Development of sub chronic heart failure possible: myocardial fibrosis
- Stomach/rumen contents: yew plant parts
26
Q
Yew: PM lesions
A
- No lesions in acute poisoning
- Subacute: myocardial hemorrhage, epicardial hemorrhages, pericardial effusion, pulmonary edema and congestion
27
Q
Yew: management
A
- Often unrewarding
- If animals alive
o Low stress handling
o No true antidote
o Supportive care: atropine, fluids, other anti-arrhythmics
28
Q
Yew: diagnosis
A
- History of access to yew (ex. plant clippings)
- Presence of yew in stomach/rumen contents
- *confirmatory testing: detection of taxine alkaloids in animal tissues (liver, heart, others)
- DDx: same as cardiac glycosides
- *prognosis: grave to poor
29
Q
Sago palm
A
- Often household plants, but found in tropical and subtropical regions as native plants
- *mostly DOGS
- All parts are toxic, especially SEEDS (seeds only by female plants)
30
Q
Sago palm: toxicity and target organ
A
- A few seeds, chewing one palm
- *LIVER, CNS, kidneys
- Multiple toxins: CYCASIN
31
Q
Sago palm: mechanism
A
- Methylation of DNA + RNA = inhibition of protein synthesis = acute hepatic necrosis
32
Q
Sago palm: clinical features
A
- Onset: within 15mins to several hours
- GI: vomiting, anorexia, diarrhea, hypersalivation
- *within 2-3 days=development of ACUTE HEPATIC NECROSIS
o Vomiting, diarrhea, melena, abdominal pain
o Ascites, icterus
o Hepatic encephalopathy
o Clin path: increased liver enzymes, indicators of liver failure
33
Q
Sago palm: PM
A
- GI hemorrhage and necrosis
- Severe centrilobular hepatic necrosis with hydropic degeneration
34
Q
Sago palm: management
A
- No antidote
- GI decontamination
- Symptomatic and supportive care
o Liver: hepatoprotectants, vitamin K, plasma, IVFT
o Gastroprotectants
o Frequent monitoring of liver values
35
Q
Sago palm: diagnosis
A
- History of ingestion of a palm or palm seed
- Plant parts/seed in vomitus
- NO confirmatory test is available
36
Q
What are some toxic differentials for acute liver failure in dogs?
A
- sago palm
- microcystin
- acetaminophen
- xylitol
- aflatoxin
37
Q
Sago palm: prognosis
A
- Variable: reported mortality rates up to 67%
- Poor prognostic indicators: thrombocytopenia, multiple clinical signs at admission, ALT, hypoalbuminemia
- Improved prognosis: initial ALT <125U/L, treatment with activated charcoal
38
Q
Insoluble oxalates
A
- Numerous plants
- Ex. peace lily, philodendron, monstera, dumbcane
39
Q
*Insoluble oxalates: mechanism
A
- Physical damage
o Mucosal irritation
o Raphides in specialized cells called idioblasts
40
Q
Insoluble oxalates: clinical features
A
- In general, they do NOT cause systemic clinical signs
- Onset: within minutes
- Salivation, head shaking, pawing at mouth, vocalization
- Pain and swelling of tongue, oral mucosa, pharynx
- +/- vomiting/diarrhea
41
Q
Insoluble oxalates: management
A
- Oropharynx only: rinsing mout with milk or water, pain management, anti-inflammaotry
- Laryngeal swelling: anti-inflammatories, may need to intubate if severe
- GI irritation gastroprtectants, analgesics, anti-inflammatories, IVFT
- *prognosis=excellent
42
Q
Tulips and Hyacinths
A
- Exposure: access to bag of bulbs for planting, digging up newly planted bulbs
- Clinical features
o Oral and esophageal irritation
o Vomiting and diarrhea
o Large ingestions: v/d, tachycardia - Management
o Oral irritation: similar to insoluble oxalates
o v/d: IVFT, gastroprotecants
43
Q
Mistletoe
A
- toxic principles: glycoprotein lectins
- mechanism of action: inhibition of protein synthesis=cell death
- clinical features
o most common: vomiting, depression
o uncommon: diarrhea, hypotension
o *generally MILD, SELF-LIMITING
44
Q
Poinsettia
A
- Toxicity in animals has been overexaggerated
- Toxic principles: irritating sap
- Clinical features
o MILD and SELF-LIMITING
o Dermal: erythema, irritation, pruritus
o GI: hypersalivation, vomiting, rarely diarrhea
45
Q
Holly
A
- toxic principles: saponins, triterpenes, polyphenols, methylaxanthines, cyanogens
- mechanism: GI irritation
- clinical features:
o GI: hypersalivation, vomiting, anorexia, dirrhea
o Oral irritation
46
Q
Holiday plant: management
A
- Supportive care: IVFT or SC fluids, gastroportectants
o Rinse mouth with water or milk
o Monitor hydration and electrolyte status
o Most cases do NOT require hospitalization
o Home care: client withholds food and water for a few hourse, then gradually re-introduces water, bland food
47
Q
Holiday plant: diagnosis and prognosis
A
- History of ingestion and plant parts in vomitus
- *prognosis: excellent
48
Q
Castor plant
A
- All parts toxic, especially seeds
- Exposure: ingestion of seeds, feed contaminated fertilizer
49
Q
*Castor plant: toxin and toxicity
A
- *RICIN
o Inactivates ribosomes=inhibition of protein synthesis=cell death - Toxicity: *1-3 seeds can be lethal
- ONLY TOXIC WHEN CHEWED
50
Q
*Castor plant: onset
A
- Latency period of several hours up to multiple days
o Miss decontamination period
51
Q
Castor plant: clinical features
A
- GI: abdominal pain, profuse vomiting, profuse severe diarrhea
- CV: hypotension, hypovolemia, arrhythmias
- CNS: depression, incoordination, terminal seizures and coma
- Liver and kidney damage
52
Q
Castor plant: PM
A
- Multiple-organ hyperemia, ulcerations, hemorrhages
53
Q
Castor plant: management
A
- No specific antidote
- GI decontamination if not contraindicated
- Aggressive support care
o GI: gastroprotectants
o CV: ECG/BP monitoring
o Liver: hepatoprotectants
o Kidney: IVFT
o Seizures: diazepam
o Monitoring of CBC/chemistry/UA for liver, kidney, electrolyte parameters
54
Q
Castor plant: diagnosis
A
- Detection of ricinine in urine or blood
55
Q
Castor plant: DDx
A
- Severe gastroenteritis
o Zinc phosphide
o Inorganics As and Hg
o DON
o Death cap mushroom - Liver damage
o Xylitol, zinc phosphide, death cap mushroom - Cardiotoxicty
o Cardiac glycoside plants, rhododendron, yew, death camas, ionophores
56
Q
Castor plant: prognosis
A
- Good with aggressive supportive care
- No treatment=grave
57
Q
Autum crocus
A
- All plants toxic, especially tubers and seeds
- *COLCHICINE
o Human med: gout, immune mediated diseases, cancer
o Vet med: off-label for glaucoma
o Microtubule inhibitor: anti-mitotic agent, PGP substrate, undergoes EHC
58
Q
Autum crocus: clinical features
A
- GI: diarrhea, abdominal pain, vomiting, drooling
- CNS: depression, weakness, ataxia, hypothermia
- Cardiorespiratory: bradycardia, pale MM, hypotension, tachypnea
- Recumbency, seizures, collapse
- Death due to shock, respiratory failure, CV failure or multi-organ failure
- PM: GI hemorrhage and congestion
59
Q
Autum crocus: diagnosis
A
- history of ingestion
- plant ID from vomitus
- *detection of colchicine in blood and urine: limited availability
60
Q
Autum crocus: management
A
- NO antidote
- Decontamination
- Supportive care
o IVFT, anti-emetics, seizure control, atropine for bradycardia
o Mannitol for cerebral edema
o Antibiotics for bacterial translocation
o Monitoring of cardiorespiratory system, liver and kidney function, intracranial pressure - If animal survives=continue to monitor CBC for a few weeks
61
Q
Autum crocus: DDx
A
- Bone marrow suppression
o Chemotherapeutics, immunosuppressive drugs, estrogen, radiation, neoplasia - Multi-systemic failure: ricin, sepsis
62
Q
Autum crocus: prognosis
A
- poor
