Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

TOXICOLOGY > 17 – Toxic Ornamental Plants and Houseplants > Flashcards

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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

True Lilies: toxin and mechanism

A
  • Unknown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

True Lilies: toxicity

A
  • *any ingestion or exposure is clinically significant to cats
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

True Lilies: target organ

A
  • Kidneys
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

True Lilies: post mortem

A
  • Swollen and congested kidneys
  • Peri-renal hemorrhage and edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

True Lilies: DDx

A
  • Ethylene glycol poisoning
  • Vit D
  • NSAIDs
  • Aminoglycosides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

True Lilies: prognosis

A
  • Fluids before anuric renal failure=good
  • Delayed treatment and/or anuric renal failure=poor
  • No treatment=grave
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cardiac glycosides: exposure

A
  • Clippings
  • Fallen leaves
  • Hay contamination
  • Access to garden
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cardiac glycosides: clinical pathology

A
  • Hyperkalemia
  • Increased CK, LDH
  • Increased cardiac tamponins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cardiac glycosides: postmortem

A
  • Cardiomyopathy and necrosis
    o Pulmonary edema and congestion, cardiac petechiation and ecchymoses, gastroenteritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Cardiac glycosides: DDx

A
  • Ionophore toxicity
  • Rhododendron
  • Yew
  • Acute selenium toxicosis
  • Death comas
  • Endocarditis
  • Colic (horses)
  • Fluoroacetate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Cardiac glycosides: prognosis

A
  • Livestock typically found dead
  • Response to treatment and supportive care dictates prognosis
    o Survival >24hrs improves prognosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

*Yew: target

A
  • Heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Yew: mechanism of action

A
  • Inhibit sodium and calcium exchanged in the myocardium
    o Decreased electrical conduction=acute heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Yew: clinical features
- 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
Yew: PM lesions
- No lesions in acute poisoning - Subacute: myocardial hemorrhage, epicardial hemorrhages, pericardial effusion, pulmonary edema and congestion
27
Yew: management
- Often unrewarding - If animals alive o Low stress handling o No true antidote o Supportive care: atropine, fluids, other anti-arrhythmics
28
Yew: diagnosis
- 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
Sago palm
- 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
Sago palm: toxicity and target organ
- A few seeds, chewing one palm - *LIVER, CNS, kidneys - Multiple toxins: CYCASIN
31
Sago palm: mechanism
- Methylation of DNA + RNA = inhibition of protein synthesis = acute hepatic necrosis
32
Sago palm: clinical features
- 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
Sago palm: PM
- GI hemorrhage and necrosis - Severe centrilobular hepatic necrosis with hydropic degeneration
34
Sago palm: management
- No antidote - GI decontamination - Symptomatic and supportive care o Liver: hepatoprotectants, vitamin K, plasma, IVFT o Gastroprotectants o Frequent monitoring of liver values
35
Sago palm: diagnosis
- History of ingestion of a palm or palm seed - Plant parts/seed in vomitus - NO confirmatory test is available
36
What are some toxic differentials for acute liver failure in dogs?
* sago palm * microcystin * acetaminophen * xylitol * aflatoxin
37
Sago palm: prognosis
- 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
Insoluble oxalates
- Numerous plants - Ex. peace lily, philodendron, monstera, dumbcane
39
*Insoluble oxalates: mechanism
- Physical damage o Mucosal irritation o Raphides in specialized cells called idioblasts
40
Insoluble oxalates: clinical features
- 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
Insoluble oxalates: management
- 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
Tulips and Hyacinths
- 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
Mistletoe
- 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
Poinsettia
- 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
Holly
- toxic principles: saponins, triterpenes, polyphenols, methylaxanthines, cyanogens - mechanism: GI irritation - clinical features: o GI: hypersalivation, vomiting, anorexia, dirrhea o Oral irritation
46
Holiday plant: management
- 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
Holiday plant: diagnosis and prognosis
- History of ingestion and plant parts in vomitus - *prognosis: excellent
48
Castor plant
- All parts toxic, especially seeds - Exposure: ingestion of seeds, feed contaminated fertilizer
49
*Castor plant: toxin and toxicity
- *RICIN o Inactivates ribosomes=inhibition of protein synthesis=cell death - Toxicity: *1-3 seeds can be lethal - ONLY TOXIC WHEN CHEWED
50
*Castor plant: onset
- Latency period of several hours up to multiple days o Miss decontamination period
51
Castor plant: clinical features
- GI: abdominal pain, profuse vomiting, profuse severe diarrhea - CV: hypotension, hypovolemia, arrhythmias - CNS: depression, incoordination, terminal seizures and coma - Liver and kidney damage
52
Castor plant: PM
- Multiple-organ hyperemia, ulcerations, hemorrhages
53
Castor plant: management
- 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
Castor plant: diagnosis
- Detection of ricinine in urine or blood
55
Castor plant: DDx
- 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
Castor plant: prognosis
- Good with aggressive supportive care - No treatment=grave
57
Autum crocus
- 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
Autum crocus: clinical features
- 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
Autum crocus: diagnosis
- history of ingestion - plant ID from vomitus - *detection of colchicine in blood and urine: limited availability
60
Autum crocus: management
- 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
Autum crocus: DDx
- Bone marrow suppression o Chemotherapeutics, immunosuppressive drugs, estrogen, radiation, neoplasia - Multi-systemic failure: ricin, sepsis
62
Autum crocus: prognosis
- poor

TOXICOLOGY (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions