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Toxicology > Unit 2 - Toxic Plants in Small Animals > Flashcards

Unit 2 - Toxic Plants in Small Animals Flashcards

1
Q

What species are affected by rhododendron?

A

Dogs, cats, and ruminants

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2
Q

What do rhododendrons look like?

A

Large shrubs to small trees - terminial clusters of large, attractive pink to purple flowers

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3
Q

What parts of rhododendrons are toxic?

A

All parts - especially leaves

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4
Q

What is the toxic principle of rhododendron species?

A

Andromedotoxin

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5
Q

What is the MOA of andromedotoxin?

A

Binds and blocks the inactivation of sodium channels in cell membranes which results in prolonged neuronal depolarization and excitation

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6
Q

When do most cases of rhododendron toxicosis occur?

A

Most ruminant cases occur in the winter and early spring

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7
Q

When is the onset of clinical signs for rhododendron toxicosis?

A

Within 6 hours

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8
Q

What clinical signs are associated with rhododendron species?

A

Depression, salivation, abdominal pain, vomiting
Arrhythmia, abnormal heart rate, hypotension
High fever, seizures

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9
Q

What typically causes death in rhododendron toxicosis cases?

A

Death - aspiration pneumonia/uncontrolled seizures

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10
Q

How is rhododendron toxicosis treated?

A

Emesis, activated charcoal + cathartic
Supportive therapy
No specific antidote

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11
Q

How is rhododendron toxicosis diagnosed?

A

Clinical signs and leavs in GI tract - detection of grayanotoxins in serum/urine/GI contents

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12
Q

Macadamia nut toxicosis is only reported in what species?

A

Dogs

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13
Q

What is the toxic principle of macadamia nuts?

A

It is unknown

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14
Q

When is the onset of clinical signs for macadamia nut toxicosis?

A

They generally begin within 12 hours and last less than 24 hours

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15
Q

What clinical signs are associated with macadamia nut toxicosis?

A

Non-fatal paralysis; weakness, ataxia, reeversible paresis and paralysis

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16
Q

What chemistry changes are associated with macadamia nut toxicosis?

A

Increased triglycerides and lipase

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17
Q

How is macadamia nut toxicosis treated?

A

Supportive care

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18
Q

What do oleander plants look like?

A

Smooth green stems, dark green leathery flowers, white or colored flowers, and they can be in bush or tree forms

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19
Q

How are small animals exposed to oleander? Large animals?

A

Small animals - common ornamental plant in the southern states
Large animals - may be baled with hay or chopped into silage

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20
Q

What toxin does oleander produce?

A

Oleandrin

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21
Q

What type of toxin is oleandrin?

A

It is a cardiac glycoside

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22
Q

What parts of oleander are toxic?

A

Stems, leaves, and flowers

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23
Q

What is the MOA of oleander?

A

Inhibition of Na/K-ATPase pump: increased intracellular sodium and hyperkalemia

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24
Q

T/F: Oleander is highly toxic.

A

True - 0.005% of the BW is toxic

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25
Q

What clinical signs are associated with oleander toxicosis?

A

Acute gastroenteritis, vomiting and/or diarrhea, weakness, colic
Bradycardia followed by tachycardia;arrythmia
Death following 2-48 hours post ingestion

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26
Q

How is oleander toxicosis diagnosed?

A

History of exposure and presence of plant parts in feed or vomitus
Confirmed by detection of oleandrin in body fluids/GI contents

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27
Q

How is oleander toxicosis treated?

A

Supportive therapy and removal of the offending material

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28
Q

What are the toxic principles of foxglove?

A

Cardiac glycosides - digitoxin and digoxin

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29
Q

Where is foxglove absorbed?

A

in the GI tract

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30
Q

When is foxglove toxic?

A

When it is dried - it is also water soluble

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31
Q

What is the MOA of foxglove toxicosis?

A

Inhibition of Na/K-ATPase pump: increased intracellular sodium and hyperkalemia

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32
Q

When does the onset of clinical signs occur for foxglove?

A

2-4 hours post ingestion

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33
Q

What clinical signs are associated with foxglove toxicosis?

A

Local irritation of the mouth and stomach, abdominal pain, nausea, vomiting
Cardiac irregularities - Bradycardia and then tachycardia and arrythmias
Peripheral vasoconstriction
Mydriasis, dizziness, ataxia, and respiratory paralysis resulting in coma and death

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34
Q

What lesion is possible with foxglove toxicosis?

A

Epicardial hemorrhage

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35
Q

What does Lily-of-the-valley look like?

A

Slightly cupped, spear-shaped green leave

Flowers are white, bell-like and drooping

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36
Q

What is the toxic principle of lily-of-the-valley?

A

30+ cardiac glycoside compounds

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37
Q

What is the toxic principle of the allium species?

A

n-propyl disulfide

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38
Q

T/F: N-propyl disulfide is only present in raw onions.

A

False - it is present in raw, cooked, and dried onions

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39
Q

What is the MOA of n-propyl disulfide?

A
  1. Increased free radical formation
  2. Direct RBC membrane damage and denatured hemoglobin
  3. Heinz body formation and acute hemolysis
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40
Q

What does the amount of toxin in allium species vary depending on?

A

Species, time of year, growing conditions, raw/cooked/dried

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41
Q

What laboratory findings are consistent with allium toxicosis?

A

Hemolytic anemia - max will be 7-12 days post exposure
Heinz body formation
Ecccentrocytes that occur secondary to oxidative stress

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42
Q

What species are most offen affected by allium toxicosis? What other species are susceptible?

A

Dogs most affected; cats and cattle are susceptible

43
Q

What clinical signs are associated with allium toxicosis?

A

Acute hemolytic crisis - weakness, tachypnea, tachycardia, pale mm, icterus, anemia, and hemoglobinuria

44
Q

How is allium toxicosis treated?

A

Supportive care - transfusion may be needed if severe

45
Q

What plants belong in the Araceae family?

A

Dumbcane, Philodendron, ceriman, elephant’s ear, calla lily, arum lilly, peace lily, and caladium

46
Q

What is the toxic agent of the Araceae family?

A

Insoluble calcium oxalates

47
Q

What is the MOA of insoluble calcium oxalates?

A
  1. Local reactions are from kinins which may be aggravated by calcium oxalate crystals
  2. Mechanically damage cells in the mouth
  3. Local inflammatory response of the mouth
48
Q

What clinical signs are associated with Araceae toxicosis?

A

Immediate pain and irritation upon chewing
Headshaking, intense hypersalivation, swelling of mucous membranes of pharynx and tongue, severe dyspnea, but rarely obstruction

49
Q

What clinical signs are associated with severe cases of Araceae toxicosis?

A

Nausea, vomiting, diarrhea, secondary dehydration, electrolyte imbalance, and shock

50
Q

How is Araceae toxicosis treated?

A

Symptomatic and supportive care - rinse mouth, activated charcoal, oral calcium, antihistamines/anti-inflammatory drugs, IV fluids if vomiting or diarrhea are persistent

51
Q

What do castor beans look like?

A

Black or mottled with grey or brown

52
Q

What is the toxic principle for Castor bean? Rosary pea?

A

Lectins - found in moost beans
Castor bean - ricin
Rosary pea - abrin

53
Q

What parts of the castor bean and rosary pea plants are toxic?

A

All parts of the pant, but especially seeds

54
Q

T/F: Does castor oil contain ricin?

A

No it does not

55
Q

What is the MOA of the castor bean toxin?

A

A-B toxin
B-chain: binds to proteins on cell surface and facilitates internalization
A-chain: Enters the ER and depurinates rRNA which inactivates ribosomes and inhibits protein synthesis

56
Q

What clinical signs are associated with castor bean toxicosis?

A

Vomiting with blood and diarrhea

57
Q

When do clinical signs due to castor bean toxicosis occur?

A

Few hours to days

58
Q

What lesions are associated with castor bean toxicosis?

A

Catarrhal to hemorrhagic gastritis
Petechial hemorrhages on serosal surfaces
Necrotizing enteritis
Edematous mesenteric lymph nodes

59
Q

How is castor bean toxicosis diagnosed?

A

History of exposure
Leukocytosis with increased AST and ALT
Detection of toxin in gastric contents

60
Q

How is castor bean toxicosis treated?

A

No specific antidote, supportive care

61
Q

How is castor bean toxicosis prevented?

A

Do not plant where animals may have access
Clip seed heads before maturity when used as an ornamental
Moist heat destroys ricin

62
Q

What plants are spurges?

A

Poinsettia, Snow-on-the-Mountain, spotted surge, and leafy spurge

63
Q

What is the toxic principle of spurges?

A

Diterpenoid phorbol esters

64
Q

What do diterpenoid phorbol esters do?

A

They are direct irritants/blistering compounds

65
Q

What parts of the spurges plants are toxic?

A

All parts

66
Q

What clinical signs are associated with spurges toxicosis?

A 
Irritation of the mouth and GI tract
Blistering
Periocular and perioral swelling
Excessive salivation, vomiting, diarrhea
Sap may cause contact dermatitis
67
Q

What treatment is associated with spurges toxicosis?

A

Supportive care - dilute toxins orally with water or milk, wash topical exposure with alcohol

68
Q

What is the prognosis of spurges toxicosis?

A

Generally very good

69
Q

What trees are mistletoe commonly associated with?

A

Oak, walnut, or other deciduous trees

70
Q

What is the toxic principle of mistletoe toxicosis?

A

It is unknown

71
Q

What clinical signs are associated with mistletoe toxicosis?

A

Acute GI upset - vomiting, nausea, and diarrhea

Other systemic signs - hypotension, weakness, bradycardia, and collapse

72
Q

How is mistletoe toxicosis treated?

A

Supportive care - removal from GI tract

73
Q

What is the major toxin associated with sago palm?

A

Cycasin

74
Q

What are the toxic parts of the sago palm?

A

All of the parts of the plalnt - the seeds are especially toxic

75
Q

When is the onset of clinical signs for sago palm toxicosis?

A

Usually within 12 hours

76
Q

What clinical signs are associated with sago palm toxicosis?

A

Acute: vomiting +/- blood, diarrhea, salivation
Depression, weakness, tremors, and seizures
Abdominal pain, jaundice, bruising, and dark tarry stool

77
Q

What clinical pathology abnormalities are associated with sago palm toxicosis?

A

Elevated ALT, AST, Alk phos, and bilirubin

78
Q

What lesions are associated with sago palm toxicosis?

A

Hemorrhage and necrosis of the GI mucosa

Liver: centrilobular and midzonal necrosis

79
Q

How is sago palm toxicosis treated?

A

Aggressive decontamination of the GI tract, GI protectants, and fluids as needed

80
Q

What is the prognosis for sago palm toxicosis?

A

Guarded to poor

81
Q

What lilies are toxic?

A

Easter lily, tiger lily, and day lily

82
Q

What species are uniquely sensitive to lily toxicosis?

A

Cats

83
Q

T/F: The water from a flower vase with a lily is toxic.

A

True

84
Q

Lilies are _____ excreted, so _____ hours of fluid diuresis can prevent death.

A

rapidly; 24

85
Q

What gross lesions does lily toxicosis cause?

A

Pulmonary and hepatic congestion

Perirenal edema and swollen kidney

86
Q

What microscopic lesions are associated with lily toxicosis?

A

Diffuse acute renal tubular necrosis typically in the proximal tubules with intact basement membraines
Granular and hyaline casts in collecting ducts

87
Q

What clinical signs are associated with lily toxicosis?

A

Both renal and GI: vomiting and salivation, depression and anorexia, polyuria for 12-24 hours or until anuria develops, dehydration, weakness, recumbence and death

88
Q

What laboratory results are associated with lilies?

A

Proteinuria, glucosuria, isosthenuria, casts, anuria
Stress leukogram
Increased BUN, Creatinine, P and K
Late in syndrome - increased ALT and ALP

89
Q

What treatment is recommended for lily toxicosis?

A

GI decontamination - emesis, activated charcoal, cathartic

Fluid therapy prior to anuria to prevent dehydration

90
Q

What is the prognosis for lily toxicosis?

A

IV fluid treatment prior to anuria is good

No treatment/late treatment is grave

91
Q

How is lily toxicosis prevented?

A

Owner education

92
Q

What species are most commonly affected by grape and raisin toxicois?

A

Dogs

93
Q

Are raisins or grapes more toxic?

A

Raisins

94
Q

What is the mechanism for grape/raisin toxicosis?

A

It is unknown

95
Q

What clinical signs are associated with grape and raisin toxicosis?

A 
Vomiting and/or diarrhea within a few hours of ingestion
Anorexia
Lethargy and weakness
May show signs of abdominal pain
Polydipsia
Tremors
Anuria in advanced cases
Once anuric - death due to renal failure
96
Q

What clinical pathology abnormalities are associated with grape and raisin toxicosis?

A

Hypercalcemia, hyperphosphatemia, and azotemia

97
Q

What microscopic lesions are associated with grape and raisin toxicosis?

A

Degeneration and necrosis of PCT epithelium - intact basement membranes, +/- regeneration, mineralization

98
Q

How is grape and raisin toxicosis treated?

A

Early - emetics and activated charcoal
Hospitalization with IV fluids
Monitor serum chemistries and urine output closely for 3 days

99
Q

When is the prognosis for grape and raisin toxicosis guarded?

A

When there is evidence of renal failure

100
Q

What species are primarly effected by stinging nettles?

A

Hunting dogs

101
Q

What do stinging nettles do? What do they contain?

A

Plants express fine stinging hairs; contain varying amounts of acetylcholine, histamine, serotonin, and formic acid

102
Q

What clinical signs are associated with stinging nettles?

A

Salivation/pawing at the mouth, emesis, respiratory distress, bradycardia/arrhythmia, and muscle weakness

103
Q

How is stinging nettle toxicosis treated?

A

According to signs: atropine, antihistamines, and supportive care

Toxicology (32 decks)

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